Some infectious

principles of immunostimulatory therapy?

1° goal: to induce production of both type I IFN (IFN-α, IFN-β) & type II IFN (IFN-γ)

subtypes of FeLV

3 main subtypes- FeLV A (receptor- FeTHTR1- thaimine transporter protein), FeLV B (receptor- FePit1 or FePit2, inorganic phosphate transporter protein), FeLV C (receptor- FLVCR heme transporter protein) All FeLV B and C cats coinfected with FeLV A and only FeLV A transmitted between animals FeLV B and C are more pathogenic - FeLV B arises from recombination of FelV A proviral DNA with endogenous FeLV sequences present in host cellular DNA; FeLV C arises from accumulations of mutations or insertions into env gene of FeLV A

hyalomma tick bite necrosis?

cytotoxin producedd in salivary gland of tick in Africa

bartonella treatment?

macrolides, aminoglycosides if have endocarditis amox+baytril will decrease titers over time, doxycycline needs to be used long term to clear

what can cause vaccine failure?

maternal antibodies are most common cause of vaccine failure

FeLV and immunodeficiency?

may occur from viral envelope peptide (p15e) that inhibits T cell and B cell function, inhibits cytotoxic lymphocyte responses, alters monocyte morphology and distribution, has been associated with impaired cytokine production and responsiveness Affected cats may develop lymphopenia, atrophy of thymus, depletion of lymphocytes within lymph node paracortical zones Impaired neutrophil function, kittens have impaired T cell function (less impaired B cell function)

feline pancreatitis dx?

#1 lethargy and anorexia, less common: weight loss, vomiting, labored breathing, PU/PD CBC: usually normal, can see neutrophilia, nonregenerative anemia, leukopenia Chem: hypercholesterolemia, hyperbilirubinemia, elevated liver enzymes, hypokalemia, hypoalbuminemia. * hypoglycemia and ionized hypocalcemia seen with necrotizing pancreatitis dx: increased PLI (mod sensitivty and spec), AUS- mod sensitivity with variable spec

confirm diagnosis of toxo?

1) Serologic evidence of recent or active infection consisting of high IgM titers (1:64) OR Fourfold or greater, increasing or decreasing, IgG or other antibody titers(after treatment or recovery) 2) clinical signs+Exclusion of other causes of the clinical syndrome 3) Beneficial clinical response to an anti-toxoplasma drug bc dont clear organism- most animals are seropositive for life, recurrence can also occur T. gondii-specific IgA, IgG, and organism DNA can be detected in aqueous humor and CSF of both normal and clinically ill cats, T. gondii-specific IgM has only been detected in the aqueous humor or CSF of clinically ill cats and so may be the best indicator of clinical disease. Because T. gondii DNA can be detected in blood of healthy cats, positive PCR results do not correlate to clinical disease

classification of IBD

1. Type of inflam: lymphoplasmacytic (#1), eosinophilic, rarely granulomatous or neutrophilic 2. Resp to tx: food-responsive diarrhea, antibiotic-responsive diarrhea, steroid-responsive diarrhea 3. Breed specific: Basenjis - immunoproliferative enteropathy; Wheaten terriers - PLE, PLN; Norwegian lundehunds - IBD; Boxers - granulomatous colitis

what percent of pericardial effusion in cats is associated with FIP?

10% FIP may be responsible for over half of neurologic cats in one study due to infectious/inflammatory disease

clinical signs of lyme disease

70-90% seropositive but only 5-10% show cliicals signs; clinical disease within 2-5 months of infection - fever, inappetence, lymph nodes, shifting leg lameness lyme arthritis or lyme nephritis (labs, goldens) are main clinical manifestations, myocarditis and arrhythmias also have been reported

canine cryptococcus?

<4yo, american cockers, labs, great danes, dobies CNS (50-80%- vestib, depression, CN V, VII, VIII deficits, sz, paresis, blindness, hypermetria, cervical pain), upper resp, (nasal cavity- 50%, frontal sinus also) ocular, cutaneous (15%- ulcerative draining lesions- head, nailbeds, feet, mm)

Canine anaplasmosis

A. phagocytophilum Ixodes ticks -vectors, small rodents (white footed mouse)- reservoir in nature, acute disaese in fall months when Ixodes active most Fever, lethargy, reluctance to move laboratory - lymphopenia, thrombocytopenia, increased ALP and amylase, hypoalbuminemia dx: PCR, ELISA (4Dx SNAP- doesnt speciate, very sen and spec), titers ELISA and IFA tests using E canis will not detect cross reacting antibodies in dogs with anaplasmosis likely tx: doxy

ddx for vector/non vector causes of polyarthropathy in dogs?

A. phagocytophilum, Bartonella, Borrelial borgdorferi, Mycoplasma spp, RMSF (R. rickettsia), E. canis, E. ewingii

canine cyclic thrombocytopenia

A. platys ixodes is the vector A. platys causes cyclic bacteremia, accompanied by thrombocytopenia, at approximately 10 to 14 day intervals (nadir 20-50k plts, plts are hypofunctional) mild normocytic, normochromic, nonregenerative anemia, leukopenia, hypoalbuminemia, and hyperglobulinemia Sera from A. platys-infected dogs does not cross-react serologically with E. canis, A. phagocytophilum, or N. risticii antigens tx: doxy

diagnosis and treatment of coccidiomycosis?

AGID: detects IgM antibody against the tube precipitin(TP) antigen of Coccidioides spp. And IgG against the complement fixing (CF) antigen Other serology: ELISA (IgM, IgG), Latex agglutination (IgG) All have low sensitivity for disease Most definitive is cytology/histopathology rads- peribronchiolar and interstitial nodular lesions are associated with hilar lymphadenopathy Skeletal lesions: productive lesions are more common than lytic lesions treatment- azoles effective (fluconazole, itraconazole, ketoconazole), amphotericin very effective for progressive disease

what cats are more susceptible for FIP?

Abyssinians, Australian mists, Bengals, birmans, Burmese, British shorthairs, Himalayans, ragdolls, rexes, scottish folds Siblings of cats with FIP may be more at risk

E. ewingii infection?

Acute infections only Replicates in neutrophils and delays neutrophil apoptosis- morulae in synovial fluid, CSF, blood smear Lethargy, fever, joint pain, neuro signs, muscular stiffness, stilted gait, reluctance to rise, kyphosis, joint swelling (polyarthropathy and meningoencephalitis common) anemia, thrombocytopenia, neutropenia, lymphocytosis, monocytosis, eosinophilia

cryptococcus diagnosis

Ag by latex agglutination- serum, CSF, urine- can use to monitor treatment bc correltaes with extent of dz CSF- organisms in 90% of canine CSCF samples; mononuclear and neutrophilic pleocytosis, increased protein cytology- organisms in 75% of cases; may need special stains

age related resistance phenomena with FeLV?

Age related resistance phenomena with FeLV, younger cats get infected and die, older cats that get exposed may not have infection 60-70% of kittens <6mo will get FeLV if exposed compared to 5% infected during same 5 month period, over 2 year period only 40-50% develop FeLV Infection can occur after exposure in adult if immunocompromised or high viral load Outcome variable- strain involved, challenge dose, host immune function (age, genetics, coinfections, stress, treatment with immunosuppressants) kittens infected in utero usually dont survive more than 2 weeks, failure to thrive, thymic atrophy

coccidia treatments?

Amprolium Amprolium/Sulfadimethoxine Diclazuril Furazolidone Ponazuril Quinacrine Sulfadimethoxine Sulfadimethoxine/Ormetoprim Toltrazuril Trimethoprim/Sulfonamide

What tick borne disease has been associated with elevations in ALP?

Anaplasma phagocytophillum Clinical signs: Nonspecific: fever, lethargy, anorexia Polyarthritis (more common with E. ewengii) Musculoskeletal pain Splenomegaly, hepatomegaly, CNS signs Rare GI and respiratory signs Lymphadenopathy Diagnosis: Blood cytology: insensitive Serology: anaplasma platys cross reactivity; not with E. canis, E. ewengii

morulae in neutrophils/eos (granulocytes)?

Anaplasma phagocytophilum: (Ixodes spp) Erhlichia ewingii: Amblyomma americanum, central, southern, and SE US

FeLV and diagnostic testing continued?

Antigen tests- ELISA, detects soluble p27 capsid protein antigen in blood, presence of circulating antigen typically presents viremia, sensitivity ranged from 92-96.8% and spec 95.4-99.2%- screening test (positive plus clinical signs, then likely progressive infection) Confirmatory testing due to false positive possible in healthy cats- use a different ELISA from different manufacturer, IFA on peripheral blood smears or bone marrow - positive IFA on blood have infection in bone marrow and less sensitive than ELISA so dont screen with this one Retest with ELISA 6 months later and if still positive then progressive infection likely False negative within first month of exposure, before antigen detectable in peripheral blood, retested in 1-2 months PCR assays developed-and must be careful not to detect endogenous FeLV genes May detect RNA or propviral DNA (detects RNA- active infection), proviral DNA- nonproductive viral infection) positive proviral but negative antigen- regressive disease

ticks and babesia?

B. canis rossi (high path strain)- haemaphysalis B. canis canis (moderate path stain)- dermacenter reticulatus B canis vogeli- least pathogenic - rhipicephalus B. gibsonii- rhipicephalus

types of babesia in US?

Babesia gibsoni (small, pleomorphism, and lack of paired piroplasms in the canine red blood cell, associated with american pit bull terriers) Babesia canis vogeli (large, paired intraerythrocytic piroplasm, associated with greyhounds) Babesia conradae (looks like B. gibsoni, only in dogs in California) North Carolina Babesia species

treatment for canine infectious respiratory disease complex

Bordetella - may have cough for 10-30 days Antibiotics if evidence of bacterial infection: mucopurulent discharge, fever, lethargy, decreased appetite, xrays, OR puppies < 6-8 weeks Good blood bronchus penetration: fluoroquinolone and clindamycin Prevention: vaccinations! Only CDV can prevent infection/shedding, others just lessen severity of disease; Shedding of bordetella, mycoplasma and CDV can last 2 months, keep affected dogs isolated; One study showed intranasal vaccines were more affective than parental antigen extract vaccines intranasal vaccine given parenterally can lead to severe injection site reactions, hepatic necrosis and death

primary bacterial pneumonia agents?

Bordetella, Mycoplasma, S. equi, S. canis, Yersinia pestis (primarily cats in Western US) Secondary bacterial

what virus is associated with staggering disease in cat?

Bornavirus, enveloped -ssRNA virus characterized by "staggering gait", depression, progressive ataxia, paresis, anorexia, increased salivation, behavior changes, hyperesthesia, impaired vision, and seizures, and high fatality Shrews- Crocidura leucodon- infectious virus and viral RNA can be demonstrated in saliva, urine, skin, tears and faeces; forested areas - ticks potentially Infection starts in the olfactory nerve cells and then spreads to the CNS, leads to LP inflammation and neuronal degeneration; strong T-cell response believed to be responsible for the development of clinical signs, other factors may also be important Dx: RT-PCR in pooled samples of blood, CSF and body secretions (urine, conjunctival, or rectal swabs); most reliable diagnosis is path/histopath with clinical signs seroprevalence in cats with neurological diseases in different countries 0-67%, healthy cats, seroprevalence - 2-40+% may be in the united states in cats because horses have gotten

Aspergillus fumigatus

Branching fungal hyphae Not yeast! Inhalation Hematogenous Worldwide Immunosuppressed, GERMAN SHEPHERDS (2-8 yo), cats <2yo with other disease, Disseminated disease, IgA deficiency can be implicated Cytology, serum and urine antigen - fungal hyphae observed on cytologic examination of urine sediment, serum, synovial fluid, lymph node centesis, bone biopsy, or intervertebral disc aspiration. confirmed by culture on Sabouraud's dextrose agar Azoles, amphotericin B GRAVE if disseminated, if in nose (GSD, rotties most common, can be primary or secondary-FB, neoplasia; mesaticephalic and dolichocephalic breeds)- clotrimazole/enilconazole infusion, usually once is curative but may need multiple treatments and can get reinfected, can consider systemic antifungals as well- terbinofine

infectious causes of stillbirth/abortion?

Brucella in dogs (zoonotic) Coxiella burnetti in cats (Q fever, zoonotic) Toxoplasma or Neospora Exposure to herpesvirus during parturition can lead to neonatal death (fading puppies/kittens) FeLV in utero transmission

Hepatitis

CAV-1 (Dogs) Direct contact with urine, saliva, feces --> oral-nasal, fomites Worldwide distribution Infection tonsils/peyers patches --> viremia --> infection in hepatocytes/endothelial cells (liver, kidney, eye) --> cell lysis Peracute (coma, shock, death) - acute (fever, hemorrhage, icterus, vomiting, etc) - subacute/chronic (immune complexes kidney/eye --> blue eye, glomerulonephritis) Dx- Clinical suspicion, histopath (intranuclear inclusions), serology Supportive Peracute die within hours, acute cases die/recover in 2 weeks, subacute/chronic die hepatic failure weeks/months Vaccination (CAV-2 vaccine protects against CAV-1 too)

diagnosis and tx for PLE

CBC & chemistry - panhypoproteinemia, hypocholesterolemia, hypocalcemia, lymphopenia; UA & UPC; Bile acids assay, ammonia testing, +/- liver biopsy; Coagulation measurements (antithrombin, D-dimers, thromboelastogram); Serum Vit D status assessment; Thoracic radiographs & abdominal ultrasound - sample effusion if present Endoscopy & biopsy Tx: Nutritional support Ideal (highly digestible, mod to high protein (20-25%), low fat (<10%), <5% insol fiber Royal Canin GI Low Fat/Vegetarian = lowest in fat; Homemade diets (nutritionist input recommended, TPN, PPN, canine albumin in severe hospitalized patients; Elemental diets available lack certain amino acids (taurine, arginine) and fatty acids (arachidonic acid) -> do NOT meet nutritional needs of cats +/- Vit B12 or fat soluble vit supplementation Reverse edema and ascites- Improved nutritional status will increased serum protein, leadfs to increased osmotic pressure Colloid therapy or plasma in severe hospitalized cases Colloids > plasma Reduce inflammation 1st line: anti-inflammatory to immunosuppressive dose of prednisone 2nd line: cyclosporine 5mg/kg PO q12hr Secondary infection (fungal most common) Azathioprine 1mg/kg PO q24hr Hepatopathy, BM suppression, pancreatitis Mycophenolate Address complications Intestinal dyspiosis - metronidazole or tylosin; probiotics Thromboembolism - aspirin or clopidogrel (concurrent gastroprotection) Prognosis: guarded; relapse common

diagnostic abnormalities with FIV?

CBC - can see anemia, lymphopenia, neutropenia (occasionally thrombocytopenia, thrombocytosis, monocytopenia, leukocytosis) Chemistry - hyperproteinemia with increased gamma globulin concentrations (direct result of FIV infection)- 4.5-11g/dL protein levels Bone marrow- mild dysplasia, ineffective hematopoiesis, maturation arrest, erythroid hypoplasia, myeloid hyperplasia despite peripheral leukopenia, sometimes with left shift Mildly prolonged PTT, thrombin time, and low fibrinogen concentrations; PT and plts normal

diagnostic tests for RMSF?

CBC- thrombocytopenia, mild (most consistent hematologic finding) Leukopenia generally occurs during the early stages of infection (first 24 to 48 hours), followed by progressive leukocytosis, which increases in proportion to the severity of vascular injury mild anemia pancytopenia can accompany fulminant canine RMSF Serology, IFA on tissue, PCR are available Prior initiation of antibiotic therapy can cause a false-negative test results with both direct immunofluorescent testing and PCR

Diagnostics for polyarthropathy? tx?

CBC/chem, joint taps, joint cultures, thoracic CXR, AUS, UPC, urine culture, echocardiogram, ANA/RF ideally radiographs of joint to evaluate for erosive vs non erosive doxycycline while workup is completed, antiinflammatory doses of pred if needed if primary IMPA and no infectious agent found then need to use second immunosuppressant typically

labnormalities with lepto?

CBC: neutrophilia, lymphopenia, monocytosis, anemia (if blood loss), thrombocytopenia Chem: azotemia, hyperphosphatemia, hyperbilirubinemia; elevated ALP, ALP, AST, and CK Elytes: hypoNa, hypoK, hyperK Acid/base: metabolic acidosis Coag abN poss

FIV into CD4 cell?

CD134 receptor on cell membrane binds with gp41 and gp120 on surface Fuses with Viral envelope fuses with cell membrane and capsid enters cytoplasm where reverse transcription occurs and dsDNA copy of retroviral genome made Long terminal repeats added to either end of viral genome and virus passes in nucleus where dsDNA copy integrates into host genome dsDNA is provirus- may be latent (no transcription host immune evasion) or transcriptionally active Transcription of DNA controlled by long terminal repeats and leads to synthesis of new virion components and virus assembly and budding occurs Tumor formation can result due to insertion near proto oncogene or variably inserted DNA leading to abnormal cell growth Survive minutes outside of host and are easily disinfected

coccidians and infective oocysts?

Cryptosporidium spp. oocysts are immediately infectious when passed by the host T. gondii, N. caninum, and Cystoisospora spp. must sporulate outside the host to be infectious

Toxoplasma

Cat (+dog) Cat ingests infected intermediate host cats produce oocytes, dogs can trasmit oocytes if ingest cat poop Sporozoite develops into oocyts 1-5 days-->tachyzoites rapidly dividing stage where replicate intracellularly and disseminate--> bradyzoites are tissue stage (CNS, muscle, organs); all stages are infective animals infected by ingesting sporozoites, tachyzoites, or bradyzoites, transplacental transmission occurs as well cats shed oocysts for 3-21 days after eating, sporulated oocysts survive in environment for a long time bradyzoites mayt persist in tissue for life- serum and ab titers unlikely to decrease after treatment 2 weeks following ingestion Adult cat (self limiting diarrea, ocular, or none), disseminated disease (everywhere --> death, can occur in animals that are immunocompromised), dogs (neuromuscular or disseminated form) dx- PCR on fresh tissue, Serology (IgM/IgG --> +IgM = shedding, paired IgG titers), PCR, fecal (if shedding) Clindamycin x 4weeks (may not clear tissues, clinical improvement 1-2d), TMS if CNS signs (or both, TMS may be better if intact BBB)- topical glucocorticoids for ocular disease; can also use sulfonamides, pyrimethamine Reduce roaming, don't feed raw meat 31% seroprevalence in all ill cats, 20% of dogs seropositive zoonotic

infectious causes of gingivostomatitis?

Cats: feline calicivirus most common. Feline herpesvirus 1 ~10%. Conflicting evidence for Bartonella

canine chronic pancreatitis

Challenging to diagnose - based on clinical signs, AUS, cPLI Presence of predominantly monocellular infiltrates, fibrosis and sporadic neutrophil infiltrates Manage with an ultra-low-fat diet (RC Gastrointestinal LF) Some may need immunemodulating therapy Prednisone - careful use due to development of DM; Dogs with DM - try managing with diet alone; Cyclosporine

can you treat babesia gibsoni with any other antibiotics?

Clindamycin—reduce morbidity and mortality, but does not eradicate infection Tetracyclines TMS—interference of protozoal folate production clinda+doxy+metro?some dogs drop under detection limit but ultimately dont know efficacy

botulism

Clostridium botulinum gram positive, sopore forming, saprophytic, anaerobic rod, ubiquitous neurotoxin that causes flaccid paralysis Naturally occurring botulism in dogs bc eating of carrion or raw meat No natural disease in cats All canine cases to date have been caused by subtype C toxin (two cases of subtype D reported from Senegal)

tetanus organism?

Clostridium tetani neurotoxin motile, gram positive non encapsulated anaerobic spore forming bacteria dogs have natural resistance caused by inability of toxin to penetrate and bind to nervous tissue, but still can get disease Most tetanus from spores that are introduced into wounds or penetrating injuries but tetanus has also been described in post-partum or post-OVH

concentration dependent antibiotics?

Cmax:MIC and AUC that is above the MIC (AUC:MIC) are determinants of efficacy have post antibiotic effects that allows for once daily dosing antibiotics- fluoroquinolones, aminoglycosides, metronidazole, azithromycin most have AUC:MIC>25 or Cmax:AUC > 10

types of coccidia

Toxoplasma, Neospora, Isospora (also called Cystoisospora), Hammondia, Besnoitia, Sarcocystis, Cryptosporidium, and Cyclospora

antibiotics for lower respiratory infections?

Community acquired in dogs: Bordetella, Mycoplasma, Streptococcus equi zooepidemicas (necrotizine and hemorrhagic pneumonia), Pasteurella, E. coli Community in cats: Bordetella, Mycoplasma, Streptococcus, Pasteurella, E. coli, C. felis. Hospital acquired: E. coli, Klebsiella, Pasteurella, streptococci, staphylococci, anaerobes, Bordetella, Pseudomonas, Mycoplasma Empiric therapy of critically ill patient: broad spectrum parenteral antibiotic Gram (-) rods: potentiated sulfonamides, gentamicin, chloramphenicol, 3rd generation cephalosporins (cefpodoxime), fluoroquinolones. Bordetella: Clavamox, tetracyclines, azithromycin Gram (+) cocci: Clavamox, chloramphenicol, cephalosporins, azithromycin.

what systemic disease reported commonly with candida cystitis? what drugs are associated? how do you treat?

DM antibiotics (tetracyclines), steroids fluconazole >> itraconazole, localized infusions of clotrimazole (US guided)

neospora caninum pathogensis

Definitive host = domestic dog + coyotes no clinical disease associated with natural infection in cats Intermediate host = herbivores (deer + cattle) Ingestion of bradyzoites in tissue cysts from intermediate host (bovine placenta, deer or cattle meat) = infection in definitive host Definitive host will pass unsporulated oocytes in feces Transplacental infection common in dogs prevention- avoid raw foods, avoid contact with bovine tissue and aborted fetuses, do not breed infected bitches zoonotic- risk in immunosuppressed, no link to abortion but avoid in pregnant women

what ticks associated with tick paralysis?

Dermacentor or Ixodes spp Neurotoxin released by gravid female ticks that prevents release of acetylcholine at the neuromuscular junction

diagnosis of mycoplasma sp?

Diagnosis: PCR is gold standard; pre antibiotics Antigen can become sequestrated during therapy in tissues; may become positive again Blood smears are poor diagnostic test Treatment Doxycycline Consider enrofloxacin, marbofloxacin or imidocarb for refractory cases; use serial PCR to evaluate Steroids?Coombs positive or refractory cases

treatment for IBD

Diet - novel or hydrolyzed protein +/- probiotics +/- O3 & O6 FA (10-12 weeks) Antibiotics - tylosin, oxytetracycline, metronidazole (28 days); enrofloxacin (Boxer GC) Immunosuppressive therapy Prednisolone 2mg/kg PO q24hr 10 days, then tapered over 8 weeks, Cyclosporine 5-10mg/kg PO q24hr, tapered after 8-10 weeks (K9), Chlorambucil 2-6 mg/m2 PO q24hr (fel), Budesonide - HPA suppression + steroid hepatopathy Sulfasalazine - adverse effect KCS, +/- Low dose or clopidogrel in pt w/alb <1.5 g/dL (hypercoagulable), +/- Cobalamin 20µg/kg SQ q7d x6 weeks, then q28d for 3mo Poor prognosis - remission rate 26% (K9) w/intermittent c.s. in half Neg px indicator = hypoalbuminemia (#1); severity of c.s., duodenal, hypocobalaminemia, inc PLI

blastomycosis?

Dimorphic fungi that can cause systemic mycosis, moisture is important for transmission (rain, dew, fog, mist) Upper Mississippi River Valley (ohio, missouri, mississippi river drainage) and mid atlantic states young (2-4), male, large breed dogs (Bluetick coonhounds, treeing-walker coonhounds, pointers, and Weimaraners have the highest risk of infection) living near water are at an increased risk immune response determines severity of disease anorexia, depression, weight loss, fever, cachexia, pulmonary (cyanosis poor prognostic indicator), perihilar LN, interstitial to alveolar pattern, cutaneous draining tracts, ocular dz, epiphyseal disease, orchitis, CNS (cats), large abscesses (cats) dx- BUA, cytology, Antibodies to WI-I antigen are more sensitive (antibodies not considered protective, need CMI to recover from dz), zoonotic when cultured, PCR, special stains (periodic acid schiff, Gridley's fungal, and Gomori's methenamine silver) tx- itraconazole, amophotericin B

Neospora

Dog Ingestion, transplacental, farm dogs Tachyzoites (acute infection, any tissue), bradyzoites (cysts, muscle/neural tissue only); Sporozoites develop in oocysts within 24 hours of passage. Tachyzoites (rapidly-dividing stage) and tissue cysts containing hundreds of bradyzoites (slowly-dividing stage) are the other two life stages. Dogs are infected by ingestion of bradyzoites but not tachyzoites Adult dogs can have reactivation from chronic infection Neuro/muscular signs, most severe in puppies --> granulomatous inflammation (multifocal CNS involvement; ascending paralysis with hyperextension of hindlimbs +/- myocarditis, dysphagia, ulcerative dermatitis, pneumonia, hepatitis) Serology (paired titers IgG >1:200, can cross react with toxoplasma at >1:50), CSF- pleocytosis with mixed cells (monos, lymphs, neuts, eos), oocysts in feces- PCR or fecal flotation, cytology, histopath Clindamycin, sulfadizine, pyrimethamine --> variable response, treat all pups in affected litter! Cook meat, dogs can get it from eating infected bovine placental tissue, don't let dogs crap around feed pens and livestock grave prognosis if neuro involvement

Babesia

Dog (+cat) --> B. canis (greyhounds), B. gibsoni (APBT) Ixodid tick feeds 2-3d --> sporozoites in saliva --> attach to RBC RBC parasite Hemolytic anemia --> pallor, icterus, hemoglobinura (may be subclinical) Cytology (feathered edge, capillary blood), serology, PCR (very sensitive!) B. canis (imidocarb; other diamidine derivatives not approved by FDA), B. gibsoni (azithromycin+atovaquone [synergistic together], supportive care, transfusions); if cannot afford atovaquone and azithromycin then can try immmidocarb (premunition occurs- immune protection from infection without clearing infection; clinical remission) Tick control monitoring during treatment- negative PCRs consecutively 2-4 weeks apart sarting 60 days or longer after treatment

Leishmania

Dogs (rodents also reservoir) Sandfly Leishmania donovani infection was confirmed in multiple dogs in a foxhound kennel in New York State. clinically affected cat in Texas was infected by L. mexicana mexicana Can be asymptomatic carrier Progressive immunosupporession and immune complex deposition (depletion of T lymphoid organs, proliferation of B cells) --> skin/nail lesions, GN, cachexia, etc- dogs develop visceral form Dx- Amastigote detection (2.5 to 5.0 μm × 1.5 to 2.0 μm), IFAT serology (IgG titers develop 14-28 days post infectiuon and decline 45-80 days after treatment, bc dogs cant clear- positive Ab means positive infection), PCR on bone marrow or LN (BEST) tx- Pentavalent antimonials, allopurinol --> relapse common, pulse therapy or lifelong treatment may be needed Sandfly repellant

Hepatozoon (H canis, H americanum)

Dogs HC --> brown dog tick/rhipicephalus (Africa, SE europe, Asia), HA --> amblyomma maculatum containing sporulated oocytes (southern US- texas gulf coast, mississippi, alabama, georgia, florida, arizona, oklahoma) dog must eat tick, clinical signs 3-5 weeks post exposure Pyogranulomatous myositis, periosteal reaction, fever (HA --> hyperesthesia, painful gait, mucopurulent ocular discharge, uveitis, ataxia, PU/PD, leukocytosis) (HC --> mild signs or severe depending on # parasites) Dx: HA: rads with periosteal bone reaction, clinical history/clinical signs supportive, rare gamonts (in WBCs in blood smear), muscle biopsy, HC: gamonts in WBC numerous; serum antibodies against H. americanum were compared with tissue biopsy; the sensitivity and specificity were 93% and 96%- definitive diagnosis with seeing gamonts in neutrophils or monocytes with Geimsa or Leishman's stianed blood smears or organisms in muscle biopsy tx- HA: TMS, clindamycin, pyrimethane OR decoquinate x 2years- decreases freq of relapse (no tx eliminates tissue phase) - HC: imidocarb And again...tick control

clinical signs associated with leishmaniasis

Dogs generally develop visceral leishmaniasis. Subclinical infection may persist for months or years. Hx: Weight loss, normal to increased appetite, polyuria, polydipsia, muscle wasting, depression, vomiting, diarrhea, cough, epistaxis, sneezing, and melena are common presenting complaints. PE: Splenomegaly, lymphadenopathy, facial alopecia, fever, rhinitis, dermatitis, increased lung sounds, icterus, swollen painful joints, uveitis, and conjunctivitis Cutaneous lesions are characterized by hyperkeratosis, scaling, thickening, mucocutaneous ulcers, and intradermal nodules on the muzzle, pinnae, ears, and footpads. Cats are usually subclinically infected. One cat had cutaneous nodules on the ear pinna

infectious causes of pollakiruia?

Dogs usually UTI, cats usually sterile Dogs: 75% gram negative (E. coli, Proteus, Klebsiella, Pseudomonas, Enterobacter) Cats: E. coli Rarely Mycoplasma, ureaplasma, Blastomyces, Candida.

Trypanosoma

Dogs, cats, humans, raccoons, opossums, armadillos Kissing bug (triatomine, reduviid bugs) Trypomastigote (blood, infectious, flagellated), amastigote (intracellular, non flagellated), epimastigote (intravector, flagellated) - Acute (myocarditis, CNS disease), chronic (DCM or asymptomatic) Cytology, serology (usually correlates wiht infection in N. America), PCR, culture, tryptomastigotes (1 flagellum, 15-20 um long) on blood film, LN aspirate or abdom. effusion cytology, histopath of cardiac tissue- reveal amastigotes (1.5-4um) no direct treatment, treat CHF and arrhythmias, Anti-parasitics (not useful in chronic stage), heart failure/DCM medications --> poor prognosis

antiobiotics for bacteremia/septicemia?

Dogs: Gram (-) especially E. coli most common, then Gram (+) cocci and anaerobes. Cats: primarily Gram (-) enterics or anaerobes IV cephalosporins or beta-lactam/aminoglycoside or beta-lactam/enrofloxacin combos Concentration-dependent once daily Time-dependent: CRI or q6h

canine and feline monocytotropic ehrlichiosis

E. canis- transmitted by rhipicephalus sanguineus; can have concurrent infections with A. platys, b. canis, H. canis, bartonella, E. chaffeensis, e. ewingii clinical findings tends to be more severe in GSD clinical signs- uveitis, splenomegaly, polyarthritis, polymyositis, CNS signs bloodwork- thrombocytopenia, mild anemia (regen), granular lymphocytosis reported, hyperglobulinemia, hypoalbuminemia and proteinuria (GN)- pancytopenia <25%, hyperglob 50-75% severe anaemia, severe leucopenia, pancytopenia, a tendency to bleed (especially epistaxis) and being a German shepherd dog were important indicators of poor survival in cases of monocytic ehrlichiosis in dogs

gram negative bacteria?

E. coli (rod), proteus, klebsiella, enterobacter, pateurella

common bacteria associated with bilary infections?

E. coli, enterococcus, bacteroides, strep, clostridium

Why do vaccines for the virulent feline caliciviruses not work?

Each outbreak has been associated with a new mutant and therefore protective immunity with vaccines is not possible (FCV-Ari, FCV-Ari, FCV-Diva)

Diagnosis of Cytauxzoon felis

Early diagnosis generally require fine needle aspirates (liver, spleen, lung, kidney, LN) Blood smears unreliable for early diagnosis PCR testing is available; high sensitivity/specificity reported treatment- azithromycin and atovaquone

effusive vs non effusive FIP?

Enters macrophages via lectin receptor fDC-SIGN (feline dendritic cell specific intercellular adhesion molecule grabbing non-integrin receptor) → replication within macrophages determines which form of disease will have due to host immune response mounted Noneffusive form- occurs in cats that mount partial CMI response characterized by pyogranulomatous to granulomatous inflammation with variety or organs, - mesenteric LN, kidneys, liver, lungs, brain, eye; solitary or multifocal granulomas of intestinal wall my develop, especially at ILC, Effusive form- unable to mount immune response and characterized by accumulation of high protein exudates in thorax and/or abdomen, low cellularity effusion, infection results in immune dysregulation and virus induced CD4+ and CD8+ cell depletion (profound), production of TNFalpha, granulocyte macrophage CSF, VEGF, granulocyte colony stimulating factorby infected macrophages, impaired IFN gamma production, hypergammaglobulinemia (infection of DCs thought lead to apoptosis of T cells, unknown mechanism of T cell depletion), concurrent infections with opportunistic invadors can occur (rare, toxo, retroviruses, sporothrix)

FeLV virus information

Enveloped RNA virus belongs to Gammaretrovirus in Retroviridae (oncornavirus) causes immunosuppression, bone marrow disorders, and hematopoietic neoplasia more pathogenic than FIV and progresses more rapidly- some animals can eliminate infection but this is rare

three retroviral diseases in cats?

FIV, FeLV, Feline foamy virus

what virus associated with feline progressive polyarteritis syndrome? cat vs dog IMPA?

Feline foamy virus (spumvirus) Common retrovirus (90% seroprevalence) that may require coinfection with FeLV for expression of disease In cats, unlike dogs, infectious causes of arthritis are much more common than primary immune-mediated disorders- Infectious causes: bacteria, bacterial L-forms, Mycoplasma species, calicivirus, feline infectious peritonitis virus, fungi (primarily cryptococcal and Histoplasma species), and some tick-borne rickettsiae (most non erosive besides Mycoplasma species) Infectious disorders primarily cause arthritis by direct infection of the synovium, but occasionally systemic infections give rise to circulating immune complexes that are deposited in joints, resulting in a sterile synovitis known as reactive polyarthritis

infectious causes of dyspnea from pleural effusion?

Feline infectious peritonitis and pyothorax most common Cats: usually history of fighting or upper respiratory tract infection Dogs: bite wound, migrating plant foreign body, trauma

Crypto

Filamentous, yeast Inhalation Thick capsule, narrow based budding Worldwide Cats >>> dogs Nose, skin, CNS, eyes Cats (upper resp, nasal deformity, skin, ocular, CNS) - dogs (CNS mostly) Cytology, LATEX CRYPTO ANTIGEN AGGLUTINATION TEST (monitor titers) Itraconazole, fluconazole for CNS/cats, amphotericin if failure (6-18mo) - treat until 2 negative tests Good if no CNS disease

clinical signs of botulism?

Flaccid paralysis, cranial nerve motor responses are affected, causing mydriasis, decreased jaw tone, decreased gag reflexes, and excess salivation. Megaesophagus may be present. Pain perception is intact; muscle atrophy and hyperesthesia do not develop recovery occurs by development of new terminal axons with functional NMJ ascending paralysis and descending recovery

mycoses and diagnoses:

For yeasts such as Cryptococcus or Candida, or for dimorphic fungi that have a yeast phase in tissue, such as Blastomyces dermatitidis or Histoplasma capsulatum, the diagnosis can usually be made cytologically. For other fungi that grow as hyphal organisms in infected tissue, the diagnosis is usually dependent on histopathology, culture, or molecular techniques

infectious causes of epistaxis?

Fungal: Aspergillus, Cryptococcus, Penicillium, Sporothrix schenckii Infectious agents causing thrombocytopenia usually not severe enough to cause bleeding unless also vasculitis: Bartonella, E. canis, R. rickettsia

Bartonella? Transmission? Diagnosis? Clinical signs?

G- fastidius bacteria, transmitted by hematophagous arthropods (biting flies, fleas, keds, lice, sandflies, ticks [ixodes, rhipicephalus]) intraerythrocyte localization, strategy for bacterial resistance lesions: heart, liver, LN, joints, eye, nasal cavity, CNS, skin and SQ; utaneous vasculitis, anterior uveitis, polyarthritis, meningoencephalitis, and immune-mediated hemolytic anemia, thrombocytopenia, and eosinphilia Diagnosis: PCR (blood, tissue- FN common bc low levels of circulating organisms) Seroconversion variable (only 33-50% of dogs have antibody response), culture- best to culture tissue, can do blood cultures (low bacteremia so FN is possible), +/- ANA titers, microscopy - modified silver stains, enrichment PCR (shortening processing time for results and broadened spectrum of species detected, still have FN), warthin starry stain- stains for spirochetes; thrombocytopenia, anemia, neutrophilic leukocytosis most common Dogs: henselae (#1 in dogs, also cat scratch in humans) Endocarditis (aortic valve, large breeds most common; B vinsonii ssp berkhoffii- myocarditis, anterior uveitis), IMT, IMHA, Polyarthritis, thrombocytopenia, granulomatous inflammation, peliosis hepatitis, lymphadenitis, sialoadenitis, panniculitis tx: azithromycin and doxycycline (long term abx), pradofloxacin, amikacin Jarisch-Herxheimer reaction due to endotoxins- systemic reaction observed after getting abx for spirechete or other bacterial infections- associated with systemic release of cytokines (TNFa, IL6, IL8)- similar clinical presentation as sepsis - fever, tachycardia, tachypnea, increased BP, leukopenia

pathophysiology of IBD

Genetics (Loss of tolerance to Ags of the microbiome & resulting misrepresentation of commensal bacteria as pathogens-> aggressive CMI response; Polymorphism in TLR5 (& TLR4 in GSD) assoc w/IBD in 38 different dog breeds) Altered intestinal mucosal immunity (skewed cytokine profile, Th1 in cats, decreased CD11c (possible dendritic cells in dogs), Th1 & Th17 profile (humans w/Crohn's dz) Upregulated TLR 2, 4, 9 expression in the duodenum and colonic mucosa in dogs- TLR2 expression correlated w/severity of disease Intestinal dysbiosis (decreased bacterial species in microbiome, Result: PAMPs recog by innate immune system -> exaggerated adaptive immune response in lamina propria of mucosa [increased Enterobacteriaceae, decreased Clostridia spp dogs; increased Enterobacteriaceae, E. coli, Clostridium; upreg Th1-cytokines in cats])

What vector borne infection has been associated with this lesion?

Hepatozoan americanum

what trematode is associated with hypercalcemia and gastrointestinal/hepatic trematode infiltration?

Heterobilharzia americana Diagnosis Generally histopathology Fecal centrifugation PCR TAMGI-Lab Treatment: Praziquantal and fendbendazole TAMU paper- When the biopsies were examined there were numerous white nodules noted in the wall of the small intestine (Figure 1). Microscopically these nodules contained numerous trematode ova, approximately 45-90 um in diameter, located within the deep muscular layers of the small intestine. Surrounding the trematode ova were thick strands of fibrous connective tissue entrapping infiltrates of multinucleated giant cells, macrophages, lymphocytes, and plasma cells. The trematode ova were histologically compatible with Heterobilharzia americana.

diagnostic testing for leishmaniasis and treatment

Histologic or cytologic evaluation (liver, spleen, bone marrow, and lymph nodes) Serology: IFA (gold standard; cross reactivity 1:64), ELISA, CF, DAT, indirect hemagglutination, western K39 antigen testing treatment- antimonials (sodium stibogluconate or meglutamine antimoniate), allopurinol, amphotericin B vaccination

vector and transmission of hepatozoon americanum, tx?

Host ingests infected tick (Amblyoma maculatum) or infected meat Zoites liberated in GI tract → dispersed to tissues (mech unknown) → mostly striated muscle → merogony → meronts found w/in WBC b/t muscle fibers after several weeks Meront-containg WBC encysted w/in host cell-derived concentric layers of mucopolysaccaride ("onion skin" cysts) Meronts mature, inc in size, rupture → release merozoites → local inflammation (pyogranuloma) and invasion into new host WBC, or develop into gamonts (infective to feeding larval and nymphal A. maculatum) Most effective therapy: Decoquinate(Decoxx)- Decoquinate decreases freq of relapse & may reduce risk of transmission by preventing infection of susceptible ticks in the environment NSAID + [TMS + clindamycin + pyrimethamine, aka. TCP] OR [ponazuril]; + long term decoquinate

Dx hepatozoon americanum?

Hx tick exposure, c.s., lab findings, rad evidence of periosteal bone proliferation Parasitemia rare (<0.1%) - can be seen 5 wk after exposure Rare gamonts = likely H. americanum Numerous gamonts = likely Hepatozoon canis Muscle biopsy to evaluate for merogony Biceps femoris or semitendinosus muscle Onion skin cysts & pyogranulomata Real-time PCR (Hepatozoon spp. 18S rDNA)

treatment for parvovirus?

Hydration is core of treatment, crystalloids preferred for replacement Monitor electrolytes (low potassion and glucose common) Oncotic support can be needed if hypoprotenemia (edema, TS < 3.5 mg/dL or albumin < 1.5); NB: Plasma has low oncotic pressure, and may have proinflammatory cytokines, author prefers synthetic colloids (hetastarch, dextran) which are also cheaper. 20ml/kg/day, and monitor coags. Nutrition: early feeding w/in 12 hours, consider NE or E tube if needed Antiemetics - Cerenia is best, metoclopramide can cayse hypermotility Antibiotics to preent bacterial translocation: use if leukopenic Antivirals show some promise - specifically Recombinant feline interferon-omega, though not available right now

Dx ehrlichia canis? tx?

IFA- takes 7-28 days to become positive after infection (If titer is between 1:10-1:80, retiter in 2-3 weeks)- can cross react with E. chaffeensis and ewingii, also RMSF, b. canis, a. platys, a. phagocytophilum SNAP 4Dx is positive at 1:100, Cross reacts with E. ewingii, Sens: 96.2 and spec 100% To determine active infection: blood culture, morulae on cytology, and PCR. PCR is positive 4-10 days after infection doxycycline, chloramphenicol in puppies (resistant to fluoroquinolones), +/- immunosuppressive steroids, can use imidocarb monitor- another PCR 2 weeks after treatment to see if cleared

steroids and disseminated/miscellaneous infections?

IMHA and ITP- typically steroids and abx FIP juvenile cellulitis (facial swelling, lymphadenopathy, deep pyoderma, fever, polyarthritis)- immune response to bacterial angtigens- abx and steroids

FIV and CD4:CD8 ratios

In the first few weeks of infection, numbers of both CD4+ and CD8+ cells decline -> strong immune response characterized by the production of anti-FIV antibodies and a rebound in CD8+ cells above pre-infection levels which results in a persistent inversion of the CD4/CD8 ratio. Over time, numbers of both CD4+ and CD8+ cells gradually decline. Decrease of CD4+ cells is caused by a shortened life span in infected lymphocytes and apoptosis of uninfected cells

clinical signs of neospora caninum infection?

In utero = ascending paralysis (+/- dysphagia & megaesophagus), rigidity of affected muscles; stillbirth/neonatal death Older dogs (>6mo) = musculoskeletal, cardiopulmonary, CNS (cerebral ataxia & atrophy); Chronic infections possible - asymptomatic; Immunosuppresion may cause sponaneous illness

tritichomnas blagburni

Infection via direct fecal oral route à no oocyst form & 1-stage asexual lifecycle Suspect colonic bacteria facilitate infection à nutrient source for T. blagburni or other potentiation Mucinase activity allows penetration thru mucus layer? May degrade mucus Ig and lactoferrin for nutrients Contact with epi à ameboid transformation, adherence & upregulation of virulence factorsBinds sialic acid portion of epi cell glycoconjugates OR may cleave it to use other adhesins after initial bindngTrichomonad surface carbohydrates à lipophosphoglycanCysteine proteases Ameboid form à cytotoxicity via disruption of tight junctions, detachment & apoptosisCysteine proteases probably both adhesins and cytotoxic mediatorsPhospholipases and porins Subepithelial invasion and host immunity evasionInduce apoptosis in host innate immune cells & phagocytose leukocytesInhibits NF-kB activity à decreased TNFa and IL-12 activity Enhances expression of anti-inflammatory cytokines IL-10, TGFbCysteine protease-mediated degradation of surface bound complement C3, IgGs, fibrinogen, albumin, others Phenotypic variation & antigenic heterogeneity à not recognizable to immune system BUT still characterized by influx of neuts, lymphs, plasma cells in to lamina propriaLikely contributes to diarrhea from T. blagburni

botulism pathogenesis

Ingested -> from the stomach and upper small bowel and enters -> lymphatic system -> binds rapidly and irreversibly to neuromuscular junction of cholinergic nerves and prevents the presynaptic release of acetylcholine at the neuromuscular junction incubation 0-6 days and earlier onset indicates more severe disease lasts 14-24 days

blastomycosis pathognesis?

Inhaled -> conidia are phagocytized by alveolar macrophages and transform from the mycelial phase to the yeast phase -> yeasts stimulate local cell-mediated immunity (marked suppurative to pyogranulomatous inflammatory response) which either controls dz locally or transports it to pulmonary interstitium, where they gain access to both the lymphatics and the vascular system -> multisystemic pyogranulomatous disease: dogs- lymph nodes, eyes, skin, bones, subcutaneous tissues, and prostate are common organs affected cats- skin, subcutaneous tissues, eyes, CNS, and lymph nodes

What oomyces has been associated with great vessel rupture, sublumbar lymphadenopathy, edema?

Lagenidium Serology cross react with phythium Culture possible Negative phythium IHC

lagenidiosis

Lagenidium caninum, most are parasites of algae, fungi, nematodes, crustaceans, insect larvae progressive cutaneous or subcutaneous lesions (often multifocal) involving the extremities, mammary region, perineum, or trunk as firm dermal or subcutaneous nodules or as ulcerated, thickened areas with areas of necrosis and numerous draining tracts Regional lymphadenopathy is often noted and may occur in the absence of cutaneous lesions. majority of dogs with lagenidiosis have been found to have lesions in distant sites, including great vessels, sublumbar and inguinal lymph nodes, lung, pulmonary hilus, and cranial mediastinum visible with H and E stain (differs from pythium which isnt)- pyogranulomatous and eosinophilic inflammation with broad irregularly branching sparsely septate hyphae Immunoblot serology for the detection of anti-Lagenidium antibodies in canine serum can provide a presumptive diagnosis of lagenidiosis but must be interpreted in conjunction with results of serologic testing for P. insidiosum infection. The definitive diagnosis of Lagenidium spp. infection is best made by culture, but requires ribosomal RNA gene sequencing or specific PCR amplification in addition

What bacterial pathogen was recently reported to be associated with small intestinal intussussception?

Leptospira australis

FeLV and clinical signs? blood work changes?

Lethargy, tachypnea, tachycardia (thymic lymphoma can cause difficulty breathing), abdominal distention (hepatosplenomegaly), uveitis can occur CBC- anemia, neutropenia, lymphopenia, monocytopenia, thrombocytopenia, aplastic anemia possible chemistry- IMHA changes UA- proteinuria BMA/Bx- if pancytopenic, lymphoma, MDS, can do IFA for confirmation on bone marrow; Myelophthisis secondary to leukemia, myeloid and/or erythroid dysplasia or myelofibrosis (50% of cats in one study with MDS and 36% of cats with leukemia were FeLV positive)

pathogenesis of coccidiomycosis

Life cycle and infection: alkaline sandy soil normal habitat -> mycelia produced during seasonal rainfall -> Arthroconidia (arthrospores) develop with soil drying -> airborne with dry/windy conditions -> inhalation of arthroconidia is the major route of infection Pathogenesis: Arthroconidia -> spherule in tissue -> internal division (endosporulation) -> ruptures -> endospore can become an endosporulating spherule (continuation and expansion of the parasitic phase) spherules or endospores can revert to the mycelial form of growth (under appropriate environmental conditions, such as might be found under bandages covering a draining tract) Dissemination: Dissemination is defined as spread beyond the tracheobronchial and mediastinal lymph nodes --> the axial and appendicular skeleton and overlying skin, abdominal viscera, CNS, ocular, pericardium, myocardium, and prostate

clinical signs suggestive of virulent calicivirus

Limb edema, head/limb ulcerations/crusting, pulmonary edema, pleural effusion, icterus, epistaxis, hematochezia Hypoalbuminemia, elevated liver values, hyperbilirubinemia Hepatocellular necrosis, penumonia, pancreatic necrosis

catagories of PLE

Lymphangiectasia or crypt disease- Yorkshire terriers, rottweilers IBD - lymphoplasmacytic, eosinophilic, granulomatous Breed associated forms or idiopathic - besenjis, soft coated wheaten terriers, Norwegian lundehund, Maltese, shar-peis Lymphogranulomas around lymphatic vessels; most severe changes to the lymphatic vessels Misc - infectious (histoplasmosis, parvovirus, severe parasitiscm), neoplastic (lymphoma) GSD- predisposed to PLE secondary to IBD, lymphoma or infectious

diagnose lepto? tx?

MAT- serum incubated with live leptospires and examined via darkfield microscopy for evidence of agglutination, cant distinguish IgG and IgM (highest dilution of patients serum with 50% agglutination- serovars- canicola, icterohemorrhagica, pomona, grippotyphosa, hardjo, bratislava (no autumnalis)- cross reactivity between serovars cant usually tell primary infective serovar; >1:800 or 4 fold increase in titer between samples (4-6 weeks apart)- MAT titers become positive after about l week, peak at 3 to 4 weeks, and remain positive for months after both natural infection and vaccination (can affect antibody results for lyme disease if have coinfection) PCR on blood and urine- best- blood within 5 days, urine within 10 days - cannot ID serovar ELISA- IgM/IgG- IgM antibodies increase within the first week of infection (before the MAT titer); the maximum IgM titer develops within 14 days and decreases thereafter. IgG antibody tests turn positive 2 to 3 weeks after infection and persist for months, with a maximum titer after l month (if vaccinated and got booster than high IgG and no IgM)- cant tell difference between serovars tx: doxy! elimites leptospiremia and renal carrier phase if cannot tolerate doxy- ampicillin (eliminate leptospiremia) and follow up with doxy for renal carrier phase

diagnosis of brucella?

ME-RSAT: 2-mercaptoethanol rapid slide agglutination test (ME-RSAT); Preferred screening test (good NPV)- false positive rates in specific breeds like irish wolfhounds and old english sheepdogs AGID- sensitive fod Ab, 2 antigens used (cell wall or cytoplasm- Cp) better CpAg-AGID uses cytoplasmic antigens and is highly specific for Brucella infection in dogs, should be used as a confirmatory antibody testing procedure culture is only way to definitively diagnose- blood best for isolation of organism (leukocyte fraction), bacteremia within 2-4 weeks of oronasal infection, can persist for 5 years if not treated (can also culture urine and semen [collect via ejaculation within first 3 mo of infection])

polyarthropathy secondary to what vaccine?

MLV for calicivirus

diagnosis of babesia? clinical manifestation?

Molecular diagnostics: PCR (B. canis, B. gibsonii; others require specialty labs) IFA for B. canis vogeli and gibsonii Definitive diagnosis is based on organism demonstration in RBCs using Wright's or Giemsa stains on thin blood smears. B. canis is typically found as paired, piriform bodies measuring 2.4 × 5.0 μm. B. gibsoni is typically found as single, annular bodies measuring 1.0 × 3.2 μm. Serology can be negative with acute disease Blood smears: cannot differentiate large types and rarely can differentiate small types and depends on parasitemia organism replicates intracellularly in RBCs, causes hemolytic anemia

three groupings of polyarthritis in dogs?

Mononuclear polyarthritis: primary osteoarthritis Septic, suppurative polyarthritis: organism causing disease in joint Non-septic, suppurative polyarthritis: 1° immune disease (SLE/idiopathic), an infectious cause, or 2° immune reaction to noninfectious cause

Feline Ehrlichiosis, Anaplasmosis, and neorickettsiosis

Morulae-like inclusion bodies have been observed in monocytes, lymphocytes, or granulocytes of cats Antibody reactivity to E. canis or N. risticii antigens has also been reported several laboratories have amplified A. phagocytophila DNA from the blood of acutely ill cats with fever, lethargy, inappetence, and thrombocytopenia Serologic evidence of ehrlichiosis was reported in 12 sick cats with clinical and laboratory abnormalities including fever, malaise, weight loss, anorexia lymphadenopathy, nonseptic suppurative polyarthritis, anemia, thrombocytopenia, neutropenia, and polyclonal or monoclonal gammopathy - all responded to doxy Based upon PCR amplification and DNA sequencing, E. canis-like infection has been reported in cats with polyarthritis or bone marrow suppression accompanied by anemia, thrombocytopenia or pancytopenia but IFA testing using E. canis antigens was negative. Antibody reactivity (IFA and Western immunoblot) to N. risticii antigens was described in five cats from California. Hematologic abnormalities included leukopenia, anemia, and thrombocytopenia All in all of unknown significance in cats

clinical manifestation of chagas disease (dogs)?

Most common clinical features Cardiac disease (arrhythmias or myocarditis, acute and chronic) Rarely neurologicdisease Many infected dogs remain asymptomatic for life

feline enteric CoV and FIP?

Multi cat households cats can be repeatedly infected and clear infection but some cats remain persistently infected and shed FeCoV in absence of clinical signs > 6 cats are likely to have FeCoV <10% develop FIP in multicat households FIP - sporadic disease, does not spread from cat to cat, epidemics occur in shelters or catteries with mortality up to 10% Readily disinfected, doesn't survive readily in environment or at room temperature

feline leprosy organism?

Mycobacterium lepraemurium usually introduced via bite wounds from rodents with greater incidence in winter systemic dz rate- FIV or FeLV can play role in pathogenesis and predispose to septicemia young cats, clinical syndrome has been described in older cats as well Strong Th1: Tuberculoid response, few organisms Weak Th1: Lepromatous response, many organisms, much worse prognosis

Which acid fast organism has been associated with panniculitis in cats and dogs?

Mycobacterium smegmatis (most common but others possible) Generally of the rapid growing mycobacterium group

What are the three reported feline haemoparasites?

Mycoplasma haemofelis Candidatus Mycoplasma haemominutium (Generally assymptomatic) Candidatus Mycoplasma turicensis (Often associated with other haemoparasites or illness Can be associated with disease) Reported in the dog: Mycoplasma haemocanis Generally requires splenectomy or immunosuppression Candidatus Mycoplasma haemoparvum

FeLV and opportunistic disease?

Neoplasia (lymphoma), PRCA, aplastic anemia, immune mediated diseases, peripheral lymphadenomegaly, reproductive failure, neurologic disease, GI disease, infections (LUT and UUT infections, URIs, FIP, stomatitis, toxoplasmosis, hemoplasmosis, dermatophytosis, cryptococcus Fibrosarcomas can develop due to FeLV-A recombining with cellular oncogenes (c-fes, c-fms, c-fgr) to form feline sarcoma virus, this is inserted into oncogenes causing malignant transformation (cutaneous masses that met to lung and poor prognosis, must have FeLV A in order to get FSV) Feline olfactory neuroblastomas, cutaneous horns, osteochondromatosis FeLV responsible for myelogenous leukemias, erythroleukemias, megakaryocytic leukemia, and lymphoid leukemia in cats, but not all cats with these cancers test positive for FeLV Ag, most FeLV leukemias are acute but can be behind CLL, chronic eosinophilic leukemia, myelomonocytic leukemia

lab findings with hepatozoon americanum?

Neutrophilic leukocytosis (neutrophilia most common, left shift 20-200k neuts) Mild normocytic normochromic nonregenerative anemia Mild inc ALP, hypoalb, hyperglob, +/- hypoglycemia, +/- dec BUN Chronic infections → glomerulopathy + renal failure Periosteal bone proliferation in dogs

treatment for chagas disease?

Nifurtimox or benznidazole steroids prognosis- if survive acute disease (progression to chronic stage tends to occur more quickly (1-2 years) in dogs diagnosed younger (<2 yo), older age at diagnosis (>4 yo) survive longer

calicivirus

Nonenveloped; ssRNA transmitted by direct contact, not aerosol FCV carriers shed virus continuously and are therefore always infectious to other cats- shedding NOT linked to stress, more prevalent in long term sanctuaries/populations virus persists in tonsil and other oropharyngeal tissues. In some cats the carrier state appears to be lifelong, but most spontaneously recover at some point and appear to eliminate virus. FCV carriers appear to be very common, with approximately 20% to 30% of cats in the general population shedding FCV clinical signs- URI, mouth ulceration (tongue), lameness and pyrexia can occur, chronic stomatitis, pneumonia

infectious causes of cardiac murmur or arrhythmia?

Often accompanied by fever, other systemic signs Aerobic and anaerobic bacteria: Staphylococcus, Streptococcus, Enterococcus, Corynybacterium, E. coli, Salmonella, Klebsiella, Enterobacter, Pseudomonas, Proteus, Pasteurella, Clostridium, Fusobacterium, and Bacteroides Usually have primary site of infection (often skin, UTI, oral) Bartonella spp. Recently associated w/ endocarditis (aortic valve) Ventricular arrhythmias from Trypanosoma cruzi, T. gondii, N, caninum

what antigen is the lyme vaccine against?

OspA: produced as borreliae enter the tick vector and remains a major surface antigen during midgut colonization

diagnose GI lymphoma cats

PARR or TCRG (determine clonality of lymphocytes, helpful to distinguish SCLSA from IBD (lymphoma mono or oligoclonal), endoscopy treatment- low grade; chlorambucil + pred; high grade- COP/CHOP prognosis based on histologic grade, initial response to therapy

what is the recommended way to monitor effective therapy for E. canis? what are 3 classic phases of E. canis?

PCR based assays; serology may be positive for years following therapy Acute, Subclinical (hyperglobulinemia, thrombocytopenia), Chronic

lyme nephritis

PLN; Immune-mediated glomerulonephritis, tubular necrosis and regeneration, and lymphoplasmacytic interstitial nephritis Proteinuria, hypoalbuminemia, hypercholesterolemia, ascites, thromboembolic disease, and systemic hypertension Sterile nephritis Dx; renal biopsy

parvovirus dx

POC ELISA that detects viral antigen in feces, FN and FP possible False negatives if CPV-2c - controversial if we can trust it Quantitative PCR may be useful in future to tell naturally infected from vaccinated (qualitative may test positive following vaccination)

feline exocrine pancreatic disorders

Pancreatitis, EPI, pancreatic cancers (adenocarcinoma, lymphoma), pancreatic pseudocyst, abscess, parasites and nodular hyperplasia Causes of pancreatitis: Cancer, infections (FIP, FIV, calicivirus, Toxoplasma gondii, Amphimerus psudofelineus, organophosphates Often have concurrent hepatic lipidosis, cholangitis, obstructive jaundice, IBD, DM, interstitial nephritis, and pleural effusion

Distemper

Paramyxovirus, outer membrane proteins (H = hemagglutinin, F = fusion) canines, aerosol transmission predominantly, found in other secretions, transplacental 7 days post infection, up to 60-90d post infection Greatest 3-6mo Multiplication tissue macrophages, spread to lymph nodes/tonsils --> replication in lymphocutes --> infection systemic lymphoid organs --> hematogenous spread Clear virus with good immunity Delayed immunity results in delayed clinical signs No immune response results in widespread infection/death CNS: acute (CHEWING GUM SEIZURES), subacute/chronic (MYOCLONUS), old dog encephalitis - general: kennel cough-like, KCS, vomiting/diarrhea, pneumonia - skin: pustular dermatitis, hyperkeratosis - ocular (gold medallion lesions) - other: enamel hypoplasia, HOD Clinical suspicion, inclusion bodies, radiology IFA for ANTIGEN, IHC for ANTIGEN, PCR, serum antibody testing (GOLD STANDARD --> IgM/IgG), CSF tap (anti-CDV Ab) Supportive, symptomatic, palliative Poor with CNS signs Modified live vaccine q3-4wks between 6-16 wks (waning maternal antibodies)

most common clinical signs of pneumocystis carinii

Pneumonia; commonly asymptomatic, young dogs diagnose via Lung aspiration or lung histopathology, TTW. Rare BAL findings of eosinophilic foamy alveolar casts and organisms treatment- Trimethoprim/sulfamethoxazole, Sulfadimethoxine/ormetoprim, Pentamidine isethionate, combo clinda+primaquine, dapsone+TMS at risk breeds: Dachshund, Shetland sheepdog, CKCS; associated with immunodeficiencies

antibiotics for URIs?

Primary bacterial uncommon, secondary common Dogs: Bordetella Cats: Bordetella, mycoplasma, Chlamydophila felis Treat underlying cause Empiric therapy: amoxicillin, Clavamox, cephalexin, cefadroxil, doxycycline, or azithromycin Reserve fluoroquinolones for resistant infections

pythiosis

Pythium insidiosum aquatic pathogen, more like algae than fungus have cellulose and beta glucan in cell wall, ergosterol not principle sterol in cell membrane motile biflagellate zoospore in water, encysts in damaged skin or GI mucosa

Coronavirus

RNA virus FeCoV --> type 1 predominant over type 2 Cats Oronasal exposure via feces/fomites Can have chronic shedders Any cat with FeCoV can develop FIP --> immune suppression and breed may predispose Mutation of FeCoV --> infection/replication within macrophages --> FIP (systemic pyogranulomatous vasculitis) --> antibody dependent enhancement Inadequate CMI (wet form), partially protective CMI (dry form) Aggressive CMI (less likely to develop FIP --> may be latent and shed) Wet form (exudation of plasma proteins from immune complex damage to vessels), dry form (granuloma formation, organ dysfunction) --> vague and varied, ocular signs (eyes, brain, kidneys, omentum, liver) Polyclonal gammopathy, abdominal and/or pleural effusion, IHC (GOLD STANDARD FOR DETECTING VIRUS), IFA (GOLD STANDARD FOR ANTIBODY DETECTION), CSF Supportive --> pred may help, poor prognosis, respond well to GS-441524 (remdesivir) Test "herd" using antibody test, queening in clean room, test queen and kittens --> vaccine isn't recommended (antibody dependent enhancement) tx: environment enrichment, high quality diet, GI intestinal parasites, FortiFlora greatly reduced prevalence rate of nonspecific diarrhea in shelter

what is the most sensitive test for brucella canis?

RSAT (rapid slide agglutination test) Highly sensitivity, low specificity, Best screening test More specific tests included ME-RSAT, TAT (tube agglutination), AGID, IFA, Blood cultures

african horse sickness?

Reoviridae, genus Orbivirus dogs only ingesting infected horsemeat but can also be infected by vector- culicoides midges fever, cough, diarrhea, lung disease, death no treatment

what retinal lesions can be seen with feline panleukopenia?

Retinal folding, dysplasia, degeneration, optic nerve hypoplasia May be incidental finding in recovered adult

Rabies

Rhabdovirus structural proteins Mammals Bite from infected animal --> saliva (Briefly before CNS signs until death) Bite wound --> enters peripheral nerves --> replication --> spreads via intraaxonal flow --> enters spinal cord/brainstem --> ascends to forebrain --> LMN disease --> acinar cells in salivary gland Current vax (revaccinate, quarantine 45d) - overdue/no vax (vaccinate, quarantine 180d) Prodromal (CNS spread --> mood change), furious (forebrain --> hyperesthesia), paralytic (apoptosis --> LMN signs), death Clinical signs, histopath (negri bodies), direct immunofluorescence on nervous tissue (BEST) No treatment Completely screwed vaccine- Killed vaccine at 3mo old, revax q1 or q3 years

Coccidiomycosis

San Joaquin Valley fever, endemic fungus in deserts of southwest (So Cal, Az, SW TX)- C. immitis (within California) and C. posadasii (in all other endemic Southwestern regions) inhalation is route of infection- spores cant be killed by neutrophils and small amount to lodge in alveoli (3-5 um) most common clinical signs- respiratory (coughing, dyspnea)- hilar lymphadenomegaly, pulmonary inflammation, effusion most common disseminated site- bone (lameness, swelling) fever, lethargy, weight loss, anorexia, lymphadenomegaly, CNS, ocular, skin

characteristics of semen in dogs with brucellosis

Semen: immature sperm, deformed acrosomes, swollen midpieces, detached tails, and head-to-head agglutination of sperm, often accompanied by neutrophilic and mononuclear inflammation

FIV diagnosis?

Serology- ELISA- highest overall sensitivity; must have no recent history of vaccination, tested cat greater than 6 months old (maternal antibodies)- positive is positive, rarely animals test positive; can confirm testing with western blotting; detects antibody to FIV provided no history of vaccination and not less than 6mo- positive is positive (assays detect p24 core protein and gp40 transmembrane protein) Should retest positive kittens after 6 months of age, but negative is negative Can do PCR on blood but sensitivity and specificity vary between laboratories - can be insensitive if viral loads are low Indications to test cat: Sick cats, even if negative in past; newly acquired cats and kittens; exposure to retrovirus infected cat or unknown cat (especially after bite wound); cats in household with other retroviral cats; before initially vaccination with FeLV/FIV vaccines; blood donors; shelter animals; group housed cats With sick cat that is FIV positive, can assume that FIV is playing some role in illness Vaccinated with be FIV positive for 4 years - infection can occur in vaccinated cats, so positive in sick cat may represent infection; false negatives if in terminal phase due to low Ab production

steroids and respiratory disease?

Short course of anti-inflammatory doses of steroids may be effective in reducing cough with uncomplicated infectious tracheobronchitis does not shorten the course of disease Initial treatment w/ anti-fungal leads to worsening symptoms due to increased inflammation w/ death Coughing from hilar lymphadenomegaly resolved more quickly with steroids (3 wks vs 9 wks)

Coccidio

Spores --> spherule --> endospores Inhalation Endospore-filled spherules Southwest US (rain then drought) Dogs >>> cats 1-3 weeks incubation pd Lungs, bones Pulmonary form (one spore = lots of inflammation), MOST SUBCLINICAL OR MILD, disseminated (bones --> chronic signs) - skin lesions in cats Tube precipitation (IgM) and complement fixation (IgG) --> hard to find on cytology Fluconazole, itraconazole, ketoconazole (~12mo or lifelong) - NO STEROIDS Good if localized, poor if disseminated

Histo

Spores --> yeast Inhalation, ingestion Small, round, thin halo, intracellular Phagocytized by mononuclear cells --> vessels and lymphatics Ohio, Mississippi, Missouri rivers Cats, dogs, humans 2 week incubation pd Lungs, intestine Mycotic pneumonia, GI signs, lymphadenopathy (SUBCLINICAL COMMON) dx with Cytology tx with Itraconazole (4-6mo), NO STEROIDS - can be self limiting, still treat Good if localized, poor if disseminated

Blasto

Spores --> yeast Inhalation Big blue broad based budding yeast Vessels and lymphatics Central atlantic, southeast states Dogs and people --> young, healthy 1-3 months Lungs, eyes, skin, bone: Mycotic pneumonia, ocular lesions, osteomyelitis, skin lesions (RARELY SUBCLINICAL) Cytology Itraconazole (~6 months), amphotericin may be necessary, NSAIDS or steroids early 75% - worse if severe lung dz, CNS (poor to fair)

What pathogen has been associated with endemic outbreaks of cutaneous and disseminated disease in Rio Di Jenero? The agent is potential zoonotic

Sporothrix schenckii Tends to be associated with cutaneous lesions and occasional respiratory involvement in about 40-50% of cases (predominantly upper airway) Treatment is via oral azoles; most cases responsive itraconazole or sodium iodide, +/- terbinafine

pyoderma most common etiologic agent in dogs? cats? treatment?

Staph pseudintermedius in dogs as primary skin disease, or secondary (fleas, food, seasonal allergies) Can also have secondary E. coli, Proteus, and Pseudomonas infections Cats only have secondary infection Systemic and topical antimicrobials. Treat underlying cause tx- clavamox, cephalosporines (first gen, save third gen for if have more serious infections, macrolides and licosamides, TMS effective as well

MOA of using steroids for infectious disease?

Steroid-receptor complex --> inactivate pro-inflammatory transcription factors and increase production of proteins that inhibit cytokine production (decreasing half life of mRNA for inflammatory cytokines) Induce lipocortin-1 --> inhibits PLA2 --> reduce production of PG, leukotrienes and eicosanoids physiologic doses- shift in cytokine production from pro to anti-inflammatory pattern Pharmacologic doses are immunosuppressive and inhibit cellular and humoral responses (Decrease phagocytic and oxidative functions of phagocytic cells in a dose dependent manner -->compromise clearance of organisms)

clinical signs of hepatozoon americanum infection?

Stiff painful gait, lameness, ataxia, weakness, muscle atrophy, mucopurulent ocular discharge Uveitis, retinal scarring, hyperpigmentation, papilledema possible

feline panc tx?

Supportive care with IVF, antiemetic, pain control, prokinetic, nutritional support Supplement with pancreatic enzymes if postprandial pain is detected Feeding tube (esophageal or PEG) should be considered if 3-4 days of inappetence Jejunostomy feeding tubes if persistent gastroduodenal ileus and drug-resistance vomiting - avoid pancreatic stimulation associated with gastric feeding Severe cases: Colloid therapy - FFP and hetastarch; Vasopressors (Dopamine may increase pancreatic blood flow and reduce microvascular permeability Epinephrine, norepinephrine and vasopressin) Surgical rarely indicated only if progressive hyperbilirubinemia secondary to an obstructive jaundice from EHBO- Cholecystoduodenostomy and cholecystojejunostomy - multiple complications including cholangiohepatitis, stricture of the stoma, recurrence of EHBO, EPI and chronic vomiting; Choledochal stenting uses a red rubber catheter Antibiotics Bacterial infections common with cholangitis/cholangiohepatitis: E choli Clavamox, amoxicillin, clindamycin ticarcillin Corticosteroids Beneficial if concurrent IBD or sterile cholangiohepatitis; Associated with significant adverse effects: insulin antagonist and unmasking or worsening DM, immunosuppression, development of infection and thromboembolism; Used in chronic pancreatitis Antithrombotic: Low-molecular weight heparin (dalteparin, enoxaparin) Morphine should be avoided due to concern for spasm of pancreatic duct

diagnose EPI?

TLI: spieces and pancreas specific, high sensitivity and specificity for EPI cTLI strong < 2.5 ug/L, gray zone: 2.5 - 5 ug/L g (unless GSD, then positive), normal > 5.7 Vary from normal to abnormal depending on the degree of pancreatic tissue loss Canine fecal elastate: species and pancreas specific, high sensitivity but low specificity Great than 20 ug/g is valuable for excluding EPI in dogs with chronic diarrhea treatment- enzyme replacement therapy (Raw pig's pancreas should be avoided in areas endemic with Aujeszky's disease -> can cause psuedorabies)- non enteric coated can cause gingival bleeding, enteric coated enzymes available as well antibiotics initially (tylosin, metro), cobalamin supp (SIBO causes low cob) prognosis- lifelong treatment but generally favorable long term prognosis if positive response to treatment (weight gain)

lyme and C6 quantification?

Tests for invariable region of OspC (VisE) molecule on spirochete anti-C6 antibody response is highly specific for B. burgdorferi and is more sensitive than whole-cell tests in early infection, detecting antibodies as early as 3 weeks post exposure Dogs with leptospirosis, Rocky Mountain spotted fever, babesiosis, ehrlichiosis, and heartworm disease do not have antibodies to C6, not affected by Lyme vaccines, also C6 levels seem to correlate with bacterial loads

tetanus neurotoxins?

Tetanolepsin - hemolysis of erythrocytes in vitro but is not considered clinically significant. tetanospasmin enters wound site -> to axons of the nearest motor nerves at endplate and migrates by retrograde transport within motor axons to the neuronal cell body in the spinal cord or brain stem (can also can be transported in the bloodstream from the area of the wound to nerves at distant sites), Tetanospasmin blocks inhibitory transmission to motor neurons (inhibits glycine and GABA release - inhibits the inhibitor NT)- binding of tetanospasmin to presynaptic sites of inhibitory neurons is irreversible; recovery depends on sprouting of new axon terminals

what is the most common bloodwork abnormality with neorickettsia helminthoeca? most common clinical sign?

Thrombocytopenia Fever, depression, weight loss, vomiting, diarrhea, lymphadenopathy Diagnosis: Cytologic visualization in LN, tissue Documentation of flukes in stool (nanophyetus salmincola)

time dependent antimicrobials?

Time where antimicrobial concentration exceeding MIC (T>MIC) determines efficacy Penicillins, cephalozporins, most macrolides and lincosamides, tetracyclines, chloramphenicol, and potentiated sulfonamides Unknown how much over MIC or percentage of dosing interval that should be above MIC. Typically exceed by 1-5X for 40-100% of interval Want closer to 100% for bacteriostatic antimicrobials, or immunosuppressed patients More frequent dosing or CRIs may be necessary Cefovecin maintains above target MIC for 7 days due to high degree of protein binding Sequestered infections may require higher plasma concentrations (may also need to use AUC:MIC or Cmax:MIC)

actions of tetanus toxins?

Toxin actions: inhibits release of glycine and gamma-aminobutyric acid (GABA) NTs of inhibitory neurons of the brain and spinal cord affinity for gangliosides in the gray matter of the CNS, which may explain the cerebral signs that appear in some cases without obvious spinal cord involvement affinity for binding at the neuromuscular junction, which can induce direct neuromuscular facilitation before the migration of toxin to the CNS. may affect sympathetic preganglionic neurons in a manner similar to that in the lower motor neurons in the spinal cord and cause signs of autonomic dysfunction can be local reaction at first

parasites causing a cough?

Toxocara in puppies and kittens (pulmonary migration) Aelurostrongylus abstrusus in cats Oslerus osleri (tracheal nodular worm) in dogs regurgitation? spirocirca lupi in esophagus

African Trypanosomiasis

Trypanosoma brucei and congolense transmitted by tsetse fly, dogs may be infected by eating fresh meat relapsing fever, anemia, emaciation, anasarca, conjuntivitis, keratitis, neuro signs, death (if not treated in 1-3mo) regenerative anemia, leukopenia, thrombocytopenia dx- IFA, seen in blood smear is best, ELISA treat- diminazine (most effective), difluoromethylornithine, ethidium, isometamidium, and quinapyramin

Chagas disease organism? geographic distribution?

Trypanosoma cruzi Southeastern texas, southern states, virginia south america, central america triatomene bug is vector

steroids and CNS infection?

Tx of bacterial organisms can result in lysis and release of inflammatory cell wall components (lipopolysaccharides and outer membrane vesicles) CSF Pleocytosis and elevated protein + consistent MRI --> abx and anti-inflammatory (pred 0.5 mg/kg BID) while waiting for bacterial culture or PCR for viral or protozoal (get CSF tap prior to therapy)

what hypersensitivity is most commonly associated with vaccine reactions?

Type 1 most common Dose-dependent relationship between number of vaccinations given at one time and likelihood of hypersensitivity reactions (Limit number of vaccines given at same time, especially in small dogs) Increased risk in dachshunds, pugs, miniature pinschers, Boston terriers, Chihuahuas, boxers, weimaraners (genetic predisposition to rapid mast cell degranulation) Clinical signs - periorbital edema, wheals, urticaria, pruritis, hypotension, vomiting, diarrhea, resp distress Treat with H1 blockers and glucocorticoids (e.g. dexamethasone)

types if interferons

Type I IFN: can suppress replication and increase intracellular killing of most pathogens, including viral, bacterial, and fungal pathogens (repeated activation of innate immune system can cause generation of pathogen specific T cell reponses) IFN-α produced by all nucleated cells , in response to viral entry and replication, suppresses viral replication in the host cell and augments cellular immunity, especially natural killer cell activity and CD8 T-cell responses Type II IFN: IFN-γ, regulating both early and late immunity to bacterial and fungal pathogens Production is restricted to primarily NK cell and T lymphocytes Early: NK cells Late: CD4 and CD8 T cells Direct suppression of intracellular replication as well as induction of effective intracellular killing mechanism by macrophages and neutrophils

pathogenesis of polyarthropathy in dogs?

Type III hypersensitivity with deposition of immune-complexes deposited in tissues or free antigen can bind to membranes and react with circulating antibodies→complement is fixed→inflammatory reaction→neutrophils/platelets attracted to the area→release lysosomal/vasoactive substances→↑ in vascular permeability

FeLV diagnosis?

Usually diagnosed as screening in healthy cats ELISA - same rules apply for testing for FeLV as FIV (92-96% sensitive, 95-99% specific IFA- serum, bone marrow - less sensitive than ELISA, positive result indicates progression to marrow Do full blood work even on healthy cat to look for underlying CBC abnormalities and look for evidence of common diseases associated with FeLV Blood profile (anemia, glomerulonephritis), radiology (neoplasia), ELISA, IFA (definitive test), seroconversion after 3 negative tests 30 days apart

What do I do if atovaquone and azithromycin treatment fails in a Babesia-gibsoni-infected dog?

Usually mutations in cytochrome b genes Stop immunosuppressive drugs before retreatment Imidocarb or clinda-doxy-metro

vaccine associated adverse effects dogs: innate immune response?

Vaccine components can stimulate innate immune reponses (DNA, peptides, carbohydrate, adjuvants) Localized reactions develop within minute-hours (Inflammation, pain, erythema, swelling) Risk increases with increased antigen exposure (dose) NSAIDS prevent or mitigate these local reactions

why is vaccination controversial for FIP?

Vaccine controversial because FIP is immune mediated disease and antibody production against disease can accelerate disease as well should FIP develop after vaccinated Antibodies may bind Fc receptors on macrophages and accelerate virus uptake (antibody dependent disease enhancement) There is intranasal mutant serotype II FIP vaccine, however efficacy and ability to induce immunity against heterologous strains controversial (study shows no difference in prevalence of disease between vaccinated and non vaccinated animals between breeders)

FeLV vaccine?

Vaccine- no sterilizing immunity produced, will get regressive or may even see progressive infections, no abortive disease Recommended for all FeLV negative kittens be vaccinated, cats that enter shelters or likely to be held with other cats should be vaccinated Testing should be performed before each booster Indicated for at risk cats

infectious causes of lameness (polyarthritis, osteomyelitis, discospondylitis, polymyositis)?

Vector borne: Anaplasma phagocytophilum, B. burgdorferi, Bartonella, E. canis, E. ewingii, R. rickettsia Polymyositis in dogs: T. gondii, N, caninum, Hepatozoon canis Hepatozoon americanum carried by Amblyoma maculatum (Gulf Coast Tick): reactive signs in periosteum next to inflamed muscles characteristic Osteomyelitis: from any bacterium - inoculation w/ hematologic spread Bartonella, All systemic fungal agents (Coccidioides in Southwest is most common) Discospondylitis: Brucella canis, Staphylococcus, Streptococcus.

diagnosis of calicivirus during outbreak? what disinfectant kills calicivirus?

Virus isolation is more sensitive; PCR primers not broad enough sodium hypochlorite

presentation of PLE

Weight loss, muscle loss, diarrhea; less often vomiting and inappetence Signs of hypoproteinemia: ventral edema, ascites, chylothorax, pleural effusion Loss of antithrombin -> inc risk of thromboempolism Malabsorption of fat-soluble vitamins (A, D, E, K) Decreased absorption of divalent cations (Ca, Mg)

infectious causes of ataxia, sz, neuro stuff?

Young: distemper (can also be chronic, typically had GI or respiratory disease previously) Rabies Aerobic & anaerobic bacteria Bartonella, E. canis, and R. ricketsii cause vasculitis, diffuse meningioencephalitis Fungal: Blatomyces dermatidis, coccidioides immitis, Cryptococcus, Histoplasma capsulatum in endemic areas Protozoal: Toxoplasma gondii, Neospora caninum

feline panleukopenia infection during pregnancy?

abortion, congenital abnormalities, infertility viral destruction of perkinje cells and granule precursor cells in cerebellar external granular layer leads to cerabellar hypoplasia (permanent damage, late in opregnancy or up to 1 week old neonates this can occur) Severity of infection varies between kitten, can lose whole litter or only portion, portion that survive develop neurologic signs Hydrocephalus, porencephalopathy (cystic lesions in cerebrum), or hydraencephalopathy (completely replace cerebrum with cysts) Seizures and behavioral abnormalities can occur Infection early in pregnancy may lead to fetal death and resorption; cerebellar hypoplasia if middle third or gestation to immediately post natally infected

clinical signs of E. canis infection

acute: depression, anorexia, fever, severe loss of stamina, weight loss, ocular and nasal discharges, dyspnea, lymphadenopathy, and edema of the limbs or scrotum (resolved 1-2 weeks without treatment) subacute: Thrombocytopenia and leukopenia generally occur 10 to 20 days after infection. CNS signs can occur from bleeding chronic: bleeding tendencies, pallor due to anemia, severe weight loss, debilitation, abdominal tenderness, anterior uveitis, retinal hemorrhages, and neurologic signs consistent with meningoencephalitis

UTIs

alkaline urine - g+ cocci staph, g- rods proteus acidic urine- g+ cocci enterococcus or streptococcus canis, g- rods E. coli if uncomplicated most first line abx will treat amoxicillin (staph, strep, enterococcus, proteus, first gen cephalosporins (staph, strep, E coli, proteus, klebsiella), nitrofurantoin (E. coli, enterococci, staphylococci, Klebsiella, and Enterobacter), tetracyclines (cna develop plasmid resistance), TMS (staphylococci, streptococci, E. coli, and Proteus), fluoroquinolones (staph and G- bacteria, variable against strep and enterococcus- not for empiric use in uncomplicated UTIs) complicated UTIs, complicated UTIs, pyelonephritis w/ Gram (-) bacteria, or in intact male dogs (prostate)- fluoroquinolones

FHV1

alpha herpesvirus, dsDNA, enveloped virus in carriers- the virus persists in a latent form largely in trigeminal ganglia; reinfectious upon reactivation with stress- see shedding week 2 of stress/stay at shelter clinical signs- URI, oculonasal discharge, conjunctivitis, sneezing, hypersalivation, coughing, pneumonia, corneal ulceration (dendritic), keratitis, corneal sequestration, uveitis

vaccine associated sarcoma

aluminum adjuvent- 5x more likely in 2002 report 93% of tumors develop within 4 years of vaccine ("3-2-1" rule: mass persists longer than 3 months, is larger than 2 cm in diameter or is increasing in size 1 month after injection) not just vaccines but anything that can cause local inflammation can lead to tumorigenesis cats over other species (more susceptible to oxidative injury) histo- fibrosarcomas are 80%, intratumoral lymphoplasmacytic inflammation, giant cells, intracellular basophilic material and myofibroblastic differentiation 5% met rate by diagnosis

morulae in neutrophils?

anaplasma

diagnosis of FIP?

antemortem diagnosis is suspected Diagnose via IHC staining for CoV antigen within lesions characterized by pyogranulomatous to granulomatous vasculitis IFA, antibody testing, ELISA, virus neutralization (titers >1:1600 for CoV with clinical signs are suggestive of FIP; 94% specific; Positive antibody titers on effusion in one study had PPV of 90% and NPV of 79% - magnitude of titer did not correlate with FIP diagnosis) CBC- mild non regenerative anemia, thrombocytopenia (DIC), lymphopenia in 50% of affected cats Hyperproteinemia (hyperglobulinemi, 50% of effusive and 70% of non effusive), hypoalbuminemia due to liver involvement, urinary loss, or inflammation (negative acute phase) Polyclonal gammopathy, but monoclonal can occur Albumin:globulin usually >0.8 (sensitive but not specific) Alpha 1 acid glycoprotein exceeds 1500 ug/mL in cats with FIP, suggested for diagnosis, but can also be increased with other inflammatory diseases Effusion with alb:glob 0.5- PPV 89%, NPV 91%, viral RNA can also be amplified by RT PCR definitive diagnosis with histopath- CoV in tissue with IHC

botulism treatment?

antitoxin may prevent further toxin binding if intestinal absorption and circulation are still occurring. Most cases in dogs are type C; thus type C antitoxin should be given. 10,000 to 150,000 IU/dog IV or IM, two doses 4 hours apart antitoxin remains in circulation for 40 days after administration, no repeats antibiotics only if secondary infection (aspiration pneumonia) develops. Aminoglycosides should be avoided because they also have the potential to block neuromuscular function.

Coccidian life cycle

asexual and a sexual cycle, resulting in the production of an environmentally resistant stage,the oocyst unsporulated oocyst shed in feces, oocysts sporulate in presence of moisture/oxygen/temperature and become infective at this stage, these are ingested by animal, sporocysts and then sporozoites released in GIT (excystation) and penetrate gut cells to initiate development of asexual intracellular schizonts, schizonts produce larger numbers of merozoites that penetate other gut cells and produce further schizonts (asexual reproduction results in exponential increase in population), following asexual lifecycle, then have sexual lifecycle where male and female gametes formed that fuze to form zygote that develop into immature unsporulated oocyst that shed into feces

what is artemisia?

asian wormwood, antimalarial activity inhibition of calcium dependent ATPase and produciton of ROS after activation by iron source (like Hgb)

what is this?

aspergillus

feline babesiosis

babesia felis anorexia, weight loss, anemia, vomiting, pica, respiratory signs, increased ALT, hyperbilirubinemia tx: primaquine phosphate- 1mg/cat q36hrs x 4 treatments then 1mg PO q7days for 4 doses; doxycycline- 5mg/kg PO BID for 21 days

anthrax

bacillus anthracis local inflammation, necrosis, edma of tissue of upper GIT (whichever first comes in contact with organism) death by asphyxiation ingestion of meat from contaminated carcasses of animals that have died from anthrax tx: penicillins

zoonoses?

bartonella, echinococcus, visceral larval migrans (Toxacara canis/cati or baylisascaris), cutaneous larcal migrans (hooks), salmonella, campylobacter, cryptosporidium, toxoplasma, lepto, coxiella, brucella, yersinia, bordatella, mycobacterium tuberculosis (more often human to pet), microsporidium canis, sporotrichosis, notoedres cati, sarcoptes sacbiei var canis, cheyletiella, ctenocephalides felis/canis can bite humans immunocompromised or no spleen- cryptosporidiosis, toxoplasmosis, salmonellosis, and bartonellosis, babesia, C. canimorsus

antibiotics for septic arhritis, tenosynovitis, osteomyelitis

based on culture and susceptibility! Aggressive empiric antimicrobial therapy Wounds: variety of Gram (+) and (-) Iatrogenic: Staphylococcus (increasingly MRSP) Osteomyelitis most commonly: Staph pseudintermedius Cat fights: Pasteurella multocida and anaerobes Pseudomonas in devitalized tissue tx: MRSP/MRSA: clincamycin initially, but may induce resistance even if susceptible initially Anaerobes: clindamycin, metronidazole Aminoglycosides and fluoroquinolones good against staphylococci, excellent against Gram (-)

FIP distribution? risk factors?

bimodal distribution- 3mo-3yo (most <12mo) and then >10 yo infected, males and sexually intact cats have been predisposed, immunosuppressed cats, siblings (genetic) risk factors? new cats introduced, immunosuppression, proportion of cattary that shed FeCoV mutated corona virus (alpha coronavirus, mutations in 3c gene)- mutations can occur shortly or years after FeCoV infection FCoV spike (S) gene mutations contribute to change in virulence by enabling infection of and replication in macrophages- multiplication in macrophages without hinderance of immune system and incites pyogranulomatous vasculitis hallmark of FIP- monocyte mediated granulomatous phlebitis and systemic endothelial activation, lymphocyte depletion + clinical signs indicate an excessive + inappropriate immune response

diagnose chagas disease?

blood smear- acute disease only (buffy coat smearp concentrates organism) serology- conversion at day 21 and positive for life, cross reacts with leishmaniasis PCR- blood, plasma, lymph node aspirate, ascites (specific but not sensitive without multiple samples)

Cytauxzoon

bobcats are natural host Cats Dermacentor tick, southeast US clinical signs after 5-20 day incubation period Tissue phase (meroziotes invade mononuclear cells --> occlude vessels --> organ failure), erythrocytic phase (destruction and phagocytosis of RBC) - Infected macrophages line the lumen of veins throughout the body and merozoites released from the infected macrophages infect erythrocytes. Clinical disease results from obstruction of blood flow through tissues by mononuclear infiltrates and from hemolytic anemia Prepatent period 2-3 weeks, rapid course --> icterus, pallor), dyspnea, CNS signs --> high fatality histology (schizonts), cytology (piroplasms in RBC --> 50% sensitivity), PCR (high sensitivity & specificity) Atovaquone and azithromycin x 10d (60% survival) Tick control, keep cats inside

ddx for secondary immune disease from infectious disease causing polyarthropathy in dogs (i.e. cause type III hypersensitivity with immune complex deposition in joints)?

brucellosis, ehrlichiosis, bacterial endocarditis, otitis externa, pyometra, actinomycosis, coccidiomycosis, leishmaniasis

exocrine pancreas testing

can also see exocrine pancreatic neoplasia (very high lipases, like thousands), rare- lymphoma and pancreatic adenocarcinoma

trypanosoma clinical signs

cardiomyopathy primarily develops from parasite induced damage to myocardial cells or immune mediated reactions generalized lymphadenomegaly, pale mm, tachycardia, hepatomegaly, pulse deficits, abdo distention, anorexia, diarrhea dogs that survive acute infection- can present for evalutaion of chronic dilative cardiomyopathy; right sided cardiac disease, conduction disturbances, ventricular arrhythmias, supraventricular arrhythmias ECG findings- ventricular premature contractions, heart block, t wave inversion

most common body system affected by toxoplasmosis in cat vs dog?

cat- pulmonary (97.7%), CNS (96%), hepatic (93%(, pancreatic (84%), cardiac (86%), ocular (81%) canine - respiratory, NMJ, GI, generalized infections can occur in younger or immunocompromised animals, ocular form is uncommon in dogs

infectious causes of uveitis in cats? dogs?

cats - FeLV, FIV, FIP, Toxoplasma, Bartonella, fungal organisms dogs- systemic fungal agents (Blastomyces, Coccidioides, Cryptococcus, Histoplasma), toxoplasma, vasculitis agents (Bartonella, E. canis, R. rickettsia) any chronic infection can cause immune complex deposition to choroid

poxvirus infection

cats susceptible to cowpox reservoir hosts are small wild mammals such as voles and woodmice rural cats that hunt rodents, and most cases are seen in summer and autumn when opportunities for contact with the reservoir hosts are highest. Cat-to-cat transmission rare and causes subclinical infection dx: virus culture, EM, PCR, serology, histopath (intracytoplasmic, eosinophilic inclusion bodies)

mycobacterium avium and cats

cats>dogs siamese and basset hound more susceptible present in acidic soil high in organic matter (acidic swamps, coastal plains, brackish coastal waters) organisms remain viable in environment for 2 years birds shed large numbers or organisms and infeciton occurs from eating meat or contact with infected soil contaminated with poultry carcas or feces disseminated disease in dogs and cats is reported tx: rifampin, enrofloxacin, and clarithromycin

autoimmune disease and vaccines?

cause and effect in IMHA and ITP not established in dogs and retrospective studies have conflicting results dont vaccinate dogs with IMHA or ITP until in remission and immunsuppressive drugs reduced below immunosuppressive levels

hypertrophic osteodystrophy and vaccines?

cause and effect unclear, disease most common in young animals and association may be coincidental

what is most important host defense mechanism in B. canis infection?

cell mediated immunity- Persistent, nonprotective antibodies are characteristic of such infections; they appear to have little influence on the level of bacteremia or the number of organisms in tissues but cause hyperglobulinemia Dogs can recover spontaneously and have low or negative antibodies and yet are immune to reinfection, which also suggests that protective immunity is cell mediated

Giardia treatment?

challenging to treat albendazole, febantel, fenbendazole, furazolidone, ipronidazole, metro, ronidazole, tinidazole, etc. If spore forming rods present (clostridium) then choose metrodniazole (Cats chose metronidazole benzoate over USP) Save ronidazole for Tritrich Eosinophilia present: consider fenbednazole for 5 days Fiber in diet may help by inhibiting organism attachement to microvilli Bath dog on last day of treatment Controversial if we should treat asymptomatic dogs who test positive, test for cysts, not fecal antigen test

diagnosis of neospora caninum? tx?

chemistry- increased LEs +/- CK CSF- increased protein, mixed pleocytosis +/- tachyzoites IFA- >1:50 indicates exposure, >1:800 in clinical patients typically tissue bx- tachyzoites or bradyzoites (light microscopy w/IHC or PCF to distinguish vs. T gondii) grave prognosis tx- no drug will eliminate tissue infection, goal to reduce disease progression with either TMS + pyrimethamine; sequential tx w/clinda, TMS, pyrimethamine; clinda alone

EPI in dogs

clinical signs do not occur until 90% of secretory capacity lost 1-5 yo, but can be older animals pancreatic acinar atrophy- most common reason (GSD, rough coated collies, eurasians)- autoimmune atrophic lymphocytic pancreatitis leads to total destruction, endocrine pancreas is not affected; subclinical - marked lymphoplasmocytic inflammation with cytotoxic T cells; clinical- pancreas thin and transparent with no increase of fibrotic tissue chronic pancreatitis- most common cause in cats and people, progressive destruction of exocrine and endocrine pancreas due to fibrosis rarely can be associated with pancreatic neoplasia

how does lepto make its way into body?

close contact through urine, venereal routes, placental transfer, bites, or ingestion of infected tissues as the organism penetrates mucosa or broken skin recovered animals can excrete organisms intermittently for months to 4 years after infection- must eliminate the renal carrier state! optimum survival conditions- neutral to slightly alkaline pH, dilute urine iodophor disinfectants work

FeLV transmission?

close contact with saliva- grooming, licking, sharing food/water dish, biting, milk, +/- fleas, blood transfusions Once infection of epithelial cells in salivary glands occu, virus shed in massive quantities in saliva, low quantities in urine and feces easily killed with disinfectants outside of host Infection rate declined in past 20 years with extensive testing and vaccination: Current prevalence 1-6%, used to be 30% of cats, Prevalence reduced from 30% in 90s to 7% in 2006 at risk cats? access to outdoors, have close contact with other cats, intact, male, aggressive, coinfected with FIV are more at risk of FeLV infection, older cats likely (median age 3 yo)

gram positive bacteria?

cocci- staph, strep, enterococcus bacilli- clostridium, cornybacterium, listeria, bacillus, nocardia,

what is this?

coccidiodes immitis

zoonotic protozoal diseases?

cryptosporidium, giardia, E. histolytica, B. coli, T. gondii

treatment for cryptosporidium? cystoisospora?

cryptosporidium- paromomycin, tylosin, azithromycin - no treatment eliminates oocyst shedding cystoisospora- TMS, sulfadimethxine, furazolidone, amprolium. no drug eliminates infection

what is this?

cytauxzoon felis

RMSF

dermacenter, rhipicephalus, amblyomma, haemaphysalis R felis- transmitted by fleas R rickettsii- most pathogenic Rickettsia-induced endothelial cell damage results in vasculitis, altered vascular permeability, edema, and necrosis Antiplatelet antibodies were detected in the sera of dogs with naturally occurring and experimentally induced Rickettsia rickettsii and Ehrlichia canis infections

IBD diagnosis?

diagnosis of exclusion CBC, chem, UA, fecal, TLI, PLI, ACTH stim vs basal cortisol, folate, cobalamin, T4, FeLV/FIV, AUS Unremarkable testing → diet trial 1st → antimicrobial trial 2nd → steroid trial 3rd Failure to response to empiric tx → endoscopy + bx (prior to steroid trial) Subnormal serum cobalamin or hypoalbuminemia → endoscopy + bx 1st New tests: C-reactive protein high- dogs w/ mod to severe IBD but not specific to GIT), Perinuclear antineutrophilic cytoplasmic Abs (pANCAs) (serologic marker in humans), Calprotectin (serum & fecal) currently being evaluated in dogs (increases seen in human IBD), Genetic testing for TLR mutations

Rivalta test?

differentiates exudate from transudate- drop of 98% glacial acetic acid mixed with 7-8mL distilled water in transparent tube and drop of effusion added to tube, if keeps shape then FIP if dissipates into solution then not FIP - PPV 58%, NPV 93%, PPV is higher in younger cats bc diseases like lymphoma or bacterial peritonitis is less common (can also cause positive rivalta test)

histoplasmosis?

dimorphic fungus, small organisms 2-4um Mississippi, Missouri, Tennessee, and Ohio RIver Valleys Found in intestinal tracts of guano bats (primary reservoir) Cats more susceptible than dogs, younger animals- dx- normocytic-normochromic nonregenerative anemia is the most common CBC abnormality, hypoalbuminemia, histo urine antigen, also cytology; In the cat, BM, LN, TTW, BAL most likely to yield organisms. In the dog, rectal scrapings BM, liver, LN, spleen, TTW, BAL most likely to yield organisms tx- itraconazole, amphotericin B prognosis- good for pulmonary, poor for GI/disseminated

sporotrichosis

dimorphic saprophytic fungus; yeast is pleomorphic round, oval, or cigar-shaped cells that measure 2 by 3 μm to 3 by 10 μm and is fairly characteristic = dx on cytology sporothrix schenckii cats>dogs- dogs get cutaneous disease and cats usually systemic

poxvirus pathogenesis

disease typically starts with a single primary lesion, generally on the head, neck, or forelimb, which may be ulcerated or scabbed and can become secondarily infected -> widespread secondary skin lesions also develop after 1 to 3 weeks as randomly distributed, small epidermal nodules that increase in size over a few days to well-circumscribed ulcers about 1 cm diameter. These gradually become scabbed and heal over a period of 4 to 5 weeks, and most animals recover uneventfully

clinical signs of disseminated prototheca? cutaneous?

disseminated- weight loss, large bowel diarrhea (hematochezia), CNS dz, uveitis; neurologic disease, blindness, and less frequently, polyuria and polydipsia- colon is likely primary site of infection and then algea disseminates cutaneous- draiing ulcers and crusts of trunk, extremeties, mucous memnbranes- dog; nodules on limbs, feet, head of cats

what is acid fast bacteria?

distinctive property of retaining hot carbolfuchsin and other stains after subsequent treatment with acid or alcohol, a property that facilitates diagnosis. This acid-alcohol fastness is due to the high lipid content of mycolic acid in the cell wall

disseminated toxoplasmosis in cats?

documented in cats concurrently infected with feline leukemia virus (FeLV), feline immunodeficiency virus (FIV), feline infectious peritonitis (FIP) virus, and after renal transplantation Transplacentally or lactationally infected kittens develop the most severe signs of extraintestinal toxoplasmosis and generally die of pulmonary or hepatic disease.

pythiosis dog? cat?

dog- young, large breed dogs, invasive masses containing ulcerated nodules, draining tracts (involving extremeties, tail head, ventral neck, perineum), GI transmural thickening of stomach, SI, colon, rectum +/- esophagus or pharyngeal region, mesenteric lymphadenomegaly (duod, ILC most often affected) cats- nasopharyngeal wounds and invasive masses contain ulcereated nodules, draining tracts, most often on extremeties, tail head, ventral neck, perineum; eosinophilia, anemia, hyperglob

diagnostics for lyme? tx?

dogs vaccinated have positive ELISA and IFA for months after vaccine, have high IgM levels for months so does not indicate active infection Experimentally infected dogs have ELISA-positive results by 4 to 6 weeks after exposure. Titers were at their highest levels by 3 months after exposure. Titer increases almost always precede clinical lameness and fever in experimentally infected dogs,45 therefore a negative titer in an animal with clinical signs rules out Lyme disease with a high probability dx: positive serology, clinical signs and response to treatment (lyme C6 quant); culture is most specific test but not sensitive and requires special medium (Barbour-Stoenner-Kelley), culture skin near site of attachment ; PCR highly specific (on skin near site of bite or joint affected) Determination of IgM titeres independent of IgG titers is not needed because Dogs are not ill until after serocvonersion to IgG and IgM peaks can reoccur in carriers OsPA, OspC, and OspE; OspA is not seen commonly after natural exposure tx: doxycycline 4 weeks, may need longer treatment for nephritis; can also use cephalosporines (3rd), ampi/amoxi, erythromycin; chronic infection? 30 day antibiotic courses for 4-5 times in 3 month intervals, can be curative Monitor C6Quant( more than 30 confirms exposure, 50% decline or more may indicated decreased antigenic load and possible clearance)- may need immunosuppressive + proteinuria therapy for nephritis Antibody prevalence in dogs in endemic areas correlates with living in forested and urban areas and time spent outdoors

clinical signs of histoplasmosis in dogs? cats?

dogs- <4 yo, male >females typically; pointers, weimeraners, brittany spaniels overrepresented; GI signs (large bowel diarrhea early in dz and small bowel late in diease), fever, anorexia, weight loss (severe), depression, +/- organomegaly, pulmonary <50% cats- <4yo, depression, anorexia, fever, pale mm, weight loss, lungs affected, hepatosplenomegaly, lymphadenomegaly, ocular signs, osteomyelitis/bone lesions

treatment for RMSF?

doxycycline 2 weeks, can also use fluoroquinolones Defervescence should be anticipated within 24 hours after the initiation of antibiotics (decrease in temp) immunity is likely permanent if survive After infection with R. rickettsii, the duration of rickettsemia is brief, approximately 5 to 14 days. Therefore infected dogs do not play an important reservoir role and pose a minimal zoonotic threat to humans

canine colitis

dx: fecal, rectal cytology, fecal culture, ultrasound, colonoscopy with biopsy considered IBD- lymphoplasmocytic enteritis most common has been associated with increased CD3+ T cells, IgA, IgG, plasma cells, upregulation of TNFa and IL2 treatment? fenbendazole or metronidazole first, diet triel (novel protein, hydrolyzed protien, highly digestible), +/- psyllium husk diet fails- add tylosin (5mg/kg PO SID), can try sulfasalazine (immune side effects), immunosuppressants as needed

Feline upper respiratory tract disease?

eline herpesvirus 1 (+/- conjunctivitis or keratitis), feline calicivirus (+/- stomatitis), Bordetella bronchiseptica can be primary pathogen in cats Chlamydia felis associated w/ conjunctivitis in cattery cats Mycoplasma normal commensal, but can be associated w/ rhinitis, conjunctivitis, bronchitis, pneumonia Molecular diagnostics have poor positive predictive value Cryptococcus, Sporothrix, Aspergillus, Cuterebra are possible

FIV virus type etc?

enveloped RNA virus, t lymphotropic Lentevirus genus of Retroviridae; Virion core proteins- capsid p24, nucleocapsid, and matrix Surface virion glycoprotein gp120 Transmembrane virion envelope glycoprotein gp41 Three layered structure- inner most genome nucleocapsid complex with helical symmetry, icosahedral capsid, and envelop with glycoprotein spikes Three major genes: gag, (encodes virion core proteins), pol (encodes reverse transcriptase, protease, and integrase enzymes), env (encodes surface and transmembrane virion envelope glycoproteins) establishes chronic, persistent infection that culminates in immunodeficiency FIV invades cells via primary CD134 receptor expressed on feline T cells (CD4+), B cells, activated macrophages and have secondary receptor CXCR4 that is a chemokine receptor

pythiosis diagnosis?

eosinophilic pyogranulomatous inflammation, stains with GMS- broad rarely septate branching stuctures inflammation in GI pythiosis centers on the submucosal and muscular layers and can be missed with endoscopy ELISA (antibodies are highly sensitive and specific) treatment- surgery is treatment of choice, itraconazole and terbinafine recommended for 2-3 months after surgery monitoring- ELISA antibodies should be gone in 3 mo if surgery and meds success

recommended treatment for campylobacter?

erythromycin or azithromycin and recommended if treatment is necessary

cryptococcus treatement?

feline- fluconazole fluconazole, amphotericin B - canine +/- flucytosine if CSF involvement (not cats) treatment should be continued until the Ag Latex Agglut is negative or for at least 2 tests 1 month apart Animals with 32 fold decrease in Ag titer can have tx d/c and monitored

RMSF clinical signs?

fever, anorexia, depression, mucopurulent ocular discharge, scleral injection, tachypnea, coughing, vomiting, diarrhea, muscle pain, neutrophilic polyarthritis, and a diverse group of neurologic signs including hyperesthesia, ataxia, vestibular signs, stupor, seizures, and coma, retinal hemorrhage (may be absent in early disease), Epistaxis, melena, hematuria, and petechial-to-ecchymotic hemorrhages occur in some dogs Scrotal edema, hyperemia, hemorrhage, and epididymal pain are frequently observed in male dogs

diagnosis of botulism?

find toxin in feces, serum, vomit, or on food ingested identify toxin with neutralization test in mice, serum or extract is injected alone and in combination with specific antitoxin into peritoneal cavity of mice, mice observed for clinical signs of botulism (Survival of one group protected with one type of antitoxin and death of the other groups with signs consistent with botulism confirm the presence of botulinal toxin)

leishmania pathogenesis?

flagellated promastigote in sandfly --> injected into vertebrate host, promastigotes engulfed by macrophages and disseminated throughout body and incubation pd of 1 month to 7 years possible --> non flagellated amastigote in mammal (macrophages) --> dissemination and cutaneous lesions form intracellular organism induces extreme immune responses; polyclonal gammopathies (and occasionally monoclonal), proliferation of mononuclear cells in lymphoreticular organs and immune complex formation resulting in GN and PA

giardia and cryptosporidium mechanism of disease?

found on surface of enterocytes- production of toxins, disruption of normal flora, induction of inflammatory bowel disease (IBD), inhibition of normal enterocyte enzymatic function. blunting of microvilli, induction of motility disorders

Phaeohyphomycoses?

fungi that produce hyphae that have thick walls, vary in diameter, have yeast-like swellings, and are pigmented Localized lesions, such as subcutaneous nodules and abscesses, ulcerations, and/or draining tracts, often occur on the face and paws and frequently migrate to regional lymph nodes most common Dissemination is uncommon species- Alternaria alternata, Bipolaris, (Drechslera) spicifera, Brachycladium speciferum, Cladosporium (Cladophialphora, Xylohypha) bantiana, Exophiala jeanselmei, Fonsecaea pedrosoi, Moniliella suaveolens, Phialemonium obovatum, Phialophora verrucosa, Pseudomicrodochium suttonii, Scolecobasidium humicola, Stemphyllium spp., Cladosporium trichoides, Curvularia geniculatu, Curvularia lunata, Exophiala spinifer, Ochoroconis (Dactyylaria) gallopavum, Ramichloridium spp.

mycobacterium tuberculosis in dogs

get from humans aerosolized droplets primary means of transmission clinical signs- bronchopneumonia, pulmonary nodule formation, and hilar lymphadenopathy are seen, causing fever, weight loss, anorexia, and harsh, nonproductive coughing dx: culture- % Ogawa egg yolk media- can identidy specific species involved (fast growing takes 3-5 days, slow growing can take 4-6 weeks) tx: fluoroquinolones pending dx, if systemic or regional spread- initial phase for 2 months (rifampin, enro, azithro), continuation phase or rifampin plus either baytril or azithro (if resistance develops- rifampin, isoniazid, ethambutol [or can use pyrazinamide or dihydrostreptomycin)

feline bartonellosis

gram negative bacteria, fastidious cat fleas- intradermal exposure of flea feces, ticks may also have role as well as other arthropods Intracellular bacteria; detected within erythrocytes and endothelial cells dependent on species Cats (reservoir host): Cat scratch disease (henselae), endocarditis (koehlerae) most infections are subclinical Non-specific: fever, lethargy Lymphadenopathy, uveitis, endocarditis, stomatitis/gingivitis, reproductive failure Bacteremia is prolonged and systemic inflammation is documented in infected cats Blood of febrile cats have a higher prevalence than that of blood in afebrile cats coinfection with mycoplasia, rickettsials, FeLV, FIV Histopath changes: myocarditis, cholangitis, nephritis tx: Long Term Abx admin; Doxycycline and enrofloxacin-mixed efficacy, Rifampin and doxycycline, azithromycin-NO SET GOLD STANDARD Concern for resistance

lepto? pathogenesis?

gram negative spirochete, leptospira interrogans sensu lata Reservoir host = vole, raccoon (grippotyphosa); rat (icterohaemorrhagiae + bratislava) Incidental hosts = humans, dogs (urinary excretion) Optimal organism survival- wet, warm environment with stagnant water Direct or indirect transmission - water, soil, food, bedding Dogs in regions of midwestern US at higher risk for lepto if they live in urban areas (despite previous believe that working/outdoor dogs carried a greater risk) Feline lepto is rare, but they can be experimentally infected with the organism, seroconvert, and shed leptospires in their urine- not clinical typically

brucellosis info

gram negative, aerobic, coccobacilla B. canis is most likely but dogs also are susceptible to infection with Brucella abortus and Brucella suis from ingestion of contaminated placentas and aborted fetuses from livestock Shedding of B. canis may occur for up to 6 weeks after an abortion

helicobacter

gram negative, microaerophilic spiral bacteria urease enzyme -> ammonia production, increased pH microenvironment allows bacteria to colonize acidic environment pathogenesis of ulcers related to host cytokine response to bacteria (genetic)- gastric ulceration rare dx: brush cytology- spiral bacteria, rapid urease test (detects bacterial ureases) tx: Triple therapy: metronidazole, amoxicillin, bismuth subsalicylate, +/- omeprazole (quadruple therapy) - resistance has been detected to metro, clarithromycin, amoxi improved clinical signs of vomiting after treatment for helicobacter

what are the two canine influenzas? what type of virus is influenza?

h3n8 (horse) h3n2 (avian) orthomyxoviridae, ssRNA, segmented

brucella canis treatement?

hard because inside of leukocytes and can relapse after abx stop, bacteremia can recur days to months after treatment stops shedding less likely in neutered animals infected males rarely recover and become sterile combination therapy with tetracyclines and aminoglycosides - best known regimen minocycline plus dihydrostreptomycin (cant get dihydrostreptomycin anymore, substitute gentamicin)- gentamicin (5 mg/kg subcutaneously every 24 hours for 7 days) administered twice in the first and fourth week and minocycline (25 mg/kg orally every 24 hours) for 4 weeks. Prevention is accomplished by quarantine of all new acquisitions until two antibody test results at l-month intervals are negative

FIP treatment?

historically- pred, supportive care and goal to improve QOL negative prognostic indicators- hyperbilirubinemia, effusion, lymphopenia effusive form is worse than non effusive, tends to have shitty prognosis, euthanasia within days to months of diagnosis Inhibition of FIPV replication- ribavirin, human interferon-a, feline interferon-omega, adenine arabinoside, amphotericin B, cyclosporine (potentially worsen FIP due to potent T lymphocyte inhibition) Potential tx - siRNA target different regions of the coronavirus to inhibit replication Immunomodulatory therapy - aspirin, prednisolone, dexamethasone, chlorambucil, administration of GC in to pleural or peritoneal cavities Antibiotics - doxycycline and azithromycin may have immune modulation effects Other drugs: pentoxifylline/propentofylline, ozagrel hydrochloride, thromboxane A2 synthase inhibitor, polyprenyl immunostimulant (inc Th-1 cytokines to aid in viral destruction), anabolic ateroids (stanozolol), ascorbic acid

bartonella pathogenesis?

immediate access to erythrocytes- can infect dendritic cells, microglial cells, monocytes, macrophages invasion mediated by adhesins (adhesion to extracellular matrix) and type IV secretion system (transporting DNA and effector proteins to target host cell) - BadA (bartonella adhesin A, adherence to endothelial cells and ECM proteins); VirB/VirD T4SS- inhibition of host cell apoptosis, bacterial persistence in erythrocytes and endothelial sprouting sustained suppression of peripheral blood CD8+ lymphocytes, accompanied by an altered cell surface phenotype and an increase in CD4+ lymphocytes in the peripheral lymph nodes erythrocyte infection waves in 5 day intervals primary niche outside of circulating blood

vaccine associated autoantibodies

immune response to virus in vaccine and also any remnants of cell line used to propogate virus

prognosis hepatozoon americanum?

improved response to treatment when implemented early in disease course guarded prognosis when presenting with chronic illness prior to tx

Trypanosomiasis pathogenesis

infected kissing bugs defecate during feeding -> epimastigotes enter the vertebrate host -> epimastigotes engulfed by macrophages and myocytes -> transform into amastigotes -> amastigotes divide by binary fission -> host cell ruptures, releasing trypomastigotes into circulation -> vector is then infected by ingesting trypomastigotes transmission: bitten by vector, ingetion of vector, blood transfusions, ingestion of infected tissue or milk, transplacentally

Hyalohyphomycosis

infections caused by nondematiaceous fungi (nonpigmented fungi), or fungi whose hyphae appear to have transparent (hyaline) walls in tissues rare disease- Focal infections are most often seen in the nose, cornea, and skin Disseminated disease may affect the lungs, lymph nodes, kidneys, liver, spleen, bones, bone marrow, and CNS Diagnosis: cytology and culture (common environmental contaminants) species- Acremonium (Cephalosporium) spp., Chrysosporium spp., Fusarium spp., Geotrichum spp., Paecilomyces spp., Paecilomycosis spp., Pseudallescheria (Allescheria, Petriellidium) boydii, Scedosporium spp.

pathogenesis of histoplasmosis

inhalation or ingestion -> conidia transform from the mycelial phase to the yeast phase -> phagocytized by macs -> grow as facultative intracellular organisms. -> hematogenous and lymphatic dissemination results in multisystemic disease lungs, GI system, lymph nodes, liver, spleen, bone marrow, eyes, and adrenal glands are common organs affected in dogs (incubation pd 12-16 days) lungs, liver, lymph nodes, eyes, and bone marrow are most commonly affected in cats.

vasculitis and vaccinations?

ischemic dermatopathy reported with rabies vaccine (months acter vx, poodles most commondly affected (possible genetic component) tx- pentoxifylline

Canine infectious respiratory disease complex?

kennel cough, canine infectious tracheobronchitis Viral: Canine adenovirus type 2, distemper virus, respiratory coronavirus, herpesvirus, canine influenza virus, canine parainfluenza virus Bacterial coinfections can occyr: Bacterial co-infections can contribute to severity: Mycoplasma, Bordetella, Streptococcus dx: Most cases are self limiting, look for cause if signs persist >7-10 days, or signs of secondary bacterial pneumonia - difficult to interpret test results because pathogens can be present in healthy animals; PCR is best in first 1-3 days of illness, or exposed dogs before signs develop

bunyaviridae?

kittens and puppies hentavirus, ssRNA aedes mosquito common vector hepatic and myocardial necrosis, meningitis, diffuse petechial hemorrhage and death no tx

cryptococcus pathogenesis/pathophys

large capsule surrounding the cryptococcal organism contributes to pathogenicity by inhibiting phagocytosis, plasma cell function, leukocyte migration CMI most important bc antibodies non protective Inhalation of dessicated,small yeast into alveoli -> dissemination by local extension to CNS or hematogenous -> skin, eyes, and CNS are most commonly affected

feline CoV?

large enveloped ssRNA virus, coronavirus canine CoV can infect cats as well type I (worldwide) and II (recombination of canine and feline enteric CoV) oral fecal route of exposure- replication of low pathogenicity strains in epithelial cells in tips of intestinal villi

babesia treatment?

large form- imidocarb diproprionate, diminizene aceturate smaller forms- atovaquone and azithromycin

cordylobia athropophaga

larvae of tumbu or mango fly (cordylobia anthropophaga) produce myiasis adult fly deposits the eggs on skin that usually is soiled with urine or feces -> 2 days the larvae hatch and penetrate the skin to form a furuncular lesion with a small central opening Tx: removal, cover hole with petroleum jelly, wound care

bloodwork changes for feline panleukopenia infection?

leukopenia (65% of cats), anemia, thrombocytopenia, hypoalbuminemia +/- hypoglobulinemia, electrolyte abnormalities (low or high Na, K, acid/base) diagnose? canine parvo fecal antigen 5080% sensitivr, 94-100% specific, EM on feces, PCR on tissue or feces, histopath (crypt necrosis in GIT with intranuclear inclusions, FPV antigen via IHC or IFA) tx? supportive care

FIV and immune dysfunction

loss of ability of lymphocytes to proliferate in response to stimulation perturbation of cytokine production Cell-mediated immunity is more profoundly affected than humoral immunity as no changes in number or proportions of B cells occur after FIV infection thus chronic inflammatory conditions, neoplasia, and infections with intracellular organisms are more common than infections controlled by antibodies. FIV-infected cats respond adequately to vaccinations and frequently develop a polyclonal hypergammaglobulinemia characteristic of nonspecific stimulation of humoral immunity

Borrelia burgdorferi

lyme disease unicellular microaerophillic, gram negative motile spirochete, can survive freezing and storage ixodes tick transmission (requires >48 hours on dog- organisms multiple cross gut epithelium of tick then into hemolymph then salivary glands to infect host), most common form is subclinical asymptomatic carrier immune response to specific antigens include flagellin (nervous tissue inflammation in humans)

astrovirus?

mild diarrhea in kittens that has been described as persistant (4-14 days) watery diarrhea, may be accompanied by vomiting, pyrexia, depression

feline GI lymphoma

most frequently diagnosed feline cancer, GI is most commomn site of lymphoma +/- associated with FeLV (incidence 0-38%, cats with GI LSA tend to be older and FeLV and FIV neg) median age 9-13 years grades: SCLSA- low grade; intermediate; large cell- high grade, immunoblastic, lymphoblastic low grade tends be associated with T cell, some studies dont show survival diff between B and T cells clinical signs- weight loss, anorexia, vomiting, diarrhea, PU/PD, hypoalb/hypocob

clinical signs with leptospirosis?

most severe with non host adapted serovars acute, chronic, acute on chronic kidney disease (acute interstitial nephritis, renal swelling, vasculitis with decreased renal perfusion and GFR)- persists in renal tubular epithelial cells, causing shedding from the kidneys for months to years after clinical recovery PU/PD- can be only clinical sign and may not be azotemic, due to decreased GFR leadign to loss of renal concentrating ability or may be an NDI acute liver injury- marked ALT and ALP increases, minimal histo changes- cholestasis of sepsis most likely; CAH and hepatic fibrosis has been demostrated as sequella to grippotyphosa infection vasculitis, thrombocytopenia, pulmonary hemorrhage (lepto lungs- caudodorsal interstitial pattern, likely due to hemorrhage secondary to endothelial damage and vasculitis), uveitis coag abnormalities- lepto LPS stimulates neutrophil adherence and plt activation, can lead to DIC young dogs more affected than older dogs and develop hepatic dysfunction with any outbreak

FIV transmission?

mostly by bite wounds, virus shed in high concentration in saliva Seropositive cats associated with: History of bite wounds, older, male sex (4.7x more likely sero+ than females), illness, outdoor access Mean age of diagnosis 6-8 years old, 90% >2yo 1-12% prevalence, higher in feral and free range cats, higher in sick cats; 2.5% in one 18k cat study; 18.2% prevalence in sick feral cats and 0.7% in healthy indoor cats Occasionally coinfection with FeLV occurs Transplacental transmission can occur and only some kittens may be infected (highest transmission rate when queens that have less than 200 CD4+ cells, those with signs of immunodeficiency, and those infected within past 15 months), Leads to arrested fetal development, abortion, stillbirth, low birth weights, T cell deficient kittens

treatment for vaccine associated sarcomas?

multimodal surgery (30-70% recurrence rate), wide margins (3-5cm) and 2 fascial planes [wide margins 16mo, marginal excision 9mo until recurrence] RT- rarely curative alone, in combination 650 days until recurrence chemo may or may not help depending on literature - carboplatin, vincristine, can use TKI as well because do express PDGF

what is this?

mycoplasma haemominutium, haemocanis

treatment for FIV?

no specific treatment, no systemic steroids unless absolutely necessary because can correlate with increased viremia supportive care mostly dont use griseofluvin for fungal disease because can cause bone marrow suppression in patients wtih FIV AZT can be used, but can cause myelosuppression in cats, will see AZT resistant virus in few months after treatment

oomycetes?

nonphotosynthetic fungi that resemble algae and that reproduce by forming oospores Soil or water-dwelling organisms that are members of the Kingdom Stramenopila NOT true fungi in that they produce motile, flagellate zoospores (the infective stage) Have cell walls that contain cellulose Have fundamentally different nuclear division Plasma membranes also lack sterols, which are typically the target of many antifungal drugs

candidiasis

normal inhabitants of GI, genitourinary, upper resp tracts, may overgrow if immunsuppressed or prolonged broad spectrum antibiotic use (esp in wounds, oropharynx, GIT) neutropenia predisposes to infection Localized candidiasis (nonhealing ulcer covered by a whitish-gray plaque) Disseminated disease (fever and acute, multiple raised erythematous skin lesions in dogs with less disseminated dz in cats); leukopenia and thrombocytopenia Renal involvement is common, and yeast may be found in the urine, especially in cats Tx: Itraconazole and amphotericin B (ABLC)

cryptococcus

opportunistic, systemic fungal infection, narrow based budding yeast (crying crypto), originates in nasal cavity, paranasal tissue, lungs; most commonly eye, skin, CNS but can disseminate C. neoformans var. neoformans most commonly causes disease and is associated with pigeon droppings C. neoformans var. gattii is capable of causing disease and is associated with bark and leaf litter of certain eucalyptus trees respiratory, nasopharyngeal, cutanous, ocular, CNS involvement most common feline- nasal cavity 50-80%, skin/sq 40-50%, eyes 20-25% (posterior segment dz), CNS 20%

pathogenesis of FeLV?

oronasal exposure leads to virus replication in oral lymphoid tissue then circulates to monocytes and lymphocytes in peripheral blood FeLV exposure (negative for all Ag and PCR testing) → week 1 → 1. Strong immune response- abortive infection where virus eliminated, angiten and PCR tests negative (no viremia occurs, virus cannot be detected at all but have FeLV antibodies), 2. Variable immune response- focal/atypical infection, antigen negative or transiently positive, blood PCR negative, tissue proviral PCR positive; week 3 → 1. Good immune response- regressive infection (antigen tests negagtive, proviral PCR weak positive, RTPCR negative, 2. poor/absent immune response or immunosuppression for regressive infection can lead to progressive infection (antigen tests and PCR tests positive) → FeLV related disease Focal infections- evidence of proviral DNA in some tissues but not in blood or bone marrow Progressive infection once involves bone marrow and cellular destruction by virus exceeds ability of host immune system to suppress viral replication and persistent viremia results (bone marrow infection is critical for pathogenesis of infection) some animals can clear active infection before getting to bone marrow, proviral DNA is found in genome and disease can recrudesce with immunosuppression, may also develop neoplasia not related to FeLV based on where inserted into genome

lyme disease and Osps?

outer surface proteins used for subgrouping OspA- predominant surface protein on borreliae in midgut of nymphal tick, helps adhere to midgut epithelial cells Warm blood during feeding stimulates OspC production over OspA OspC correlates with migration of spirochete from midgut to salivary glands of tick Sufficient numbers of spirochetes are in salivary gland >53 hours after starting to feed reactivity to OspA but not OspC occurs in vaccinated dogs but not in natural infection Lyme C6 quant looks at OspC

what part of villi attacked by Parvo, CoV, rotavirus

parvo- crypt, helicobacter also CoV- tip of villi rotavirus- top 1/3 of villi others: villi- rotavirus, coronavirus, enterphatogenic E coli, giardia, cryptosporidium crypts- parvo, helico both- salmonella and campylobacter

mycobacterium bovis and cats

pathogen of classic feline tuberculosis cats>dogs infected by drinking unpasteurized milk, uncooked meat, offal from infected cattle clinical signs- GIT can excrete organism in feces as well dx: culture- % Ogawa egg yolk media- can identidy specific species involved (fast growing takes 3-5 days, slow growing can take 4-6 weeks) tx: fluoroquinolones pending dx, if systemic or regional spread- initial phase for 2 months (rifampin, enro, azithro), continuation phase or rifampin plus either baytril or azithro (if resistance develops- rifampin, isoniazid, ethambutol [or can use pyrazinamide or dihydrostreptomycin)

treatment of canine pancreatitis?

pathophys- exocrine pancreas source of numerous inflammatory cytokines (high risk MODS, SIRS, increased mortality) tx: IVF (replacements, colloids may be needed for hypoalb and plasma- FFP (clotting factors, albumin, high molecular weight proteins), hetastarch; pain control (opioids), emetic control (NK1 antagonists, 5HT3 antagonists, dopamine antagonists), glycemic regulation/control (may have hyperglycemia, tx with IVF first then may need insulin), nutritional support (early enteral nutrition associated with better outcome- LF formulation, feedings tubes if needed otherwise oral if tolerate/eating)

public health and FIV?

positive cats should be kept indoors (helps prevent spread and coinfections [other infections can increase viral transcription and accelerate disease progress], vaccinate if around other cats [inactivated vaccines, may activate viral transcription]) Vaccine? protected 60-80% of cats from infection - vaccine is controversial; Existing serological assays cannot differentiate vaccine from natural infection, vaccination only provides partial protection from infection, PCR assays can't be relied upon in vaccinated cats in terminal illness (when not producing antibodies), owners need to be warned that can still get FIV with vaccine Increased risk of sarcoma formation with adjuvant vaccines as well, so non core vaccine and only given if test negative initially for FIV

sporotrichosis treatment?

potassium iodide, ketoconazole, or combinations of the two (55% of treated cats in the literature responded to one or both of these drugs) Itra is treatment of choice in people and is effective in dogs and cats. OK prognosis if not disseminated feline is significant zoonotic disease

clinical signs of Brucella canis

primary disease in intact male dogs- epididymitis, scrotal enlargement, scrotal dermatitis, antisperm antibodies (inflammation in epipdidymis and testes causes sperm to leak -->immune response making antisperm agglutinating antibodies and delayed-type hypersensitivity reactions against sperm that are unrelated to the antibodies against B. canis; immune responses produced against spermatozoa contribute to the epididymitis, infertility, and eventual spermatogenic arrest) bitches late in gestation 40-60days- abort dead puppies, bot no other clinical signs- no effect on estrus cycle discospodylitis, uveitis with corneal edema, GN, meningitis

what is this?

prototheca zopfii: P. wickerhami (cutaneous dz) and P. zopfii (disseminated) are recognized as pathogenic to humans, cattle, and dogs, cats caused by a type of green algea; organism found in sewage and animal waste and transmitted by ingestion of contaminated food, water, soil reproduce asexually by internal cleavage (endosporulation), resulting in the formation of 2 to 20 small endospores within the sporangium, which expand until they are released when the sporangium rupture 31 canine cases in the primary literature, largely arising from the United States, most cases are immunocompromised or those with decreased CMI ocular+neuro+chronic diarrhea dx- cytology, histopath, culture and documenting organisms in CSF, rectal scraping, rectal biopsy Tx: itraconazole and amphotericin B has been effective, grave prognosis with only 2/31 of the US cases reporting survival, individual case reports with survival, but also did not develop systemic dz

sarcocystosis

protozoal disease, dogs and cats definitive host cattle, sheep- intermediate hosts ingests meat containing sarcocysts -> bradyzoites develop into macrogametocytes and microgametocytes in the epithelial and goblet cells of the intestine -> oocysts then form, which sporulate in situ within the intestinal wall; they are released into the intestinal lumen -> in feces dx: sporocysts in feces using supersaturated NaCl solution usually asymptomatic, but acute to chronic diarrhea may occur -> sulfas are tx

infectious causes of azotemia?

pyelonephritis from aerobic bacteria most common lepto, lyme E. canis, RMSF can see vasculitis and azotemia

systemic illness and vaccine?

rare but can happen possible with MLV- no MLV to pregnant or very young inadvertant parenteral administration of topical vaccine increases risk of systemic infection

Encephalitazoon cuniculi

rare dz Schizonts and sporonts are found intracellularly in many cell types including renal tubular epithelial cells, endothelial cells, tissue macrophages, and hepatocytes. Spores are the extracellular stage of the organism that is passed in urine. Transmission: probably from oronasal exposure to spores passed in urine in utero -> infected puppies are weak, have stunted growth, and develop renal failure and CNS disease. Muscle spasms, depression, paralysis, and death have been reported in naturally infected cats, can see azotemia, increased LEs, CSF pleocytosis (neuts) and increased protein no effective treatment

acantoamoeba sp.

rarely cause disease in dogs Acanthamoeba castellanii and A. culbertsoni are free-living amoeba rarely associated with disease in dogs greyhounds young dogs affected more clinical signs like CDV infection- consists of oculonasal discharge, fever, anorexia, lethargy, dyspnea, CNS

lyme vaccine?

recombinant OspA available OspA converted to OspC when warm (i.e. bloodmeal), when tick is feeding, vaccine provides OspA antibodies that help neutralize borellia before it gets into host! Antibodies to OspA from the host cause an arrest of growth and salivary gland invasion in the ticks. Spirochetes either are killed instantly by antibody-induced complement lysis or their mobility is reduced such that they cannot continue their migration to the salivary glands of the ticks risk of developing immune complex disease from vaccine is less than with whole cell borellia vaccines bc cant bind OspC borrelia organisms in body, no type III hypersen can occur Amitraz-impregnated collars prevented transmission of B. burgdorferi in 4 of 4 treated dogs and may be a useful management tool for prevention of borreliosis in dogs

lyme arthritis?

release of proinflammatory cytokines esp. interleukin-8 (IL-8) plays an important role in the pathogenesis of acute arthritis, acts as neutrophil chemotactant pathologic changes in the joints are progressive. Chronic nonerosive polyarthritis is the primary condition after prolonged infection, and it may persist despite antimicrobial therapy- may need roids intact B. burgdorferi or fractions of the bacterium can induce the local up-regulation of TNF-alpha, IL-1 alpha, and IL-1 beta in the synovium but that the interaction of viable spirochetes with synovial cells leads to the release of IL-8, which probably is a prime initiator of PMN migration during acute Lyme arthritis

clinical signs of hepatozoon?

results from pyogranulomatous inflammation, GN, amyloid deposition Fever, weight loss, severe hyperesthesia (paraspinal regions), anorexia, pale mucous membranes, depression, oculonasal discharge, and bloody diarrhea Cats often require co-infection with viral disease

pneumocytosis carinii?

saphrophytic organism, in alveoli of some normal animals, immunosuppressed cats disease occurs in immunosuppressed individuals replication of the organism in the alveoli induces infiltrates of lymphocytes, plasma cells, and macrophages that induces an alveolar-capillary blockage mini dachs, CKCS,- affected dogs mostly 1 year of age, predominant findings are dry cough, dyspnea, progressive weight loss (interstitsial to alveolar pattern on rads)- P. carinii pneumonia occurring in the miniature dachshund is a result of both a T- and B-cell deficiency

what is essential for clinical signs to occur in feline panleukopenia infection?

secondary bacterial infections seem to be essential peracute form of disease causes death without perimortem clinical signs, then fever, lethargy, weakness, inappetence, GI signs death due to dehydration, low BG, electrolyte abnormalities, hemorrhage, endotoxemia, bacteremia fecal shedding for 6 weeks

seropositive vs seronegative dogs for bartonella- paper?

seropositive dogs were more likely to be herding dogs and to be female, whereas toy dogs were less likely to be seropositive. Seropositive dogs were also more likely to be lame or have arthritis-related lameness, nasal discharge or epistaxis, or splenomegaly

lepto serovar infection based on location?

serovar grippotyphosa is a predominant serovar in dogs east of the Mississippi River. northeastern states, pomona has predominated; on the western coast, bratislava and pomona

diagnosis of tetanus?

serum antibody titers to tetanospasmin, clinical signs typically enough to diagnose tx: tetanus antitoxin to bind any free toxin, equine formulation so give slowly IV- therapeutic blood level of antitoxin persists in dogs for 14 days after injection; penicillin G, metronidazole may be more active than PenG bc bacteriocidal against anaerobes slow and progressive recovery,

feline panleukopenia

similar to CPV2- ss non enveloped DNA virus panleukopenia and enteritis in wild an domestic cats- preference for rapidly dividing cells can have mixed infections with CPV2, CPV2b, CPV2c, ad FPV fecal oral transmission vs fomites (most important route)

protozoa causing small bowel diarrhea? large bowel?

small - giardia, cryptosporidium, toxoplasma gondii, cystisospora large- E. histolytica, B. coli, Tritrichomonas blagburn, cystosospora

feline leprosy clinical signs?

soft, fleshy, focal nodules in skin and SQ of head and extremities, lesions develop rapidly and usually freely movable and panless haired or ulcerated lesions, regional lymph nodes may be enlarged dx: PCR Mycobacterium lepraemurium

spirocercosis

spirocerca lupi nematode parasite of carnivores found primarily in dogs adult parasite found embedded in nodule in hosts thoracic esophagus adult worm passes larvated eggs into the lumen -> hatch only after being ingested by an intermediate host (coprophagous beetles) -> transport hosts (birds, amphibians, reptiles, and small mammals) infected if they ingest the intermediate -> definitive host becomes infected by ingestion of the intermediate or the transport host -> larvae are liberated in the stomach -> larvae penetrate the stomach wall and enter an arteriole -> migrate in the wall of the gastric and gastric-epiploic arteries to the celiac artery -> migrate to thoracic aorta -> emerge and migrate to the adjacent esophagus (takes 6 months nodule can turn into sarcoma) vomiting, regurgitation, weight loss, salivation, dysphagia dx: esophagoscopy, larvated eggs on fecal tx: doramectin

canine parvovirus

ssDNA virus, non enveloped- environmentally hardy; CPV2 most pathogenic strain, CPV2b can cross to cat Clinical syndrome: Spread Fecal-orally, Ingested -> replicates in lymphoid tonsils -> intestinal tract -> viremia (3 days) Viremic phase: fever, malaise, lethargy, fecal shedding 5-7 days makes it to rapidly dividing cells in intestinal crypts and bone marrow leading to hemorrhagic diarrhea, vomiting, GI hypermotility (risk of intussusceptions) CBC: Leukopenia +/- neutropenia and lymphopenia (due to myelo destruction), +/- anemia or thrombocytopenia, hypoglycemia +/- Sepsis secondary to bacterial translocation

flaviviridae?

ssRNA virus, vector borne dogs and cats (transient neuro disease) aedes mosquitoes are vector yellow fever- transient viremia with transient febrile reaction wesselsbron disease- reported in dog that died from encephalitis

FeLV treatment?

supportive care, IFN omega initially improved clinical scores and survival times in cats with FeLV over 2 months in one study Antivirals that may help- fozivudine, raltegravir- safety has yet to be studied variable prognosis but all cats develop FeLV related illness within 5 years of diagnosis- MST weeks with leukemias MST 2.4 years compared to 6.3 years for age matched controls May live for several years with good QOL

lagenidiosis treatment

surgery, search for distant disease, prognosis is grave

treatment for feline leprosy?

surgical removal of granulomas treatment of choice complete excision of all nodules beneficial to many cats, fluoroquinolone pending diagnosis if cant do surgery- rifampin, clarithromycin, clofazimine

feline URI

syndrome linked to stress, crowding, poor husbandry mainly viral- 80% FCV or FHV1- Both maintain carrier states, spread by fomites, can spread 5 ft w/ sneeze Clinical signs: rhinitis, stomatitis, conjunctivitis (think FHV), oral ulceration (think calici)

phases of FIV infection?

targets CD4 cells, also infects CD8 cells, B cells, macrophages, DCs, microglial cells, astrocytes FIV can be isolated from lymphocytes, at the earliest, 10 to 14 days after infection -> viremia rapidly increases until day 21 and peaks between weeks 7 and 8 -> decreases gradually until the virus load increases in the terminal stage acute- virus replicates in lymphoid tissue after inoculation, high concentrations present 2 weeks post infection, peak viremia at 8-12 weeks post infection, decline in CD4+ and CD8+ T cells in periphery; Upregulation of T Regulatory cells (CD4+/CD25+) that inhibit proliferation of activated CD4+ and CD8+ cells and cause then to undergo apoptosis- cat survive this stage because rebound in CD8 cells subclinical- asymptomatic, CD4 cells rebound, plasma virus load declines; virus production continued at low levels and there is slow progressive decline of CD4+ T cells, reduction in CD4:CD8 ratio, hyperglobulinemia (B cell hyperactivation), altered lymphocyte expression of cell surface molecules (CD4, cytokine receptors, MHC II antigens) and alteration of dendritic cell and neutrophil function contribute to immunosuppression- cats can remain subclinical for many years terminal- clinical signs of opportunistic infections, neoplasia, myelosuppression, neurologic disease, moderate to severe periodontal disease/stomatitis, fungal infections, parasitic infections, demodicosis, lymphoma most common tumor type (5x more likely to develop than non FIV cat, SCC and others can develop)- 1 year MST at this pt CD4 cell population decerases as viral load increases

pathogenesis of tetanus?

tetanus- clostridium tetani, enter tissue where germinate and reolicate producing toxin in anearobic conditions, binds presynaptic terminals of lower motor neurons and travels up axons by retrograde axonal flow, enters inhibitory neurons in brain and SC where interferes with release of GABA (brainstem) and glycine (cord) Tetanospasmin: (H-chain) affinity to ganglioside surface receptors on NM endplates and causes internalization L-chain transynaptically to inhibitory interneurons on motor and autonomic centers Autonomic loss: increased symphatetic or parasympathetic activity

Hepatozoon americanum pathogenesis

tick feeds on fected dog ->oocysts develop->dog ingests tick --> sporozoites liberated in GIT --> invade monomuclear phagocytes and endothelial cells of spleen, liver, muscle, lungs, bone marrow, dispersed between tissues mostly striated muscle -->merogony-->meronts found within WBCs between muscle fibers after several weeks- Meront-containg WBC encysted w/in host cell-derived concentric layers of mucopolysaccaride ("onion skin" cysts)-->Meronts mature, inc in size, rupture → release merozoites → local inflammation (pyogranuloma) and invasion into new host WBC, or develop into gamonts (infective to feeding larval and nymphal A. maculatum)

pathogenesis of botulism? most common type in canine?

toxin cleaves a presynaptic membrane protein needed for fusion of synaptic vesicles containing acetylcholine to the terminal membrane --> flaccid paralysis Type C and rarely Type D

relative adrenal insufficiency

transient lack of reponse to endogenous/exogenous ACTH and occurs in patients with systemic inflammation (SIRS, ARDS, MODS) hypotension despite appropriate hydration (CVP 5-10) and vasopressor dependency (dobutamine, norepinephrine)- responsive to hydrocortisone

leishmaniasis

transmitted by female sandflies causes fever, weight loss, cutaneous lesions, immune complex deposition (GN), hyperglobulinemia foxhounds at risk breed

brucellosis transmission?

transmitted venerially via penetration of mm --> taken up by phagocytic cells and taken to lymphatics and genital tract tissues --> leukocyte associated bacteremia occurs 1-4 weeks after infection and can last 6-64 months can go to non reproductive tissue like eyes, intervertebral discs, and kidneys infection rate is high during breeding or after abortion with highet number of organisms found in aborted material Milk has organisms but most pups get in utero Seminal fluid and urine of dogs can have organisms from persistently infected prostate and epididymus Transmission via fomites has been reported after vaginoscopy, blood transfusion, artificial insemination, and use of contaminated syringes

sporotrichosis pathogenesis?

trauma that results in inoculation of infective conidiophores or yeast from cutaneous lesions can be infective and is a potential zoonotic source of infection -> skin infection first and can disseminate esp. in cats/immunosuppressed animals 3 forms- cutaneous (dogs), cutaneolymphatic (dogs and cats), disseminated (cats) subcutaneous or dermal nodular lesions that occur most commonly on the head, neck, trunk, and distal limbs characterize the cutaneous form of the disease- dissemination to nodes, spleen, liver, lungs, eyes, bones, muscles, and CNS can occur

Tritrichomonas foetus treatment?

tritrich blagburn- susceptible to 5 nitroimidazoles, resistance prevalent to metro. ronidazole, If diarrhea persists after 2 weeks, retest for T. Foeteus with PCR of fecal sample (colon saline flush). If positive can consider higher doses with increased frequency, just keep in mind neurotoxicity If PCR negative, try fenbendazole 88% of cats untreated will have resolution of diarrhea within 2 years (median 9 months)

Pseudomonas (Burkholderia) pseudomallei

ubiquitous soil saprophyte melioidosis chronic nodular or purulent generalized systemic inflammatory disease in dogs, cats infection route through inhalation, ingestion, direct transmission into wounds or tissues by bites of arthropod vectors or by direct contact with contaminated soil tx: one paper - Intravenous meropenem injections (20 mg/kg twice daily) were given for 14 days to prevent death from sepsis prior to treatment with oral sulfamethoxazole-trimethoprim (25 mg/kg twice daily) for 20 weeks to eliminate the bacteria

when is immunotherapy indicated for chronic infections?

use in cases where site of infection is not super accessible and use immunotherapy to reach site Chronic viral infections in cats (feline herpes, coronavirus, FIV) Chronic intracellular pathogens in dogs (toxo, mycobacterium, ehrlichiosis, coccidioides, papilloma) some infections cause super inflammatory response in body and may need brief anti-inflamm/immunoruppressent course of steroids: ↓ host inflammatory response & ↓ damage while not interfering with effectiveness of treatment/antimicrobial drugs Active immunotherapy can be an alternative/adjunct to antimicrobial therapy

granulomatous colitis

usually infectious etiology, culture biopsies histiocytic ulcerative colitis- histopath: mucosal infiltration with lots of macrophages that stain for PAS and mucosal ulceration and loss of goblet cells FISH for 16s RNA - may detect e. coli fluoroquinolones- can have antibiotic resistance

how does feline panleukopenia virus get into cells?

via transferrin receptors, replicates in cells in S phase initially replicates in oropharygeal lymphoid tissue then disseminates into bloodstream affects lymphoid tissue (necrosis), bone marrow (leukopenia), intestine (virus replicates in intestinal crypts, neutrophils recruited to site causing neutropenia) disease severity deoends on age, immune status and concurrent other infections (FeLV, FeCOV, clostridium piliforme, salmonella spp, astrovirus) 2-10 day incubation pd

feline respiratory viruses- diagnosis? tx?

virus isolation from oropharyngeal and conjunctival swabs, PCR, RTPCR, viral culture tx: most resolve within 2 weeks and may not need treatment, doxycycline for secondary bacterial infections, give abx until clinical signs resolve, famcyclovir, L-lysine may be helpful Prevention: limit crowding, give them more space, decrease length of stay in shelter Vaccination: to decrease severity of disease, doesn't prevent infection or carrier state

clinical signs of tetanus?

within 5-10 days of injury, but because resistance in dogs and cats onset may be delayed 3 weeks wounds closer to hear assocaited with more rapid onset and more generalized tetanus stiff gait, high temps due to muscle activity, risus sardonicus (always smiling due to tetany), protrusion of third eyelid and enophthalmia, trismus (lockjaw), Increases in salivation and the respiratory rate, laryngeal spasm and dysphagia (parasympathetic and somatic cranial nerve nuclei). Regurgitation and GERD from esophageal hiatal hernia and megaesophagus signs may proceed to periodic generalized tonic contraction of all muscles with opisthotonus or grand mal convulsions cardiac- bradycardia likely from vagal hyperactivity blocking inhibition of cardiac inhibitory center of nucleus ambiguous, so increased vagal tones and bradyrhythmias; can get increased catecholamine release with adrenergic stimulation so can also have tachycardia or hypertension Death is from resp px: rigidity of the respiratory musculature, reflex spasms of the larynx, increased airway secretions, and central respiratory arrest from medullary tetanospasmin effects or anoxia