Tyzzer’s Disease in a Foal-Clostridium piliforme

Tyzzer’s Disease in a Foal-Clostridium piliforme

History: A 1 month-old female intact Quarterhorse foal. She was depressed, with an increased respiratory rate. Later that day,her temperature increased to104.5 F so 37 mg Banamine PO was administered. The animal refused to eat grain. On 4/6/09 the filly had watery foul smelling diarrhea soaking its tail and hindquarters, andwas wide stance, stiff-legged, ataxic, its head tilted to the left, and fell down after a few steps. During the day, the filly was recumbent and did not attempt to get up. The results of the serum assays were increased liver enzymes and numerous electrolyte abnormalities. The foal died on that afternoon.

Gross findings:

The foal was in fair body condition. Her mucous membranes were pale and slightly icteric. There was green fecal staining on the hind legs, tail and perineum. The abdominal cavity contained 100 ml of yellow serous fluid.

The liver was diffusely enlarged with coalescing yellow areas of necrosis in all the lobes.
Liver, capsular surface: There are coalescing pale yellow areas of necrosis

Liver, cut sections: The pale yellow necrotic areas contrast to the congested dark red areas. Within the dark red areas are multifocal areas of necrotizing, hemorrhagic hepatitis.

The ventral colon had several 3 mm multifocal ulcers with clotted blood and ingesta adhered to them. The rest of the mucosa was diffusely red(congestion).  No formed feces was found in the descending colon.

The lungs failed to collapse and had a rubbery texture.  The tracheobronchial lymph nodes were enlarged and edematous. The pericardium contained approximately 20 ml of yellow serous fluid.
There were mild, multifocal subendocardial hemorrhages.

The following structures were grossly normal: Oral cavity, guttura lpouches, pharynx, larynx, trachea, thyroid glands, pancreas, stomach,small intestine, cecum, dorsal colon, kidneys, ureters, adrenal glands,urinary bladder, uterus, ovaries, brain, and skeletal muscle.


Liver: There are multifocal to coalescing areas of necrosis and hemorrhage affecting approximately 60 % of the liver. Necrotic areas have a central zone of pale eosinophilic hepatocytes with loss of cellular and nuclear detail, and this is surrounded by a zone of necrotic cellular and nuclear debris with degenerate and intact neutrophils, macrophages and lymphocytes. Many hepatocytes in and adjacent to the areas of necrosis contain numerous intracytoplasmic bacterial rods resembling sheaves of wheat (consistent with Clostridium piliforme). Multifocally, the portal areas contain fibroblasts, macrophages, lymphocytes, and plasma cells, and bile ductile proliferation. The capsule is thickened with moderate amount of collagen and proliferating fibroblasts.

Liver, low power: There are multifocal pale eosinophilic (pink) areas of hepaticyte necrosis which are immediately surrounded by the darker basophilic stippling of degenerate and intact neutrophils

Liver, high power: Numerous hepatocytes surrounding the necrotic areas contain long bacterial rods (arrows) which appear to stack on top and cross eachother (Clostridium piliforme)

Liver, high powe Warthin-Starry Silver stain: The intracytoplasmic bacterial rods appear as long black sticks (arrows)

Heart: There are multifocal areas of myocardial necrosis and neutrophilic infiltration with mineralization.

Heart, high power: There is multifocal cardiomyocyte necrosis and mineralization with moderate numbers of degenerate neutrophils

Spleen: Multifocally, there is depletion of follicular lymphocytes.

Large intestine: There is a focal hemorrhage and ulceration of the mucosa. Multifocally the mucosa contains cross sections of adult nematodes.

There are no microscopic lesions in the lungs, kidneys, pancreas, adrenal glands, thyroid glands, tongue, skeletal muscle, ovary, small intestine, stomach, lymph nodes, or brain.


1. Liver: Necrotizing hepatitis, neutrophilic, multifocal to coaleascing, chronic with intracellular bacteria, mineralization, and bile duct proliferation.

2. Heart: Multifocal necrotizing myocarditis, neutrophilic with mineralization

3. Large intestine: multifocal mucosal ulceration, and intramucosal nematodes

Laboratory results:

Anaerobic culture: Spleen: Clostridium perfringens

Clostridium piliforme PCR (UC Davis): Postitive (liver)


The histological changes in the liver are diagnostic for Tyzzer’s disease(Clostridium piliforme infection).  The PCR test was positive for Clostridium piliforme.  C. piliforme is an obligate intracellular bacterium, and is very difficult to grow in laboratory setting, so it is no surprise that the anaerobic cultures failed to grow it.  The C. perfringens grown from the spleen was considered a post-mortem contaminant.

The pathogenesis of this disease probably begins with the bacteria colonizing the intestinal epithelium, then causing transmural necrosis leading to hematogenous dissemination to the liver and in this case probably to the heart.  Although no bacteria was visible by histopathology in the heart it is possible that small numbers were able to colonize the myocardium causing necrosis and subsequent mineralization.  The necrosis caused by the bacteria is presumed to be caused by mechaninsm other than an exotoxin alone, but the exact mechanism of cell death has not been well characterized.  In foals diarrhea can be associated with Tyzzer’s disease, but it is an inconsistent finding.  The liver lesions are the most consistent finding, which lead to acute liver failure and hepatic encephalopathy.  The nematodes found on histopathology are probably small strongyles (Cyathostomes).

About Brian

Anatomic Pathologist, VetPath Services, Stone Ridge, NY- musculoskeletal, oral/dental, and sinonasal diseases www.vetpathservices.com
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1 Response to Tyzzer’s Disease in a Foal-Clostridium piliforme

  1. Jimmy S Kalianda says:

    I really enjoy veterinary pathology forum, here 1 can reinforce my knowledge and experience.Thank you

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