Contagious state

10. Chlamydiosis, prevention and control, measures in outbreak, current epizootological situation. Proceeding of competent authorities in the case of disease outbreak, control and prevention

- Chlamydia is a genus of pathogenic G- bacteria that are obligate intracellular pathogens, growing in eukaryotic host cells (within cytoplasmic vacuoles) - They're unable to produce ATP (restricted metabolism) and rely on the host metabolism - Chlamydia infections are the most common bacterial venereal disease in humans. Present worldwide. - Many Chlamydia coexist with the host organism without producing clinical signs - Sheep, goats and cats are most commonly affected Special reproductive cycle · Elementary bodies: Infectious form. Small, metabolically inert, osmotically stable · Reticulate bodies: Intracellular replicating form. Divide by binary fission within the host (inclusion body). Leave the host cell by lysis. Chlamydiosis: Respiratory disease, eye infections and abortions in animals and sometimes humans. Etiology: Family: Chlamydiaceae. Genus: Chlamydia Species: 9 spp (abortus, caviae, felis, muridarum, pecorum, pneumoniae, psittaci, suis and trachomatis) Agent/host: o Chlamydia trachomatis: Human venereal disease o Chlamydia suis: May cause asymptomatic or systemic disease in pigs. o Chlamydia muridarum: Cause pneumonia and enteritis in mice o Chlamydia pecorum: Associated with abortion, conjunctivitis, encephalomyelitis, enteritis, pneumonia, and polyarthritis in domestic animals o Chlamydia abortus: Venereal disease of many mammals. Cause abortions. o Chlamydia felis: Cause conjunctivitis (feline contagious conjunctivitis), rhinitis and resp. problems in cats o Chlamydia psittaci: Infects mainly birds Resistance: Escape recognition by T-cells. But not resistant to ATB treatment. Latency is a common feature of chlamydial infections; may be activated by stress and concurrent infections. Persistent antigenic stimulation provokes chronic inflammation in host tissues. In case of confirmation à close the farm. At the focus of infection (farms): Protection and surveillance zone, quarantine for 28 days, mechanical cleaning, remove bedding, rendering plant. Chlamydia psittaci (avian chlamydiosis) A systemic lethal intracellular bacterial species that may cause endemic avian chlamydiosis, epizootic outbreaks in mammals and respiratory psittacosis in humans. OiE- notifiable. Poultry, turkeys and ducks are more susceptible than chickens. Among domestic species; turkeys, ducks and pigeons are most often affected. There are 8 avian serotypes where 6 (A-F) infect avian species (each serotype tends to be associated with certain types of birds - e.g. A and D are highly virulent for turkeys). Epizootology: Worldwide, particularly in psittacine birds in tropical and subtropical regions. Pigeons are the main reservoir in Europe (highest seroprevalence in the end of winter/beginning of spring) IP: Typically, 3-10 days (may be up to several weeks in older birds or after low exposure). Transmission: Ingestion or inhalation of infectious material (dust, feces, discharges from GIT and respiratory tract). Vertical transmission possible in some birds (turkeys, chickens, ducks). Arthropod-borne transmission by blood sucking ectoparasites. Respiratory discharge or feces of infected birds contain elementary bodies that are resistant to drying - can remain infective for several months when protected by organic debris (e.g. litter and feces). Pathogenesis: Elementary bodies are taken up by the host cells via endocytosis. Once inside it forms an inclusion body in the cytoplasm, turning into the reticular body which cause lysis of the cell and release of the bacteria. C. psittaci strains in birds infect mucosal epithelial cells and macrophages of the respiratory tract. Septicemia eventually develops and the bacteria becomes localized in epithelial cells and macrophages of most organs, conjunctiva and GIT. Stress will commonly trigger onset of symptoms, starting with flu-like symptoms resulting in a life-threatening pneumonia. Carriers à stressors/immunosuppression à intermittent shedding and recurrence of clinical disease. Clinical signs: Inappetence, depression, ruffled feathers, purulent nasal and ocular discharge, severe yellow-green diarrhea. Respiratory signs from sneezing to respiratory distress. In chronic cases; neurological signs (e.g. torticollis, opisthotonus, tremors, convulsions, paresis or paralysis of the lungs) · The disease varies from asymptomatic to high mortality and morbidity. · Can be inapparent subclinical infection or acute, subacute or chronic disease of wild and domestic birds. Pathology (anatomy): Severity depends on the virulence, infectious dose, stress factors, susceptibility of the bird species. Necropsy findings are non-specific (serofibrinous polyserositis, bronchopneumonia, hepatic necrosis, hepatomegaly, splenomegaly = similar as other systemic bacterial infections). Diagnostics: · Cultivation in 6-day-old embryos or monolayer McCoy or HeLa cell culture. · Staining by Stamp, Ziehl-Nielsen, Giemsa stains. Staining of the elementary bodies à immunofluorescence · ELISA, complement fixation test and PCR. Serology (ELISA, CFT, IFAT) may be false negative. · Flocks: Serologic testing, necropsy and PCR · Confirmatory tests: Ag detection test, PCR or culture (practical diagnostic scheme). PCR is the most sensitive and specific test. Stain purple with Giemsa and red with Macchiavello and Gimenez stains. · Differential diagnosis: Other respiratory and systemic diseases of birds (?) Prophylaxis: · Treatment prevents mortality and shedding but cannot eliminate latent infection; shedding may occur. · Vaccines: No effective vaccine for use in birds is available Control and prevention: Quarantine and examination of all new birds, buy from sero-negative flocks, prevention of exposure to wild birds, traffic control (minimize cross-contamination), isolation and treatment of affected and contact birds, thorough cleaning and disinfection (all-in/all-out), good ventilation, immersion of dead birds in disinfectant (prevent aerosolization), buy uncontaminated feed, records of all birds movements, continual monitoring of presence of chlamydial infection. It is susceptible to heat (destroyed in <5 min at 56°C) and most disinfectants. Resistant to acid and alkali. Control: Flocks of birds à elimination (eradication). Pet birds à treatment. Treatment: Tetracyclines (chlortetracycline, oxytetracycline, doxycycline). Bacteriostatic, only effective against actively multiplying organisms à extended treatment times (2-8 weeks). Chlamydia pecorum Found in ruminants, koalas and swine. In the koala, C. pecorum causes reproductive disease, infertility and urinary tract disease and death. In other animals, associated with abortion, conjunctivitis, encephalomyelitis, enteritis, pneumonia and polyarthritis. Chlamydial arthritis and conjunctivitis in sheep. Mammalian chlamydiosis Chlamydia abortus: Enzootic abortion of small Ru. OiE notifiable. Prevalence can be 40% Chlamydia felis: Respiratory problems and conjunctivitis (feline infectious conjunctivitis) Chlamydia suis: Respiratory and gastrointestinal problems Chlamydia pneumonia: Respiratory chlamydiosis Transmission by inhalation, ingestion, vertical. Shed in large numbers in reproductive discharges, milk, feces and nasal discharges. Pathogenesis: Similar to avian chlamydiosis, but some Chlamydia spp. are capable of causing abortion by infecting the placenta, damaging it à stopping/affecting development of the lamb; Enzootic abortion of ewes: Entry via ingestion of the infected afterbirth and vaginal discharge, bacteria travels to the placenta where it infects its cells and multiply within them à lysis à release of bacteria àinflammation. This interferes with placental function, shutting down the vital support that it offers the unborn lamb. Placentomes produce a diffuse inflammatory response, including thrombotic vasculitis and tissue necrosis, resulting in death of the fetus due to impaired nutrient and gaseous exchange. Symptoms: · Ruminants: Late term abortion, stillbirths, low birth weight, red-brown vaginal discharge. · Humans: Flu-like symptoms and late-term abortion · Cats: Conjunctivitis, occasionally rhinitis (sneezing and nasal discharge) Pathology (anatomy): Lesions related to the respiratory system (bronchiolitis, severe focal pneumonia, pulmonary edema may occur). Chronic (often subclinical); mild lesions, or a few foci of atelectasis, predominantly affecting the apical lobes. Diagnostics: Anamnesis and clinical signs (abortion rate >2%). Isolation and identification. Microscopy, serology, laboratory methods (?) · Differential diagnosis of enzootic abortion of ewes: Coxiella burnetii Prophylaxis: Vaccination. Purchase stock from clean flocks, quarantine, isolation, disinfection after abortion, veterinary surveillance. NB! Professional zoonoses. To be declared negative: No clinical signs in the past 2 years, diagnostic tests of a certain number of animals. Treatment: Tetracycline and fluoroquinolones or oxytetracyclines. a. Sanitation measures and focal disinfection at these diseases. Preventative disinfection. Once Chlamydia is shed to the environment it can only remain viable for a few days (longer if freezing temperatures), exception is slurry (can survive for months). It is susceptible to most disinfectants (except acids and alkalis) as well as dry heat (160-170°C for 1 hour or longer) and moist heat (121°C for minimum 15 minutes). Preventive sanitation measure types, control Preventive sanitation is a complex of measures directed to the removal, inactivation or killing of the agents of infection in the external environment. Disinfection, rat control, insect control, disposal of cadavers, removal of excrements, adequate hygienic level on the farm. Disinfection means the process of eradication of infectious and hygienically harmful microorganisms in the external environment: Elimination (removal, inactivation, killing) of all microorganisms that may cause a disease or affect adversely the health of animals and humans using disinfectant preparations. Types of disinfection · Preventive: Eradication of pathogens, decreasing counts of MOs, improving hygiene in animal houses - 2x/year · Focal: Eradication of pathogens in focus of infection, interruption of disease transmission. Stages are: o Continuous: Performed during the shedding of the pathogen by the sick animal into the environment. All contaminated places must be disinfected. o Final: Carried out before the place is declared free of infection. No infectious agent can be present in the environment. Observation time - minimum 21 days, but it depends on when the infection occurred. Rat and insect control. Steps: · Mechanical cleaning (removal of 80% of MOs). · Disinfection: spray preparation on surfaces (e.g. formaldehyde). 2-hour exposure time · Deactivation o Neutralization: carried out after recommended exposure time o Removal of chemical residues: by washing with water or chemical deactivators. · Finishing work: protocol of disinfection procedure. Interruption of the pathways of disease transmission · Adequate decontamination of animal buildings and pens prior to their occupation · Provision of a clean air supply by ventilation · Exclusion of vectors of infection (birds, insects, rodents, dogs, etc.) · Appropriate disposal of sewage, slurry, farm waste and animal carcasses · Provision of a safe water and food supply b. Pathological states of the foetus and its adnex from a forensic point of view Placenta accesoria: The accessory lobe from the main disc of the placenta. Found in ruminantsMola hydatidosa: The placenta contains grapelike vesicles (small sacs) that a usually visible with the naked eye. They arise by distension of the chorionic villi by fluid- hyperplasia of the trophoblastic tissue. If left untreated, a hydatidiform mole will almost always end as a spontaneous abortion (miscarriage)Hydroallantois: Caused by a defective placenta (the chorioallantois). Condition is characterized by rapid accumulation of watery clear fluid, usually in the last trimester. Usually condition results in a sick cow with anorexia, decreased rumen motility, dehydration and weakness. The foetus is normal, but the placenta is thick. The condition usually ends in death or intervention. If the cow survives, postpartum metritis is common. The prognosis is guarded to poor for life and fertility. Hydramnios: Caused by a defective calf, usually attributed at least partly to a defect in swallowing. The condition is characterised by a gradual accumulation of thick, viscous fluid during the last half of gestation The cow has a pear shaped caudal view, but is otherwise clinically unaffected. The pregnancy usually goes to term, and frequently a small, deformed foetus is delivered. Good prognosis. Post-partum metritis is uncommon, no treatment required.Oligohydramnion: The result of excessive absorption of amniotic fluid in the last period of pregnancy. The foetus is small, and has deformities.Anomalies of the umbilical cord: Not diagnosable during pregnancy. Result in infirmity of blood conduction and death of the foetus.Defects in fertilization- Superfetation: the simultaneous occurrence of more than one stage of developing embryo in the same animal. It manifests as the formation of a foetus from a different menstrual cycle while another embryo is already present in the uterus- Superfecundation (heteropaternal superfecundation): Ovas during one oestrus are fertilised by two sperms or more from males. Common in stray dogs and cats- Hyperfetatio: abnormal fertility (a lot of embryos)Foetal mummification- Mummy: carcass with at least some preserved soft tissues- Mummification: all natural and artificial processes, that bring about preservation of the body.Foetal mummification: When necrotic foetus is retained in uterus. Can be caused by failure in blood supply, infectious disease, anomaly of the umbilical cord, inbreeding (in Su), metabolic disorders of the foetus, trauma. There is no involution of the CL and fetal expulsion àfoetus is exposed to autolytic changes, absorption of the foetal fluids and involution of the placenta. Diagnosis: Based on presence of CL, lack of fremitus in uterine artery and lack of foetal fluids in the uterus. Prognosis is good if foetus is removed à conception usually 1-3 months later. Maceratio foetus:Foetal maceration results from death of the foetus followed by dilation of the cervix and incomplete abortion or dystocia, usually during the last half of gestation. The condition can be due to a variety of miscellaneous organisms. Macerated foetus in second gestation described with implantation in both horns.

25. Trichinellosis, prevention and control, measures in outbreak, current epizootological situation. Proceeding of competent authorities in the case of disease outbreak, control and prevention.

10. · Trichinella spp are the agents of trichinellosis · Trichinellosis is a worldwide zoonosis · Associated with low indicidence of human cases and high cost for prevention · OiE notifiable Etiological agent Trichinella is the only genus in family Trichinellidae. The larval stages (in striated muscle) can be either encapsulated or non-encapsulated. Species Distribution Principal host Resistant to freeze Capsule forming T. spiralis Worldwide Pig, rat, man No T. nativa Arctic & subarctic Wild car, seal, polar bear, walrus High T. nelsoni Tropical Africa Wild car & omnivores No T. britovi Temp zone, EU Wild car, fox, wild boar, horse & man Low T. murrelli North America Wildlife, horse & man No Non-capsule forming T. pseudospiralis Worldwide Mammals & birds No T. papuae Papua New Guinea Wild pig & man No Morphology Very small! Males: - 1.5 mm - Slimmer at the anterior than at the posterior end. - The stichocytes are arranged in a row following a short muscular esophagus Females: - Twice the size of males, viviparous - Slimmer towards the anterior end like male - Esophagus is a third of the body length. Has a single uterus Life cycle Trichinella spp use the same individual organism as final and intermediate host. IH: Adult worms inhabit the small intestine where females release L1, which are distributed via blood and lymph vessels and infect striated muscle cells. Larvae which invade muscle cells transform cells into nurse cells which provide nutrition for the larvae and clear waste products. In some species, the infected muscle cells encapsulates larvae within the cell membrane by various types of collagen forming capsules. FH: The infection of a carnivorous or omnivorous host occurs by ingestion of striated musculature containing encapsulated infectious larvae (L1). The larvae are released in the GIT and settles in epithelial cells of the small intestine. Here they molt 4 times and develop to adults. Shed in feces. Transmission · Through the consumption of animal meat infected with the parasite · Animals in close contact with rodents (typically hogs) are at the highest risk of contracting the infection. · Human contraction of Trichinosis is usually from consumption of raw or undercooked domesticated swine infected with Trichinella larvae · Human to human transmission is not possible unless ingestion of contaminated human meat occurs Pathogenesis In animals, trichinella infections are mostly inapparent. 2 phases can be distinguished in the course of trichinellosis · Intestinal phase: L1 of T. spiralis is released from their capsule and infestate the intestinal epithelial cells which subsequently are transformed to syncytia (multinucleated cell). The intestinal infection may be asymptomatic or associated with a catarrhalis, haemorrhagic enteritis · Muscle phase: L1 infecting striated muscle cells initially induce degenerative processes, but also modify the cells gene expression. Cellular infiltration develops in the interstitial tissue causing a transient non-purulent interstitial myositis. This disappear after completion of capsule formation The migrating L1 reaching unsuitable tissues die and may induce heavy local inflammatory reactions. Clinical signs Naturally acquired trichinella infections in animals are usually asymptomatic and remain undetected. Pigs, puppies and kittens may develop severe catarrhal enteritis with diarrhea and vomiting. Later: Myositis, stiffness, pain, convulsions, edema, heart dysfunction and difficulties in swallowing. In humans, infections with 50-70 trichinella larvae may cause clinical symptoms: · Intestinal phase: Nausea, vomiting, gastrointestinal disorders, low fever · Muscle phase: Muscular pain, difficulties breathing and swallowing, fever, edemas of face. Treatment - Not in meat producing animals - Albendazole/mebendazole/pyrantel in carnivores and humans. - Corticosteroids to reduce inflammation from dead larvae. Analgesics and anti-pyretics for myopathic phase Diagnosis · Pigs: o Direct identification of agent- digestive method (pepsin/HCl), trichoscopy (compression) o Indirect identification via serological tests (ELISA, latex agglutination test) · Humans: Serology, muscle biopsy, PCR Epizootiological situation In many regions, trichinella spp are transmitted in wildlife (sylvatic) cycles, but T. spiralis is mainly transmitted in synanthropic cycles, including domestic pigs. · Various species occur in certain geographical areas (see table above) except T. spiralis which has a wider distribution. · Trichinella spp is one of the most widespread parasites infecting people and other mammals, though Trichinella spp infections in humans are relatively rare · Normally larger groups of people are often involved in one outbreak as they consume meat from the same source. · Domestic pigs which are maintained under good hygienic conditions in stables are generally free of trichinella. Prevention, control Control · Mandatory monitoring in EU countries (OiE): Serological testing, slaughterhouse examination - Seven methods are accepted: 6 digestive methods and trichonoschopy - Sampling: All slaughtered/hunted swine, horses, bears: Pillars of diaphragm, tongue, jaw muscle (1g/pig) · Outbreak - Positive case must be reported! - Official restriction of herd, food chain information, test animals at positive farm at slaughter for 12 months, test products from site of origin, if meat have been exported or traded within EU, a rapid alert will be issued. - Positive animal: Seized and destroyed (category 2) - Search for source: Vectors, wild animals, purchase history, hygiene, feed storage Prevention · Food safety regulations include controls of carcasses and meat intended for human consumption. · Meat preparation: cook all meat (curing, salting, drying and smoking is not enough), freeze for 20 days · Do not feed pigs and wild animals uncooked meat · Rodent and wildlife control. a. Sanitation measures and focal disinfection at these disease. Using of chronic rodenticides. Resistance Trichinella spp., can survive for 6 weeks in undercooked meat and for several days in frozen food. Sanitation · Rodent control: Mechanical (traps), physical (water), biological (cats, dogs), chemicals (rodenticides). - Acute rodenticides: zinc phosphide, aluminium phosphide - Chronic rodenticides: anticoagulants · Interrupt life cycle: cooking (80°C for 30 min) or freezing (2 months) Using of chronic rodenticides Chronic rodenticides are slow-acting poisons causing death within 4- 10 days. They belong to a class of cumulative poisons and all are anticoagulants- causing alterations to blood coagulation and death due to haemorrhages. Products · 1st generation - Kumatox (1% warfarin)- risk of resistance with frequent use. Toxic baits · 2nd Generation (superwarfarins) - Talon (0,005% brodifacoum): easy to handle and resistant to humidity, but can cause secondary poisoning and thus require pulsation methods. Wax, pellets, grains · 3rd generation - Borik (0,0025% difethialone) - Antidote is injection of Vitamin K Pros and cons · Pros: No bait shyness, good control, multi-dosing decrease chance of accidental poisoning, palatable, low concentration of AS, antidotes available · Cons: Bodies not visible, non- selective, slow action, secondary poisoning, large quantities/rodent, resistance b. Determination of age in tissue helminthoses After swallowing meat infected with trichinellos: · 3 days: Enteritis or peritonitis · 14 days: Migrating Trichinella is completely straight and reach the size of 0.5mm long · 21 days: Parasite reaches the normal size and begin to twist · 24 days: Parasites are encapsulated · 6 months: Capsule is calcified · 9 months: The parasite is completely processed

28. Anisakidosis, Toxocarosis, prevention and control, measures in outbreak, current epizootological situation. Proceeding of competent authorities in the case of disease outbreak, control and prevention

ANISAKIDOSIS = the accidental ingestion of species of anisakidae family by ingesting raw or undercooked fish or crustaceans where the larvae will be found in the stomach or stomach wall. Most commonly found in the stomach or intestine of the fish, but can be found in the flesh and of higher risk to humans consuming raw fish. Main species · Anisakis spp, A. simplex · Pseudoterranova spp, P. decipiens · Contraceum spp Morphology - In fish, they have a characteristic "watch-spring coil" shape, roughly 2 cm long uncoiled - In mammals they are longer, thicker and more sturdy Susceptible agents Dolphins, seals, sea lions, whales, aquatic birds and turtles. Life cycle (Anisakis spp) · Adult stages reside in the stomach of FH: marine mammals à unembryonated eggs produced by adult females are passed with the feces of mammals · Eggs become embryonated in the water, undergoing 2 developmental molts (L1 à L3) · They hatch as L3 larvae (free-swimming) and are ingested by crustaceans (1 IH) · 1 IH crustaceans ingested by 2IH fish à 2 IH fish infective to FH marine mammals + PH humans · L3 moult 2 times and develop into adults inside FH or inside PH L3 die (dead-end host) PathogenesisWhen the infected raw fish enters the host stomach, it is resistant to gastric acid and can burrow into the gastric wall, it rarely enters small intestine. Tissue invasion is facilitated by release of hydrolytic enzymes from the parasite. In humans, it dies within a few days and provoke an eosinophilic granulomatous reaction. Clinical signs (in humans) Usually asymptomatic, but can cause acute abdominal symptoms, may occur within hours. These symptoms can often be mistaken by; food poisoning, appendicitis or peptic ulcer, if the larvae makes it through to the bowel, it can cause a severe eosinophilic granulomatous response (after 1-2 weeks after infection) which may cause symptoms similar to Crohn's disease. If the larvae penetrate the stomach it usually causes abdominal pain, nausea and vomiting. Occasionally, the larvae is coughed up.Usually self-limiting in humans as larva is unable to survive in the PH for long periods. Ag's that remain in fish muscle after larvae are killed (e.g. after freezing) can cause allergic reactions in some individuals. Treatment Usually self-limiting. No drugs available, only physical removal w/ gastroscopy, can help easier healing of host organs, but is rarely necessary. Supportive therapy may be sufficient enough. Diagnosis Inspection of fresh fish for visible parasites and transillumination (candling) of fish filets. DNA analysis, immunodiagnostics, serology (IFA, ELISA, CFT), gastroscopic examination to visualize the larva - most used dg. method, but also possible to use histopathologic examination from tissue (after biopsy or surgery). May be coughed up and identified as well. Lactophenol cotton blue for species differentiation. Differential diagnosis: food poisoning, appendicitis or peptic ulcer Epizootological situation - Over 90% of cases of anisakidosis in humans are from Japan, it represents 2-3000 cases pr year. - There has been a tremendous increase in the number of cases in the western world due to an increased consumption of dishes from the japanese cousine. - The parasite is found in many species of saltwater fish, also along the coast of Norway, but in Norway people rarely develop anisakidosis as it is uncommon to consume raw or undercooked wild-caught fish. - In Norway mainly Anisakis simplex and Peudoterranova decipiens is present. In Norway only 2 cases of anisakidosis have been reported in recent years where raw or undercooked fish was consumed. - For de interesserte: Norwegian farmed Atlantic salmon and rainbow trout reared in floating cages/ onshore tanks the anisakis risk is negligible and thus do not need to be treated before consumed raw or undercooked. That is if the fish is reared on dry pelleted food throughout the production cycle, the farm have assessments and routines limiting working in such a way that parasites are not a threat to the food safety and reports any changes related to control of parasites to the food safety authority. Control and prevention - Most important is public health education, to discourage consumption of raw or uncooked fish, to inform about precautions and preparation of fish. - Can be prevented by freezing or cooking. - Boiling/frying/grilling must reach a core temp of 60°C or more for 1min, freezing below -20°C or lower for 24h or -35°C or lower for 15h. - The parasite can be found in eggs of fish, but will not be present if the eggs have been removed from the sac (skein) and rinsed. Measures in outbreaks (public education and to imply the measures of properly preparing the fish) TOXOCAROSIS___________________________ T. canis and T. cati, roundworms of dogs and cats, predilection site: SI, zoonotic, cause widespread and common human infection. Ingestion of T. eggs or larvae can lead to clinical disease, called toxocarosis. Several toxocara spp play an important role as parasites of the SI of domestic animals Main species · Toxocara canis- canines · Toxocara cati- felines · Toxocara vitulorum- calves · Toxascaris leonina- carnivores Morphology · Toxocara canis: large white worm, female up to 18 cm. Elliptical head due to presence of long and narrow cervical alae and esophagus with ventricle. Mouth is surrounded by three lips. No buccal capsule and esophagus lacks bulb. Small finger like process on male tail and two spicules. · Toxocara cati: large white worm, female bigger than male, up to 10 cm. Cervical alae have arrow head form and is broader and more convex than that of t. canis. Life cycle Adult parasites inhabit SI of various carnivores. Females release unsegmented eggs that are passed in the feces. In environment infective L3 develop in the eggs. FH may contract the infection by various transmission routes- horizontally (ingestion), vertically (prenatal or lactogenic transmission), or fecal- oral transmission from puppy to bitch. In dogs, prenatal infections are of particular epidemiological importance. In the FH the parasite migrate via different routes: · Infection through PH: Dogs eat (rodent, bird etc) with L3 inside, without migration it moults to adult in SI · EHP - entero - hepatic - tracheal migration: after oral ingestion and hatching of L3, the larvae penetrate the intestinal wall, enter the bloodstream and reach the liver - causing tissue damage. They then migrate to the lungs where they invade the alveoli, moult into L4 and migrate via trachea and pharynx to the SI where they go through a final moult and attain sexual maturity. This route occurs predominantly in young individuals, up to 3 months of age. · Somatic migration: this route is taken after infection of older dogs with infective eggs. L3 invade the gut wall, enter the blood circulation and are transported to the lungs where they migrate through the tissues to re-enter the blood stream, which carries them to various organs. Approximately 1 week after infection, they accumulate in striated muscles, where they can survive for years in a hypobiotic stage. In a female dog, the larvae now has 2 options: - Prenatal (transplacental) transmission: only performed by toxocara canis. Hypobiotic larvae are hormonally activated 42 days after impregnation. They then invade the bloodstream, pass through the placenta to the foetus and infect various organs. In puppies, the cycle is completed immediately after birth by migration to the intestine. - Lactogenic (transmammary) transmission: migrating toxocara larvae can reach the mammary gland of a female host and may subsequently be transmitted to her offspring via milk. Pathogenesis and clinical signs Toxocara infections can cause different types of disease in final and paratenic host. Clinical signs in final host · Light to moderate infections: asymptomatic or occasional vomiting, diarrhoea and retarded development in young individuals. · Heavy infections in puppies - Tissue damage: caused by migrating larvae with formation of granulomas in various organs. - Intestinal infection: hypertrophy of the t. muscularis, atrophy of villi, crypt hyperplasia è Vomiting, bloated abdomen, colic, obstipation, diarrhoea, bloody faeces and anaemia. IN HUMANS: Larve migrans visceralis Is a type of toxocariasis that occurs due to the systemic migration of toxocara larvae throughout the thoracic and abdominal cavity and their respective organs and tissues. Affected organs include liver, heart and CNS, with matching symptoms. This type is most common in preschool children with a history of pica. Mechanism of infection When contaminated soil (or food) is ingested by humans, the larvae hatch in the SI and invade the mucosa. From there, it enters the portal blood and is carried to various visceral organs. Some remain trapped in the liver, others proceed to the lungs or other organs. In these organs, the larvae enters a hypobiotic stage, in which it persist in the tissues until it dies. The presence of the larvae causes a granulomatous reaction. Clinical signs In general, clinical signs are rare and are predominantly observed in children, including eosinophilia, leucocytosis, hepatomegaly, splenomegaly, fever, asthma, pneumonia, urticarial and rarely CNS disorders. Death has been associated with myocarditis, encephalitis and respiratory syndromes. Larva migrans ocularis Aka. ocular toxocariasis, is the ocular form of the larvae migrans syndrome that occur when toxocara spp larvae invade the eye. It may develop in any age, but most commonly older children and young adults, and is often caused by a single larvae. Mechanism of infection During its somatic migration, the larvae reaches the posterior segment of the eye through the blood vessels of retina and choroid, and occasionally through the optic nerve. (larvae has no predilection for the eye, and its migration is a matter of chance). Pathogenesis Ocular invasion by the larvae may produce retinal granulomas, inflammation, retinal scarring and decreased visual activity. When the macula or optic nerve is involved, the larvae may also cause partial or permanent vision loss. IN CATTLE: Toxocara vitulorum Occurs in cattle particularly in warm climates, very rare in central Europe. Lactogenic transmission Life cycle After ingestion of eggs infected with L3 from the environment, the larvae hatch and start migration following the somatic route to liver and lungs, settle in the parenchyma and undergo hypobiosis. Larvae become activated in pregnant animals a few days before calving and invade the udder. The majority of them are shed with the milk in the first 2 days of lactation. There is no tissue migration in the calf following milk-borne infection. Pathogenesis and clinical signs Heavily infected calves may suffer from variable intestinal disorders and large amounts of worms can obstruct the gut and even perforate it. Can cause diarrhea (often putrid), colic, enteritis, loss of appetite and weight. Treatment · Animals: deworming with fenbendazole, mebendazole or ivermectin · Humans: albendazole or mebendazole, in addition to anti-inflammatory and corticosteroids. Diagnosis · Animals: flotation methods · Humans: ELISA, western blot, liver biopsy Occurrence and epidemiology The parasite is found worldwide. In Europe approximately 20% of young dogs were reported to shed toxocara eggs. The contamination of the environment with toxocara eggs is a relevant epidemiological risk for humans and other paratenic hosts. Daily egg production of T. canis is 25-85 000 eggs. Eggs containing L3 of toxocara canis and cati are infectious for many animal species and humans. Larvae take a somatic migration route in these hosts and infect various organs. In tissues they can persist for many years. Several forms of larvae migrans (unapparent, visceral, ocular and neural) Proceedings of competent authority, control and prevention Control and prevention- Anisakidosis · Public education about raw fish · Visual examination of fish- condemnation of heavily infested fish · Immediate evisceration after catching Food processing: heating 60°C for 1 min, salting, freezing (-20°C for 24h or -35°C for 15h). Control and prevention- Toxocarosis · Prevent human infection - Wash hands/fruit and vegetables, hygienic precautions - Avoid children eating dirt - Educate public · Reduce risk of infection to pets - Deworm puppies regularly - Prevent contamination of environment with dog faeces - Animals imported from endemic areas should be controlled (quarantine/coproscopical exam) - Keep cows off contaminated pastures, alternate grazing with other animals a) Sanitation measures and focal disinfection at these diseases. Treatment of the fish ponds. Anisakidosis · Food processing - Heating to 60°C for 1 min - Freezing (-20°C for 24h, -35°C for 15h OR -4°C for 7d). - Salting and smoking is not reliable · Disinfection - NaOH (1%) Toxocarosis Eggs are highly resistant due to sticky outer coat and can survive for months or possibly even years. The larvae require temperatures of >10°C to mature and temperatures above 30°C and sunlight will kill them. Toxocara eggs survive sewage processing and they're very resistant to chemical disinfectants. · Disinfection: aqueous iodine, UV light (direct sunlight), high temperatures - Feaces: lime (calcium hydroxide) - Soil: broken up and flamed repeatedly, or 20cm of upper layer of soil can be removed and replaces. - Sand: steam-sterilised or replaced Treatment of fish ponds/lakes 1) Before disinfection: empty pond, remove sediment 2) Disinfection: lime (calcium hydroxide) applied on the bottom of the pond - Lime is used for fertilisation and disinfection for disease prevention. - It improves production factors, accelerate circulation of substances, improves O2 ratios, uptake of plant nutrients, Ca and Mg for plants and at the same time also prevents fungal infection of gills. - Lime contains 80-95% calcium oxide, which adjust alkalinity and pH (antiseptic effect). - It lasts 2-3 weeks and is suitable for disinfection of a smaller area. - Calcium cyanamide has a longer effect, but is toxic. It cause destruction of resistant parasites and germs. Methods - Liming bottom: application for wintering/summering by spreaders. Most effective - Air liming by airplane - Liming water - Liming Ice Types: Calcium fertilizers, Crushed Limestone; Quick lime; Waste lime - lime dust b) Keeping and ownership of animals Pet keeping is a relatively recent phenomenon. Until the 19th century, most animals owned by households were working animals that lived alongside humans and were regarded unsentimentally. More recently, however, several countries have moved to change the legal status of animals (recognised animals as sentient beings, in effect declaring them no longer property) Keeper VS owner · Main difference: owner can sell or donate the animal, keeper cannot · Keeper (someone who is taking care of an animal at a certain moment) - Cannot decide on the euthanasia: unless there has been an emergency and euthanasia is beneficial for the animal, the keeper can give permission without the owners decision - Responsible for the animal behaviour - Obliged to compensate the owner for the damage caused to him, for example, by the unlawful possession, non-achievement of possible expected increases in fattening animals, abortion due to inappropriate treatment of animals etc. · Owner - Must instruct the keeper (in the case you ask somebody to walk your dog - at this moment the keeper is responsible for the animal) - Responsible to notify the authorities of the place where the dog bite somebody. Then the dog will be marked as a dangerous dog - Must give the keepers vaccination cards or the passport in the case they are going on holiday - If something happens when the keeper is taking care of the animal, the owner is responsible for the damages è If the dog ran into the neighbour's garden and attacks animals è In the case of an infectious disease the owner is responsible not the keeper The owner and keeper are entitled to same right in relation to benefiting from the animal (companionship) Property Rights The owner is within the bounds of the law entitled to: · Ius possidendi: the right of ownership is one of the owner's fundamental rights · Ius utendi et fruendi: the application of this right the owner of the matter consists of the use, which is appropriation of the essence and utility of the matter, including the change of the substance of the matter, the consumption of the things as well as the utility of the goods and fruits · Ius disponendi: the owner's right to dispose of the subject matter of ownership, for example owner has the right to sell, to donate, to exchange it, or to found, lease or lend it, to establish a covenant

3. Anthrax, tetanus, botulisms and other anaerobic infections, prevention and control, measures in outbreak, current epizootological situation. Proceeding of competent authorities in the case of disease outbreak, control and prevention

Anthrax Bacillus anthracis. Gram +, spore forming, facultative anaerobic or aerobic. Primarily in herbivores. High mortality. OIE listed. Zoonotic. Epidemiology Endemic areas with more frequent outbreaks. Sporadic outbreaks many places, often due to the old practice of burying dead animals in the ground. Bacterial spores reside in the soil and after floods or heavy rainfall they are washed to the surface à meet oxygen à become virulent. This "awakening" can occur after 100s years. Transmission · Inhalation of virulent spores · Ingestion of virulent spores · Carnivores can eat infected meat Pathogenesis Spores enter body à infect macrophages where they proliferate à causes lymphadenitis and lymphangitis. Why is anthrax so dangerous? It has 2 big virulence factors; A capsule that protects against phagocytosis and a toxin (Tenk, anthrax må nesten ha et toxin siden det er så sykt dødelig!) Toxin consists of 3 protein parts: · Protective antigen (evade immune system) · Edema factor · Lethal factor This allows bacteria to proliferate and kill cells, ultimately killing the host animal. Local reaction: Necrosis and severe edema Systemic reaction: Toxemia, bacteremia as bacteria proliferates in the lymphnodes Increased toxin production à tissue destruction à organ damage is high à widespread hemorrhages Animal dies due to lack of oxygen!!!!!!!!! There are 4 forms of anthrax depending on route of infection Cutaneous: Blister - swelling - ulcer with black center. Painless Inhalation: Fever - chest pain - shortness of breath (choking) Intestinal: Bloody diarrhea - abdominal pain - nausea - vomitus Injection: Fever - abscess around injection site Clinical signs Often no clinical signs due to the rapid onset and progession of the disease (in peracute and acute forms). Ruminants are often found dead on the field with no prior signs. If any, there is fever, muscle tremor and dyspnea shortly before death. Unclotted blood coming from body openings and no rigos mortis! (No rigor mortis because the blood doesn't clot). In subacute cases there can also be depression and inappetence (if there is any time before to see this) Horses have signs of digestive upset and colic, fever and depression up to 4 days before death Carnivora have the intestinal form with abdominal pain and cramps. Diagnosis Examine blood and look for agent à smear and MacFadyen (methylene blue). Sample is ear (tissue) or blood. Selective agar for cultivation and then identification by PCR. Ascoli test can be used + AB suceptibility test. Treatment, prevention and control If there is any time, antibiotics will help. Most important is to properly dispose dead animals by incineration or bury >2m deep and cover with lime, no field necropsy and systematic disinfection of property. Vaccine in endemic areas. Tetanus - lock jaw Infection by Clostridium tetani. Gram positive, anaerobe. Produce toxins causing painful muscle contractions. Transmission Clostridium tetani is found in soil, dust, manure, saliva à problem is when it enters through break in skin, e.g. through bite wound (saliva) or contaminated object (piercing injury) (Tenk, vi tar tetanus shot hvis vi blir bitt av hund) Etiology Clostridium tetani is found all over the world. Higher incidents in warm, wet climates where there is more organic, decaying matter in the soil for the bacteria to feed on. · Cats are very resistant! · Dogs and birds are fairly resistant · Horses and humans are most sensitive Pathogenesis Entry: Fex deep puncture wound OR docking + castration. Infection can only be produced in tissues with LOW BLOOD PERFUSION therefore tissue necrosis is the best. Bacteria come to necrotic site à reside and multiply there à neurotoxins released when bacteria undergo autolysis. Neurotoxin - tetanospasmin = Zn-binding protease - cleave synaptobrevin. Usually: Toxin is absorbed by local motor nerves in the areaà travel to spinal cord à ascending tetanus (up) - Causes: Spasmodic, tonic contractions of skeletal muscle due to interference with release of ACETYLCHOLINE (too much) - The toxin blocks inhibitor impulses - inhibitory effect of inhibitory interneurons à constant contractions Excess toxins that can't be absorbed by motor nerves à lymph à blood à descending tetanus (downwards) Clinical signs · Spasms start in jaw à progress to rest of body · One spasm = five minutes. Can continue for weeks · Spasms are so strong they can cause bones to break · Sudden movements or other excitements can cause more severe spasms There can also be fever, sweating, tachycardia. Mortality rate up to 80% Diagnosis · Symptoms · Swab from entry wound à culture on agar and make smear to gram stain · Find toxins in serum Prevention Vaccine!!!! And protect wounds from being contaminated Treatment There is a tetani anti-toxin Barbiturate sedatives (diazepam) and tranquilizers - Vaccination (horses, Equivac-T) - Active immunization can be accomplished with tetanus toxoid - If the animal has not been immunized previously, it should be treated with 1,500-3,000 IU or more of tetanus antitoxin, which usually provides passive protection for up to 2 weeks https://www.youtube.com/watch?v=zHpbzlbVdLY Botulism - C.botulinum An intoxication, not an infection! By toxins produced by Clostridium botulinum that proliferates in decaying food and plant material (including spoiled silage, hay, grain) Gram positive, spore forming, anaerobic. The toxin - Exotoxin - Neurotoxin - severe paralysis - Type A-G o A and B in humans o C in waterfowl and animals o D in cattle - The most potent toxin known to mankind!!!!! - Prevents release of acetylcholine which prevents contraction of muscle cell Botulism in waterfowl Transmission cycle It is concentrated in MAGGOTS that filter feed on sediments or water OR on already dead birds. When birds eat the maggots they get a concentrated package of toxins. Maggots are resistant to toxin and thus it concentrates in their body. Waterfowl consume the maggots and other toxin-laden invertebrates. Birds die from botulism and their carcass is infested with maggot - and we have the carcass-maggot-cycle. Also a possibility of direct infection if animal feeds on decaying plant- or animal material. Not contagious between animals! Prevalence - higher in warm summer months, when ponds are anaerobic and thus clostridium multiply faster. Clinical signs Severity depends on amount of toxin ingested and susceptibility of bird. Pigeons and birds are sensitive compared to mammals. Paralysis and paresis occur and bird is not able to fly, walk or hold eyes open. Death due to drowning when bird is unable to hold head above water due to neck paralysis. No lesions upon necropsy. Diagnosis Clinical signs and the absence of lesions, time of year and location of bird. Detection of toxin in blood and GIT content must be done relatively fast after death, before clostridium start feeding on carcass and the presence of toxins are a post-mortem finding. Botulism in mammals Dogs and cats are usually quite resistant. However, infections can occur if they ingest food containing the toxin produced by clostridium botulinum. Mostly they occur when dog/cat has eaten dead animals. If dose is high enough there can be intoxication. Often hind legs are the first to be affected, and we see weakness and later paralysis. Thereafter, the same happens in front legs and muscles of head and face. Inability to swallow causes salivation and inability to blink causes eye inflammation. If diaphragma is paralyzed there is death. Ruminants can suffer from botulism if high quantities are ingested or if they suffer from protein or phosphorous deficiency. Spoiled silage or hay are ways of ingesting toxins. Toxicoinfectious botulism = disease where Clostridium botulinum grows in tissue of live animals and produce toxins there, spreading it to the body from the lesions. Colonize + grow + release toxins.(1st some soil or contaminated feed is ingested) Predilection sites are - gastric ulcers - necrotic foci in liver or GIT - abscesses in lungs. = BECAUSE THEY CANNOT PRODUCE INFECTION IN TISSUES HIGHLY PERFUSED WITH BLOOD bcs anaerobes. As before, patient shows progressive muscle paralysis, inability to masticate and swallow. Clinical signs therefore include drooling, dysphagia, recumbency and loss of reflexes. Death due to paralysis of myocard and/or diaphragma. https://www.youtube.com/watch?v=6astF1cU5SU Prevention and control · Control: remove source, correct dietary deficiencies and dispose of carcass. · Prevention: good husbandry (protect food from contamination, remove spoiled silage, rodent control, vaccination- botulism toxoid). Infectious enterotoxemia (clostridium perfrigens toxins) Clostridium perfrigens. Gram positive, spore forming, strain A-D. Normal in GITs, soil, decaying vegetation. Gas gangrene/emphysematous inflammation/necrosis Lamb enterotoxemia · Clostridium perfrigens type D · Bacteria is found in healthy sheep/goat GIT and in soil · Certain conditions à rapid multiplication + rapid toxin production · Epsilon toxin is the most significant one in this disease Pathogenesis · Intestinal hypomotility due to OVERINGESTION of pasture/milk/grain · Clostridium in intestines show rapid growth and produce high amounts of toxins (alpha and epsilon) · ALPHA = NECROTIZING, MYONECROSIS, GAS GANGRENE EPSILON = PORE FORMING (CELL LEAKAGE) Clinical signs Rapid course; Peracute with convulsions and death only minutes after overfeeding. In slower course, there is opistotonus, hypersalivation, tachypnea, convulsions and coma. Lesions in necropsy Ecchymosis and petechiae on serous surfaces and abdominal muscles (toxin causes myonecrosis). Rumen, reticulum, omasum and intestines are gas distended. Necrotic enteritis in chicken · Clostridium type A or type C Transmission Bird is infected by ingesting contaminated food and water, by inhaling spores or by contact with fomites. Pathogenesis · GIT imbalance in microflora allowing bacteria to multiply · Rapid multiplication and production of toxins alpha and beta which causes damage to intestinal wall o Necrotizing agent, myonecrosis and gas gangrene (as above) o Necrotizing agent, catecholamine release causing hypertension Clinical signs Rapid deteriation of health Loss of appetite and weight loss, depression Passing of undigested food and bloody feces (not surprising when there is necrosis in enterocytes). Necropsy · Bloody necrosis of intestine · Small white foci on liver Humans (type C) Food poisoning when eating raw or undercooked meat/food with enterotoxins on them. Diarrhea, vomitus, cramps https://www.youtube.com/watch?v=h_A8yVY1kBg&t=22s a.) Sanitation measures and focal disinfection at these diseases. Physical disinfection. Anthrax Anthrax spores are extremely resistant and can survive for centuries in soil, one year in slurry and two years in milk. Disinfection of animal housing by Chloramine T (10%), NaOH (10%), formalin (10%), 1% peracetic acid, and chlorinated lime (10%) · Manure: 3% lime, 1% phosphoric acid, 0.3% peracetic acid · Slurry: Disinfect with formalin 35% · Housing: fumigation with formaldehyde · Soil: flooding with disinfection- lime, phosphoric acid, peracetic acid. 8-10l/m2, 20cm depth Tetanus Spores can survive for years in faeces, water and feed. Destroyed by sterilization (autoclave at 121°C for 15 min or ionizing radiation) or by disinfectants (10% chlorinated lime, 3% formaldehyde). Botulism The vegetative bacteria are relatively susceptible to many disinfectants (sodium hypochlorite, HCl, ethanol), though spores are resistant in environmental conditions and require autoclaving, gamma radiation or formaldehyde. The botulinum toxin is inactivated by exposure to sunlight for 1-3 hours or heating to 80°C for 30 min or 100°C for 10 min. Physical disinfection Heat 1. Moist heat: the most efficient method. It cause death due to coagulation of proteins. At 80°C for 10 min most vegetative organisms will be destroyed. Spores require ≥100°C.Autoclaving and pasteurisation are the most efficient methods. 2. Dry heat: used for disinfection of surfaces (floors, walls, tools) and cause death by oxidation.100°C for 1 hour is not enough for all vegetative microbes and spores may survive up to 150°C. Irradiation 1. Ionising radiationGamma ionising radiation is most frequently used and cause death by suppressing multiplication and viability of microbes. It is used in food industry to sterilise and pasteurise food stuffs, as well as for some pharmaceutical and surgical products that could be damaged by heat sterilisation. 2. Non-ionising radiation (UV radiation)Cause death by denaturation of proteins. Commonly used in labs, food industry, veterinary surgeries and for disinfection of water. b.) Removal of carcasses and exhumation of animals Removal of carcases Burial: there should be no groundwater after digging (depth of at least 1 m) and plot should be located at least 500m from nearest watercourse. Carcass should be buried in decomposable packaging and treated with disinfection. · Owner of companion animal: consent from owner of land, at least 5m from building and 2 m from adjacent land. Should be marked appropriately. · Keeper of dead animal (eq): only with consent of veterinary authority if animals were kept as companion animal, owns the land or has written consent and site is 100m from building, 500m from well. Map. Who can bury animal? · Owner of pet: and prove animal didn't have communicable disease · Burying company: must be legally approved, own land for at least 50 years in the future, fenced land, located 500m from nearest building and 500 m from spring. Burn off: open burning of animal carcasses is not allowed, incineration is only approved in an approved incineration facility or with a mobile air curtain incineration approved by the state. Rules of disposal Animal waste must be disposed within 48 hours, perished (omkomne) animals within 24 hours · Animals can be disposed at rendering plants or special digging places- fences, one locked entry, etc. · Holes must be covered with soil (2m) · Place for burial cannot be used for other purposes for 20 years after last burial Exhumation (oppgraving) Is less important in animals then humans and of little relevance to veterinary forensic medicine other than taxonomic purposes and paleontological studies (evolution of primates). Cases of special consideration include very expensive animals whose death in the case of crime suspicion are screen and the evidence are developed within pathologic necropsy.

21. Bluetongue and other notifiable sheep diseases, prevention and control, measures in outbreak, current epizootological situation. Proceeding of competent authorities in the case of disease outbreak, control and prevention

Blue tongue A non-contagious, viral disease affecting domestic and wild ruminants (sheep, cattle, goats, buffalo, antelope, deer) transmitted by insects, particularly biting midges of the Culicoides species (small flies). OIE notifiable! Etiological agent The virus which causes BT is identified as a member of the Reoviridae family. Transmission Transmission through vector: Biting midges mostly of spp Culicoides. NO transmission through contact with animals, premises, wool or consumption of milk. Spreads by semen, transplacentally from mother to fetus and by blood. The insect vector is the key to transmission of BT virus between animals! Cattle may serve as a source of virus for several weeks, while displaying little or no clinical signs of disease and are often the preferred host for insect vectors. Pathogenesis After infection à multiplication of virus in regional lymph nodes followed by a primary viraemia with subsequent infection of target tissue (endothelium of all organs and tissue). Virus multiplication at these sites gives rise to a secondary viraemia of variable duration. Virus causes destruction of endothelium (blood vessels) resulting in effusions into body cavities and edematous changes of various tissues (particularly head), as well as serosal and visceral haemorrhages. Viremia peak around 7-8 days post infection. There is no chronic infection. Clinical signs In highly susceptible sheep, morbidity can be 100%. Mortality averages from 2-30% but can be 70%. Outcome of infection ranges from inapparent (in most infected animals) to fatal. - Acute form (sheep and some species of deer) o Pyrexia (up to 42°C), excessive salivation, depression, dyspnoea and panting o Discharge from nose, hyperaemia and congestion of head leading to edema (bluetongue from cyanosis) o Hyperemia of coronary band à lameness o Ulceration and necrosis are seen of the mucosae of the mouth o Death due to heart attack - Inapparent infection: Frequent in cattle and other species for certain serotypes Treatment No treatment. Kill infected animals and isolate/test the rest Diagnosis · Clinical signs, post- mortem lesions and seasonality · Samples o Blood in heparin from living animals o Spleen, liver, red bone marrow, heart blood, lymph nodes collected at necropsy (preserved at 4°C, not frozen) · Identification by ELISA, IFA, VN. · Serology with CF, agar gel immunodiffusion, competitive ELISA. Epizootological situation BT has a significant global distribution in regions where the insect vector is present, including Africa, Asia, Australia, Europe, North America and several islands in the tropics and subtropics. The virus is maintained in areas where the climate allows biting midges to survive over winter. Occurrence of BT generally parallels vector activity during periods of high temperature and rainfall and diminishing with the first frost or severe cold weather. Commonly mostly during April - October. Measures during outbreak Prevention, control In endemic areas Sentinel monitoring programs actively sample animals in sentinel herds to monitor for presence of the virus. This in combination with active surveillance programs to identify location, distribution and prevalence of insect vectors in an area. Other control measures - Identification, surveillance and tracing of susceptible and potentially infected animals - Quarantine and/or movement restrictions during insect activity period - Vaccination o New-born animals receive antibodies from mothers that protect them from the disease for 3 months. However, these antibodies may interfere with vaccination à vaccination is ineffective during this period. Immunity starts in most cases 21 days after the second dose of the basic vaccination scheme. Insect control measures Enthomological monitoring by „traps of vectors". Elimination of vectors. Other notifiable sheep diseases · Contagious agalactia · Contagious caprine pleuropneumonia · Nairobi sheep disease · Ovine epididymitis (Brucella ovis) · Salmonellosis (S. abortusovis) · Chlamydia abortus infection · Scrapie · Sheep/goat pox · Caprine arthritis/encephalitis · Maedi-visna virus · Peste des petits ruminants virus infection VISNA/MAEDI Etiological agent Visnavirus; Lentivirus of Retroviridae Maedi = lung = pneumonitis. Visna = neuro = encephalitis. 2+y Transmission Fecal-oral: Virus shed in feces and contaminates feed and water Milk/colostrum: Most sheep are infected when they are fed infected milk as lambs Inhalation: Virus found in aerosols (higher incidents during winter when sheep are inside) Pathogenesis A retrovirus: Hence, virus RNA is inserted into leukocyte genome (mainly lung macrophages but also lymphocytes and monocytes) which carry virus to the brain, lung and other organs. After 2-6 years, T cell have reaction causing an immune complex disease which deposits AbAg complexes in target organs. This causes chronic inflammation - Maedi à Ly and macrophages infiltrate alveoli, causing its enlargement and emphysema - Visna à demyelination and meningitis Clinical signs Seen mostly in sheep older than 2 years due to long incubation time Maedi à Progressive dyspnea, dry cough, wasting. Death due to anoxia Visna à In beginning signs are subtle; Lip trembling, head tilt, weakness of limbs. Later signs become more severe; Ataxia, muscle tremor and paresis. Most have subclinical infection of milder respiratory signs, few develop the progressive, fatal outcome mentioned above. Treatment No treatment. Diagnosis Suspicion of disease when sheep aged 2-6 years show slow but progressive wasting and respiratory distress or neurological signs. - PCR - ELISA - Agar gel immunodiffusion AGID (formation of AbAg complex) Epizootiological situation Worldwide distribution Measures during outbreak Prevention, control Serological surveillance and always remove positive animals. Isolation of lambs from seropositive mothers. Due to slow progression of the disease, it is recommended to test animals 2 times per year since antibodies may appear at any time. No vaccine. Caprine encephalitis and arthritis Closely related to the visna-virus! Only found in goats! Is also a lentivirus à visna = slow (develops slowly) Etiological agent Caprine encephalitis and arthritis virus, lentivirus (Adults = arthritis, young = encephalitis). Transmission Like above: - Drinking infected colostrum and milk - Contact with infected material, feed, water, bedding - Inhalation of aerosols Pathogenesis Virus-infected macrophages are in the milk à taken up whole from the gut mucosa à monocytes, lymphocytes and macrophages carry the virus and spreads it around the body. CAE virus persists in the host because of its ability to sequestrate (become hidden by being provirus inside host cells; having its genome in their DNA) as provirus. The infection induces a strong immune response (both humoral AbAg and cellular leukocytes) but neither will destroy agent, because it is hidden inside hosts own cells. - Arthritis due to mononuclear cell infiltration and consequently proliferation of synovial vili - Encephalitis due to mononuclear cell infiltration causing demyelination Clinical signs Most infections are without clinical signs. 2-6 months - encephalitis - Early = ataxia, hind-limb placement problems and hypertonia - Later = Progression into paresis and paralysis. Circling, torticollis and opisthotonus Adults - arthritis - Joint capsule is distended (by mechanism mentioned above, the MNC-infiltration) and there is varying degrees of lameness. Clinical course is always progressive with loss of condition and rough coat. Treatment No treatment Diagnosis Same as visna-maedi Epizootiological situation Worldwide distribution Measures during outbreak Prevention, control No vaccine. Same as visna-maedi (transmission via colostrum is important to stop) Peste des petits ruminants virus (is rinderpest in small ruminants) Etiological agent Paramyxoviridae, morbillivirus (=parainfluenza). Virus have H hemagluttinin and N neuraminidase proteins on surface. Transmission Every excretion and secretion of infected sick animal is contagious; so inhalation, ingestion and direct contact. Pathogenesis and clinical signs (Fever à oral ulcers à diarrhea/pneumonia à death) - Sudden fever above 40°C which causes general depression, anorexia and dull coat - Nasal discharge, can form crust that blocks airway; dyspnea - Few days after onset of fever, the ulceration starts - Gums become hyperemic and erosive lesions develop in oral cavity - excessive salivation - Bronchopneumonia and coughing is often seen - General state involves dehydration, emaciation, dyspnea and death - If they survive, there is a long recovery period Treatment There are no medications available to treat the disease, but supportive treatment may decrease mortality. Diagnosis Isolation of agent in cell culture. Identify by virus neutralization test, AGID, PCR. Epizootiological situation Found in Africa, Middle East, south-west Asia and India. Measures during outbreak - Quarantine - Movement control - Sanitary slaughter - Cleaning and disinfection are applied - The virus is susceptible to most disinfectants. Prevention, control Vaccination programs in endemic areas, quarantine and control of movement. OIE has goal to eradicate it within 2030! Main diff from Rinderpest is the involvement of respiratory system. a. Sanitation measures and focal disinfection. Preventative insect control. Blue tongue: Resistance of virus: Survive in presence of proteins: - In blood for several years at 20°C. Inactivation - 50°C for 3 h or 60°C for 15 min. - pH sensitive (6-8) Disinfection of surfaces - 3-5 % NaOH or 0.5 % Peracetic acid Visna/maedi + CAE Lentiviruses can be destroyed with most common disinfectants including lipid solvents, periodate, phenolic disinfectants, formaldehyde and low pH (pH < 4.2). Peste des petits ruminantes Virus is susceptible to most disinfectants, sanitary focal disinfection after slaughter in outbreak. Preventative insect control Involves the following mechanism: prevention of insect reproduction, hygiene, removal and disposal of waste, composting of manure, and prevention of access of insects to house/feed/food Life cycle · Complete metamorphosis: egg, larvae, pupa and adult - Mosquito, flies è Mosquitos breed in wet, swampy areas, where they lay their egg in water. Thus, a key factor in mosquito prevention is the elimination of standing water. · Incomplete metamorphosis: egg, nymph, adult - Cockroaches, lice, bugs Prevention 1) Preparatory work 2) Investigation work 3) Selection of insecticide and method of insect control - Mechanical: window screens, adhesive substances, light, and fall traps - Physical: temperature, steam, heat, UV light, radiation, ultrasound - Biological: deliberate introduction and establishment of natural enemies into areas where they didn't previously occur. Include parasites and pathogens - Chemicals: based on the use of chemical preparations insecticides that are commonly available as fungicides, aerosols, sprays, smokes, dusts, granular pellets, residual fumigants and baits. They are applied into the soil, plant leaves or directly on animals or in their houses. - Classification è Effect on life cycle: ovicides, larvicides, adulticides è Entry: contact, stomach respiratory è Mode of action: systemic or residual è Formulation: sprays, dusts, powders, granules, aerosols, fumigants, baits, repellents è Origin: plant derived or synthetic- pyrethroids (axonic poisons), organophosphates (cholinesterase inhibitors), carbamates (cholinesterase inhibitors) b. Types of necropsy - Also called autopsy, postmortem or obduction à necropsy is specifically used when examinations are performed on non-humans à autopsy is used for humans - Necropsy is a postmortem examination that can provide important information about the cause of death, and this information can be used in a wide variety of ways - The body presented for necropsy in forensic cases is more than a carcass. It is evidence. Necropsies on animals · Are routinely performed when a new disease breaks out to determine which animals carry the disease and what the effects the disease has on animals · Necropsy may be ordered on any suspicious animal death, to determine what the animal died of · To see if the death should be a cause for concern · Might not determine why the animal died, but it can still determine what the animal didn't die from. Types of necropsies: Anatomical necropsy Performed at veterinary universities in the teaching of normal and comparative anatomy animals. It's used to study anatomy. Animals of old age may be used, animals who has no economical value or animals whose health condition was not caused by an infectious disease. Medical necropsy Pathological-anatomical examination. Each breeder should be interested in knowing the cause of an animal's death that occurred on his farm. He should ask for an autopsy, even if the legislation does not explicitly oblige him to do so. Forensic necropsy Unlike when people die in suspicious circumstances, only very sporadically the authorities will order a necropsy of an animal. But if there is suspicion of a deliberate action aimed at causing death to the animals and thereby causing damage to property to their owner, it might be ordered. There can be a need to identify not only the causes of an animal's death (medical autopsy) but there is also a need to clarify the circumstances in which death has occurred. Forensic Veterinary necropsy does not only give a clinical diagnosis and determine the cause of death, but mainly explains the conditions under which death has occurred

5. Campylobacteriosis, prevention and control, measures in outbreak, current epizootological situation. Proceeding of competent authorities in the case of disease outbreak, control and prevention

Campylobacterioses Special things about campylobacter jejuni: Cytolethal distending toxin that 1) Stops host cell's cell cycle 2) Stops activation of immune system AND the fact that there are no antibody detection during diagnosis! Gram neg. Comma shaped with flagella. Main reservoir is poultry but all animals can be infected Campylobacter jejuni, campylobacter fetus veneralis, c. coli Current epizootological situation Campylobacteriosis worldwide distribution, peaks in summer months. Most reported zoonotic infection since 2005 and numbers are only increasing. Gastrointestinal campylobacteriosis - campylobacter jejuni Transmission Fecal-oral by ingestion of contaminated food and water. Direct contact, fomites, vector (common housefly) Humans ingest raw poultry or contaminated meat. Birds and asymptomatic carriers are important sources of infection. Pathogenesis · Campylobacter invade cells of jejunum, ileum and colon · Most strains produce CYTOLETHAL DISTENDING TOXIN which will stop cell cycle in the affected cells. Cell becomes enlarged and distended and later undergo apoptosis. · This toxin also hinders the activation of the immune system and thus enhances bacterial survival · As a consequence of the mentioned pathogenesis, there is o Destruction of brush border o Destruction of goblet cells (produce protective mucus) o Thickening of intestinal mucosa · This causes bloody, exudative enteritis · Dystentery (bloody diarrhea), pain and cramps Clinical signs The signs are usually most severe in young animals of all species affected. · Dogs: mucous, watery and/or bile-streaked diarrhea with or without blood, reduced appetite and occasional vomitus. Sometimes intermittent diarrhea persists for more than 2 weeks. · Calves: thick, mucoid diarrhoea with occasional blood flecks. The signs vary from mild to moderate. Diagnosis Sample: Fecal or intestinal sample, rectal/cloacal swab. Culture on selective culture medium. Identify agent by PCR, bacteriological appearance. No serology antibody detection! Bovine genital campylobacteriosis - campylobacter fetus fetus / campylobacter fetus veneralis Transmission · Veneral disease - transmitted during copulation · Artificial insemination using infected semen o Older bulls can be chronically infected o Younger bulls seem to have only transient infection o They think this is because old have deeper crypts in preputial and penile epithelium · Instruments, bedding Clinical signs · Mucopurulent endometritis causing · Early embryonic death · Low fertility · Irregular estrous · Usually no systemic disease! Presents as clinically healthy Low pregnancy rates are often the only clinical sign, together with prolonged gestation periods and early embryonic death. Abortions are less common. Diagnosis Vaginal mucus agglutination test VMAT (Ab) and ELISA. Dark-field or phase-contrast microscopy detect the darting motility of pathogen. Necropsy: congested and edematous colon, hemorrhagic colitis, edematous lymphnodes, placentitis, autolyzed fetus. https://www.youtube.com/watch?v=HsyrOicubso Prevention and control Control Analysis of control measures at food chain, isolation of infected animals, antibiotic treatment, isolation and sensitivity testing Poultry is the most significant public health concern and accounts for about 50-70% of all human cases. Vaccination (after diagnosis of disease) Vaccination of genital campylobacteriosis is performed 30 days prior to breeding in order to prevent abortion. Vaccination hastens elimination of the agent and improve fertility. Additional antibiotic treatment of infected bull by streptomycin can break transmission cycle. Outbreak is usually due to the introduction of an infected male/semen. Prevention · Artificial insemination and examination of bull semen · Hygiene: black and white system, all-in all- out, quarantine, heat treatment of feed pellets, proper disposal of aborted foetuses, vector control · Food industry: cook all meat thoroughly, wash hands with soap, prevent cross contamination by using separate cutting boards and do not drink unpasteurized milk a.) Sanitation measures and focal disinfection at these diseases. Disinfection in food industry Survival Campylobacter spp. has relatively low resistance in the environment though it can survive for weeks- months, especially in moist environment with faeces, milk, water, vaginal discharge and poultry litter. Can only grow in places with less oxygen than the atmosphere. Freezing reduces numbers in raw meat. Disinfection · Chloramin T (4%), peracetic acid (0,3%), formalin (2%), NaOH (2%), suspension of fresh slaked lime (20%), cresol- sulphuric mixture (3%) - Water: chlorination - Food processing: pasteurization, autoclaving, dry heat (160-170°C), radiation - Manure: 3% lime, 0.3-0.5% peracetic acid - Improvement in animal housing: daily mechanical cleaning, remove waste Disinfection in food industry There are 4 types of cleaning and disinfection in food industries- continuous, daily, weekly and general. Cleaning 1. Mechanical cleaning - Most important step: NaOH, caustic soda, quaterinary ammonium compounds 2. Pre- rinsing - Preferably with high pressure water 3. Chemicals - In order to remove sticky layers of fats and biofilm (alternate acids/alkalis) - Alkaline cleaning agents: remove organic dirt, protein, residues and fat - Acid cleaning agents: remove encrusted residues of dirt, protein or inorganic deposits - Neutral cleaning agents: less effective 4. Rinsing 5. Drying - Important as concentration of disinfection is lowered if water is left on surfaces. Chain of contamination Productive hygiene is a complex of permanently applied measures to protect products against contamination with pathogens by interrupting the chain of contamination. 1. Primary contamination: contamination of product, packaging material, air, insects, rodents, persons 2. Second contamination: contamination of workplaces, material, water, towels, clothes, wastewater 3. Biofilm: layer of organic material protecting potential pathogenic and spoilage bacteria - prevent by alternating acids and alkalis Factors affecting hygiene include raw material, technology, man, environment, etc. b.) Reasons for seizing the animal Existing law requires a police officer, humane society officer or animal control officer to take possession of a stray or abandoned animal, or any animal when the officer has reasonable grounds to believe that very prompt action is required to protect the health and safety of the animal or the health and safety of others. · In the case of taking possession of a stray or abandoned animal, existing law required the officer to provide care and treatment for the animal until the animal is deemed to be in suitable condition to be returned to the owner · Law permits the return of an animal only when the owner can demonstrate to the satisfaction of the seizing agency or hearing officer that the owner can and will provide the necessary care for the animal · Law makes it a misdemeanour (foreseelse) for every owner, driver or keeper of an animal to permit the animal to be in any building, enclosure, lane, street, square, or lot of any city, county, city and country, or judicial district without proper care and attention · Existing law, in cases involving cats and dogs, allows a seizing entity (gripende enhet) or prosecution (tiltale) attorney to file a petition (begjæring) in a criminal action to request that the court issue an order forfeiting an animal prior to the final disposition of the case

30. Cryptosporidiosis and giardiosis, prevention and control, measures in outbreak, current epizootological situation. Proceeding of competent authorities in the case of disease outbreak, control and prevention

Cryptosporidiosis Genus cryptosporidium includes around 30 species. Three subgroups are recognized based on molecular differences and oocyst morphology. The species show different host specificities. 1. Gastric group: parasites of stomach 2. Intestinal group: small intestine 3. Marine and freshwater group Cryptosporidia cause predominantly intestinal infections in vertebrates. Some are zoonotic. Cryptosporidium shows several peculiarities a) The various stages are localized intracellularly, but extracytoplasmic location b) Multimembrane attachment layer- feeder organelle c) Small oocysts without sporocysts Main species Mammals Birds C. Hominis C. galli C. Felis C. meleagridis C. Canis C. baylei C. Parvum C. Bovis C. suis Life cycle Direct developmental cycle. Transmission by means of contaminated feed, water or objects. · Merogony: after ingestion of oocysts, sporozoites are released and infect enterocytes (intracellular but extracytoplasmic position). Here they form a parasitophorous vacuole and develop type I/ II meronts. · Gametogony: type II meronts develop to gamonts (macrogamonts and microgamonts), which fuse together to form a zygote. · Sporogony: zygote, oocyst, sporulate in the host cell without forming sporocysts. - Thin- walled oocyst (20%): when sporulated cause release of sporozoites directly within the host's intestine and in this way is responsible for continuous endogenous autoinfection. - Thick- walled oocyst: exit host in feces Pathogenesis Cryptosporidiosis in immunocompetent hosts cause usually self-limiting, unapparent infection. In very young, old and immunosuppressed individuals, it may induce severe, long-lasting diarrhea and sometimes death due to damage to epithelial cells, focal necrosis and atrophy of villi, which is associated with malabsorption. Clinical signs Often unapparent infections. · Young calves: C.parvum may cause catharrhalic enteritis with water or profuse diarrhea, fever, acidosis, weight loss and occasionally death · Other hosts (particularly young animals): enteritis · Birds: respiratory system Therapy - Symptomatic treatment of diarrhea (fluid replacement). - Treatment of calves with halofuginone and humans with nitazoxanime. Diagnosis · Flotation: difficult · Faecal smears by special staining techniques: modified Zielh Nielsen stain (red), Kinyoun stain (pink), carbol- fuschin (colourless). · Marking with labelled antibodies, DNA analysis, ELISA, PCR Epidemiology Worldwide prevalence is around 10%, though up to 20% of the general population is considered high risk. There was an outbreak in UK in 2015 and first reported outbreak in Slovakia was in 2012 (12-fold higher incidence in gypsies). Many cryptosporidium spp have a broad host spectrum, while others are more host specific. GIARDIA Giardia spp. are worldwide distributed internal parasites of mammals, birds, reptiles and fish. Considered to be a water-borne pathogen rather than foodborne. In moist cool environment it can survive for several weeks and in dry warm environment with direct sunlight only a few days. Morphology Giardia species have a direct life cycle consisting of 2 stages. · Replicative stage: trophozoite · Infective stage: cysts The trophozoites have bilateral and symmetric structure and resemble half a pear with a convex dorsal and a flat ventral side, which carries a large adhesion disk in its anterior part. The cell contains 2 nuclei at its apical end, 4 pairs of flagella and a characteristic tubulin-based crescent shaped median bodies. Each of the nuclei contains a complete diploid genome. Main species Based on morphological features and host, several species can be distinguished · Mammals: G. duodenalis complex (intestinalis, lamblia) · Birds: G. ardeae, G. psitacia · Amphibians: G. agilis Giardia infection of domestic mammals and humans are caused by g. duodenalis, a species complex consisting of various subgroups- described from A-H - Assemblage A (g.duodenalis): humans, livestock, dogs and cats. Zoonotic - Assemblage B (g. enterica): humans, dogs, cats and birds. Zoonotic - Assemblage C/D (g. canis): canids - Assemblage E (g.bovis): cattle and other ungulates - Assemblage F (g.cati): cats - Assemblage G (g.simondi): rodents - Assemblage H: marine mammals Life cycle Trophozoites colonize the mucosal surface of the duodenum and jejunum, where they multiply by binary fission and form cysts. During encystment, the adhesion disc and flagella are broken up into fragments and the nuclei divide, resulting in a cyst with four nuclei. These cysts are excreted into the environment. Hosts become infected by swallowing cysts in contaminated water or food. The free trophozoites divides, resulting in two trophozoites from each cyst. The prepatent period is usually short (4-10 days) Pathogenesis Massive infections with trophozoites can be tolerated by intestinal mucosa without apparent disorders or may lead to changes, such as epithelial damage, pressure atrophy of mucosa, inflammation of mucosa, irregular formation of cysts, enteric loss of fluids and electrolytes, etc. Clinical signs Infections are often asymptomatic. Disease occur mainly in young animals and manifest as acute or chronic, usually intermittent diarrhea and often malabsorption. In dogs and cats are soft to watery faeces, containing high amounts of mucus and fat. Treatment - Calves: Halofuginone - Dogs, cats: metromidazole, fenbendazole and ronidazole, vaccination Diagnosis · Trophozoites: fecal smear, gastric probe · Cysts: flotation method with faust for 3 consecutive days. · ELISA and IFA Epizootology and epidemiology · Cyst excreted in host faeces are responsible for spreading the infection. This lasts for several weeks to months. Cyst remain infective for up to 3 months. Min infective dose is 10-100 cysts. · Worldwide distribution, with higher prevalence in developing countries (20%). In UK around 52 000 people contract giardia (g.lamblia) each year. It is the most common protozoan found in stools, and is more prevalent in places where lot of animals come together (shelters)- 10% in healthy dogs, 50% in puppies and 100% in shelters. Proceeding of competent authority, control and prevention. Cryptosporidiosis · Control - Water: control contamination of water supply- introduce additional on-site water measures at risk zones · Prevention - Hygiene measures and good husbandry (avoid overstocking and overcrowding) - Food and water containers should be high enough to prevent fecal contamination - Young animals should receive colostrum within 24h of birth (keep colostrum supplies) - Isolate and treat calves with diarrhea, clean boxes daily - Food: heat processing, milk pasteurization, cook meat for 2min at 70°C - Infected people: do not swim, do not prepare food for others and do not attend nurseries - If manure from infected cattle is to be used as fertiliser, must 1st be treated - Personal hygiene Giardiosis · Control and prevention - Personal hygiene: hand wash and food hygiene, do not touch animal feces, wear gloves when gardening - Food hygiene: wash all fruit and vegetables - Pet: take to vet, isolate, prophylaxis - Water: treat and protect - Pet: clean and disinfect household regularly, bath pets following treatment, limit access to untreated water to avoid infection or contamination, clean and disinfect toys, bedding, bowls regularly a) Sanitation measures and focal disinfection at these diseases. Disinfection of water. Cryptosporidium Resistance Sporulated oocysts in the faeces may survive for 2-6 months in a moist environment, surface water, drinking water, soil and wastewater. As most other protozoal cysts, they're resistant to common disinfectants- also chlorination of water (killed by chlorine dioxide). The parasite is removed by coagulation, boiling, disinfection, UV light and filtration through reverse osmosis filter. Control of contamination in the water supply Disinfection · Ammonia (5%), hydrogen peroxide (5%) - Water: filtration is keys (removes up to 99%) and new approaches are needed to determine if the organisms in water are infectious. - Heating to 65°C for 30 min (incl. composting) - Manure: composting or disinfection with ammonium (3%), peracetic acid, phosphoric acid - Soil: lime, peracetic acid, phosphoric acid - Milk: pasteurization effective - Meat: 70°C for at least 2 min Giardiosis Resistance Cysts of giardia can survive in water for weeks to months (prefers wet and cool conditions) Disinfection - Surfaces: heat treatment, Na hypochlorite (5%), H2O2 (6%), ammonia - Leaving disinfectant on surface for 5-20 min before rinsing aids inactivation - Water: chlorination, UV light, ozone, filter, boiling - Manure: composting Treatment of water: Filtration, centrifugation, coagulation and sedimentation. Disinfection of water All water used for mass consumption must be treated before consumption. · Ground water: processes used to treat ground water involves removal of excess iron and manganese, sedimentation, filtration and disinfection. · Surface water: processes used to treat surface water involves mechanical pre-treatment (rakes), odour removal, coagulation of colloidal substances, sedimentation, filtration and disinfection (chlorination, UV-lights and ozone). Factors affecting disinfection include time, pH, water temp, conc of killing agent, conc of MO, nature of killing agent and nature of suspended medium. Disinfectants 1) Chlorine and chlorine preparations - Mechanism: disruption of protein synthesis in bacterial cells, disruption of outer membrane of G- bacteria and protein coat of virus.Disinfection under slightly acidic conditions recommended as HOCl more potent than OCl è Advantages: leave residual protection (0,05-0,3mg/l). Cheap è Disadvantage: formation of trihalomethane precursors and chloramines. - Local water supply: chloramines, chlorine lime, hypochlorite - Mass water supply: gaseous chlorine 2) Cl dioxide - Advantage: more effective against bacteria and virus than free chlorine, no trihalomethane or chloramines, destroys biofilms - Disadvantage: toxic chlorate ions 3) UV light - Absorption of UV energy by microbes lead to photochemical damage to nucleic acids. - Advantages: Efficient against bacteria, virus and cysts. No carcinogenic or toxic by-products. No taste and odour problems. Higher cost than chlorination. - Disadvantages: dose calculation is difficult and it is not effective towards biofilms 4) Ozone - More expensive, no residues, more powerful oxidant than Cl2 and affects permeability of cell walls, enzymatic activity and DNA of bacterial cells, causes rupture of the cell wall Total coliform, E. Coli and enterococci: indicator of hazards in EU. 0/100ml in mass supply and 0/10ml in local supply/ well/ for individual consumption (mass supply = more than 50 people - individual supp = less than 50) b) Definition of forensic veterinary medicine = the application of the broad spectrum of sciences, including veterinary medicine to answer questions of interest to a court of law Can be used to: - Establish if a crime has or has not been committed which involves an animal - Solve an animal related crime Case investigation is a multidisciplinary approach and the responsibility to "prove" a case does not lie on the veterinarian alone. The veterinarian should simply present the facts of the case and their interpretation or conclusion drawn from such facts. A veterinary forensic medical examination is a detailed exam done in order to methodically document physical findings and facilitate the collection of evidence from the patient's body. It starts at the scene as one cannot fully interpret exam findings without crime scene information. Forensic necropsy Of a deceased victim is also known as veterinary forensic pathology. The goal is to determine: - Cause of death - Manner of death - Contributory causes - Mechanism of death - Estimate the postmortem interval

27. Cysticercosis of cattle and swine, prevention and control, measures in outbreak, current epizootological situation. Proceeding of competent authorities in the case of disease outbreak, control and prevention

Cysticercosis of farmed and wild animals is caused by the larval stages (metacestodes) of cestodes (tapeworms). The adult stages occur in the small intestine of dogs, wild Canidae and humans. Etiological agent Taenia saginata with metacestode called cysticercus bovis. Human is FH and cattle is IH. Taenia solium with metacestode called cysticercus cellulosae. Human is FH and pig + human are IH. OIE. Morphology Taenia saginata Adults: large, yellowish tapeworm capable of reaching 10m in length - Scolex: Small with 4 suckers, but without rostellum. - Strobila: Many thick proglottids, which can be equipped with two rows of large and small rostellar hooks. Gravid proglottids are longer than they are wide. The genital pores are in irregular sequence on either side. Metacestodes: Cysticercus bovis. Small, fluid filled bladder with single invaginated scolex. Taenia solium Adults: Large, yellowish tapeworm capable of reaching 3-4m in length. - Scolex: Small with 4 suckers and a rostellum armed with a double row of hooks. - Strobila: Many proglottids, which can be equipped with 2 rows of large and small rostellar hooks. The number of branches of the uterus is smaller than that of Taenia saginata. · Metacestodes: Cysticercus cellulosae. Small, fluid filled bladder with single invaginated scolex. Life cycle Taenia saginata Location in IH: Muscle, liver, kidney etcLocation in FH: Small intestine 1. Embryonated eggs passed in feces of FH 2. IH ingest contaminated grass with eggs/proglottids → oncospheres hatch in IH → circulate in blood and lymph to muscles → develops to larval stage cysticercus bovis 3. In FH: Human ingests raw/undercooked meat from IH → Cysticercus bovis goes to SI → In SI the cysticercus evaginates the protoscolex à attaches itself to the mucosa of the upper SI and develops into an adult tapeworm → shed proglottids/eggs Taenia solium Location in IH: Muscle, kidney, liver etcLocation in FH: Small intestine Same as Taenia saginata, but if human becomes accidental IH from ingesting eggs → autoinfection: - The adult Taenia is in SI as described above, and during anti-peristaltic movements the gravid proglottis can be transported to the stomach. Here the eggs are released (as well as oncosphere), which penetrate the stomach wall and then travel to the striated muscle or brain via blood (= cysticercosis). Pathogenesis Taenia saginata Humans - Parasite located in GIT Cattle: - Cysticercus located in the connective tissue of striated muscle. Viable cysts are oval, translucent, and filled with a clear fluid. Heavy infections can cause cellular infiltration of the surrounding connective tissue. - Cysticerci are mainly found in the masticatory muscles, heart, diaphragm, tongue, limbs and body muculature. Usually, the infection is asymptomatic. - Adverse effects are mainly due to loss or impairement of meat from infected cattle. Taenia solium Humans - Intestinal infection: None or only minor disturbances, similar to the infection with T. saginata. - Cysticercosis: Much more serious. People can be infected by taenia solium eggs by autoinfection or from other hosts, resulting in various forms of cysticercosis, including cysticercosis of the CNS (neurocysticercosis), the eye, muscles and subcutaneous tissue. Pigs - Often heavily infected. The metacestodes are predominantly located in the muscles of the sacrum, shoulder blade, diaphragm and tounge. Less often in other organs. Clinical signs Taenia saginata Humans: Abdominal pain, nausea, hunger, weight loss, diarrhoea, constipation and unpleasent sensations due to discharge of proglottids from anus. Cattle: Fever and stiff gait. Very rare and may only appear in massive infections. Taenia solium Pig: Symptoms are generally not observed. Include respiratory disorders, stiff gait, difficulties with food intake and nervous disorders Humans: Intestinal disease like above, and extra-intestinal depends on location of cysticerci. Transmission Taenia saginata - Humans: Ingestion of improperly cooked beef infected with cysticercus bovis - Cattle: Swallow egg when grazing contaminated pasture or feed Taenia solium - Humans: Ingestion of improperly cooked pork infected with cysticercus celluloase (à taeniasis) - Pigs: Ingestion of eggs when eating contaminated feed (à cysticercosis) The major risk factors related to transmission of eggs to pigs: • Extensive or free-range pig rearing; • Outdoor human defecation near or in pig rearing areas; • Never use untreated sewage or sludge for fertilization of pastures and soil for food crops; Treatment Taenia saginata Humans: Praziquantel and niclosamides Cattle: chemotherapy is not feasible. Vaccination is possible, but not available. Slaughtered cattle with metacestodes are unsuitable for consumption Taenia solium Intestinal infection of humans: Praziquantel or niclosamide Pigs: Oxfendazole. Diagnosis Segments may creep out of anus. Detection of eggs in faeces and perianal region by a swab. Gravid segments in faeces Cysticercosis (soleum) in humans by imaging techniques, serology (ELISA) Cysticercosis (cattle and pigs) meat inspection and investigation of slaughtered cattle and pigs. Epizootiological situation Taenia saginata Is distributed globally but the infection is particularly important in Africa, Latin America and Asia as well as in some Mediterranean countries. Low prevalence in Europe in humans. Taenia solium Endemic in large areas of Latin America, Asia and sub-Saharan Africa. Low prevalence in Europe, sporadic occurrence. Prevention, control Risk factors · Poor hygiene of farm staff · Defecation by man in places frequented by cattle · Application of human sewage slurry on pastures or where there is risk of contamination of drinking water. Control · Condemnation of carcasses with severe infection Prevention · Keep animals indoor all their lives · Feed animals only with feed guaranteed free from Taenia eggs. (This means that no feed from pastures or crops can be used unless treated) · People handling animals should be free from Taenia. The more people on farm, the higher risk of infection · Certification of the herd through sero-surveillance / monitoring as free from cysticercosis · Meat inspection: All bovines older than 6 months. Longitudinal cuts into masseters, cardiac muscle, diaphragm and muscles of trunk. è Heavy infestation: Generalized infection (2 or more sites) à unfit for human consumption and carcass + offal must be incinerated. è Light infestation: Small number of dead/degenerated cysticerci à removed, rest of carcass is treated either boiled or frozen (10 days -10°C). · Wastewater treatment, repair damaged sewers, sanitation of sewage sludge by pasteurization · Vaccination: Possible, but not yet available · Not using sludge for fertilizing soil, grazing or feeding cattle · Cooking meat · Wash your hands with soap and warm water after using the toilet, before handling food · Wash vegetables a. Sanitation measures and focal disinfection at these diseases. Sewage and sludge treatment Resistance: • Eggs are resistant to outer environmental conditions (up to 1,5. years in favourable conditions) • Survive in feces for 2-3 months • In wastewater for 2 weeks • In sludge and on pasture for several months Eggs are also resistant to several common disinfectants. However, they can't survive in a dry environment and is destroyed by drought and pasteurization. Freezing will also kill the parasite Sanitation: · Tapeworm eggs are resistant to a number of common disinfectants. · T. solium and T. saginata are inactivated by 1% sodium hypochlorite or 2% glutaraldehyde · Sterilisation of meat: 60°C for 10 min · Salination: in 25 % NaCl for 5 days · Temperature above 57°C devitalises cysticercus · They do not survive in a very dry environment Sewage and sludge treatment Activated sludge process This process imitates natural self-cleaning processes, however in a more intensive form. An important characteristic of this process is the recycling of a large portion of the biomass. 1) Aeration tank: where the wastewater is mixed with activated sludge and the activation system can remove substantial portion of the carbonaceous and nitrogenous pollution after the retention time 2) Secondary tank: used for the sedimentation of microbial flocs (sludge) produced during the oxidation phase in the aeration tank. A portion of the sludge is recycled back to the aeration basin and the remainder is „wasted" and processed 3) Activated sludge: a natural mixture of floc-producing micro-organisms (pseudomonas, protozoans, rotifers, and zooalgea) composed of live and dead organisms and suspended, colloidal, and dissolved organic (70-90%) and inorganic substances (10-30%) - Two main goals of the activated sludge system are: oxidation of the biodegradable organic matter and flocculation, i.e. separation of the newly formed biomass from the treated effluent. Nutrient removal by the activated sludge process 1) Nitrification - 1st stage: conversion of NH4+ to NO2+: Nitrosomonas,Nitrosospira, Nitrososcoccus, Nitrosobolus. - 2nd stage: conversion of NO3+ to NO3+ : Nitrobacter, Nitrospira, Nitrococcus 2) Denitrification: NO3 à NO2à NO à N2O à N2(gas). Denitrifiers= Pseudomonas, Alcaligenes, Bacillus Removal of phosphorus · Chemical precipitation during the primary treatment · Polyphosphate accumulation: Acinetobacter, Pseudomonas, Aerobacter and other so-called poly-P bacteria have the ability to accumulate intracellulary P up to 5 to 6 times in excess of the normal requirement Pathogen removal by activated sludge · Retention time= 24 to 30-34 hrs result in inactivation - Bacteria: 80 - >99 %. Inactivation by protozoa, adsorption, encapsulation and sedimentation - Viruses: 93-99 % removal. More than 90 % are solid-associated, inactivation, ingestion - Parasitic protozoa: 80-98 % .E.histolytica, Giardia cysts and Cryptosporidium. Oocysts are not inactivated by the process. They are entrapped in flocs and concentrate in the sludge Solid fraction (sludges) treatment · Sludge treatment: very costly procedureProcessing usually starts with thickening to increase concentration of solids to about 12%, the drying on sludge beds. Then stabilisation of sludge by one of the following methods: - Anaerobic digestion: 30-40°C (mesophilic temp), followed by belt pressing (dewatering). - Composting: aerobic thermal decomp of organic wastes to a relatively stable humus - Lime stabilisation: controlled dose of liquid lime, hydrated lime or quick lime to raw sludge. This dries the sludge and converts it to a biosolid product b. Determination of age in tissue helminthoses Cysticercus cellulose 8 days: parasite reaches the size of 0.33-0.034 mm approximately. They are as oval vesicles. 20 days: the parasite reached the size of 0.8 mm 40 days: the parasite is size of grain of mustard seed or a little smaller, surrounding membrane is distinctly seen and scolex is clearly visible with size 1 mm. 3 months: parasite reaches the size of lens or larger and mature completely. Cysticercus bovis Development of this parasite is slower than C.cellulosae 14 days: haemorrhages can be seen which are later absorbed. 33 days: education and caseation mass around of cysticercus is seen around parasite 4 weeks: cysticercus reaches the size 4 mm x 3.5mm 8 weeks: size of 4.5mm x 3.5mm 12 weeks: the size is 5-6 mm x 3.5-4 mm 28 weeks: the size is 7.5 mm x 5.5mm

15. Aujeszky diseases and other swine notifiable diseases, prevention and control, measures in outbreak, current epizootological situation. Proceeding of competent authorities in the case of disease outbreak, control and prevention

DNA viruses (Herpesviridae) with subfamilies alpha-herpesviridae (all those we talk about). All herpesvirus share the same structure; This is the virion It has envelope with glycoproteins Capsid protects DNA. Tegument protects capsid - All herpesviruses are nuclear-replicating, in that the viral DNA is transcribed to mRNA within the infected cell's nucleus. - During symptomatic infection, infected cells transcribe lytic viral genes. - In some host cells, a small number of viral genes termed latency-associated transcript (LAT) accumulate, instead. - In this fashion, the virus can persist in the cell (and thus the host) indefinitely. - While primary infection is often accompanied by a self-limited period of clinical illness, long-term latency is symptom-free. · They are polytropic known to infect both GIT, respiratory tract, reproductive tract and CNS. · Herpesvirus are relatively little resistant in the environment Some general info: · In beginning of disease, there is a self-limiting period of clinical illness. From there, there is a long-term latency where there are no clinical signs. Latency interrupted e.g. during stress à disease · Herpesvirus are polytrophic; Causes disease in RT, GIT, reproductive tract and CNS. Species Herpesviridae has 3 subfamilies; Alpha-, beta- and gammaherpesvirinae. 1. Porcine herpesvirus 1 (Aujeskys disease) 2. Bovine herpesvirus 1 (IBR/IPV) 3. Gallid herpesvirus (Mareks disease) 4. Equine herpesvirus 1 +4 5. Canine herpesvirus 1 6. Feline herpesvirus 1 Suid alphaherpesvirus 1. Pseudorabies. OIE notifiable. Virus resistant as always, pH sensitive. Young = CNS à why the name pseudorabies. Adult = respiratory. Pregnant = abortion. Etiology The main reservoir of SAHV1 is swine (wild and domestic) because they are the only species that survive infections. Other species may be infected after contact or ingestion of infected pigs meat, but they develop fatal neurological disease and die few days later. In wild and domestic swine, it can cause persistent and latent infection, thus serving as reservoirs. Dogs, cats, wildlife = dead-end-hosts (survive for only 2-3 days, but can transmit the virus between farms). Epizotlogy - Worldwide distribution - Emerged as major pathogen in USA since 1960s but eradicated from most USA - now only cases in Mexico - Current situation: Outbreak in France in wild boar intended to be released for hunting and 1 case in Finland in wild boar per 2020 Transmission Contagious!!! Respiratory, ingestion and veneral route. Carnivora infected when eating meat. Can travel 2 km as aerosol! Pathogenesis and clinical signs Primary site of viral replication is nasal, pharyngeal or tonsillar epithelium à lnn, lymph vessels = cont. replication. Nasal/pharyngeal mucosa + tonsils à infects olfactory/glossopharyngeal/trigeminal nerves à brain. Spreads within CNS via synapses like in rabies. Injures CNS by destroying neurons. 1. Young pigs develop CNS disease and die from encephalitis. 100% mortality. a. Hyperthermia and ataxia, opistotonus, seizures 2. Older pigs develop respiratory disease a. Hyperthermia, anorexia b. Respiratory signs are mild to severe; Rhinitis, sneezing, may progress to pneumonia 3. Pregnant sows suffer abortions and reproductive disease a. Because virus cross placenta, infects fetus and kills it Severity of disease depends on virulence of strain, route of infection, immune status and age of host In other susceptible species (dogs, cats, cattle, sheep, rabbit, not humans) the disease is fatal. Main sign is intense pruritus causing severe self mutilation. "Mad itch" was old name. Diagnosis Based on findings from necropsy: · Focal necrotic lesions found in CNS and viscera (lung, liver, spleen) · Piglets and fetuses have white spots on liver from the viral infection Sample for testing are tonsils and brain sample if neurological signs were present. Virus isolation in cell cultures and identification of agent - Immunofluorescence (Ag - serum Ab - Ab2 with fluorescein) - Virus neutralization test and ELISA (OIE requirement) - Latent infection by immunoblotting to find proteins in tissue Prevention and control OIE NOTIFIABLE so screening should be performed and culling of all positive is favorable Vaccines only used in enzootic areas under permission from state vet (marker vaccines) Control - At the focus of infection Quarantine of infected herds, vaccination and removal of latently infected animals. Strategies to eradicate the disease from a herd; test and removal (test breeding herd monthly and remove [eradication] the positive animals), offspring segregation (vaccinate breeding herd, remove young weaned pigs), depopulation and repopulation (premises cleaned and disinfected, left empty for 30 days). Prevention in an endemic region: - Isolation and testing of new breeding animals - Biosecurity measures to prevent entry via contaminated fomites, people and roaming animals (including rodents and birds) The virus is carried in wild swine. Thus, domesticated herds must be kept separate from wild swine. Closed herd system in pigs is very important measure. · Good hygienic level in housing, and good hygiene and disinfection of empty areas · Good housing conditions with adequate climate control · All-in-all-out management systems · Good biosecurity to keep farms as a closed system, restricting contact with other farms · Only buy from Aujeszky's disease-free herds Other swine notifiable diseases OiE-listed diseases, infections and infestations in force in 2020: · Infection with African swine fever virus (question 22) · Infection with classical swine fever virus (question 22) · Infection with porcine reproductive and respiratory syndrome virus · Infection with Taenia solium (porcine cysticercosis) (question 27) · Nipah virus encephalitis · Transmissible gastroenteritis Porcine reproductive and respiratory syndrome (PRRS) Aka. blue ear disease. Widespread disease affecting domestic pigs. Caused by virus in the family Arteriviridae, genus Arterivirus (enveloped virus); two related strains - genotype 1 (Europe) and 2 (North America). Pathogenesis: Ingestion or inhalation. Acute phase - replicates mainly in macrophages of the lymphoid tissues and lungs. The virus has a tropism for macrophages (compromises cellular immune response and damages mucosal surfaces). Current situation: Ecuador and Uruguay in 2017, ongoing case in Switzerland 2014- present time Clinical signs Adults: Reproductive failure Piglets: Pneumonia and cutaneous cyanosis Increased susceptibility to secondary infections No treatment (only for the secondary infections), but commercial modified live vaccines have been licensed and have been effective in controlling outbreaks, reducing shedding and preventing economic loss. Nipah virus (NiV) encephalitis aka Barking pig syndrome or Porcine respiratory and neurologic syndrome NiV: Family Paramyxoviridae, genus Henipavirus. Occur naturally as virus of fruit bats (flying foxes). NiV appeared in the human population (zoonosis) between September 1998 and April 1999 in Malaysia as the cause of fatal acute encephalitis, after spreading primarily as a severe respiratory disease of unknown etiology in the pig population. Highly contagious. Affect companion animals. Pathogenesis Transmitted via ingestion/inhalation/vertical - the virus enters the bloodstream (viremia) leading to vasculitis, thrombosis and ischemia. Further spread cause parenchymal infection and cellular injury of the CNS. Clinical signs Characterized by fever with respiratory and often neurological involvement, but many infections are subclinical. Some infected animals display an unusual loud barking cough. Sows - abortion. Peracute death (sows and boars). Naturally infected dogs - distemper-like syndrome, high mortality rate. Cats - pulmonary disease. No treatment. Transmissible gastroenteritis (TGE) Common viral disease of the small intestine. Etiological agent: TGE virus (TGEV), a member of Coronaviridae. - TGEV is shed in feces - Transmission is orofecal Epizootiology Still reported on an occasional basis from parts of Europe, North America and Asia. Last reported case was in Argentina 2014. Vaccination is carried out in several countries. Pathogenesis: Multiply (+damage) in enterocytes à villus atrophy and enteritis à diarrhea and vomitus in pigs of all ages. Mortality highest in neonates. Extra-intestinal sites are RT and mammary tissue. Clinical signs In non-immune herds vomiting is the initial sign, followed by profuse watery diarrhea, dehydration and polydipsia. Feces of nursing pigs often contains curds of undigested milk. Mortality: Nearly 100% in piglets <1 week, pigs over 1 month old seldom die. Lactogenic immunity (very important) and herd size (important) - self-limiting in herds <300 pigs. Diagnosis by PCR and ELISA. Treatment: Supportive, non-specific. Prevention and control Control · Radical method: Kill them all · "Blanket vaccination": Norway, France and the USA o Vaccinate all 8-12-week-old slaughter pigs (inactivated) and breeding pigs (marker) o ELISA to monitor natural infection o Isolation and culling of infected animals · Movement restriction · Observation for 30 days after disinfection · Vaccination of dogs is not recommended - risk of latent carrier Prevention · All-in-all out, quarantine/isolation · Age group management, proper husbandry and sanitation · Marker vaccines (pseudorabies) - practiced in enzootic countries o Vaccination also prevent the virus from going transplacentally and the piglets get antibodies from the milk · Regular testing (blood sampling): ELISA (pseudorabies) a. Sanitation measures and focal disinfection at these diseases. Protection of the farm from diseases Disinfection: Sensitive to disinfectants and detergents (the virus has "fat"). · 2-3% Sodium hydroxide 70-80°C (3 hours, 2 x) · 0.5% Peracetic acid · 6% Chloramine T (3 hours, 2 x) · 1% Formalin (3 hours, 2 x) · 20% Slaked lime · 1% Virkon Protection of the farm · The farm should be kept as a closed system (must be fenced in). · At the entry to animal farm and houses: Disinfectant ford and mats provided with active disinfectants, usually chlorinated lime 5%. It must be freshly prepared as it is unstable and the active chlorine decreases (new solution must be prepared every 2-3 days) o Veterinary filter (prevention of spreading disease by infected animals) o Hygienic filter for protection, to prevent the introduction of diseases by people (protective clothing and footwear, changing rooms, showers) · Preventive disinfection, rat and insect control, all sanitation measures · Newly purchased animals must be quarantined · Animals susceptible to infection must be isolated! · Black and white system: o White objects: Animal houses, and in some cases storage of feed. Persons only enter through hygienic filter. o Black objects: Storage of food, administration, transport, vehicles, machinery, storage of manure (freedom of movement) (?) o Carcass box: Special entry from outside the farm for vehicles collecting the carcasses · Emergency supply of disinfectant b. Xenotransplantations Refers to any procedure that involves the transplantation, implantation or infusion into a human recipient of either; live cells, tissues, or organs from a nonhuman animal source, or; human body fluids, cells, tissues, or organs that have had ex vivo ("which takes place outside an organism") contact with live nonhuman animal cells, tissues or organs. The motivation for using animal sources for organ or tissue transplantation is driven by supply and demand. EU legislation: Since 1999 there is a moratorium (delay or suspension of an activity of a law) on xenotransplantation in the EU. A Europe-wide moratorium on clinical xenotransplantation trials is needed - until absolute safety can be guaranteed. Scientists known too little about the transplantation of animal viruses to man, citing the animal origins of HIV and the transmission of Creutzfeldt-Jakob disease through bovine spongiform encephalopathy as existing cases causing concern.

26. Echinococcosis, prevention and control, measures in outbreak, current epizootological situation. Proceeding of competent authorities in the case of disease outbreak, control and prevention

Etiological agent Echinococcus multilocularis, Echinococcus granulosus Echinococcus are flatworm endoparasites, also called platyhelminths. They belong to class cestoda, order cyclophyllidea, family taeniidae and genus echinococcus. Morphology The adult echinococcus is the smallest cestode with the strobila containing only 3-5 proglottids; mostly one immature, one mature and one gravid proglottid. The mature proglottid have functional ovaries and testes, while the pregnant proglottid has uterus filled with eggs. Echinococcus have no digestive system or anus. The adult parasite is small, granulosus is up to 9 mm long while multilocularis is even smaller, up to 5.5 mm. Scolex has 4 suckers and a rostrellum with hooklets. The eggs are typical taenia type. Small, round, thick shelled and embryonated (hexacanth larvae = oncosphere) The encysted larval stage is called metacestode and they are in the form of a hydatid cyst, but the two species differ in structure of the cyst: E. granulosus larvae is a bladder-like structure (hydatid cyst) It has a hydatid cyst wall with 2 layers, surrounded by a collagen capsule produced by the host. The cavity is filled with hydatid cyst fluid. Inner germinal layer gives rise to cellular buds that becomes brood capsules, that bud and produce protoscoleces. Daughter cysts can be found inside the main cyst E. multilocularis is similar but instead of the cavity there is a labyrinth (alveolar cyst) of small chambers which is mixed with the fibrous reaction of host' parenchyma of the affected organ. The cyst performs exogenous budding to form multiple cysts. In this way the cyst is very invasive on the organ. Transmission E. granulosus is found mainly in sheep and cattle, but IH are all omnivorous animals. The FH where we find the adult worms are canids, including dogs, wolves, coyotes and more. Humans can be accidental IH. Dogs infected when fed fresh offal/scavenge infected sheep/cattle à feces contaminate pasture and sheep/cattle are re-infected as they graze. E. multilocularis have a narrower host range, where only rodents serve as IH with hydatid cyst formation. However, humans can be accidental, aberrant IHs if they ingest eggs, and the hydatid cysts will form inside of them. Mainly transmitted within the predator-prey relationship between foxes and small mammals. Life cycle IH ingest the embryonated egg. The hooklets from larvae attaches to SI and they help it migrate to their predilection site which is liver and lung of the IH. Here they start formation of the hydatid cyst. When the FH ingest the IH uncooked, they also ingest the hydatid cyst and the protoscoleces (larvae) it contains. Protoscoleces will evaginate and attach so the SI of FH and grow to adult larvae. The parasites lie deep into the intestinal mucosa, causing a lot of damage to the IH. The FH will have the adult worms in their SI and whole gravid proglottids are shed in feces and eggs will be released. The eggs survive for a long time in the environment, in moist and cold conditions up to a year. The eggs are ingested by the IH, often during grazing and the cycle repeats itself. Clinical signs Disease in animals For the FH, having the tapeworms in the SI causes few ill effects. For the IH on the other hand, the effects can be detrimental. - As hydatid cysts grows, they displace or induce fibrosis in normal tissue - In livestock animals, we often see reduced growth and decreased production - When hydatid cysts are found in PM inspection, organs will be condemned which gives economical losses - However, production animals are mostly slaughtered before the cysts cause disease problems. This is unless the cysts are located in the brain or testes, where visible signs may arise sooner. Disease in humans Hydatid disease (E. granulosus) One or more hydatid cysts grows in the liver and lungs, sometimes in bones, kidney, spleen, muscles and CNS. There are no symptoms for many years as the cysts grow, until they reach a substantial size. Signs depends on location of cyst, e.g. when in the liver there is abdominal pain and nausea, while if in the lungs there will be chronic cough, chest pain and dyspnea Alveolar echinococcosis (E. multilocularis) The incubation period without symptoms are much longer, it ranges from 5-15 years. The primary tumor has a slow development and is usually found in the liver, causing weight loss, abdominal pain and in the end hepatic failure. Metastases can occur via the blood and lymph and the disease is fatal if not treated. Treatment Humans: Surgery removal of mass (not usually 100% effective). Long term chemotherapy, benzomidazole for 2 years (alveolar echinococcosis = difficult). Albendazole (hydatidosis = easier). Animals: Deworming with praziquantel Diagnosis Final host: Flotation or adhesive tape technique. Copro-antigen and copro-DNA detection. IH/accidental host: Imaging techniques combined with specific serum ABs. DNA analysis of biopsy material Epizootiological situation The real prevalence of echinococcosis is difficult to estimate, due to the patchy distribution within transmission areas, the high proportion of asymptomatic infected individuals and symptomatic patients living in poor areas. E. granulosis which is found worldwide E. multilocularis is widespread in the northern hemisphere Prevention, control, measures during outbreak · Prevention and control of echinococcosis is mainly performed by surveillance · Carcasses of heavily infected animals are condemned in a proper manner · Further control is performed by breaking life cycle between FH/IH, especially in pets and humans · Meat inspection at slaughter · Education of the public by means of proper cooking and not feeding offals to dogs · Livestock vaccines exist and are recommended in endemic areas · Deworming a. Sanitation measures and focal disinfection at these diseases. Preventive measures against parasitic infections Resistance Eggs are very resistant and survive in - 4°C water for 10 months (hence many eggs survive winter) - Freezing at -26°C for 2 months - 40°C for several months Eggs are well adapted to survive in environment for over 1 year in cool, moist conditions. Resistant to all disinfectants effective against viruses and bacteria, but a portion may be destroyed by Na hypochlorite (at low concentrations). Disinfection Sodium hypochlorite (min. 3,75%- 1 hour) - Equipment: moist or dry heat - Soil: lime (3%), peracetic acid (0,3%) - Composting: eggs are killed at temperatures above 60°C - Drying: eggs are very sensitive to dehydration. Preventive measures against parasitic infections Integrated approach - Education of public - Maintain animal hygiene in housing and on pasture - Meat inspection - Do not feed cats and dogs raw meat - Wash forest fruits and hands - Deworming - Rodent and insect control - Vaccination when available b. Determination of age in tissue Helminthoses 4 weeks: Bluish nodules with shape of round ball and 1mm big 2 months: Nodules 1.5-2mm. Parasitic follicles 1-1.2 mm are found in these nodules. 5 months: Parasite reaches the size of 15-20 mm at 5 months age. Scolex develops in cyst. First: Prepatent period: Period between infection with a parasite and the demonstration of the parasite in the body especially by recovery of an infective form (as oocysts or eggs) from the blood or feces. Communicability in final host - FH can transmit echinococcosis to susceptible intermediate hosts, via eggs shed in the feces. - E. granulosus becomes prepatent in 32 to 80 days in the FH. This period varies with the species or strain. - Although the parasites stop laying eggs after 6 to 10 months in dogs, the adult worms may survive for up to 3 years in some cases. - E. multilocularis usually becomes prepatent in foxes or dogs in 28 to 35 days - Experimentally infected dogs and foxes shed eggs for 1 day to 4 months. The adult worms are estimated to survive in the definitive host for approximately 5 months. Communicability in intermediate hosts - IH only transmit infections to FH if tissues contain mature cysts with protoscolices and cysts are ingested. - The percentage of viable cysts can vary with the host and the species/strain of Echinococcus. - Most E. granulosus cysts in sheep are fully infectious - Feeding the viscera of IH to dogs will spread the cycle in domesticated animals - IHs cannot transmit echinococcosis by casual contact.

17. Influenza (avian and others), prevention and control, measures in outbreak, current epizootological situation. Proceeding of competent authorities in the case of disease outbreak, control and prevention

General about the agent Orthomyxoviridae (RNA) 7 genera, where 4 causes influenza in animals ABCD A = Horse, swine, fowl and other animals B = only humans C = humans and swine D = swine and cattle Influenzavirus is good at being pathogenic because of its ability to mutate. The virus is sensitive to mutations which makes it impossible to eradicate the disease and why they make new influenza vaccines every season. The mutation occurs through a process called antigenic shift and drift. This is possible because: RNA proofreading enzymes are absent, thus RNA transcriptase makes an error every 10.000th nucleotide à a new mutation in the genome of every new influenza virus. Influenza surface molecules Influenza RNA genome encodes 11 proteins and the 2 most important ones are hemagglutinin (H) and neurominidase (N). These can be found on the surface of the virus. Neurominidase = release progeny viruses from infected cell Hemagglutinin = binding of virus to target cell + viral genome entry Influenza viruses are classified based on type of H/N present! H = 18 subtypes H1-H18 N = 11 subtypes N1-N11 Influenza virus A infection. Important subtypes include H1N1 = swine flu H1N2 = human, swine and avian flu H5N1 = avian flu H7N7 = horse flu destroy cilia in lungs and trachea, highly increasing susceptibility to secondary infections. Exudative nasal secretions, can turn into pneumonia. Swine flu Influenzavirus A H1N1 Transmission - airborne from nasal discharge. Sneeze, cough, nose-nose contact. Pigs have receptors for many types of Influenzavirus - high chance of mutations - high chance to develop a zoonotic strain!! Pigs are mixing wells for influenza virus. Epizootology: 2009 swine flu pandemic (WHO calls it A(H1N1)pdm09). April 2009 a new strain of H1N1 which resulted from a previous triple reassortment of bird, swine and human flu viruses further combined with a Eurasian pig flu virus (leading to the term "swine flu"). Pathogenesis - virus replicates in cells of upper and lower RT à this AND the immune response elicited causes destruction and loss of cells in the lining of RT à Inflammation of mucosa with excessive secretions + bronchitis + bronchopneumonia + lung abscesses. When infection subsides, the epithelium will regenerate (can take months) Clinical signs - depends on form of swine flu Epidemic. Quick disease progression and rapid recovery as long as no 2ndary infection occur Endemic. Less obvious CS, lasts longer. Some pigs show no clinical disease. Other: Coughing, sneezing, rhinitis + nasal secretions, tachypnea. Systemic: Fever, lethargy, anorexia Diagnosis - Sample is lung tissue or nasal swabs. Isolate in cell line, embryo. RT-PCR, VNT, ELISA. Avian influenza - fowl plague (fowl = galliformes + anseriformes = høns og ender) Influenzavirus A subtype H5N1. Natural reservoir in aquatic birds but is also zoonotic. Kill millions/year. Avian Influenzavirus A subtype H5N1 Divided into high pathogenicity types HP and low pathogenicity types LP LPAI causes mild to no disease, only signs may be decreased egg laying and ruffled feathers HPAI causes severe disease and has high mortality Both types spreads fast through a flock! Epizootiology LPAI occurs worldwide (wild birds and poultry). HPAI: Eradicated from domestic poultry in most developed nations. Epidemic ongoing in parts of Asia, the Pacific, Middle east and Africa. Domesticated poultry: HPAI morbidity and mortality rates approach 90-100% Wild birds: Typically asymptomatic (some H5N1 viruses may cause death). Current situation: Reported in Hungary in 2020, 53 outbreaks and a few cases in Slovakia Transmission High amounts of virus are shed in feces, saliva and nasal secretions. Main route of transmission is fecal-oral, aerosols and fecal contamination of fomites Pathogenesis LP strains are carried in wild birds. Once they are introduced to domestic poultry, they recombine by mutation from LP to HP and then causes severe disease. Inhaled à virus replicates in epithelial mucosa of both upper and lower RT à cell destruction itself and the immune response it elicits àsevere cell damage in RT Inflammation with high secretions seen in bronchi + bronchopneumonia + purulent pneumonia and lung abscesses. This can cause severe breathing difficulties. Infection subsides and healing starts, epithelium can take months to regenerate (by this time they are dead or culled often). Clinical signs · Depends on HP or LP strains! HP which causes severe disease includes · Anorexia, diarrhea, apathy · Coughing, reduced vocalization, dyspnea, cyanotic comb · Discharge from nose and eyes, swelling of head and sinuses · Can develop into nervous signs like ataxia · High morbidity with increasing mortality! · Less severe in ducks; Upper respiratory signs, diarrhea and increased mortality in flock · More severe in humans; Acute respiratory distress, severe pneumonia, multiple organ dysfunction Postmortem lesions Chickens and turkeys: Swollen sinuses, edematous comb and wattle, subcutaneous edema, petechia in trachea, lungs and proventriculus Diagnosis Swab from nasal cavity, orophagyngeal or lung tissue. Isolation in cell culture, identification by RT-PCR. ELISA for Ag detection. Main serology in surveillance is HIT. Prevention Vaccine, all in all out, no contact with wild birds, rapid elimination of all birds in an outbreak Control and Prevention Control Suspected outbreak: Holding where the competent authority suspects the presence of influenza Warning system, send samples to reference lab, notify OiE (HPAI), investigation Bring animals inside, no materials/eggs/animals should leave the building, authorized enter to the building Count animals (dead, sick, likely to be sick), culling of animals upon confirmation, carcass disposal and disinfection Outbreak (focus of infection): Holding where influenza has been confirmed by competent authority · Protection zone: 3 km · Surveillance zone: 10 km · Entry: Active disinfectant ford · Prevention of contact with wild birds · Radical elimination of animals (slaughtering using CO2 and burning/burial - 2 m deep). · Contaminated eggs and products sent to rendering. Prevention Good hygiene practices, prophylaxis with antiviral drugs (people), vaccination, all-in-all-out systems and preventing contact with wild birds or their water sources. Hygienic filter, control of movement of man and animals, use of protective clothing, face masks, goggles, gloves and boots. Outbreaks can be controlled by rapid elimination of infected and exposed flocks, strict biosecurity measures. HPAI vaccines are not used routinely in most countries; however, nations may consider vaccination as a preventive or adjunct control measure during an outbreak. a. Sanitation measures and focal disinfection at these diseases. Hygiene of air in animal houses. Resistance Environmental survival is influenced by temperature, pH, salinity and presence of organic matter Temperature: 30 days at 4°C, 7 days at 20°C, 28 days at room temperature On eggs for 8 days Stable at pH 7-8, whereas acid kills the virus Inactivation of viruses: 70°C for 1 hour (survives freezing). By ionizing radiation or low pH (2). Sensitive to jodonals, QAS, ether. Focal disinfection Preliminary cleaning and disinfection: All parts of the farm (houses, runs...) contaminated by movement of animals or killing places. Disinfectant need to be applied for minimal 24 hours Final cleaning and disinfection: Surfaces must be cleaned using washing soda and removed by cold water Next disinfection after 7 d. Surfaces must be cleaned again using washing soda and removed by cold water. Manure and bedding: Disinfected and covered for 42 days (heating) Sludge: Storage minimum 42 days Disinfection of surfaces: 2-4% NaOH 2-4% Chlorinated lime 4-8% Chloramine T 10% Formalin 0.5% Peracetic acid Aerosol: Peracetic acid or formalin (both 25 ml/m3) Excrements: 0.3% Peracetic acid or 1.5% H3PO4 Water sources: Chlorination Rodent control: Acute, chronic rodenticides of 2nd and 3rd generations Insect prevention and control: Screens, nets on the windows Hygiene of air in animal houses Gases, dusts, liquid droplets and microorganisms - airborne particulates in animal houses are the principle risk factors for respiratory diseases Gases: A criterion of the level of hygiene in the stable - related to aerogenic infections CO2: Indicator of ventilation. 0.3% by volume Ammonia: Indicated decomposition of organic substances, 25 ppm (0.0025% by volume) Effects on the organism: Primary: Irritation of mucous membranes of the eyes, and respiratory mucous membranes Secondary: Aerogenic infections, penetration into the blood Metatoxic: Accumulation at long-term exposure, decreases immunity Hydrogen sulphide: Irritation of the mucous membranes of the respiratory tract Effect on CNS 10 ppm (0.001% by volume) Dust particles: Determination of amount and size. Microorganisms: 103-106 x m3 of the air. Evaluation of the contamination of air with microorganisms Determination of the total number of microorganisms, coliforms, fungi Quality of air MOs: Airborne disease is affected by the stocking density, animal age, ventilation system, microclimate, level of dust particles, removal of dirt Airborne diseases: Anthrax (food), bovine viral diarrhea (BVD), FMD... Bacteria: Brucella (food), Listeria (tick, rats, food), Leptospira (water, rats), Pasteurella, Salmonella (water, rats, food, insects), Q fever (ticks, rats), Tuberculosis (food, rats), on small droplets, dust particles... Airborne particulates in animal houses: Feed particles, proteins, feces, mold spores, grain, mites, insect parts. Pathogens can be transmitted by dust, aerosol to the respiratory system. Factors of their presence in animal houses: Cattle: Mycoplasma bovis - crowding, poor feeding, high humidity, stress Mastitis: E. coli, Streptococcus - contaminated bedding, poor hygiene Pigs: Diarrhea (Rotavirus, E. coli) - poor hygiene, cold stable Poultry: Mycoplasmosis - high temperature, poor ventilation, high gas/dust levels, low humidity, high density Prevention and control: Regular cleaning and disinfection of animal houses, removal of excrements, good ventilation systems, no mixing feeds in the house, good quality bedding. Way of disinfection to suppress airborne diseases: Aerosol disinfection. b. Determining the state of pathological processes (inflammation) Inflammation is the vascular and cellular response of living tissue to injury. It is a reaction of the microcirculation characterized by the movement of fluid and WBCs from blood to extravascular tissue. The role of inflammation includes the elimination of pathogenic factors and damaged tissue, border pathogenic agent and reparation and proliferation of new cells. Exudative inflammations; various diseases, various character and a huge exudate. Tissue changes: 1st-2nd day: Serosis (xerosis?) - turbidity, loss of shine, laying of fibrin floccules 6th-8th day: Fibrinous sticks, possible to detach from the underlying tissue 7th day: Mucous membranes matting, rough, bumping - formation of granulation tissue >3 weeks: Granulation tissue is of pink color, mature to fibrinous tissue From 4th week: Fibrinous adhesion Fibrinous inflammation 1-2 days: Serous surfaces are hyperemic and cloudy caused by the presence of a few leukocytes 3-4 days: Edema and desquamation of the cells on the inflammatory surface. The cloudiness of the surface is gradually depressed and small amounts of fibrin clinging to the involved surface can be seen. In some cases, the fibrin surface can be removed. 1 week: Some nodules can be found on the serous surfaces during the fibrinous inflammatory process. This is the first sign for initiation of proliferation of granulation tissue from the subendothelial layer. Microscopically, distinct granulation tissue infiltrates into fibrinous exudate which cannot be removed without removing a superficial layer with bleeding of after 1 week (?). In this period fibrinous adhesions between serosa is easy to remove. In the period of 3 weeks: Granulation tissue is differentiated into early form of granulation tissue, which is rosy and wet. Gentle fibrinous adhesions. >4 weeks: Interstitial adhesions composed from the mature granulation tissue are found at least 4 weeks later. The tissue at this stage is pale, avascular, and smaller than in the vascular stage. It is the characteristic period for scar formation Purulent inflammation: Mucous (membranes?), cavities (empyema, pyothorax, pyometra), tissues (phlegmon, abscess). Pus is different according to species; Ruminants, pigs and horses: Pus similar to human pus Rabbits and birds: Dense (like cheese) Dogs: Less concentrated and more serous Aging - based upon the migration of neutrophil granulocytes and the character of the demarcation zone around the purulent focus: 2-3 hours: Emigration of neutrophils 2-3 hours after affection of the pathogen (fresh process) 7 days: The number of neutrophils gradually decrease when the proliferation is in progress 7 days of the duration of the process 2-3 days to 2 weeks: Eosinophils appear in 2-3 days and their emigration increase till 2 weeks. After this period eosinophils gradually decrease. Basophils are detected in small amounts and have no practical significance

13. Mycosis, prevention and control, measures in outbreak, current epizootological situation. Proceeding of competent authorities in the case of disease outbreak, control and prevention

In general about mycoses = fungal infections: - The soil reservoir is the primary source of most infections - Can also be acquired by inhalation, ingestion or traumatic introduction of fungal elements Opportunistic fungi usually require a host that is debilitated or immunosuppressed to establish infection. Prolonged administration of antimicrobials or immunosuppressive agents increases likelihood of infection by the opportunistic fungi that cause diseases such as aspergillosis and candidiasis, which may be focal or systemic. Clinical findings and gross lesions are often suggestive of systemic mycoses, but definitive diagnosis requires microscopic identification, culture of the organism or PCR. Dermatomycoses Fungi that rely on keratin as growth factor; Found on skin, hair, nails. Caused by dermatophytes · Anthropophilic dermatophytes o Humans are primary hosts, causes mild inflammatory reaction, chronic in many humans · Zoophilic dermatophytes o Transmitted by contact in animals, pets. Elicit stronger inflammatory reaction in humans · Geophilic dermatophytes o Live in soil and can cause disease in animals and humans Transmission · Direct contact with asymptomatic animals or the lesions of infected animals · Indirect contact with bedding · Fungal spores can be found in dust particles and on fomites, and will persist for many years · Increased susceptibility in young, old, immunosuppressed or those with poor nutritional status Dermatophytosis - Ring worm · A superficial fungal skin disease · Most common etiological agents are microsporum spp and trichophyton spp · Contagious, infectious. Zoonotic! Common! · Self-limiting in immunocompetent hosts (within weeks-months) Species Host Microsporum canis Cat and dog Microsporum nanum Pig Trichophyton verrucosum Cattle Pathogenesis Infection à penetrates hair follicles à produce hyphae and spores à feed by enzymatically decomposing tissue. 4 stages of natural infection: Multiplication à maturation à crust formation à regression 1. Incubation. Multiplication in hair follicle. Day 7-17 2. Maturation a. Fungi grow through hair and produce spores inside the hair b. Autolysis causes hair to break off. Small round patches appear. Skin is inflamed and swollen 3. Crust formation. Patches turn scaly, flaky, covered by crust = parakeratosis. Day 28-49 4. Regression. Takes 1-4 months before lesions are self-limiting. Pruritus can be present or absent. When present, self-mutilation and introduction of bacteria in wound is common and problematic. Clinical signs Are as mentioned the lesions. Predilection site is head, neck, limbs. Alopecia in affected area. Diagnosis Woods lamp - UV light that fluorescence on the fungi of Microsporum canis o Due to metabolite present in hair shaft. Debris, scales of and around infected area - Fixed in KOH seen under microscope Culture fungi on Sabourad agar (21d) Also a special dermatophyte agar that can be used (6-7d) Treatment Large animals: Thiabendazole, lime-sulfur baths (for 3-8 weeks), iodophors. Small animals: Myconazol or clotrimazole. Systemic therapy with Griseofulvin in severe cases. Preventive measures, prophylaxis Some European countries have live vaccines (M. canis and T. mentagrophytes). Preventive measures for pet owners include food personal hygiene (zoonotic), regular diagnostic testing and/or repeated proper treatments. Systemic mycoses (aspergillosis, candidiasis) In systemic mycoses the fungi have infected internal organs. How does it happen? Patient is immunosuppressed, stressors (overcrowding, poor nutrition) - fungi enter body (lungs, gut, paranasal sinuses, skin) - via bloodstream it reaches organs - multiple organ failure and death can follow. · Blastomycoses - candidiasis (and other) · Hyphomycoses - aspergillosis (hypha has real septa) (moulds) · Phycomycoses - (hypha has not real septa) Aspergillosis in birds (mould) · fumigatus, flavus, niger · Opportunistic pathogen o In immunosuppressed individuals or when large quantities of aerosol spores are inhaled · Higher incidence in poor hygiene, warm, humid, dirty, dusty environments with little ventilation · Most infections are aerosol routes and occurs in lungs, air sacs and upper respiratory tract · Eggs can be infected and embryo killed, when fungi colonize shell and penetrates through pores Clinical signs Respiratory signs include dyspnea, tail bobbing, tachypnea, gaping, voice change. There can also be anorexia. In chronic case signs include cyanotic wattle, yellow feces, anaemia. Necropsy shows granulomas of air sacs and in body cavity, as an attempt to stop the disease. Diagnosis Fungi can be isolated and grown on Sabourad agar. ELISA test on blood to detect antibodies. Aspergillosis in mammals can have grey-yellow lungs with pea-sized nodules on them. It can have a reproductive significance: Aspergillus reach placenta and can causes abortion (mycotic abortion) Aspergillosis in cattle: A.fumigatus, A.niger, A.nidulans, A.flavus = ASPERGILLOSIS OF THE RESPIRATORY SYSTEM Clinical signs: cough, kachexia, dyspnoe. Necropsy: Peanut caseous nodules with yellow content in lungs. Candidiasis - candida albicans In general Often presented as a secondary infection after antibiotic treatment. Occurs because AB has removed also commensal bacteria that help suppress the growth of fungi. · Mucus membrane - thick, white coat, cheese pseudomembrane. Inflammation o Oral lesions - white crusts (à stops eating à crop stasis à problem) o Vaginal - white, creamy discharge, white coating on walls · Skin o Folliculitis, moist red lesions (papules, vesicles) covered with white crusts Candida in birds "sour crop" · Common in birds, both exotic, pets and poultry · Candida albicans · Mostly related to poor husbandry, unsatisfactory hygiene · Most common in young birds In adult birds - mild disease, may include mild weight loss and dull plumage In young birds - white plaque in oral cavity, anorexia and thus crop stasis. Regurgitation and weight loss. Severe infection in young birds can cause complete stasis in crop and GIT. Diagnosis: Finding the fungi has little value (ppt says). Smears taken and native or stained perform cytology. Control: Isolation, treatment (topical and/or systemic antifungals - NB! Liver damage), clipping of hair coat, cleaning and disinfection of the environment, rodent control elimination of the source and prevent access to infected soil. Prevention: Proper husbandry and sanitation (prevent immunosuppression), quarantine/isolation, vaccination, good personal hygiene, rodent control, treatment of infected animals, do not touch skin lesions (gloves), improve animal hygienic conditions (humidity, density, etc.). Prevention of personnel: Personal hygiene, disinfection of the environment and equipment, wash clothes in hot water with fungicidal soap, avoid sharing clothes, use protective footwear, avoid touching pets with bald spots. a. Sanitation measures and focal disinfection at these diseases. Application of the acids in disinfection practice. Sanitation measures, focal disinfection Fungal species are extremely resistant in the environment Removal of hair is important as spores may survive for 12 months (or even 2 years) on hair clinging to surfaces Elimination of fungi in case of pets: - Wash the household's hard surfaces with sodium hypochlorite bleach solution (effective in killing the spores), but this is too irritating to be used on hair and skin - For the pets themselves; fluconazole and itraconazole and lime sulphur dips. Disinfection: Peracetic acid (1%. And 0.2% in the presence of animals, or in case of skin treatment), alkaline formalin (3%), mycolastanox (0.5%). Important to mechanically remove material containing keratin (skin, nails, hooves, hair). Application of acids in sanitation practice Inorganic and organic acids. Acids are the strongest disinfectants. Inorganic acids: Strong corrosive effect Hydrochloric acid (HCl) 2.5% + 15% NaCl is used for skin contaminated with anthrax spores Sulphuric acid is used in the form of a sulphuric acid : cresol mixture (1:3 - three parts cresol mixed with one part sulphuric acid) is used for focal disinfection (tuberculosis, clostridium). Nitric acid (HNO3) 0.3-0.5%; Used in the food industry (milking equipment). Phosphoric acid: Manure, soil (not mentioned in the book) Organic acids: Less corrosive. Lactic acid - aerosol - used for disinfection of air; 10-15 mg/m3 air Peracetic acid (CH3COOOH). Corrosive, unstable. Bactericidal, viricidal, sporicidal and fungicidal effects. Effective at low temperature. Preventive disinfection: Low concentration is used 0.1-0.5%. Focal disinfection: 1% is used. Persteril: Contains minimum 15% peracetic acid Pedox: 30% peracetic acid Lactic acid and peracetic acid can be used in the presence of animals. Acetic acid (CH3COOH); concentrated (95% glacial acid) - corrosive to skin and lungs. Household vinegar (4-5% acetic acid by volume). Spraying, misting of immersing items. Mechanism of effect: o Oxidation: Linked with the pH. Dehydration: Of viruses and fungi. Destruction of enzymatic systems b. Occupational diseases and objective liability for them The term "occupational disease" covers any disease contracted as a result of an exposure to risk factors arising from work activity. Definitions, however, have two main mandatory elements in common; Causal relationship between exposure in a specific working environment or work activity and a specific disease; and the fact that the disease occurs among the group of exposed persons with a higher frequency rate than in the rest of the population, or in other worker populations. Definitions concerning occupational and work-related diseases Reportable occupational diseases: Occupational diseases mentioned in national list as part of national laws or administrative provisions liable for compensation and subject to preventive measures. Reported occupational diseases are reportable diseases already passed through the legally required reporting process. Recognized occupational disease: A recognized case of an occupational disease is a case accepted as such by a competent national authority in an administrative proceeding. Work-related diseases: All illnesses that can be caused, worsened or jointly caused by working conditions. · A case of work-related illness does not necessarily refer to recognition by an authority, whereas occupational diseases have a specific or a strong relation to the occupation, generally with only one causal agent while work-related diseases have a complex etiology. · Among their multiple causal agents, factors arising from the work and/or working environment play a role in the development of such diseases · A more precise distinction between occupational diseases and work-related diseases can be made by evaluating their attributable fractions. o It is suggested that the attributable fraction is >50% for occupational diseases and <50% for work-related diseases Occupational diseases caused by exposure to agents arising from work activities: · Diseases caused by chemical or physical agents · Biological agents and infectious or parasitic diseases Occupational diseases by target organ system: Respiratory diseases Skin diseases Musculoskeletal disorders Mental and behavioral disorders Occupational cancer and other diseases. The occupational safety and health convention: The provisions of the Protocol, state that the competent national authorities shall establish and review requirements for the recording and notification of occupational diseases. The requirements shall determine (among others); · The responsibility of employees to keep records on occupational diseases · The use of these records to establish preventive measures at the workplace · The maintenance period of these records · Measures to ensure the confidentiality of personal and medical data · The responsibility of employers to notify the competent authorities To provide appropriate information to workers and their representatives concerning notified cases

35. Leishmaniosis, prevention and control, measures in outbreak, current epizootological situation. Proceeding of competent authorities in the case of disease outbreak, control and prevention

Leishmaniosis Species of genus leishmania are parasites of mammals and humans, have an indirect (heteroxenous) life cycle and are transmitted cyclically by sand flies (phlebotaminae), it is an obligate vector-borne disease and it is widespread in tropical, subtropical and temperate regions. OiE notifiable disease Morphology and location Exist in 2 forms, in the mammalian host, the parasite exists in an amastigote form in the cells of the mononuclear phagocytic system (macrophages, monocytes, Langerhans cells) and in the promastigote form extracellularly in the intestine of the insect vector. Amastigotes when inside host, intracellularly: ovoid organisms, which possess a rod-shaped kinetoplast associated with a rudimentary flagellum. The promastigote has an elongated ovoid cell body with a long motile flagellum. Hosts Occurs primarily in mammals, but may also occur in lizards and are transmitted by sandflies of subfamily Phlebotominae: genus Phlebotomus in the Old World and genus Lutzomyia in the new world. Clinical signs 1) Cutaneous leishmaniosis: Affect skin, cause skin lesions, nodules and ulcers. After inoculation the agent remain at site where it attracts macrophages, causing inflammation and destruction of tissue at site. Usually painless with swollen lnn near sores, can heal as a scar with dark pigments, IP = 2 weeks 2) Mucocutaneus leishmaniosis: similar to cutaneous form, but affect the mucosa. Partial or total destruction of MM of nose, mouth and throat. 3) Visceral leishmaniosis (black fever): fatal if untreated, affect reticuloendothelial system, causing hepatomegaly, splenomegaly, lymphadenopathy, anaemia, fever and weight loss. IP = 2-6 m. Main species Various leishmanial species and strains are morphologically indistinguishable and are often referred to as "species complex". Their differentiation is based upon biological criteria (clinical picture, host, vectors) and molecular characteristics. In humans, leishmanial species cause different forms of disease, which can be roughly classified into 3 main groups · Visceral leishmaniosis (most dangerous): l.donovani, l.infantum, · Cutaneous leishmaniosis (most widespread): l.tropica, l.major · Mucocutaneous leishmaniosis: l.mexicana Leishmania infantum- Lieshmanosis in dogs Life cycle In the vertebrate host, L. infantum infects cells of the mononuclear phagocytic system, in which they multiply as amastigotes. During a blood meal, female sand flies acquire leishmanial amastigotes. In the midgut of the insect vector, amastigotes transform to promastigotes, which multiply intensively by binary fission. The metacyclic promastigotes are transmitted during the next blood meal to a new mammalian host. In the skin, the promastigote stage is phagocytised, turn into its amastigote form and multiply by binary fission. After the multiplication, the cell disintegrates and release the parasite, which then can infect new cells in various organs. Pathogenesis Leishmaniosis is transmitted by sand fly. Only females feed on blood and they are most active at dawn, dusk and during night. After inoculation of promastigotes by vector, a primary reaction occurs (nodule formation, inflammation) in the skin. Recruited macrophages are infected and spread the parasite to other organs (lymph nodes, spleen, liver, bone marrow, etc.). This cause widespread inflammation and organ damage. Clinical signs · Visceral form: clinical signs develop gradually during a chronic course, ranging from low-grade lymphadenopathy to severe visceral disease. The main sings include apathy, spleno-and hepatomegaly, fever, renal insufficiency, diarrhea, muscle atrophy, osteolysis, espistaxis, etc. · Cutaneous signs: skin lesions (start on head), alopecia, nodules, pustules and excessive growth of claws. · Dermatological: (start head) muscle atrophy, excessive scaling, massive loss of hair and cachexia. Treatment Most cases heal without treatment (cutaneous)- other forms are very difficult to treat (long course + relapse). - Humans: pentavalent, antimonials - Dogs: not possible to cure. Parasitaemia and clinical signs can be decreased by milteforan, glucantime, allopurinol Diagnosis Diagnosis is based on anamnesis, clinical signs, detection of specific serum antibodies, detection of parasite in lymph nodes or bone marrow. · Direct confirmation: amastigote in smears from skin scrapes, biopsy, bone marrow aspirates · Serology: ELISA, IFAT, western blot, direct agglutination assay · Delayed hypersensitivity test (leishmanin skin test): intradermal inoculation of leishmanin in humans · PCR Epizootology Worldwide prevalence, being most active from June to September and endemic in subtropical and tropical area (areas where the sand flies are present), mostly include South and Central America, Africa and Middle East. Major risk factors: poverty, malnutrition, poor housing, weak immune system, open sewers, overcrowding, HIV co-infections, environmental changes and climate changes It is estimated that 12 million cases worldwide exist and 1-2 million new infections occur each year. - Cutaneous leishmaniasis: Most common form, 95% of cases occur in Americas, Mediterrian area, Middle East and Central Asia. 600 000 to 1 mill new cases worldwide annually. - Mucocutaneous leishmaniasis: 90% of cases occur in Bolivia, Brazil, Ethiopia and Peru. - Visceral leishmaniasis: Fatal if left untreated in 95% of cases. Most occur in Brazil, East Africa and India. 50-90 000 cases worldwide annually, but few (25-40% cases) reported to WHO. Prevention of competent authority, control and prevention 5- pronged approach (WHO) 1) Facilitation of early diagnosis and prompt treatment 2) Support for control of sand fly population through residual insecticide spraying of houses and use of insecticide-impregnated bed nets 3) Provision of health education and production of training materials 4) Detection and containment of epidemics in the early stages 5) Early diagnosis and effective management of leishmania/HIV co-infections Control Control methods are divided into 2 groups 1) Methods aimed at infectious dogs (direct control measures) - To identify what dogs should be subjected to control methods - Dogs in canine leishmania endemic regions should be divided: sick and healthy dogs è Removal of positive dogs (euthanasia) è Anti- leishmania dog vaccine: only licensed in Brazil 2) Methods aimed at vectors (indirect control methods) - Prevention of sand fly bites: insect repellents (synthetic pyrethroids, permethrin, deltamethrin), collars, sprays and spot-ons (anti- feeding or insecticide effect) - Prevention of sand fly bites in dogs also reduce the risk for human infections - Movement control Prevention · Health education and protection: avoid sandfly bite - nets, repellents or insecticides · Vector control · Stray dog control · Keep susceptible animals indoor between dusk and dawn · Killing symptomatic and sero+ dogs (uneffective)- nonsympt. dogs + wild canids are source of inf. · Vaccination a) Sanitation measures and focal disinfection at this disease. Main groups of insecticides Leishmanias are unable to form cyst, thus cannot survive free in the environment. This makes focal disinfection unnecessary as the disease is strictly vector borne Main approach is to reduce the reservoirs of infection and the presence of the sandfly. 1. Protection of dogs: control of stray population, vaccination 2. For man: repellents, wear long sleeves tucked in shirts long, pants, shoes, boots and hat. 3. Vector control: traps, screens, insecticides. Main groups of insecticides 1) PYRETHRUM: · From flower Chryzantenum, natural, not stable on light (hm,ja?) · Contact, rapid knock-down effect on flying insect, low toxicity to mammals, short residual effect. · Commonly used as an aerosol spray. 2) SYNTETIC PYRETHROIDS: · Synthetic, rapid knock-down effect, contact, stomach, low toxicity to birds and mammals, but toxic to fish and bees. · They are degraded rapidly in the soil. Sodium channel blockers - Axonic poisons (disruption of axonal transmission), affect both peripheral and CNS. Long lasting residual effect. · Resistance to synthetic pyrethroids may develop in insect - rotating various pyrethroids and other insecticides. · May be used in public health and industrial pest control, grain protection and in horticultural and agricultural crop protection. · Allethrin, Cypermethrin, Deltamethrin, Permetrin 3) ORGANOPHOSPHATES: · Synthetic, contain phosphorus (Bromophos, Diazinon, Dichlorvos), stomach, contact, respir. · Many working as systemic insecticides. · Cholinesterase inhibitors: paralysis nervous system. · Short residual effect, high efficiency, low toxicity to man. Act as systemic insecticide, rapid degradation in the soil. 4) CARBAMATES: · Cholinesterase inhibitors, Long residual effect. Act as systemic insecticide, rapid degradation in the soil. Most are solid substances used as dusts or surface sprays. · Longer lasting residual effect: Carbaryl, Pirimicarb · Fumigants - gases or volatile liquids · Respiratory poisons, empty building of animals: Hydrogen cyanide, Methyl bromide, Hydrogen phosphate, Sulphur dioxide · Repellents, attractants, chemosterilants and hormones to prevent maturity. b) Killing an animal from the cause of self-defence and extreme urgency Self Defence Is the defence of one person or interests, especially through the use of physical force, which is permitted in certain cases as an answer to a charge of violent crime. - A person claiming self-defence must prove at trial that the self-defence was justified - A person may use reasonable force when it appears reasonably necessary to prevent injury - A person using force in self-defence should only use so must force as is required to repel the attack - A person who is under attack should attempt to retreat or escape, but only if an exit is possible Extreme Urgency Any offence punishable by any person directly threatening the interest protected by this law, is not a criminal offence. It must be a diversion of a danger. Danger may be caused, for example by natural forces (earthquakes, floods etc.) can even be cause by the animal (the exception is the situation where the animal is to be coursed), but also can lead to human action,

8. Pasteurellosis and yersiniosis, prevention and control, measures in outbreak, current epizootological situation. Proceeding of competent authorities in the case of disease outbreak, control and prevention

Pasteurellosis Pasteurella spp. Gram negative, multiple shapes (pleomorphic), facultative anaerobic, cause of primary and secondary infections. Naturally found in humans and animals à disease appears in immunocompromised individuals RESPIRATORY TRACT DISEASE! · Ship o hoi Pasteurella multocida- respiratory disease and septicemia · Pasteurella hemolytica - pneumotic pasteurellosis (in sheep) Bovine respiratory disease - "shipping fever" in calves Pasteurella A multifactorial disease. Bacterial species involved are Pasteurellamultocidaand Pasteurellahemolytica(mannheimia hemolytica). Etiology When large groups of calves coming from different geographical, nutritional and genetic backgrounds are assembled together into feedlots. Peak morbidity 7-10 days after assembly. Stress factors are thought to play a role, including weaning, transportation, exhaustion and a new surrounding. Pathogenesis Disease occurs when the host immunity is compromised, for example during · Viral disease · High stress situations (stress factors mentioned above) The commensal bacteria of the upper respiratory tract are allowed to freely replicate and multiplies at a high rate. After some time, they move to the lower respiratory tract and bronchopneumonia is produced. Clinical signs · Peracute: sudden death, severe resp. failure · Acute: Anorexia, dyspnoe, depression. Ocular and nasal discharge, fevere > 40C. spesific sound on ascultation · Chronic: Normal appetite, chronic cough, recurrent pneumonia Haemorrhagic septicaemia- cattle, sheep, pig Caused by Pasteurella multocida manifested as an acute and highly fatal septicaemia of cattle, sheep and swine. Pathogenesis The initial site of proliferation is the tonsils. From there, septicaemia develops rapidly and death occurs due to endotoxemia. There is widespread haemorrhages and edema. The endotoxin of Pasteurella multocida cause fever, changes in WBC counts, activation of inflammatory mediators (can destroy endothelium DIC), disseminated intravascular coagulation, hypotension, shock and death. Clinical signs Not present or nonspecific due to the rapid course of the disease. Fowl cholera (not like cholera in humans) · Pasteurella multocida · Zoonosis · The most common pasteurellosis of poultry · Adults and old are most susceptible · When disease has entered a flock, it will not be removed until culling · High morbidity and mortality · Can easily be removed from environment by disinfection!! Transmission Oral or nasal by transmission of nasal exudate, feces. Also indirect by infected bedding, soil and equipment. Pathogenesis and clinical signs Acute form: Find dead birds. Fever, depression, anorexia, rough plumage Chronic form: Accumulation of fibrinosuppurative exudate causes swollen wattle, joints and footpads. Can also see torticollis and exudate from eyes Diagnosis Bacterial cultivation from swabs of viscera Impression smear of liver with Giemsa stain PCR and serology (agglutination tests, ELISA). Pasteurellosis in rabbits Many pet rabbits suffer from respiratory disease by Pasteurella multocida. Mostly rhinitis, but lower respiratory tract can also be affected. Pathogenesis The initial site of proliferation is the tonsils. From there, septicaemia develops rapidly and death occurs due to endotoxemia. There is widespread haemorrhages and edema. The endotoxin of Pasteurella multocida cause many pathophysiological reactions. Clinical signs Conjunctivitis can also occur. Sneezing, discharge, wet face. · Acute form is characterized by a rapidly fatal septicaemia · Chronic form respiratory lesions like fibrinopurulent bronchopneumonia, pleuritis and pericarditis. Swine pasteurellosis Disease in swine depends on which strain of Pasteurella multocida is present. Nontoxigenic strains are the predominant isolates from cases of pneumonia. Toxigenic strains are associated with atrophic rhinitis Pathogenesis · Pneumonic pasteurellosis: Associated with other resp. disease. P. multocida spread to the lungs, multiply and produces exudative bronchopneumonia, sometimes with pericarditis + pleuritic pneumo. In piglets, the bacteria enter the bloodstream where it either multiply rapidly or localise in the liver and spleen where initial multiplication occurs before a massive bacteraemia. Meningitis is occasionally observed · Atrophic rhinitis: Bordetella bronchoseptica adhere to the nasal mucosa, probably by attaching to the ciliated epithelial cells. It produce a toxin that diffuses into the turbinates and cause osteopathy and hypoplastic rhinitis. Toxigenic P. multocida colonizes the nasal mucosa and produce a potent toxin that causes a rhinitis with progressive osteopathy of facial and turbinate bones. Clinical signs · Pneumonia: coughing, dyspnoea, fever and prostration. Swine with well-developed pneumonia or extensive adhesions between lungs and rib cage often have a marked expiratory lift ("thump"). · Atrophic rhinitis: sneezing, snorting and a serous or mucopurulent nasal discharge are early signs of AR. Yersinioses (yes eg e inni'a! Intracellular enteropath) Yersinia genus. Family Enterobacteriaceae, gram negative, facultative anaerobic. Orofecal route or vector. - Yersinia enterocolitica: most important cause of yersiniosis in animals. Zoonotic - Yersinia pestis: characterised by septicaemia, pneumonia and bubonic plagues - Yersinia pesudotuberculosis: Low pathogenicity. May cause pyogranulomatous lesions in cats 1. Yersinia enterocolitica · Most important cause of yersinosis in animals à pigs and cattle are main · Zoonotic · Intracellular pathogen · Not pathogenic in dog and cat Transmission Fecal-oral route: Ingestion of contaminated feed, water and bedding. Humans by ingesting undercooked meat and unpasteurized milk. Pathogenesis Ingestion à Yersinia colonize ileum and colon à virulent Yersinia attach to and penetrate into intestinal cells. They prefer M cells of the Peyers Patches. Once inside these enterocytes à Yersinia is taken by phagocytes à Yersinia replicate inside macrophages and thus transported to lnn à triggering inflammation. Once inside macrophages and disseminated to lnn, liver, spleen à Yersinia continue replication extracellularly and produce small abscesses à inside abscesses bacteria replicate further. (Prøv å huske at yersinia lager byllepest og derfor er det naturlig at det blir abscesses også her) Clinical signs No clinical disease in adult pigs and cattle. However in piglets there is - Watery diarrhea - Dehydration, weightloss, weakness - If not treated (antibiotics) it can be deadly. Diagnosis Necropsy micro-abscesses Clinical signs and rectal/fecal swab culture. In dead animal, sample can be taken from lnn, blood 2. Yersinia pestis (svartedauden) - bubonic plague (bubo = inflammation of lnn) · Plague/black death · Zoonotic · Primarily a pathogen of rodents, accidentally transmitted to other via flea bites · Inhalation of aerosols from infected humans transmits disease to other humans · Virtually all mammals can be infected via flea bites Pathogenesis Yersinia inoculated during flea bite à ingested by macrophages à survives inside macrophage and multiplies à infected macrophage travel to lnn causing ds. à also go to the liver and spleen. Macrophage lysis à bacteria grow extracellularly in parenchymatous organs (lnn, liver, spleen, lung). Especially in the lnn, they replicate and cause buboes (black, inflamed lnn) which is hot, swollen, hemorrhagic and painful and typical for disease. There is now bacteriemia which can develop to septicemia and death. Clinical signs · Non-specific: Malaise, depression, vomitus, diarrhea, dehydration, fever, enlarged lnn, soreness · In septicemic cases there is shock and death · Not all courses of disease has buboes Diagnosis Typical lnn changes upon necropsy - Smears of buboes or sputum à Giemsa stain à see bipolar "safety pin" rods - Serology for antibody detection Prevention and control Control · Pasteurella: Culling of affected animals in breeding colonies. Treatment is difficult and may not eradicate the organism. ATB are temporary remission (next stress may cause relapse). Vaccines have been used but efficacy appears to be low (cattle). · Yersinia: Isolate and treat affected animals or humans (prevent spread within population). Yersinia pestis is a notifiable disease. · Focal disinfection, quarantine, movement restrictions, tracing activity Prevention · Vaccination - Pasteurella: not all are effective, intra-nasal vac for rabbits is in development but is not commercially available - Yersinia: none for domestic animals but vaccination for adults at high risk (severe inflammatory reactions are frequent and its only protective against bubonic form) · General - Pasteurella: proper husbandry, prevention of stress, remove carriers - Yersinia: flea prevention in endemic areas, decrease rodent habitat, wear gloves a.) Sanitation measures and focal disinfection at these diseases. Methods of rodent control Survival Pasteurella survive for a few days in the environment, but up to 3 weeks in water. Yersinia can survive months in organic matter. Sanitation · Pasteurella (aerosol): Chloramin T (2%), NaOH (2%), formaldehyde (0,5%), peracetic acid (0,5%), slaked lime (20%). Aerosol disinfection, temperature over 60°C kills in several minutes. · Yersinia: vector control, Chloramin T (4%), formaldehyde (2%), NaOH (2%), peracetic acid (0,5%). Manure composting, disinfection of water. Methods of rodent control 1) Mechanical - Snap traps, live traps, electronic traps. è Benefits: reduce use of rodenticides, rodents do not die in wall or feed storages è Disadvantages: need to be checked regularly, less rodents are caught 2) Physical - Close all holes and gravel 3) Biological - Dogs, cats and ferrets- banned in food places. Encourage birds of prey to nest at site 4) Chemical - Acute rodenticides: Zinc or aluminium phosphide: pre- baiting - Subacute: Vitamin D - Chronic: anticoagulants (1. Warfarin, 2. Brodifacoum, 3. Difethalone) b.) Litigation (prosedyre) in cases of the purchase of animals, food and feedstuffs, products of animal origin (responsibility for defects of the sold item) · Civil code legislation distinguishes between the liability for defects which the product had at the time of purchase and the responsibility for defects which occur during the warranty period. · Agreeing to the purchasing agreement is understood to mean that the item being sold is without defects, and that it is of such a quality and has such properties as the manufacturer state in the purchase agreement or the products advertisement. · It must be of such quality and properties that are normally expected for the time, be of the required quantity, dimension or weight and the item must correspond with either the purpose claimed. The scope of the liability of defects (Omfanget av ansvar av defekter) · When the item being sold is new: vendor is responsible for all defects, which are in conflict with the agreement and which occur within the warranty period. · The warranty period is set at 24 months. The warranty period can be contractually extended beyond the statutory time. · If the defective items are sold at a discount: For defects of either new or used goods where the item's price was decreased, the vendor is not responsible if the sale occurred. (Items with defects, which do not hinder the normal use). · With used items the vendor carries no liability for defects that occur after purchase. The vendor is responsible for only the defects that were present during the sale of the item. · If the item is discounted below the usual price as a result of a sale or post-seasonal sale, it is significant if the item being sold is new and defect-free, and not a used item; the vendor is responsible in full for all defects. Liability for damage caused by defective product vs liability of defect · The liability for defects of a sold item is distinguished from the claim based on the liability for defects that cause damage to the consumer's health or property. · The application of the liability for defects is an attempt to address the situation where the consumer paid the full purchase price but did not acquire the product stipulated by the purchase agreement and obtained a defective product and in this way was "injured" up to the maximum amount of the purchase price. · This, however, may lead to a further claim, if the defect to the purchased product caused damage to another party (which does not necessarily have to be the purchaser, and can lead to damages far in excess of the purchase price).

23. Poxviral infections, prevention and control, measures in outbreak, current epizootological situation. Proceeding of competent authorities in the case of disease outbreak, control and prevention

Poxvirus infection Poxviridae family One of the largest viruses DNA viruses Makes specific, typical lesions that has same development and stages in all diseases 2 subfamilies; Chordopoxvirinae and Entomopoxvirinae. We only speak about spp in Chordopoxvirinae; - Orthopoxvirus (cowpox, smallpox) - Suipoxvirus - Leporipoxvirus (myxomatosis) - Avipoxvirus (fowlpox) - Parapoxvirus (bovine popular stomatitis- zoonosis). - Capripoxvirus (sheep pox) Etiological agent - Smallpox (variola virus) is human poxvirus. It has no animals involved, no vectors/reservoirs. Therefore, it was eliminated in 1979 (vaccine = vaccinia = from a cow. Hence name of vaccine and poxvirus) - Cowpox (variola vaccinia) is poxvirus in animals including cattle. It produces the typical lesions on skin, lip, udder, teat and scrotum. Vaccine against smallpox was development when Jenner realized milk maids did not contract the disease à injected kids with fluid from cow pox vesicles, humans developed immunity. - Cats often contract cowpox. We are most worried about secondary infection of the ruptured vesicles! - Capripoxvirus in ruminants. Among the most serious poxvirusinfections in animals. OIE notifiable. Genus contains 3 species · Sheep-pox virus · Goat-pox virus · Lumpy skin disease virus LSDV - Avipoxvirus Transmission - Aerosol after close contact with severely affected animals with ulcerated papules on the mucous membranes - There is no transmission in the prepapular stage (before skin papules) - Indirect transmission by contaminated vehicles occurs - Chronically infected carriers do not occur (develop strong immunity) - LSD, fowl pox, myxomatosis are transmitted mechanical by arthropod vector (flies/mosquitoes). Diagnosis - PCR - Virus isolation in cell culture - Antigen by immunoperoxidase or immunofluorescence staining techniques - Serological testing includes virus neutralization test, IFA, ELISA. Samples from live animals: Full skin thickness biopsies, vesicular fluid, scabs, skin scrapings and lnn aspirates. Myxomatosis Myxomatosis is a fatal viral disease of wild and domestic rabbits caused by the Leporipox virus (poxviridae). The virus is originally from South America, and when introduced in Europe, caused a rapid decrease of the rabbit population. Affected rabbits develop skin tumors, and in some cases blindness, followed by fatigue and fever. The disease is mostly fatal. OiE notifable Pathogenesis Infection by insect vector (fleas, mosquitos) mostly. Tumor development at site of dermal inoculation. Viral replication is also here. It is taken to regional lnn and is spread in lymph and blood à viremia. By this, virus is spread to all organs in the body. Typical site for lesions is orifices; Anus, mouth, eyes. There are 3 known forms of disease manifestation: · Acute Form: Edema of head, eyelids and genitals, followed by the appearance of myxomes. This form is usually fatal and death occurs within 14 days · The chronic, nodular form shows edematous swellings called pseudotumours which develop after 10-15 days on the ears, nose and paws and is not so fatal (<50%), but mean survival time is 40 days. Lesions develop into hard scabs which heal into scars. · A specialised form is seen in Angoras which have been vaccinated and then depilated: Lesions can be found on the torso after vaccination and are considered to be a type IV hypersensitivity Clinical signs After skin nodules have developed, there is more generalized infection with swelling of eyes (big head) and genitals, and secondary infections occur. At the same time there is immunosuppression and pneumonia and accommodating rhinitis, coughing is often present. Disease progress and animal is in general bad state Pneumonia often develops and death after 14 days in the most pathogenic strains Respiratory form has no lesions! Treatment None? Epizootiological situation Mild disease in original hosts native to South America, but aggressive disease in Europe. Measures during outbreak Kill sick animals, remove safely Prevention, control Vaccines are used for farmed/pet rabbits in the UK Insects/ mosquito protection! When infection occurs, isolation of the infected animals is necessary to prevent the disease from spreading to other animals. Lumpy skin disease virus Poxvirus infection in cattle. Subfam chordopoxviridae. Genus Capripoxvirus, lumpy skin disease virus. Virus is very stable, surviving in environment for a long time. Survives particularly well inside scabs. Pathogenesis Infection by insect vector (fleas, mosquitos) mostly. Tumor development at site of dermal inoculation. Viral replication is also here. It is taken to regional lnn and is spread in lymph and blood à viremia and lymphadenopathy. Clinical signs include: Systemic signs High fever develops Depression, emaciation, enlargement of all superficial lnn, agalactia (economic importance!) Abortion Cutaneous signs Up to 5 cm Ø painful nodules appear all over the bodyParticularly on head, neck, udder, perineum Nodules are deep and penetrates into dermis too - hide is ruined (economical importance!) The nodules ulcerate and secretions contains virus (contact transmission) The pox-lesions can also develop in oral mucosa, GIT and on the lungs, and cause pneumonia and open up for secondary infections. Treatment Epizootiological situation Morbidity rate varies between 5 and 45%. Mortality rate is up to 10%. Hosts include domestic cattle and some African wild animals. The disease is mostly limited to Africa. Measures during outbreak Prevention, control Animals that recover from one capripoxvirus infection generate a lifelong immunity that protects them from subsequent reinfection with any Capripoxvirus. If country is free from disease, they should not import. If country has disease, they should use quarantine. Vector control! Slaughter all sick and infected animals and incinerate. Pathogenesis - RT à lymph/blood à MPS à skin, mucosa Transmission is close contact between sick animals, by aerosol route. Transmission only when vesicles has developed! Also, less transmission when vesicles have become necrotic. Virus replicates in epithelial cells of upper and lower RT à induce a strong immune reaction (damage) à disseminated in blood and lymph throughout the whole body à viremia à intense replication inside macrophages and monocytes àvirus reach skin and mucosa. Clinical signs Early clinical signs include fever above 40°C, loss of appetite, papebral edema, secretions from orifices. Skin lesion stages: Pink red spots (stadium erythematosum) in hairless zones, which rapidly transform into round or oval papules (stadium papulosum). These create vesicles (stadium vesiculosum) characterized by blisters that after several days form yellowish, round crusts (stadium crustosum), which in the end is followed by the desiccation of the pustule (stadium decrustations). Acute phase: within 24 hours after papules. Affected animals develop rhinitis, conjunctivitis and enlargement of all superficial lymph nodes. Papules ulcerate, creating mucopurulent discharge. Mucosae of the mouth, anus, and prepuce or vagina become necrotic. Treatment, prevention, control Sanitary prophylaxis. Slaughtering of infected herd and proper disposal of cadavers and products stringent disinfection. Can survive for many years in dried scabs at ambient temperatures. Virus remains viable in wool for 2 months and- in premises for as long as 6 months. Epizootiological situation Sheep pox and goat pox are endemic in Africa north of the Equator, Middle East and Asia. Some parts of Europe have experienced outbreaks recently (2017). Morbidity rate in endemic areas 70-90%. Mortality rate in endemic areas 5-10%. Measures during outbreak Kill sick animals. Avipoxvirus The fowl pox virus produces 2 forms of disease; Dry (pox) and wet (diphteria). Again, virus is very resistant and survives a long time, especially inside scabs. Worldwide occurrence. Dry form. More typical pox virus with skin lesions. Spread by biting insects Wet form. Thick (diphteric) membrane of oral and RT mucosa. Spreads by inhalation Transmission is via - Scabs or lesions come in contact with lacerated skin - Biting insects - Inhalation (aerosols) Pathogenesis Inoculation site - lnn - viremia - whole body. The virus will replicate in skin/mucus membrane where it entered the body. From there it is carried to regional lymph nodes, which gives access to the blood and whole body. Clinical signs Dry form (fowl pox) Lesions are like the common pox virus lesions; Erythema becomes risen and filled with fluid and pus, and then a thick, dark scab develops. - Lesions around nostrils - nasal discharge - Lesions around eyes, eyelids - complete closure of eyes Usually birds recover from this disease and maintain normal production after. Low mortality. Wet form (diphteria) Lesions develop in mucus membrane of mouth, esophagus, pharynx, larynx and trachea. Diphteric membranes often develop and they severely interfere with feeding and breathing. In the end, there may be death due to suffocation. Mortality is much higher and many do not recover on their own. Epizootiological situation Measures during outbreak Prevention, control Control primary vector (mosquitoes). Feeders, waterers, birdbaths and cages should be decontaminated a 10% bleach solution. Vaccine is recommended, especially in endemic areas. Disease develops slowly, therefore vaccination can be done in a flock even after infection has occurred. 1 week after vaccination, check if chicken have scab/lesion - they should have it! If not, the vaccine lacked potency, vaccination was wrongfully done or the chicken have immunocompetence already. a. Sanitation measures and focal disinfection at these diseases. Main group of preparations for insect control. Sanitation measures in diseases Poxvirus infections in general Housing: NaOH (2%), peracetic acid (0,5%), Chloramin T (4%), formalin (1%) Slurry: 3% lime Soil: peracetic acid (0,3%), lime (3%) Bird housing equipment: bleach (10%) Protection - Limit direct contact between people and infected animals, bedding, personal hygiene, using of protective clothing, gloves, goggles, masks. - Rat and insect control Main group of preparations for insect control: Plant derived - Pyrethrum: Rapid short time in environment, contact insecticide. - Alkaloids: Contain morphine, cocaine, strychnine. Nicotine affects the nervous system à paralysis, death - Rotenoids: Important against aphids, caterpillars, wasps and sawflies. Synthetic Insecticides - Synthetic pyrethroids: Affects sodium channels, bad for bees and fish. Allethrins and Esbiothrin. - Organophosphates: Cholinesterase inhibitor, floods synapse dies due to overstimulated nervous system. They kill a variety of animals and act as stomach, contact and respiratory poisons. Short residual effect. - Carbamates: Cholinesterase inhibitor that result in convulsions and death. Longer residual effect than organophosphates. - Neonicotinoids: Mimics Acetylcholine and overstimulates the nervous system - Chlorinated hydrocarbons: DDT nerve poison acts on peripheral nerves a lot of hazards. - Fumigants: Gases and liquids - Hydrogen cyanide, Methyl bromide, Hydrogen phosphate ++ b. Care of the entrusted animals under the custody agreement At the concluding of the custody agreement, on the one hand, the agent (the person who handles the custody - custodian) and, on the other hand, the custodist (the person in custody) takes over. The subject of the contract can only be movable (animal, food, etc.). The basic duty of the custodian is to properly take care of the matter. The depositor is required to compensate the resident for the necessary costs suffered by the custodian. The custodian is obligated to take the case back in the agreed manner, after the expiry of the custody period, returning it together with what has come to it (offspring, weight gains). In cases where a custodian would use a retrieved thing if he could use it for another (huntable dog in custody), if he gave it without the permission of the co-worker to someone else in custody or is in delay with his return, he is also responsible for accidental damage. From Ingrid: ??? Responsibility of shelter If somebody brings an animal to a shelter the shelter must keep and care for the animal and try to find a new owner. How long must they look after the dog? It depends: · The owner of the shelter can kill the animal if there is no place for it to go - Slovak law states that only the owner can say if the dog can be killed or not because it belongs to them - Difficult when nobody knows whether the owner is lost or abandoned - If you know an animal is abandoned then the shelter is allowed to euthanize the animal If an animal in shelters has been neutered - then the owners can ask for money because the animal was damaged by the shelter. Because shelters have no money, there is a problem for them to pay for these incidents and the case can go to court. De-helminthisation and vaccination of stray dogs costs money and when the owner isn't found the shelter pay these costs. Therefore, when the animal is rehomed the new owner must pay the shelter some money (fee) If you find a stray dog and you take it in you are then taking responsibility for it.

16. Transmissive encephalopatiest, BSE, scrapie and others, prevention and control, measures in outbreak, current epizootological situation. Proceeding of competent authorities in the case of disease outbreak, control and prevention

Prions are misfolded proteins causing fatal neurodegenerative diseases in humans and animals. PrPC (healthy form) and PrPSc (infectious form). PrPC are found on the surface of normal cells, including on neurons. The pathogenic form PrPSc will be degraded by proteases to inhibit any danger. However, when there is conformational change on the secondary level (3D shape) no proteases are able to degrade them. The inability to degrade faulty proteins causes dangerous accumulation of these proteins, which leads to vacuolization of nervous tissue. This makes the neural tissue "spongiform" in texture, hence the name of diseases (TSE transmissible spongiform encephalopathy). The disease is deadly. Prions are extremely resistant against temperature, dessication, pH, ionization and UV radiation. It can even survive incineration. Therefore, outbreaks started when ruminants were fed meat-bone-meals of infected cattle. Transmissible spongiform encephalopathy A group of progressive conditions that are associated with prions affecting the brain causing encephalopathy. Current situation Classical BSE: One reported case in Scotland in 2018 Atypical BSE: Detected in a 13 yo cow in Switzerland in 2020, a 18 yo cow in Spain 2019 and a 6 yo cow 2019. Brazil and Poland in 2019. Norway: Only one case; 2015 - subclinical infection of atypical BSE. Transmission - unique. Genetic, sporadic or infectious by eating infected tissues and iatrogenically e.g. in blood transfusions. Most cases of TSE occur sporadically with no other prion mutation of proteins. Pathogenesis - when a PrPSc enters an organism, it will induce the pathological change (misfolding) in existing, properly folded proteins. The newly formed prions will go on to induce the same change in other proteins, and a chain-reaction occurs resulting in a high amount of prions proteins. Prion proteins accumulates in the tissue and cause damage and death of cells. This chain reaction depends on the presence of properly folded (healthy) proteins. Animals that do not express the normal form of the prion proteins, cannot develop the disease. Tissue damage includes - Spongiform change of structure - Loss of neurons - Astrocytosis (abnormal increase in the number of astrocytes due to the destruction of nearby neurons. Will cause neural dysfunction and disease too. Astrocytes are glial cells) - Amyloid plaque (protein breakdown forming plakk between neurons) TSE diseases include - BSE - Scrapies - Chronic wasting disease - Kreutzfelt jacobs - Feline spongiform encephalopathy Bovine spongiform encephalopathy Mad cow disease. fatal. Can infect humans also causing Creutzfelt-Jacobs disease. OIE notifiable. Etiological agent - PrPSc , a misfolded prion protein. We distinguish between classical BSE (after ingestion of infected material) and atypical BSE (spontaneous mutation). Transmission - meat bone meal ingestion or spontaneous mutation Pathogenesis - when a PrPSc enters an organism, it will induce the pathological change (misfolding) in existing, properly folded proteins. The newly formed prions will go on to induce the same change in other proteins, and a chain-reaction occurs resulting in a high amount of prions proteins. Prion proteins accumulates in the tissue and cause damage and death of cells. (Replication actually starts in PP of ileum, and then travels via peripheral nerves to the CNS). Clinical signs - takes 2-8 years between infection and appearance of clinical signs. Hence, only found in adults 1. Gait abnormalities, hindlimb ataxia 2. Hyperresponsiveness to stimuli 3. Tremors 4. Behavioral change a. Aggression, nervousness even frenzy The combination of abnormal gait, behavioral change and hyperresponsiveness is a good indicator of disease. However, some animals only show one of these mentioned signs. In atypical form there is usually no clinical signs! Found in animals during routine surveillance or when cattle are found dead. Thus the above mentioned signs goes for classical form. Diagnosis Sample is CNS. Perform histology to find the amyloid plaque and vacuoles of prions. To detect the specific PrP we use western blotting which identify proteins in a sample - WB has proteinase K à digest the normal PrPs and leave only PrPSc . PrPSc is bound to Ab, electrophoresis There is also a rapid test available that detects SAF (scrapie associated fibrils). Prevention · PM inspection of cattle older than 4 years old if there are any AM indications. · Obligatory PM inspection of all cattle older than 6 years old · No feeding MBM · Banning the feeding of SRM to humans, including bovine brain, tonsils, spinal cord and intestine. Scrapies Classical scrapie is a naturally occurring progressive, fatal, infectious neurodegenerative disease of sheep and goats. Found in Europe, North America, Asia and Africa. It is a type of the TSEs. Atypical scrapie (Nor98) is also a neurodegenerative disease of sheep and goats. First described in Norway in 1998. The difference is that Nor98 has not been shown to be naturally transmitted to other animals. Widespread occurrence throughout Europe. Found in sheep of genotypes considered to be relatively resistant to classical scrapie and in goats. = TSE in sheep and goat. It is not zoonotic, but it can cause BSE in cattle which again can cause CJD in humans. Etiological agent - is the misfolded prion protein PrPSc. (Sc is for scrapie. PrP means prion protein). Genetic importance - Codon 171 of the PRNP gene of sheep is involved in scrapie susceptibility Transmission - via exposure to birthing fluids. Main is offspring after birth but also other animals that come in contact with the material. The transmission to adults has much lower frequency than that to offspring. Chance of transmission/infection also depends on the mentioned genetic susceptibility. Pathogenesis When a PrPSc enters an organism, it will induce the pathological change (misfolding) in existing, properly folded proteins. The newly formed prions will go on to induce the same change in other proteins and a chain-reaction occurs resulting in a high amount of prions proteins. Prion proteins accumulates in the tissue and cause damage and death of cells. (Replication actually starts in PP of ileum, and then travels via peripheral nerves to the CNS). Clinical signs Starts with behavioral change - like in bovine; Aggression, nervousness, hyperexcitability Then later pruritus (scraping) - animal will rub and scrape itself vigorously towards objects and nibble its skin. This leads to visible loss of wool especially on flanks and hindlimbs. The typical nibble reflex if you touch sheep. Also neurological signs like hindlimb ataxia, swaying, stumbling and falling. Seizures can also occur. There is an atypical form in which pruritus is absent! Different breeds show different signs. Some die without any clinical signs. 100% mortality. Situation 2018-2020 (some of the cases): Iceland (20 cases 2019 and 1 case 2020), Italy (many cases), Norway (3 cases in 2019), Romania (many cases 2018), Portugal (1 case 2020), Slovakia (1 case 2019) and Spain (12 cases 2019). Diagnosis like before Clinical signs, CNS sample, histology and WB. Prevention Surveillance and genetical screening. Kill those who are genetically susceptible in flocks where scrapies has been detected. There is an ongoing work to eradicate scrapies, by genetic screening of susceptibility and breed on them only. Chronic wasting disease Affects deer and other cervids (deer, elk, moose, reindeer), primarily in North America but also detected in 2016 in Norway (eradication was done, over 1000 reindeer was killed 2017). Fatal, progressive neurodegenerative disorder affecting both wild and farmed animals. Primary signs are significant weight loss (wasting), ataxia and hypersalivation. TSE Diagnosis Sample: CNS (customized instrumentation for sampling) Histology: Show TSE-specific vacuolation at several different levels of the brain (not diagnostic) Differential diagnosis (BSE): All types of neurological diseases (infectious encephalitis, metabolic disorders, toxicosis, neoplasia and trauma) Detect disease-specific forms of PrP: Immunohistochemistry and/or PrP-detection methods = Western immunoblot Rapid tests for screening (BSE, scrapie): Rabid Western immunoblot, ELISA techniques, or lateral flow assays (BSE) Prevention and control measures Surveillance of occurrences of clinical neurological disease, transparency in reporting findings, safeguards on importation of live ruminant species and their products in accordance with the OiE terrestrial code: · Removal of specific risk material (SRM) - brain, spinal cord - at the slaughterhouse/processing of carcasses · Prohibit inclusion of SRM in animal feed, thus removing potentially contaminated material from the food chain · Humane destruction of all suspected and susceptible animals exposed to contaminated feed · Appropriate disposal of carcasses and all animal products · Livestock identification to enable effective surveillance and tracing of suspected livestock a. Sanitation measures and focal disinfection at these diseases. Treatment of cadavers Resistance Prion is resistant to commercial inactivation, heat, UV, chemicals; long biodegradation. Procedures like heat may not be completely destroyed in rendering processed (incineration needed) Laboratory workers handling tissues of BSE-suspected animals should wear appropriate protective clothing and observe a strict code of practice to avoid exposure to the highly resistant agent. Sanitation measures in focus Confirmed BSE: Focus of infection, protective zones, disinfectant ford, active disinfection Quarantine and movement control. All suspected animals must be killed and their bodies must be destroyed in a rendering plant (first sprayed with disinfectants). From carcass box; cadavers must be transported by specific cars to the rendering plant. Processing under specific conditions (described below). Specific risk material (SRM) - cattle: Skull including brain and eyes, tonsils and the spinal cord of bovine animals >12 months. Intestine from duodenum to rectum of all ages. SRM must be removed at slaughterhouses, cutting plants, high-risk processing plants under the supervision of a designated agent appointed by the competent authority. Disinfection Everything must be disinfected (vehicles, car wheels...) · 2-4% NaOH (70-80°C) · Chlorinated lime 2-3%. Exposure time: >1 hour at 20°C for surfaces. Overnight for equipment · Chloramine T 5% (50-60°C) for vehicles Procedure: Preliminary disinfection: Apply disinfectant for 24 hours Final cleaning and disinfection: · Remove mechanical waste (fats, proteins) using washing soda (4% sodium carbonate) · Apply disinfectant · After 7 days, removal of mechanical waste · Repeat applying of disinfectant, control Agent can spread through manure, disinfection of manure: CaO - lime 3%, minimum 42 days composting, covered. Water, well: Chlorine compounds. Rodent control: Acute rodenticides Treatment of cadavers The cadavers/carcasses are collected in a carcass box and transported by special vehicles that do not enter the farm (special entry from outside the farm) to a rendering plant. The carcasses, the bodies of dead animals, are processed under specific conditions: · Time: 20 minutes · Temperature: 133°C · Pressure: 0.3 MPa Bodies are destroyed - semiproduct: Meat bone meal (MBM). Specific risk material (SRM) from infectious diseases must be burned at a temperature of 1350°C (incineration) - mixture to concrete. b. Animal identification, expert opinion Animal identification is necessary in several situations: Examination of live and dead animals, in cases of legal relationship, from which participants enforce the law and corresponding obligations. Animal identification can be based on height determination, mass, growth, coat, skin color, hair, feathers age. Identity confirmation in animals: · Dogs - according to teeth; trauma, teeth extract, fillings, developmental anomalies · Scars: Number, presence, size, shape, consistency, nature · Tattoo · Marks from: Tethering devices, saddle, yoke (wooden beam on animals to let them to pull something) · Ring the birds · Chipping Identification and registration of animals Cattle: Individual animal identification that allow producers to keep records on an animal's parentage, birth date, production records, health history. Combination of letter and numbers Sheep and goat:Registration, identification and accurate recording supports traceability, helps to minimise the risk of disease transmission and maximize possibility of controlling the spread during an outbreak. Housed indoors; marked within 6 months, housed outdoors; 9 months. o If they are kept for longer than 12 months farmer must apply two identifiers (ear tags). Both will bear the same unique individual ID number (one must be electronic). o If intended for slaughter within 12 months of age they can be marked with a single ear tag. Pigs: Slapmark (a permanent herd mark applied to each front of shoulder areas). Ear tag that is stamped or printed. Tattoo of herd mark on ear. Temporary paint mark (must last until the pig reaches its destination). o All pigs going to slaughter must be identified with herd mark. o All pigs over one year old moving to another holding must also the identified with a herd mark. o Imported from outside EU - must not apply a new ID if the pig is to be slaughtered within 30 days of arrival. Companion animals (cats, dogs, ferrets): Pet passport created by European Commission which can only be issued by an authorised veterinarian. Over 5 animals = commercial movement Horses: Single lifetime identification document. A method to ensure a link between the ID document and the horse. Unique equine life number - UELN (database recording).Passport: Owner, identification (must be done by competent aurhority), records of identity checks, vaccination records, laboratory health tests and medical treatment Expert opinion A relatively informal technique that can be used to serve a variety of purposes and may be used to assist in problem identification, in clarifying the issues relevant to a particular topic, and in the evaluation of products. Individual experts can be consulted, but usually better to bring groups of experts together so that a wide range of experience can be drawn on. Experts may be personally interviewed or given questionnaires and may also be asked to discuss their observations in a group setting with other experts. The "expert" must take a showing of the necessary background through questions in court, and the trial judge has discretion to qualify the witness or rule he/she is not an expert or is an expert on limited subjects. Opinion testimony that is based on facts is usually considered incompetent and inadmissible If the fact finders are well qualified as the witness to draw conclusions from the facts. Expert testimony: Opinions stated during trial or deposition (testimony under oath before trial) by a specialist qualified as an expert on a subject relevant to a lawsuit or a criminal case.

9. Q fever and other rickettsiosis, prevention and control, measures in outbreak, current epizootological situation. Proceeding of competent authorities in the case of disease outbreak, control and prevention

Q-fever and other rickettsioses (all are tick borne, intracellular) Rickettsia. Rickettsiaceae family. Gram negative. Obligate intracellular pathogens = will not grow on culture media and must be grown in cell lines or embryos. Vector borne - by ticks, fleas, lice. Family causes several, similar diseases that all include fever and rash: · Q-fever · Rocky Mountain Spotted Fever - ricket = rocket = rocky mountain spotted fever · Ehrlichiosis · Typhus Q-fever (Q = ku = ruminants) (Ku = cow = cox = coxiella). Some have baby fever (baby abortus) we have Q-fever · Coxiella burnetii · Zoonotic!! Important in developing countries and for vets, farmers · Two antigenic phases: o Phase 1: virulent- infected animals or nature o Phase 2: less pathogenic- lab · Infects all animals (mammals, birds, reptiles and arthropods) but we speak of infection in ruminants · Survives long in environment because it forms a spore-like structure that is very resistant · Important because of abortions in small ruminants Transmission Bacteria is shed in urine, feces and milk. Most important is the huge load of bacteria during parturition, found in birthing fluids and placenta. This causes contamination of environment and spread to new host. · Feed, water and dust particles can be infected with the "spore" and then be ingested or inhaled · Infected arthropods can also transmit the disease upon feeding. TICKS- ixodes, dermacentor · Humans or baby animals drinking unpasteurized milk Pathogenesis · Of lower importance is the mild clinical disease that develops following infection by Coxiella o Animals shed during this period · More important is the abortus in late gestation which is seen in sheep and goat · Humans may have none or mild clinical signs which resolve themselves. Some can develop flu-like symptoms and require prolonged antibiotic treatment Diagnosis · History of serial-abortions · Sample is vaginal discharge, milk, placenta or tissue from aborted fetus · Isolation of pathogen in chicken embryo, cell lines or laboratory animals. Identification by PCR · Smears: Giemsa or Ziehl Neelson (vaginal or tissue) · ELISA, IFA or CFT can prove antibodies post-infection Therapy Oral tetracyclone up to 2-4 weeks for RU. Tetracycline in water prior to parturition can reduce spread. Prevention and control · Good husbandry, tick prevention and disposal of birth fluids. Pasteuraztion of milk · Separate new or sick animals · Vaccination of animals and humans Eradication not practical- too many reservoirs, constant exposure, great stabillity of agent in · Environment o Coxiella burnetii has a number of distinctive characteristics, including a sporulation-like process that protects the organism against the external environment, where it can survive for long periods Rocky mountain spotted fever · Rickettsia ricketsii · Tick borne (American dog tick and Rocky mountain wood tick) · Seasonal: March to September when adult tick feeds · Bacteria live in endothelial cells and replicate here. Causes vasculitis and damage to vessel walls In dogs: Unspecific signs of fever, vomitus, diarrhea, muscle pain, depression. Petechiae and ecchymosis can be seen in mucosa in more severe cases. Disease can be self-limiting or fatal. In humans: Severe flu-like symptoms of fever, chills, headache, muscle ache. Rash can develop = spotted. Diagnosis is based on 1) History of travels to tick habitat and/or tick bite. Also season of year! 2) Clinical presentation (rash seldom in dogs) 3) IFA to find antibodies in blood Typhus Rickettsia prowazekii. Found naturally only in a species of flying squirrel. Generally, humans are the only species affected by typhus. Transmitted by body lice when its feces enter body through breaks in the skin. Humans have severe flu-like symptoms and develops a rash after few days. Untreated can be fatal in some. ATB. https://www.youtube.com/watch?v=Owv-S-_BFzQ https://www.youtube.com/watch?v=JynGH6bXaw4&t=5s Ehrlichiosis - Rickettsia- like bacteria Tick-borne infections, also known as canine haemorrhagic fever. · Ehrlichiosis canis and Ehrlichia chaffeensis Infect monocytes dogs. (AMBLYOMMA AMERICANUM) · Erlichia ewingii infects granulocytes (zoonotic). · Anaplasma marginale cause bovine erlichiosis. (IXODES) Epizootological situation Found worldwide, incidence is related to tick population. Due to global warming, there's a shift of borders to the north, and the disease is now found in Spain, Portugal, Italy, Greece and France. Pathogenesis These bacteria inhabit WBCs and may cause widespread blood clotting (DIC), severe malfunction (failure) of several organs, seizures and coma. In acute cases, there is reticuloendothelial hyperplasia, fever, generalized lymphadenopathy, splenomegaly and thrombocytopenia. Clinical signs Fever, chills, muscle aches, weakness, nausea/vomiting, cough, headache and rash. Diagnosis · Anamnesis and clinical signs · Blood sample: platelet count · Microscope and cultivate: bacteria in peripheral blood smears or impression smears from tissues. Intracellular inclusion bodies are found in white blood cells and platelets. · PCR and serology: immunofluorescent assay, complement fixation test, ELISA, WB Treatment Antibiotics- doxycycline, tetracycline and supportive therapy. Animal should be tested after treatment (if still carrier- oxytetracycline). Medication can be given during vector season (oxytet) or during the entire year (chlortet). Prevention and control · Proper disposal of waste: remove placenta and birth fluids- burn or bury · Cleaning and disinfection: prevention of spread · Awareness: education of public and relevant work groups · Surveillance: mandatory in EU · Tick control program: permethrin (dogs), fipronil (cats), prevent contact with ticks and infected animals · Vaccine: in endemic areas or following outbreaks, human and animals · Farm management: manure, parturition areas, quarantine, isolation, disinfect areas where animal give birth. a.) Sanitation measures and focal disinfection at these diseases. Excrements and soil disinfection. Resistance Rickettisa spp., survives for months in the environment and can spread over large distances via aerosols Disinfection Q-fever · Chloramin T (4%), formaldehyde (2%), NaOH (2%), ethanol (70%), heat - Manure: composting - Slurry: lime (3%) and H3PO4 - Pasture: lime (3%), no grazing for 90 days - Vector control: acute or chronic rodenticides (zinc phosphide then 3 generation baraka). Insecticides- pyretroids on the farm, for animals, people and dogs. Rocky mountain spotted fever - Disinfection of tick bite: 70% isopropyl alcohol - Destroyed by moist heat (121°C 15 min) and dry heat (160-170°C 1 hour) Excrements and soil disinfection Definitions - Manure: organic fertilizer after 1 month storage in correct conditions - Farmyard manure (fresh manure): manure unsuitable for soil application as nutrients are not available. - Dung water: liquid released from stored farmyard manure - Slurry: liquid manure from housing without bedding after 6 months storage. Storage conditions Minimum 15 m from milking parlour and 50 m from well. Treatment · Biothermic treatment (composting): 70°C, 40-60% RH, pH 6,5- 8,5 · Chemical decontamination: - Farmyard Manure: lime 3% or peracetic acid 0.3-0.5% - Slurry: Ammonium hydroxide 3%, Fresh slaked lime 3-6%, peracetic acid 0.3-0.9%, phosphoric acid 1.5-3%, formalin 1%, sodium hydroxide 2% · Burning or Burying · Combinations Disinfection of Soil: · 3% Ca(OH)2 or CaO - lime - 8-10 l.m-2 · 1% phosphoric acid - 8-10 l.m-2 · 0.3% peracetic acid - 8-10 l.m-2 b.) Damages caused by animals and on animals Damages caused BY animals · Owners of domestic animals will be responsible for any harm they cause others due to negligence - The owner of a dog who bites another person or an animal (other than a trespasser) is liable for the damage caused by the dog bite - Dogs can cause damage to horses, cattle or other valuable livestock. In these situations, there are various laws that add to the general dog bite rules - While general "negligence" principles apply that require animal owners to take reasonable precautions, there are often additional legal issues when animals are involved, particularly in cases involving livestock and farmland. · Dog bites are so common and potentially serious, that many laws specific to dogs have been implemented to protect against the dangers posed by dogs- "Leash laws" Naturally dangerous animals Some types of animals are naturally dangerous. If you own one of these types of animals (called ferae naturae) and it hurts someone, you are totally responsible. It does not matter how careful you were Other animals Owners will only be responsible for injuries caused by these animals if they were in some way negligent or if they knew that the animal had previously hurt someone, or was likely to hurt someone If you keep an aggressive dog to protect yourself or your property, at the very least you should put up a sign warning people about the dog If your dog escapes from your property and bites a person or another animal, you will be liable for that action and subject to fines and possible damages claims Animal trespass If your animals stray onto your neighbour's land, it is likely that you will be responsible for any damage that they cause. It does not matter that you were not negligent or didn't know what was happening. Damage includes damage to land, crops, people and livestock Animals on the highway People who own animals (including dogs) are under a duty to take reasonable care to see that their animals do not cause any damage by straying onto a highway. If reasonable care is not taken and damage results, the owner is liable to pay compensation. Damages caused ON animals Damages compensated for animals include damage caused to a domestic animal, farmed animal, honey crop and fences, buildings and other similar structures used for the keeping of animals. Damage to a dog caused by a large carnivore may be compensated only if the dog was in a controlled circumstance in the yard or garden of its owner or holder when the damage occurred. No compensation will be paid for damage to a hunting dog, if the damage was caused by a large carnivore that was the object of the hunt in which the dog participated

22. Classical swine fever, African swine fever, Rinderpest and peste des petits ruminants, prevention and control, measures in outbreak, current epizootological situation. Proceeding of competent authorities in the case of disease outbreak, control and prevention

Quick comparison: CSF and ASF. Both are OIE notifiable, both are not zoonotic. CSF = neurological signs. ASF = bloody diarrhoea CSF is an RNA virus ASF is a large and complex DNA virus For CSF, vaccines exist For ASF, no vaccine exists Classical swine fever (classical swine fever) Etiological agent RNA virus, pestivirus, Classical swine fever virus. High morbidity, high mortality. Hunt! Kill as many as you can! Survives well in pork meat, even frozen. Is killed during cooking. Transmission Virus found in tissue, blood, secretions from nose, semen, excretions like feces and urine. Most common route of infection is ingestion Other: Direct contact between animals (snout to snout, mucus membranes), copulation and artificial insemination. Pathogenesis Oral ingestion of virus à virus go to tonsils to replicate à from tonsils to lnn/lymph à blood to cause viremia. Virus has affinity towards endothelial cells and immune cells and they replicate there (and in kidney, spleen and bone marrow). This causes severe leukopenia and internal hemorrhages. Death. (ASF has mostly same) Clinical signs Acute infections in virulent strains or in young animals Fever, diarrhea, coughing, swollen lnn Crusty eyes, skin discoloration from cyanosis on ears, tail, snout and limbs Pigs huddle together, might show neurological signs like ataxia. Death Chronic infections in less virulent strains and in adult animals Growth retardation and general malaise Diarrhea for a limited period, button ulcers in colon. Also causes death Abortions in pregnant sows Treatment No treatment; animal must be killed. Diagnosis- Is clinically indistinguishable from ASF. Sample: Tonsils and lnn. Blood from live animals. Culture virus, RT-PCR and immunofluorescence. Serology can be performed after 3 weeks of disease. Virus neutralization, ELISA. Epizootiological situation Measures during outbreak In case of outbreaks in the EU, one needs to resort to the slaughtering of all pigs in the infected farms and the destruction of cadavers. Farm is closed, restocking can occur after 30 days. A protection zone (3 km radius) and surveillance zone (10 km radius) are established around each outbreak, with restrictions on pig movements. An epizootological investigation with the tracing of the source of infection and the possible spread is carried out. Prevention, control Prevention can be achieved through - Effective communication between veterinary authorities, veterinary practitioners and pig farmers - Effective disease reporting and animal identification system - A strict import control of live pigs, fresh and cured meat - Prohibition of feeding pigs with waste food - Virological and serological surveillance African swine fever LOW MORBIDITY AND HIGH MORTALITY so don't hunt, wait and rather remove dead animals after. Etiological agent DNA-virus - asfivirus, African swine fever virus. Is an arboviral infection because replication is inside a tick!! Transmission · Direct between pigs · Infected fomites like clothes, premises · Indirect by ingestion of infected meat (cannibalism in wild boar) · Soft ticks (transstadial, transovarial) · Recovered individuals are carriers and persistent shedders Pathogenesis Similar to hog cholera: Virus replicates in the MPS (macrophage, lymphocyte, monocyte) and cause splenomegaly (due to leukopenia and hemorrhages) and petechial hemorrhages on all organs. Affinity to endothelial cells. Clinical signs Acute disease/high virulence Abortions may be the first sign Fever, anorexia Bleeding from body openings, hemorrhages on skin, redness on ears, legs and abdomen Up to 100% mortality SPLEEN ENLARGEMENT, CONGESTION Post mortem findings; - Petechial hemorrhages on lnn, kidney and other organs - Splenomegaly (leukopenia and hemorrhages causes this) - Excessive fluid in pericard, pleura and peritoneum Chronic disease/low virulence Intermittent fever Weight loss, emaciation Chronic skin ulcers Mortality rates are lower, but still ranges from 30-70% Post mortem findings; Enlarged lnn Lungs have focal necrosis and mineralization Treatment No treatment. Diagnosis Should be done on basis of 2 blood samples from each animal; 1 with and 1 without anticoagulant. Suspected case should have 10 samples form the farm. - Hemadsorption test à positive here is guaranteed positive ASF! - Antigen detection by FAT à positive FAT and clinical signs gives a probable diagnosis of ASF - Viral isolation and PCR - Sample from dead is lnn, spleen, kidney, tonsil Epizootiological situation Measures during outbreak - Slaughtering all pigs and destruction of cadavers and litter - Cleaning and disinfection - Designation of infected zone and control of pig movement, as well as epidemiological investigation (tracing of sources and possible spread of infection) - Restocking 40 days after ended disinfection Prevention, control There is no treatment or vaccine for ASF Prevention in countries free of the disease depends on: - Strict import policies, ensuring neither infected live pigs nor pork products are introduced into free areas - Biosecurity (fencing the farm, avoid contact with wild boards, their contact with feed and bedding This includes ensuring: o Proper disposal of waste food from aircraft, ships or vehicles coming from infected countries. In endemic areas: Difficult to eliminate the natural reservoir; - Control of the tick vectors is important in preventing the disease - Ensure that meat from infected animals is not fed to pigs Rinderpest -ERADICATED in 2011 Etiological agent Paramyxoviridae, morbillivirus (=parainfluenza), rinderpest virus Virus have H hemaglutinin and N neuraminidase proteins on surface. Transmission Virus in expired air and all discharges à Transmission via direct or close indirect contact with infected animals No fomites because virus is killed in sunlight thus not resistant in environment! Can remain viable for long periods in chilled or frozen tissues. Stable between pH 4.0 and 10.0. Pathogenesis and clinical signs (fever à necrotic mouth ulcers à watery, bloody diarrhea à terminal stage, death) The classical form: - Acute fever above 40°C occurs together with depression, reduced rumination, reduced production - Next the necrotic mouth lesions develop and they spread inside mouth; Tongue, cheek, palate. - Next - fever drops a few days after mouth lesions has occurred - and then the GIT signs start: - Diarrhea is watery, but becomes bloody later The severe diarrhea leads to dehydration, abdominal pain and weakness Terminal stage of disease; - Animal becomes recumbent and die 1-2 days after recumbency - The exact day of death depends on the virulence of strain and the cattle breed etc. - Mortality can be 100% in highly virulent strains, and 20-30% in less virulent strains - In a few, rare cases, the clinical signs regress and recovery occurs Other forms of the disease are either without diarrhea or with only fever and subsequent sudden death. Treatment No effective treatment, rely solely on prevention. Diagnosis Virus detection and identification by RT-PCR. PV virus can be cultured from whole blood (heparin or EDTA) or uncoagulated blood Virus can also be isolated from samples of the spleen, prescapular or mesenteric lymph nodes of dead animals Detect Ag by agar gel immunodiffusion Detect Ab by competitive ELISA and virus neutralization. Epizootiological situation Is eradicated, but remains a notifiable disease and adequate surveillance systems must be maintained for the early detection of clinical cases should there be any accidental escape of the virus.Was widespread in Africa, India and middle East. Measures during outbreak Infected and exposed animals will likely be slaughtered and this can account for significant economic losses. Prevention, control Vaccine was developed giving lifelong immunity. To prevent future outbreaks: - Quarantine, testing, and vaccination of introduced animals - Prevention via sanitary prophylaxis - Appropriate destruction of cadavers - Disinfection of equipment and facilities - Serologic monitoring of wild ungulates, sheep and goats. When monitoring small ruminants, the use of a rinderpest vaccine must be taken into consideration. (The vaccine is often used to protect against peste des pestis ruminant because it provides cross-protection against this virus - Heightened awareness of and surveillance for RPV and restricted movement of animals and meat into rinderpest-free zones. Peste des petits ruminants (is rinderpest in small ruminants) - OIE listed Etiological agent Paramyxoviridae, morbillivirus (=parainfluenza), PDP virus Virus have H hemagluttinin and N neuraminidase proteins on surface. Transmission Every excretion and secretion of infected sick animal is contagious; - Inhalation of droplets from coughing, ingestion of feces, direct contact. Bedding/surroundings from feces. Pathogenesis and clinical signs (Fever à oral ulcers à diarrhea/pneumonia à death) - Sudden fever above 40°C which causes general depression, anorexia and dull coat - Nasal discharge, can form crust that blocks airway; dyspnea - Few days after onset of fever, the ulceration starts - Gums become hyperemic and erosive lesions develop in oral cavity - excessive salivation - Bronchopneumonia and coughing is often seen - General state involves dehydration, emaciation, dyspnea and death - If they survive, there is a long recovery period Treatment There are no medications available to treat the disease, but supportive treatment may decrease mortality. Diagnosis Isolation of agent in cell culture. Identify by virus neutralization test, AGID, PCR. Epizootiological situation Found in Africa, Middle East, South-west Asia and India. Measures during outbreak - Quarantine - Movement control - Sanitary slaughter - Cleaning and disinfection are applied - The virus is susceptible to most disinfectants. Prevention, control Vaccination programs in endemic areas, quarantine and control of movement. OIE has goal to eradicate it within 2030! Main diff from Rinderpest is the involvement of respiratory system. a. Sanitation measures and focal disinfection at these diseases. Main groups of disinfectants Classical swine fever Virus is stable at pH 5-10, but is rapidly inactivated by pH 3 or less or higher than 11. Focal disinfection: - 2 % NaOH with content of 3-5 % milk lime • 4 % Chloramin T • 2 % Formalin • 0.5 % Peracetic acid • 20 % Slaked lime • 3 % cresol-sulphuric mixture Elimination of viruses in blood/2 hours, • Urine/15 min. • Floor, walls/1 hour This virus is sensitive to drying and ultraviolet light. Preliminary cleaning and disinfection: Must be done of all parts of farm, houses, runs, contaminated by movement of animals or killing places.... Minimum 24 hours apply disinfectant. Final cleaning and disinfection: • Organic materials (fats and dirt) removed by washing soda • (4% sodium carbonate) and then by cold water and next disinfection • After 7 days surfaces must be cleaned again using washing soda and removed by cold water • Next disinfection and removed by cold water • Manure and bedding - disinfection and covered for 42 days (heating) • Sludge: Storage min. 42 days African swine fever · Treatment of contaminated materials, wastes and food by disinfection including equipment, vehicles, cars. · Cadavers disinfection and removal · Disinfection of all houses, vehicles, transport car, all equipment, bedding · Disinfection of manure (composting) à 3 % lime · Slurry à 1.5 % phosphoric acid. 0.3 % Persteril · Soil à 3 % lime, 1.5 % phosphoric acid, 0.3 % Persteril (8-10 l/m2) Peste des petits ruminants Virus is susceptible to most disinfectants. Rinderpest Susceptible to lipid solvents and most common disinfectants - Sodium hydroxide 2% for 24 hours. Survival: Quickly inactivated in environment, sensitive to light, drying and ultraviolet radiation. Main groups of disinfectants Alkalis (hydroxides)Stable disinfectants with a wide microbiological effect. They are the first choice against virus. Work by saponifying lipids inside envelopes of MOs à destruction by hydrolysis of proteins and the destruction of the enzymatic system. Activity of alkali can be increased by raising the temperature. They are very corrosive. - Sodium Hydroxide: already described - Potassium Hydroxide: similar to NaOH. Used as a component in some cleaning preparations. - Calcium Hydroxide: simple disinfectant. Provides an effective means of white-washing surfaces. - Ammonium Hydroxide: effective against coccidial oocysts. AcidsAcids are the strongest disinfectants. They cause oxidation, dehydration, and destruction of nucleic acids and enzymes by changing the pH. There are 2 main groups of acids: - Inorganic acids: have a strong corrosive effect and require safety measures è HCl: 2,5% hydrochloric acid with 15% NaCl is used to disinfect skin è Sulphuric acid: found in cresol mixture (3 part cresol + 1 part sulphuric acid) è Nitrogen acid: act on bacteria and spores, used to disinfect equipment in food industry - Organic acids: less corrosive and can be used to disinfect air and in presence of animals. è Lactic acid: easily evaporated, aerosol disinfection è Peracetic acid: the most frequently used organic acid. It is non- stable, highly corrosive towards metals, and effective against bacteria, spores, and fungi. Chlorine compoundsThey oxidise peptide links and denature proteins and are considered broad spectrum, effective against bacteria, enveloped and non-enveloped viruses. Their action is markedly reduced in the presence of organic matter, thus they must be applied to thoroughly cleaned surfaces. - Chlorine: strong oxidizing agent. Corrosive to metals. - Hypochlorites: Less effective against spores. Chlorinated lime contains 33-36% active chlorine. Iodine compounds Skin disinfectant. Denature proteins and interfere with the enzymatic systems of microbes. Irritating to skin, damage rubber and some metals. Iodonal A, B and M. AldehydesBroad spectrum disinfectants. Denature proteins and disrupt nucleic acids. Effective against bacteria, spores, mycobacteria, fungi and viruses. Potentially carcinogenic. - Glutaraldehyde: lethal to bacteria, their spores, fungal spores and various types of viruses. - Formaldehyde- used against Anthrax. Formalin contains 38-40% formaldehyde. Metal compounds: tin, mercury, silver Phenols: Affect cell permeability and cause denaturation of proteins b. The pattern of the document declaring the outbreak to be extinct To declare the freedom from a disease - When will freedom from a disease be achieved? Freedom from a disease is declared - Only when all known infected animals have recovered (or in some cases been destroyed) - And surveillance shows livestock are clear of residual infection - Observation period - Final disinfection o Surveillance has to include proper survey of all exposed livestock, it may take weeks or even months. o Countries may also demand that a certain amount of time (observation period) passes before they will recognize freedom from the disease and reopen export markets.

18. Rabies, prevention and control, measures in outbreak, current epizootological situation. Proceeding of competent authorities in the case of disease outbreak, control and prevention

Rhaboviridae. Lyssavirus. Classical rabies virus (RABV). · Many lyssaviruses but RABV is the most important · Many strains of rabies virus, each strain is maintained in their own reservoir(s) · Neurotrophic · Extremely wide host range! Can cause disease in any mammal · Main reservoirs are carnivores and bats (chiroptera) · 100% preventable but still 70.000 human deaths per year (Asia, Africa) Epidemiology Rabies is maintained in 2 epidemiological cycles; sylvatic cycle and urban cycle · Sylvatic = main reservoirs are bats, foxes (Europe, Northern hemisphere) · Urban = main reservoirs are dogs (Asia, Africa) · Cases: Norway (Svalbard, Jan Mayen): 5 cases in 2018, France (2 dogs), Morocco 1 dog and many cases in Malaysia Transmission Virus is in saliva. Transmission through biting, saliva in open wound. Virus is also in CNS and CSF so carnivores eating infected animal will be sick. Virus can NOT penetrate intact skin! Pathogenesis · After infection, virus enters eclipse mode to go unnoticed · It travels to non-neural tissue (muscles) and replicates without stimulating immune response. · After days/months, virus cross neuromuscular junction by acetylcholine receptors. · They travel from peripheral nerves to the CNS by retrograde flow of axons (from periphery to central). · After dissemination in the CNS neurological signs develop as neurons are severely damaged · Via cranial nerves, the virus travels to the salivary glands (Longer time to develop neurological signs when bite site is long away from the brain - neck vs paw) Pathology There are no characteristic lesions. The stomach can contain various abnormal objects (e.g. sticks and stones). Microscopic lesions are found principally in the CNS - non-suppurative encephalomyelitis. Lesions are in the cerebral cortex, hippocampus, Amon's horn, medulla, cerebellum and cervical spinal cord. Glial nodules (called Babes nodules) are present in both white and grey matter. Neuronal degeneration can be present in a greater or lesser extent. The most diagnostic feature is the presence of Negri bodies. These inclusion bodies are intracytoplasmic. Clinical signs Animals Beginning: Non-specific signs - restlessness, vomitus, hyperreactions to stimuli, excessive salivation Later: After 2-5 days, either dumb or furious form i. Dumb form (also called paralytic form) Animal is calm, quiet, lethargic. Paralysis develops. Starts with throat and masseter, inability to swallow and tongue paralysis causes profuse salivation. Ataxia - paresis - limb paralysis - death due to respiratory failure. ii. Furious form Limbic system is infected. 3 stages are involved · Prodromal stage with sudden change in temperament. Pupils dilated, loss of corneal reflex · Excitation stage with restlessness, catch imaginary objects, drooling, attacks objects, fury · Paralytic stage with ataxia, convulsions and death Humans Have much of the same non-specific signs in beginning: Flu-like signs, pain, pruritus and discomfort. Develops into anxiety, hypersensitivity and agitation. Furious form = hyperexcitability, hydrophobia. Paralytic form = paralysis Death within 10 days without vaccines. Diagnosis Sample is brain and can be done by 3 ways; Open skull (on mice), retrobulbar by needle or occipital foramen. Gold standard: Fluorescence antibody test (FAT). Tissue stained with conjugate and viewed in fluorescent microscope. When labelled antibody is incubated with rabies-suspect brain tissue, it will bind to rabies antigen. Unbound antibody can be washed away and where antigen is present can be seen as fluorescent apple-green areas using a fluorescence microscope. If the rabies virus is absent, there will be no staining. This method is fast and the result is available within 1 hour Histology: Negribodies (viral protein) in CNS tissue All lyssavirus infection gives similar clinical disease, so use RT-PCR to identify virus Vaccine: IM in domestic and oral in wild animals Prevention and control measures · Endemic: Measures address and reduce the risk of infection in susceptible populations (wildlife, stray and domestic animals) and create a buffer between the animal source of the disease and humans. · Surveillance and reporting of suspected cases of rabies in animals. · Vaccination programs for domestic animals · Wildlife rabies control programs including vaccination (trap - vaccinate - release), or delivery of oral vaccines. Oral rabies vaccination of reservoirs (modified live vaccine); oral vaccine is dropped in endemic areas from a plane · Hunters shoot and kill foxes and allow State Vets to perform regular tests - cooperation with hunters. · Population control and vaccination programs for stray animal populations. · European countries implementing effective wildlife rabies control programs that include oral vaccination campaigns have successfully eliminated the disease in wildlife · Population control and/or oral vaccination programs for domestic and stray animals are being implemented in several developing countries where rabies is endemic. a. Sanitation measures and focal disinfection at these diseases. Prevention of secondary poisons. Disinfection The virus is resistant in the outer environment. Survives in tissues at 4°C for weeks and 23 days at a 18°C. Can survive for 5 weeks in buried carcasses. At the place of the dead body and vehicles in contact. 5% NaOH 5% Chloramine T 4.5% Formalin 1% Peracetic acid Rabies virus can be inactivated by lipid solvents (soap solutions, ether, chloroform, acetone) Also susceptible to UV radiation or heat (50°C for 1 hour), boiling water (2 minutes) Rapidly inactivated by sunlight and does not survive for long in environment except in a cool dark area. In focus Prohibition of movement of animals. Transport susceptible animals. Disposal of milk from susceptible cows Prevention of secondary poisoning Secondary poisoning is when one animal, e.g. a dog, consumes a rodent which still has undigested bait in its gut or mouth. The dog directly consumes the bait along with the carcass, the effect would be the same as if the dog were to eat the bait directly. Secondary ingestion is much more of a concern with rat carcasses than with mice. An adult rat can consume up to 30 grams of bait per day, whereas a mouse typically ingests only up to 4 grams of bait. In order to limit the risk of secondary poisoning a "pulsation method" is recommended to prevent accumulation of excessive dose of coagulant in the rodent body. Pulsation method: Consists of placing low quantities of toxic baits (20-80 g for rats, 2-25 g for mice). The repeated placing of baits is practiced after 6-7 days. Diseases transmitted by rodents Salmonellosis, Tularemia, Listeriosis, Leptospirosis, Toxoplasmosis, Rabies, Mycobacteriosis, Black plague Hantavirus pulmonary syndrome, rat-bite fever How the diseases spread Salmonellosis: Eating or drinking food or whatever that is contaminated by rat feces Lassa fever: Breathing in dust that is contaminated with rodent urine or droppings. Direct contact with rodents or their urine and droppings. Eating food that is contaminated with rodent urine or droppings Leptospirosis: Breathing in dust that is contaminated with rodent urine or droppings. Direct contact with rodents or their urine and droppings. Listeriosis: Infected milk, meat, soil Hantavirus pulmonary syndrome: Breathing in dust that is contaminated with rodent urine or droppings. Direct contact with rodents or their urine and droppings b. The procedure for human bitten by a dog Guide for post-exposure prophylaxis Local treatment of the bite wound, followed by vaccine therapy immediately following a transdermal bite or scratch by an animal suspected of being rabid or when possibly infectious material, usually saliva, comes into direct contact with the victim's mucosa or with fresh skin wounds. Treatment may be discontinued if the animal involved (dog or cat) remains healthy throughout an observation period of 1-5-10 days; or if the animal is killed humanely and found to be negative for rabies by laboratory examination.

32. Babesiosis and theileriosis, prevention and control, measures in outbreak, current epizootological situation. Proceeding of competent authorities in the case of disease outbreak, control and prevention

The families babesiidae and theileriidae are the most important blood parasites of domestic mammals. Babesia spp replicate by merogony exclusively in erythrocytes, whereas Theileria spp multiply in mononuclear leukocytes (lymphocytes) and subsequently erythrocytes. The intracellular stages develop directly in the cytoplasm of host cell without parasitophorous vacuole. Gamogony and sporogony occur in the ticks. Babesia infect all domestic mammals. BABESIA Morphology It has a characteristic drop-shaped, mononuclear merozoite, which is usually pairwise located in erythrocytes. Based on its morphology, babesia are described as "large species" or "small species". Babesiosis of cattle 1) Babesia bovis: small babesia lying in centre of the erythrocyte. It has a wide distribution and high pathogenicity, making it the most important babesia species in cattle. Found in southern Europe, Africa, Australia and America. Transmitted by Rhipocephalis spp 2) Babesia divergens; a small babesia characterized by paired, divergent forms found in marginal positions in the erythrocytes. Transmitted by Ixodes spp. 3) Babesia bigemina: a large babesia lying in pairs at an acute angle. Transmission by Rhipocephalis spp. Dog babesiosis Main species- large babesia 1) Babesia canis: pleomorphic, pyriform stages. Geographical distribution depends on occurrence of dermacentor reticulatus, which occurs in Europe. Characterized by high fever, apathy, anaemia, haemoglobinuria and cerebral disorders. DIC can cause multiple organ failures. 2) Babesia vogeli: transmitted by dermacentor variabilis and rhipicephalus sanguineis found in USA and tropical areas. 3) Babesia rossi: most pathogenic species. Found in Africa Main species- small babesia 1) Babesia gibsoni: rarely found in Europe. Transmitted by haemaphysalis spp. 2) Babesia annae: transmitted by ixodes hexagonus Life cycle Infection of vertebrate occurs through the bite of tick. Inoculated sporozoites exclusively infect erythrocytes where they initially develop to ring-shaped trophozoites that multiply asexually by binary fission, forming mostly two drop-shaped merozoites. They are released from the host cell and enter other erythrocytes. Some merozoites transform into spheroid stages, the gamonts. Blood-feeding ticks ingest the infected erythrocytes, which disintegrate in the ticks intestine. The gamonts differentiate into gametes (ray-bodies). By fusion of two uninucleated gametes (syngamy), a zygote is formed. Zygotes enter intestinal cells, multiply and form sporokinetes, which pass into the haemolymph and infect haematocytes. Following the infection of ovary and oocytes Babesia stages may be transmitted in the egg (transovarial transmission) to the next tick generation (vertical transmission). After hatching of tick from infected egg, sporokinetes infect salivary glands in which they can be transmitted. Mechanisms of pathogenicity · Anaemia and haemoglobinuria: changes in osmotic fragility cause lysis of erythrocytes · Systemic inflammatory reactions: associated with DIC. Enhanced platelet aggregation and degranulation and release of vasoactive molecules reduce blood pressure · Cytoadherence: infected RBC adhere in capillaries of various organs · Neurological disorders: result of hypoglycaemia, hypoperfusion, hypoxia and hypermetabolism. · Fever: due to presence of antigens Clinical signs Acute babesiosis is associated with apathy, high fever, anorexia, parasitaemia, haemolytic anaemia, thrombocytopenia, icterus, circulatory disorders and neurological disorders resulting in a multiple organ dysfunction syndrome (MODS). Therapy Acute babesiosis is a medical emergency- imidocarb, combo of atovaquone and azithromycin. Cattle- diminazene, humans- clindamycin Diagnosis · Case history and symptoms · Direct demonstration of parasite in Giemsa stained blood smear · ELISA, PCR, haematology and histopathology Therapy Acute babesiosis is a medical emergency- imidocarb, combo of atovaquone and azithromycin. Cattle- diminazene, humans- clindamycin Epizootological situation The location of babesia can be classified into 3 zones: 1) Free zones: areas where the tick vector doesn't occur- Canada, Iceland, Greenland 2) Areas of enzootic instability: locations with well-defined cold seasons- no ticks 3) Endemic areas: locations with year- long prevalence of ticks. THEILERIA Members of the genus theileria are parasites of domestic and wild ruminants, equids and some other mammals. They are responsible for important diseases such as East Coast fever and theileriosis. Characteristic stages in the mammalian hosts are meronts in mononuclear leukocytes and erythrocytes. Main species · Theileria parva- cattle · Theileria mutans- cattle · Theileria orientalis- cattle · Theileria ovis- sheep and goat · Theileria equi- horse Morphology The leukocyte form are small bodies of circular-irregular shape, containing a few large nuclei or many small nuclei. These are known as Kochs bodies. The erythrocyte form are oval rod shaped, sometimes also forming a maltese cross. Life cycle · Vertebrate host: infected ixodes ticks inoculate sporozoites during feeding into a mammalian host. The sporozoites infect mononuclear leukocytes, multiply by merogony and generate merozoites, which invade erythrocytes- gametogony. · Tick: During subsequent feeding, infected erythrocytes are ingested by larval/nymph ticks and parasites released in the ticks intestine. Here the gamonts develop to gametes (ray-bodies) that form zygotes by syngamy. Zygotes undergoes a complicated developmental cycle, resulting in formation of infective sporozoites. After moulting of the tick and commencement of feeding, the parasite is transferred to a new host. Theilleria is only transferred trans-stageal (vertical) in ticks! Not transplacental as Babesia spp. Pathogenesis The members of the genus theileria can be grouped into transforming and non-transforming species. a) Transforming theileria: highly pathogenic as they immortalize the infected leukocyte host cells and stimulate them to continuous proliferation. In these species the leukocytic phase continues even after the initiation of the erythrocytic phase. Three main phases: 1) After incubation period, a massive hyperplasia of mononuclear leukocytes develops. This is followed by lymphocytolysis. This produce tumor-like infiltrations 2) Infected macrophages are activated and show enhanced phagocytic activity and upregulated TNF synthesis- fever, chronic inflammation and emaciation. 3) Progressive lymphocytolysis and suppressed leukopoiesis resulting in lymphoid depletion and disorganization of lymphoid organs associated with necrosis and hemorrhages of GIT. b) Non-transforming theileria is usually associated with low number of meronts and low parasitemia levels. Disease symptoms are limited to erythrocytic phase and resembles that of Babesia spp. Clinical signs · Transforming theileria: the pathogenic stages are the meronts in leukocytes. These cause fever, leukopenia, dyspnea and necrosis of GIT. · Non- transforming theileria: the pathogenic stage is the erythrocyte stages, which induce fever, erythropenia, haemoglobinuria and icterus. Diagnosis · Case history, clinical signs and laboratory examinations · Giemsa stained blood smear, DNA analysis, serology Therapy, control Chemotherapy of cattle- buparvaquone Chemotherapy of horse- parvaquone Live vaccines are available for sheep and goat. Epidemiology Widely distributed in Africa, Asia, Oceania and Europe. Various mammalian hosts serve as reservoir hosts, in which erythrocytic stages may persist for years East coast fever- theilerioses of cattle East coast fever is caused by Theileria parva, a highly pathogenic parasite. Mortality rates can reach up to 100% and only young and immune animals survive the infection. Typical symptoms include: swelling of lymph nodes, fever, dyspnea, constipation and bloody diarrhea. Death occur after 2-4 weeks or in peracute cases- within 4-5 days. Necropsy shows emphysema and edema of lungs and ulcers of GIT. Corridor disease Resemble east coast fever (both is caused by t.parva), but differ in epidemiology. The distribution of east coast fever is East and Central Africa, while corridor disease is found in South Africa as well. It is usually associated with less severe clinical symptoms- still very pathogenic. Equine theileriosis Only the erythrocytic stages of Theileria equi are pathogenic. Clinical signs in acute phase resembles those of Babesia. Chronic infections are associated with low-grade anaemia, splenomegaly and moderate decline in performance. Proceeding of competent authorities, control and prevention. Babesiosis Control · Acaricides: to prevent further exposure- prevent tick attachment · Babesiacide: in case of severe outbreak · Carcasses with icterus or emaciation is condemned · Vaccine, only live vaccine, may be virulent in adult animals Prevention · Tick- control: ascaricides and habitat destruction, insect repellent · Cross- breeding European cattle with babesia resistant breeds Theilleriosis Control · Tick control · Chemotherapy · Cull affected animals: carcass is approved for consumption unless in acute febrile condition · Movement control Prevention · Tick control: spray (amitraz), dips, pheromone traps, window nets · Vaccination · Import animals from free countries. a) Sanitation measures and focal disinfection at these diseases. Using of organophosphates and carbamates Babesia and Theilleria are unable to form cyst, thus cannot survive free in the environment. This makes focal disinfection unnecessary as the disease is strictly vector borne. Main approach is to reduce the reservoirs of infection and the presence of the ticks. · Protection of cattle: pastures far from sources of ticks · For man: repellents, wear long sleeves tucked in shirts long, pants, shoes, boots and hat · Vector control: traps, screens, ascaricides Using of organophosphates and carbamates Organophosphates • Synthetic organic compounds containing phosphorous in their molecules, they kill a wide range of insect, act as stomach, contact and respiratory poisons. • Have a short residual effect, high efficiency, low toxicity to man and other animals of many preparations. Easy and inexpensive way of application, rapid degradation in soil (less risk of chronic effects in ecosystem) and act as systemic insecticides. • They are cholinesterase inhibitors (cause paralysis of NS) resulting in that acetylcholine (ACh) is not broken down, causing neurons to continually fire, leading to overstimulation of the nervous system and later, death Frequently used · Bromophos: very effective against ectoparasites in livestock and acaricide · Malathion: important contact insecticide and acaricide used for control of mites on vegetables Dichlorvos: volatile contact and stomach insecticide and acaricide, effective fumigant (flies) · Diazinon: non-systemic insecticide with some acaricidal effect with better residual activity. · Pirimiphos: wide spectrum, effective against flies, cockroaches, mosquitoes, lice, bed bugs and fleas · Chloropyriphos: moderate persistence, effective for mosquito, cockroaches and other household pests · Azamethiphos: against flies, long residual effect if applied to inorganic supports like walls Carbamates · Cholinesterase inhibitors, some have a systemic effect and longer residual effect than OP. They are related to carbamic acid, are stomach and contact poisons, and have a rapid degeneration in soil. · Majority are solid substances, used as dusts and surface sprays. Treated insects show initial hyperactivity, followed by convulsions and paralysis. Examples: • Dioxacarb - effective against cockroaches, flies, fleas • Bendiocarb - against household pests, flying and crawling • Pirimicarbic - systemic insecticide with rapid action Three main classes of carbamates 1) N-methylcarbamates of phenols and hydroxyheterocyclic compounds - Dioxacarb: effective against cockroaches, flies, fleas, other insects. - Bendiocarb: against household pests, flying and crawling 2) N-methylcarbamates of oximes - Methomyl: soil and seed treatment but high mammalian toxicity 3) N,N-dimethylcarbamates of hydroxyheterocyclic compounds - Pirimicarb: specific systemic insecticide with rapid action, only moderate mammalian toxicity b) Investigation of blood traces Since blood evidence associated with crime can provide information in a case, it is essential to correctly document, collect and preserve this type of evidence. If blood evidence is documented, collected and stored suitably, it can be presented to a judge or jury several years from the time of the criminal act. The most powerful application of blood evidence is the ability to absolutely eliminate a person as a potential suspect in a crime. Collection of samples 1) Dried blood stains - If the bloodstained item is small and transportable, pack it in a paper bag or envelope. - If the bloodstained item is large or not easily transported, then following techniques can be used for collecting the blood strains. è Cutting out the portion(s) of item with the bloodstain è Tape lifting bloodstains è Scraping bloodstains into a paper packet è Absorbing stains into moistened ½" long threads or 1/2x1/2" cotton square. 2) Wet blood stains - If the item is small and transportable, pack it in a paper bag (or plastic). Bring to secure location, allow to air dry. - If bloodstained item is large or not easily transported, then absorb the stain onto a 1"X 1" square of cotton muslin. Pack it in paper (or plastic to prevent contamination of other subjects). Bring to secure location, let air dry. Bloodstain pattern analysis Is the examination of the shapes, locations and distribution of pattern of bloodstains. It's performed in order to provide an interpretation of the physical events that gave rise to their origin. The following information may be obtained from a proper bloodstain pattern analysis - The distance from the blood source to the target - Direction of travel and impact angles - Nature of the force used to cause the bloodshed - The object used to cause the bloodshed - Sequencing of multiple bloodshed events - Interpretation of contact or transfer pattern

20. Tick encephalitis, prevention and control, measures in outbreak, current epizootological situation. Proceeding of competent authorities in the case of disease outbreak, control and prevention

Tick-borne encephalitis (TBE) is a viral infection of the central nervous system. There are 3 main types of TBE: o Western European o Far Eastern (Russia, China, Japan) o Siberian (Siberia, Mongolia) Etiological agent Caused by group B arboviruses, which belong to family Flaviviridae. Natural reservoir is wild animals and ticks. Transmission Spread ticks - the virus lives in tick saliva. Ticks live in forests, woods, grasslands, riverside, meadows, marshes, brushwood. They usually live in the undergrowth, where they can easily get onto the clothes or skin (0.5-1m above soil). - Virus is found naturally in small animals (mice and voles (klatremus) and in host (sheep, goats, cattle, birds, carnivores, horses and humans) - Disease is transmitted by the bite of several species of infected ticks o Ixodes scapularis, Ixodes ricinus, Ixodes persulcatus.; Dermacentor. Can also be zoonotic: Ruminants and dogs providing the principal source of infection for humans. Humans become infected when they are bitten by an infected tick or when drinking non-pasteurized milk. Pathogenesis The virus replicates at site of inoculation before entering the lymphatic system and bloodstream, causing viraemia. Later it is transported to the central nervous system. 1/3 of infected people get encephalitis. Clinical signs Ruminants: Inapparent but shed virus in milk (7-10 days following infection) Dogs: Nervous signs with apathy, hyperexcitability, ataxia, paresis/paralysis of limbs, abnormal spinal reflexes, nystagmus and paralysis of facial nerve. Humans: - Inapparent (abortive form- refers to end of disease before clinical signs) - Viremic phase: Flu-like symptoms, headache, weakness, nausea during - Meningitis or meninigoencephalitis with vomiting, confusion and paralysis - In acute cases there is death Treatment There is no specific treatment for tick-borne encephalitis. The patient is treated symptomatically depending on the symptoms: - Indomethacin or paracetamol (for pain and inflammation) - Diazepam (sedative) - Prednisone (anti-inflammatory - when the course of the disease is very severe) Intravenous solutions are constantly given to restore the electrolytic balance. Mannitol, which reduces the accumulation of excessive fluids in the brain, is also administered. Diagnosis Clinical signs, seasonality and epizootology situation Histology: meningoencephalitis Biochemistry - Phase I: leukopaenia, thrombocytopaenia - Phase II: increased WBC in blood and CSF Serology: VNT, ELISA Reverse Transcriptase PCR Epizootiological situation Tick activity depends on factors such as temperature, moisture and humidity. Wet summers and mild winters increase tick activity. In central Europe the main periods of tick activity are May/June and September/October. In the mountainous and colder areas of northern Europe, ticks only tend to be active in summer and are rarely found in areas above 1,200 meters. Measures during outbreak Prevention, control Tick control, monitoring of ticks: - Make maps showing infestation with ticks is very important because they spread to areas in higher places - Remove of ticks - Vaccination - Prevented by using insect repellents, protective clothing - Treat your clothes with insecticides such as permethrin - Avoid eating/drinking milk and unpasteurized dairy products in countries where there is a high risk of TBE. Vaccine exists! Recommended for those who spend much time in the forest and for the rural population. a) Sanitation measures and focal disinfection at these diseases. Ticks, lifecycle, methods of treatment Sanitation - Insect control - Using of permethrin on farm - Permethrin products can be applied to clothing/boots (not to skin) - Kill ticks that come in contact with the treated clothing, and usually stay effective through several washings. Inactivation of virus by higher temperature - 56° C 30 min - 72-85° C during 10 seconds - By pasteurization Ticks, lifecycle and methods of treatment - Incomplete lifecycle (larvae, nymphal stages, adult). - Ticks are main carriers of the virus (feed on the blood of infected animal) - The virus is transmitted both o Transstadially (from larva to nymph to adult ticks) o Transovarially (from adult female tick through eggs) Treatment to kill ticks: Acaricides - Chemical ascarids (fipronil, imidacloprid, amitraz, etc.): spot-on, dipping bath, spray, etc. - Organophosphate and pyrethrioid (not for cats!) insecticides. Are used in form of plunge dips, spray races, pour on/spot on, ear tags and tail bands impregnated with tick-killing chemicals. Using permethrin on farm: Permethrin products can be applied to clothing/boots (not to skin) à kills ticks that come in contact with clothing. b) Simulation by animals = The occurrence of problems for which clinical or anatomical evidence is lacking in human medical practice. The reasons for the simulation are very diverse (trying to avoid punishment, unwillingness to perform some of the activities in the job, getting insurance benefits, etc.) While a person simulates pursuing a certain goal, animals, if not mimics, are not capable of simulating themselves. However, their breeder may be interested in concealing some of the animal's properties or the opposite; In causing some conditions that would not have occurred in the animals without their killing. The breeder may be interested in raising claims to get "damages" for damaging the animals that were the object of a contractual relationship (rent, borrowings) or to obtain a discount on the price of the animal that he took as the object of the purchase or for some other reason. Examples includes: - Hemoptoe (bleeding from the lungs) by spreading the blood of the facial part of the head of the animal or wounding the nose - Albuminuria - Achieved by adding a dry egg white to urine (can be distinguished serologically) - Glykosuria - Sugar in urine is achieved by adding fruit juice to the urine) - Haematuria - Blood in urine is achieved by the administration of higher doses of urotropin, rhubarb exhilarants or by the addition of foreign blood to the urine - Emesis - vomiting is achieved by administering ements. Bloody vomiting, especially in carnivores, can be imitated with potassium permanganate (vomits are positive to benzidine reaction, but excrements are negative) - Intoxications (poisoning) - Atropine - Administered to dogs to disguise breathing issues during sale. At the time of selling the animal looks okay but after some time the problems can become visible - Animals can, after training, be forced to experience hives, ataxia, pain manifestations

29. Toxoplasmosis, prevention and control, measures in outbreak, current epizootological situation. Proceeding of competent authorities in the case of disease outbreak, control and prevention

Toxoplasmosis Toxoplasma gondii only species of the genus Toxoplasma. Cyst forming coccidial parasite with worldwide distribution with a facultative heteroxenous lifecycle. FH are domestic cats and other felids. Numerous warm-blooded vertebrates can serve as IH carrying tissue cysts. Humans are frequently infected as aberrant hosts. Forms T. gondii has 3 main forms in its host 1. Tachyzoites: rapidly multiplying. Endopolygony reproduction. 2. Bradyzoites: slowly multiplying. Endodygony reproduction. 3. Tissue cysts: walled structures often found in muscles and CNS. It is the infective form and contains bradyzoites. Life cycle · Environment: Unsporulated oocysts are passed by the FH to the environment. Here they sporulate within 1-5 days. Sporulated oocysts contain 2 sporocysts with 4 sporozoites. · IH: Numerous species of vertebrates are natural IH. Both sporozoites and bradyzoites are infective to these hosts. After ingestion of sporulated oocyst (humans- vegetables) or by tissue cysts, the released sporozoites or bradyzoites penetrate into the intestinal wall and infect cells. In the host cell they induce the formation of a parasitophorous vacuole. Inside this vacuole, rapid asexual extraintestinal proliferation by endodygeny (tachyzoites) occur. The released tachyzoites are spread to various organs until the onset of immune response cause stage conversion to bradyzoites and cyst formation. · FH: Cats acquire the infection by oral ingestion of bradyzoites (in tissue cysts in IH) or by sporozoites (in sporulated oocysts). https://www.researchgate.net/figure/Life-cycle-of-Toxoplasma-gondii-Shown-are-the-biology-infection-and-replication-of_fig2_223973212 - Bradyzoites: Infection with bradyzoites is followed by an enteroepithelial phase with merogonies, gamogony and oocyst formation. Excretion of unsporulated oocysts in the faeces. - Sporozoites and tachyzoites: infection with sporulated oocysts is followed by extraintestinal asexual tachyzoite proliferation and subsequent bradyzoite formation in cysts. - Some extraintestinal parasite stages may return to the intestine and finish the development by merogonies, gamogony and oocyst formation. Pathogenesis Characterized by focal necrosis due to cell damage during parasite proliferation. Associated with adjacent inflammatory and immunopathological lesions in many organs. Clinical signs Most of the natural infections are asymptomatic. Clinical signs occur predominantly in young or immunosuppressed animals. · Cats: anorexia, pneumonia, hepatitis, icterus, diarrhoea, encephalitis, nephritis, myositis · Other animals: transplacental transmission of the parasite may cause abortions or damage to the foetus. Change of behaviour- rodents stop being afraid of cats. · Humans: abortion, hydrocephalus, mental-ocular- and aural disability of the child. Idiopathic epilepsy, schizophrenia, behavioural changes- love cats. Reduced reaction time. Therapy - Clindamycin, sulfadiazine (nb dangerous for cats) + trimetrhoprim. Humans- pyrimethamine. Diagnosis - Cat: flotation method (Faust)- detection of oocysts in faeces (only possible during the first 2-3 weeks). Serology and animal inoculation. Sample- blood, sputum, tissue biopsy. - IH: direct demonstration of cysts in tissues- histology, DNA analyses. Indirect- serology Epizootological situation Toxoplasmosis have a worldwide distribution and is the most frequent parasitic zoonosis. In UK up to 1/3 of the human population will have toxoplasmosis at one point during their life. The seroprevalence in sheep is up to 20-75% and toxoplasmosis caused 30% of diagnosed abortions. Proceeding of competent authority, control and prevention Control · Rodent control · Treatment of infected animals · Composting of infected excrement · Burn and disinfect placenta and associated material following abortion Prevention · Cats - Prevent access to farm housing, keep cat indoors, don't get a new cat while pregnant - Feces should be removed daily - Feed with dry, canned or boiled food, discourage hunting and scavaging · Intermediate host - Keep cats away - Vaccination of sheep (live attenuated) - Surveillance programmes (tokowise)- free blood testing. · Humans - Public education- especially pregnant women - Do not handle stray cats, regular cleaning of litter box with gloves + wash hands after (esp if pregnant or immunocompromised), regular disinfect tray with boiling water, fence children's sandpits - Food hygiene: cook and freeze meat products, don't drink raw milk, wash fruit/vegetables and hands, wear gloves when gardening. Wash cutting boards, dishes, counters, utensils and hands with hot soapy water after contact with raw meat, poultry, seafood, or unwashed fruits or vegetables Seropositive cats- no risk, immune a) Sanitation measures and focal disinfection at these diseases. Protection and disinfection of the sand pit. Resistance Oocysts of t. gondii can survive for 3 weeks after infection in feces, the zygote form (unsporulated) is also highly resistant and is able to survive at 4°C and in water pipelines and moist soil for more than one year. Tissue cysts remain infective in meat for as long as it is edible and uncooked. Disinfection Ethanol (70%), formalin (1-2%), Na hypochlorite (1%), chloramine T (3%) / Use only drinking water, no disinfection with chemicals - Litter box: disinfect once a month by wiping it out and applying boiling water - Cooking: Whole meat: 63°C, ground meat: 71°C and poultry 74°C - Freeze meat - Cooking (5min at 66°C) or freezing (-15°C for 3 days, or -20°C for 2 days) Protection and disinfection of sand pits Protection · Keep clean and dry, daily removal of wastes, leaves and excrements · Cover when not in use to prevent entry of cat · Rake regularly to remove rubbish and airing of sand, fence pits Disinfection When disinfecting a sand pit it is important to use a mild detergent or household disinfectant diluted in water, for example Na hypochlorite. There should be no salmonella or parasites present in the sand box, and not more than 10 CFU/g of faecal coliforms and 1 CFU/g enterococci. b) The difference between an abandoned and a lost animal Definitions · Lost property: all tangible personal property which does not have an identifiable owner and which has been mislaid on public property or premises used for public recreation or other places open to the public in a substantially operable, functioning condition. · Abandoned property: all tangible personal property that does not have an identifiable owner and that has been disposed on public property in a wrecked, inoperative, or partially dismantle condition or has no appearing intrinsic value to the rightful owner. - The term "abandonment" means to forsake entirely or to neglect or refuse to provide for an animal by its owner or the owner's agent. Such abandonment shall constitute the relinquishment of all rights and claim by the owner to such animal. Abandonment of animals by owner- procedure for handling - Any animal left with veterinarian or in a boarding kennel for treatment/care and is abandoned by its owner for more than 10 days can be turned over to custody of nearest humane society or dog pound in area (after written notice to owner) - The notice given to owner or agent of owner shall relieve veterinarian or kennel operator of any further liability for disposal. Such procedure by a licensed vet shall not constitute grounds for disciplinary procedure. Reporting lost or abandoned property - Whenever any person finds any lost or abandoned property, such person shall report the description and location of the property to law enforcement officer. - The officer taking report shall ascertain whether the person reporting the property wishes to make a claim to it if the rightful owner cannot be identified or located. - If the person want to make such claim, he or she shall deposit with the law enforcement agency a reasonable sum sufficient to cover the agency's cost for transportation, storage and publication of notice. This sum shall be reimbursed to finder by the rightful owner should he or she identify and reclaim the property. - It is unlawful for any person who finds any lost or abandoned property to appropriate (tilegne) the same to his or her own use or to refuse to deliver the same when required. - Any person who unlawfully appropriates such lost or abandoned property to his or her own use or refuses to deliver such property when required commits theft.

1. Tuberculosis and paratuberculosis, prevention and control, measures in outbreak, current epizootological situation. Proceeding of competent authorities in the case of disease outbreak, control and prevention

Tuberculosis Mycobacteriosis, genus mycobacterium. Oie notifiable. Gram + bacilli. Acid fast (ZN, kinyoun). Intensive testing à disease and bacteria in animals is partially under control. Public health risk = low. Mycobacterium tuberculosis complex M. bovis (most warm blooded animals and humans) M. caprae M. tuberculosis (most host spesific, humans) Mycobacterium avium complex (causes non-tuberculous disease) M. avium subsp. avium (M. avium subsp. paratuberculosis = paratuberculosis) M. avium subsp. intracellulare Bovine tuberculosis Chronic disease of animals caused by M. bovis. General illness, inflammatory changes, coughing and presence of tubercles. Transmission Contagious. Direct contact between animals, or indirectly by ingestion of contaminated material Inhalation: of infected droplets expelled by coughing (90%) Ingestion: of contaminated milk and colostrum by humans or by calves from their mothers Tropism Disease mainly affects the lungs and liver (as main parenchymatous organs). However, bacteria can "escape" and infect body cavities (à generalized disease). Pathogenesis Bacteria in lung à invade alveolar macrophages à macrophage is surrounded by other immune cells (Ly and other macrophages) àfuse together and form giant multinucleated cells: The granuloma/tubercle. The tubercles work to Prevent spreading of mycobacterium Evade destruction by immune system Promotes host immunosuppression There is central necrosis and later fibrotic encapsulation of the tubercle. Primary site of infection = primary focus. This focus + other similar lesions forms in the regional lnn, and together they form the primary complex of the disease. Bacterium enters blood à dissemination à multiple foci of infection. Then = generalized disease (pearl, miliary) which can be rapidly fatal Forms of tuberculosis Respiratory tuberculosis (Bronchopneumonia. Chronic, wet cough. Tachy/dyspnea). Miliary tuberculosis (tiny 1-5 mm lesions, "millet seeds", many and widespread) Pearl tuberculosis (tuberculosis of the serosal surfaces like pleura and peritoneum) Clinical signs Disease is long-term, takes years to develop. Therefore, typical clinical signs are non-specific and general. · Weakness, non-persistent fever · Anorexia, weight loss · Non-persistent coughing, dyspnea, signs of bronchopneumonia · Enlarged lnn · Diarrhea Remember two things: a) Bacterium can also lie dormant and NOT cause disease b) Infected animal sheds bacteria all those years with subclinical disease! Diagnosis 1) Intradermal tuberculin test - based on delayed hypersensitivity reaction a. Tuberculin is a purified protein derivate of M. bovis b. Test is either simple (just bovine tuberculin) or complex (bovine + avian tuberculin) c. Injected intradermally on the neck (one on each side if complex) d. Wait 72 hours and measure size of skin, compare it to pre-injection size e. 2-4 mm dubious, 4+mm positive 2) RGT shows the radiodense tubercles 3) Laboratory tests a. Bacterial culture on L-J agar, cauliflower appearance (min 8w) b. PCR or ELISA on sputum or tissue samples 4) Necropsy a. Tubercles on lnn in relation to lungs (mediastinal, bronchial) b. Can also be on lungs, serosal surfaces, liver, spleen, GIT c. Miliary, pearl BCG vaccine for bovine tuberculosis but has limited effect Differential diagnosis Lung worms, actinomycosis, CNS disease, diarrhea, traumatic reticuloperitonitis, etc. Avian tuberculosis by M. avium subsp. avium (not resp disease!) Important disease in birds and mammals. Of mammals, pigs are most susceptible but they rarely show disease. · Infected birds usually show no clinical signs - they become lethargic and emaciated · Diarrhea, comb + wattle becomes pale and small · Affected birds are often older than 1 years old which is rare... Sometimes sudden death occurs, and they find lesions during PM inspection: · Almost always in GIT · Deep ulcers filled with caseous material containing mycobacterial cells (almost like the tubercles) · Caseous material is discharged into lumen of intestines and is shed in feces à transmission · Liver and spleen are enlarged due to formation of this tuberculous tissue Pigs No clinical signs. At PM inspection the meat on head and mesenteric lnn can have tuberculous lesions. Diagnosis also by ZN stain of smear (sputum, swab? Tissue.), culture and PCR. Tuberculin test to ensure healthy animals before movement and ensure healthy flock. No vaccine for avian TB (BCG is for T. bovis) Human tuberculosis M. tuberculosis Tuberculosis infect 1/3 of the human population, however only 5-10% develop clinical illness (immunosuppression). There is an increased incidence of human tuberculosis due to increased immigration, resistant bacteria, increased circulation in wildlife and stop of obligatory vaccination. Majority of cases occur in south- east Asia (35%) and Africa (30%). Clinical signs Loss of appetite, fatigue, chest pain, wet productive cough https://www.youtube.com/watch?v=0qFiflLL21U Prevention and control Veterinary filter: protect animals to prevent infectious diseases. Quarantine and isolation. Hygienic filter: for protection from personnel: protective measures for man, clothes, gloves, footwear. Black and white system. Carcass box with special entry for cars. Window nets prevent entry of insects that may transmit disease. No treatment of infected animals: radical or elimination method. Pasture: lime (800-1000 kg/ha), recultivation. Rodents are TB reservoir: At first use acute rodenticides and then of 2nd and 3rd generations. Avian tuberculosis Prevention of avian tuberculosis into the flock of animals, include control of transport, purchase of animals from farms free of disease, quarantine of purchased birds and poultry. No treatment or vaccination of avian tuberculosis. Tuberculosis of swine Protection of herds against introduction of disease agents (free-living birds), control of animal transport, purchase of animals from disease-free herds. No treatment and immunoprophylaxis. Radical elimination of sick animals. Paratuberculosis M. avium subsp. paratuberculosis. Johne's disease in ruminants (»Chron's disease in humans) · OIE notifiable · Chronic, usually fatal · Contagious · GIT; Mainly small intestine · Bacterium very hardy; survive heat, cold and desiccation · Not zoonotic! Transmission · Bacteria shed in feces, milk and colostrum · Calves less than 6 months are most susceptible · Oro-fecal route · Ingestion o In calf by milk/colostrum (calf is sick from birth and sheds bacteria for years and years) o Feed and water contaminated by feces o Soiled udders · Intrauterine vertical transmission Pathogenesis Main site of infection is ileum à In ileum there is Peyers Patches containing clusters of macrophages and lymphocytes à these macrophages engulf bacterium to kill them, but bacterium survives à Inside macrophage they multiply until it ruptures àmycobacterium is spread and infects new cells. The following immune response is to recruit more lymphocytes and macrophages, and these cells infiltrate the intestinal mucosa. This causes thickening of mucosa and damage to enterocytes à prevents nutrient absorption à diarrhea à emaciation over time. (Thus, tissue destruction is bcs of immune response). Clinical signs Chronic disease developing over time. Clinical signs appear in young adulthood from 4-7 years of age. Stress and malnutrition are predisposing factors. Paratuberculosis causes hypertrophic enteritis ultimately causing weight loss and unthriftiness · Watery diarrhea and weight loss but normal appetite and normal temperature · Ruminants other than cattle may not have diarrhea · Protein loss = intermandibular edema = bottle jaw · Clinical signs develop and become more serious over time, will in the end be fatal Diagnosis Can be difficult because animals don't show signs of disease! · By clinical signs · Upon necropsy Isolate mycobacterium from feces · Culture on special medium · Must have mycobactin a siderophore used by Mycobacterium to shuttle free extracellular iron ions into the cytoplasm · Confirm by PCR Impression smear from lesion in intestine · ZN/kinyoun acid fast staining · Confirm presence in microscope Confirm presence of antibody with serology · ELISA · Compliment fixation test · Agar gel immunodiffusion test There is also an intradermal skin test Johnin test, same as before. Has limited value. Vaccine exists it seems (OIE). Prevention and control There is no known treatment for the disease. · Control involves good sanitation and management practices including screening tests for new animals · Test and slaughter (only assured approach to the eradication of the disease) · Test and segregate: Infected herds are usually quarantined and animals that have been in contact with reactors are traced General prevention of young animals should be prevented from contacting manure from adults. - Contaminated pastures should be tilled and reseeded or used for animals that will not become herd replacements. - In herds affected with paratuberculosis, calves, kids or lambs should be born in areas free of manure and removed from the dam immediately after birth. - Bottle-fed pasteurized colostrum (or tested disease-free colostrum) and raised separately from adults until at least one year old. Also, reduce faecal contamination of feed a.) Sanitation measures and focal disinfection at these diseases. Activation of disinfectants. Mycobacterium spp. are very resistant to disinfectants due to the production of spores that can survive in the environment for up to 4 years (soil-4y, water and pasture- 2y, manure-200d). Because of this it requires long contact time and higher concentrations. Disinfection · Focal disinfection (aerosols): Chloramin T (6-10%), peracetic acid (1%), alkaline formalin (3%) · Environmental disinfection: glutaraldehyde (2%), formaldehyde, lime powder (1100g/m2) · Disinfection of organic material: sodium hypochloride (2%)- long contact time · Disinfection of excrements: 0,3% perestril (peracetic acid), 3% lime. · Manure composting is not enough because TBC can survive for 6 months in liquid slurry.Slurry should be stored for longer than 6 months before applying to field- important to thoroughly clean equipment before and after. ParaTBC can survive water treatment and in some cases pasteurization. Sanitation measures Elimination of animal, final disinfection, observe for 110 days. · Rodent control (reservoirs): at first use acute rodenticides, then later chronic rodenticides of 2nd and 3rd generation. · Protective measures · Prevention and control Activation of disinfectants Heating · NaOH: 70-80°C · Chloramines: 50-60°C Addition of detergents · Addition of 2% sodium carbonate (washing soda- mechanical cleaning) · 3% alkaline formaldehyde (for mycobacteriae and fungi) Organic matter and decreased temperature can decrease the efficiency b.) Determination of the age of pathological process (age of TBC process) The age of a TBC process is not uniform and duration of nodule formation depends on, among others, way of infection. In general: · Milliary nodule: 14 days · Caseation (necrosis): 4 weeks · Calcification: 3 months · Conglomeration: 5 months · Acute cavern in lung: 8 days · Chronic cavern: determined by nature and composition of connective tissue · Shape - Pinhead: 3-4 weeks - Hazelnut: 5-6 weeks - Pearl: 75days to ½ year

6. Tularemia and borelliosis, prevention and control, measures in outbreak, current epizootological situation. Proceeding of competent authorities in the case of disease outbreak, control and prevention

Tularemia , ¯, ¯¯ Francisella tularensis. Zoonotic. Tick/mosquito borne. (Det er bare tull med den flåtten og milten) · Gram negative · Many subspecies with different virulence · Natural disease of lagomorphs and rodents · Other mammals, birds and invertebrates are also susceptible Francisella tularensis subsp. tularemia (Type A) - humans and rabbit. North America Francisella tularensis subsp. holarctica (Type B) - Aquatic rodents and voles in NA, Lagomorphs in Eurasia. Transmission Main is vector transmission; ixodes and mosquitos Ingestion (oro-fecal route) and inhalation (direct contact) Pathogenesis Facultative intracellular pathogen à Multiply in macrophages à Induce apoptosis à escapes to re-infect Like this, it evades the immune system and spreads throughout the body. Course of disease and spread inside body also depends on route of exposure. Epizootology Endemic in Northern hemisphere. In Europe it is mainly transmitted by ticks, while in the USA it is known as "deerfly fever". Infective dose is low and bacteria is shed in urine and feces. High chance of human infection! Wear gloves etc. Clinical signs Depends on the host and their susceptibility and sensitivity to the pathogen 1. High susceptibility, high sensitivity - Severe disease. Septicemia with fever. Enlargement of lnn and spleen. High mortality, death within 12 days a. Brown hare, rabbit, hamster, water rat 2. ¯ High susceptibility, low sensitivity - reservoir group. Sheds bacteria over long periods a. Squirrel, hedgehogs 3. ¯¯ Low susceptibility, low sensitivity - mild or no apparent disease. a. Horse, cattle, dog, cat In humans it looks different. At the site of inoculation there is often ulcers or abscesses. Depending on the route of infection there are several forms of tularemia in man: Internal form has Thoracal form (cough, dyspnea, pneumonia = lung) and abdominal form (abdominal pain, diarrhea) External form has Ulceroglandular (most common), oculoglandular, oralglandular. Lnn enlarged and reaction at bite site Diagnosis In necropsy we find round, grey, necrotic lesions on viscera and caseous necrosis on lnn (in septicemic cases). Identification of agent by · Bacterial culture of special Francis medium · Impression smear · Tissue sections for histopathology From there we use PCR to confirm bacterium. Serology is good in human cases but useless in animals, because death occurs before the development of Ab. Remember to use gloves and masks when handling samples! Vaccine in humans is possible. Responds to certain antibiotics. Borelliosis - Spirochetoses; Borellia burgdorferi sensu stricto is spiral, endocellular flagella, motile. Gram negative. Zoonotic. Tick borne. Lyme disease, and cause erythema chronicum migrans in humans. Main reservoir= birds - Other species: B. afzelji, B. garinji also cause lyme disease - Vector: Eggs are mostly not infected. Grow to larvae. - May be infected transstadially making larvae already infected, but they think larvae feeding on rodents and birds (main reservoir) is when they get infected for the first time. - Tick nymphs are main transmitters: Feed on humans, mammals at spring and summer - Adult ticks continue to feed on mammals and humans and infecting them. - Therefore we see that Lyme disease is seasonal and that Ixodes ticks have wide host range Pathogenesis Inside tick the bacteria move from midgut to salivary glands and are deposited during feeding. From site of inoculation, the bacteria can migrate via lymph or blood to its preferred organs. It replicates in the skin and will reside in tissues; skin, heart, nervous system etc. Bacteria elicit a strong inflammatory response which is thought to be the cause of the severe disease, rather than the work of the bacteria itself. (Immunocomplexes deposited in joints and kidney) Clinical signs Very few dogs (only few % of seropositive individuals) develop clinical disease after infection. If present there is · Non-specific signs o Lethargy, anorexia, fever, depression o Disappears after few days · No erythema migrans but can be reddening around bite site that disappears after tick removal · Later we can see more specific signs o Lameness, seizures, encephalitis and joint swelling starting in the limb closest to bite site · "Lyme nephritis" in dogs with severe, untreated long-lasting disease Humans get "erythema migrans": A non-itchy, painless often bulls-eye shaped rash that resolves in 4 weeks. Diagnosis Can be hard. Depends on history of travelling to tick habitat, clincal presentation and in humans the rash. Sample is blood, urine, CSF. Isolate agent: Barbor-Stoner-Kelly 2 medium. Identify by PCR. Detect antibodies with ELISA or indirect IFA. There is a snaptest available! Treated by antibiotics. Prevention and control General prevention · Insect control: insect repellent and removal of ticks. - Ascaricides: permethrin spray, amitraz collar, fipronil spot-on · Protection of pets: prevent ingestion of carcasses, tick bites and contact with wild animals. Tularemia · Single case: disinfect cage, early treatment to prevent deaths/ losses (may be prolonged). · Several cases: cull animals, disinfect area, notify OiE · Control: difficult, limited to reduction of tick infestation, keeping pets inside, not feeding raw meat. · Prevention: vaccine, gloves Borelliosis · Prevention: tick avoidance- permethrin spray, amitraz collar, fibpronil spotVaccination of young dogs. - Pre- vaccination infection: long incubation, persistence of infection after ATB treatment may lead to disease in immunised dogs. a.) Sanitation measures and focal disinfection at these diseases. Insect control methods Sanitation measures and disinfection Tularemia Is very resistant and can survive in environment for months, it is also resistant to freezing (3 years). Viable bacteria can be found for weeks to months in carcasses, hides, urine, feces, bedding and fomites. Disinfection · Hypochlorite (1%), chloramine T (1%), formaldehyde, peracetic acid, ethanol (70%), heat - Water: chlorination - Vector: insect and rodent control, pyrethroids, organophosphates Borrelia Killed by common disinfectants, heat and UV light. Insect control methods Insect control involves the following mechanism: killing of insects outright, reduction of reproductive capacity, slow growth and development of insects. 1) MechanicalLabour- intensive and require special material and devices, for example: window screens, adhesive substances, light and fall traps 2) PhysicalTemperature, steam, heat, UV light, radiation and ultrasound 3) BiologicalInvolves the deliberate introduction and establishment of natural enemies into areas where they didn't previously occur. a) Parasites: aphid parasites, egg parasites, caterpillar parasites, beetles and flies.Nematodes- can parasitize spiders, leeches, annelids, crustaceans, etc. b) Pathogens: fungi- enter through cuticles, colonize haemocoel and produce toxin. Viruses- nuclear polyhedrosis virus. Bacteria- Bacillus thuringiensis 4) ChemicalsChemical methods of insect control are used preventatively and as part of focal sanitation. Chemical insect control is based on the use of chemical preparations insecticides that are commonly available as fungicides, aerosols, sprays, smokes, dusts, granular pellets, residual fumigants and baits. They are applied into the soil, on the soil, onto plant leaves or directly on animals or in their houses. Classification a) Effect on life cycle: ovicides, larvicides, adultcides b) Entry: contact, stomach respiratory c) Mode of action: systemic or residual d) Formulation: sprays, dusts, powders, granules, aerosols, fumigants, baits, repellents e) Origin: plant derived or synthetic - Pyrethroids (axonic poisons) - Organophosphates (cholinesterase inhibitors) - Carbamates (cholinesterase inhibitors) - Fumigants (respiratory poison- hydrogen cyanide) - Neonicotinoids (neuroactive systemic insecticides) - Midacloprid (mimics action acetylcholine) - Chlorinated hydrocarbons (DDT, extremely stable). b.) Advise of gunshot wounds An animal's carcass may contain bullets, shots or pellets from different guns. Interpretation can be complex and far from straightforward. When examining a gunshot wound it is important to determine: 1. Entrance and exit wound - Entry wound: they are typically smaller than exit wounds, many have stellate or irregular appearance (over a bony prominence), though generally are round or oval. The animal's hair may be pulled inward into the opening. A "collar" of abrasion and discharge residue may be visible. It has the same size or is smaller than the bullet - Exit wound: often ragged edges, irregular shape, collar and discharge residue rarely present. Variable size 2. Type of bullet 3. Range - Contact wounds (less than 2cm): ragged wound, soot or gunpowder may be obvious and carbon monoxide may be detectable in the tissues. - Close range (2-50cm): the wound is likely to be circular and concave, soot or gunpowder are unlikely to be detected macroscopically, but can seen microscopically in histological sections, feathers or hairs may be singed (svidd) by the weapon. - Long range: entrance wound is likely to be circular and concave, there may be grease-soiling on the bullet and soot or gunpowder are not usually visible macroscopically or microscopically 4. Type of weaponThere are important differences between the damage caused by a low-velocity weapon (hand gun), and those from a high-velocity rifle. The latter cause severe injury and shock waves created by energy of the bullet and can destroy tissues that are not in the pathway. It is crucial that the pathologist removes, handles and stores all ballistic material with care 5. OtherIt may also be necessary to ascertain whether only one or more people was involved in a shooting incident (during a hunting expedition or a street fight).

24. Haemorrhagic fevers, prevention and control, measures in outbreak, current epizootological situation. Proceeding of competent authorities in the case of disease outbreak, control and prevention

Viral hemorrhagic fevers (VHFs) are a diverse group of animal and human illnesses caused by 4 families of viruses. These diseases have common features: they affect many organs, they damage the blood vessels and they affect the body's ability to regulate itself. The main clinical signs are haemorrhages and fever. Diseases caused by these viruses are classified as emerging diseases; they are newly identified and previously unknown, causing public health problems either locally or internationally. Factors increasing prevalence of emerging diseases includes: Changes in agent, development of drug resistance, demographic change, immunosuppression, social inequality, climate change, globalization, immigration, urbanization and travel. Etiological agents Arenaviridae: Lassa fever, South American haemorrhagic fever Filoviridae: Marburg, Ebola Flaviviridae: Dengue fever, yellow fever Bunyaviridae: Rift Valley Fever, Crimean- Congo, Hantavirus Rift valley fever OIE notifiable Etiological agent Rift valley fever virus family Bunyaviridae. Resistant in alkaline environments but inactivated at pH <6.8. Survives in freeze dried form and aerosols at 23°C and 50-85% humidity. Transmission and epidemiology Disease occurs in sub-Saharan Africa. Animals: Mosquito bite (Aedes spp), rodents, ticks or inhaling aerosols. Mosquitos thrive after heavy rainfall giving higher incidence of disease at these times. Humans: Infected when inhaling air around slaughtered infected animal, touching infected blood, drinking untreated milk from infected animal or by mosquito bite. Mortality for RVF is extremely low at 1%, with the most common complication after recovery being permanent visions loss in about 10% of cases. Pathogenesis Entry into blood à virus replicates in macrophages à is transported via blood to various organs in which they continue replication. Main organ of infection is the liver but also kidney, spleen, pancreas and lung. Affinity to endothelial cells This is reason why lnn have necrosis and hemorrhages (also liver has this) Massive hepatic necrosis, hemorrhages, inflammation and enlargement is seen. Clinical signs Clinical signs are age- and species dependent! (Listed as 1 = highest susceptible, 3 = less susceptible) Lambs, kids - High fever, weakness, anorexia, death. Mortality 70-100%. Calves, sheep - High fever, weakness, anorexia, bloody diarrhea and icterus. Mortality 20-70% Goats, humans - Often inapparent. In acute disease there is fever, weakness, bloody diarrhea. Pregnant animals have abortion rate of 85%!! Clinical signs are non-specific and hard to distinguish from a range of other diseases. Diagnosis Blood, plasma, serum. Aborted fetus. Isolate virus by cultivation in cell line or embryo. AGID, PCR, virus neutralization test, ELISA, hemaglutination test Necropsy we find lesions: Hepatic necrosis, congestion and hepatomegaly. Widespread cutaneous hemorrhage and lnn has necrotic hemorrhages too Measures during outbreak Prevention, control Control animal movement and have vector control. For human infection it is about hygiene in contact with raw/slaughtered animals, boil milk, cook meat and use mosquito net during night time, wearing long sleeved clothes. Vaccination programmes for animals prevents outbreaks - no vaccination after outbreak has occurred. There is no specific treatment for RVF. Sanitary prophylaxis includes control of animal movement (extension of disease). Control at slaughterhouses (exposure to disease). Ebola and Marburg hemorrhagic fever The Ebola virus disease is a severe, often fatal febrile haemorrhagic illness in humans. The virus is transmitted to people from wild animals and spreads in the human population through human-to-human transmission. Average EVD fatality rate is around 50%. Case fatality rates have varied from 25% to 90% in past outbreaks. Etiological agent · Ebolavirus from family filoviridae. It's a notifiable disease, though not to OiE · Marburg virus of family filoviridae is morphologically indistinguishable and induces symptoms similar to Ebolavirus Transmission The hosts of ebola include several species of mammals, including chimpanzees, gorillas, fruit bats, monkeys, forest antelope, porcupines and humans. Natural reservoir is believed to be fruit bats Transmission is by all routes- via direct contact (through broken skin or mucous membranes) with the blood, secretions, organs or other bodily fluids of infected people, and with surfaces and materials (e.g. bedding, clothing) contaminated with these fluids. Contact with sick people is extremely risky. Pathogenesis · Following infection, immune cells carry virus to nearby lnn where further replication takes place. · From there the virus can enter the bloodstream and lymphatic system and spread throughout the body. · Macrophages infected first à results in apoptosis. Other types of white blood cells also undergo apoptosis àlymphocytopenia and immunosuppression · Endothelial cells may be infected within 3 days after exposure · Endothelial cells breakdown leads to blood vessel injury and widespread bleeding à swelling and shock · There is also liver damage, leading to improper clotting and activation of the coagulation cascade Treatment No treatment, no vaccine. Only supportive therapy. Clinical signs After an incubation period of 2-21 days the affected person experience: · Acute fever, weakness, muscle pain, headache, sore throat, vomiting, diarrhea, rash, and internal and external bleeding (epistaxis, melena, haemorrhages everywhere!). Diagnosis Laboratory methods- the virus pose an extreme biohazard risk. · Isolation, PCR and ELISA · Biochemistry: lymphopenia, elevated liver enzymes Epizootiological situation The first big outbreak of Ebola was in 1976 at Ebola river, in which an entire village was infected. Up to 2013, ebola occurred mainly in remote rainforest areas of Central and East Africa. However, a severe epidemic, starting in 2013-14 affected a large West African region Since 2014, 3 new outbreaks have occurred in the Democratic Republic of Congo. Prevention, control, measures during outbreak Ebola: Prevention: Sanitary measures, patient isolation, decontamination of used equipment, quarantine, It is important to follow simple sanitary measures: Strict decontamination of all materials and tools used in patient care, compliance with the quarantine measures and adherence to the transport and import standard rules on imports of primates. Marburg: Barrier methods include the use of gloves, gowns, goggles, masks. High observation of hygiene in hospitals! Hantavirus Hantaviruses are rodent-borne viruses causing clinical illness in humans of varying severity caused by hantaviruses from the family Bunyaviridae. Hosts are micromammals and humans, reservoir is rodents. Viruses are maintained by different species of rodents, in which they produce chronic, inapparent infections. Humans become infected through contact with urine, saliva or faeces from infected rodents, mainly via the aerosol route. In humans, clinical disease occurs in the form of 2 major syndromes: haemorrhagic fever with renal syndrome (HFRS) or hantavirus pulmonary syndrome (HPS). Hantavirus renal syndrome - Transmission among rodents, transmission to man - Infected animals: virus in saliva, urine and feaces à direct contact with man. Signs include low blood pressure, acute shock, vascular leakage and acute kidney failure à can cause severe fluid overload. Hantavirus pulmonary syndrome - No symptoms in rodents, but transmits to humans - Humans have infection of pulmonary system - Seasonal occurence: High in spring and summer because of increase in reservoirs (rodents) - Transmission also possible by aerosol (dust) Signs include coughing and shortness of breath Treatment No specific treatment Epizootiological situation Hantaviruses are found throughout Europe, Asia and the Americas. Renal syndrome mainly occurs in Europe and Asia and pulmonary syndrome has only been reported in the Americas. Prevention, control, measures during outbreak Prevention by elimination of rodents, • Prevent their contact with people, housing/house, foods, feed, water • Prevent direct contact with rodents and their excretes, secretes • Removal of excrements - aerosol from feces Protection of people by masks, gloves Rodent control: Acute rodenticides (later in this question) Lassa fever Etiological agent Lassa virus of family arenaviridae Transmission Horizontal and Vertical · The infected rodents are not clinically sick! · People get infected by direct contact with rodent excretions (urine, feces) o Special rodent mastomys natalensis = multimammate rat · Touching soiled objects · Direct contact with blood, urine, fecal and other body secrets of sick people · Not airborne (in comparison to Ebola) Clinical signs · Incubation period: Average of 10 days (range 2-21 days). Mild form 80%, severe form 20%. · Non-specific signs: Fever with headaches, sore throat and muscle pain, weakness · Severe form of disease, after 7-8 days: Epistaxis, sub conjunctival haemorrhage, bleeding from the gums and neurological conditions (shock, seizures, coma and deafness). · After several days, in severe form: Multiple organ failure, renal failure associated with generalized edema and hemodynamic shock. Possibility of death between the second and third week. · High mortality rate among women in late pregnancy Source Epizootiological situation Lassa fever is limited to rural areas of West Africa, with areas of hyperendemicity in eastern Sierra Leone, Guinea, Liberia and Nigeria. Prevention, control, measures during outbreak Prevention in people: Protection mask, gloves, protective clothes when in contact with patients. Elimination of rodents, good hygiene levels. Treatment Ribavirin, an antiviral drug, has been successful when given soon after a patient becomes sick. Patients should also receive supportive care Crimean-Congo hemorrhagic fever virus An important zoonosis! Etiological agent Crimean-Congo hemorrhagic fever (CCHF) is caused by infection with a tick-borne virus (Nairovirus) in the family Bunyaviridae. Transmission The virus circulates in a tick-vertebrate-tick cycle, but can also be transmitted horizontally and vertically within the tick population. Transmission to humans through contact with infected ticks or animal blood (typically in facilities processing animal products). CCHF is transmitted from one infected human to another by contact with infectious blood or body fluids. Susceptible groups include people working in agriculture, forests, slaughterhouses, vets. Natural reservoirs (and important vectors) are ticks Hyalomma, Ixodes, Dermacentor. Virus persist in nature particularly by transovarian and trans-stage spreading within tick population. Pathogenesis At present, the pathogenesis of the disease in humans is not well understood. Clinical signs No signs in animals! Only in humans! Initial signs: - Headache, high fever, back pain, joint pain, stomach pain and vomiting - Red eyes, flushed face, red throat, petechiae and jaundice - Neurological signs Later signs: Severe bruising, severe nosebleeds and uncontrolled bleeding at injection sites Treatment Only symptomatic. Diagnosis ELISA, PCR. Epizootiological situation Found in many countries of Asia, Africa, the Middle East and South-eastern Europe. The distribution of CCHFV coincides with the distribution of its main vector, ticks of the genus Hyalomma. Prevention, control, measures during outbreak No vaccine. Main is tick control! Tick repellents. Focus on prevention. a. Sanitation measures and focal disinfection at these diseases. Using of acute rodenticides. Rift valley fever Disinfection: Inactivated by -lipid solvents (i.e. ether, chloroform) Low concentrations of formalin, strong solutions of sodium hypochlorite, 1% Peracetic acid. Ebola/Marburg Hantavirus Chlorinated lime is used for treatment of the environment. 2 % NaOH, 0.5% Peracetic acid. Crimean-Congo HF virus Peracetic acid, chlorine compounds. It is necessary to decontaminate all equipment. Using of acute rodenticides Principle of use Acute rodenticides are used when a rapid, high level of rodent control is required (during an epizootological outbreak). They cause death 12-24 hours after ingestion. Only once yearly. Due to neophobia, pre- baiting is required (bait boxes). Rodents will also learn to avoid toxic substances. Acute rodenticides have low specificity and high toxicity, thus caution is required. Chemicals Zinc or aluminium phosphide: cause death within 1 hr due to formation of hydrogen phosphide when combined with HCl- heart attack, liver and kidney damage. Red squill: acts on the central nervous system. It is emetic to other species. Pros and cons Pros: rapid killing, bodies visible, require small amounts Cons: pre-baiting, bait shyness, high conc., poor selectivity Sub- acute rodenticides Used in situations where rodents have developed resistance to anti- coagulants. Includes vitamin D preparates (induce hypervitaminosis and alteration of calcium metabolism) b. Unpublished contracts for veterinarians (authorization and instructions) Contraca inominata · Unpublished contract for the provision of services by veterinary surgeons involved in the treatment · Reflected in a contract in writing, which would include the terms and conditions (procedure(s)) proposed by the service provider (vet) and accepted by the service purchaser (owner). · The veterinarian is also protected by preparing the "Consent and instruction" document (consent form), any adjustments or additions (including any procedures that could be additionally necessary (e.g. extractions found to be needed in dentals) should be made before signing of the contract, especially if the surgery is to be performed on the animal

19. Other notifiable viral encephalitis (West Nile, equine encephalitis), prevention and control, measures in outbreak, current epizootological situation. Proceeding of competent authorities in the case of disease outbreak, control and prevention

West Nile encephalitis OIE listed Etiological agent West Nile Virus (WNV) flavivirus Host range is extremely wide (birds, reptiles, amphibians, mammals, mosquitos and ticks). Most animals do not show symptoms and clinical disease is seen mostly in humans and horses. Humans and horses are dead-end hosts and disease cycle in a mosquito-bird-mosquito cycle. Transmission - Reservoir of virus are birds - Mosquitoes (Culex, Aedes) are vectors spreading the virus from infected bird to other birds and animals o Mosquito bite infected bird à feed on animal - Some birds are more susceptible to the virus than others, especially the crow family (Corvidae). Pathogenesis First replication probably in macrophages of skin where inoculation occurred à macrophages travel to lnn à viremia and dissemination to the organs. In particular it attacks CNS and cause hemorrhages and congestion. Clinical signs Birds - WNV cause encephalitis (inflammation of the brain). The signs include fever, neck stiffness (at least in other species), stupor, disorientation, coma, tremors, convulsions, muscle weakness, paralysis and death. Horses - WNV causes encephalomyelitis (brain-spinal cord infection). Most horses will not develop clinical disease. However, when clinical disease occurs, signs include: listlessness, weakness, inability to swallow, anorexia, depression, stumbling, lack of coordination, fever and death. Humans: West nile fever: non-specific clinical signs. West nile encephalitis: convulsions, paralysis and coma. Treatment Symptomatic and supportive Diagnosis Identification of agent by virus isolation (in vivo, in vitro) and RT-PCR. ELISA for Ab detection. Seasonality, mosquito population and clinical signs. Epizootiological situation The occurrence of disease in humans/animals/birds and mosquito surveillance, demonstrates that virus range has dramatically expanded including North, Central and South America as well as Europe (Romania, France, Greece, Germany). Prevention, control Key to preventing the spread of West Nile fever is to control mosquito populations. Horses should be protected from exposure to mosquitoes: - Avoid exposure to mosquitoes especially at dusk and dawn, very active - Use insect screens and insect repellents - Limit places for mosquitoes to breed, remove all stagnant waters In areas where the disease is common, vaccination of horses is considered to be an effective control measure. Insect control for people: - using repellents, protective clothes, net on windows and traps. Further preventative measures are monitoring, storage of manure not close to animal house (horses) and in nature: eliminate wet places on pasture (hatching of eggs). Western WEE, Eastern EEE Equine and Venezuelan VEE encephalomyelitis. Etiological agent RNA virus - Togaviridae, alphavirus, Western Equine Encephalitis virus RNA virus - Togaviridae, alphavirus, Eastern Equine Encephalitis virus RNA virus - Togaviridae, alphavirus, Venezuelan Equine Encephalitis virus Transmission Eastern + Western: · Main routes of transmission are vectors mosquitos · Birds are the primary source of virus during an outbreak · Horses are dead-end hosts with viral load too low to infect a vector, so disease is spread from birds to vectors and then to the horses/humans (dead-end) · The epidemiological cycles of EEEV and WEEV are maintained in nature within a transmission cycle between ornithophilic mosquitoes (feed on birds) and birds Venezuelan: · Mosquito (rodents- reservoir) · Have found both contact-, aeorogen and ingestion spread of disease · For VEEV, horses and humans act as amplifying hosts, and develop a high- titre viraemia which is capable of transmitting the disease via mosquitoes to other horses or humans Pathogenesis Virus inoculated à travels to lnn and replicates inside macrophages and neutrophils which causes lymphocytopenia and neutropenia and fever. Viremia develops and further viral replication occurs in brain to which virus has travelled via blood and lymph. This virus favors the CNS and causes damage and death to most of its hosts. Most pathogenic for equines and humans. Damage to cerebral cortex, brain stem and thalamus (which works as a control board for many functions of the brain). Clinical signs Horses - In the beginning they show non-specific signs like fever, depression and anorexia. They are calm. They have neurological signs like head pressing, circling, inability to swallow, ataxia. This will progress and turn into paresis, convulsions, paralysis, lateral recumbency, paddling and death. Mortality depends on species; Eastern has the highest (up to 90%). Venezuelan has less and Western 20-50%. Humans - Sudden onset of fever. Muscle pain and headache. Many people progress into seizures and coma. Of people who develop clinical disease with Eastern, 1/3 will die. For Western and Venezuelan mortality is low. Treatment No specific therapy, only supportive. Surviving horses develop lifelong immunity but may have permanent neuropathology. Diagnosis Clinical signs, geographical location, season of year. Virus isolation and identification. Serology: HI, VN, CF and ELISA. Prevention, control - Control of equids by quarantine and movement controls - Vaccination of equids - Stabling horses in screened housing especially during prime daily mosquito activity - Use insect repellents - Vector control measures includes elimination of mosquitoes breeding locations Japanese encephalitis Etiological agent Japanese encephalitis virus, family Flaviviridae, genus Flavivirus. Transmission - Spread by mosquitos, mainly Culex spp that feed on birds, pigs, horses and humans - Because of low titres and short duration of viraemia, humans and horses are usually inadequate to maintain the virus (=dead-end hosts. No high viremia à do not transmit disease when mosquito feeds on them). Pathogenesis - Horses are the primary affected domestic animals of JE though essentially a dead-end host; other equids (donkeys) are also susceptible - Pigs act as important amplifiers of the virus producing high viraemias that infect mosquito vectors - The natural reservoir for JE virus are birds of the family Ardeidae (herons and egrets) - Although these birds do not demonstrate clinical disease, they do generate high viraemias upon infection, acting as an amplifying host - Humans are vulnerable to this disease and this disease is a primary public health concern in Asia - Humans are considered a dead-end host Clinical signs In horses: Subclinical disease is most common. Clinical signs, if present, vary; disease usually presents itself in sporadic or localised clusters. 3 syndromic manifestations have been described: 1. Transitory type: Moderate fever 2-4 days. Inappetence, impaired locomotion. Swift recovery of 2-3 days 2. Lethargic type: Febrile periods (up to 41°C), with lethargy, paresis and paralysis. Recovery in 1 week. 3. Hyperexcitable type: High fevers (41°C +) with profuse sweating and muscle tremors, aimless wandering, behavioral changes (aggression), loss of vision, collapse, coma and death. In pigs: Mostly a reproductive disease; reproductive losses can reach 50-70%. Abortions in sows à stillbirths at term. Reduced number/motility of sperm in boars Live born piglets often demonstrate neurologic signs of tremors and convulsions and may die soon after birth Treatment Non-specific, symptomatic, supportive. Diagnosis - On clinical signs - Isolate agent, serology. Like always. Epizootilogical situation JE is widespread in Eastern/Southern Asian countries and has spread to western India and to the western Pacific region and Australia. It is most often associated with areas of intensive rice farming and swine production. Prevention, control - Vaccine for swine in Japan and Taiwan - Stagnant water control - Kill the vector and destroy mosquito habitats Control: Since Japanese encephalitis virus is spread by certain species of mosquitoes, proper mosquito control programs help minimize the spread of the disease. a. Sanitation measures and focal disinfection at these diseases. Mosquitoes, lifecycle, methods of treatment West Nile Virus Virus is inactivated at - 60 oC for 10 min or at 37 oC for 7 hours - Low pH - Radiant sunlight, heat (moist, dry), drying - Pasteurisation 72-85o C/10 seconds Stable, equipment, vehicles and surfaces must be disinfected in case of outbreak: • NaOH-2%,70-80 °C, • Ca(OH) 2-20% solution, fresh • Peracetic acid-0.5-0.9% • Chlorinated lime - 2-5% activated Cl • Chloramín T - 2-3%, 50-60 °C • Dikonit - 2% Japanese encephalitis - 1% sodium hypochlorite (NaOCl) - Ethanol - 2% formaldehyde - UV Equine encephalitis virus - Inactivated by various common disinfectants - Sensitive to o Organic solvents and detergents o 1% sodium hypochlorite o Quaternary ammonium compounds o Phenolic disinfectants o 70% ethanol o 2% glutaraldehyde and formaldehyde o 50% ethanol for 1 hour o UV-light Mosquitoes, lifecycle and methods of treatment. The most important mosquito genera are: - Anopheles (malaria, filariasis, encephalitis) - Aedes (yellow fever, dengue fever) - Culex (Culex pipiens − „house mosquito") (West Nile Virus, encephalitis etc) · Mosquitoes breed in wet areas · Lifecycle includes undergoing complete metamorphosis · Females lay eggs on stagnant water · Eggs hatch in the water about 5 days and larvae moult 4 times. After the last moulting, they are transformed to pupae from which the adult forms emerge. Most mosquitoes live for an average of about 2 weeks in their adult form. · Different mosquito species prefer different host species; Some will seek blood meals from birds, others from mammals and some are generalists · Only female mosquitoes bite à They require a blood meal to acquire the protein needed to produce eggs. · A key factor in mosquito prevention is the elimination of standing water in an area. Control: Pyrethroids (Allethrins, Esbiothrin, Permethrin) à Wide-spectrum, knock-down insecticides with very rapid action, with long-lasting activity elimination of breeding sites. Wash hands with soap, water after using. b. Tissues and organs taking from the point of view of the forensic veterinary medicine Deciding about organ and tissue donation usually comes after a sudden and unexpected death · Individual who is brain dead but is on respirator and has a beating heart is an acceptable donor for: liver, heart, pancreas, eyes/corneas, kidneys, intestine, heart valves, skin, bone and lungs. · Dies of cardiac arrest: acceptable for eyes/corneas, blood vessels, cartilage, skin, bone, pericard, soft tissue The procurement process is a complex series of events that involves medical profession. State legislation has been authorized to help ensure that the process is carried out in a fair and efficient way, leading to an equitable distribution of donated organs. This legislation recommended the establishment of national computer registry. In vet practice · Tissue or animal organ procurement is not routinely done for medical or scientific purposes (the collection of biological material does not apply to use in the pharmaceutical industry). There are no legislation limits for such activity. · The complexity of transplantation in human medicine practice is the reason for ongoing discussion about the potential for xenotransplantation, to which a moratorium is currently in place in the EU.

2. Brucellosis, differential diagnostics of abortions, prevention and control, measures in outbreak, current epizootological situation. Proceeding of competent authorities in the case of disease outbreak, control and prevention

Brucellosis Malta fever in humans (not abortions etc). Gram negative coccobacilli These species are zoonotic and therefore OIE listed: B. abortus (cattle) B. suis (pig) B. melitensis (sheep and goat) Brucella bovis is not zoonotic Brucella canis is zoonotic but very few cases have been reported, extremely seldom it transmits to owners · Disease caused by multiple species of the genus Brucella · Facultative intracellular pathogens · Abortions and reproductive failure are typical for animal Brucellosisà survive but sheds for life · Malta fever (b. melitensis) in humans à farmers, vets and all who handle aborted material is at high risk Transmission · High level of bacteria in birth fluids · Aborted material or during birth releases masses of bacteria · Bacteria survives in environment for several months o Infection by ingestion of contaminated feed, water, bedding o Infection by drinking milk coming from or feeding directly from contaminated udders o Infection by contamination of wounds in skin or mucus membranes o Inhalation Pathogenesis Infection via a mucosal surface (GIT, RT, skin) à regional lnn drains mucosa for bacteria à bacteremia à survive intracellularly either in phagocytic - or non-phagocytic cells à in phagocytic cells, they evade the lysosome fusion and thus are not killed by phagocytosis. Brucella, living intracellularly, evades innate immune system and second bacteremia occurs à pathogen is spread to its preferred sites via the blood and there is generalized infection. Brucella abortus · Huge economic importance for farmers because of the poor reproductive performance · High affinity for the pregnant uterus · In pregnant cow it produces o Chronic infection o High bacterial replication in placenta à placentitis, fetal death and abortion o Cow shows few clinical signs until she aborts! · In bulls it produces o Orchitis often together with epididymitis and vesiculitis o Chronic orchitis often causes impaired semen production and permanent infertility · Veneral transmission during intercourse is not major route · Artificial insemination with contaminated semen is a source of infection Horses get swelling of neck or back (fistulous withers) Humans get febrile disease; Intermittent fever, muscle ache, joint ache, night sweats Diagnosis · Clinical signs · Examination of aborted material; Placenta has hemorrhages and necroses. Altered colour of the cotyledons · Culture sample from placenta, swab from aborted fetus or udder secretions on selective media (Modified Farrell's medium) · Agglutination tests o In serum, milk and semen · ELISA detects antibodies in serum and milk · Screening tests "Brucella milk ring test" but it is not so good o Principle is the same as always with agglutination tests Differential diagnosis · Ruminants: Campylobacter foetus, Listeria monocytogenes, Coxiella burnetti, Leptospira interrogans. · Cattle: aspergillus spp, Trichomoniasis, pestivirus (BVDV), IBR, rinderpest, blue tounge, q- fever If positive: Lipophilic antibodies (attached to milk fat globules) will fix the blue stained BRT antigen. This will float up and form a BLUE CREAM LAYER Pig:Aujeszky's, Leptospira interrogans · All: toxoplasma spp., salmonella spp., Borrelia spp., Therapy, prevention and control Animals: No treatment, kill them all. Humans: Long AB treatment (2 types, one for 14 d and other for 45 d). Surveillance and necropsy of suspected cases. Good hygiene, gloves on for vets and workers! · Vaccination (modified live) in endemic areas (not Europe) · Pasteurization of milk hinders infection to humans. a. Sanitation measures and focal disinfection at this disease. Biothermic treatment of manure. Brucella spp., are capable of surviving in cool, moist environments (manure, slurry) for months (70 days). In soil and manure they can survive more than 1 year. Disinfection The agent is readily killed by most commonly used disinfectants and temperatures around 50-60°C · Housing: Peracetic acid (0,3-0,9%), chloramine T (4%) · Surfaces: formalin (2%), NaOH (2-3%), sodium hypochlorite (2,5%) · Skin: ethanol, ionophores, diluted hypochlorite · Equipment: autoclaving (moist heat 121°C for 15min), dry heat (160-170°C for 1 hr) · Manure: composting with/without lime or peracetic acid, burning · Slurry: 6 months storage with phosphoric acid or lime (3%) Sanitation measures · Carcasses: incineration at rendering plant at 133°C for 20min · Rodent control: traps, acute and chronic rodenticides · Insect control: pyrethroids, fumigation Biothermic treatment of manure (composting) - Composting is the biological decomposition and stabilization of organic substances under biologically produced thermophilic temperature. It takes organic matter (manure, woodchips), minerals, water and microbes and turn it into organic matter (carbon, nitrogen, phosphorous, proteins, and humus). - This process conserves chemical nutrients in raw waste material and enhances its availability for plants. - The main factors are aeration, moisture of 50%, carbon/nitrogen ratio of 25/1 and pH of 5,5-8,0. - Contaminated manure is placed on a surface layer of non- infected manure, straw and dry leaves and covered with non- infected manure and earth. - The temperature must be above 55°C for more than 3 days. - A temperature of 70°C for a minimum of 4 weeks (months- slurry) is considered sufficient to kill pathogens in manure, however this is not enough for devitalisation of spores- disinfectants (3% lime, 0,5% peracetic acid). 70°C, 4 weeks (6 months- slurry) b. The legal liability for the spread of infectious diseases Minimising the transmission of infectious diseases is a core function of public health law. · Where public health laws authorise, interferences with freedom of movement, the right to control one's health and body, privacy, and property rights, they should balance these private rights with the public health interest in an ethical and transparent way. · Public health powers should be based on the principles of public health necessity, reasonable and effective means, proportionality, distributive justice and transparency · The appropriate role of criminal law in national efforts to prevent transmission of transmissible infections is often controversial § Public health laws often contain penalties for failing to comply with PH orders made by authorities or for engaging in behaviours that place PH at risk The Slovak Republic · Those whose negligence causes danger of introduction or spread of contagious disease of domestic or economically important animals, shall be punished by imprisonment for up to 1 year · The offender shall be liable to a term of imprisonment of between 6 months to 3 years if he commits the offense referred to in the above point a) And causes more damage b) And causes the spread of such a disease c) A more serious conduct

4. Salmonellosis, prevention and control, measures in outbreak, current epizootological situation. Proceeding of competent authorities in the case of disease outbreak, control and prevention

Salmonella genus. Gram negative rods. Family Enterobacteriaceae. There are 3 forms of salmonellosis: 1. Septicemic salmonellosis a. Fever, depression, hemorrhage, death b. In neonate calves and poultry 2. Acute enteritic salmonellosis a. Fever, depression, dysentery (mucus, blood), watery diarrhea 3. Chronic enteritic salmonellosis a. Persistent diarrhea, fever, dehydration, emaciation Salmonella species are S. enterica and S. bongori à (Salmonella dublin causes abortions) Transmission Orofecal route by contaminated feed and water. Salmonella survive in wet and warm environment for a long time, so dirty barns and such are perfect. Humans can be infected by eating contaminated meat, milk and eggs. Pathogenesis Ingestion à salmonella multiply in enterocytes à enteritis à may invade bloodstream and invade · Brain and meninges · Pregnant uterus · Bone Salmonella can also persist in lnn and tonsils, thus being a continuous source of bacteria for fecal excretion. Diagnosis Samples taken are rectal swabs, feces. Culturing salmonella requires multiple steps: Pre-enrichment (non-selective broth), enrichment in selective broth MKTT and RVS and thereafter plating out on XLD agar. Several biochemical tests are performed. We also perform serological confirmation of presence of special H, O and Vi antigens. Salmonellosis in cattle Disease in cattle depends on age of the infected individual 1. Neonates: septicemia and death within 6-12 hours 2. 2-6 weeks old calves a. Dull b. Depressed c. Diarrhea and wont suck milk 3. Older calves a. Bloody diarrhea with mucus b. Dehydration and general ill feeling c. Survivors have slow growth 4. Adult cattle a. Salmonella dublin causing abortions Salmonellosis in poultry 1) Salmonella pullorum - pullorum disease Pullorum disease is a highly fatal disease of young chicks and turkey caused by Salmonella pullorum. OiE- notif. Clinical signs May have no signs due to acute septicaemia and death. · Somnolence, weakness, anorexia and have accumulation of chalk-white excrement · Infection may localise in joints and adjacent synovial sheaths producing lameness and severe swelling · Transovarial infection and thus infection of chick is the most important route of transmission o We find moribound or dead chicks in the incubator or shortly after hatching o If they survive, we see depression, dyspnea, diarrhea, weakness and feces adhering to vent · Highest mortality in birds 2-3 weeks old · Survivors have low BW, poor feathers and likely not mature into well-developed laying/breeding hens Diagnosis is the same as above. Sample can be most tissues, including caecum swab. Isolate agent as described above. Blood can be used for serology; ELISA to detect antibodies. 2) Salmonella gallinarum - fowl typhoid Fowl typhoid is a lethal disease caused by the bacteria Salmonella enteritis serotype Gallinarum. OiE- notif. Clinical signs · Lesions are similar to pullorum disease, however there is a much more spread in mature flocks with higher mortality in older birds compared to pullorum · Older birds may be pale, dehydrated and have diarrhea 3) Fowl paratyphoid (salmonella typhorium) Paratyphoid is a disease caused by Salmonella typhimurium var. typhimurium. This bacteria is capable of infecting several organs- most commonly the joints and GIT. It also cause suppurative encephalitis and swelling of eyelids. High mortality in turkey and ducklings the first days of life. Clinical signs · Depression, poor growth, diarrhoea and dehydration. Enlarged liver and enteritis Salmonellosis in birds can only be diagnosed by isolation and ID of the causative agent, due to similar and non-pathogenic signs. Salmonella in pigs There are three main subspecies found in pigs: a) Salmonella cholerasuis var kunzendorf: cause septicaemia- skin discoloration on head, petechial haemorrhages, pneumonia and congestion of visceral organs. b) Salmonella typhimurium: acute/chronic enterocolitis c) Salmonella typhisuis: ulcerative enterocolitis- nonsuppurative inflammation of intestines, button ulcers Salmonella is mainly found in feeder pigs and is uncommon in suckling and adult swine. Salmonella in horses There are two main subspecies found in horses: a. Salmonella abortus- equi: cause septicaemia in foal and abortion in adults b. Salmonella typhimurium: gastroenteritis in adult Pathogenesis The origin of infection is typically the alimentary tract and through umbilicus (ascending infection through poorly disinfected umbilicus post- partum). Many horses are also carriers of salmonella and disease occurs when they become stressed. Prevention and control Control · Collection of epidemiological, microbiological, environmental and veterinary information · Risk assessment and risk management of foodborne diseases · Serological monitoring: Slide agglutination test- carrier animals should be identified and isolated, then treated (retest several times) or culled · Obligatory bacteriological monitoring of breeding flocks with more than 250 birds and hatchers · Culture of DOC/chick of 4 weeks/2 weeks prior to laying/ adults every 2 weeks o Slaughter of positive flocks o Eggs from positive flocks should not be sold as fresh table eggs o Limited access to site- only authorized personnel with disinfection o Carcasses should be removed via special entrance and transported to rendering plants · Vector control: acute or chronic rodenticides, insecticides Prevention · National schemes are implemented in many countries to control salmonella infections in animals · Mandatory serological and bacteriological monitoring · Mandatory vaccination of layers in EU member states with a prevalence above 10% · Hygiene: black and white system, all-in all-out, quarantine, proper collection and storage of eggs, proper disposal of positive carcasses and vector control · Treatment: contradicted- anti microbials are not permitted in EU · Humans: roast meat, pasteurize milk, wash raw vegetables a.) Sanitation measures and focal disinfection at these diseases. Black and white system and prevention of diseases Salmonella spp. are quite resistant in the environment and can survive for a long time in dry faeces, 1-4 years in dust, months in wet environment (biofilm) and survive on insects (cockroaches, flies, fleas) and rodents. However, it is destroyed at 50°C, high pH, pasteurization, sunlight, ozone and by common disinfectants. Disinfectants Chloramine T (6%), NaOH (2%), sodium hypochlorite (1%), peracetic acid (0,5%), formalin (2%), glutaraldehyde (2%), ethanol (70%), ionophores, hydrogen peroxide, quaternary ammonium compounds. · Housing: chloramine T, peracetic acid (aerosol disinfection in layer houses) · Manure: composting at 65°C · Slurry: peracetic acid (0,3%), lime (3%), ammonia · Soil: lime, peracetic acid · Water: chlorination, nb. Biofilms · Eggs: formaldehyde (2%) vapours · Meat: cook properly (steak- 63°C, ground beef- 71°C, poultry- 77°C) Black and white system Black and white system is a hygiene system dividing food processing houses, animal houses, etc into "clean" and "dirty" zones in order to avoid cross-contamination of animals and food products. · Black zones (dirty zone): waste storage area, fuel store, carcass box, office, changing rooms · White zones (clean zone): productive and reproductive zoneFeed storage can be in either black (complete protection system) or white zone (incomplete protection). Between these zones there is a protection zone (hygienic filter- protection against introduction of diseases by people/ veterinary filter- protection against introduction of diseases by animals). Contact point is protected by disinfectant ford and mats that protects animals and act as a reloading point and exit for removal of carcasses and excrements. b.) Salmonella-related contingency proceeding - carriers of infection Carrier of infection An asymptomatic carrier (healthy carrier or just carrier) is a person or animal that has contracted an infectious disease, but displays no symptoms. Although unaffected by the disease themselves, the carrier can transmit it to others. The carrier state has been described in livestock animals and is responsible for food-borne epidemics. Identification and treatment of carriers are crucial for the control of disease outbreaks. Typhoid fever Typhoid fever is a disease cause by Salmonella enterica ser. Typhi An individual can acquire this infection from consuming risky food or drinks, or by consuming food or drinks prepared by an infected individual. Those who recover from this infection can still carry the bacteria in their cells and therefore be asymptomatic. Approximately 2-5% of typhoid patients fail to fully clear the infection within 1 year of recovery, instead progressing to a state of carriage. To establish long-term infection, evasion of intestinal barrier and innate immune system have to occur with successful establishment in gallbladder. As shedding of the organisms is intermittent and sometimes occurs in low levels, methods to detect the organisms in faeces have limitations and are not amenable to large-scale screening. Standard practice has been to detect typhoid carriage through analysis of serial stool and urine samples, which is logistically difficult to perform at a population level and is associated with low sensitivity. In order to break the transmission cycle of S. Typhi and S. Paratyphi A, new strategies to identify chronic carriers that are specific, sensitive and cost-effective are needed.

31. Trypanosomosis of cattle, prevention and control, measures in outbreak, current epizootological situation. Proceeding of competent authorities in the case of disease outbreak, control and prevention

Trypanosomosis Nagana is a protozoan disease caused by Trypanosoma spp, the most economically important disease of livestock in Africa, especially cattle. Morphology Trypanosomas are unicellular parasites with leaf-like or rounded body containing a large vesicular nucleus (for quick growth and reproduction) and one mitochondria. There is a single flagellum arising from a kinetosome. This flagella is in some genera attached to a cytoplasmic membrane - undulating membrane. There exist some morphological variations: · Trypomastigote (infective) form: long flagella and undulating membrane. Posterior kinetosome. · Amastigote (intracellular) form: subspherical cell without flagella. · Epimastigote (vector) form: short undulating membrane. Kinetosome/plast- anterior end. · Promastigote (vector) form: no undulating membrane- kinetosome/plast- anterior end. Location and transmission Members of trypanosoma are found in the bloodstream and tissues of vertebrates. All members, except one (t. equiperdum- ventrally) have an arthropod vector. Transmission is either cyclical or non- cyclical. 1) Cyclical transmission: an arthropod is a necessary IH where the trypanosomes multiply and undergo morphological transformations before becoming infective. - Salivaria: when the multiplication occurs in the digestive tract and proboscis, so that the new infection is transmitted when feeding, the process is known as anterior station development. All is transmitted by the Tsetse flies (T.vivax, etc). - Stercoraria: when the multiplication occurs in the gut and the infective form migrate to the rectum and are passed with the feces, it is known as posterior station development. These are relatively non- pathogenic (the exception being T. cruzi). 2) Non- cyclical transmission: mechanical transmission in which the trypanosomes are transferred from one mammalian host to another, through interrupted feeding or biting insects- tabanids. Life cycle During a blood meal from the host, the trypomastigote is taken into its vector. It then moves to the gut and develops into the epimastigote, which then moves either to the salivary glands or rectum and matures into the trypomastigote again, making the vector infectious. During a blood meal the parasitic stage are either injected into the host or passed with feces and later introduced into the host during scratching. The parasite reproduce in the site of injection by binary fission. They then invade the blood stream and migrate to the lymphatic system and later CNS. Main species Salivaria group · Animal African Trypanosomosis = Nagana disease. · Human African Trypanosomosis = Sleeping sickness. Stercocaria group: · American Trypanosomosis = Chagas disease. Trypanosoma spp. Distribution Disease and hosts Vectors and transmission T. congolense Sub-Saharan Africa Nagana Bovinae, equidae, Glossina: cyclic T. vivax Sub-Saharan Africa Nagana Bovinae, equidae, Glossina: cyclic Haematophagous flies: non-cyclic T. brucei brucei Sub-Saharan Africa Nagana Equidae, car, bovinae, suis, Glossina: cyclic T. brucei rhodesiense Sub-Saharan Africa Sleeping sickness - acute Humans, impala), zebra, etc Glossina: cyclic T. brucei gambiense Sub-Saharan Africa Sleeping sickness - chronic Humans, pig, cattle dog, antelopes Glossina: cyclic T. cruzi Central and South America, USA Chagas disease Humans, dog, cat, opossum Triatoma: cyclic T. theileri Worldwide Apathogenic in cattle Tabanidae: cyclic Ixodidae: cyclic T. brucei euiperdum Dourine Horses and other equines Venereally (sexually) Epizootological situation Commonly found in Africa, though they are also common in South- and Central- America, middle east and Eurasia. In 2009 there were less than 10 000 cases of sleeping sickness in the world, however it is estimated that 60 million people and 100 million farm animals are at risk. In 2017 WHO started a program in order to eliminate human trypanosomes by 2020. There was around 3000 cases in 2015 and 2184 cases in 2016. The disease is found in Spain and Portugal in Europe. African animal trypanosomosis - nagana - surra (from contagious PP) Chronic trypanosomosis caused by: T. brucei brucei, T. congolense or T. vivax Pathogenesis - Disease occur 7-10 days after infection - Body temperature increase, heart and respiratory rate increase Clinical signs - Permanent loss of fitness - Clearly sick with variable appetite - Diarrhea in initial stage - Animal anemic (pale mucosa) - Enlarged lnn. - Increased tear secretion - Emaciation associated with weakness, inability to stand, severe anemia and death Salivarian trypanosomes I. Trypanosoma vivax- animal trypanosomiasis Trypanosoma vivax causes the disease Nagana, also known as animal trypanosomiasis, affecting blood vessels of CATTLE and wild mammals. Life cycle After ingestion of a blood meal from the final host by the vector (Tsetse fly- glossina spp.), the development takes place in the proboscis (mid gut). The trypanosomes first turn into the epimastigote form, and then later into the metacyclic infective trypomastigote, which pass to the hypopharynx (salivary glands) and infect a new host when the tsetse flies bite and feed. Inside the host the parasite reproduce asexually and spread to the entire body (CNS). Pathogenesis This parasite cause anaemia by releasing phospholipases that damage erythrocyte membranes. There is formation of circulating immune complexes, which damage organs. Immunosuppression. Clinical signs The disease has 3 phases: progressive emaciation, lethargy and death + enlarged prescapular lnn First clinical signs is an inflammatory focus at the inoculation site, after migration intermittent episodes of fever occur. The main sign of infection is progressive anaemia. Animals may also show edema, locomotor disorders, emaciation, ascites, jaundice and death + diarrhea. II. Trypanosoma brucei- human trypanosomiasis In humans T. brucei causes African trypanosomiasis, or sleeping sickness- endemic in 36 countries. Epizootology There exist 2 morphologically indistinguishable subspecies, which cause distinct disease patterns in humans: · T. b. gambiense causes West African sleeping sickness. Chronic, most common. · T. b. rhodesiense causes East African sleeping sickness. Acute. Cause asymptomatic disease in animals, but they are important reservoir hosts. Life cycle After ingestion of a blood meal from the final host by the vector (Tsetse fly- glossina spp.), the development takes place in the proboscis (mid gut). The parasites transform into procyclic trypomastigotes, which multiply by binary fission, then leave the midgut, and transform into the epimastigote form, and then later into the metacyclic trypomastigote with a glycoprotein coat (infective). This form pass to the hypopharynx (salivary glands) and infect a new host when the tsetse flies bite and feed. Inside the host the parasite enters the bloodstream where they transform into bloodstream trypomastigotes and reproduce asexually. Later they spread throughout the entire body (extracellular parasitemia). Clinical symptoms Infection occurs in 3 stages. 1. Primary lesion: occur at the site of inoculation, 2-3 days after the bite. The metacyclic form multiply locally and produce a raised cutaneous inflammatory swelling. 2. Parasitemia: the parasite appears in the bloodstream and produce irregular fever waves, as well as insomnia, generalised erythema and pruritus. 3. Invasion of CNS: can cause headaches, somnolence, abnormal behaviour, and lead to loss of consciousness and coma. https://www.youtube.com/watch?v=mKnlRVfjl-o Stercorarian trypanosomes I. Trypanosoma cruzi (not technically trypanosome of cattle) The protozoan parasite, Trypanosoma cruzi, cause Chagas disease, a zoonotic disease that can be transmitted to humans by blood-sucking Triatoma (kissing) bugs. Epizootology This parasite is endemic in Latin America, with the highest prevalence being in rural areas. The main host is humans, while the reservoir host is dogs. Life cycle The vector becomes infected by feeding on blood that contains circulating parasites. Once ingested, the trypomastigote form pass to the midgut, where they transform into epimastigotes. These multiply by binary fission, and then migrate to the rectum, where they turn into the metacyclic trypomastigote form, which pass out into the feces. An infected triatoma insect vector takes a blood meal and release trypomastigotes in its feces near the site of the bite wound. Trypomastigotes enter the host through the wound. The infective trypomastigote enter cells in the muscles, especially the heart, where they form rounded intracellular amastigotes. These multiply by binary fission, and turn into trypomastigotes that re-enter the blood. Trypomastigotes infect cells from a variety of tissues and transform into intracellular amastigotes in new infection sites. The bloodstream trypomastigotes do not replicate. Pathogenesis The disease has 3 phases: · Acute: asymptomatic, fever, romana (edema of eyelids) or chagoma (edema) · Latent: low parasitemia, characterized by an asymptomatic chronic form. · Chronic: up to 10-20 years, heart failure, mega colon, weight loss. Dogs: during the acute infection, there is a risk of heart failure. The surviving dogs develop hepato-splenomegaly, anaemia and edema. The acute phase is followed by a transitional phase (8-36 months) with no clinical signs. The progressive chronic form is characterized by myocardia and destruction of ganglia cells. Humans: have a largely inapparent acute phase with a 10-20 year pause, then serious pathological changes- damage of tissue cells and ganglia. Therapy · Cattle, sheep, goat: diminazene, isometamidium (prophylaxis) · Camels, equids, dogs: malarsomine (diminazene is toxic) · Chemotherapy is difficult. Benznidazodos (helminths), vector control Diagnosis Diagnosis can occur through several methods · Direct demonstration of the parasite with wet mount, giemsa stain, thin or thick smear from chancre aspiration, lymph glands, blood and cerebrospinal fluid (chronic phase). · Concentration technique: HCT (haematocrit centrifugation) · PCR, serology, ELISA Proceeding of competent authorities, control and prevention Control There is no universal method of control. The trypanosomosis eradication campaign aim to eliminate vector. Control can be through control of the principal reservoirs of infection (livestock and wild) and through reduction of vectors (destroy habitats, flytraps, sterilized waters). Other methods include health education, improvement of human dwellings, culling/isolation, movement control. Prevention · Vector: insecticides on cattle (pyrethroids), proper clothes, sterilization of male tsetse fly, minimise contact, avoid bushes, spray land, fly trapping, pheromone-baited traps, resistant cows · Agent: gentian violet for blood transfusion, no vaccine or prophylactic drug a) Sanitation measures and focal disinfection at these diseases. Classification of insecticides. Trypanosomas are unable to form cyst, thus cannot survive free in the environment. This makes focal disinfection unnecessary as the disease is strictly vector borne. Main approach is to reduce the reservoirs of infection and the presence of the tsetse flies. - Protection of cattle: pastures far from sources of flies - Animal houses: have nets in windows - For man: repellents, wear long sleeves tucked in shirts long, pants, shoes, boots and hat. - Vector control: traps, screens, insecticides, sterilisation of male tsetse flies Classification of insecticides Chemical methods of insect control are used preventatively and as part of focal sanitation. Chemical insect control is based on the use of chemical preparations insecticides that are commonly available as fungicides, aerosols, sprays, smokes, dusts, granular pellets, residual fumigants and baits. They are applied into the soil, on the soil, onto plant leaves or directly on animals or in their houses. Classification according to: 1. Origin - Plant derived or synthetic 2. Effect on life cycle - Ovicides, larvicides + adulticides 3. Mode of entry - Contact, stomach + respiratory 4. Mode of action 1. - Systemic or residual Additional classification: Formulation Sprays, dusts, powders, granules, aerosols, fumigants, baits, repellents Agents · Pyrethroids (axonic poisons) · Organophosphates (cholinesterase inhibitors) · Carbamates (cholinesterase inhibitors) · Fumigants (respiratory poison- hydrogen cyanide) · Neonicotinoids (neuroactive systemic insecticides) · Midacloprid (mimics action acetylcholine) · Chlorinated hydrocarbons (DDT, extremely stable). Resistance management Use of pesticides only when needed, avoid pesticide residues, alternate pesticides with different modes of action, use recommended rates of pesticides, use other controls where possible, time pesticides sprays for the most vulnerable stage (larvae rather than adult) Interruption of development of resistance Non-insecticidal control methods, such as eliminating breeding sites and using natural insect predators, help kill or prevent development of resistant insects along with the susceptible ones. By rotating to a new chemical class you are likely to kill the resistant population so the cycle of resistance development must begin a new. a) General rules for animal transportation General provisions - Pregnant animals likely to give birth during carriage or animals having given birth during the preceding 48 hours and newborn animals, in which the navel has not completely healed, shall not be considered fit for transportation. - Animals shall be provided with adequate space to stand in their natural position and, when necessary partition to protect the animals from motion of the means of transport. - Unless special conditions for the protection of animals require otherwise, room to lie down shall be provided. - The means of transport and containers shall be constructed and operated so as to protect animals from weather and marked differences in climate conditions. - Ventilation and air space shall be in keeping with the conditions of transport and appropriate for the species of animals. - Sufficient space should be provided inside the animals' compartment and at each of its levels to ensure that there is adequate ventilation above the animals when they are in a naturally standing position without on any account hindering their natural movement. Watering and feeding intervals, journey times and resting period. · Journey time shall not exceed 8 hours. · The maximum journey time may be extended where the transporting vehicle meets the following additional requirements: - Sufficient bedding on floors - Appropriate feed and water for the animal species and journey time - Direct access to animals - Adequate ventilation that is adjustable (temperature) - Movable pens to create separate compartments - Unweaned calves, lambs, kids, foals that are still on milk, after 9 hours are give rest period of 1 hour. (Then another 9 hours) - Vehicles are equipped for connection to a water supply during stops · Pigs: max transport is 24 hours. Continuous access to water, sufficient water carried for watering · Unweaned calves, lambs, kids and foals which are still on a milk diet and unweaned piglets must, after 9 hours of travel, be given a rest period of at least 1 hour sufficient in particular for them to be given liquid and if necessary fed. After this rest period, they may be transported for a further 9 hours. · Domestic soliped ungulates: max 24 hours. Need liquid during journey and fed every 8 hours. · All other animals: after 14 hours require a rest period of 1 hour. Give liquid and feed. · After the journey time laid down, animals must be unloaded, fed and watered and rest at least 24h.

12. Leptospirosis and other spirochetosis, prevention and control, measures in outbreak, current epizootological situation. Proceeding of competent authorities in the case of disease outbreak, control and prevention

Leptospirosis infection by any pathogenic spp of g. leptospira. Zoonosis. Rodents are reservoir à spread disease. Etiology and epizootology Leptospira interrogans. 23 serovars! For dogs = L. interrogans serovar canicola Gram negative, spirochete, motile, endocellular flagella. · Lives well in water, so floods, lakes and muddy riverbanks are favorable · Natural and focal; higher incidents in times of heavy rainfall o Year-round incidents in tropical climates and seasonal in temperate climates · Professional disease, often given to vets! · Occurs mostly in dogs! Rarely in cats. Can occur in all mammans - zoonosis Transmission Leptospirosis is shed in urine of infected animals (because bacteria reside in kidney). New animals are infected when · Urine enters mucosa by wounds · Urine contaminates grass, feed, water, soil, bedding, puddles - animal ingests it · Other routes include o Semen, bites, transplacentally, eating infected carcass Pathogenesis Bacteria enters mucosa à leptospiremia when bacteria replicate in the blood à bacteria have affinity to the kidneys and continuous replication there. Then 3 things can happen (and it depends on vaccination status): 1. High antibody titer = body eliminates leptospirosis and there is no disease 2. Moderate antibody titer = there is mild kidney disease. Infection persists and then either a. Antibody production is increased and leptospirosis is eliminated b. Antibody production is not increased and there is mild disease 3. No antibodies = leptospira replicate in nephrons and the liver and there is severe disease a. Renal failure, toxic hepatitis and death There is peracute infection which is lethal, and we see fever, dehydration, tachypnea and vomitus. There is chronic infection which is most common, there is diarrhea/vomitus, nephritis, hepatitis and icterus. Kidney damage due to leptospirosis has many causes 1. Rhabdomyolysis à myoglobin à tubular damage 2. Vomitus, diarrhea à dehydration à hypotension à tubular hypoxia (decreased perfusion) 3. Direct toxicity of leptospira à kidney injury Clinical signs · Fever, shivering, muscle tenderness (à rhabdomyolysis) · Increased thirst, changed patterns of urination, dehydration, vomitus · Lethargy · Jaundice Humans: · Mild: Fever, muscle pain, head ache. Severe: Internal hemorrhage, kidney failure (Weils disease) Diagnosis Sample is blood, urine or CSF. In dead animals also kidney, liver or brain. Grow bacteria on agar (special, need BSA and Tween 80) and identify by PCR. Gold standard is the MAT - microscopic agglutination test. - Use live leptospirosis (recent isolates). Dilution series of patient serum - mixed with the isolates - Agglutination = AbAg is clumping = antibodies present = positive sample - Need to be done at intervals of 3-4 weeks! Because we want to see if Ab is rising or dropping Other Spirochetoses (syphilis/treponema and brachyspira) Includes leptospira, borrelia, treponema/syphilis and brachyspira. Gram negative, spiral, endocellular flagella, motile, many species cause disease. Treponema - syphilis (rabbit) Treponema cuniculi · Veneral disease - transmitted by copulation · Through milk from mother to offspring · Bacteria often lie dormant (up to years) and triggered by stress à clinical disease Clinical signs Typical form is lesions: Ulcers that is later covered with a thick crust develops in muco-cutaneus junctions (where mucus membranes meet skin) of the anus, genitalia and face (nose, mouth, eyes). Atypical form is same lesions but only on the face. Lesions are deep, inflamed, may bleed and have white exudate. They may disappear then reappear, but treatment with antibiotics is recommended. Brachyspira - swine dystentery · Large intestine · Small intestine is not affected! · Muco-hemorrhagic enteritis · Diarrheal disease · Brachyspira hyodysenteriae Pathogenesis Brachyspira proliferate = degeneration, inflammation of mucosa à hypersecretion of mucus, hemorrhage. Damaged mucosa à inhibited resorption à watery diarrhea Clinical signs The development of the diarrhea: (becomes increasingly more mucoid, bloody, watery) 1. Soft feces 2. Mucoid, has blood spots 3. Watery and very mucohemorrhagic 4. Brown feces with spots of fibrin. Now pigs are emaciated, dehydrated and weak. This bacteria produce hemolysin = causes lysis and damage to RBC Diagnosis Samples: Rectal swab, mucosa from colon, feces. Isolate by cultivatation on agar plate (TSA tryptone soya agar) Identification of agent by PCR During necropsy we find the mentioned damages in LI which is indicative Brachyspira pilosicoli Disease of the large intestine caused by the intestinal spirochetosis. It is transmitted orally and survives extremely well in the environment. Prophylaxis, control and prevention Control: · Leptospirosis: Isolation, treatment, proper husbandry and sanitation, rodent control · Intestinal spirochetosis: Prevent movement of the agent between groups of animals, all-in-all-out, thorough cleaning and disinfection, rodent control, waste management · Borrelia anserine: Tick control Prevention: Annual vaccination, prevention of contact with vectors and wildlife, prevent contact with contaminated environment, prevent access to contaminated water or waste, selective breeding, chemoprophylaxis, quarantine/isolation, proper husbandry and sanitation, tick removal within 12 hours. a. Sanitation measures and focal disinfection at these diseases. Preventative rat control Leptospira spp. survive for several weeks in wet environment, soil, water, feces, cold polluted water and slurry. Do not multiply outside its host. Need humidity for survival and are killed by dehydration. Brachyspira spp. survive outside its host (pigs) for up to 7 weeks in cold moist conditions. Sensitive to dehydration and most disinfectants Brachyspira pilosicoli is extremely resistant in the environment. Disinfection - 2-3% NaOH, 4-6% Chloramine T, 2% formaldehyde, 0.3% Peracetic acid. - Sensitive to moist heat (121°C for min. 15 minutes). Killed by pasteurization. - Chlorination of water. Composting excrements. Personal hygiene (protective clothing, treatment of wounds, clothing, face mask, gloves, glasses). Treatment of fishponds (lakes) - empty the pond, remove sediment, treatment by applying lime (calcium hydroxide) disinfectant. Preventive measures - rodent control Prevent access of rodents to the animal houses: Proper organic waste disposal, removal of excrements, carcasses, making the building rodent proof, closing rat holes with concrete or metals. Nets on windows. Limiting access to the food by having proper food storage - avoid them entering the food stores. Sanitation of the environment, disinfection, insect and rat control, hygiene in animal houses and on pasture. The presence of rats can be seen by the presence of droppings, gnawing on debris, runways (paths formed through vegetation), greasy rub marks and holes. Rat mechanical trapping: Traps use baits to capture rats. Types: Cage traps, glue, electronic. Before placing the traps, the following should be known; action of rodenticide, biology of rodents, selection of suitable type and form of rodenticide, how to properly place baits, quantity, frequency, location, bait boxes and warnings. b. Animal cruelty as a criminal act Cruelty to animals, forms of cruelty - Neglect. Animal cruelty is often broken down into two main categories; active and passive (commission and omission): Passive: Is typified by cases of neglect in which the cruelty is a lack of action rather than the action itself. Active: The intentional withholding of basic necessities and care. Examples of neglect: Starvation, dehydration, parasite infestations, allowing a collar to grow into an animal's skin, inadequate shelter in extreme weather. Act of Slovak National Council No 39/2007 Coll. on Veterinary Care: Cruelty to animals is prohibited. These prohibitions shall apply only to vertebrates. Cruelty to animals means any procedure, except reasoned medical and approved reason, which causes: · Permanent or long-term damage to health · Permanent or long-term violation of exhaustible parts of the body except for female sterilization and castration of males or tail docking of dogs · Permanent or long-term animal behavior disorder · Crossing the biological capacity of the animal or causing excessive pain, injury or suffering · Restriction of food and water, which is harmful to animals' health · To the animal pain or suffering by using them as live bait It is also prohibited to: · Dope animals/feed them drugs and chemicals harming their health or inducing a non-physiological condition · Use suggestions, materials or devices inducing pain · Interfere in childbirth with methods which increase the pain or damage the health of the animal · Badger animal to animal, train or test an animal on another live animal, except falcon training · Use animals as a price in competitions and animal exhibitions · Use live animals in artistic production/advertising without giving notice to local competent veterinary authority · Promote animal cruelty · Leave the animal with the intention of getting rid of it · Killing an animal without adequate reason The owner or keeper of the animal is obliged to ensure measures to prevent the escape of the animal, unplanned reproduction or unwanted reproduction. Breaking the law = only a fine. The owners/keepers cannot be imprisoned. Criminal Code (in the Slovak Republic); a person who abuses an animal, although he/she was affected for a similar offense in the past 12 months or he/she was convicted for the same offense in the previous 24 months. Abuses an animal in an especially cruel and brutal way. Fags (abuse to death) an animal out shall be punished by imprisonment for up to 2 years. Basic merits of the crime: The offender shall be punished with imprisonment for 1-5 years if he/she commits one of the follow offenses: · On more animals · In public, or in a place accessible to the public · On the animal especially protected by the law · In a serious manner Qualified merits of the crime: The neglect of an animals' care; A person who negligently causes death or permanent injuries to more animals which he/she owns, or is required to take care of, by neglecting the necessary care of animals, shall be punished by imprisonment for up to 2 years.

11. Listeriosis and bacterial encephalitis, prevention and control, measures in outbreak, current epizootological situation. Proceeding of competent authorities in the case of disease outbreak, control and prevention

Listeriosis sauen lister seg rundt med ataxia og lammet fjes (CNS) og en sandwich i hånden (food borne) Listeria spp, listeria monocytogenes. G+. Big food borne disease of humans. Severe disease!! CNS, GIT, sepsis. Etiology Gram positive (most pathogens are gram negative). Dangerous because it is very resistant and survives freezing, drying and heat. Multiplication at fridge temperature! Inactivated by pasteurization. Epizootology Found worldwide; Soil, plants, animal and water. Can infect many species but sheep listeriosis is main here. Higher incidence in winter and spring when ruminants are inside and fed on silage infected with bacteria. Used to be the most important foodborne human pathogen but is now decreasing. Elderly people, pregnant women, newborns and immunocompromised people are in risk. Transmission Ingestion of bacteria via infected food is most common. (Humans: Same but disease in young, elderly, immunosuppressed). Shedding from infected animals; feces, milk, uterine discharges, aborted fetuses, nasal discharges and urine of symptomatic animals. Ingestion, inhalation or direct contact. Pathogenesis Ingestion à bacteria reach small intestine à bacterium and epithelial cells of Peyers Patches in ileum share special bond (bacteria has d-galactose residue, epithelial cell has d-galactose receptor) à bacterium gains access into Peyers Patches and invade immune cells (macrophages, leukocytes) and gets in host blood. Listeria monocytogenes survives inside immune cells. It spreads to organs (CNS, parenchymatous organs like liver, kidney) and fetal fluids. Listeria monocytogenes travels via peripheral nerves to reach the CNS. Clinical signs are divided into 3 1. Septicemic form a. Death within 24-48 hours. Fever, weakness, anorexia. Calves, kids, lambs, piglets, immunosupp. animals. 2. Encephalitic form a. Stiff gait, face- and limb paralysis, opistotonus, Very common in sheep!! 3. Abortion a. If infection is in late gestation 4. Humans a. Fever in pregnant women. Neonatal infection cause sepsis and in utero premature birth. Encephalitis, gastroenteritis and cutaneus form. Diagnosis Microbiological methods First enrichment broth, then culture on ALOA medium and PALCAM or Oxford medium Confirmation by CAMP test or beta-hemolysis on blood agar. Necropsy shows lesions · Hemorrhages in epicardium and necrotic lesions on liver is seen in septicemic form · Slight changes like edema in brain in encephalitic form · Necrotic lesions of placenta in abortions caused by listeria monocytogenes Other PCR to identify agent. ELISA to detect specific antibodies Treatment: If signs of encephalitis are severe, death usually occurs despite treatment. L. monocytogenes is susceptible to penicillin = the drug of choice (but also ceftiofur, erythromycin, trimethoprim/ sulphonamide). Prevention: Spoiled silage should be avoided. Corn ensiled before being too mature and grass silage containing additives are likely to have a more acidic pH, which discourages multiplication of L. monocytogenes. Vaccines are available but the results are equivocal (tvetydig). Control: In an outbreak, affected animals should be segregated. If silage is being fed, use of the particular silage should be discontinued on a trial basis. Other bacterial encephalitis Streptococcus suis cause suppurative meningitis of pigs in addition to other syndrome such as pleuritis, pericarditis and arthritis. It is a zoonotic disease. Transmission Clinically healthy pigs can carry the bacteria in their tonsils, nasal mucosa and vagina for many months. Transmission via ingestion, inhalation or nose-to-nose contact. Pathogenesis Management and husbandry stressors may predispose. After oral/respiratory entry, streptococci pass to the crypts of the palatine tonsils. From there they invade via lymphatics to the mandibular lymph nodes where they can remain localized or become septicemic. Some organisms may survive within phagocytes and gain access to cerebrospinal fluid, brain, meninges, lungs and joints where they localize and cause meningoencephalitis, arthritis or pneumonia. Clinical signs Sudden death of piglets, or death after signs including fever, anorexia, depression, tremors, ataxia, convulsions and blindness. Arthritis (if present) - lameness and swelling. Endocarditis of older pigs - death without clinical signs. Diagnosis Clinical signs, necropsy, and isolation of the organism from CSF, brain, lungs, synovial fluid or heart. Many Mycoplasma cause nonspecific encephalitis in their natural hosts such as goats (M. mycoides), poultry (M. gallisepticum), cats (M. felis), dogs (M. edwardii) and rodents (M. pulmonis). Others: Escherichia coli, Pasteurella multocida, Rodeococcus equi, Tuberculosis a. Sanitation measures and focal disinfection at these diseases. Microbiological control of the disinfection Quite resistant in the environment (especially when present in a biofilm), being capable of growing in a wide range of temperatures (4-45°C) and can tolerate pH values between 5.5-9.6. Survives in slurry for 1-3 months, manure 1 month, soil 300 days, water 7 days and silage 450 days Survives conservation by low temperatures and can grow at refrigerator temperatures. Prevention Avoid spoiled silage, isolate sick animals, thoroughly wash vegetables, cook raw meat, do not drink raw milk, good hygiene and sanitation. ControlIsolation, vector control, regular disinfection, treatment by antibiotics, remove poor silage, handle suspected material with caution. Live attenuated vaccines are available in some countries. Control of disinfection can be divided into chemical control (determination of concentration of active substance by chemical swabs) and microbiological control. Microbiological control of disinfection The most objective method of determining effectiveness of disinfection is based on taking microbial swabs. A total number of microorganisms or the presence of indicator germs (endobacteria, coliforms, E. coli) is established by microbiological control. This is carried out at both preventive and focal disinfection. The data can be used to establish resistance of microorganisms. A minimum of 30 swabs from different surfaces must be taken from the disinfected object. Preventive disinfection Swabs are taken before and after disinfection, to compare and assess the efficiency of the disinfectant used. Dilutions of samples are performed if necessary. Samples are plated on culture media (selective media such as Endo-agar for the growth of indicator bacteria - total coliforms). Colony forming units/area are calculated. A minimum of 90% of the swabs must be negative after preventive disinfection. Focal disinfection All swabs must be negative after final focal disinfection b. Regenerative processes in the CNS from a forensic point of view Regeneration of ganglion cells and nerve fibers is negligible in the CNS, even in the prenatal period or in early adolescence. Reparative processes in the CNS appear only in the form of neuroglia that can partially replace damaged nerve tissue. After 2 days of inflammatory processes in the brain, proliferation of glial cells is observed and after 10-14 days, glial cells from small foci. Why does the CNS lack the ability for nerve cell regeneration? Lack of neurolemma, axon regrowth inhibition, and scar tissue formation.

34. Scabies and myiasis, prevention and control, measures in outbreak, current epizootological situation. Proceeding of competent authorities in the case of disease outbreak, control and prevention

SCABIES The scab (mange) cause chronic contagious animal dermatitis characterised by typical changes in the skin: The formation of massive yellow scabs, wet wool squeezed excoriations, falling wool, hair and feathers, strong pruritus and weight reduction. It is caused by ten species of mites - Psorptes, Chorioptes, Sarcoptes, Demodex and Psorergates, which can also induce a scab or pseudoscab in humans. Sarcoptosis Is a parasitic disease caused by sarcoptes scabiei or the itch mite, which is a type of burrowing mite: stationary, permanent parasites whose morphology is adapted to living in the epidermis. It is the causative agent of sarcoptic mange of animals and scabies in humans. Morphology Adult mites are small and circular. Only the 2 front pairs of the short legs protrude from the body edge. These carry a long, unstructured pretarsus with a small bell-shaped sucker-like pulvillus. The dorsal surface has transverse ridges, scales and bears long bristles. They have no eyes. Main species The genus has only one species, sarcoptes scabiei. The varieties of s. scabiei are usually host specific, so they do not colonize permanently other hosts (and do not reproduce). Genus sarcoptes · Sarcoptes scabei var. bovis, equi, ovis, suis, canis, vulpes and hominis Life cycle After copulation on the skin of the host, the females dig burrows of up to 1cm length in the epidermis where the cytoplasm of the epidermal cells serves as feed for the mites. In the tunnels only one female reside, which lay 1-3 large eggs per day. A six legged larvae hatch, which develops in the tunnels or hair follicles via the nymphal stages to the adult. After copulation, the male dies. Mites initially infest the sparsely hairy skin of head, neck and especially the auricle. From there, they spread to other body regions. Pathogenesis Sarcoptic mange develops in 3 different phases: · Incubation: minor local skin reactions · Hyperergic phase: severe itching, erythema, papules, parakeratosis, etc. · Desensitization: allergic reactions, clinical symptoms decrease and animal remain carrier. Skin changes and symptoms of sarcoptic mange are primarily triggered by allergic reactions to mite antigens. Clinical signs Itching, erythema, papular and inflammatory lesions, parakeratosis, hyperkeratosis with crusting, skin damage from scratching and rubbing, alopecia and secondary infections. Severe changes lead to weight loss, abnormal behaviour, systemic diseases and death (piglets, fox). Differences in the course of disease and predilection sites of mange in the host species. · Pig: lesions located in inner ear, behind ear, nose, neck and bends of joint. Hyperkeratosis. · Cattle: edema, inflammation, formation of vertical skin folds, scratching (mechanical lesions), hyperkeratosis and extensive alopecia · Small ruminants: head mange, lesions on head and legs, thick crysts and pruritus · Dog: changes on ears and head, spreading to chest, abdomen and legs. Puppies get more sick. Therapy and control · Amidines fex amitraz (Not for equines!) · Pyrethroids fex deltamethrin · Macrocyclic lactones (ivermectin, doramectin, selamectin-dog) and some organophosphates. Diagnosis Mite detection in deep skin scrapings (until capillary bleeding) in transition zone to healthy tissue and specific antibody detection. Occurrence and epidemiology · Worldwide distribution of sarcoptic mange in domestic and wild animals. In Europe, it is common among domestic pigs and less common in dogs. Dogs in contact with foxes are more often infested. · Transmission of mites is by direct contact or indirectly via contaminated environment. Sheep scab Infestation with the mite Psoroptes ovis leads to a common and destructive skin condition in sheep. It is the most severe ectoparasitic infection of sheep and it is extremely contagious. It affects woolly areas of the body and the mites are present at the periphery of the lesions. The mites are transferred by contact, either from one sheep to another, or from fence posts or stubs of infected wool. The mites are fairly hardy and can live up to 37 days off host, so even areas that have contained infected animals that have been reared may remain infective for 3-4 weeks. Clinical signs - Moist and pruritic lesions measuring a few mm, often on back - Itching is intense - Scratching causes reddening of the skin, bleeding and loss of wool over large areas - Skin is dry and scaly - Loss of body condition - In rare cases affected animals can die Diagnosis - CS provide a good indication that sheep scab is present - Definitive dg. requires the visualisation of the lesion and confirmation of the presence of mites - Superficial skin scrape (WITHOUT capillary bleeding) Treatment/control - By dipping or by the use of macrocyclic lactone injectables - The use of synthetic pyrethroid (SP) dips (cypermethrin) - Injectable drugs for scab: ivermectin, moxidectin and doramectin Notoedres Notoedres cati is the causative agent of notoedres mange in cats, which is very similar to sarcoptes mange, and usually starts on the head and then may spread to the legs and other body areas. Life cycle and clinical signs is similar to sarcoptes spp. Mites initially infest the sparsely hairy skin of head, neck, and especially the auricle. From there, they spread to other body regions. Skin changes and symptoms of notoedres mange are primarily triggered by allergic reactions to mite antigens and include severe itching, lesions on tip of ear which rapidly spread to entire head and neck. Knemioptes Mites of the genus knemidocoptes are burrowing mites that parasitize birds causing disfiguring dermatitis and thickening of the skin, and potentially life-threatening lesions. Main species · Knemidocoptes pilae: scaly leg and face mite of psittacine birds - mite burrow into feather parts of the beak. There is loss of feathers, scaliness, mild pruritus. · Knemidocoptes mutans: scaly leg and face mite in domestic fowl - mite burrows beneath leg scales, causing them to loosen and rise. There is distorted legs and claws, lameness, pruritus · Knemidocoptes gallinae: depluming mite of chickens, pigeons and pheasants. - mite a burrows into the feather shaft, which cause intense pain and irritation prompting the bird to pull out its feathers. There is loss of feathers, depression, anorexia and weight loss. MYIASIS The invasion of organs and tissues of humans and other vertebrate animals with dipterous larvae, which for at least a period feed upon the living or dead tissue, or in the case of intestinal myiasis, on the hosts ingested food. Principle of pathogenesis - Mechanical damage of tissues - Proteolytic enzymes dissolves tissues, results in deep and extensive damage and strong exudate formation - Bacterial infection, inflammation and the animal may die Types of myasis - Accidental or pseudomyiasis, facultative and obligatory Main species The larvae of several fly species are causative agents of myiasis in sheep and other domestic animals. Family Oesteridae- botflies · Hypoderma spp · Oestrus spp · Gasterophilus spp Family Sarcophagidae (fleshflies) · Sarcophaga spp · Wohlfarthia spp Family Caliphoridae (blowflies) · Lucilia spp- blowfly myasis · Phormia spp · Calliphora spp · Chrymosoma spp · Cochliomyia spp- screwworm myasis Hypoderma bovis (cattle grub) Cattle botflies or ox warbles, Hypoderma spp are flies whose larvae develop in the body of ruminants and other mammals. Adults are bumblebee-like flies with dense bristles and rudimentary mouthparts. Life cycle The fly is active from June to September. Mating occurs immediately after emergence of adults. During the flight period the female flies attach eggs to the hair of grazing cattle, preferable on the distal part of the body. Within few days the hatching larvae (L1) penetrate the skin and migrate along the fascial and perineural tissue of larger nerve fibers to the spinal canal. Following this phase, the larvae migrate through muscle to the dorsal skin, especially in the lumbar region. There they develop into L3 and form warbles with breathing holes in the skin. The L3 leaves the warbles in spring or early summer and pupate in soil Pathogenesis The panic escape reactions of cattle (gadding) during the approach from h.bovis can cause injuries. Hypoderma larvae damage the skin and partly also the back muscles. They can also cause reduction in performance and suffering of the host. Occasionally aberrant larvae invade other organs causing different types of damage. Clinical signs Rarely seen during migratory phase, except if larvae are killed during their passage through the spinal cord, as paralysis may then occur. Nodules within an opening usually seen in the skin of the back. These cysts contain a larva. When the adult flies attack cattle, stampeding may occur. Therapy and control - Hypodermosis can be eliminated by systemically acting insecticides. - Ivermectin (spot-on, pour-on) - Avoid late fall treatment, because bloat/hind end ataxia may result, due to host reaction around killed larvae in esophagus or spinal canal. - In endemic areas: treatment of all 3 month cattle with systemically active insecticides (eprinomectin). Epidemiology They occur in temperate regions in northern hemisphere. Hypodermosis can spread rapidly if no countermeasures are taken. Warble flies of wild ruminants do not pose a threat to cattle. Oestrus ovis Oestrus ovis, or the sheep bot fly, is a widespread species of fly known for its parasitic predation and damage to sheep, goat, deer and sometimes cattle. Adults are slightly hairy, brown-ish flies with a broad head and small eyes. The mouthparts are greatly reduced as the adult do not feed. Life cycle Adults occur from May to September. After mating, gravid females swarm and deposit batches of L1 to the nostrils of sheep. The larvae migrate directly into the nasal cavity and settle later at the nasal conchae and nasal sinuses. Here they firmly attach to the mucosa and feed on mucous secretions and inflammatory products. Several proteases are secreted by the larvae to liquefy tissue. The larvae grow and moult twice to L3, which are equipped with mouth and caudal hook, as well as spines and papillae. The L3 that is ready to pupate, detach and leave the host actively, or are discharged by sneezing and coughing. On the ground, the larvae pupate. In temperate zones, only one fly generation develop each year. Pathogenesis The first weeks of infestation is usually inapparent. The deposition of L1 and their migration into the nasal cavity can cause restlessness, rubbing the head on objects and shaking the head. At their place of attachment, larvae can cause inflammatory changes, bacterial infections and nasal discharge. In case of strong infestation, colonization of the larynx, trachea and large bronchi may occur. Clinical signs Inflammatory reactions in head and nasal cavity. Nasal discharge (rhinitis), haemorrhagic, sneezing, wheezing breath, snorting, head shaking, rubbing nose against grown, nervous excitability, pneumonia, lacrimation, dyspnoe, coughing, impaired food uptake, weight loss and loss of condition. Therapy Cosantel, Nitroxynil, Ivermectin, Doramectin and Moxidectin. Differential diagnosis Scrapie, psoroptic otoacariasis or sheep scab. Traumatic myasis- screw-worm myiasis (OiE notifiable) Main species · Cochliomyia hominivorax: new world screwworm · Cochliomyia macerllaria · Cochliomyia bezziana Pathogenesis Female flies lay their eggs at the edges of wounds or on mucous membranes. When they hatch, the larvae enter the body. As the larvae feed, the wound gradually enlarges and deepens. Infested wounds often have a serosanguineous discharge and sometimes a distinctive odor. By the third day, the larvae may be easily found. If left untreated, infestations can be fatal and animal may die in 7 to 14 days. Clinical sings Animals may appear dull and lethargic. Smelly wounds will be observed during inspection. - Small infection: little to no clinical effect - Heavy infection: irritation, discomfort, pruritus, weight loss, loss of general condition, hemorrhage, bacterial infection, anaphylaxis and toxemia. - Animals may become anemic and suffer from severe toxemia (adult flies excrete ammonia that is absorbed by the skin). Affected sheep usually stand outside the main herd. Treatment and control - Subdermal larvae: surgical removal - Cutaneous myasis: removal of larvae and cleaning of wounds. Topical organophosphates. Diagnosis Post mortem finding of larvae Others - Traumatic myasis (blowfly myasis): infestation of sheep skin causing dermatitis. - Gastrophilus spp: obligate parasitism of the larval stages in equine species. They cause inflammation and ulceration of the stomach, colic, anemia and cachexia. Proceeding of competent authority, control and prevention Scabies Control · Isolation and treatment of affected animals · Quarantine of new animals · Mechanical cleaning · Ascaricide application (dipping tanks, spraying, topical application or systemic treatment) Prevention · Access to safe water · Treatment of animals ASAP · Sanitation of environment - clean and disinfect animal accomodation · Personal hygiene · Treatment of wounds · No vaccine available Myiasis Control · Surveillance in non- endemic regions · Isolation and treatment · Movement control · Meat judgement · Insect/vector control - is preventative and aims to eradicate adult flies before they can cause any damage o Insecticide - application in the environment where the target livestock is kept o SIT - Sterile Insect Technique - a significant number of artificially reared sterilized (usually through irradiation) male flies are introduced · Treatment once the infestation is present Prevention · Removal of larvae: physical (tweezers), larvicide, removal of necrotic tissue · Wound treatment: cover air hole with petroleum jelly · Removal of tail/docking - to remove the environment most favourable to the flies · Crutching of sheep - removal of wool from around the tail and between the rear legs, which is a favourable environment for the larvae · Mulesing - more permanent practice, used in some countries, skin is removed from young animals to tighten remaining skin - leaving it less prone to fly attack L a) Sanitation measures and focal disinfection at these diseases. Using of pyrethroids The survival of flies dependents on temperature, relative humidity, food sources, host availability and other ecological factors. Ambient temperature of 25-30°C with relative humidity of 30-70% are ideal parameters for screwworm flies, enabling them to survive for up to 1 month off the host. The larvae can survive for 2-5 days at normal indoor temperatures, but are only infective the first 2 days. Prevention of these parasites are best achieved by general hygiene (mechanical cleaning) and spraying of housing with insecticides (organophoshpates). Use of pyrethroids Synthetic pyrethroids are a modern group of insecticidal substances with high insecticidal activity which are derived from pyrethrum but chemically prepared. Mechanism of action Sodium channel blockers. Their biological effect is defined as a knock-down or killing effect. The major biochemical effect of pyrethroids concerns the interference with sodium channels and disruption of axonal transmission - resulting in continuous nerve impulse transmission, tremors and eventually to death. Most products are formulated with synergists such as piperonyl butoxide to enhance the pesticidal properties of the product. These compounds have no insecticidal effects themselves but enhance the effectiveness of the pyrethrins. Usage May be used in public health and industrial pest control, timber protection, mothproofing, grain protection and in horticultural and agricultural crop protection. Cypermethrin has especially high activity against veterinary ectoparasites and is used as a spray of dip-bath. Not active against mites. Resistance among insects may develop but can be avoided by rotating various pyrethroids and other insecticides. Products Important pyrethroids include: • Allethrins and Esbiothrin - Against houseflies, mosquitoes, midges, moths, bees, ants, cockroaches, earwigs, crickets etc - Effective wide-spectrum knock down insecticides with very rapid action. May be used alone or in combination with other insecticides. • Permethrin • Deltamethrin • Cypermethrin - against vet. ectoparasites, including ticks, lice, sheep scabies Toxicity These substances are 2250 times more toxic to insect than mammals, as insects have increased sodium channel sensitivity, smaller body size and lower body temperature. Become more toxic to insect with decreasing temperature. Biological toxicity to mammals and birds is very low, however they have high toxicity to bees and fish. Penetration into soil and water must be prevented. b) Donating an animal Donation The subject of donation can be anything that can be subject of civil relations (ie animals and other movable or immovable things). A donor transfers the property without expecting anything in return. The donation takes place by delivery and acceptance of the gift. Donation can only occur only between living people. Donation cannot be decided after the donor's death. - Donor is obliged to draw attention to the defects when presenting gift. If a thing has got defects, which the donor has not warned, the gift may be returned. - Donor, who has not warned the recipient of defects of the gift of which he knows, is responsible for the damage that will arise as result of defect of the gift. - Donor can demand the return of the gift if the donee does not behave correctly to him/her or his/her family members so that the donee grossly violates good morals. The return of the gift - Donor who has not warned the recipient of defects of the gift of which he knows, is responsible for the damage that will arise as a result of the defect of the gift. - Donor can demand the return of the gift if the donee does not behave correctly to him/her or his/her family members so that the donee grossly violates good morals. The european convention for the protection of pet animals No pet animal shall be sold to person under the age of 16 without the express consent of their parents or other persons exercising parental responsibilities.

7. Mycoplasmosis, prevention and control, measures in outbreak, current epizootological situation. Proceeding of competent authorities in the case of disease outbreak, control and prevention

Mycoplasmoses Diseases caused by mycoplasma; the smallest prokaryotes. Bacteria without cell wall à fried egg appearance · Opportunistic pathogens · Found on wet surfaces, typically RESPIRATORY tract · Lacks cell wall! Thus very RESISTANT to treatment · Mycoplasmosis in cattle and poultry in this question (det e så mjuk og god plass her, sier kuen og hønen som ligger og chiller) Epizootology Mycoplasmosis worldwide occurrence, endemic in Africa. · Eradication programmes exist for chronic bovine pleuropneumonia, resulting in no cases in Europe since 1999. Mortality in this disease is high and it cause significant economic losses. · Contagious caprine pleuropneumonia outbreaks often occur after heavy rains, cold spells or transport. · There was a case of avian mycoplasmosis in Finland 2015. · Mycoplasmosis in humans have a high prevalence worldwide, especially in babies post-weaning. Diagnosis · Samples (live): nasal swabs, pleural fluid, blood · Samples (necropsy): lung lesions, lymph nodes, synovial fluid · Clinical signs, lesions · Isolation and identification of organism: special agar- cloudy, fried egg appearance. · Serology: PCR and ELISA Treatment Antibiotic treatment is not recommended (tetracycline, tylosin). Respiratory mycoplasmosis in cattle 1. CONTAGIOUS BOVINE PLEUROPNEUMONIA Mycoplasma mycoides mycoides (OIE listed). · Long incubation period; 1-4 months · Spread by inhalation of droplets from coughing · Direct contact (saliva, urine, fetal membrane, transplacental) Pathogenesis: Morbidity may be up to 100% and mortality 30-80%. 25% recovered animals may become carriers with chronic lung lesions, including hydrothorax, fibrin deposits on thoracic organs, enlarged and carnified lung tissue. In chronic cases, the lesion has a necrotic centre sequestered in a thick, fibrous capsule. Clinical sign: · Acute form: o Early signs include depression, moderate fever, coughing and tachypnea o Pneumonia progresses, to dyspnea. Elbows abducted to decrease thoracic pain, extended neck · Chronic form: o Less obvious signs of pneumonia, cough with exercise, emaciation etc. o Calves: polyarthritis, pneumonia Without treatment, mortality can be high Non-clinical individuals, those with chronic infection are major carriers o Viable organisms encapsulated in lung lesions for many years! Sheds Diagnosis by samples from nasal swab, tracheal wash or pleural fluid (by puncture). Cultured on agar and has "fried egg" appearance. PCR, CFT and ELISA. 2. ENZOOTIC PNEUMONIA IN CALVES (CUFFING PNEUMONIA) Mycoplasma spp causing chronic, catarrhal bronchitis over a course of many months. Production of lymphofollicular sheats around airways = "cuffing pneumonia". Mucus and neutrophils accumulate in the lumen of airway. Causes can include: · Partial failure of maternal antibody transfer · Stressors altering normal microflora · Viral respiratory infection · Crowding in dairy houses (less outbreaks in hutches). Avian mycoplasmosis - Chronic respiratory disease Caused by several pathogenic mycoplasmas; Mycoplasma galliseptum and Mycoplasma synoviae (OIE listed). Causes chronic respiratory disease, especially during stressors or concurrent disease. Birds will suffer from decreased egg laying and meat production (economic loss) in chronic infections. Clinical signs · Subclinical disease in chronic disease (only seen as decreased production) · Obvious respiratory signs in more acute disease o Runny nose, coughing and sneezing o Open beak breathing o Sinusitis o Conjunctivitis with frothy exudate; soiling of feathers from trying to remove exudate o Secondary infection e.g. by virus will worsen clinical picture Lesions in respiratory tract includes excess exudate which later becomes caseous and deposits are masses in the air sacs. Diagnosis As above. Swabs taken from choanal cleft, esophagus, trachea, cloaca or oropharynx in live birds. Same but also air sacs in dead birds. Mycoplasmosis in goat- Contagious caprine pleuropneumonia Mycoplasma capricolum subsp. capripneumoniae is causative agent. Important in Africa and Asia with great economical loss. Associated with heavy rain and transportation. · Morbidity often 100% and mortality 60-100% Transmission: Highly contagious by direct contact (inhalation of resp. droplets). IP: 6 - 10days sometimes as long as 3 - 4 weeks. Clinical signs: · Peracute: None · Acute: High fever, anorexia, wide stance, extended neck · Chronic: Cough, nasal discharge Pathogenesis: Granular lung appearance, fibrinous pneumonia, chronic changes (pleuropneumonia, pleuritis and adhesions) Respiratory mycoplasmosis in swine Mycoplasma hyopneumoniae and hyorhinis are the number one cause of Enzootic pneumonia in pigs, a chronic, usually non-fatal disease of young pigs. Morbidity in a herd is up to 70-100%. Pathogenesis The attachment of mycoplasmas to the ciliated cells is followed by a cytopathic effect and exfoliation of epithelial cells. Later during the course of disease, the epithelium is completely ulcerated. Simultaneously, cellular reactions occur, consisting mainly of increased peribronchiolar and perivascular mononuclear cell accumulation. The result is exudative bronchopneumonia or lobar pneumonia. M. hyosynoviae has a special affinity for joint tissue and may cause arthritic disease, leading to economic losses. Clinical signs Coughing. Chronic disease is seen only at slaughter or after dying from another disease (secondary bacterial infection by mainly Pasteurella multocida) Prevention and control Control · Treatment: due to the lack of cell wall, treatment with antibiotics is difficult as not all is effective. Tetracycline, erythromycin, streptomycin · Radical method: stamping out all serologically positive and susceptible animals · Disease free countries: quarantine, movement restriction, serological screening (agglutination and ELISA, HIT is confirmatory). · Positive countries - Slaughterhouse surveillance: efficient method of detection of clinical cases - Milk: milk infected animals at end of milking line - Vector control Prevention · Vaccination: contraindicated as it leads to carriers (only approved in USA and Africa). · Good husbandry: preventative disinfection, ventilation, decreased density, quarantine. · M. gallisepticum: test a small nucleus of breeding flocks. ATB treatment of embryonated eggs. a.) Sanitation measures and focal disinfection at these diseases. Aerosol disinfection. Sanitation Mycoplasmas do not survive long in the environment and is readily destroyed by light, heat (55-60°C) and pH (acids/alkalis). M.mycoides may survive for 10 years if frozen. Disinfection · Chloramin T (4%), NaOH (2%), formalin (2%), peracetic acid (0,5%), chlorinated lime (3%) - Aerosols (air): peracetic acid and formaldehyde vapours - Physical disinfection: dry pasture and burn waste Aerosol disinfection Aerosol disinfection is the distribution of very small particles (0,5-10um) of disinfectants using special equipment. Requirement include electricity, tap water supply, RH of 70-90% and temperature above 15°C. The disinfectant is prepared according to air volume and only unstable agents are used. 5-25ml/m3 of concentrate disinfectants is used. Exposure time min 6 hours or overnight, prevent aerosol to escape from the house. · Peracetic acid (5ml/m3): can be used in presence of animals if added lime (?). · Formaldehyde (25ml/m3): addition of 25g potassium permanganate result in exothermic reaction Ppt disinfection page 17+18 b.) Potential consequences in increasing the risk of dismantling the disease Dismantling = spreading · Any person who (even by negligence) creates the danger of introducing or spreading a contagious disease of farm or other animals of economic importance shall be liable to a term of imprisonment of up to 1 year. · The offender shall be liable to a term of imprisonment of 6m-3y if he commits the offence referred to in paragraph 1. - And causes larger damage through its commission - And causes the spreading of such disease, or - Acting in a more serious manner · The offender shall be liable into term of imprisonment of 1-5 years if he comments the offence referred to in paragraph 1 and causes substantial damage through its commission. - Acting in more serious manner, or - Causes grievous bodily harm or death through its commission

14. Foot and Mouth disease and vesicular stomatitis complex, prevention and control, measures in outbreak, current epizootological situation. Proceeding of competent authorities in the case of disease outbreak, control and prevention

Vesicular stomatitis complex: A group of indistinguishable diseases characterized by the formation of blister-like sores in the oral cavity. Diseases belonging to this complex: · Foot and mouth disease (FMD) · Vesicular stomatitis · Swine vesicular disease · Vesicular exanthema of swine Foot and mouth disease OIE listed. Cattle and pig (all spp with cloven feet!). Severe. Highly contagious. High economic losses. Picornaviridae (RNA). Very small (pico). Aphtovirus = causes aphthae which are ulcers in the mouth. Etiological agent FMD virus has 7 strains (O, A, C, SAT1, SAT2, SAT3, Asia1) - No cross-immunity! Vaccine has only 1 serotype covered, can still be sick from rest Resistent and survives in frozen, desiccated and pasteurized products = survives well inside the body of live animals But it is pH sensitive and dies in muscles during rigor mortis when pH falls below 6 Epizootology Endemic in Asia, Africa and south America. Sporadically occurs all over the world. Not a public health risk. Outbreaks in the UK in 2001 and 2007. In Israel, South Africa and Columbia in 2018. Transmission Virus is in all excretions and secretions of infected animal which is why FMD is so contagious! · Semen, milk, cough, feces, urine, breath (aerosols) · Direct contact or contact with contaminated bedding, feed, water etc. (ingestion, inhalation) · Humans harbor virus in RT for up to 48 hours which helps transmission a lot Pathogenesis 1. Replication in mucosa of throat (pharynx) 2. Distributes in lymphatic system à replicates in epithelium of mouth, muzzle, feet 3. Inside the epithelial cells the virus replicates profusely and cell eventually bursts 4. Burst = virus disseminated in blood Clinical signs Severity of disease depends on virulence of strain, dose of inoculated virus, age and species of host. Morbidity can reach 100% (very contagious) but mortality is generally low, slightly higher in young. · Blisters (vesicles) on nose, tongue, lips, oral cavity, between cloves, above hooves · When blisters rupture there is extreme pain causing lameness and reluctance to move · Ruptured blister may heal but secondary infections are common · Reduced milk production Higher mortality is seen in pigs because they tolerate stress of disease/pain less than cattle Differential diagnoses are the other vesicular diseases of swine; Vesicular stomatitis, swine vesicular disease and vesicular exanthema of swine. Diagnosis · Necropsy = tiger heart. Found in young animals due to necrosis and degeneration of myocard · Virus isolation · PCR, ELISA, Virus neutralization test · Sample is lesions, liquid in vesicles https://www.youtube.com/watch?v=V1HbJ8xlQXY Prevention: Protection zones, clean premises, quarantine, slaughter of positive animals Vesicular stomatitis · Indiana vesiculovirus (vesiculovirus) · Zoonotic · OIE notifiable · Horses and cattle mostly but other spp are susceptible o Horses are immune against FMD so this is their vesicular disease Transmission Directly through transmucosal/transcutaneous route (piercing through layers from outside to inside). Can also be vector borne by blood sucking arthropods like mosquitos and sand flies. Virus found in saliva, vesicle fluid and inside vectors Hosts are equines, bovines, suidae and camelids. High morbidity in herd, low mortality. America. Epizootology Disease is present in and limited to America. Pathogenesis Is unclear. Virus enter mucosa or skin and a vesicle is formed. The vesicle will rupture and leave painful ulcers which are open for secondary infections. Clinical signs First manifestation is excessive salivation due to the painful ulcers in mouth. We see vesicles or broken vesicles in mouth, gingiva, on tongue, lips, hard palate and sometimes on muzzle and around nose. - Horse, cattle and pigs = also on feet - Dairy cows = also on teats à lameness à mastitis à secondary infections Many have subclinical disease with no signs!! Differential diagnoses are also here the other vesicular diseases (swine exanthema, FMD, swine vesicular disease) except when it is in horses. Diagnosis Sample taken from vesicular fluid, epithelium of unruptured vesicle or swab from ruptured vesicle. Virus isolation in cell culture, ELISA to detect antibodies, CFT and PCR. Prevention Restrict animal movement. If moved, use quarantine. Disinfect trucks and premises. Wait at least 21 days after lesions are healed before movement. Insect control to limit vector. https://www.youtube.com/watch?v=sVqXTWlEyOY Swine vesicular disease Also, picornavirus but genus is enterovirus. Swine vesicular disease virus. Fever and vesicles! Epidemiology Outbreaks are often seen after transport and movement of pigs with subclinical infection. During transport or crowding in general, pigs often get small lesions. This is a portal of entry for virus into body! Morbidity is high within pens, between pigs in close contact. Can also be contracted by sheep. Virus is very stable and resistant! Similar to FMD virus and vesicular stomatitis. Epidemiology The disease is found worldwide. Endemic in some areas of Europe (Italy - first identified, 1966) and Asia (Japan and Hong Kong). Sporadic outbreaks in Portugal 2003, 2004, 2007. Transmission Virus is found in blood - feces - vesicles - saliva. · Direct contact between pigs · Orofecal route with ingestion of contaminated feed · Feeding of pork meat (undercooked) or pork products · Open skin/mucosa (viremia > generalized vesicles > rupture > more virus in body) Clinical signs Severity of disease (subclinical, mild or severe) depends on - Host: Immunocompetence, age, housing conditions - Virus: Virulence of strain, dose of infection In acute form, there is fever, lameness (painful vesicles) and vesicles forming in mouth, snout, feet and teat. They rupture and form deep ulcers prone to secondary infection. In severe viremia animal can develop neurological signs indicating encephalitis. Sometimes, the only evidence of infection is a dark horizontal line on hoof that shows growth was temporary interrupted. Differential diagnoses are as before; FMD, vesicular exanthema and vesicular stomatitis. Diagnosis Same as before. Liquid in vesicles and epithelium from unruptured vesicles, or skin flap from freshly ruptured vesicles. Can also swab ulcer. Virus isolation in cell culture, ELISA, virus neutralization test and RT-PCR (bcs rna-virus). Prevention · Surveillance programmes · Slaughter of all seropositive animals and those in contact with them · Disinfection of premises, trucks and equipment · Strict rules about import and movement of animals. Quarantine! Also for animal products. · Prohibition of garbage feeding (pigs being fed pigs?) or make sure thorough cooking first. Vesicular exanthema of swine Vesicular exanthema of swine virus. Caliciviridae, Vesivirus. Fever, vesicles (snout, mouth, feet, toes) Epizootology Only reported in USA (not since 1959) - but remains historic due to its clinical similarity to FMD (indistinguishable). The virus was globally eradicated in swine in 1959, but the virus is still present in sea mammals and fish, so it could occur again. Transmission Blisters contains large amounts of Vesivirus. When they break, virus remains in environment for months and can infect new hosts. Virus is also found in saliva and feces. If pig has damaged skin, virus from vesicle fluid/saliva/feces can enter and pig is infected. Pig to pig transmission is common thus high morbidity within a herd Before, many outbreaks started with feeding of uncooked pork scraps, and when they stopped doing that, incidences was reduced a lot. Clinical signs Clinical disease is indistinguishable from FMD, swine vesicular disease and vesicular stomatitis. - Itching vesicles with clear fluid - Vesicles erode into deeper tissues - Fever Can also see pneumonia, encephalitis and abortions (possible due to viremia). Diagnosis · Identify agent as before, same sample as before. · Complement fixation test, ELISA, RT-PCR · Slaughter all positive and those in contact. Disinfect premises and equipment · Samples include vesicle fluid, epithelium of unruptured vesicles, epithelial flaps or freshly ruptured vesicles (or swabs of these vesicles), or from oropharyngeal fluid. Disease Species Transmission Etiological agent Foot and mouth Cattle + pigs Cloven hoofed All - direct, indirect, excretions/secretion, inhalation Picornaviridae Aphtovirus RNA Vesicular stomatitis Horse + cattle (wild + human) Direct + vector Rhabdoviridae Vesiculovirus RNA Swine vesicular disease Pigs Direct, orofecal, vesicles Picornaviridae Enterovirus RNA Vesicular exanthema of swine Swine (eradicated) Still: sea mam + fish Blisters, in env, direct, ingestion Caliciviridae Vesivirus RNA Prevention of these diseases Proper husbandry and sanitation through disinfection of premises, transport vehicles and equipment. Surveillance program for vesicular diseases with tracing and slaughter of all seropositive animals and contacts. Animal movement restrictions: Strict import requirements, movement controls and quarantine for animals and animal products. Vector control (birds, dogs, cats, all sick animals). Either prohibition of feeding food scraps (pigs) or enforcement of thorough cooking of wastes used to feed animals. FMD: Emergency vaccine Dampening down: Aimed at reducing the amount of virus in areas where it is not possible to slaughter animals fast enough to prevent spread. Protective: Aim to produce an "immune belt" of vaccinated animals around an infected area. All vaccinated animals should be marked and not moved out of the zone. Control The basis of any policy to control FMD is to limit access of the virus to susceptible animals. Method of control depends on the prevalence of the disease in particular regions/states, geographical considerations and the desire to eradicate or simply control. Disease eradication - "stamping out" - Slaughter of all infected animals and in-contact animals, cleaning, disinfection + other measures necessary in case of outbreak in an FMD-free country, region or zone. Sanitary prophylaxis: Protection zones, quarantine measures, slaughter, clean and disinfected premises. Personnel should wear protective clothes. Infected animals: Should be killed (avoid unnecessary movement), covered with plastic bags to minimize environmental contamination. The carcass should be disposed of by burial (method of choice) - NB! There are requirements for place of burial (distance from water, buildings...). Recommended pit dimension for 20 bovine or 60 sheep/pigs, is 6 x 3 x 4-meter-deep. Incineration/cremation (second choice) or rendering (if no other methods are available). FMD control polices: Increased awareness, staff training in recognition and surveillance, detailed contingency plans (contingency = a possible circumstance which is not able to be predicted with certainty). Community Reference Laboratory for FMD diagnosis. National vaccine banks. Trucks and fomites should be disinfected, and sub-clinically infected animals should be isolated. a. Sanitation measures focal disinfection diseases. Application of the sodium hydroxide in disinfection practice. FMDV is very resistant to environmental factors and survives freezing, drying, and pasteurization. It can survive in the lymph nodes and bone marrow at neutral pH but destroyed when pH <6 (e.g. rigor mortis). It is also able to survive in contaminated fodder for up to 1 month. At the focus of infection: Closed farm, fenced, 3 km protection zone, 10 km surveillance zone. Disinfection Sodium hydroxide (2%), sodium carbonate (4%), citric acid (0.2%), peracetic acid (higher concentration), ethanol (70%) and formalin. Sensitive to acids, alkalis, chlorine, formaldehyde. · Premises and infected material: Milk-pasteurization, burial (spray with disinfectant) · Preliminary (preparatory) cleaning and disinfection: When all parts of the farm is considered contaminated · Final cleaning and disinfection: Sodium carbonate for organic material, then cold water, followed by disinfection. Clean again after 7 days and observe for 21 days. · Manure and bedding: Disinfect and cover for 42 days (composting). Manure must be added quick lime, slaked lime (20%), then stacked for warming and added 100 kg of granulated calcium oxide. · Sludge: Storage for 42 days, NaOH · Vehicles: Never use NaOH · Rodent control: Acute rodenticides (zinc phosphide) with pre-baiting Application of sodium hydroxide (NaOH) in disinfection practice NaOH (lye, caustic soda) have strong alkaline properties. Very strong, highly corrosive to aluminum, metal, textiles. Unstable during storage: To prevent conversion of sodium hydroxide (NaOH) to sodium carbonate (Na2CO3) under the action of carbon dioxide (CO2) present in the air, NaOH granules should be stored in tightly closed containers. Wide microbicidal effect: Effective against · G- bacteria: At 1% concentration · G+ bacteria: 3-5% · Viruses: 2-4% (1-2 hours exposure time) · Spores: 5-10% It is used in the form of spray. Focal disinfection: Also used in combination with formaldehyde · 3% alkaline formaldehyde - good effect on mycobacteria and fungi Activation at 70-80°C b. A veterinarian as an expert, the responsibility of a veterinarian As an expert or witness (or forensic assistance) Veterinary involvement: Assessment of welfare, animal behavior and nutrition. Determination of cause, time and circumstances of death. Verification of origin and history of live/dead animals. Postmortem examination when abuse and violence of humans appear to be linked. Food safety (includes welfare at slaughter to meat inspection standards, detection of contaminants). Human welfare (zoonoses, personal injuries e.g. kicks, bites). Miscellanesous (various) cases relating to liability, negligence, nuisance, fraud, environmental pollution, damage. · A witness has seen with his/her own eyes · An expert must be a specialist in the field, finishing with an exam (at least in Slovakia) Non-criminal cases · The veterinarian may have to testify in court proceedings. · Determination of the circumstances of death (cause, mechanism, manner); how, why, when, and where did it die, who might have been involved. Witness of fact · Evidence may arise from daily life. E.g. observation done during veterinary clinical examination · Knowledge gathered by the veterinarian from any other source is considered to be "hearsay" and would have to be provided by a person who observed the ill-treatment of the animal. Professional witness Veterinary surgeons can be asked at the end of their factual evidence, in a prosecution for causing an animal unnecessary suffering, whether they thought that the animal suffered and whether the suffering was necessary. Expert witness Veterinary surgeons, by way of specialized knowledge, qualifications and experience, are sometimes called upon to act as expert witnesses before the court. All expert witnesses must · Refer to any material fact or matter of relevance (regardless of whether they have been asked to comment on that particular matter) · Indicate if their opinion is not supported by sufficient research or data · Inform the engaging party via supplementary report if their opinion about a material matter change · Provide a copy of their resume alongside all reports Duties of veterinarians · Examination of animals in clinics and on farms to check for signs of illness or disease and to establish overall health of animals · Examination, diagnosis and create treatment plans for a wide range of problems · Patient education - keeping animal owners informed about the best practice for care of their animals. Suggest healthy diets, how to deal with behavior problems, explain how to monitor animals for signs of disease. · End of life - when the animal is sick, in pain or if treatment cannot prolong the life of the animal, euthanasia is the kindest thing to do. Veterinarians handle the euthanasia, comfort owners and dispose of the remains. · Legal - recognizing and reporting zoonotic diseases (report to a public health department). Taking biological samples. · Ethical - standards for humane and ethical treatment of animals (professional behavior, patient relations, e.g. client privacy). Transfer of treatment records when the client change to another veterinarian. Maintain a professional relationship with colleagues

33. Trichomonosis, prevention and control, measures in outbreak, current epizootological situation. Proceeding of competent authorities in the case of disease outbreak, control and prevention

Members of the family trichomonadidae are usually pyriform, uninucleated organisms with 2-5 anterior flagella and one posterior flagellum, which pass along an undulating membrane. There is NO cyst stage! Several genera can be distinguished by the number of anterior flagella: - Tritrichomonas: 3 flagella - Trichomonas: 4 flagella - Pentatrichomonas: 5 flagella Bovine trichomonosis- Tritrichomonas foetus B (bovine strain) Tritrichomonas foetus is a sexually transmitted parasite of the reproductive tract of cattle. It is an OIE-notifiable disease Morphology Pear to spindle-shaped cell bodies, 3 anterior flagella, 1 posterior flagellum with undulating membrane and thick axostyle. Life cycle Direct life cycle, involving mobile trophyzoites, which multiply by binary fission. These are transmitted during sexual contact between cattle. In some cases, pseudocyst might be formed. These are rounded cells without free flagellum, but with internal flagellar movements. Contain two or more nuclei. Capable of budding. Pathogenesis After infection of female animals, tritrichomonas initially multiply on the vaginal mucosa. Thereafter, the flagellates migrate through the cervix into the uterus and may reach the oviduct. In the vagina, they might cause mild catarrhal infection. Characterized by early abortion. In male animals, the parasite colonize the preputial cavity and sometimes the urethra and testicles. Visible lesions do not occur in infected bulls and potency and semen quality are not compromised Clinical signs · Cows: early abortion, fetal death, uterine discharge, pyometra, endometritis, reproductive disorders and sterility · Bulls: inflammation of preputial sac, small nodules, no gross lesion, lifelong carrier Treatment and control · No legal treatment in cows. Maybe symptomatic treatment and sexual rest in cows, though cannot be used for breeding. Control of bulls and artificial insemination. Inactivated vaccines- not very common Diagnosis · Clinical history (early abortion, irregular estrus) · Stained smears · Native preparation (nb sensitive to cold): typical jerky movement · Culture procedure: commercial culture kit · PCR and ELISA Avian trichomonosis- Trichomonas gallinae Trichomoniasis is a cosmopolitan disease of pigeons, poultry and raptors caused by the protozoan parasite Trichomonas gallinae. These flagellated protozoa live in the MM of mouth, throat, esophagus, liver, etc. In pigeons, transmission occurs when infected adults (carriers) feed "pigeon" milk to newly hatched birds. In chickens, source is often contaminated water. Morphology Roughly pear-shaped parasite with 4 anterior flagella, thin axostyle and short undulating membrane. Geographical distribution Worldwide in domestic pigeons and other types of birds. Rare in chickens Life cycle Infected adult pigeons transmit trichomonas with the crop milk to their offspring. Older birds acquire the infection through drinking water that has been contaminated with trichomonas from the beak cavity of infected pigeons. Birds of prey becomes infected by ingestion of captured birds. Pathogenesis Mainly a disease of young birds- fatal in pigeons The early lesions appear as small white to yellowish areas in the mouth cavity, especially the soft palate. The lesions consist of inflammation and ulceration of the mucosal surface. The lesions increase in size and number and extend to the esophagus, crop and proventriculus. The lesions may develop into large, firm necrotic masses that may block the lumen. Occasionally, the disease may spread by penetrating the underlying tissues to involve the liver and other organs. Lesions consist of circumscribed, yellowish, caseous, necrotic foci. Recovery leads to partial immunity- asymptomatic carrier. Clinical signs Birds lose weight rapidly, become weak and listless and sometimes die within 8-10 days. Treatment Metromidazole Diagnosis · Live animal: Crop swabs- wet or stained smears · Post mortem smears Proceeding of competent authorities, control and prevention Control · Positive animals: cull bulls and repeat testing negative animals. Its recommended to cull positive cows as they will remain carriers · Movement restriction: breeding animals and semen · Birds: sanitation Prevention · Vaccination (cattle): 2 doses 2-4 weeks apart prior to breeding seasons · Repeated testing · Prevent reinfection: use only negative animals for breeding and insemination (both bull and cow) · Imported animals and semen: arrive with veterinary certificate declaring negative results · Birds: prevent contact between birds a) Sanitation measures and focal disinfection at this disease. Personal hygiene. Resistance Tritrichomonas foetus can survive the process of freezing semen (-79°C), as well as being viable in urine, slurry, semen and wet stool for 3-14 days. It is killed by drying or high temperatures. Trichomonas gallinae does not survive long outside the bird and transmission must occur rapidly. Disinfection - Equipment: NaOH (2%), peracetic acid (0,5%), chlorine compounds - Hands: septonex Personal hygiene Is very important, especially in zoonotic and highly contagious diseases. Rules: · Wash hands between animals, when leaving farm, before eating and smoking · Disinfect boots and equipment between farms to prevent spread of disease · Change overalls between farms Put stress on increased hygiene of the house and workplace concentrating on personal hygiene, disinfection of the environment and equipment Wearing appropriate protective clothes, boots, gloves, masks, glasses in animal housings Washing used clothes in hot water with soap (antibacterial and anti-fungal), after suspected exposure to disease agents Washing and cleansing/disinfection of footwear, is important to prevent spreading the infection Avoid sharing clothing, towels Washing hands after animal contact before eating, drinking, preparing food After being exposed to places where the potential of being infected is great, you should wash your hands with an antibacterial and anti-fungal soap Avoid touching pets as they are often carriers of contagious diseases Minimize contact with disease agents b) Sexual abuse of animals Bestiality is a word describing sex between a human and an animal. In most countries, bestiality is illegal under animal abuse laws or laws dealing with buggery or crimes against nature. The only EU countries where zoophilia remains legal are Finland, Hungary and Romania. In Norway it has been illegal since 2008, while in Sweden it is legal in circumstances where it doesn't cause harm to the animals. As of 2017, bestiality is illegal in 45 U.S. states. Laws surrounding bestiality and zoophilia Some jurisdictions list laws very clearly, such as UK, which specifically prohibits penetration of a human being by the penis of an animal, and penetration of an animal by a human's penis. By contrast, many countries and US states are less precise about the scope of law in that they outlaw sex with animals, without defining what constitutes "sex". Even if bestiality is not explicitly prohibited, there are often many other laws which can be used to effectively prosecute cases. For example, most countries have animal cruelty laws, and a prosecutor will argue that all zoophilia activity is animal abuse. Under the Sexual Offences Act 2003 (UK) Prohibits the deliberate or accidental but objectively reckless penetration of the penis anally or vaginally of or by a living animal. This also involve: - Oral stimulation of or by an animal - Acts involving dead animals - Manual stimulation for the purposes of animal husbandry Criminal Justice and Immigration Act 2008 (UK) This act bans an "extreme image". An extreme image is an image which falls within or is grossly offensive, disgusting or otherwise of an obscene character. An image falls within this subsection if it portraits, in an explicit and realistic way any of the following: - An act which threatens a persons life - An act which results or is likely to result in serious injury to a persons anus, breasts or genitals - An act which involves sexual interference with a human corpse - A person performing an act of intercourse or oral sex with an animal (whether dead or alive) - And a reasonable person looking at the image would think that any such person or animal was real A person commits an offence · If he intentionally performs an act of penetration with his penis into the vagina or anus of a living animal and he is aware of what is being penetrated · If they intentionally cause or allows the vagina or anus to be penetrated by the penis of a living animal and they are aware of what they?/he is being penetrated by Ethical arguments - Involves animal cruelty so must be prohibited to safeguard their welfare - Since animals cannot give their consent, bestiality must always be equivalent to rape