An adaptation of the Adams cephalostat for use with standard hospital X-ray equipment.
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Biomedical subjects
Publications and source records attributed to J D Clark.
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Parasitological, clinical, and histopathological observations on 54 baboons infected with Schistosoma mansoni are presented. The baboon and S. mansoni constitute a compatible host-parasite system, evidence by the infectivity of cercariae (98% penetration, 42% adult worm recovery), and the long, fertile life of the worms. Baboons tolerated the infection well, with clinical illness a rarity in moderately infected baboons. Pathological findings were generally unremarkable. An acute "toxemic" phase occurred 66 days or less following a large cercarial exposure in three baboons. Worm burdens were not significantly reduced during the course of prolonged infection, but prolonged infections resulted in decreased oviposition by the worms and in an anterior shift in egg deposition from the colon to the small intestine. Concomitant immunity was also a feature of baboon infections. Decreased oviposition and the anterior shift are probably manifestations of a second phase of immunity, distinct from concomitant immunity. The baboon is similar to man and the grivet monkey in that in all three species immunity is slow to develop.
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Candida albicans, administered by gastric intubation, persisted in the gastrointestinal tract of gnotobiotic mice for long periods but was eliminated within a relatively short period of time in pathogen-free mice. Oxytetracycline administered by mouth had no reproducible effect on the persistence of C. albicans in the gastrointestinal tract of either germ-free or pathogen-free mice. Prolonged administration of streptomycin extended the time that C. albicans could be recovered from feces of pathogen-free mice when compared to mice not receiving the antibiotic or those receiving a single large dose. There was a brief interval of time during which C. albicans could not be recovered from the feces of gnotobiotic mice contaminated with certain intestinal bacteria, but eventually all mice began to shed the fungus again. C. albicans administered by mouth was not pathogenic for germ-free or pathogen-free mice. It can be concluded from these findings that mice do not possess an innate resistance to C. albicans but that pathogen-free mice do possess some ecological mechanism which prevents establishment of the fungus in their gastrointestinal tract. The reason for the difference in colonization of C. albicans in germ-free or gnotobiotic mice and pathogen-free mice was not determined.
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