GI3- SA Infectious Diarrhea

  1. What are the major viral causes of canine enteritis? (3)
    canine parvovirus-2, canine coronavirus, canine rotavirus
  2. What are the major viral causes of feline enteritis? (2)
    feline parvo/panleukopenia, feline coronavirus/FIP
  3. Describe parvovirus characteristics.
    • high contagious, stable in the environment
    • fecal-oral transmission
  4. Describe the timeline of parvovirus infection.
    • incubation 4-14 days
    • viremia 1-5 days post infection
    • fecal shedding 7-10 days
  5. What happens to dogs that get parvo <8 weeks of age?
    myocarditis and death
  6. What happens to dogs that get parvovirus >8 weeks of age?
    enteritis--> diarrhea-->mild recovers, severe causes sepsis, DIC, and death
  7. Describe the pathogenesis of parvovirus.
    • affects rapidly dividing cells- radiomimetic
    • intestinal crypt epithelial cells--> crypt necrosis and shortened villi
    • bone marrow--> neutropenia
    • lymphoid tissue--> lymphopenia
  8. What are clinical signs of parvovirus? (4)
    vomiting, bloody diarrhea, +/- neurologic signs, +/- myocarditis (if <8weeks old)
  9. Why does parvo sometimes cause neurologic signs?
    • severe acid-base or electrolyte abnormalities
    • hypoglycemia
  10. Describe the usefulness of the parvo snap test.
    detects parvo antigen, if the animal isn't shedding at that moment, it might be a false negative; if the animal has clinical signs, negative does not rule out
  11. What is the treatment for parvo? (6)
    QUARANTINE, IV fluids, anti-emetics, gastroprotectants, nutritional support, +/- antibiotics (if risk for bacterial tanslocation from gut, if severe neutropenia)
  12. Under what circumstances do you give antibiotics to an animal with parvo? (2)
    • risk of bacterial translocation (a lot of GI bleeding)
    • severe neutropenia
  13. Describe prevention measures for parvovirus. (3)
    • vaccination
    • isolation of affected dogs
    • infection may confer immunity but this is NOT  a reason to stop vaccinating after infection
  14. What cell populations are affected by panleuk?
    rapidly dividing cells- intestinal mucosal crypts, lymphoid tissue, bone marrow
  15. What happens when neonatal kittens are infected with panleuk?
    cerebellar hypoplasia
  16. What are the syndromes and clinical signs associated with panleuk? (3 syndromes)
    • peracute- death due to septic shock
    • acute form- fever, depression, anorexia, vomiting, diarrhea
    • final stage- hypothermia, DIC
  17. How is panleuk diagnosed? (4)
    clinical signs, leukopenia, pancytopenia, +/- snap parvo test (may be false negative if not shedding)
  18. What is the treatment for panleuk?
    supportive care (survival >5 days is a good sign)
  19. What is the best way to prevent panleuk infection?
    • 2 shots, 3-4 weeks apart, starting at 5 weeks of age
    • booster every 1-3 years, depending on vaccine
  20. Describe Giardia characteristics.
    binucleate flagellated protozoan, trophozoite is motile form in body, cyst shed in feces is infective form
  21. How is Giardia transmitted and who is at highest risk?
    • fecal-oral
    • high prevalence in kennels, young and immunocompromised are at highest risk
  22. What are clinical signs of giardia? (2)
    acute-to-chronic diarrhea that is mucoid, weight loss
  23. What are methods of diagnosing Giardia? (3)
    • fecal smear
    • zinc sulfate fecal floatation
    • SNAP Giardia (best, easiest)
  24. Describe the treatment of Giardia. (2)
    • Fenbendazole
    • Metronidazole (be careful- side affect of neurotoxicity)
  25. Describe the prevention of giardia. (2)
    proper disinfection, frequent bathing (if you don't disinfect the environment, the animal will just keep re-infecting itself...don't confuse with resistance)
  26. What is the difference b/w Giardia and Tritrichomonas on a fecal smear?
    • Tritrichomonas: jerky, random movement
    • Giardia: "falling leaf"
  27. Tritrichmonas is more common in ________.
    cats (as opposed to dogs, where giardia is more common)
  28. What is a major difference b/w tritrichmonas and giardia as far as life cycle?
    tritrichomonas only exists in trophozoite form
  29. How is tritrichomonas transmitted? Where does it have highest prevalence?
    • fecal-oral
    • catteries (esp siamese and bengals)
  30. Co-infection is common b/w tritrichomonas and... (2)
    giardia, cryptosporidium
  31. What are clinical signs of tritrichomonas? (4)
    waxing and waning large bowel diarrhea, hematochezia, mucus, malodorous
  32. How is tritrichmonas diagnosed? (3)
    PCR (litter-free feces, off antibiotics for 2 weeks before), fecal culture, +/- direct fecal smear (not recommended b/c looks the same as giardia and not sensitive)
  33. What is the treatment for tritrichomonas?
    • [resistant to most antibiotics] Ronidazole
    • spontaneous resolution (9months-2 years)
    • subclinical infection may persist
  34. Describe the prevention of tritrichomonas.
    control environment- isolate infected cats, disinfect litter boxes, reduce housing density, improve husbandry
  35. Fungal enteritis is usually caused by... (2)
    Histoplasma, Pythium (more like an algae, not common in ohio)
  36. Describe Histoplasmosis characteristics. (3)
    soil-borne dimorphic fungus- mycelial form in environment, yeast form in body
  37. Describe the pathogenesis of Histoplasmosis.
    inhalation of spores--> hematogenous and lymphatic dissemination--> spreads throughout body (unclear how primary GI disease occurs)
  38. What are clinical signs of Histoplasmosis? (4)
    respiratory signs (cough, dyspnea), GI signs (depending on extent of disease), hepatosplenomegaly, lymphadenomegaly
  39. How does Histoplasmosis appear on minimum database? (5)
    non-regenerative anemia, stress leukogram, hypoalbuminemia, +/- hypercalcemia, +/- elevated liver enzymes
  40. How does fungal disease cause hypercalcemia?
    macrophages express 1alpha-hydroxylase, which converts vitamin D to calcitriol, which stimulates calcium absorption in the gut; with fungal infection--> granulomatous inflammation--> hyerpCa via vitamin D activation
  41. How is Histoplasmosis diagnosed? (2)
    • Organism identification (definitive but difficult)
    • MiraVista urine antigen titer
    • culture is not recommended because lab worker with get sick (highly pathogenic in culture)
  42. What is the treatment for Histoplasmosis? (2)
    • itraconazole, fluconazole (PO- be careful of hepatotoxicity)
    • Amphotercin B (IV- be careful of nephrotoxicity)
    • treatment is usually >6 months
  43. What is the ACVIM consensus on bacterial enteritis? (4)
    • usually associated with self-limiting diarrhea
    • antimicrobials could be more harmful than beneficial
    • do provide supportive therapy and hygiene control
    • only give antibiotics to animals with systemic signs (exception is E. coli with granulomatous colitis)
  44. Describe disease caused by C. diff in SA.
    disease caused by toxins A and B (found in healthy animals); colonization progression to disease depends on age, immune status, antibiotic exposure, co-morbidities
  45. What are risk factors for C. diff? (4)
    living with an immunocomp owner, antibiotic administration to dog or owner, visiting human hospitals, contact with children
  46. What are clinical signs of C. diff?
    subclinical carrier usually, maybe acute hemorrhagic diarrhea
  47. How is C. diff diagnosed? (3)
    • detection of fecal toxins (not usually utilized)
    • ID organism in stool (culture, PCR, ELISA)
    • combination testing (ELISA toxin test + organism detection)
  48. How is clinical C. diff treated? (3)
    supportive care, fecal transfuantation, probiotics
  49. Describe Salmonellosis in SA.
    • isolated from healthy animals, more common with raw diets
    • clinical signs: vomiting, diarrhea, fever, anorexia lethargy, maybe chronic disease
  50. How is Salmonellosis diagnosed?
    5 serial samples for fecal culture
  51. What is the treatment for clinical Salmonellosis? (2)
    supportive care, antibiotics for systemic illness or immunocomp animals
  52. What does E. coli cause in SA? (2)
    granulomatous colitis, histiocytic ulcerative colitis of Boxer dogs
  53. What are clinical signs of E. coli in SA? (2)
    large bowel diarrhea, weight loss
  54. What are clinicopathologic findings associated with E. coli diarrhea in SA? (2)
    hypoalbuminemia, +/- microcytic anemia (if blood loss through GI)
  55. How is E. coli definitively diagnosed?
    Histopathology: macrophagic (histiocytic) mucosal infiltration, mucosal ulceration, loss of goblet cells
  56. What is the treatment of E. coli?
    antibiotics- Baytril (try to get culture and sensitivity b/c resistance is increasing)
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GI3- SA Infectious Diarrhea
vetmed GI3