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Enterotoxemia attributable to Clostridium perfringens type D in goats is difficult to diagnose because of a lack of specific clinical signs or postmortem lesions, on which to base the diagnosis. This report describes the clinical signs, postmortem lesions, and clinical responses to treatment and vaccination in 4 goat herds, in which a diagnosis of enterotoxemia was confirmed. Four clinical cases had the diagnosis confirmed on the basis of signs of diarrhea or sudden death and the isolation of C perfringens and epsilon toxin from the feces at the time of admission. The 10 necropsy cases were diagnosed on the basis of the isolation of C perfringens (not typed) or epsilon toxin from the intestinal contents of goats that died with clinical signs compatible with enterotoxemia and without lesions associated with a second serious disease. Enterocolitis was the most consistent lesion reported at necropsy in the 10 goats with enterotoxemia. Ovine enterotoxemia vaccines were of limited value in preventing enterotoxemia. These observations imply that naturally induced enterotoxemia in goats involves a different pathophysiologic mechanism than that associated with enterotoxemia in sheep.
Two double sandwich enzyme-linked immunosorbent assays (ELISA) for Clostridium perfringens beta and epsilon toxins were assessed for routine diagnosis of enterotoxemias on intestinal contents of 151 sheep that died suddenly. Conventional tests (mouse assay and culture of organism) showed that 21 specimens were positive for Clostridium perfringens type C (beta toxin) and 39 were positive for Clostridium perfringens type D (epsilon toxin) enterotoxemias. Comparison of the ELISA results with conventional assays gave sensitivity and specificity rates respectively of 90.5% and 89.2% for beta toxin assay and 97.4% and 94.6% for epsilon toxin assay. With further refinement to improve the performance of the assay for beta toxin these tests could serve as a substitute for conventional tests in the laboratory diagnosis of Clostridium perfringens types B, C and D enterotoxemias.
Maturing lambs, eight to nine months old, were dosed by the intraduodenal route with various preparations of Clostridium perfringens type C. Whole cultures of this organism or cells suspended in fresh medium, both supplemented with soybean flour as a protease inhibitor, produced acute fatal hemorrhagic enterotoxemia in these animals. The latter preparation was more effective than the former in causing disease. Without the soybean supplement the inocula did not produce fatal disease. Dosing with toxic cell-free culture supernatant fluid, with or without soybean supplement, had no lethal effect. Animals that died showed severe hemorrhagic enteritis with necrosis and sloughing of the mucosal epithelium, involving jejunum, ileum and part of duodenum. These lesions were similar to those seen in natural cases of hemorrhagic enterotoxemia in neonatal animals. This experiment demonstrated that nonimmune animals are normally protected against C. perfringens type C enterotoxemia by adequate levels of pancreatic proteases in the intestine, and that factors which inhibit or reduce these enzymes predispose animals for the development of this disease.
Enterotoxemia was induced in 4 lambs and 4 goat kids by continuous intraduodenal infusion of a whole culture of Clostridium perfringens type D. Clinical signs, hematologic values, biochemical alterations, and postmortem lesions in the lambs and goat kids were compared. The 4 lambs and 4 goat kids died within 25 hours of beginning the infusions. Lesions were not observed in the gastrointestinal tract of the 4 lambs; however, severe hemorrhagic enterocolitis was found in the 4 goat kids. This difference between the lambs and goat kids in the lesions caused by experimentally induced enterotoxemia may explain the discrepancies reported between sheep and goats in clinical signs, response to treatment, and efficacy of vaccination observed in naturally induced enterotoxemia in the 2 species.
Experimental colibacillary (Escherichia coli) enterotoxemia as described in this report mimics natural edema disease both clinically and in gross pathology. The histopathology is characterized by accumulations of non-inflammatory edema and by arteriopathy. The smaller arterial and arteriolar changes recorded here are similar to those described in natural edema disease. The vascular changes described in recovered cases of experimental colibacillary enterotoxemia concur with those reported in so-called subacute and chronic edema disease. The arteriolar changes that occur in colibacillary enterotoxemia of swine are comparable to those associated with hypertension. Thin sections of cerebral cortex from four pigs with acute experimental edema disease were examined by electron microscopy in an attempt to demonstrate brain edema. Sections from one pig taken during the convulsive phase of disease revealed dilatation of perivascular glial processes. However, examination of sections taken from three other pigs during an earlier phase of the neurological disturbance revealed no significant lesions. We were unable to ascertain the role of brain edema in the pathogenesis of the nervous system disturbance in these experiments.
The effects of intraduodenal administration of Clostridium perfringens cultures and culture products in goats were evaluated to develop a reliable experimental model of enterotoxemia in this species. Five conventionally reared, 11-16-week-old Angora goat kids were dosed intraduodenally with whole cultures of C. perfringens type D; five similar animals were dosed with C. perfringens type D filtered culture supernatant; and a third group of five kids was dosed with C. perfringens type D washed cells. Two kids were used as controls and received sterile, nontoxic culture medium intraduodenally. All animals received starch solution into the abomasum. All five kids inoculated with whole culture and three of five dosed with culture supernatant and with washed cells developed central nervous system signs. Diarrhea was observed in two of five kids inoculated with whole culture, in all five of those dosed with culture supernatant, and in three of five of those that received washed cells. The most striking postmortem findings consisted of lung edema, necrotizing pseudomembranous colitis, and cerebral vasogenic edema. The protocol thus provided a reasonable model of naturally occurring enterotoxemia in goats, producing a range of clinical signs and postmortem changes similar to those observed in the natural disease.
C. perfringens type A was isolated from different organs and intestines from breeding and racing camels which died from peracute and acute enterotoxemias in two separate outbreaks. Pathological changes in the digestive tract were mild in breeding camels, and severe in racing camels. A polyvalent clostridial antiserum of bovine origin given intravenously had a life-saving effect on breeding camels, but not on racing camels. In the two outbreaks, fifty percent of the breeding camels were suffering from an acute Trypanosoma evansi infection, and 25% of the racing camels had developed a salmonellosis. It is suggested that both infections played an important role as predisposing factors for the outbreak of C. perfringens enterotoxemias.
The coli enterotoxemia caused by Coli serotype 0139 occurred in contrary to the generally observed course of this infection through several weeks and was exceedingly detrimental. Almost exclusively the shock and oedema form of coli enterotoxemia was seen. The application of usual schemes of prophylaxis and therapy did not effect durable reduction of animal losses. With the daily oral application of Rhodovet, a drug containing thiocyanate, in doses of 3.5 kg/t feed during 5 weeks the morbidity resp. mortality could be decisively reduced.
The incidence, bacterial characteristics, disease syndromes, diagnosis, treatment, and prevention of enterotoxemia of neonatal calves caused by Clostridium perfringens (Types A, B, C, D, and E) are reviewed.
Staphylococcal enterotoxin B (SEB) injected intravenously is rapidly cleared from the circulation and deposited in tissues. Type-specific antiserum administered after toxin has left the circulation can influence the course of enterotoxemia, and this observation suggests that toxin antigens may either be returned to the circulation or reside on cell surfaces readily available to antibody. If SEB toxin or its fragments regain access to the extracellular space, they might react with circulating antibody and be detected and quantitated by the reduction in antibody titer. Accordingly, 1 h after toxin or saline injection, animals were given type-specific enterotoxin B antiserum, and the difference in titers between the animals was used to compute the amount of enterotoxin immediately available to antibody. Further, by measuring differences in titers over a 48-h period, an estimate was made of the amount of SEB antigen that gained access to antibody. The data indicate that rats, which are relatively resistant to the lethal effects of enterotoxin, clear toxin from the circulation promptly and that very little toxin reenters the circulation. Monkeys, who are highly susceptible to SEB, also clear toxin promptly. However, in contrasts to rats, monkeys have greater quantities of SEB immediately available to antibody and in addition return significant quantities of toxin antigens to the extracellular space.
The official methods of control of vaccines against sheep enterotoxemia are indirect in two ways : on the one hand they are carried out on animals for which the vaccine is not intended, and on the other hand they test only an immunological serum reaction. Another method consisting of direct testing by intravenous injection of toxin has been carried out on mice previously vaccinated with different doses. It has been shown that it is possible to obtain a certain level of protection giving a good dose-effect relation. However, immunity provided by this direct method is weak although the vaccine utilized is considered very efficacious with regard to the official norms of the direct test. These results, which are both encouraging and disappointing, will be the subject of a more intensive study of the different parameters in question.
Two Quarter Horse foals from different premises died from enterotoxemia. Clostridium perfringens toxins alpha and beta were demonstrated in the foal's intestines by mouse protection tests. Clostridium perfringens type C was isolated from the intestines of each foal. Histologic examination revealed hemorrhage, necrosis, and massive numbers of C perfringens.
Necrotising enteritis had been the cause of death of 4.9 per cent in 5,177 nursed piglets, which was established by pathological examination. The number of piglets, in that context, which had come from industrialised sow breeding units was equivalent to 92 per cent. The nursed piglet held the third position, next to smaller ruminants (19.4 per cent) and fowl (6.0 per cent), with regard to the occurrence of Clostridium perfringens enterotoxemia or necrotising enteritis in 112,218 animals which were pathologically examined after death. Necrotising enteritis so far has been rare in the GDR. No regional accumulation has been observed. Several outbreaks on industrialised sow breeding units actually remained stationary. The occurrence of the disease may be favoured by a number of factors which are conducive to accumulation of Clostridium perfringens Type C in a given stock. Group keeping of pregnant sows, simultaneous farrowing of larger groups of sows, group treatment of nursed piglets, using neomycin, chloramphenicol, oxytetracycline, and other antibiotics to which Clostridium perfringens is primarily resistant or has acquired resistance in the course of time are some of those contributive factors. Transmission of Clostridium perfringens Type C through feedstuff is possible, though it would lead to a real outbreak only by high intensity of the contamination, and it played a minor role in proliferation of the disease. 3479 Clostridium perfringens strains were isolated from 9,481 animals, both clinically intact and after death, with 30 species being included. Type classification revealed 2454 strains of Type A (70 per cent), 204 of Type D (5.88 per cent), 164 of Type C (four per cent), and 48 of Type B (1.34 per cent). There were 688 atoxic strains (17 per cent). Swine is the major carrier of Clostridium perfringens Type C, with 87 per cent of all Clostridium perfringens Type C strains having been isolated from swine. Swine was followed by fowl (four per cent), sheep (four per cent), cattle, rabbit, and dog (1.27 per cent each). Clostridium perfringens Type C was obtained from the faeces of clinically intact sows in seven instances, including two cases with sows (0.46 per cent) from farms with no previous record of necrotising enteritis.
Eleven Clostridium perfringens type C strains isolated from fatal cases of hemorrhagic enterotoxemia of Canadian calves, a piglet, and a foal were studied for the production of soluble antigens. All the isolates from calves and a foal failed to produce delta toxin, but were capable of producing large amounts of lethal beta toxin. A strain isolated from a piglet produced delta, but very little beta toxin. Other differences were relatively minor. The results indicated that young domestic animals may be susceptible to all subtypes of C. perfringens type C. A simple method of using blood agar plates coated with type A antiserum for demonstration of hemolytic patterns was found advantageous in differentiation of C. perfringens strains.