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

Abstract

A 5-year-old Dutch Warmblood gelding was referred to the University of Pennsylvania George D. Widener Hospital for the evaluation of abdominal discomfort and acute onset of neurologic deficits. The horse was imported from Holland 10 days before admission and was intended to be used for dressage. Vaccination for rhinopneumonitis, influenza, and tetanus was performed 11 months before importation, and the horse had no medical history that was relevant to this study. The day before presentation, the horse was depressed, febrile, and anorexic and showed mild abdominal discomfort. Treatment with 500 mg of flunixin meglumine IV and 2 g of phenylbutazone PO improved the horse's clinical signs. The following day, the horse became increasingly depressed and tachycardic and showed signs of abdominal discomfort. Progressive development of ataxia was also reported by the referring veterinarian. The horse received an additional 500 mg of flunixin meglumine IV and was referred for further medical evaluation and treatment.Upon arrival, the gelding was very depressed and showed signs of severe symmetric ataxia in all 4 limbs with hindlimb extensor rigidity. The horse was head pressing, leaning against walls, and propulsively circling. Rectal temperature, heart rate, and respiratory rate were 99.8ЊF, 60 beats/min, and 24 breaths/min, respectively. His mucus membranes were hyperemic and tacky with a capillary refill time of 1.5 seconds. The peripheral pulses were weak, the distal extremities were cold, and hypalgesia was present. No menace response was obtained in either eye, and pupillary light response was slow bilaterally. Cardiac and thoracic auscultation were normal. Borborygmi were decreased, and abdominal distention was present bilaterally. The horse showed intermittent signs of mild abdominal discomfort characterized by a regular pawing and looking at his flanks. Rectal palpation revealed a gas-distended large colon. Nasogastric intubation did not yield marked reflux. Abdominocentesis yielded grossly and cytologically normal peritoneal fluid. Urinalysis was unremarkable. Attempts to perform a sonographic evaluation of the abdomen were unsuccessful because of the horse's behavior. A CBC showed a PCV of 61% (reference range, 32-52%), a total protein concentration of 7.4 g/dL (reference range, 4.6-6.9 g/dL), and a white blood cell count of 1.39 ϫ 10 3 cells/L (ref-Medicine 0891-6640/03/1702-0019/$3.00/0 erence range, 5.5-12.5 ϫ 10 3 cells/L) with 26% segmented neutrophils (reference range, 30-65%) and 6% band cells (reference range, 0-2%) with toxic changes. Hypochloremia (91 mg/dL; reference range, 94-102 mg/dL), hypocalcemia (9.99 mg/dL; reference range, 10.7-13.4 mg/ dL), hypomagnesemia (0.91 mg/dL; reference range, 1.6-2.5 mg/dL), and hyperglycemia (191 mg/dL; reference range, 72-114 mg/dL) were shown on clinical chemistry evaluation. The plasma creatinine concentration was increased at 2.23 mg/dL (reference range, 0.6-1.8 mg/dL), and the lactate concentration was 13.6 mol/L (reference range, Ͻ2 mol/L). Because the horse's...

Postmortem diagnosis of idiopathic hyperammonemia in a horse

“…Bacteria that produce ammonia in the gastrointestinal tract are gram‐negative aerobic bacilli, such as Escherichia coli , Klebsiella , Proteus , and Pseudomonas 3. Clostridium sordelli is a gram‐positive spore‐forming bacillus that also has been implicated as a potential cause of hyperammonemia associated with colitis in the horse because of its urease activity 1. Salmonella agona , the bacterium isolated in this case, is not known to be a urease‐producing bacterium 8…”

“…Hyperammonemia in the absence of liver disease has been reported as a cause of encephalopathy in 11 horses, 9 of whom had signs of gastrointestinal disease 1–7. The majority of these horses were either euthanized, or died shortly after developing signs of encephalopathy.…”

“…The majority of horses with idiopathic hyperammonemia died or were euthanized soon after the onset of clinical signs 1–7. The acute nature of this disease in horses often does not provide sufficient time for an antemortem diagnosis.…”

“…However, the sample sat at room temperature for approximately 2 hours before being stored at 4°C for 10 hours, at which time it was analyzed for ammonia concentration using a colorimetric assay (Vitros 5,1 FS Chemistry System, Ortho‐Clinical Diagnostics). Although the ammonia concentration was markedly increased (958 μmol/L; reference interval 11–55 μmol/L1), the results were considered questionable because of the delay in analysis. We hypothesized that ammonia concentration also would be increased in cerebrospinal fluid (CSF) and aqueous humor and that these might be appropriate samples to confirm a diagnosis of hyperammonemia postmortem, since additional antemortem samples were unavailable.…”

Uroperitoneum secondary to rupture of the urachus associated with Clostridium spp. infection in a foal: a case report

“…sordellii is a soil organism and is able to penetrate the wounds and mucous membranes. It has been demonstrated that C. sordellii induces haemorrhagic enteritis in equine neonates and oedema, infection of wounds and hyperammonemia in adult horses (Desrochers et al, 2003;Ortega et al, 2007). C. perfringens is a life-threatening bacterium in 1-10 day old foals, inducing necrotizing enterocolitis (East et al, 1998).…”