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Postmortem examination of a Boer buck kid that died peracutely revealed diffusely congested, edematous bowel. Clostridium perfringens Type A was isolated. Some isolates carried the gene for beta2 toxin, suggesting a role for beta2 toxin in caprine enterotoxemia, a common cause of death in growing kids.
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.
A vaccination trial involving 72 goats was designed to compare the epsilon antitoxin titres and local reactions at the injection sites, of two commercial enterotoxemia vaccines. Three dosage regimens were used for each vaccine (12 goats per group). Although no significant differences were noted in humoral immune response between the two vaccines (P = 0.05), one vaccine regime resulted in low titres (P = 0.05) on two occasions. Local tissue reactions at injection sites persisted for six months in 53% of the goats regardless of vaccine used or dosage administered. No immunological basis for the reported differences in vaccine efficacy between sheep and goats was observed in this trial.
Hepatic and renal electron microscopic investigations were carried out in 10 chickens that had experimental intraduodenal infection with Clostridium perfringens Type A. Fourteen days postinfection, there were ultrastructural changes in hepatocytes and renal tubular epithelial cells; these included mitochondrial lesions (swelling, cristolysis, rarefication of the matrix, myelin figures), glycogen loss, and capillary endothelial cell swelling in both organs, as well as thickening of glomerular basement membrane. The findings are discussed with particular reference to the pathogenesis of Clostridium perfringens Type A enterotoxemia.
Twenty-one pigs were divided into three groups. Pigs in one group were inoculated with the intestinal contents which included bacteria from a pig with edema disease. Pigs in another group were inoculated with a culture of Escherichia coli serogroup O 139:K12(B):H1 isolated from the aforementioned contents, and pigs in a third group served as uninoculated controls. The infection was similar following both inocula. Enterotoxemia developed in 11 of the 14 pigs allowed to survive for more than two days. The onset varied from two to seven days after inoculation. There were maximal viable counts of E. coli in the intestine from the second day post-inoculation and thereafter. In frozen and paraffin sections, as well as by scanning electron microscopy, the organisms were seen on the surface of the small intestinal epithelium where they formed either isolated colonies or continuous layers. They colonized the lower small intestine more intensely than the upper section. The intestinal epithelium and the villi of infected pigs were indistinguishable morphologically from the tissues of three uninoculated control pigs. The diarrhea which was observed in controls and inoculated pigs before inoculation and the villus atrophy in controls and inoculated pigs indicated a preexisting infection with at least one other agent.
Outbred Mongolian gerbils from a United States commercial source were examined for colonization with naturally occurring enterohepatic Helicobacter spp. Helicobacter spp. were identified in the cecum and colon by culture and by using genus-specific primers in polymerase chain reaction (PCR) assays. Nutritionally balanced triple-antibiotic wafers (containing amoxicillin, metronidazole, and bismuth) used previously to eliminate helicobacter infections in mice were administered in an attempt to eradicate the naturally occurring novel helicobacters in the gerbils. After 7 days of antibiotic treatment, two of the experimental animals died due to Clostridium difficile-associated enterotoxemia. However, at 3 weeks after antibiotic cessation, the surviving three animals had no Helicobacter spp. in the cecum or colon according to PCR analysis. Eradication of Helicobacter spp. using dietary administration of antibiotics was complicated by the presence of toxin-producing C. difficile. An alternate method to develop helicobacter-free gerbils (such as Caesarian rederivation) may be necessary.
The clinical symptoms and the morphologic picture of calf enterotoxemia are described. Studied were a total of thirty-two dead and slaughtered animals. Bacteriologically, the disease was shown to be caused by types A, D, and C of Clostridium perfringens. Types C and D proved pathogenic for guinea pigs, while type A did not. Isolated was a strain of Clostridium perfringens, which had high toxigenicity. It was found that calves were fairly often affected with the disease. Most severe were the infections caused by type C of Cl. perfringens, with most pronounced morphologic lesions. There were differences in the changes caused by all three types of the organism in calves, which made it possible to distinguish them as causative agents. Type A induced slight icterus and slightly manifested hemosiderosis of the liver, kidneys, and spleen; type D was responsible for severe injury and hyalin dystrophy of the kidneys; and type C caused necrotic enteritis, pronounced hemorrhagic diathesis, degenerative changes in the ganglial cells, and demyelinization of the brain.
Four specific-pathogen-free rabbits with anorexia died peracutely; decreased fecal output, nasal exudate, and labored breathing were the only other clinical abnormalities observed in two of the rabbits before death. The animals, three juveniles and one adult, were on a standard polyclonal antibody production regimen and had received immunizations approximately 2 weeks before presentation. External examination revealed distended abdomen and perineal fecal staining. At necropsy the small intestine was distended with fluid, and the cecum was distended with chyme. The small intestines and cecum had marked serosal hyperemia. Anaerobic bacterial culture techniques were used to isolate Clostridium difficile from the small intestine (3/4) and cecum (2/4). In all cases C. difficile toxin B was detected at high titers (10(2) to > 10(5)) in the small intestine by cytotoxicity assay with HeLa 229 cell culture. In two of the four rabbits C. difficile was isolated, and cytotoxin titers were detected at 10(1) and 10(4) in the cecum of affected rabbits. Toxin B was neutralized with C. sordellii antiserum but not C. spiroforme antiserum. In addition, toxin A was detected in each of the cytotoxin B-positive samples by a commercial toxin A enzyme immunosorbent assay. In vitro production of toxins A and B was detected from each culture isolate after incubation in chopped meat broth. These cases are noteworthy because spontaneous (nonantibiotic-associated) C. difficile enterotoxemia has not been previously reported in rabbits. Also the toxins of clostridial organisms are usually documented in the cecum, not the small intestine, of rabbits.(ABSTRACT TRUNCATED AT 250 WORDS)
Clostridial infections are found worldwide in almost all species of animals and may involve a variety of body systems and present with a diversity of clinical signs. Most damage done through clostridial infections is due to the action of toxins released from the bacteria.Thus, disease caused by Clostridium spp should more correctly be called intoxication. Two prominent clostridial infections are associated with neurologic signs: Clostridium botulinum and C tetani. In both infections, the mechanism that is responsible for causing the problem is similar, despite the remarkable difference in clinical presentation. In addition, neurologic signs are described with C perfringens types C and D but are not the dominant feature of these diseases.
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Bovine enterotoxaemia is an acute to peracute syndrome occurring mainly in calves and characterized by the sudden or very rapid death of the calf, with colics, convulsions and nervous disorders as clinical signs, if any. The most pronounced lesion is a necrohaemorrhagic enteritis of the jejunum, the ileum, and sometimes the colon. Suckling beef calves are the most frequently affected ones. In 67% of the 78 field cases investigated, some kind of stress was observed 24 to 36 hours prior to the death: change in diet or pasture, vaccination... The most frequently isolated bacteria, and the one isolated in highest numbers, was non-sporulated non-enterotoxigenic toxinotype A Clostridium perfringens. Reproduction of the lesions was successful in a ligated intestinal loop assay in one calf with a few of these strains, more especially with one of them, which was shown later to produce another recently described toxin, the beta 2 toxin. A role for this beta 2 toxin in bovine enterotoxaemia is thus speculated for future research.
Broth culture filtrate containing endotoxin, prepared from serotype O 139:K82(?):H1 was given by the intra-enteric route with and without dimethyl sulphoxide, and with or without blockade of the RES by intravenous injection of trypan blue, using about five piglets for each of the four combinations. Clinical signs, blood pressure, ECG, respiration, temperature, haematology and pathological findings were recorded. Coli enterotoxaemia manifested by fatal endotoxin shock developed in all ten piglets given toxin plus dimethyl sulphoxide, and in 4 of 5 similarly treated after RES blockade. The sondrmoe did not develop in piglets given large amounts of toxin without dimethyl sulphoxide, whether the RES was blocked or not. When enteric absorption of toxin was promoted by dimethyl sulphoxide, RES blockade increased the sensitivity of the animal to toxin (shortening of the time till death). The results show that there are two functional barriers to endotoxin: - the intestinal barrier, which normally prevents large amounts of toxin from entering the circulation; and RES, which plays a part in detoxifying and eliminating endotoxin which has been absorbed. Application of these findings to the pathogenesis of coli, enterotoxaemia is discussed.
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