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What are the major viral causes of canine enteritis? (3)
canine parvovirus-2, canine coronavirus, canine rotavirus
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What are the major viral causes of feline enteritis? (2)
feline parvo/panleukopenia, feline coronavirus/FIP
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Describe parvovirus characteristics.
- high contagious, stable in the environment
- fecal-oral transmission
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Describe the timeline of parvovirus infection.
- incubation 4-14 days
- viremia 1-5 days post infection
- fecal shedding 7-10 days
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What happens to dogs that get parvo <8 weeks of age?
myocarditis and death
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What happens to dogs that get parvovirus >8 weeks of age?
enteritis--> diarrhea-->mild recovers, severe causes sepsis, DIC, and death
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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
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What are clinical signs of parvovirus? (4)
vomiting, bloody diarrhea, +/- neurologic signs, +/- myocarditis (if <8weeks old)
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Why does parvo sometimes cause neurologic signs?
- severe acid-base or electrolyte abnormalities
- hypoglycemia
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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
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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)
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Under what circumstances do you give antibiotics to an animal with parvo? (2)
- risk of bacterial translocation (a lot of GI bleeding)
- severe neutropenia
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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
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What cell populations are affected by panleuk?
rapidly dividing cells- intestinal mucosal crypts, lymphoid tissue, bone marrow
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What happens when neonatal kittens are infected with panleuk?
cerebellar hypoplasia
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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
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How is panleuk diagnosed? (4)
clinical signs, leukopenia, pancytopenia, +/- snap parvo test (may be false negative if not shedding)
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What is the treatment for panleuk?
supportive care (survival >5 days is a good sign)
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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
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Describe Giardia characteristics.
binucleate flagellated protozoan, trophozoite is motile form in body, cyst shed in feces is infective form
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How is Giardia transmitted and who is at highest risk?
- fecal-oral
- high prevalence in kennels, young and immunocompromised are at highest risk
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What are clinical signs of giardia? (2)
acute-to-chronic diarrhea that is mucoid, weight loss
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What are methods of diagnosing Giardia? (3)
- fecal smear
- zinc sulfate fecal floatation
- SNAP Giardia (best, easiest)
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Describe the treatment of Giardia. (2)
- Fenbendazole
- Metronidazole (be careful- side affect of neurotoxicity)
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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)
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What is the difference b/w Giardia and Tritrichomonas on a fecal smear?
- Tritrichomonas: jerky, random movement
- Giardia: "falling leaf"
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Tritrichmonas is more common in ________.
cats (as opposed to dogs, where giardia is more common)
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What is a major difference b/w tritrichmonas and giardia as far as life cycle?
tritrichomonas only exists in trophozoite form
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How is tritrichomonas transmitted? Where does it have highest prevalence?
- fecal-oral
- catteries (esp siamese and bengals)
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Co-infection is common b/w tritrichomonas and... (2)
giardia, cryptosporidium
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What are clinical signs of tritrichomonas? (4)
waxing and waning large bowel diarrhea, hematochezia, mucus, malodorous
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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)
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What is the treatment for tritrichomonas?
- [resistant to most antibiotics] Ronidazole
- spontaneous resolution (9months-2 years)
- subclinical infection may persist
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Describe the prevention of tritrichomonas.
control environment- isolate infected cats, disinfect litter boxes, reduce housing density, improve husbandry
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Fungal enteritis is usually caused by... (2)
Histoplasma, Pythium (more like an algae, not common in ohio)
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Describe Histoplasmosis characteristics. (3)
soil-borne dimorphic fungus- mycelial form in environment, yeast form in body
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Describe the pathogenesis of Histoplasmosis.
inhalation of spores--> hematogenous and lymphatic dissemination--> spreads throughout body (unclear how primary GI disease occurs)
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What are clinical signs of Histoplasmosis? (4)
respiratory signs (cough, dyspnea), GI signs (depending on extent of disease), hepatosplenomegaly, lymphadenomegaly
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How does Histoplasmosis appear on minimum database? (5)
non-regenerative anemia, stress leukogram, hypoalbuminemia, +/- hypercalcemia, +/- elevated liver enzymes
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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
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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)
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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
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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)
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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
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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
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What are clinical signs of C. diff?
subclinical carrier usually, maybe acute hemorrhagic diarrhea
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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)
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How is clinical C. diff treated? (3)
supportive care, fecal transfuantation, probiotics
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Describe Salmonellosis in SA.
- isolated from healthy animals, more common with raw diets
- clinical signs: vomiting, diarrhea, fever, anorexia lethargy, maybe chronic disease
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How is Salmonellosis diagnosed?
5 serial samples for fecal culture
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What is the treatment for clinical Salmonellosis? (2)
supportive care, antibiotics for systemic illness or immunocomp animals
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What does E. coli cause in SA? (2)
granulomatous colitis, histiocytic ulcerative colitis of Boxer dogs
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What are clinical signs of E. coli in SA? (2)
large bowel diarrhea, weight loss
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What are clinicopathologic findings associated with E. coli diarrhea in SA? (2)
hypoalbuminemia, +/- microcytic anemia (if blood loss through GI)
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How is E. coli definitively diagnosed?
Histopathology: macrophagic (histiocytic) mucosal infiltration, mucosal ulceration, loss of goblet cells
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What is the treatment of E. coli?
antibiotics- Baytril (try to get culture and sensitivity b/c resistance is increasing)
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