EqMed, Q2, IV

  1. what is the most common sertype of salmonella to infect the horse?
    S. typhimurium (no enteric host adapted species in horse)
  2. Salmonella has zoonotic potential, 1 in 17 healthy horses are shedding, and it has established resistant infections in hospitals. which horses are more susceptible to infection?
    • young (foals more likely to become septic)
    • old and sick
  3. what is pathophysiology of disease caused by salmonella?
    bacteria invade mucosa - engulfed by macrophages - prod. toxin that damages mucosal barrier and Na/Cl secrete into lumen - inflammatory response and can be absorbed into blood stream
  4. what are the most common signs associated w/salmonellosis?
    • fever
    • endotoxemia
    • diarrhea (may be absent or in small amounts)
  5. how is salmonella diagnosed? when is horse considered unlikely to be shedding?
    • PCR of feces, tissue or body fluid (blood in foals)
    • bacterial culture
    • 5 neg fecal cultures or 3 neg PCRs taken 24 hr apart
  6. what worsens prognosis for salmonella patient?
    • prolonged diarrhea or sepsis
    • fibrin formation - adhesions - irreversible/poor absorption/damaged mucosal barrier
  7. what are signs a patient being kept in hospital has developed salomella infection?
    • decr. appetite and attitude
    • elevated PCV w/low TP (PLE and dehydration)
  8. what kind of bacteria is clostridium? which species are problematic in the horse? when?
    • gram +, spore forming rod, anaerobic (normal intestinal flora)
    • C. perfringens and C. difficile (when stressed, immunosuppressed, Ab-induced)
  9. which antibiotics are more likely to cause diarrhea/disrupt intestinal flora? which Ab should NEVER be used in horses?
    • erythromycin, neomycin
    • TMS
    • ceftiofur
    • ampicillin
    • never use Lincomycin
  10. any antibiotic can cause diarrhea in horses so what are signs that problems are arising?
    • decr. appetitie/attitude
    • mild fever
    • decr. water intake
  11. how do you test for clostridium? what type of diarrhea is often seen w/clostridium infection?
    • ELISA for c. difficile toxins A and B
    • PCR, cytotoxin assay
    • culture from feces (inferior test)
    • hemorrhagic diarrhea
  12. how is clostridium treated? prognosis?
    • metronidazole
    • DTO-smectite/biosponge (binds toxins)
    • laminitis prophylaxis
    • high mortality
  13. what is causative agent of Potomac Horse Fever? which cells does it infect? which seasons are associated w/disease?
    • neorickettsia risticii - carried by aquatic flukes
    • late summer, early fall (warm water)
    • trophism for monocytes and enterocytes
  14. clinical signs of PHF are similar to salmonella and clostridium, but what other sign can be noted in late disease?
  15. how is PHF diagnosed? treatment?
    • PCR on blood or feces; paired serology titer
    • Oxytetracycline (dilute/NO bolus- avoid chelation of Ca - heart stop)
  16. what are the 2 most common complications associated with PHF? is there a vaccine available?
    • laminitis and abortion
    • vaccine exists but don't use it, not efficacious
  17. what is cause of cantharidin toxicosis?
    • blister beetles contain this toxin; often encountered in alfalfa hay - mucosal irritant
    • 4-5 beetles = signs within hours
  18. what other organ system is affected by blister beetles?
    • GI + *renal* (hematuria, stranguria) + oral ulceration (salivation)
    • myocarditis may also be present
  19. what is the most distinguishing feature of blood work of cantharidin toxicosis patient?
    • *hypOcalcemia* (and hypomagnasemia) so incr. TPR
    • synchronous diaphragmatic flutter/thumps
  20. what is treatment and prognosis for cantharin toxicity?
    • no specific antidote, supportive care
    • mineral oil to help evacuate
    • poor; mortality >50% (if survive first couple days, prog. improves)
  21. how does grain overload cause colitis?
    not enough amylase to digest high CHO load - undigested CHO reaches colon - bacillus/lactobacillus/strep proliferation - prod. lactate and proprionate - acidic pH - decr. fermentation/motility and laminitis
  22. what are presenting signs of grain overload?
    • severe colic pain
    • endotoxemia
  23. what is treatment for grain overload?
    • gastric lavage if caught early
    • mineral oil via NGT
    • anti-endotoxemic therapy; laminitis prophy
    • trocharize cecum to relieve distention (right side)
  24. feeding how many kg of oats/day will increase risk? what is recommended amount to feed per meal?
    • >2.7kg of oats/day
    • feed <2g/kg of body weight per meal
  25. Horse in Michigan is seen laying down more and passing normal consistency feces then watery diarrhea. What is likely diagnosis? what do you expect peritoneal fluid to be?
    • sand enteropahty
    • normal fluid; careful not to penetrate colon when collecting!
  26. what would US show with sand colitis?
    stretched colon so loss of haustra
  27. how is sand colic treated if only mild signs present?
    • over hydrate w/oral and IV fluids
    • NSAIDs + analgesia
    • psyllium (metamucil) to encourage movement over time
  28. what should be done for sand colic patient that is not responding to therapy?
    • surgery to remove sand - pelvic flexure enterotomy
    • cecal trochar prior to sx to improve respiration/venous return
    • (if sand in R dorsal colon, cant exteriorize, more difficult)
  29. what is the difference between cox 1 and cox 2?
    • cox 1: consistently being produced; maintain mucosa
    • cox 2: inducible during pain/injury - inflamm. mediators
  30. where is NSAID damage most likely to occur? what dose is considered excessive? which NSAID in particular is dangerous?
    • right dorsal colon
    • >8.8 mg/kg/day in face of water deprivation (lesser doses can cause problems too)
    • phenylbutazone
  31. what is diet treatment for right dorsal colitis?
    • pelleted feed, no long stem fibers
    • corn oil
  32. what other supportive care things can be done to treat right dorsal colitis?
    • may require colloids
    • synthetic prostaglandins
    • psyllium to promote movement of ingesta
    • opioids + Lidocaine CRI
  33. Cyathostomes infect the large intestine. What is their life cycle?
    • ingest L3 - migrate into cecal/colonic mucosa - go back into lumen as L4 after 5-6 weeks
    • OR L3 can encyst in mucosa for months - when excyst release inflammatory products (end winter/early spring)
  34. what are clinical signs of acute cyathostome infection?
    severe diarrhea, rapid wt. loss and marked hypoproteinemia; passing larva in feces
  35. what are clinical signs of chronic cyathostome infection?
    • *wt. loss*
    • chronic diarrhea (so no CV deterioration or volume depletion)
    • intermittent colic
  36. cyathastomes have resistance to which drug?
  37. what are the 2 licensed products for treatment of cyathastomes? how is successful treatment determined?
    • fenbendazole (power pack)
    • moxidectin (quest)
    • >90% reduction in FEC after 1 wk therapy
  38. what drug can be given to PREVENT mucosal invasion of cyathastomes?
    daily pyrantel tartrate
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EqMed, Q2, IV
EqMed, Q2, IV