Brief SummaryRead full entry
Babesiosis is caused by unicellular apicomplexan parasites in the genus Babesia. Although more than 100 Babesia species have been described, only a few have been identified as causing human infections, including B. microti, B. divergens, B. duncani, and several other forms that have not yet been formally named. Human Babesia infections occur worldwide, but little is known about the prevalence of Babesia infection in malaria-endemic countries, where misidentification as Plasmodium (the apicomplexan parasite causing malaria) probably occurs. In Europe, most reported cases have generally been attributed to B. divergens and believed to occur only in splenectomized patients. In the United States, reported babesiosis cases have been concentrated in the northeast and midwest, have been generally attributed to B. microti, and have clearly not been limited to splenectomized individuals.The recently described B. duncani (Conrad et al. 2006) has been isolated from patients in Washington and California (U.S.A.). (Centers for Disease Control Parasites and Health website) Although this presents the picture of babesiosis that has prevailed for decades, beginning in the 1990s it has become increasingly clear that the diversity of Babesia is much more complex than previously realized, with undescribed species and broader host and geographic ranges than recognized. Babesia microti, for example, is now recognized to actually represent a complex of distinct species. (Gray 2006; Hunfeld et al. 2008; Leiby 2011).
The normal Babesia microti life cycle involves two hosts, a rodent (often the White-footed Mouse, Peromyscus leucopus) and a tick in the genus Ixodes. During a blood meal, a Babesia-infected tick introduces sporozoites (an active, infective developmental stage) into the mouse host. Sporozoites enter erythrocytes (red blood cells) and undergo asexual reproduction (budding). In the blood, some parasites differentiate into male and female gametes, although these cannot be distinguished at the resolution of a light microscope. The definitive host (i.e., the host in which sexual reproduction occurs) is the tick. Once ingested by an appropriate tick, gametes unite and undergo a sporogonic cycle resulting in sporozoites, which can then be transmitted back to a rodent fed on by the tick. Transovarial transmission ("vertical" transmission across tick generations) has been documented for “large” Babesia species but not for the “small” babesiae, such as B. microti. (Centers for Disease Control Parasites and Health website)
Humans enter the cycle when infected ticks bite them in lieu of a rodent host, introducing sporozoites, which enter erythrocytes and undergo asexual replication (budding), as in a rodent host. Multiplication of the blood stage parasites is responsible for the clinical manifestations of disease. However, humans are essentially dead-end hosts and there is probably little, if any, subsequent transmission that occurs from ticks feeding on infected persons. Human-to-human transmission can occur through blood transfusions. (Centers for Disease Control Parasites and Health website)
The primary vector for B. microti in the U.S. is Ixodes scapularis (Black-legged Tick or Deer Tick), which also transmits the bacteria causing Lyme disease (Borrelia burgdorferi). The white-tailed deer (Odocoileus virginianus) is not a competent host for B. microti, but serves as a maintenance host for adult ticks and thereby transports the infected ticks to previously uninfected areas. In a range of geographic locations worldwide, the tick vector implicated in the transmission of Babesia is often the ixodid species locally responsible for the transmission of Bo. burgdorferi. (Hunfeld et al. 2008 and references therein; Leiby 2011 and references therein)
Hunfeld et al. (2008) and Leiby (2011) provides wide-ranging reviews of biological and medical aspects of babesiosis. Hunfeld et al. (2008) review what is known about reservoir hosts and tick vectors with respect to babesiosis.