Babesiosis pathophysiology: Difference between revisions
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{{Babesiosis}} | {{Babesiosis}} | ||
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==Overview== | ==Overview== | ||
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[[Category:Parasitic diseases]] | [[Category:Parasitic diseases]] | ||
[[Category:Apicomplexa]] | [[Category:Apicomplexa]] | ||
[[Category:Infectious disease]] | [[Category:Infectious disease]] | ||
[[Category:Disease]] | [[Category:Disease]] |
Revision as of 15:35, 20 November 2012
Babesiosis Microchapters |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Babesia parasites reproduce in red blood cells, where they can be seen as cross-shaped inclusions (4 merozoites asexually budding but attached together forming a structure looking like a "Maltese Cross") and cause hemolytic anemia, quite similar to malaria.
Note that unlike the Plasmodium parasites that cause malaria, Babesia species lack an exo-erythrotic phase, so the liver is usually not affected.
Pathophysiology
Pathogenesis
The Babesia microti life cycle involves two hosts, which include a rodent, primarily the white-footed mouse, Peromyscus leucopus, and a tick in the genus Ixodes.
- During a blood meal, a Babesia-infected tick introduces sporozoites into the mouse host.
- Sporozoites enter erythrocytes and undergo asexual reproduction (budding).
- In the blood, some parasites differentiate into male and female gametes, although these cannot be distinguished by light microscopy.
- The definitive host is the tick. Once ingested by an appropriate tick
- Gametes unite and undergo a sporogonic cycle resulting in sporozoites.
- Humans enter the cycle when bitten by infected ticks. During a blood meal, a Babesia-infected tick introduces sporozoites into the human host.
- Sporozoites enter erythrocytes and undergo asexual replication (budding).
- Multiplication of the blood-stage parasites is responsible for the clinical manifestations of the disease.
- Humans usually are dead-end hosts. However, human-to-human transmission is well recognized to occur via contaminated blood transfusions.