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Basics ⬇

Outline

BASICS

Overview!!navigator!!

  • A rapidly progressive, highly fatal disease of foals caused by Clostridium piliforme (previously Bacillus piliformis) characterized by peracute progressive hepatitis
  • Worldwide distribution

Signalment!!navigator!!

  • Can be sporadic or occur in outbreaks
  • Foals of any breed and sex are affected
  • Age ranges from 5 days to 6 weeks old; average age 20 days

Signs!!navigator!!

  • Usually normal at birth and then develop rapidly progressive signs including lethargy, loss of suckle reflex, diarrhea, tachycardia, and dehydration
  • Icterus, fever, seizures
  • Foals are usually found dead without significant premonitory signs

Causes and Risk Factors!!navigator!!

  • Ingestion of spore-containing feces with subsequent colonization of the intestine and liver via the portal circulation
  • C. piliforme, a Gram-negative, endospore-forming, obligate intracellular bacterium found in soil and feces
  • Foals born to nonresident mares and/or mares <6 years of age are more likely to develop disease, possibly owing to differences in colostral quality and specific protective immunoglobulin

Diagnosis ⬆ ⬇

Outline

DIAGNOSIS

Presumptive diagnosis may be made on history, physical examination, diagnostic imaging, and clinicopathologic data. Definitive antemortem diagnosis requires demonstration of C. piliforme on liver biopsy.

Differential Diagnosis!!navigator!!

  • Neonatal septicemia
  • Neonatal isoerythrolysis
  • Viral hepatitis
  • Toxic hepatopathy (rare)

CBC/Biochemistry/Urinalysis!!navigator!!

  • CBC—hemoconcentration, hyperfibrinogenemia, and normal to low leukocyte count
  • Biochemistry—hypoglycemia, metabolic acidosis. Elevated serum sorbitol dehydrogenase, γ-glutamyltransferase, alkaline phosphatase, bilirubin

Other Laboratory Tests!!navigator!!

  • PCR testing on samples of liver and/or cecum
  • Coagulation profiles—prolonged prothrombin time/activated partial thromboplastin time, increases in fibrin degradation products, decreases in antithrombin

Imaging!!navigator!!

  • Abdominal radiography may reveal hepatomegaly
  • Transabdominal ultrasonography may reveal hepatomegaly with diffuse hyperechogenicity

Other Diagnostic Procedures!!navigator!!

  • Percutaneous liver biopsy and demonstration of characteristic histopathologic findings (see Pathologic Findings)
  • C. piliforme is extremely difficult to culture in vitro

Pathologic Findings!!navigator!!

  • Hepatomegaly with coagulative necrosis surrounded by degenerate hepatocytes and neutrophilic (suppurative) inflammatory cell migration
  • Confirmation of Tyzzer disease is achieved by histologic demonstration of intracellular interlacing bundles of filamentous bacilli (C. piliforme) at the periphery of the lesions within the liver

Treatment ⬆ ⬇

TREATMENT

  • Limited reports exist of successful treatment in confirmed cases
  • Fluid therapy is essential. Volume resuscitation, glucose provision, and electrolytes to assist in correcting metabolic acidosis

Medications ⬆ ⬇

Outline

MEDICATIONS

Drug(s) of Choice!!navigator!!

  • Broad-spectrum antimicrobials, including Gram-negative anaerobic coverage such as penicillin (22 000 IU/kg IV every 6 h), tetracycline (10 mg/kg IV every 12 h), erythromycin (25 mg/kg PO every 6 h), sulfamethoxazole–trimethoprim (15–25 mg/kg PO every 12 h), and metronidazole (10 mg/kg PO every 12 h)
  • Seizure management using diazepam (0.1–0.4 mg/kg IV) or midazolam (0.02–0.06 mg/kg/h constant rate infusion)
  • Anti-inflammatory drugs, e.g. ketoprofen (1.1–2.2 mg/kg IV every 12 h)
  • Lactulose (0.1–0.25 mL/kg PO every 6–8 h) to help reduce intestinal ammonia production

Contraindications/Possible Interactions!!navigator!!

  • Barbiturates should be given with caution for seizure management given their extensive hepatic metabolism. Benzodiazepines have the potential to worsen hepatoencephalopathy owing to potentiation of GABA-induced sedation
  • Metronidazole is given at a lower dose owing to reduced hepatic metabolism

Follow-up ⬆ ⬇

Outline

FOLLOW-UP

Patient Monitoring!!navigator!!

  • Monitor plasma ammonia, acid–base status, and glucose frequently during therapy
  • Consider decreasing doses of any medication that undergoes hepatic metabolism

Prevention/Avoidance!!navigator!!

None specific. Ensure adequate transfer of passive immunity.

Expected Course and Prognosis!!navigator!!

  • Grave prognosis. Most foals die within 24 h from the onset of clinical signs. Early recognition, referral to an intensive care facility, and therapeutic intervention are required to have any chance of clinical resolution.

Miscellaneous ⬆ ⬇

Outline

MISCELLANEOUS

Zoonotic Potential!!navigator!!

Unknown

Pregnancy/Fertility/Breeding!!navigator!!

N/A

Abbreviations!!navigator!!

  • GABA = γ-aminobutyric acid
  • PCR = polymerase chain reaction

Suggested Reading ⬆ ⬇

Borchers A, Magdesian KG, Halland S, et al. Successful treatment and polymerase chain reaction (PCR) confirmation of Tyzzer's disease in a foal and clinical and pathologic characteristics of 6 additional foals (1986–2005). J Vet Intern Med 2006;20:1212–1218.

Fosgate GT, Hird DW, Read DH, et al. Risk factors for Clostridium piliforme infection in foals. J Am Vet Med Assoc 2002;220:785–790.

Swerczek TW. Tyzzer's disease in foals: retrospective studies from 1969 to 2010. Can Vet J 2013;54:876–880.

Author(s) ⬆

Author: Samuel D.A. Hurcombe

Consulting Editor: Margaret C. Mudge