Bovine Week 4 VIN

Thromboembolic meningoencephalitis (TEME)

- Histophilus somnus = gram (-), opportunistic ( part of Bovine Respiratory disease complex & shipping fever) - HIGH FEVER; may see resp. .signs before CNS signs, myocardial infarcts - NEUTROPHILIC PLEOCYTOSIS on CSF tap, xanthochromic (evidence of prior hemorrhage) - vaccination and metaphylaxis important - DfDx for polioencephalomalacia

Peak lactation for cows

4-8 weeks post parturition

Hypocalcemia

AKA Milk Fever AKA Parturient Paresis Hx - periparturient cows - most common in high-producing dairy cows, cows on their 3+ lactation, Jersey cows, multiparous mature dairy or beef cows - Occurs w/in 72 h post-parturition - associated w/ rapid-onset milk production - weak cow that recently calved or is about to calve Clinical Stage 1 signs (mild) - ambulatory, weak, ataxic, or down w/ normal head posture - hypersensitive, excitable, restless, aggressive - fine muscle tremors, starting in flanks & triceps, ear twitching, head bobbing - bellowing Clinical stage 2 signs (moderate) - sternal recumbency - obtunded - cool extremities - low temperature - anorexic - tachycardia & decreased heart sounds w/ weak pulses - smooth muscle paralysis which can lead to bloat, failure to defecate, loss of anal sphincter tone, inability to urinate (distended bladder on rectal palpation) - neck in S-curve Clinical Stage 3 signs (severe) - comatose - opisthonus - muscles flaccid - tachycardia w/ no pulses Death can occur w/in hours if no intervention Dx: - hx & signs - total blood calcium (< 8 mg/dL) - ionized blood calcium (< 4.5 mg/dL) - rule out sepsis on any down cow who calved recently - check uterus (for possible dead twin) - check udder quarters/milk (for possible septic mastitis) - hyperglycemia can occur b/c low extracellular Ca inhibits insulin secretion Rx: - Calcium is cardiotoxic - IV Calcium given carefully - Auscult heart & palpate pulses during infusion - stop & wait if bradycardic, arrhythmic, pulse weakens or cow begins to pant - signs of improvement are decreased heart rate, strong pulses, eructation, able to rise, urination/defecation - re-treat if not standing w/in 4-8 hrs - float cow in a water tank if refractory - Correct lateral recumbency as cow may regurgitate & aspirate Prevention - low calcium diet during dry peeriod - use dietary cation difference (DCAD) during late-dry & early-milking period to decrease blood pH - Feed vitamin D3 late-dry - Administer PTH just before parturition - Avoid diets high in potassium & low in anionic ions prognosis - good to excellent if no concurrent disorder - 75% of cows stand up w/in 2h of tx & 30% of those relapse pearls: - also risk factor for uterine prolapse, retained fetal membranes, abomasal displacement - practice of completely milking them out to increase calcium reabsorption from mammary gland leads to mastitis & is no longer recommended

Selenium &/or Vitamin E deficiency

AKA White Muscle Disease (WMD) AKA Nutritional Myodegeneration hx: - horses, ruminants, pigs, poultry - animals fed poor quality hay (vit E deficiency) - soil-deficient in selenium Clinical Signs ● Cardiac Form - sudden onset; animal may be severely debilitated or found dead. Animals frequently die w/in 24 hours despite medical therapy. Lesions may be found in the heart, diaphragm &/or intercostal muscles. a. Depression. b. Respiratory distress. c. Nasal discharge (from pulmonary edema). d. Rapid and possibly irregular heartbeat. e. Weakness & recumbency. ● Skeletal Form - slower onset; more responsive to medical therapy. Common muscle groups affected include the biceps, semitendinosus, semimembranosus, gluteal muscles & neck musculature a. Muscular weakness &/or stiffness. b. Recumbency, may be unable to stand. c. If able to stand, muscle weakness & trembling, stiff gait d. +/- hard & painful muscles e. Respiratory difficulty/distress (involvement of the diaphragm). f. Dysphagia (muscle involvement of the tongue, pharyngeal & masticatory muscles). g. Lethargy. Diagnosis Clinicopathologic Findings ● Acute disease may demonstrate significant elevations in AST & CK along w/ hyperkalemia, hyponatremia &/or hypochloremia. ● +/- Myoglobinuria ● Decreased serum selenium concentrations; decreased glutathione peroxidase activity is a suitable means to evaluate selenium. ● Decreased whole blood selenium (can also be measured in liver samples) &/or decreased glutathione peroxidase activity. ● Decreased serum vitamin E concentrations. Gross Histologic Findings ● Grossly, affected muscles of the limbs, diaphragm, heart and tongue may appear gray to white (hence the name). Microscopically, bilaterally symmetric myodegeneration is consistently observed. Hyaline degeneration of myofibers may be observed; regeneration of myofibers may be observed in the recovery stages. Treatment ● Limit physical activity. ● Administer vitamin E & selenium. ● Anti-inflammatory medications & supportive care (nasogastric feeding, antibiotics, fluid therapy). Control - Ensure adequate vitamin E and selenium concentrations in deficient regions; - supplementation of pregnant animals if necessary. pathogenesis: - Body makes reactive oxygen species (free radicals) during normal metabolism such as hydrogen peroxide, superoxide radical, & hydroxyl ion that are normally counteracted by endogenous antioxidants. - Suboptimal concentrations of vitamin E &/or selenium impairs the animals' ability to control oxidative damage to cells, resulting in muscle damage. - Polyunsaturated fatty acids that are integral in cell membranes are predisposed to oxidative damage (lipid peroxidation). - Muscle cells are prone to damage because of their high metabolic activity. ● Vitamin E or selenium may be deficient in certain regions. a. Selenium is a cofactor for the enzyme glutathione peroxidase (reduces H2O2 to H2O). b. Vitamin E (also known as alpha tocopherol) is incorporated w/in cell membranes & is a lipid-soluble antioxidant. Vitamin E breaks the chain reaction of lipid peroxidation within the cell membrane. ● 2 main clinical manifestations of WMD are the cardiac form & skeletal form.

Vagal indigestion

Aka chronic indigestion syndrome signs: - "papple" abdominal distension of the left paralumbar fossa & ventral right abdominal wall - scant, dry feces - anorexia - weight loss - rectal palpation: rumen full of ingesta & ventral sac extends to right of midline (L-shaped) type 1 vagal indigestion = free gas bloat due to something affecting vagus nerve type 2 vagal indigestion = failure of omasal transport & appears as an enlarged fluid-filled rumen. Most often associated w/ chronic infection of the lungs dx: - really based off signs in field - essentially can go all the way to exploratory - most elect not to go this route unless really valuable cow. rx: - depends on cause (ie traumatic reticuloperitonitis, adhesions from abomasal ulcer, etc) - most elect to salvage to slaughter prognosis - depends on etiology but often poor to grave

Cutaneous Anthrax

Hx - humans enters through a break in the skin begins a papule, progresses to a vesicle, then ulcerates extensive edema around lesions may be seen A black eschar forms Cutaneous infections can rarely become systemic

Bovine Viral Diarrhea (BVD)

Subclinical Signs - many animals that have never been observed to be ill have antibody present Acute BVD signs - most common in cattle 6 to 24 months of age - after 5-7 days incubation, see fever, leukopenia, anorexia, oculonasal discharge, oral erosions, ulcers, & diarrhea - virus damages the epithelium of the mouth, esophagus, intestine & bronchi - immunosuppression & pneumonia from bacterial pathogens can occur Hemorrhagic syndrome signs - BVD virus-induced thrombocytopenia Reproductive Loss - Infertility & early embryonic death or abortion can occur at any stage of gestation & cows may show no other clinical signs - aborted fetus either normal or mummified - congenital defects are most common when infection occurs at 100 to 150 days gestation, & include hydrocephalus, cerebellar hypoplasia, hypomyelinogenesis, ocular defects, hypotrichosis, & brachygnathia - Persistent fetal infection occurs at 40-125 days if fetus is exposed to non-cytopathic (NCP) biotype -- in this form, the fetus is immunotolerant & if it survives that animal acts as a reservoir & consistently sheds virus -- These carriers are persistently infected & called PI animals. They are the main way BVD is maintained in the herd Mucosal Disease or Chronic BVD - occurs when a persistently infected animal is superinfected w/ a cytopathic (CP) biotype of BVDV or the non-cytopathic (NCP) biotype switches to the CP biotype - Mucosal dz is a peracute often fatal attack of BVD - Chronic BVD is eventually fatal Responsible for: - economic losses in cattle worldwide - loss of productivity - reproductive wastage - increased morbidity & mortality Dx: - Based on antigen detection -- fluorescent antibody, immunohistochemistry, or antigen capture ELISA can be utilized. -- Ear notches are often used for immunohistochemistry detection of carriers (PI) - PCR or serology can also be used DDX for clinical BVD: - MCF (typically has greater lymph node enlargement & bilateral corneal opacity, where as corneal opacity probably occurs in only 1% of BVD cases - Rinderpest - FMD - Vesicular stomatitis & bovine papular stomatitis (usually are associated w/ oral lesions but are not associated w/ diarrhea) Tx: - tx of acute BVD cases is generally aimed at preventing serious secondary infections such as Mannheimia hemolytica pneumonia & providing fluids & electrolytes Prevention/Control - Biosecurity, vaccination, & detection & elimination of carriers (PI animals) - Vaccination aimed at protecting young animals as maternal immunity wanes - Vaccination of cows is aimed at preventing PI calves & reproductive losses via fetal infection - Killed virus vaccines require two doses, whereas modified live virus vaccines only require one dose - Replacement heifers are vaccinated w/ modified live virus vaccines at 5-6 months of age - Cows are vaccinated prior to breeding season using modified live virus vaccine containing both type 1 & type 2 viruses - Pregnant cows can be safely vaccinated w/ killed vaccine; however fetal protection appears to be better when modified live virus vaccines are used Pearls: - Pestivirus in family Flaviviridae - RNA virus related to classical swine fever & border disease virus in sheep - BVD can reassort & change antigenically which aids in virus escaping immune mechanisms & thus remaining active. - can also cause fever, oral ulceration, diarrhea, & abortion in camelids Virus classification: - virus can be classified into type 1 & type 2 infections based on genotype - both types can exist as either Cytopathic (CP) or non-cytopathic (NCP) biotype - biotype does not indicate virulence, but only how the isolate behaves in tissue culture

Bovine Herpesvirus III

alcelaphine herpes virus (African malignant catarrhal fever)

Bovine Herpesvirus II

causes bovine ulcerative mammilitis

Bacillus anthracis (anthrax)

- Aerobic Gram Positive spore forming Rod Bacteria - spore is dehydrated w/ thick walls; can remain inactive for decades; aka endospore - spores germinate in animal host & grow rapidly in vegetative form, causing a fatal septicemia - spores are resistant to heat, drying, & many disinfectants Hx - typically infects herbivores; most frequently cattle, sheep, & goats - flooding event signs: - acute death - bloody discharge from orifices - absence of rigor mortis - rapid bloating - dark blood that does not clot - staggering - convulsions - high fever - extensive swelling - cardiac or respiratory distress - depression/stupor Dx: - If anthrax suspected, do not perform a necropsy - can be confirmed by submitting a blood, fluid, or tissue sample in red top tube in accordance w/ the procedures of the diagnostic lab (contact them first Rx: - Early antibiotic tx is essential - Ciprofloxacin, doxycycline, & penicillins are appropriate Abx - extended tx, usually 60 days, is indicated to completely eradicate the organism Prognosis: Control & Prevention - rapid detection, reporting & quarantine are key to prevention - vaccination is effective (given annually in endemic areas) - Post-exposure prophylaxis of asymptomatic animals helps control dz when seen in a herd - Suspect animals should be buried/burned w/out opening the carcass & w/out moving the animal which may spread the bacteria (opening the carcass will cause the more fragile vegetative bacteria to form resistant spores

Lactation length for cow

305 days 60 days dried off

Most desirable bulk tank milk somatic cell count in cows

< 200,000 cells/ml

Passive transfer in 3 day old calf protein refractometry value on serum

< 4.5 - failure of passive transfer 4.5-5.5 - unsure if failure of passive transfer >5.5 successful passive transfer

Brucella abortus (Brucellosis)

AKA Bang's dz gram-negative, coccobacillary, facultative intracellular bacterium hx: - mainly cattle but also found in bison, elk, feral pigs signs - abortion - 2nd half of gestation (~7 months) - +/- abortion storm - +/- endometritis (purulent vaginal discharge & decreased conception rates) Dx: - Titers will rise BUT some infected heifers may not have a titer until the abortion - screen w/ Brucella ring test (BRT) or brucellosis card (Rose Bengal) test tx: - no tx - for eradication, serologically identify infected animals, isolate & slaughter prevention: - vaccine RB51 does not cause antibody production & is used in calves; Strain 19 causes antibody production - PPE - Handle vaccines w/ care Transmission: - pregnant cows become infected by contact w/ aborted fluids & tissues from infected cows pearls: - REPORTABLE - ZOONOTIC (causes undulant fever in humans.. ingestion unpasteurized dairy product, exposure to brucella vaccine, infected animals, or in lab) - considered eradicated in US but some wildlife pockets exist & occasional transmission from Mexico - may cause poll evil & fistulous withers in horses

Clostridium perfringens Type B, C, & E

AKA Enterotoxemia Hx: - type c mainly cattle - calves, lambs, kids, piglets, or foals less than 7 days old - often associated w/ an increase in dietary intake allowing proper growth under certain conditions signs: - sudden onset, some calves may die w/out showing any - weakness - abdominal distention - bloody diarrhea - convulsions Dx: - extremely reddened secretions of fluid-filled small intestines; "purple gut" tx: - usually fatal once signs present - can attempt to tx w/ IV fluids + electrolytes & giving broad spectrum antibiotics & specific antitoxin Prevention: - herd vaccination - can administer antitoxin (antiserum) at birth or can vaccinate dam twice w/ bacterin/toxoid Transmission: - normal GI tract inhabitant that only causes disease under certain conditions

Clostridium perfringens type A

AKA Jejunal Hemorrhage Syndrome (JHS) AKA hemorrhagic bowel syndrome AKA Hemorrhagic enteritis in adult dairy cattle AKA yellow lamb dz - Intestinal clostridiosis in horses & others Hx: - cattle - lamb - horses Cow signs - dead acutely - normal to subnormal temperature - increased HR - enlarged abdomen (ileus) - small intestinal obstruction develop - if feces pass, dark & bloody (digested or clotted blood) Lamb signs - icterus - weakness - death occurs rapidly Cow dx: - abdominal US & finding increased SI diameter - hyperglycemia - hyponatremia - hypochloremia - hypokalemia - hypermagnesemia Lambs dx: - hemolysis - anemia - hemoglobinuria - icterus - fever - death occurs rapidly prevention: - it is not known whether repeated vaccination can prevent JHS - increasing the amount of long stem fiber in the diet has decreased the number of cases - No Cl perfringens type A vaccines are available in the USA prognosis: - low morbidity & high mortality

Clostridium perfringens type D

AKA Overeating Dz AKA pulpy kidney dz in sheep (rapid carcass decomposition which leads to pulpy kidneys on postmortem but not always) hx: - sheep & goats > cattle & young horses - < 2 yrs of age - high grain ration - fattening lambs on rich pasture - increase in dietary intake - associated w/ overeating signs: - decrease in appetite - weakness, incoordination - diarrhea - nervous signs, death - glucosuria common - "pulpy kidneys" due to rapidd postmortem decomposition prevention: - prevented by 2 doses of 7 way bacterin vaccine transmission: - normal GI tract inhabitant that only causes disease after excessive ingestion of feed or grain

Clostridium novyi Type B

AKA black disease AKA Infectious Necrotic Hepatitis Hx: - Primarily affects sheep, but occasionally cattle on a high grain ration. - damage to liver by the fluke Fasciola hepatica Signs: - Sheep are often found dead, with no evidence of clinical signs. - less common in cattle and clinical signs may be reluctance to move, lost appetite, and a dull and listless appearance. Dx - large areas of damaged, necrotic tissue in liver appear gray to black w/ a foul smell Tx: - no effective tx as dz often progresses rapidly Prevention: - prevented by 2 doses of 7-way bacterin vaccine Transmission - Endospores are ingested, and the bacteria lodge in the liver (similar to C. haemolyticum). - In sheep, the liver fluke, Fasciola hepatica, plays an important role in the disease in creating a desirable environment for the bacteria to grow. - Toxins released cause severe liver damage and result in red blood cell destruction.

Listeria monocytogenes (Listeriosis)

AKA circling dz hx: - silage-fed adult cow - indoors in winter - cattle, sheep, goats (possibly camelids), poultry, pet birds, humans, rare in horses signs: CNS - head tilt - circling - asymmetric sensory loss on face & weak jaw closure due to sensory, motor dysfunction of trigeminal nerve - purulent ophthalmitis, exposure keratitis - isolation from rest of herd - ocular & nasal discharge - food stuck in mouth, weak tongue, bloat - marked somnolence, tetraparesis, ataxia - poor to absent palpebral reflex - difficulty swallowing/poor gag reflex - obtunded, semicoma, death Hx: - ingesting silage stored at a pH >5 Dx: - clinical signs - CSF tap: shows mononuclear pleocytosis, increased protein - culture is difficult & usually unsuccessful DDX: PEM Rx: - Penicillin, sulfonamides, tetracyclines (avian, mammals) or ampicillin for 2-4 weeks - support: fluid therapy & dietary maintenance prognosis: - guarded to poor - poor if recumbent &/or can't swallow - 50% if standing & can swallow Prevent: - complete anaerobic rendering of silage Pearls - Zoonotic - most common encephalitis in dairy cows - no forebrain signs (seizures, aggression, blindness)

Clostridium septicum

AKA malignant edema Hx: - mainly sheep also cattle, goats, and horses of any age signs: - Localized swelling and edema that may gravitate to dependent portion of the wound - Depression, anorexia, high fever - Death often occurs within 24-48 hours Dx: - On postmortem, the infected area is darkened with a foul odor. There is swelling without gas accumulation. Tx: - Often fatal unless identified early and treated with penicillin Prevention: - vaccination with two doses of 7-way bacterin vaccine, clean surgery, and clean environment following a surgical procedure. Cause: - Clostridium chauvoei, septicum, novyi types A & B, sordellii & perfringens types C & D are also part of 7-way vaccine & cause malignant edema. - Bighead in sheep is a form of Malignant edema caused mainly by C. novyi type A . Transmission - Disease develops when an open wound is infected with bacteria. - May be introduced in deep wound from injury, castration, difficult parturition, fighting, etc.

Clostridium haemolyticum or Clostridium novyi Type D

Aka Redwater Disease AKA Bacillary Hemoglobinuria Hx: - cattle & sheep - endospores are ingested & bacteria lodge in the liver - damage to liver by the liver fluke Fasciola hepatica Signs: - Reddish discoloration of urine due to hemoglobinuria secondary to red blood cell lysis - Labored breathing - Anemia, icterus - Dehydration, fever Dx: - Extremely pale animal with red urine in the bladder and thin, watery blood. - Often a large necrotic area in the liver. due to germination of spores there & producing hemotoxin Tx: - Early treatment with antibiotics (penicillin or tetracycline) and antitoxin serum. Prevention - vaccination with two doses of bacterin with booster given every 6 months (Cl. novyi type D vaccine) - controlling liver flukes w/ controlling snails, fencing off wet areas, and fluke treatments Transmission: - Endospores are ingested and the bacteria lodge in the liver. - When damage occurs in the liver (often due to the liver fluke, Fasciola hepatica), the bacteria replicates. - The toxin released results in red blood cell lysis.

Clostridium botulinum

Aka botulism Hx: - uncommon in animals - rare in livestock, but outbreaks do occur - horses appear especially susceptible to type B toxin - foals susceptible to toxicoinfectious form where the toxin forms in the GI tract. Often called Shaker Foal Syndrome. - ingestion of preformed toxin in feed signs: - start w/ muscle tremors & fasciculations - then ascending paralysis - respiratory paralysis - death - mydriasis - ptosis - weak tongue Dx - detection of toxin in serum, intestine, or feed for confirming diagnosis & type - no specific postmortem signs tx: - no effective tx for most species. - in horses, botulism antitoxin has been used w/ varying success Prevention: - Type B vaccine available; requires 3 doses at 4-week intervals. Booster dose to mare 8 weeks before foaling - Colostrum will protect foal for 8 to 12 weeks. There is a type C vaccine approved for mink that has been used in livestock transmission: - Usually introduced through contaminated feed (dead cat or rabbit in silage or hay). where the organism has already produced high levels of toxin into the foodstuff. - wound botulism rare but can occur

Clostridium chauvoei

Black leg dz hx - mainly sheep almost always due to wound or at parturition - also cattle btwn 6 months & 2 years - after flooding where cattle ingest the soil bacteria become bacteremic then develop the clostridial myositis endogenously - damage/bruising to muscles from transport, injections, rough handling signs - sudden death w/out signs (w/in 12-48 hrs) - acute lameness - fever - depression - anorexia - +/- crepitation/crackling on palpation from gas bubbles - lack of wounds - profound depression - dark red to black muscle tissue dx: - presumptive dx based on gaseous swelling in young animal - on postmortem, the infected area is black & necrotic w/ gas bubbles w/ a foul, sweet odor (like rancid butter) tx: - often fatal unless identified early & treated w/ penicillin but survivors may have permanent deformity prevention - discard carcasses immediately w/out contaminating the environment - Vaccination (7-way bacterin vaccine: 2 doses at 1-month intervals that is often given as a "7-way" vaccine against clostridium chauvoei, septicum, novyi types A&B, sordellii & perfringens types C&D) prevention: - vaccinate all cattle w/ multivalent clostridial vaccine containing C. chauvoei in addition to prophylactically treating w/ penicillin up to 14 days transmission: - endospores are ingested then cross Gi tract into blood stream & become deposited throughout the body or enter through a wound - bacteria become activated & multiply in an anaerobic environment, particularly bruised or damaged muscle tissue - commonly occurring after transport, handling, injection, or other rough activity

The big 8 rule outs of vesicular diseases

Bluetongue Bovine papular stomatitis (BPS) Bovine Viral Diarrhea (BVD) Foot & Mouth Disease Infectious Bovine Rhinotracheitis (IBR) Malignant Catarrhal Fever (MCF) Rinderpest Vesicular Stomatitis Virus (VS)

Infectious Bovine Rhinotracheitis (IBR)

Cause: - Bovine Herpesvirus-1 w/ 3 subtypes called BHV-1.1 (respiratory), BHV-1.2 (respiratory & genital), & BHV type 5 (neurologic) 6 main forms of dz 1. Respiratory 2. Abortion 3. ocular 4. Infectious pustular vulvovaginitis 5. Generalized neonatal infection 6. Encephalitis Respiratory signs: - rhinotracheitis aka "Red Nose" (inflammation of muzzle & nostrils w/ nasal discharge +/- small white plaques in nares) - plays role in bovine respiratory disease complex - fever 104-107 - immunosuppression - decreased appetite - depression - rapid breathing - usually entire herd affected - tracheitis +/- nonproductive cough - death uncommon unless secondary bacterial pneumonia present Abortion signs: - abortion at ~5-6 months of gestation (mid term) - +/- abortion storms that may occur 100 days after last clinical case - animals can usually breed back - result of fetal death & fetus is typically partially decomposed - aborted calves may have white abomasal plaques - can induce abortion by giving modified live virus to pregnant animals or those in contact w/ pregnant animals - Dx: immunofluorescence on fetal cotyledons, fetal abomasum, & fetal lung Ocular signs: - may occur alone or in conjunction w/ respiratory form - severe conjunctivitis - pink eye - excessive clear ocular discharge w/ corneal opacity in some cases - may make surrounding haired areas look crusty - Ddx: moraxella bovis Infectious pustular vulvovaginitis signs: - Vulvar discharge - Drop in milk production - Red spots & pustules lining the vulva & vagina - Excessive tail twitching - Frequent urination - Persists for ~2-3 weeks - Males also get pustular lesions on the penis w/ exudate & inflammation (balanoposthitis) Generalized neonatal infection signs: - Respiratory tract, GI tract, liver, Kidneys, & adrenals involved - Usually fatal - can be caused by wild virus or live vaccines DDX: - vesicular stomatitis, F&MD Tx: - No effective tx - supportive care - antimicrobials to prevent secondary bacterial infections in respiratory form - Flunixin or other NSAID, shade, water & good feed Prevention: - Isolate new additions for 30 days prior to introduction to herd - Isolate infected animals immediately to prevent rapid spread - Vaccinate before outbreak but be careful vaccinate pre-breeding - vaccinate at 6 months Vaccination: - be careful which type of vaccine you use (killed vs live) to avoid abortion - Use either intranasal or IM live vaccines in feedlot aged & adult cattle - Do not use live vaccines in neonatal calves or pregnant animals Transmission: - Airborne - Contact - breeding - in utero - During birth passing through infected vagina Pearls: - one of the most common infections in cattle in the US - latent infection maintained in ganglia - rapidly spreads from those infected or recovered carriers to new arrivals - stress may result in recurrence of infection in those previously recovered

Bovine Herpes virus 1

Causes Infectious bovine rhinotracheitis ophthalmic lesions pearls - infects the trigeminal ganglia & becomes latent - when animal immunosuppressed, virus replicates & causes dz

5-8 months pregnant cow

Corpus luteum & placenta share the role of providing progesterone to keep pregnancy going so both dexamethasone & PGF2-alpha is needed to eliminate both sources of progesterone to induce abortion

Environmental Mastitis Pathogens Sources Control

Environmental Pathogens - Coliforms (most severe +/- death) - Streptococci uberis - Streptococci dysgalactiae other environmental pathogens: - Arcanobacterium pyogenes - Prototheca - Yeasts - Pseudomonas - Serratia - Nocardia - Mycobacterium - Pasteurella contagious/environmental pathogens: - Coagulase negative Staph (s. hyicus, epidermidis, etc) (most prevalent bacteria isolated from milk of cows & heifers) Sources: - bedding - fecal material - soil - contaminated water Control - Frequent manure removal - Using appropriate free stalls & managing the bedding - Providing pastured cows w/ clean locations to lie down -- sand is preferred -- avoid wood b/c predispose to Klebsiella mastitis - Pre-dipping teats & having clean dry udders at milking are important Dry cows are often infected so maintaining clean bedding areas for the herd must include the dry cows. Dry cow tx w/ intramammary antimicrobials & a teat sealant are also useful

Foot and Mouth Disease (FMD)

Hx - cattle, swine & sheep - NOT HORSES Signs: - vesicles on mouth, lips, coronary band, teats, & interdigital space that rupture & result in ulceration - painful - decrease productivity - high fever - drooling - lameness, foot stomping - weight loss - abortions: neonatal dz/death Dx: - 1st step Notify Regulatory officials (Area Vet in Charge & State Vet) - Get samples from vesicles & affected epithelium & use appropriate transport media & put in double leak-proof containners - approved labs perform initial testing, special reference labs confirm testing - Viral antigen (ELISA) - Nucleic Acids (PCR) DDX: - Bluetongue - bovine herpes 1 - Vesicular stomatitis - BVD - Malignant catarrhal fever - Bovine papular stomatitis - Infectious bovine rhinotracheitis - Orf - Swine vesicular Dz - Vesicular exanthema Prognosis: - good - survival of infected individuals - Poor - overall health of heard & economic outcome - guarded in neonates & nursing animals Tx - supportive care - euthanasia of all positive & in-contact animals & Burn or bury carcasses Prevention - maintain strict movement/entry requirements - Thorough disinfection ph <6/ >9 - Vaccination (killed, immunity only for 4-6 mo) - Quarantine - People can be temporary carriers (cannot leave for 3-5 days if exposed) REPORTABLE DZ - worldwide rare zoonotic transmission - contact: all secretions & excretions carry virus - Aerosol & wind carries - Recovered animals may be carriers for months to years Pearls: - Picornavirus - 7 serotypes - Reportable - not in US - one of the most contagious animal dzs known

Clostridium sordellii

Hx - mainly cattle predisposing factors: - unknown Signs: - sudden death syndrome

Pyelonephritis (cow)

Hx - post-partum cows signs - renal swelling - pain (grinding teeth, swishing tail, repeatedly up & down) - fever - loss of appetite - +/- blood & pus in urine rx: - procaine penicillin cause - bacteria enter via the urethra due to a post-partum uterine infection & vaginal damage at calving - most common organisms: Coliforms or corynebacterium renale

Clostridium tetani

Hx : - worldwide - affect most animals, horses & pigs most susceptible - puncture wound, castration sites, banding, & dehorning signs: - Extended "sawhorse" stance - Difficulty chewing food ("lock jaw") - Stiff tail, prolapsed third eyelid, flared nostrils - Severe muscle tremors/spasms - Sensitivity to noise and movement - general body stiffness Dx: - clinical signs - often no postmortem lesions are present Tx: - Tranquilization - Penicillin - Tetanus antitoxin - supportive care Prevention: - w/ vaccination - diligent cleaning of surgical instruments - placing animals in clean environment after surgical procedures Transmission: - Organism is found widespread in soil and is introduced through injuries such as puncture wounds, castration sites, banding, and dehorning. - Organism does not actively invade or create a larger wound - Incubation period of 10-21 days followed by production of a potent nervous system toxin.

Ketosis

Hx: - most common in lactating cows Signs: - nonspecific - depression - inappetance - weight loss - decreased milk production - decreased rumen motility - ketone breath Dx: - detection of ketones in urine (common & readily available for screening ruminants), blood, &/or milk - based on hx (recent parturition & heavy lactation) - decreased blood glucose - +/- elevated liver enzymes due to its central role in energy metabolism & gluconeogenesis Tx: - correct negative energy balance by increasing the available energy to the animal via IV & oral glucose - Correct any primary dz that may be contributing to anorexia or inappetance - IV glucose (usually marked improvement when given) - Oral propylene glycol (glucose precursor that supports gluconeogenesis) - Corticosteroids (ie Dexamethasone used to prolong hyperglycemia b/c of their gluconeogenic & appetite stimulating effects) - Insulin (adjunctive tx to IV glucose) - Force feeding (tube) - signs may spontaneously resolve w/out tx if an equilibrium btwn milk production & dietary intake is reached prevention: - Good feeding & husbandry strategies during late lactation & the dry period that aid in good body condition at calving Pathogenesis: - Central process in ketosis revolves around negative energy balance and inadequate feed intake. Fats are consequently mobilized to support energy production but, in some instances, the body is unable to utilize all these fats (and/or their metabolites) thus resulting in excess production of ketone bodies. - Ketosis occurs most commonly in lactating cows b/c the energy (glucose) necessary to support heavy milk production exceeds caloric & nutrient intake. Increased mammary uptake & utilization of glucose in high producing animals is not adequately offset by increased gluconeogenesis in the liver. The body attempts to increase energy production/precursors by mobilizing adipose stores in the form of free fatty acids (FFAs) to contribute to gluconeogenesis in the liver. - Ketosis AKA pregnancy toxemia in ewes & does; it occurs during the last 2-4 weeks of gestation when there is increased energy demands from rapidly growing fetuses (i.e. twins) combined w/ insufficient feed intake. - When liver is overwhelmed & unable to convert all the mobilized FFA glucose, excess amounts of ketone bodies remain in the blood. Ketosis is a disease that occurs when absorption & production of ketone bodies exceeds their use as energy resulting in elevated ketones in the blood, elevated fatty acids & decreased blood glucose. Other primary dz that may result in secondary ketosis: - displaced abomasum - metritis - peritonitis - mastitis Ketosis is characterized by elevated concentrations of ketone bodies - Acetoacetic acid - Acetone - B-hydroxybutyric acid Simplified Major Pathways of Energy Metabolism & Ketone Body Formation - Efficient oxidation of Acetyl CoA requires adequate amounts of oxaloacetate. Oxaloacetate is generated from precursors such as pyruvate (from glycolysis) and propionate (from rumen). During ketosis, supplies of oxaloacetate are reduced and are unable to keep up with the demand necessary to supply the citric acid cycle; therefore, the citric acid cycle slows down and the backlog of acetyl CoA is diverted into the formation of ketone bodies.

Clinical Mastitis

Inflammation of the mammary gland most frequently caused by bacteria or mycoplasma Clinical signs: - milk from affected quarter visibly abnormal - +/- gland appearing inflamed - reduced milk production - +/- systemic illness signs Detection of Clinical Mastitis: - W/ mild clinical mastitis, milk is abnormal in viscosity, color, or consistency (flakes, clots). Abnormal milk can be seen at each milking when milk is stripped onto the floor or onto a black surface called a strip plate - W/ moderate clinical mastitis the milk is similarly abnormal but gland is swollen, firm, red, & painful. Milk production is decreased. - W/ severe clinical mastitis, the changes in milk & gland described above are seen, & the cow is systemically ill - Milkers should routinely check every cow, & cows w/ clinical mastitis should be examined & treated promptly. Once infection is eliminated, SCC usually returns to normal w/in 2 weeks

Subclinical mastitis

Inflammation of the mammary gland most frequently caused by bacteria or mycoplasma Subclinical signs - most common form - reduced milk production - altered milk composition Detection of Subclinical Mastitis - Somatic Cell Count (SCC): A milk SCC of > 100,000 cells/ml is consistent w/ inflammation, but the threshold for determining the quarter is infected is at or near 200,000 cells/ml - California Mastitis Test (CMT): 2-3 ml of milk from each quarter is stripped into a paddle w/ 4 compartments. The CMT reagent is added to lyse the cells & cause gelling of the mixture. The degree of gelling is graded 0 to 3 & corresponds roughly to the number of cells present. 0 = <200,000 cells/ml - Electrical conductivity: W/ Mastitis, there is an increase in sodium & chloride & a decrease in potassium concentration in the milk, resulting in an increase in electrical conductivity. This can be measured automatically while the cow is being milked, resulting in early detection & tx

Mycobacterium avium paratuberculosis

Johne's disease in cattle (can also affect sheep, goats, deer, elk & exotic hoofstock) hx - infection usually when young as calves often incubating 2-3 years - clinical signs do not show up until stressed - primarily dairy cattle up to 20-50% of dairy herds signs: - granulomatous bowel - chronic wasting - chronic/intermitten watery diarrhea (esp bovine) - weight loss (due to hypoalbulinemia) (esp sheep/goats) - anemia of chronic dz Dx: - serology - clinical cases not hard to make dx but subclinical difficult - fecal culture (up to 16 weeks & low sensitivity) - Absorbed ELISA for antibody detection preferred test - DNA probe on feces (low sensitivity - new RT-PCR on feces excellent but costly - herd wide testing not useful Tx: - none - cull infected animals & offspring of infected animals prognosis: grave prevention: - test new animals before bringing into herd - vaccination calves <35 days to control as reduces fecal shedding by 90% but gives you positive TB test for 2 years & positive for Johne's antibody tests - all dairy cattle in US are TB tested &TB is more important - voluntary control program w/ 6 levels run by some states & USDA - cull cows test positive repeatedly - purchase from negative herd - feed calves colostrum only low risk cows &lowrisk milk or milk replacer - do not spread manure - do not share pastures w/ other herds Pearls - REPORTABLE in sheep & goats in all states & in cattle in some states - concern as a zoonosis that could be contributing to Crohn's Disease - hearty organism that survives long time in environment including soil & H20 - survives pasteurization - OIE listed - iceberg effect (for every 1 clinical case, there are many subclinical) transmission - largely vertical but also horizontal (in utero, colostrum, milk, feces) - #1 mode transmission is fecal-oral - "silent" shedders #1 mode

Bovine Leukosis

Lentivirus bovine lymphosarcoma

Leptospirosis bovine

Leptospira pomona Signs: - Young ruminants: fever, icterus - Adult ruminants: abortion prevention: - PPE face protection - Avoid contaminated environments Pearls: - spirochete bacteria - serovars are adapted to one or more mammalian maintenance hosts; host-adapted species do not tend to cause clinical signs in their maintenance host as they do in other species - shed in urine of infected animals - Worldwide

Contagious Mastitis pathogens detection control

Major contagious pathogens: - Streptococcus agalactiae - Staphylococcus aureus Minor contagious pathogen: - Corynebacterium bovis extra contagious pathogen: - Mycoplasma sp. are carried in sites other than the mammary gland, but once they gani access they become highly contagious contagious/environmental pathogens: - Coagulase negative Staph (s. hyicus, epidermidis, etc) (most prevalent bacteria isolated from milk of cows & heifers) Detection: - bacteria are detected by culture of milk samples Control: - Routine use of POST-MILKING teat dipping w/ a germicidal solution, usually iodine-based, helps prevent new infections - Treating all dry cows w/ an intramammary antimicrobial product effectively controls existing infections w/ S. agalactiae & C. bovis - Staphylococcus aureus & Mycoplasma are more difficult to eradicate, & animals infected w/ these pathogens are often culled. In some cases, cows w/ Staphylococcus aureus infection are treated & recultured, & then cases still positive are culled - Milkers wear rubber gloves - Backflush system on the milking cluster - Heifers can be milked before cows to prevent heifers from becoming infected - Sometimes, S. aureus-positive cows can be segregated into a separate string & milked last

What zoonosis are you most concerned about from drinking raw unpasteurized cow's milk?

Mycobacterium bovis

Period that requires the greatest nutritional demand w/ calving:

Period 1: calving to breeding (~70-90 days in length) - cow recovering from parturition - producing large quantities of milk

Period that requires the least nutritional demand w/ calving:

Period 3: weaning to 50 days prior to calving (~100 days) - cow no longer lactating - fetal growth relatively slow

Polioencephalomalacia (PEM)

Predisposing Factors ● High concentrate diets (pastured animals can also develop disease) ● Feed with corn or sugar cane byproducts ● High grain intake may promote proliferation of thiaminase producing bacteria ● Rations with added sulfate to limit intake ● Ingestion of plant thiaminases or thiamine analogs Clinical Signs ● Depending on the nature of the underlying cause, this can appear as isolated disease or herd problem. Acute Form ● Blindness ● Seizures ● Recumbency Subacute Form ● Initial signs a. Decreased appetite b. Twitching (ears & face) c. Separation from herd d. Hold head up in an elevated position e. Staggering, hypermetric gait ● Later signs a. Cortical blindness i. Absent menace, intact palpebral reflex & pupillary light response b. Dorsomedial strabismus c. Head pressing d. Teeth grinding e. Opisthotonus DDX: - listeriosis, nervous coccidiosis, salt toxicity, meningoencephalitis, rabies, vitamin A deficiency, pregnancy toxemia (sheep). Diagnosis ● challenging. a. Clinical presentation is useful to help differentiate PEM from many DDX ● Pre-mortem diagnostic testing can be unreliable & not available in many laboratories. a. i.e. Blood thiamine levels, transketolase activity to assess thiamine. ● Post-mortem findings. a. Gyral flattening, brain swelling. b. Brain tissue may fluoresce under UV light. c. Cerebrocortical neuronal necrosis. d. Cortical spongiosis. e. Cavitation of cortical tissue. f. Multifocal vascular necrosis, hemorrhage, & necrosis in deep gray matter. Treatment ● Early treatment critical. ● Treat w/ thiamine, regardless of cause. a. 10-20mg/kg IM or SC TID. b. Expect to see improvement w/in 1-3 days. ● If cerebral edema is suspected, can administer 1-2 mg/kg of dexamethasone. ● Supportive care. ● Animals w/ advanced disease may continue to show neurologic impairment after treatment. Prevention ● Thiamine supplementation in feed for prevention of disease in other animals, supply roughage, & investigate environment for sources of thiaminases or excessive sulfur levels.

Mycoplasma bovis

Signs: - minor bacti in cattle enzootic pneumonia (part of Bovine Respiratory Dz complex) -- thin, weaned calf w/ good appetite -- tachypnea, soft cough, sepsis -- lung auscultation: crackles & wheezes, harsh sounds no cranioventral sounds - mastitis (responsible for mycoplasma mastitis in cattle) (eventually causes fibrosis of the glandular tissue) - polyarthritis - bronchopneumonia - otitis media/interna DX: - culture DDX: pasteurella multocida type A or mannheimia haemolytica Rx: - Tulathromycin (or tetracyclines or tilmicosin) - Anti-inflammatories transmission: - highly contagious - large numbers shed in milk -cultured from respiratory & repro tracts of cattle - multifactorial - stress +/- viral infection

Actinobacillus lingnieresii

WOODEN TONGUE signs - lethargy - ptyalism - protruding tongue Dx: - Needle aspirate & gram stain (GRAM NEGATIVE) - Radiograph jaw - manual pharyngeal explore unless any neuro signs (don't want rabies) - cranial abdominal ultrasound or radiography Rx: - IV sodium iodide Sodium iodide IV as a 10-20% solution, repeat after 7 -10 day interval - +/- penicillin prognosis - excellent pearls: - wooden tongue = soft tissue getting harder - can be herd problem - can be part of normal oral flora but infect through a wound or trauma caused by sticks, straw, or barley awns

Epizootic Bovine Abortion (EBA)

aka foot hill abortion hx: - only seen in foothill regions of California, Oregon, & Nevada (WEST USA) - seen in cows (mostly heifers) signs: - last trimester abortion storms in heifers or cows new to area - up to 60% - ~60-120 days after naive pregnant heifers are moved onto contaminated pastures - fetus often has petechiae & lymphadenopathy - cows may give birth to weakened or dead calves transmitted: ground-dwelling soft tick or argasid tick (Ornithodoros coriaceus) prevention: - raise heifers in foothills & put pregnant heifers in the hills only when 6 months or more pregnant so they calve before fetal lesions occur cause: novel deltaproteobacterium (Pajaroellobacter abortibovis) pearls: - affected cattle are usually resistant to future foothill abortions - will NOT occur if pregnant cows are moved to pasture at greater than 120 days of gestation

Bovine Respiratory Syncytial Virus (BRSV)

associated w/ Bovine Respiratory Disease Complex hx: - younger calves - acute signs - pneumonia Rx: - antimicrobial drugs for secondary infection - NSAIDS - corticosteroids if pulmonary edema severe Prevention: - vaccinate all calves against BRSV - until calves build up immunity, new animals should be raised apart from & isolated from current group of calves where the virus is circulating

You are performing a routine pregnancy examination via rectal palpation on an Angus beef cow and note that placentomes of variable size, some as big as a half-dollar coin are present and also note bilateral uterine artery fremitus. At what point in gestation is the fetus?

at least 6 months. Placentomes (cotyledons on the placenta / caruncules on the uterus) will be palpable starting between 75-90 days of gestation and at 150 days can reach the size of a half-dollar coin. Three or more placentomes must be palpated to rule out that you are not palpating an ovary. Uterine artery fremitus which is hypertrophy of the middle uterine artery with fluid turbulence that gives a "buzz" feeling to the artery will be evident on the ipsilateral pregnant horn at about 120 days of gestation. From 6-7 months on, the fremitus can be felt bilaterally. Fremitus is not a positive sign of pregnancy, but can be useful in staging

Proper anatomical location for performing a lumbosacral CSF tap in cattle

between the dorsal spinous process of L6 cranially & S1 caudally & the tuber sacrales laterally

Bovine Spongiform Encephalopathy (BSE)

causative agent: - prions (abnormal protein) - extremely resistant to heat & normal sterilization procedures Hx: - ate contaminated feed w/ ingredients from rendered infected cattle (ie bone meal) - young animals most susceptible signs: - onset over several months - Hyperesthesia (mad cow); exaggerated reflexes) - fine tremors - persistent licking of muzzle - nervousness - aggression - incoordination - abnormal posture - difficulty rising - progressive ataxia - weight loss Dx - characteristic histological lesions in brain of bilaterally symmetric intracytoplasmic vacuolation of neurons. Can confirm w/ immunohistochemistry for prion protein fibrils Tx: - no effective tx - Report cases & cull animals Pearls: - REPORTABLE Creutzfeldt-Jakob Dz - chronic & fatal neurodegenerative disease of humans - 1996 new variant (vCJD) was discovered in UK & experimental & epidemiologic studies have linked these cases to consumption of food containing BSE infected cattle. - led to a ban on the use of non-ambulatory cattle in the human food chain & additional controls to inspect slaughtered cattle & forbid the use of mechanically separated meat in human food.

Inhalation anthrax

from breathing in anthrax severe respiratory z w/ near 100% mortality Flu-like syptoms progressing to massive bacteremia & shock Abx will kill the organism but not the bacillus exotoxins & death w/in 2-3 days in common

Salmonella typhimurium (cows)

gram negative rods hx: - most susceptible is fresh cow group signs - severe acute diarrhea, foul smelling (serum proteins in feces) - fever - decreased appetite - decreased milk - decreased rumen activity - scleral injection (enlarged & dark scleral vessels) - endotoxemia (neutropenia or neutrophilia) - increased plasma fibrinogen - death pearls: - zoonotic - transmission to humans: fecal oral

Vesicular stomatitis/vesicular dz

hx: - affects bovine, horses, camelids, occasionally swine - adults > 1 y/o - western hemisphere only - warm humid areas - seasonal occurrence signs: - vesicles, ulcers, lesions on mouth, lips, teats, udder, coronary bands, sheath, belly - fever - salivation, drooling - difficulty eating - lameness - secondary infection (mastitis) - hyperemic (skin) or raised blanched areas (oral) DDX: - cannot be distinguished from Foot & mouth dz (FMD), Swine vesicular disease (SVD), & Vesicular exanthema of swine (VE) by clinical signs alone - Papular stomatitis, foot rot, Orf, Trauma Dx: - Identify viral antigen or antibody - ELISA most commonly used Rx: - symptomatic care - soft feed, bedding - antibiotics for secondary infections - analgesics as needed Prognosis: - Excellent, mortality rare - economic loss significant Prevention: - Quarantine farm - Isolate affected animals - Sanitation - Insect control - Vaccines Transmission - insects: sand/black flies, mosquitoes - direct contact: saliva epithelium, exudates, fomites REPORTABLE - contact State Vet ASAP do not perform dx ZOONOTIC - humans in close contact get flu like symptoms +/- vesicles around mouth/nose Pearls - virus family Rhabdoviridae (same as rabies) genus Vesiculovirus - 2 Serotypes: New Jersey (NJ) & Indiana (IND)

Giardia duodenalis (G. intestinalis or G. lamblia)

hx: - calves 2-10 day old calf signs: - pasty, fatty, mucoid diarrhea - lethargy, depression, hypothermia, sepsis Dx: - Fecal floatation with direct smear &/or immunoassays Rx: - if calf over 5-7% dehydrated & very sick use IVF - determine type based on pH status/base deficit (usually sodium bicarbonate w/ dextrose) - If calf less than 5-7% dehydrated use enteral fluids - electrolyte replacer & milk - +/- antimicrobials & antiinflammatories prevention - good calf management - clean calving areas & hutches - provide good quality colostrum (1 gallon colostrum per 100 lb calf in first feed Pearls - protozoan intestinal parasite - Genus divided into 7 genetic assemblages: A & B are zoonotic, other most host specific - Humans most important reservoir host - human signs: diarrhea, flatulence, greasy stool that floats, nausea, abdominal cramps, dehydration - human to human transmission is more important than zoonotic transmission - unlike in animals, in humans it is a nationally notifiable dz transmission: fecal-oral (ingestion of cyst), fomite, drinking untreated water, contaminated food pearls: - protozoan intestinal parasite - causes enteritis which can be associated w/ intussusception

tetanus

hx: - cows w/ recent uterine infection (metritis) - surgical castration - hoof wounds (uncommon) signs - spastic paralysis pearls - tetanus toxin moves retrograde up the peripheral neuron into the spinal cord, where it prevents release of inhibitory neurotransmitters such as GABA (causes spastic paralysis)

Nitrate poisoning (bovine)

hx: - grazing sudan grass, Pigweed (Amarannthus), Nightshades (Solanum), Oat hay, Sorghum, Rye, Alfalfa - water contaminated - primarily a problem in ruminants (esp cattle) due to reduction to nitrite by microbes in the rumen signs: - methemoglobinemia (chocolate colored blood) - O2 carrying capacity & delivery reduced - "muddy" mucous membranes - dyspnea - tremors - convulsions - ataxia - tachycardia - death Tx: - Methylene blue IV 1%-4% solution w/ total dose of 4-15 mg/kg (to reduce methemoglobin) pathophys: - nitrate converted in rumen to nitrite & absorbed into blood causing oxidation of heme iron to the 3+ ferric state (methemoglobin) causing methemoglobinemia, leading to dark brown or "chocolate colored" blood, which has diminished oxygen carrying capacity - methylene blue restores the iron in hemoglobin to its normal (reduced) oxygen-carrying state. This is achieved by providing an artificial electron acceptor for NADPH methemoglobin reductase. The NADPH is generated via the hexose monophosphate shunt.

Winter dysentery

hx: - winter - housed cattle - 10-90% adult cows affected signs: - diarrhea - +/- fever tx - no tx, dz runs its course in weeks & herd becomes immune & recovers but milk production might not be the same pearls - coronavirus - lesions involve the colon

Uroabdomen electrolyte abnormalities

hyponatremia hypochloremia hyperphosphatemia azotemia +/- hyperkalemia

3 most common causes of colic

intussusception, cedal dilation w/ or w/out torsion, & abomasal volvulus

Right Displaced Abomasum (RDA)

ping is heard lower on the right and in front of the last rib

Spondylosis

refers to degenerative intervertebral joint space disease hx: - middle-age & older bulls (as well as sheep, horses, etc)

Interdigital necrobacillosis or infectious footrot

signs - interdigital lesions - lameness Tx: Florfenicol SQ one dose

Lead toxicosis (cattle)

signs - neuro signs - INTACT PLR Acute signs: (esp young cows) - ataxia, blindness, eyelid twitching - salivation - jaw chomping, bruxism - muscle tremors, convulsions Subacute signs (eesp sheep, older cows) - anorexia, rumen stasis, colic - constipation, then diarrhea - blindness, head pressing, hyperesthesia, incoordination - bruxism Chronic signs - Dysphagia - Aspiration pneumonia Dx: - blood lead concentration > 0.05-0.1 ppm - CBC anemia, anisocytosis, poikilocytosis, polychromasia, basophilic stippling, metarubricytosis, hypochromia tx: - do not give Sodium EDTA as it binds up all the Ca & produces a hypocalcemia - can give Ca EDTA (disodium edetate) - Thiamine Pathophys: - capillary damage/edema - irriation - immune suppression - nephrotoxic - toxic to hematopoietic system - teratogenic

cecal displacement or torsion

signs - ping heard from last rib to the pelvis high up - rectal exam distended structure palpated just cranial to pelvis that feels like loaf of bread

intussusception

signs - scant dark blackberry jam-colored feces on rectal exam - +/- palpable hard & painful mass on right

Actinomyces bovis

signs: - LUMPY JAW - gradual onset of hard, non-moveable masses on facial bones (rarely draining) - weight loss - quidding (dropping feed while chewing) Dx: - Needle aspirate & gram stain (gram positive rods) - Radiograph jaw - Manual pharyngeal exploration unless any neuro signs (don't get rabies) - cranial abdominal ultrasound or radiography Rx: - IV sodium iodide - Sometimes cull b/c of prognosis prognosis - Fair but bony deformation likely to remain prevention - remove scabrous or prickly feed Pearls - normal inhabitant of cow's oral cavity or rumen - causes dz when able to invade into damaged mucosa - Lumpy jaw = hard tissues getting softer - can be herd problem

Hypomagnesemia

tetany or grass tetany hx - cold or cool weather in pastured beef or dairy cows - lush pastures that are high in K & N & low in Mg & Na - adult, recently fresh, multiparous cow - lactating cows - also lactating ewes Signs - neuro signs - recumbency, hyperesthesia - stiffness, hypertonicity, sudden death Dx: - serum Mg < 1.5 mg/dl DDX: - PEM, Lead poisoning, Vit A deficiency, Water toxicity, BSE Rx: - give Mg & calcium slowly IV after sedation w/ diazepam (otherwise Rx may cause fatal seizure prevention: - in sheep can give daily magnesium oxide during risk period prognosis: - guarded to poor pearls - can be caused by cantharidin poisoning (ingestion of Blister beetles aka Epicauta spp) - sheep clinical signs are rare until concurrent hypocalcemia

GI anthrax

usually from consumption of contaminated meat Oropharyngeal z begins w/ a severe sore throat &/or ulcerations w/ neck swelling GI dz may cause anorexia, vomiting, abdominal pain, hemorrhagic diarrhea May become systemic & fatal