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Biomedical subjects

H BAUER

Publications and source records attributed to H BAUER.

At least 109 records · Page 6Linked to original sources

Activation of quiescent mucormycotic granulomata in rabbits by induction of acute alloxan diabetes.

In normal rabbits subcutaneous granulomata produced by the injection of a spore suspension of Rhizopus oryzae remained confined to the site of inoculation, showed no fungus proliferation, no longer yielded the agent on culture 10 weeks after inoculation, and eventually healed. Similar well established granulomata in rabbits with acute alloxan diabetes induced 8, 10, and 15 days after injection of the fungus uniformly showed activation of the infection. This occurred only in animals showing acetonuria. In these animals the skin lesions showed proliferation of the fungus frequently associated with invasion and early necrosis of the granuloma wall. In some instances, spread of the infection to adjacent tissues with invasion of blood vessels had occurred. These experiments illustrate that changes in host metabolism can activate a preexisting quiescent infection.

Animals↗

Leukopenia with granulocytopenia in experimental mucormycosis (Rhizopus oryzae infection).

Mucormycosis was produced in rabbits with sustained, severe leukopenia and granulocytopenia induced by repeated injections of nitrogen mustard. Initially, these animals developed extensive fungus lesions at the site of inoculation which later became granulomatous and tended to heal. Only the early phases of host resistance appeared impaired by the virtual elimination of the polymorphonuclear leukocyte as a factor in the host response. Despite the persistent leukopenia and granulocytopenia, the later phases of host resistance resembled those of the normal animal. Thus, the behavior of the infection in this experiment differs greatly from the unchecked progression of mucormycosis in the metabolically abnormal animal with acute alloxan diabetes. The differences in the course of the disease and in the morphologic appearance of the lesions indicate that metabolic alterations in the host affect all phases of host resistance and not only the polymorphonuclear leukocytic response.

Agranulocytosis↗