Isolates of Treponema hyodysenteriae from 25 geographically separated outbreaks of swine dysentery were tested for their ability to produce the disease. Clinical signs and lesions typical of acute swine dysentery were produced in 52 of 68 (75%) susceptible specific pathogen-free pigs that had been orally inoculated with pure cultures of 23 of 25 beta-hemolytic isolates. In addition, 13 weakly beta-hemolytic isolates of nondysentery origin with morphology similar to T. hyodysenteriae did not produce disease when orally inoculated into susceptible specific pathogen-free pigs. Two of these latter isolates, Puppy and B296, and one pathogenic, beta-hemolytic isolate failed to produce disease when orally inoculated into puppies. Swine dysentery (SD) is a mucohemmorrhagic diarrheal disease of swine. The primary lesions of inflammation, excess mucus production, and superficial necrosis of the large intestine result in hemorrhage, dehydration, and death (8). Affected swine herds may experience 90% morbidity and 25% mortality (16). The surviving animals are often unthrifty, due to decreased rate of gain and feed efficiency. The disease has been estimated to cause an annual loss of $34 million to the U.S. pork industry (35). Although SD was first described in 1921 (45), the etiology of the disease was not demonstrated until 1971 (41, 42). Electron microscopic studies on SD-affected pigs demonstrated the presence of large numbers of spirochetes in the early lesions of the disease (4, 11, 42). Subsequently, this organism was isolated in pure culture and found to induce signs and lesions of SD when orally inoculated into 6to 8-week-old pigs (10, 18, 41). The organism was propagated on blood agar plates incubated anaerobically and produced zones of beta-hemolysis. The organism was further characterized and named Treponema hyodysenteriae (18). The production of SD by oral inoculation of swine with pure cultures of beta-hemolytic T. hyodysenteriae has been reported by many workers (1, 14, 15, 20, 21, 24, 28-30, 34) and is an indication of the involvement of this organism in the etiology of the disease. Organisms of similar morphology (0.32 to 0.38 ASm in diameter; 6 to 8.5 ,um long, with seven to nine axial flagella) (19), have been reported in cases of canine diarrhea (5, 13, 23, 31, 40, 44, 46) and in normal swine (41). Isolation of the spirochetes associated with canine diarrhea has not been reported. Taylor and Alexander (41) isolated T. hyodysenteriae from normal swine (isolate 4/71) which was not pathogenic for specific pathogen-free (SPF) pigs. This nonpathogen produced less complete hemolysis than the pathogenic isolate A-1. And, in a study involving 334 clinically normal swine from five midwestern U.S. swine herds (SD free), nonpathogenic isolates of T. hyodysenteriae were obtained from 20 to 40% of the pigs. The hemolytic pattern of these isolates was like that of isolate 4/71 (J.

Clostridium difficile was investigated as a possible cause of enteritis in calves. The organism and its toxins (TcdA and TcdB), respectively, were found in 25.3% and 22.9% of stool samples from diarrheic calves. Culture positive samples were more likely than culture negative samples to be toxin positive. However, toxin positive stools were more common among nondiarrheic calves, but diarrheic calves were nearly twice as likely to be culture positive. Ribotype 078 was dominant among isolates. Salmonella sp. was isolated from both diarrheic and nondiarrheic calves, but large numbers of E. coli were found more commonly in diarrheic calves than in nondiarrheic animals. Prevalence rates for coronavirus and Cryptosporidium sp. were substantially higher in nondiarrheic calves than in diarrheic, but rates of detection of rotavirus and Giardia sp. were more nearly equal between groups. Lesions in naturally infected calves included superficial mucosal erosion with associated fibrinous exudates. Neutrophils and eosinophils infiltrated lamina propria. Large Gram-positive rods morphologically compatible with C. difficile were abundant in the colonic lumen and the organism was isolated by bacteriologic culture. Toxins were found throughout the colon. Purified toxins A and B (individually and conjointly) caused comparable lesions, as well as fluid accumulation, in ligated intestinal loops. Our findings are in substantial agreement with those of others [Rodriguez-Palacios, A., Stampfli, H.R., Duffield, T., Peregrine, A.S., Trotz-Williams, L.A., Arroyo, L.G., Brazier, J.S., Weese, J.S., 2006. Clostridium difficile PCR ribotypes in calves, Canada. Emerg. Infect. Dis. 12, 1730-1736; Porter, M.C., Reggiardo, C., Bueschel, D.M., Keel, M.K., Songer, J.G., 2002. Association of Clostridium difficile with bovine neonatal diarrhea. Proc. 45th Ann. Mtg. Amer. Assoc. Vet. Lab. Diagn., St. Louis, MO, U.S.A.] and add strength to a working hypothesis that C. difficile infection and the accompanying intoxication can manifest as diarrhea in calves. It seems clear that calves serve as multiplying hosts for this organism.

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The national incidence and extent of injection-site lesions in the muscles of the round were determined via audits conducted at retail stores and in purveying establishments. Two additional experiments were conducted to examine the subsequent effects of pharmaceutical administration on tissue histology, soluble and insoluble collagen concentration, and muscle tenderness in beef bottom-rounds. Injection-site lesion incidence in beef round cuts audited at retail (n = 3,538) and in steak-cutting facilities (n = 15,464) was 8.45 and 10.04%, respectively, with an average lesion-trim of 314.7 and 191.59 g, respectively, in these two studies. Lesion classification revealed that 93.20 and 99.91% of lesions reported for the retail and purveyor audits, respectively, were chronologically aged lesions. Overall, 19,002 round cuts were examined, and injection-site lesion incidence (nationally) was 9.74%, whereas lesion-trim averaged 211.8 g. Warner-Bratzler shear measurements taken near lesions and in areas 7.62 cm from the lesions were higher (P < .001) for lesioned, than for control bottom-round steaks. Warner-Bratzler shear values for lesion cores were 3.5 times greater than those in paired control (non-affected) steaks. Concentrations of insoluble and soluble collagen were much higher (P < .001) at the site of the lesion center in lesion-afflicted vs control steaks. Histological determinations of the relative proportions of muscle, connective tissue and fat to a distance of 5.08 cm from the site of the lesion center confirmed that severe disruption of muscle tissue constituents and architecture had occurred. Injection-site lesions occur at an unacceptable frequency in the muscles of the round, and severe tissue changes accompany these lesions that can dramatically affect tenderness of those cuts.

A USDA Early Response Team investigated deaths of several horses and a mule in northern Arizona at the request of local animal health officials. Thirteen animals (12 horses and 1 mule) housed at 5 facilities in a 7.4 square mile area died between August 1998 and January 1999. Clinical signs consisted of muscular weakness that rapidly progressed to lateral recumbency. Ten animals had paresis of the tongue, throat, or lips. Affected animals appeared alert and were interested in eating and drinking, even while recumbent. All 13 animals were euthanatized. Clostridium botulinum type C was isolated from feces or intestinal contents from 3 affected horses. Preformed toxin was detected in samples of soil and bird droppings collected from a nearby horse burial site. It was hypothesized that the outbreak was a result of birds, presumably ravens, feeding at the burial site and at horse facilities in the area that transferred toxin to the affected animals.

Sudden deaths or the sudden death syndrome are perceived as major concerns in cattle feedlots because most of these deaths occur in cattle near market weight. Etiology and preventive measures are poorly defined. The current literature indicates that sudden deaths are associated most commonly with digestive upsets. Death is thought to be the result of interactions between factors including acidosis, bloat, and endotoxemia. Trauma, peracute interstitial pneumonia, and other identifiable events are specifically defined but relatively uncommon. Enterotoxemia is of questionable significance as a cause of sudden deaths.

Nineteen of 22 female mice (CF1 strain) inoculated intragastrically with Treponema hyodysenteriae developed cecal and colonic lesions consisting of catarrhal inflammation, edema, and occasional hemorrhage.

The large intestines of pigs with swine dysentery were examined by phase, light, and electron microscopy at intervals up to 11 days after oral inoculation with mucosal scrapings from infected pigs. Large spirochetes with the structural characteristics of Treponema hyodysenteriae were found only in infected pigs and were first observed in small numbers in the lumen of the large intestine 2 days after inoculation. Numerous large spirochetes were present on the luminal surface and in mucosal crypts as lesions developed. Degenerative changes were first observed in the apical portion of epithelial cells in close contact with large spirochetes. These large spirochetes were found intact in goblet cells and epithelial cells in the early stages of the disease and were numerous within degenerating epithelial cells as lesions became more advanced. Invasion beyond the lamina propria was not detected. These observations demonstrated the relationship between pathogenic large spirochetes and the mucosa of the large intestine in a specific disease, swine dysentery.