Clostridium sordelli Infection as a Suspected Cause of Transient Hyperammonemia in an Adult Horse

Desrochers, Anne; Dallap, Barbara L.; Wilkins, Pamela A.

doi:10.1111/j.1939-1676.2003.tb02441.x

Cited by 20 publications

(31 citation statements)

References 15 publications

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“…Although liver disease is the most commonly reported cause of hyperammonemia in horses, the laboratory data and history of colic in this case were compatible with hyperammonemia associated with gastrointestinal disease 2–4. Although this interpretation is difficult to prove conclusively, the quick clinical response and resolution of hyperammonemia with symptomatic and antimicrobial treatment supported this hypothesis.…”

Section: Discussionmentioning

confidence: 48%

“…Even under normal circumstances, large amounts of ammonia are produced in the gastrointestinal tract, predominantly in the cecum and colon of horses 2. Bacterial enzymes degrade luminal amino acids, proteins, and endogenously produced urea to produce ammonia, which is carried via the portal circulation to the liver where it is detoxified by conversion to urea.…”

Section: Discussionmentioning

confidence: 99%

“…Bacterial enzymes degrade luminal amino acids, proteins, and endogenously produced urea to produce ammonia, which is carried via the portal circulation to the liver where it is detoxified by conversion to urea. Animals with liver pathology may lack adequate hepatic function to process normal amounts of ammonia, however, animals with intestinal disease may produce excessive amount of ammonia because of bacterial overgrowth or may absorb increased amounts of ammonia because of compromised intestinal barriers or ileus 2. This may overwhelm the capacity of the normal liver to detoxify ammonia, leading to accumulation of excessive ammonia in the systemic circulation.…”

Section: Discussionmentioning

confidence: 99%

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Neurologic signs and hyperammonemia in a horse with colic

Sharkey¹,

DeWitt²,

Stockman³

2006

Veterinary Clinical Pathol

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A 23-year-old Thoroughbred gelding was referred for the evaluation of acute onset of ataxia and depression, and a 2-day history of fever. On physical examination, the gelding was profoundly depressed and 10-12% dehydrated. The horse appeared very unstable, with a wide-based stance in the hind limbs, severe symmetric ataxia in all 4 limbs, and proprioceptive deficits in both hind limbs. Nasogastric intubation produced 4 L of brown, fetid reflux, and rectal examination revealed mild small intestinal and cecal distention. Hematologic abnormalities included neutropenia with toxic change, compatible with acute inflammation and endotoxemia, and prolonged coagulation times. Serum biochemical abnormalities included prerenal azotemia. metabolic acidosis, and electrolyte abnormalities consistent with enteritis. Blood ammonia concentration was markedly increased (406 micromol/L; reference interval 4-49 micromol/L), however, serum bile acids concentration and hepatic enzyme activities were within reference intervals. Histopathologic examination of a liver biopsy revealed no abnormalities and results of tests for several infectious agents were negative. Clinical signs resolved with correction of the dehydration and electrolyte abnormalities and with antibiotic therapy. The horse was diagnosed with hyperammonemic neuropathy associated with gastrointestinal disease. In such cases, hyperammonemia is caused by increased production of ammonia by organisms in the gastrointestinal tract in combination with increased gut permeability that facilitates ammonia absorption.

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Section: Discussionmentioning

confidence: 48%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Neurologic signs and hyperammonemia in a horse with colic

Sharkey¹,

DeWitt²,

Stockman³

2006

Veterinary Clinical Pathol

View full text Add to dashboard Cite

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“…Triglycerides, glucose, ammonia, AST, GGT, SDH, and BA were measured immediately in plasma from blood collected in lithium heparin tubes. Triglycerides, glucose, ammonia, 1,24 AST, and GGT were measured on a biochemistry analyzer a . BA and SDH were measured via an enzymatic colorimetric method on a different biochemistry analyzer b,c .…”

Section: Methodsmentioning

confidence: 99%

“…Surgical colic patients often experience alterations in gastrointestinal flora and mucosal barrier permeability 1–3 . Along with ileus, gastrointestinal distension, and fasting, these changes may contribute to increases in ammonia, bilirubin, and triglyceride concentrations and liver enzyme activities 1,2,4–6 . These increases may be associated with nonspecific clinical signs such as inappetence, dull mentation, and altered behavior.…”

Section: Introductionmentioning

confidence: 99%