Abstract

Lyme disease, human babesiosis, and human granulocytic ehrlichiosis are vector-borne diseases that are increasingly recognized as important pathogens in the northeast and upper midwestern regions of the United States (1-6). The etiologic agents of these human infections, Borrelia burgdorferi, Babesia microti, and Anaplasma phagocytophilum, respectively, are maintained in the same tick vector (Ixodes scapularis also known as Ixodes dammini or the deer tick) and the rodent reservoir (Peromyscus leucopus, the white-footed mouse). The definitive host of the tick vector is the white-tailed deer (Odocoileus virginianus). The proliferation of the deer populations in certain geographical areas of the U.S. during the mid-20th century has been the basis for the emergence of these infections (7). Because I. scapularis serves as the tick-borne reservoir for B. burgdorferi, B. microti, and A. phagocytophilum, mixed infections with any two, or perhaps all three, of these agents are possible. In fact, in one study (8) of 93 patients with culture-proven Lyme disease, 2% of the patients were coinfected with B. microti and another 2% were coinfected with A. phagocytophilum. Other studies (9,10) have shown that up to 10% of patients may have Borrelia and Babesia coinfections. These coinfections may cause a confusing clinical picture, and some investigators have reported that coinfected patients may have more severe or persistent illness (10,11). This case report describes a 79-yearold patient who acquired a coinfection with B. burgdorferi and B. microti while on a 2-week family camping trip in Massachusetts.

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