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Babesia microti

Microbiology > Parasitology > Protozoa
Babesia microti

Structure:
Babesia is an intraerythrocytic, sporozoan parasite that causes human babesiosis. Infected red blood cells contain ring forms that resemble those of Plasmodium falciparum, however, malarial pigment and other stages of plasmodial growth are not present.  

Epidemiology:
Over 70 species of Babesia are found worldwide, with B. microti responsible for most of the human disease in the Northeast and upper Midwest. Other species causing babesiosis in the USA include B. duncani and B. divergens. Ixodes scapularis (the blacklegged tick) is the vector for transmission in the NE.

The life cycle of Ixodes scapularis involves both deer and mice. Adult ticks feed on deer before laying their eggs in the spring. When the tick larvae hatch, they may feed on infected white-footed mice (Peromyscus leucopus), which are the primary reservoir for B. microti. B. microti is then transmitted from larvae to nymphs to adult ticks that may eventually feed on humans (incidental hosts).

Although the most common route of transmission is a tick bite, B. microti may also be transmitted via blood transfusion or transplacentally.

Pathobiology:
When an infected tick feeds on a human, it takes 36-72 hours for B. microti to reach the tick’s salivary glands and be transmitted into the host dermis. Thus, tick removal during the first 24-36 hours reduces the chance of transmission.

Once in the dermis of its host, B. microti eventually reaches the circulation, where it penetrates and lyses RBCs. Anemia is exacerbated by the production of reactive oxygen species during B. microti replication that alter RBC structure promoting removal by the spleen. The host inflammatory response and release of pyrogenic cytokines (TNF-alpha, IL-6) is responsible for other symptoms commonly associated with babesiosis, including fever, headache, fatigue and myalgia.

Co-infection with B. burgdorferi (causing Lyme Disease) and A. phagocytophilum (causing Anaplasmosis) is possible in any individual exposed to I. scapularis.


Disease Manifestations:
Following an incubation period of 1-4 weeks, clinical manifestations may range from absent/mild to severe/life threatening. Mild illness usually involves fatigue, malaise, weakness, fever and chills. As the disease progresses, hemolytic anemia develops; splenomegaly and hepatomegaly may occur in advanced disease. Severe illness (which may involve ARDS, DIC, CHF, renal failure, or splenic infarcts) is more likely to occur in patients who are asplenic, older than 50 years of age, or immunocompromised. Persistent and relapsing babesiosis is also more likely to occur in these patients.

Laboratory Diagnosis:
Diagnosis is generally made by blood smear examination for intraerythrocytic ring forms and differentiating these from Plasmodium species.  Ring forms occasionally present in a “Maltese Cross” formation and are more likely than Plasmodium species to be extracellular due to RBC hemolysis.  In addition, PCR (especially useful when circulating parasite levels are low), or serologic testing is available.  A low hematocrit and thrombocytopenia are also often associated with babesiosis.

Differential Diagnosis:
Includes anaplasmosis, malaria, leptospirosis, other tick-borne diseases, viral hepatitis, and noninfectious causes of hemolytic anemia.

Treatment:
Treatment for mild to moderate disease is with atovaquone and azithromycin or quinine and clindamycin, orally for 7-10 days.  Severe cases or cases of persistent relapsing babesiosis may require longer length of treatment, intravenous formulations and occasionally RBC exchange transfusions (parasitemia levels >10%).

Related concepts
1. Parasite
2. Protozoa
3. Babesia
4. B. microti
5. Babesiosis
6. Ticks
7. Tick bite
8. Ixodes scapularis
9. Hemolytic anemia

 
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