Signalment:  

Three-month-old, female Saanen goatA 3-month-old, unvaccinated Saanen goat was anaesthetized for the purpose of performing a laparotomy to inject 100 mls of a 20% solution of cornstarch into the abomasum, followed by inoculation of the duodenum with a 200 ml culture of Clostridium perfringens type D (approximately 1 x 10⁸ CFU per ml). The animal recovered completely from anaesthesia within 30 minutes after surgery, developed hemorrhagic diarrhea 8 hours post-inoculation, and was euthanized 12 hours later. Necropsy was performed immediately.

Gross Description:  

The wall of the colon was thickened with mild serosal and mesocolonic edema. The colon contained red fluid and the diffusely red colonic mucosa was lined by strands of tan fibrinous exudates (Figs. 3-1, 3-2). Other findings included dilatation and mucosal congestion of the small intestine, and cerebellar coning (herniation of posterior cerebellum into foramen magnum).

Histopathologic Description:

Multifocal to diffuse necrosis of superficial to mid-mucosa is accompanied by formation of a diphtheritic membrane composed of fibrin, mucus, exfoliated epithelial debris, neutrophils, erythrocytes and abundant bacteria (predominantly large bacilli) on the luminal surface of the necrotic mucosa. Clumps of similar fibrinocellular exudate and bacteria also lie free within the lumen. Crypts underlying the necrotic, eroded surface epithelium are distended with catarrhal exudate and lined by necrotic to attenuated epithelium; and associated lamina propria is markedly congested, hemorrhagic and infiltrated by numerous neutrophils. Deep crypts are frequently mildly distended with mucus or catarrhal exudate, and the deep lamina propria and muscularis mucosae are populated by occasional clusters of neutrophils. Scattered lymphatic vessels within the submucosa, tunica muscularis and serosa/mesocolon are distended with proteinaceous fluid. The submucosa is irregularly, mildly/moderately expanded by proteinaceous effusion, infiltrated by small numbers of neutrophils, and populated by scattered clusters of lymphoid cells, and the serosa is mildly, irregularly edematous.

Morphologic Diagnosis:  

Multifocal to diffuse, moderate/severe, pseudomembranous (fibrinonecrotic) colitis, etiology subacute, caprine Clostridium perfringens type D enterotoxemia

Condition:  

Clostridium perfringens Type D

Contributor Comment:  

Enterotoxemia caused by Clostridium perfringens type D occurs in several animal species but has been studied most thoroughly in sheep. The pathogenesis of C. perfringens type D enterotoxemia in sheep and goats is mostly mediated by epsilon toxin.(2,3)

In sheep, type D enterotoxemia mostly occurs following a sudden change of diet, particularly to feeds rich in fermentable carbohydrates (resulting in large amounts of undigested carbohydrates entering the small intestine). Ovine type D enterotoxemia produces acute to chronic neurologic disease (ranging from sudden death to blindness, opisthotonus, bleating, convulsions and recumbency with paddling) frequently accompanied by respiratory signs and uncommonly accompanied by diarrhea.(3) The neurologic signs are caused by cerebral perivascular proteinaceous edema (observed in 90% of cases), and in chronic cases multifocal, bilaterally symmetrical necrosis of white matter. The respiratory signs are caused by pulmonary edema. There are usually no significant gross or microscopic changes in the intestinal tract of sheep dying from enterotoxemia.(2,3)

Less is known about predisposing factors of caprine type D enterotoxemia. Cases of type D enterotoxemia have occurred in goats on a regular hay diet.(3) In goats with type D enterotoxemia, the most consistent clinical signs are diarrhea, respiratory distress and central nervous system (CNS) signs including recumbency, paddling, bleating and convulsions. Pseudomembranous colitis, similar to that observed in this goat, is the most characteristic postmortem change in caprine enterotoxemia. Histological changes in the brain are not a consistent feature of caprine type D enterotoxemia; however, cerebral vasogenic edema can be observed in some cases of subacute type D enterotoxemia such as this. Accompanying small intestinal lesions are uncommon in goats and were not observed in this case. Cerebellar coning in this goat was considered to be a consequence of cerebral vasogenic edema.(2,3)

In summary, the major difference between type D enterotoxemia in sheep and goats is the response of the intestinal tract to the disease. The reason for the caprine-specific, selective damage to the large intestine has not been determined. It is possible the caprine small intestine is simply more resistant than the large bowel to the effects of the epsilon toxin (or possibly other C. perfringens type D toxins). Antibiotic-associated pseudomembranous colitis in humans, caused by Clostridium difficile, has a similar disease pattern; however, the reason for the lesion distribution has not been identified.(2) It is also possible that the small intestinal mucosa of sheep is more susceptible to damage by epsilon toxin through facilitating absorption of the toxin into the bloodstream with more pronounced systemic effects (CNS lesions). It has also been suggested that the selective damage of the large bowel in goats is a consequence of toxin modification by enzymes in the goat colon. However C. perfringens epsilon toxin, produced as an inactive prototoxin, is activated following cleavage by trypsin. Because trypsin is secreted in the small intestine, epsilon toxin should be activated in the small intestine of both sheep and goats.(2) Transit speed of the intestinal content should not be a factor with regard to the different disease pattern of type D enterotoxemia in sheep and goats because of the similar transit time in both ruminants (normally approximately three hours for small intestine, and 18 hours for large bowel).(2)

JPC Diagnosis:  

Colon: Colitis, fibrinonecrotic, multifocal to coalescing, marked, with hemorrhage and superficial cocci and bacilli (Fig. 3-3)

Conference Comment:  

Clostridium perfringens type D, also known in the veterinary literature as overeating disease, or pulpy kidney disease, is an agriculturally important disease of ruminants. Unfortunately, this disease often affects the hardiest animals on the farm and is caused by excessive intake of starch. The two major types of toxins produced by C. perfringens type D include alpha and epsilon, with epsilon being the major contributor to disease.(1) In sheep, epsilon toxin binds to endothelial cells (especially in the brain) leading to focal symmetrical encephalomalacia (FSE). Grossly, lesions often appear in the basal ganglia, thalamus, or substantia nigra. Within the kidney, once bound to distal renal tubular epithelium, the tubules degenerate and the result is a pulpy kidney. Rapid autolysis of the sheep carcass is also thought to contribute to the pulpy appearance of the kidney. 

There are four clinical forms of Clostridium perfringens type D enterotoxemia in goats: peracute, acute, chronic and subclinical. The peracute form manifests as sudden death with little to no warning. The acute form is characterized by diarrhea and colic of a few days duration, and this turns into the chronic form if the animal does not either fully recover or die within a few days of clinical onset. Mentioned by the contributor, the distal small intestine, cecum, and large intestine are most severely affected in goats. Histologically, affected areas are hyperemic and may be covered by a layer of fibrin with a moderate number of inflammatory cells present in the lamina propria.(1)

References:

1. Brown CC, Baker DC, Barker I: Alimentary system. In: Jubb, Kennedy and Palmers Pathology of Domestic Animals, ed. Maxie MG, 5th ed., vol 1, pp. 212-220. Elsevier Limited, Philadelphia, PA, 2007
2. Uzal FA, Kelly WR: Experimental Clostridium perfringens type D enterotoxemia in goats. Vet Pathol. 35:132-140, 1998
3. Uzal FA, Songer JG: Diagnosis of Clostridium perfringens intestinal infections in sheep and goats. J Vet Diagn Invest 20:253-265, 2008

Click the slide to view.

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03-1. Colon, goat.

03-2. Colon, goat.

03-3. Colon, goat.

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