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DOI 10.1128/jcm.34.3.724-727.1996

Медицинская библиотека · Journal of clinical microbiology · 1996

Immunoserologic evidence of coinfection with Borrelia burgdorferi, Babesia microti, and human granulocytic Ehrlichia species in residents of Wisconsin and Minnesota.

Mitchell P D, Reed K D, Hofkes J M

СтатьяПоддержка исследования: вне правительства СШАПоддержка службы здравоохранения СШАПеревод пока не подготовлен

Аннотация

In Wisconsin and Minnesota, Ixodes scapularis (Ixodes dammini) ticks are the vector of three microorganisms that may cause significant disease in humans and lower mammals. These diseases include Lyme borreliosis, which is caused by Borrelia burgdorferi, babesiosis, which is caused by Babesia microti, and human granulocytic ehrlichiosis (HGE), which is caused by an apparently new species in the genus Ehrlichia. Immunoserologic testing was performed on sera from patients with a diagnosis of one of these diseases to determine if there was evidence of coinfection with one or more of the other agents. Of 96 patients with Lyme borreliosis, 9 (9.4%) demonstrated immunoserologic evidence of coinfection: 5 (5.2%) with the agent of HGE, 2 (2.1%) with B. microti, and 2 (2.1%) with both microorganisms. Of 19 patients diagnosed with HGE, 3 (15.8%) showed immunoserologic evidence of coinfection: 1 (5.3%) with B. burgdorferi, 1 (5.3%) with B. microti, and 1 (5.3%) with both microorganisms. One patient diagnosed with babesiosis was also seropositive for ehrlichiosis. These results provide evidence for coinfection, perhaps explaining the variable manifestations and clinical responses noted in some patients with tick-transmitted diseases. In certain clinical settings, laboratory testing for coinfection is indicated to ensure that appropriate antimicrobial treatment is given.

Для цитирования: Mitchell P D, Reed K D, Hofkes J M. Immunoserologic evidence of coinfection with Borrelia burgdorferi, Babesia microti, and human granulocytic Ehrlichia species in residents of Wisconsin and Minnesota.. Journal of clinical microbiology. 1996. DOI: 10.1128/jcm.34.3.724-727.1996.

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