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Tularemia is a disease of wild mammals caused by F. tularensis. Humans become infected by direct contact with infected animals or through the bite of a vector (tick or deer fly). The illness is characterized by high fever and severe constitu- tional symptoms. The epidemiology of tularemia and many features of the clinical infection are similar to those of plague.
Humans most often acquire F. tularensis by contact with an infected mammal or a bloodfeeding arthropod. Because the infecting dose is very low (< 100 organisms), many routes of infection are possible. A tick bite or direct contact with minor skin abrasion are the most common mechanisms of infection. Many wild mammals can be infected, including squirrels, muskrats, beavers, and deer. A common history is that of skinning wild rabbits on a hunting trip. Inhalation may also lead to disease. In a recent outbreak of pulmonary tularemia on Cape Cod, experts believed that lawn mowing and brush cutting facilitated inhalation. Occasionally, the bite or scratch of a domestic dog or cat has been implicated when the animal has ingested or mouthed an infected wild mammal. Infected animals may not show signs of infection, because the organism is well adapted to its natural host. The usual vectors in animals are ticks and deer flies. Ticks may also serve as a reservoir of the organism by transovarial transmission to their offspring.
Tularemia is distributed throughout the Northern Hemisphere, although there are wide variations in specific regions. The highly virulent tick/rabbit-associated strains are com-mon only in North America. In the United States 100 to 200 cases are reported each year half of which are in the lower Midwestern states (Arkansas, Missouri, Oklahoma). Tu-laremia is not found in the British Isles, Africa, South America, or Australia.
Relatively little is known of the events that occur during the 2- to 5-day incubation period. A lesion often develops at the site of infection, which becomes ulcerated. The organism then infects the reticuloendothelial organs, often forming granulomas, and the disease may sometimes follow a chronic relapsing course. These properties suggest a facultative intra-cellular pathogen; multiplication within macrophages, hepatocytes, and endothelial cells has been demonstrated with F. tularensis. This intracellular survival has been attributed to failure of phagosome–lysosome fusion and phagosome acidification. Early bacteremic spread probably occurs, although it is rarely detected. Other areas of multiplication are characterized by necrosis or granuloma production, and a mixture of abscesses and caseat-ing granulomas may be seen in the same organ.
Naturally acquired infection appears to confer long-lasting immunity. Antibody titers re- main elevated for many years, but cellular immunity plays the major role in resistance to reinfection. T cell–dependent reactions involving either CD4+ or CD8+ cell are de- tectable even before antibody responses.
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