Porcine Clostridium perfringens type A spores, enterotoxin and antibody to enterotoxin

Forty-two Clostridium perfringens type A strains isolated from cases of diarrhoea in pigs were tested for their ability to sporulate and produce enterotoxin in three different sporulation media. Enterotoxin was produced by 11 of the 42 C perfringens type A isolates (26.2 per cent). Thirteen isolates (30.9 per cent) produced spores at a frequency of 10 per cent or more. Spore production was recorded in 24 (57.1 per cent) of the isolates. The titres of enterotoxin produced by the isolates ranged from 1:2 to 1:64. The enterotoxin produced was compared with that produced by a reference strain and found to be identical. Ninety-eight of 106 sow sera from four different farms were found to possess antibodies to C perfringens type A enterotoxin with titres ranging from 1:2 to 1:64. Spores of C perfringens type A were detected in pig faeces and intestinal contents in 20 of 23 cases of enteritis at levels of up to 5 x 10(6) cells/g of faeces. Smaller numbers of spores, up to 2 x 10(4)/g were present in five of 10 samples from non-diarrhoeic pigs. Enterotoxin was demonstrated by Vero cell assay in five of the 23 samples from diarrhoeic pigs but in none of the 10 samples from non-diarrhoeic animals. It was clear from these studies that C perfringens type A strains in pigs could sporulate and produce enterotoxin in vitro and in vivo and that enteritis might be associated with sporulating organisms in vivo.     

Necrotizing enterocolitis and death in a goat kid associated with enterotoxin (CPE)-producing Clostridium perfringens type A

A goat kid died after being depressed for several days. No significant gross abnormalities were observed at postmortem examination, while histopathological analysis revealed diffuse necrotizing enterocolitis. Isolation of Clostridium perfringens type A secreting enterotoxin (CPE) and presence of CPE in the small intestine suggest that CPE contributed to the death of this kid.     

Hemorrhagic enteritis associated with Clostridium perfringens type A in a dog

A female Shetland sheep dog died suddenly with hemorrhagic diarrhea and vomitting, and was examined pathologically and microbiologically. Gross pathological change was restricted to the intestinal tract. The intestine contained watery, blood-stained fluid. Histopathologically, the principal intestinal lesion was superficial mucosal hemorrhagic necrosis at the jejunoileum. Many Gram-positive bacilli were found adhering to the necrotic mucosal surface in parts of the intestinal tract. Clostridium perfringens in pure culture were isolated from jejunal contents by anaerobic culture. These results suggested that the typical lesion of this case coincided with canine hemorrhagic enteritis and enterotoxemia due to C. perfringens infection could be the cause of sudden death.     

Enteritis associated with Clostridium perfringens type A in 9-month-old calves

Four 9-month-old Simmental male calves were presented with a history of sudden death. The necropsy and microscopic findings allowed a diagnosis of enteritis and severe intraluminal hemorrhage with blood clots in the jejunum, suggestive of jejunal hemorrhage syndrome.     

Equine grass sickness: serologic evidence of association with Clostridium perfringens type A enterotoxin.

Clostridium perfringens type A enterotoxin seroneutralization was carried out on sera from 50 horses recovered from grass sickness and from 100 other horses with no record of having had the disease. Of the affected horses, 70% had seroneutralizating titers higher than 1:64, half of these being equal or higher than 1:128. More than 88% of the horses with no record of grass sickness had titers lower than 1:64. These data support the theory of association between C perfringens type A toxins and grass sickness.     

Diarrhea associated with enterotoxigenic Clostridium perfringens in a red-footed tortoise (Geochelone carbonaria).

Enterotoxigenic Clostridium perfringens was associated with diarrhea in a 4-yr-old female captive-bred red-footed tortoise (Geochelone carbonaria). Diagnosis was based on bacterial culture, detection of C. perfringens enterotoxin in feces, and exclusion of commonly recognized pathogens. After treatment with metronidazole, normal feces were passed and C. perfringens enterotoxin was no longer detected in the feces. Although the role of C. perfringens cannot be determined definitively from this case, this pathogen should be considered in cases of diarrhea in tortoises and, perhaps, other reptiles.     

Clostridium perfringens type A enterotoxaemia in pigs: a report of five cases

Enterotoxaemia caused by Clostridium perfringens type A in five intensively managed pigs is reported. The condition was precipitated by constipative digestive disturbance. Diarrhoea was not observed in the five animals before death.     

A negative serological relationship between cases of grass sickness in Scotland and Clostridium perfringens type A enterotoxin

In an attempt to compare the equine grass sickness as reported in Europe with that described in the Republic of Colombia, sera from horses experiencing grass sickness in Scotland were used in neutralisation tests with Clostridium perfringens type A enterotoxin. The sera, from acute and chronic cases of the disease, failed to neutralise either crude or partially-purified enterotoxin. Neither were precipitin lines formed when the sera were treated against the toxin in immunoelectrophoresis. These results suggest that grass sickness in Europe and the equine disease in Colombia have a different aetiology.     

The effects of Clostridium perfringens type A enterotoxin in Shetland ponies--clinical, morphologic and clinicopathologic changes

Severe abdominal pain, classic colic signs and hemorrhagic gastro-entero-cecocolitis were induced in three conventional Shetland ponies by intravenous injection with Clostridium perfringens Type A enterotoxin. Histological examination showed marked congestion, edema and hemorrhage of the large and small intestine and sloughing of the tips of the intestinal villi. Marked vacuolar degeneration of hepatocytes with dilatation of the spaces of Disse also was found. Clinical changes consisted of severe hypoglycemia, markedly increased aspartate aminotransferase levels and leukopenia that occurred rapidly.     

The effect of enterotoxin of Clostridium welchii (perfringens) type A on fowls.

Lethal doses of enterotoxin of Clostridium welchii (perfringens) type A injected intravenously into young fowls caused immediate lassitude, with partial recovery, followed by death seven to 35 h after inoculation. Lesions found were ascites, hydropericardium, oedema of the muscles, hepatic congestion, urate deposits on the peritoneum and the pericardium, and intestinal hyperaemia. Sublethal doses produced no clinical signs or lesion. The LD50 of this enterotoxin was 74-84 mug/kg of body weight.     

Clinical and antibody responses to Clostridium perfringens type A enterotoxin in experimental sheep and calves.

Clostridium perfringens type A live cultures or sonicated sporulating cells, all containing enterotoxin, were repeatedly inoculated into sheep and calves by the intraduodenal route over periods of 30 to 35 days. Serum antibody to C. perfringens enterotoxin, tested by ELISA, developed in four of seven sheep and in two of four calves. The titers ranged from 400 to 1600. The live organism introduced into the duodenum did not become established in the bacterial flora of the intestinal tract.