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What is the usual presentation with acute colitis?
rapid onset, high-volume diarrhea
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What are infectious causes of acute colitis in horses? (6)
Salmonella, C. perfringens, C. difficile, Neorickettsia risticii, Cyasthostomiasis, Strongylosis
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What are non-infectious causes of acute colitis in adult horses? (5)
carb overload, sand enteropathy, Canthardian toxicity, right dorsal colitis and IBD
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What are some possible precipitating causes of acute colitis associated with Salmonella? (3)
stress of transportation, feed changes, antibiotics
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How is Salmonella associated with acute colitis diagnosed? (2)
5 serial fecal cultures or PCR on feces
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Due to the contagious and zoonotic potential, what is a confounding risk associated with Salmonella acute colitis?
can have active shedding without diarrhea
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Horses affected with Salmonella acute colitis often have _________ on CBC ad signs of __________.
leukopenia; endotoxemia
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What causes SIRS, and what are the associated clinical signs(6)?
Systemic Inflammatory Response Syndrome caused by endotoxemia; fever, tachycardia, tachypnea, low or high WBCs (+/-left shift, toxic changes), injected MMs, depressed mentation
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Severe, acute cases of __________ in adult horses have been referred to as Colitis X; another top differential for colitis X is ___________.
C. perfringens; Salmonella
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Characterize the disease caused by C. perfringens in adult horses.
acute, often hemorrhagic, enterocolitis +/- typhlocolitis (cecal inflammation + colitis)
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When and how do horses become infected with Potomac Horse Fever?
June-September peak; infected via primary (flukes) or secondary (snails) or paratenic (caddisflies/mayflies- ingestion) IH
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What is the etiologic agent of Potomac Horse Fever?
Neorickettsia risticii
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N. risticii infects the __________, causing clinical signs of... (6)
intestinal epithelial cells of the large and small intestines; dullness, anorexia, variable diarrhea, fever, leukopenia, monocytosis
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How is N. risticii diagnosed? (2)
serology (IFA) and PCR of whole blood or feces
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Large strongyles should be well-controlled by __________.
macrocyclic lactones, such as ivermectin
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Describe the unique life cycle of small strongyles.
emerge from hypobiotic state in late winter/ spring--> diarrhea and massive shedding
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Small strongyles are aka ____________.
cyathosomes
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Encysted cyathosomes are often assocaited with __(2)__.
weights loss and chronic diarrhea
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Why does grain overload cause diarrhea and colic?
acidification of large intestine--> intestinal inflammation--> death of normal GI flora--> endotoxemia--> diarrhea, laminitis, death
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How does sand enteropathy often present, and how is it diagnosed?
low-grade colic and diarrhea; diagnosed via fecal sand test and abdominal radiographs
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What are clinical signs of canthardian toxicity? (5)
oral ulcerations, colic, hypocalcemia, UTI, diarrhea
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What is the etiologic agent of canthardian toxicity?
blister beetle
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What are complications of acute colitis? (4)
laminitis, jugular thrombosis, intestinal ischemia/infarction, septicemia
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Describe the therapy for acute colitis. (7)
- ISOLATION
- IV fluids- treat shock, correct electrolytes, colloids if hypoproteinemic
- Banamine, bismuth
- Laminitis prevention- ice feet
- Re-establish normal GI flora- hay, probiotics, +/- transfaunation
- +/- Antibiotics
- +/- Antitoxin
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What antibiotics do you give to a horse with Salmonelosis?
none- no evidence that antibiotics alter the course of Salmonellosis in horses UNLESS there is severe neutropenia (Enrofloxacin or Gentamicin)
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What antibiotic is indicated for Clostridial diarrhea?
Metronidazole (stop atb immediately if you suspect atb-induced colitis)
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What antibiotic is indicated to treat Potomac Horse Fever?
oxytetracycline!!
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What are anti-toxins that are used in horses with acute colitis, and what organism is each directed against? (3)
- polymyxin B- binds endotoxin
- antiserum (??) for Salmonella
- Dr-tri-octahedral smectite- binds Clostridial toxins
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Anterior enteritis is aka ___________.
proximal duodenitis-jejunitis
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Anterior enteritis causes _________ from the ________ and __________ secondary to __________; there is associated ____________.
hypersecretion; SI; functional ileus; inflammation; leakage of protein
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What are clinical signs of anterior enteritis? (5)
- colic that usually improves after refluxing
- large volumes of NG reflux
- fever
- high or low WBCs
- hemoconcentration/ dehydration
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How is anterior enteritis diagnosed? (3)
- functional ileus on US
- fluid-filled SI on rectal
- abdominocentesis shows no evidence of ischemia (important to r/o strangulating lesions)
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What is a huge rule out for anterior enteritis, and how do you rule it out?
- Intestinal strangulation
- SI strangulation: continued, severe pain, serosanguinous abdominal fluid with high lactate
- Anterior enteritis: less pain after refluxing, normal to orange abdominal fluid
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What are etiologic agents of anterior enteritis? (4)
[often no definitive Dx] Clostridium, Salmonella, mycotoxins, inc risk with high conc diets
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Describe the therapy for anterior enteritis. (7)
- Gastric decompression (NG reflux every 2-4hr)
- IV fluids
- Laminitis prevention
- NSAIDs
- Anti-endotoxin
- +/- prokinetics
- +/- antibiotics
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When do you refer cases of colitis and enteritis? (6)
hypovolemic shock, uncontrollable pain, continued NG reflux, need for isolation, unresponsive to treatment, faster test results desired
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What is PLE?
malabsorption and maldigestion, most often SI IBD, leading to hypoalbuminemia (+/- panhypoproteinemia) and dependent edema--> weight loss
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Why do horses with PLE get edema?
hypoalbuminemia (responsible for oncotic pressure)--> can't keep fluid in vasculature--> edema
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What are etiologies of PLE? (7)
idiopathic granulomatous enteritis, multisystemic eosinophilic epitheliotrophic disease (MEED), lymphocytic-plasmacytic enterocolitits, lymphosarcoma, right dorsal colitis, Lawsonia intracellularis, parasitism
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What animals are usually affected by idiopathic granulomatous enteritis?
1-6 years old, usually <3 years; Saddlebreds over-represented
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What are histopathologic signs of idiopathic granulomatous enteritis?
thickened SI with villous atrophy- most severe in ileum- w/ lymphoid and macrophage infiltration
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What are clinical signs of idiopathic granulomatous enteritis? (4)
severe wasting, edema, depression, usually despite having a good appetite
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What might your lab findings be with idiopathic granulomatous enteritis? (3)
anemia, low albumin, reduced absorption (??)
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What animals are usually affected by MEED?
<4 years old; Standardbreds and Thoroughbreds over-represented
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What are histo findings with MEED?
diffuse lymphocytic and eosinophilic infiltrates in SI
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Clinical signs of MEED. (6)
severe wasting, edema, appetite may be good, mild diarrhea, recurrent colic, skin lesions and ulcerative coronitis (unique to this PLE)
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What are lab findings associated with MEED? (2)
low albumin, +/- high GGT and ALP
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What animals are usually affected by lymphocytic-plasmcytic enterocolitis?
3-26 years old, i.e. no age predilection
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What are histo findings associated with lymphocytic-plasmacytic enterocolitis? (3)
mucosal/submucosal edema, infiltration of lymphocytes and plasma cells, villous atrophy
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Clinical signs of lymphocytic-plasmacytic enterocolitis. (5)
inappetence, depression, diarrhea (low-volume), colic, edema
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What lab findings are associated with lymphocytic-plasmacytic enterocolitis? (2)
low albumin and TP
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What animals are usually affected by GI lymphosarcoma?
majority <4 years old
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What are histo findings with GI lymphosarcoma? (3)
diffuse infiltration of SI and mesenteric lymph nodes, thickened SI, villous atrophy
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What are clinical signs of GI lymphosarcoma? (5)
poor appetite, edema, depression, mild diarrhea, enlarged lymph nodes
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What lab findings are consistent with lymphosarcoma? (4)
anemia, neutrophilia (lymphocytosis is rare), low albumin, high globulin
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What diagnostic test is required to make a definitive diagnosis of lymphosarcoma?
biopsy
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What is the carbohydrate absorption test?
Administer D-xylose or D-glucose via NG tube--> serial blood sampling--> look for normal peak of absorption; delayed absorption d/t malabsorption in SI or delayed gastric emptying (impaction, functional motility); almost no absorption--> PLE
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What types of biopsies can help you with the diagnosis of PLE? (4)
- Skin lesions (MEED)
- Rectal mucosa (sometimes doesn't correlate with SI)
- Gastroscopy/ duodenoscopy (mucosal biopsy only)
- Laparotomy
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What is the general prognosis for PLE?
poor for all PLE conditions
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What are the mainstays of txt for PLEs? (3)
- dexamethasone or prednisolone at tapering dose for 8 weeks
- increased caloric intake/ decrease requirement for SI digestion
- treat GI parasites if present
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What is the major cause of right dorsal colitis?
excessive phenylbutazone administration
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Describe the pathogenesis of right dorsal colitis.
decreased prostaglandin production due to NSAIDs--> decreased mucosal blood flow, decreased mucus and bicarb secretion--> ulceration of the right dorsal colon
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What are clinical signs of right dorsal colitis? (3)
colic, ventral edema, low volume diarrhea (loose stool, cow patty- not so much water)
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What lab test results might be associated with right dorsal colitis? (3)
hypoproteinemia, neutropenia, +/- azotemia
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What additional diagnostics can help you diagnose right dorsal colitis? (2)
- mostly to rule out other causes of colic
- US- thickened RDC
- gastroscopy- concurrent gastric ulcers?
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What is the treatment for right dorsal colitis? (6)
- discontinue NSAIDs!!!
- pain management- butorphanol, morphine, xylazine, detomidine, lidocaine CRI
- misoprostol- prostaglandin analog
- sucralfate
- psylium- short chain FA that acts as a local anti-inflammatory
- nutritional- small frequent meals, corn oil
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