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  1. neospora caninum hosts, transmission
    • coccidian parasite in farm DOGS (like toxoplasma in cats - tachyzoites, bradyzoites, oocysts)
    • Dog/coyote = definitive host
    • cattle, sheep, goat, horse, cat (experimental) = intermediate hosts
    • usu congenital transmission, then shed oocysts to infect cattle (infective in 24h)
  2. neospora caninum signs
    • Young: ascending paralysis (LMN), myositis (muscle atrophy, rigid hyperextension, urinary incontinence, respiratory paralysis), Pelvic limb stiffness progressing to contracture, cerebellar atrophy to cerebellar ataxia
    • >6mo: neuro (sz, tremors, blindness), myositis (flaccid LMN, paresis, hyperesthesia), myocarditis, dermatitis (ulcers, pruritis)
  3. Neospora caninum: dx and tx
    • serology IFA best
    • poor px once contracture. Don't get better, just stop getting worse
    • Clindamycin, TMS. 
    • NOT ZOONOTIC, but dangerous to cattle--keep dogs off farms
  4. Toxoplasma gondii
    about, hosts, transmission, pathogenesis
    • coccidian protozoal parasite
    • definitive host: cats
    • intermediate: mammals, birds, fish
    • obligate intracellular with tachyzoites, bradyzoites, oocysts
    • transmission: ingest tachy or bradyzoites in meat, ingest oocysts in feces, congenital
    • infected, spread to organs. Acute rarely fatal. Chronic infection causes immunsuppression.  Often associated with other dz (FIP, FIV, FeLV)
  5. toxoplasma gondii Hx
    acute signs
    chronic signs
    • male cats esp
    • lethargy/depression, anorexia, weight loss, fever, ocular signs (keratic precipitates, uveitis), resp distress (kittens), neuro, GIT, abortion/stillborn kittens
    • acute: same, fever doesn't respond to abx. Signs reflect necrosis in major organs (resp, liver, CNS, GIT, ocular). Rapid, mainly resp and CNS
    • Chronic: Type IV hypersensitivity, Type III immune complex. Can recrudesce, causing CNS dz, pneumonia or pancreatitis
  6. Toxoplasma gondii
    dx
    tx
    prevent
    • leukopenia on CBC, leukocytosis = recovery. Nonspecific anemia and chem
    • Serology: on aqueous humor or CSF (serum first to compare). IgM up 2 weeks PI - 3months.  IgG up 2-4wks PI - 1 year.  4x in 3 weeks for dx.  Usu IgG+ for life.
    • PCR to distinguish from neospora in dogs
    • diffuse interstitial to alveolar pattern in lungs on rads. 
    • Hyperproteinemic cellular CSF.
    • Tiny bananas on cytology, tiny eggs in fecal (often missed)
    • tx: clindamicin 2+ wks, watch for GIT.  Pred drops in eye. Signs better in 2d.  Some neuro may remain, consider stopping abx 2 weeks after O says it's gone. 
    • prevent: NO RAW MEAT or cockroaches, or hunting.
  7. Toxoplasma gondii zoonosis
    • healthy cat with positive titer is NO RISK TO O
    • No Ab titer may be at risk of infection and shedding, could infect people. 
    • Pick up feces within 24h
    • avoid infection during pregnancy
    • placental transmission is rare but a big deal in first trimester
  8. Babesia overview, transmission
    • protozoal dz with merozoites infecting RBCs, causing anemia (usu immune-mediated but also damage to RBCs)
    • infection via ticks, transplacental or blood
  9. Babesia species (c/d)
    • Dogs
    • Large: Babesia canis vogeli in US, Babesia canis rossi (most virulent, Africa), Babesia canis canis (Europe)
    • Small: B. gibsoni (only relevant one in the US), B. conradae (CA), B. annae (Spain/Europe), 
    • Cats
    • small: babesia felis, not in US
  10. Which babesia infects which breeds?
    • B. canis common in greyhounds
    • B. gibsoni common in pit bulls, fighting dogs
  11. clinical signs of babesia
    • peracute, acute chronic or asymptomatic
    • worse with splenectomy and/or immunosuppression
    • Canis rarely causes signs, rossi and gibsoni worst.
    • systemically sick - lethargic, anorexic, weight loss, pale mm, fever
    • splenomegaly
    • lymphadenopathy
    • hemoglobinemia, hemoglobinuria
    • icterus
    • GI signs (v/d, dark feces)
    • cerebral: weakness, disorientation, collapse
    • renal failure
    • thrombocytopenia, anemia in some cases.
  12. dx and tx of babesia
    • cytology (blood smear)
    • b canis usu large piriforms, occasionally rings
    • b gibsoni smaller, single MO in RCB.
    • PCR is good
    • Tx: tx anemia PRN.
    • Imidocarb for b. canis
    • Azithro + atovaquone for B gibsoni
    • Tx may not COMPLETELY remove parasite
    • Screen the whole kennel!!
    • often co-infection with other vector pathogens
    • vax in Europe, not US for our strains. Tick control!  
    • Test blood donors 2-3x with PCR
  13. hemotropic mycoplasmosis - etiology, types, clinical findings
    • rickettsial bacteria (was haemobartonella felis) causing RBC destruction and anemia (esp in FeLV). More in adult males
    • Attaches to external surface of RBC, causes immune response
    • mycoplasma haemofelis: lg form in cats, more severe disease
    • mycoplasma haemominutum: small form
    • mycoplasma canis: dogs
    • signs: depression, weakness, anorexia, pale mm, splenomegaly. Icterus rare. Intermittent fever. May be asymptomatic.
  14. hemotropic mycoplasmas dx and tx
    • dx: regen anemia (unless concurrent dz), auto-agglutination. Blood smears (pre-tx, don't use reticulocyte stains)
    • feline are small blue-staining cocci, rings or rods. PCR can detect first. 
    • tx: doxy, tetracycline or oxytet. +/- pred to tx IM anemia, slow reduction as PRC goes up.
    • May remain carriers
    • px excellent in cats with early tx
  15. cryptococcus neoformans etiology, pathogenesis
    • saprophytic round yeast-like fungus that makes a capsule in tissues.  Only crypto that grows at vertebrate temps. 
    • Reproduces by budding. 
    • Found in bird poop for up to 2 years.  
    • Worldwide, mostly in cats. 
    • inhalation? nasal or pulmonary granulomas, spread through cribiform plate or blood.  Worse with immunosuppressed
  16. clinical findings of cryptococcus neoformans
    • most common systemic mycosis in cats
    • URI signs most common. 
    • Flesh colored masses in nostril or firm swelling over nose in 70%
    • submandibular lymphadenopathy
    • mouth ulcers
    • cutaneous lesions in 40%
    • CNS signs variable dep on locations.  CNs, ocular disease.
  17. Dx, Tx, zoonoses in cryptococcus neoformans
    • cytology: most rapid. Nasal or skin exudate, CSF, ocular or aspirates.  Also serology, tissue biopsy, culture/isolation
    • tx: itraconazole (NOT FOR OCULAR, NEURO), fluconazolefirst choice for ocular, neuro.  Add flucytosine.  Amphotericin B - CIDAL, eradicates CNS. May need surgical debulking. 
    • No risk to O from P, just from common exposure
  18. Histoplasmosis overview, infection/dissemination
    • systemic fungal infection caused by dimorphic fungus. Prefers warm and humid bat or bird excrement. Free-living in soil, produces macro- and microconidia
    • infection via inhalation of microconidia, convert to yeast, budding.
    • Phagocytosis by mononuclear, hematogenous and lymphatic dissemination
    • Some just respiratory, some just GI (so maybe can enter there, too?).  Most immune systems control it pretty easily.
  19. clinical signs, dx, tx, px, zoonosis of histoplasmosis
    • usu young (<4yo) dogs
    • inappetance, weight loss, fever unresponsive to abx.  Some resp, most GI. Rarely hepatomegaly, visceral lymphadenopathy, splenomegaly, icterus, ascites, ocular, skin, CNS.  
    • dx: nnn anemia from inflamm. Can find histo in monocytes/neutrophils (rare). hypoalbuminemia.  interstitial on chest rads. aspiration, exfoliative, rectal cytology show intracellular round organisms with small body and clear halo.  
    • Don't culture!  Infectious!  
    • tx: itraconazole (best), fluconazole (ocular or neuro) + amphoteracin B. 
    • px: good if pulmonary. Disseminated fair to good.
    • zoo: not transmissible from animal to animal. but CULTURES!!
  20. Blastomyces dermatitidis overview, distribution, dissemination/infection
    • dimorphic fungus (saphorphytic mycelium in nature, budding yeast in the body). thick, refractile double-contoured cell walls
    • usu in soil in Eastern US and canada, along Mississippi esp. 
    • infection: inhalation of spores from environment, turns to yeast in airways. Rarely innoculated into a wound--cutaneous almost always dissemination
    • dissemination sites: skin, eyes, bones, LN, SQ, nares, brain, testes. Lungs may be resolved by this time.
  21. Blastomyces host, clinical signs, dx
    • host: male dogs worst, esp lg breeds. 1-5yo, no season. 
    • signs: anorexia, weight loss, coughing, dyspnea, ocular, bone/lameness (osteolytic, usu distal to stifle or elbow), sometimes skin (draining ulcer, esp face, nail beds, planum nasale). Usu weeks to year, sometimes suddenly worse. espression, fever, lymphadenopathy, emaciation, lung sounds
    • rads: lung changes even without resp signs. 
    • dx: anemia of chronic dz, lymphopenia with leukocytosis, hyperglobulinemia, hypoalbuminemia. LOTS of MO on aspirates
    • don't culture - infection from mycelium
    • AGID ELISA PCR not great.  Urine Ag test best, cross rx with Histoplasma
  22. Blastomyces tx, px, zoonosis
    • Amphotericin B: nephrotoxic and phlebitis, but rapid and effective. Slow infusion with hydration and mannitol. IV.  Lipid complex best but $$$
    • Fluconazole/Itraconazole: alter ergesterol of fungal membranes.  As effective as AMB but fewer side effects (Itra $$). Fluconazole best and only one that does urine. 2-3mo usu. Rarely anorexia with hepatotoxicity. 
    • Px: brain involvement usu die. Severe lung dz - die in first 7d of tx. Serious ocular decreases px. 
    • No re-infection, but total re-tx if relapse. 
    • Zoo: not between animals, but culture and penetrating wounds can transmit.
  23. parvovirus of dogs etiology/strains
    • small nonenveloped ss DNA
    • CPV-1: "fading pups" with lethargy, loose stool, resp distress, sudden death. 
    • canine adeno-associated virus: non-pathogenic
    • CPV-2: replicates in dividing cells, esp intestinal. Severely pathogenic. Closely related to feline panleuk and mink enteritis. 4 forms (abc), can cause dz in cats. Vax cross-protect
    • resistant to inactivation, can live outside host for 5+ months.
    • Most detergents can't kill
    • CPV-2 hemoagglutinates RBCs from many species (so hemoagglutination assays best!)
  24. Parvovirus of cats etiology
    • Panleukopenia ("cat plague"). 
    • Cats can be infected by canine CPV-2 strains. Feline panleuk vax cross-protects against CPV and can be detected on the SNAP.
  25. Parvovirus hosts, predisposition, transmission, pathogenesis
    • Host: canidae, esp unvaccinated intact male. Stress and co-infections exacerbate. 
    • transmission: fecal-oral. LOTS shed in feces. Persists in environment--more likely route.  Active shedding up to 2 weeks after infection. 
    • path: oronasal exposure, replication in LN of pharynx/tonsils. Viremia on day 2, infects lymphoid tissue on day 3, intestinal epithelial cells on day 4.  Shedding on day 3, most on 4-7 as signs appear. Usu gone by day 12-14. 
    • path/signs: Rapidly dividing cells, so SI crypt cells (enteritis, villus can't be replaced), lymphatic tissue, bone marrow (necrolysis of myeloid and erythroid stem cells, so eventually anemia but major leukopenia. Leukocytosis shows tx success, left shift = survivor), myocardial (infection before 2wks, rare because mom usu vax).  
    • In-utero infection (CATS) = abortion or birth defects (cerebellar hypoplasia, retinal dysplasia, hydrocephalus).
  26. Parvovirus clinical signs
    • viral dose and strain affect (2a and 2b in pups can kill before signs).
    • depression, anorexia, vomiting +/- pyrexia initially
    • vomiting, sometimes with roundworms in vomit.
    • mucoid to bloody diarrhea
    • severe lymphopenia (helpful dx sign), also possibly neutropenia. 
    • severe dehydration, weight loss, abdominal discomfort and pain
    • endotoxic shock or DIC
    • all similar with FIP
  27. parvovirus diagnosis, mgmt/tx, client education
    • dx: leukopenia with clinical signs (when band cells appear, px improves). ELISA, but blood in stool can give false negatives (and fecal shedding of virus stops on days 8-12). 
    • mgmt: replace fluid loss (prolonged CRT, dry mm, shock, PCV, TP, UA). Estimate volume (by %), ongoing losses and maintenance (15ml/kg/day).  Balanced fluid, + Dextrose PRN. IV if possible, SQ can cause infections and PO (vomiting). replace electrolytes (K esp), correct acid/base via fluids, prevent infection (broad-spectrum abx like cephalosporin, enrofloxacin or combo like ampi+gentamicin once rehydrated, metro PO. Watch for candida). prevent further loss (anti-emetics like metoclopramide, ondansetron). oral gastric protectants (carafate and famotidine), feed asap so tube (no parenteral or steroids), recombinant feline interferon-omega (maybe?), Blood/plasma (if needed. Hyperimmune plasma may be helpful). NOT TAMIFLU, NO NEURAMINIDASE. 
    • Client: disinfect with 1:30 of 5% bleach for a few minutes. Sanitation, isolate pups until 3mo. No carrier state for parvo. VAX!
  28. Parvo prevention
    • Vaccination!  Core for all dogs and cats.  Start at 6wks, repeat q 3-4wks until 16-20 wks. First yearly, then q3y. 
    • MLV protects faster in an at-risk population.
    • Maternal immunity: causes vaccine failure. 
    • 1/32 household bleach solution. 
    • quarantine puppies! No fomites!
  29. Ehrlichia species, cells, ticks,
    • canis: in monocytes
    • ewingii: in granulocytes
    • chaffeensis: in HUMANS (monocytes)
    • Rhipicephalus sanguineus (3-host, no transovarial transmission), nymph and adult can transmit to all canids
  30. ehrlichia canis forms, signs, timeframe
    • ACUTE
    • common: lethargy, inappetance, fever, weight loss
    • less common: lymphadenopathy, splenomegaly, ocular and nasal d/c, peripheral edema, mucosal bleeding, neuro deficits. 
    • Signs 8-20d post-infection. Recovery in 2-4wks
    • CHRONIC: only some dogs get chronic. Clinical signs for acute + pancytopenia, polymyositis, secondary infections, granular lymphocytosis, hyperglobulinemia, PLN, thin BCS
  31. ehrlichia canis diagnosis, tx, prevention
    • thrombocytopenia, non-regen anemia, PANCYTOPENIA, Morulae in MONOCYTES
    • IFA Serology: Antibodies (acute and covalescent)
    • ELISA serology: like IFA but no quantification. Also ewingii
    • PCR: whole blood, DNA (also ewingii, muris), active infection, most sensitive
    • tx: doxycycline 10mg/kg x 28d, improve in 24-48h, platelets normal in 2wks
    • Cell-mediated immune response necessary, high Ab titers not protective.  No vax.
  32. ehrlichia ewingii vector, clinical features
    • amblyomma americanum (3-host, no transovarial)
    • acute dz only - 3-4wks post-infection, lethargy, anorexia, , neutrophilic polyarthritis
    • dx: thrombocytopenia, nonregen anemia, ELISA, PCR best, morulae in neutrophils.
  33. anaplasma phagocytophilum vector, clinical signs, dx, histo, tx, prevention
    • Ixodes (3-host, no transovarial)
    • most have no signs.  Lethargy, fever, inappetance 1-2wks post-infection.  Can be lameness, joint effusion, lymphadenopathy, splenomegaly, PUPD, v/d, petechia, melena, epistaxis, neuro, secondary infections
    • diagnostics: thrombocytopenia, morulae in NEUTROPHILS, mild hypoalbuminemia
    • IFA Serology: abs to all anaplasma spp. acute and coalescing required
    • ELISA: Abs, like IFA but no quantification
    • PCR: whole blood, DNA to phago... and platys.  Most sensitive. 
    • tx: doxy 5mg/kg BID for 2-4wks, better in 24-48. Not fatal. Humoral and cell-mediated immunity important.  No vax.
    • reportable
  34. anaplasma platys
    • rhiphicephalus sanguineus (3-host, no transovarial)
    • dx: thrombocytopenia worst 2-3wks post infection, cycles of bacteremia and thrombocytopenia every 7-14d. 
    • Morulae in platelets
    • usu NO CLINICAL SIGNS
  35. Rickettsia Rickettsii
    • via dermacentor (3-host, no transovarial)
    • signs: nonspecific. Lethargy, anorexia, v/d, weight loss. Fever, eyes (injection, retinal hemorrhage, d/c, inflam), lymphadenomegaly and splenomegaly, resp signs, vasculitis, orchitis, etc. 
    • thrombocytopenia, non-regen anemia, lots of urine abnormalities and coag issues. MO in joint fluid
    • dx: Micro IF (serum, IgM and IgG ABs, requires acute and covalescent)
    • IFA: cutaneous bx, looks for AG, good for acute
    • PCR: whole blood, DNA, specific
    • tx: doxy 5mg/kg BID 7-14d, often aggressive supportive care (vasculitis). Improve in 24-48
    • endothelial cells
    • cell mediated and innate required to clear.  Long term immunity?
    • REMOVE AND PREVENT TICKS
    • reportable in some countries
  36. FIP - type of virus, host, clinical signs, px
    • severe, immune-mediated coronavirus in cats.  More in young, but any age.
    • Transmitted to kittens by mom usu at 4-7wks, but horizontal too. Local epithelial infection, macrophages carry systemically.
    • <10% get FIP (persistent infection, vasculitis and pyogranulomatous reaction).
    • Sneaks up on you with persistent, non-responsive fever. 
    • Pyogranulomatous rxn in tissues, exudative fluid in abdomen or thorax. 
    • almost 100% fatal - no tx and vax is limited. 
    • most common in catteries or multi-cat facilities.  Hard to dx.
  37. FIP is (maybe) caused by (3)
    • Feline Enteric Coronavirus: intestinal viral infection of cats, common, mild enteritis or subclinical, + AB titers against FIP. 
    • Canine coronavirus: can infect cats!  + AB titers against FIP
    • Transmissible Gastroenteritis Virus: can infect cats!  Severe enteric infection of swine. + AB titers against FIP
  38. Feline type 1 coronavirus vs type 2 coronavirus
    • Antigenically similar (not serotypes), distinguished with MAbs
    • Type 1 is hard to isolate, type 2 is easy.  Type 1 = 85% of FCoV cases. Vax is type 2 virus, similar to canine coronavirus
  39. FIP incubation
    • Enhanced disease within first day after infection
    • 2-4wks usu, but can be 2-4months.  May take years for signs to appear.
  40. Feline Coronavirus
    • Pleomorphic enveloped coronavirus (ss +RNA) with nuclear protein, matrix glycoprotein, spike glycoprotein, types I and II. 
    • survives in environment for 3-7wks
    • Replication: Fusion or receptor-mediated endocytosis into cell, replicates in cytoplasm, integrates into RER membrane, transported out via golgi vesicles. Stays cell-assocated. Rupture of cells could release.
    • asymptomatic to mild intestinal infection most common, could be inflammatory abdominal or ocular.  FIP least common.
  41. clinical signs of effusive/wet FIP
    • insidious onset (gradual)
    • rough hair coat, poor condition
    • fever refractory to abx
    • progressive anorexia and weight loss
    • progressive ascites (big belly)
    • progressive thoracic fluid with dyspnea
    • depression, possible CNS
    • kidney and/or liver signs
    • FLUID: up to 1000mL of straw-colored, clear to slightly opaque, viscous, fibrinous, 1.017-1.047, 5-10 protein, sterile fluid.
  42. Diagnosis of FIP by serology
    it is MALPRACTICE to diagnose FIP in a cat by serology alone.  Dx for FCoV, not FIP!
  43. Immunoperoxidase assay for FIP
    performed on histopath on formalin-fixed tissues.  Immunoperoxidase-tagged MAbs ID specific cells containing virus.  (brown = infected).
  44. Treatment and vax for FIP
    • no sure tx. Trying antivirals
    • Only one vax (primucell--don't use), not considered core or recommended. Considering FCoV vax?
  45. Feline Leukemia
    etiology
    pathogenesis
    signalment
    • foreign horizontally-transmitted pathogenic retrovirus
    • causes persistent viremia and immunosuppression predisposing to secondary infections. Also causes neoplastic diseases like lymphosarcoma and leukemia. 
    • several vaccines and good dx tests available. Persistent infections come from outdoor and feral cats
    • MUCH more prevalent in SICK cats
  46. FeLV subgroups (4)
    • FeLV-A: in 100% of FeLV cats.  50% JUST type A (49% AB, 1% AC or ABC)
    • FeLV-B: 50% of FeLV cats, REQUIRES type A
    • FeLV-C: RARE - mutation from type A
    • FeLV-T: T-cell tropic virus, evolved from type A.  Rare. Highly cytolytic for T lymphocytes. Causes severe immunosuppression
  47. FeLV transmission
    • Vertical: milk, transplacental (death!), saliva
    • Horizontal: saliva, feces, urine
  48. FeLV
    Viremia
    antigenemia
    transient viremia
    persistent viremia
    progressive FeLV infection
    Regressive FeLV infection
    Latent infection
    sequestered infection
    • Viremia: FeLV virus particles in blood
    • antigenemia: FeLV antigens in blood
    • transient viremia: FeLV viremia <12 weeks, ELISA +, IFA -/+, VNAb -. Leads to regressive.
    • persistent viremia: FeLV viremia >12 weeks. ELISA and IFA +, VNAb negative. 30%.  95% of these get FeLV-related diseases. 
    • progressive FeLV infection: continuous increase
    • Regressive FeLV infection: viremia leads to immunity (60%). ELISA -, IFA -, VNAb +. MOST become negative with no dz. A few  (30%?) develop latent infection. 
    • Latent infection: integration of FeLV genome.  ELISA +/-, IFA -, VNAb +.  They can progress to viremia or FeLV negative lymphoma. 
    • sequestered infection: virus controlled and dormant. ELISA +, IFA -, VNAb +/-. Progresses to Persistent viremia or regression.
  49. Pathogenesis of FeLV infection
    oral/nasal mm innoculation, replication in tonsil and local lymphoid tissue, mononuclear viremia, replication in systemic lymphoid tissues, replication in bone marrow and crypt epithelium, marrow-origin viremia, infection of mucosal and glandular epithelium, leukemogenesis or aplasia in lymphoid tissues
  50. FeLV - who gets it
    • Newborn to 2 weeks, decreases by 4 weeks, then decreases again by 4 months.  Usu in young adults.  FIV in middle-aged to older adults.
    • outdoor cats, open multi-cat environments, FeLV and FIV-infected environments.  Hx of chronic illness of unknown etiology.
  51. clinical signs of FeLV and FIV
    • Chronic diseases, immunosuppression, 2ndary infections, tumors, degenerative diseases, illness of unknown cause
    • weight loss, fever, dehydration, rhinitis, oral infections
  52. Laboratory tests for FeLV
    • IFA: Ag for FeLV
    • ELISA: Ag for FeLV, Ab for FIV - SNAP
    • Western Blot: Ab for FIV
    • PCR: Ag for both FeLV and FIV
    • False + are rare
    • Retest + cats in 3-4wks with ELISA and IFA
  53. FeLV vaccines
    • inactivated, subunit or recombinant
    • Safe from producing FeLV or related diseases, won't exacerbate dz in FeLV+ cat
    • no other Ag in vax, some allergic to bovine serum, etc. Fibrosarcomas very rare
    • 2 doses 3-4wks apart starting at 8wks. Revax in 1 year, then every 1-3yrs
  54. FIV
    • lentivirus, retrovirus. Many isolates, at least 5 subtypes (A-E, A in western US, B in eastern US). Possibly no protection between subtypes. 
    • transmission: cat bites (primary), sexual (unimportant). Rarely transmitted in socially stable cats. No public health concerns. 
    • incubation period: serious clinical response in 4-6wks (transient illness, lymphadenopathy). Clinical dz in 3-5yrs.
  55. FIV stages of pathogenesis
    • acute infection: weeks/months, cyclin neutropenia, fever, lymphadenopathy
    • asymptomatic carrier: years, no clinical signs
    • Progressive generalized lymphadenopathy: months, generalized lymphadenopathy
    • AIDS-related complex: months to 1 year, weight loss, chronic diarrhea, chronic URI, chronic stomatitis, chronic skin infections, lymphadenopathy
    • AIDS: months, ARC signs plus emaciation, anemia or pancytopenia, opportunistic infections, malignancy
  56. FIV tests
    • ELISA - Ab test
    • IFA - Ab test
    • Western Blot - Ab test
    • ALL TESTS DETECT ANTIBODY, NOT ANTIGEN.  High correlation between serum Ab and viremia in UNVAX cats. 
    • Don't test before 12 weeks, you're just testing mom.  
    • double-confirm a positive test.
    • PCR for antigen is unreliable
  57. FIV vaccine
    • Inactivated whole-virus parenteral vax, subtypes A and D. Only licensed vax. 
    • Negates Ab dx tests
    • experimental recombinant vax. 
    • noncore - use only in high-risk animals that test Ab-negative BEFORE vaccination. 
    • 3 SQ doses at 2-3 week intervals, tell O that P will now test +. MICROCHIP vaccinated cats.
  58. Lyme
    • Borrelia burgdorferi(lotsof borrelia but we only care about this one)
    • spirochete, large,  lots of outer surface proteins that cause huge immune reaction
    • ”elusive”: constantly changes epitopes to hide.  OspA is major adhesive outer lipoprotein - vax and tests are based on this.  After 48h of feeding, OspA downregulated for mobility. Then expresses OspC, SUPER variable so we can’t use it (yet).
  59. How Lyme vaccine works
    Antibodies in blood sucked by tick go into her midgut and kill adhesive protein OspA before it ever leaves tick’s body.
  60. Transmission time of Lyme
    • >48h after tick attachment
    • EXPONENTIAL increase after 48-72h.
  61. How do ticks get Lyme?
    • Usu from mice!  No transovarialtransmission. 3-host ticks.
    • Nymphs are very aggressive, prefer humans.  
    • Deer don’t transmit the borrelia, they just feed the ticks.
  62. Clinical signs of borreliosis
    • Limb/joint involvement (1 or 2 joints, fibrino-purulent exudate in tap, no spirochetes)
    • lymphadenopathy
    • fever, lethargy, inappetance
    • responsive to abx
    • renal, cardiac, neuro manifestations
    • Onset in 50-123d  after tick exposure. 
    • 80% of lameness happens in quadrant of dog where TICK BIT. REGIONAL disease
  63. Canine Lyme Nephropathy
    • Distinctiverenal lesions: glomerulonephritis, diffuse tubular necrosis, interstitial inflammation
    • Rapidly progressive
    • Uniformly fatal: usu 5.6yrs, labs and Goldens at higher risk.
  64. Diagnostic tests for Lyme
    • Direct: culture & isolation, PCR of tissues (NOT BLOOD), but only for researchers
    • Indirect: IFA, Western Blot, ELISA (SNAP), C6, Novel assays (Lyme multiplex, C6 quantitative,accuplex)
    • Multiplex: ONLY OspA = vaccine, not infection.  OspC = early infection.  OspF = chronic infection.
  65. Treatment for lyme
    • Extracellular!  
    • Doxy, Amoxicillin, minocycline, cefovecin/convenia.
    • Natural infection WILL NOT PROTECT from subsequent protection!!!  Becuase OspA is only there AT infection!  Also can be really hard to get rid of, even with tx.  PREVENTION
    • Vaccines and tick control!  
    • Mow, leaf litter removal, landscape barriers like wood chips, lots of sunlight!
  66. Leptospirosis MO basics
    • gram negative spirochete
    • Flexible, motile bacteria with hook-shaped end. Can only replicate within host. 
    • L interrogate and L kirschneri cause 250 pathogenic serovars adapted to hosts. May play a role in organ involvements. Cross-reactivity makes ID complicated
    • Gryppothyphosa, icterohemorrhagiae, canicola are the big ones
  67. Lepto transmission
    • Direct: exposure to urine, bite wounds, ingestion of tissue, venereal, placental
    • indirect: contaminatedwater, soil, food, etc. Reservoir hosts can shed in urine for years. Can survive in soil or water for months.
    • Peaks in October, Nov (3mo after rainy season)
  68. Lepto signalment
    • WAS intact male, large breed and males
    • older dogs, both sexes, small breed and terriers overrepresented
  69. Pathogenesis of lepto
    • Penetrate mm
    • high ab titer, MO eliminated, no clinical signs.
    • Low/absent ab titer, leptospiremia within 4-7d.  Vascular damage and thrombocytopenia(Kidneys, liver, vasculitis, coagulopathy).  Clinical disease leads to death or increased Ab titers (chronic  active hepatitis, renal colonization, leptospiruria (carrier state).  Elimination?
  70. Clinical signs of lepto
    • Fever only at onset of disease (shivering, reluctance to move, muscle tenderness).
    • PUPD (nephrogenic DI due to ADH interference, tubular damage)
    • Gastroenteritis/pancreatitis (v/d, inappetance, abdominal pain)
    • Uncommon: bleeding/coag, icterus, tachypnea/dyspnea (Severe Pulmonary Hemorrhage Syndrome (SPHS), oliguria/anuria, uveitis, myocardial injury, infertility/abortion
  71. dx tests in lepto
    • UA: isosthenuria, glucosuria, proteinuria,  cylinduria,  bilirubinuria. MO NOT VISIBLE
    • coag: thrombocytopenia, prolonged PT/PTT, hyperfibrinogenemia, elevated D-dimers, decreased antithrombin
    • Renal US: hyperechoic cortex, pyelectasia, renomegaly, peri-renal fluid, medullary band sign. 
    • Microscopic Agglutination Test (MAT): TEST OF CHOICE. Requires live lepto cultures, subjective (amt of precipitation). Cross-rx with vax titers. 4-fold rise = + active infection.
    • Darkfield microscopy
    • blood/urine culture
    • PCR
    • Histopath (IHC or silver stains)
    • Lepto SNAP: in-clinic ELISA. Doesn’t diff. Serovars, false - in acute dz, false + in vax.
  72. Lepto Tx
    • Leptospiremia: Doxycycline (or other tetracyclines), Ampicillin, Amoxicillin/Clavamox
    • Leptospiruria: doxycycline (or other tetracyclines), streptomycin
    • supportive care: fluids, antiemetic, gastroprotectants, O2 PRN, +/- antihypertensives (amlodipine WITH ACE INHIBITOR), +/- blood products
    • Diuretics: for oliguria, anuria, polyuria - not until rehydrated!! May require dialysis
  73. Lepto px, prevention, zoonosis
    • Pxp: >50% survival, 80% with hemodialysis (lower with pulmonary  involvement)
    • may take 4+ weeks for urine concentrating ability to return. 
    • Vaccination:inactivated bacterins.  Four-serovars represented, reduce risk of Type I hypersensitive.  12 month immunity, but serovar/serogroup specific. Vax dogs in direct contact with wildlife or livestock, stagnant water exposure, urban/suburban dogs in risk areas. 
    • Zoo: most humans get mild dz from recreational water activity. No documented pet transmission!  But still PPE! Educate about environmental exposure. REPORTABLE IN SOME STATES
  74. Rabies
    etiology
    hosts
    transmission
    pathogenesis
    incubation period
    histology
    result
    • Lyssavirus from rhabdoviridae.  Bullet-shaped negative ss RNA
    • Common hosts: skunk, fox, raccoon, mongoose, bat. Dif species have different susceptibility.  Our domestics are moderate, other animals are higher. Different strains for different areas, hosts. 
    • Enters cytoplasm, uncoats, replicates in cytoplasm, buds out of cell. 
    • Transmission: bite. Have been aerosol in labs and bat caves (rare) or organ transplants (corneal, etc). Latent infections may still have salivary shedding (no signs of virus!). Also ingestion, inhalation. Maybe re-vax if they eat a fresh deer?
    • path: introduced in saliva, replicates locally, moves into nerve cells and travels up nerve sheath into SC then brain, 100mm/day
    • Incubation: widely variable.  2-24wks. More innervated exposure area = faster.
    • Histo: Negri bodies! Packed with protein and RNA, budding viruses off. 
    • Result: FULMINANT ENCEPHALITIS, widespread infection of neurons of CNS
  75. Phases and forms of rabies
    • Prodromal phase: apprehension, nervous, anxiety, withdrawal, variable fever, pupillary dilation +/- sluggish reflexes, licking or chewing at site of inoculation
    • Furious form: 1-7d. Restless, irritable, increased response to stimuli, photophobia, hyperesthesia, muscular in coordination, paralysis, death
    • dumb: 2-4d after prodromal. CN paralysis, change in tone of bark, salivation from lar par, labored respiration, dropped jaw, coma, death from resp paralysis.
    • RARELY dogs recover, shed for a few months
  76. Livestock rabies signs
    • Muzzle tremors, ptylaism, pharyngeal paralysis, anorexia/pica, bellowing/whinnying, aggression/depression, blindness/photophobia, seizures, regional pruritus, head pressing, hypersensitivity to stimuli
    • sudden-onset behavioral changes
    • NO VAX IN GOATS (use off-label)
  77. dx of rabies
    • Direct FA analysis of Brian and spinal cord.  
    • ALWAYS POST-MORTEM
    • Gel electrophoresis to determine strain
  78. post-exposure (d/c/ferret)
    • Unvax are euthanized or vax and placed in 4-6mo strict isolation. Re-vax 1mo before
    • vaccinated are treated, vaccinated and released to O for observation for 45d
    • Undocumented prior vax are treated, vaccinated, and paired serum samples show increase in abx. May need longer observation.

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XQWCat
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335293
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SA Infx Dz
Updated:
2017-11-09 14:04:33
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SA Infx Dz exam Vb
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