Fifty-five pregnant BALB/c mice received various doses of Brucella abortus virulent strain 2308 intraperitoneally on day 9 of gestation, and uteri and spleens were examined at 3, 5, 7, and 9 days post-inoculation to study the pathogenesis of infection. A dose of 10(5.7) B. abortus organisms produced a severe, necrosuppurative placentitis. Bacteria multiplied preferentially within the placenta and were identified within the rough endoplasmic reticulum of trophoblast giant cells and within the visceral yolk sac endoderm. Abortions did not occur, but infarction of the labyrinth region of severely affected placentas occasionally resulted in fetal death. The severity of infection in the spleens of nonpregnant mice receiving the same challenge dose was not significantly different from that in the spleens of challenged pregnant mice. These results suggest that the sensitivity of the pregnant mouse to placental brucellosis is not due to a generalized immunosuppression but rather may involve a combination of local suppression of the immune response and a susceptible cell population suitable for Brucella colonization and replication. Experimental murine brucellosis resembles ruminant brucellosis and provides a model to study the intracellular replication of B. abortus in trophoblasts.
Potomac horse fever is characterized by fever, anorexia, leukopenia, profuse watery diarrhea, dehydration, and high mortality. An ultrastructural investigation was made to search for any unusual microorganisms in the digestive system, lymphatic organs, and blood cells of ponies that had developed clinical signs after transfusion with whole blood from horses naturally infected with Potomac horse fever. A consistent finding was the presence of rickettsial organisms in the wall of the intestinal tract of these ponies. The organisms were found mostly in the wall of the large colon, but fewer organisms were found in the small colon, jejunum, and cecum. The organisms were also detected in cultured blood monocytes. In the intestinal wall, many microorganisms were intracytoplasmic in deep glandular epithelial cells and mast cells. Microorganisms were also found in macrophages migrating between glandular epithelial cells in the lamina propria and submucosa. The microorganisms were round, very pleomorphic, and surrounded by a host membrane. They contained fine strands of DNA and ribosomes and were surrounded by double bileaflet membranes. Their ultrastructure was very similar to that of the genus Ehrlichia, a member of the family Rickettsiaceae. The high frequency of detection of the organism in the wall of the intestinal tract, especially in the large colon, indicates the presence of organotrophism in this organism. Infected blood monocytes may be the vehicle for transmission between organs and between animals. The characteristic severe diarrhea may be induced by the organism directly by impairing epithelial cell functions or indirectly by perturbing infected macrophages and mast cells in the intestinal wall or by both.Potomac horse fever (PHF) has been reported with apparently increasing frequency during the summer months of the last 7 years in the counties adjacent to the Potomac River in Maryland and Virginia (9). Reports of the disease have recently been received from other areas in the Uni ed States (J. E. Palmer, personal communication). The cli "cal signs of the disease include fever, anorexia, leukopenia, watery diarrhea, and dehydration (9). In 1983, 42 of 116 Maryland horses affected with PHF died or were euthanatized. Among the 32 cases reported in Virginia, there were 10 deaths. In Pennsylvania, there were 4 deaths in 25 cases, and in 1984 18 of 108 horses in the same region died.Examinations for salmonellae have proved negative, and clostridial toxins do not appear to play a role in the etiology of the disease (2). From a recent epidemiological survey it was concluded that the disease is infectious, but not contagious (
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