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Erysipelothrix rhusiopathiae was isolated from the spleen, liver, lung, heart, kidney, and skin of a red-tailed hawk (Buteo jamaicensis) which had a concurrent avian pox virus infection. The hawk had been housed on a farm with domestic turkeys, providing a possible source of the E. rhusiopathiae.
Erysipelothrix rhusiopathiae was found to be the causal organism of high mortality in a colony of Little Swifts (Apus affinis (Gray), occupying the vertical walls of high-rise buildings. The mortality continued for a period of about 4 weeks. Negative post-mortem findings necessitated a diagnosis based on bacterial examination during which the causal organism was isolated in pure culture from the liver, spleen and heart blood of affected birds.
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Rats treated with carbaril (sevin) at the rate of 2 to 5 mg were infected via the feed with Erysipelothrix rhusiopathiae in the course of 30 days. Studied were the clinical picture, some paraclinical indices, the mortality rate, and the morphologic and histopathologic changes in the parenchymal organs. It was found that rats that were given carbaril for a long time in minimum amounts and were then subjected to infection developed a characteristic clinical picture and showed a high mortality rate (nearly twice as high as that with the control animals). In hemocultures the causative agent was isolated over a longer period than in the case with the controls. Both the gross and the histopathologic findings were more strongly manifested in the test (carbaril-treated) rats.
Infection of Lewis rats with Erysipelothrix rhusiopathiae represents an experimental model system of acute and chronic arthritis. We studied here the acute inflammatory phase with respect to stimulation of macrophages and lymphocytes. Intragluteal injection of viable E. rhusiopathiae (10(2) to 10(4) bacteria) rapidly induced generalized inflammation, loss of body weight, hind leg arthritis, and systemic macrophage activation within 2 to 3 days. The same symptoms could also be evoked by injection of dead E. rhusiopathiae. Ex vivo, peritoneal macrophages released large amounts of tumor necrosis factor alpha on day 2 and interleukin-1 on day 3, whereas production of prostaglandin E2 was delayed to days 5 to 7 and appeared to counteract tumor necrosis factor alpha synthesis. The inflammatory response and development of arthritis were strongly dependent on T lymphocytes, as evidenced by the following findings: (i) lymphocytes released lymphokines that activated macrophages to enhanced mediator release; (ii) treatment of rats with cyclosporin A reduced infection-induced macrophage activation; (iii) mitogen-stimulated thymocyte proliferation was enhanced, indicating an infection-induced maturation-differentiation process in the thymus; and (iv) in T-cell-deficient nude rats, a higher dose of bacteria was required for infection, the inflammatory response was less severe, and only mild, but not chronic, arthritis developed. Thus, an E. rhusiopathiae-induced inflammation in rats provides a useful tool to characterize activated macrophages and T lymphocytes during the development of acute arthritis and its transition into the chronic form.
Neuraminidase may play a role as a pathogenic factor in Erysipelothrix rhusiopathiae infection. The protective effect of active immunization with purified neuraminidase was therefore tested in an infection experiment in white mice. Mice were immunized 2, 4, 6, 8 or 10 times i.p. with Erysipelothrix neuraminidase. A control group received 10 injections with physiological saline. The infective dose varied between 7 and 7 x 10(7) cells. While all control animals infected with 7 x 10(1) germs died, the lethal effect could be reduced to 50% and 25% in animals immunized twice and 4 times, respectively. Only animals immunized 8 and 10 times were still partly protected against germ numbers of 10(3)-10(4). Germ numbers of 10(5) and more were almost always fatal even in highly immunized animals. Even a high immunization with neuraminidase could only lower the lethal by a maximum factor of 10(4) germs used.
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