17 John F. Prescott, Paula I. Menzies, and Russell S. Fraser Clostridial abomasitis is not an uncommon problem encountered mostly in young farmed pre-ruminants (calves, lambs, goat kids, and others), and it is associated with several clostridial species. The etiology is usually multiple, including, amongst others, Sarcina spp. (which are really true species of Clostridium, Chapter 1). This and the generally sporadic and multifactorial nature of clostridial abomasitis complicate understanding of the disease and consequently its effective diagnosis, treatment, and control. This chapter discusses what is currently known about clostridial abomasitis. Further research is required to understand this often frustrating and demoralizing disease process. Braxy (also known as “bradsot”) is the name used to describe abomasitis of sheep and other ruminants caused by Clostridium septicum. Braxy is caused by C. septicum, a species sometimes associated with other enteric infections as well as wounds of animals. It is not known whether the strains of C. septicum involved in braxy have any features uniquely associated with abomasitis, since no genetic characterization has been done. The organism causes severe localized abomasal infection and toxemia, and may disseminate through the bloodstream to other tissues. The toxins produced by this microorganism are described in Chapter 4. Braxy, first described in Scandinavian countries, is a disease that most commonly affects lambs post-weaning up to approximately 1 year of age. The disease is associated with grazing on cold or frozen pastures. Braxy is well recognized in more northerly countries, but it has been described in most sheep-rearing countries. The disease has also been described in calves. Speculatively, sheep may alter their grazing behavior in the winter when grasses are of poorer quality, which may increase ingestion of woody forages and soil containing spores of C. septicum. These elements may damage the abomasal mucosa, thus providing a port of entry for C. septicum. Freezing may make those high-lignin-containing plants more readily consumed. Experimentally, abomasal damage caused by an infusion of acetic acid through a cannula resulted in death due to C. septicum infection around the cannula site. This supports the importance of local trauma in the pathogenesis of the disease. In enzootic areas, losses can reach 8% of sheep at risk, with mortality being as high as 50% of affected sheep. Clinically, there is sudden onset of illness, complete anorexia, depression, and abdominal discomfort with moderate bloating. Fever may reach 42 °C. Affected animals become recumbent and die within 12–36 hours of the onset of disease. There may be bloody discharge from the nose of comatose animals. Characteristically, the abomasal wall is markedly edematous and congested. Congestion may be focal but is commonly diffuse. Focal mucosal necrosis is usual; because of the rapid progression of disease, these lesions rarely become extensive. Gas bubbles that extend from the submucosa are commonly seen on the mucosal surface (Figure 17.1). The blood-tinged abomasal content smells foul. Figure 17.1 Abomasum of a sheep with braxy. The abomasum shows generalized edema and patches of marked congestion. Large gas bubbles are visible under the mucosa. Several multifocal ulcers are also present. Courtesy of the Department of Pathobiology, University of Guelph. Microscopically, there is marked necrosis, ulceration, edema, and congestion of the mucosa and submucosa. There is heavy neutrophilic infiltration around necrotic areas and throughout the lamina propria and submucosa (Figure 17.2). Large numbers of Gram-positive rods, sporulated or not, are present in clumps or chains in the necrotic areas. Thrombosis may be present in severely inflamed areas of the mucosa and submucosa. Figure 17.2 Abomasum of a lamb with braxy. There is marked mucosal necrosis, edema, emphysema, and congestion of the mucosa and submucosa. A rim of heavy neutrophilic infiltration surrounds necrotic areas. HE, 40x. Courtesy of F.A. Uzal. Diagnosis is based on clinical signs, gross and microscopic changes, and on identification of C. septicum by anaerobic culture, PCR, immunohistochemistry, and/or a fluorescent antibody technique. C. septicum grows within 24–36 hours on blood agar incubated anaerobically at 37 °C as a swarming colony, and characteristically forms long filaments. It can, however, be a post-mortem contaminant, since the organism invades readily from the intestine after death, and it is therefore important to use material collected from freshly dead animals for identification results to be significant. Isolation (or detection by other means) of C. septicum from tissues of animals in the advanced stage of post-mortem decomposition is not considered diagnostically significant. Identification of isolated microorganisms can be performed by conventional biochemical methods, by PCR, and/or by MALDI-TOF. PCR can also be performed directly on tissues. Immunohistochemistry can be used to identify C. septicum in tissue sections, and fluorescent antibody staining can detect organisms directly in smears. Disease at the flock level is usually sporadic, but can be prevented effectively in animals at risk by routine annual immunization with commercially available clostridial bacterin–toxoid vaccines containing C. septicum (Chapter 20). In countries where the disease is endemic, sheep management practices such as feeding hay before putting animals onto frozen pasture have been found to be useful. Prevention of the sporadic disease seen in calves should take the approaches recommended under other agents of clostridial abomasitis described below. Because of the rapid nature of the disease, treatment with antibiotics such as penicillin G is usually ineffective. Clostridial abomasitis of calves, lambs, and goat kids in which C. septicum is not the causative agent is a well-recognized but not well-understood disease. It has been attributed to several different Clostridium spp. as well as to Sarcina spp. (which are true Clostridium spp., Chapter 1). It is possible that the disease may be caused concurrently by more than one clostridial species, taking advantage of host or environmental predisposition that is likely multifactorial. Although often sporadic, outbreaks associated with significant levels of morbidity and mortality may occur in animals at risk and be difficult to control. The full clinical and pathologic manifestations of clostridial abomasitis in calves, lambs, and goat kids have not been fully characterized. The condition may present as acute diffuse abomasitis, the most widely recognized presentation, but also as severe abomasal bloat or deep to perforating abomasal ulcers. Severe clostridial enteritis may occur with or without abomasitis in the same outbreak. A working assumption is that predisposition to the disease and its pathogenesis is similar in young calves, lambs, and goat kids, and the etiologic agents may vary with the circumstances, but final evidence for this is lacking. Several agents have most commonly been associated with clostridial abomasitis, including Clostridium perfringens type A, Clostridium sordellii, and Sarcina spp., or combinations of these agents. Other clostridia such as Clostridium fallax have been generally less consistently isolated. Numerous questions remain about both the etiology of clostridia-associated abomasal bloat and abomasitis in young pre-ruminants, including its microbiology. Microbiologic issues yet to be resolved include the impact of dietary components (milk replacer, stored colostrum, different carbohydrates and proteins in both milk replacer and solid “starter” feed, and the effect of feed texture in solid starter) on bacterial growth and fermentation. Additionally, the cleanliness and effectiveness of the cleaning protocols of milk-feeding equipment may play a role. Clostridia including Sarcina are notable gas producers. Nothing is known about the interaction of the agents listed above in the abomasum, for example the possible role of quorum signaling by Sarcina on growth or expression of virulence determinants of other clostridia, or the role of Sarcina in providing an anaerobic environment in which other clostridia can establish and flourish. Current understanding of the microbiology of abomasal disease and abomasitis in young farmed pre-ruminants is shown in Figure 17.3. The current knowledge of the etiology of clostridial abomasitis varies in different species. Figure 17.3 Venn diagram of current understanding of the microbiological complexities of abomasal bloat and abomasitis in young calves, lambs, and goat kids. It helps to see the circles as dynamic and changing, depending in part on the environmental and host predisposing factors. The figure also indicates our current inadequate understanding of the pathogenesis (and control) of the problem(s). C. perfringens type A is commonly isolated in large numbers from the abomasum in fatal cases of abomasitis in young calves. In the single experimental study that has reproduced the disease, inoculation of C. perfringens type A into the rumen of healthy calves resulted in anorexia, bloat, depression, diarrhea, and, in some cases, death. Necropsy showed variable degrees of abomasitis that included petechial and/or ecchymotic hemorrhages and ulcers of variable size and depth, including those that were almost perforating. Microscopically, lesions in experimental calves were similar to those described in the naturally occurring infection, except that they lacked the emphysema that is sometimes described in the latter. The experimental reproduction of a disease resembling the naturally occurring condition is convincing evidence that C. perfringens type A can cause abomasitis in calves. Isolates have been inconsistently positive for the cpb2
Clostridial Abomasitis
Introduction
Braxy (Clostridium septicum)
Introduction
Etiology
Epidemiology
Clinical signs
Gross changes
Microscopic changes
Diagnosis
Prophylaxis and control
Treatment
Other agents of clostridial abomasitis
Introduction
Etiology
Calves
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