Currently, the Golden Syrian hamster is widely considered an important model of Clostridium difficile disease, as oral infection of this animal pretreated with antibiotics reproduces many of the symptoms observed in humans. Two C. difficile strains, B1 and 630, showed significant differences in the progression and severity of disease in this model. B1-infected hamsters exhibited more severe pathology and a shorter time to death than hamsters infected with 630. Histological changes in the gut did not correlate with absolute numbers of C. difficile bacteria, but there were clear differences in the distribution of bacteria within gut tissues. Light, scanning, and transmission electron microscopy revealed high numbers of B1 bacteria at the mucosal surface of the tissue, whereas 630 bacteria were more frequently associated with the crypt regions. Both B1 and 630 bacteria were frequently observed within polymorphonuclear leukocytes, although, interestingly, a space frequently separated B1 bacteria from the phagosome wall, a phenomenon not observed with 630. However, pilus-like structures were detected on 630 located in the crypts of the gut tissue. Furthermore, B1 bacteria, but not 630 bacteria, were found within nonphagocytic cells, including enterocytes and muscle cells.

This study used gross and histological examination to highlight the large variety of naturally occurring gastric lesions in a mixed population of horses. Analysis of the pathogenesis of lesion development is now possible. Further research regarding the range of pathology in larger, more diverse groups of horses is required.

A subcellular extract prepared from nonencapsulated Diplococcus pnewnoniae type 3 protected mice against a subsequent challenge with virulent D. pnewnoniae types 1, 2, 3, and 7. Potency ratios ranged from 25 (type 3) to >1,175 (type 1). The immunity induced in mice by this preparation was best obtained by intraperitoneal inoculation followed by intravenous challenge. Mice immunized in this manner were protected up to 12 weeks and could withstand a challenge of several hundred LD50. The protection was destroyed by treatment of the preparation with ribonuclease and was decreased by treatment with protease. The preparation consisted of 60.5% ribonucleic acid, 29.1% protein, 6.3% deoxyribonucleic acid, and 4.0% hexose. Ultracentrifugation studies indicated that this extract had five constituents which are compatible with ribosomal material.

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