Human babesiosis (Piroplasmosis)
Babesiosis occurs only occasionally in man (mainly cattle farmers) and the disease is often misdiagnosed as drug-resistant malaria since the drug response significantly differs from that of Plasmodium. Thus the incidence of Babesiosis in man is not well known. What however is known is that frequently anti-babesia antibodies are found in African people, indicating that they easily contratct babesiosis without suffering from major symptoms of disease.
Humans become infected with Babesia when they accidently intrude into a natural disease cycle. In the eastern and midwestern U.S., the disease is known since 1966. Human cases often turn out to be caused by Babesia microti of rodents. Human infections tend to be mild and self limiting, and most probably are never diagnosed.
Transfusion with blood or blood componenet from asymptomatic donors may result in human babesiosis. However, such a risk is minimal.
Transmission of Babesia microti from one host to another generally takes place through direct tick-host contact. In the northeastern United States, the enzootic cycle is maintained principally by the interactions between immature blacklegged ticks and white-footed mice. In general, larvae acquire the infection when feeding on Babesia microti-infected mice. Engorged larvae overwinter and pass the parasites transstadially to the next developmental stage, the nymph, in the following spring. Nymphs infected in the larval stage pass the infection to susceptible animals upon feeding. In areas where Babesia microti is endemic, infection rates of nymphal ticks with the pathogen typically range from 5 to 40%. The role of adult ticks in transmission of the infection appears to be minimal. Adults feed predominantly on white-tailed deer, which is not a competent reservoir for Babesia microti.
The same ticks also are responsible for the transmission of lyme disease, a bacterial infection caused by Borrellia burgdorferi.
Flu-like symptoms start two to four weeks after a tick bite, and can include sweating, fever and chills, headache, fatigue, muscle pains and weight loss. They usually only become severe in persons with a weakened immune system, or whose spleen has been damaged or removed. The spleen is responsible for clearing out damaged blood cells, so when it is missing these infections can progress out of control. In spleen-intact patients, parasitaemias may range from 1 to 20%, however, a parasitaemic level of 85% in severe human babesiosis has been reported. Haemolytic anaemia and thrombocytopenia have been frequently found, and dark urine also may be observed. Patient leukocyte counts are typically in the low to normal ranges.
Diagnosis of human babesiosis relies upon the determination of the presence of the erythrocytic stage of the organism. Examination of Giemsa-stained thin blood smears is considered the most useful diagnostic procedure. The tetrad forms (Maltese-cross) of the parasite are believed to be the primary diagnostic character for the disease.
PCR has proven to facilitate the diagnosis of zoonotic babesial infections. By using genus- and species-specific primers, a definitive diagnosis can be made within a day.
Most patients infected with Babesia microti appear to experience only mild clincal manifestations; therefore, they normally require no specific treatment. If treatment is required, both pentamidine and berenil therapies can effectively control the parasitemia, but fail to eliminate the parasites completely. Currently, administration of quinine combined with clindamycin is the treatment of choice for human babesiosis. The parasitemia is consistently eradicated after the administration of the drugs and there is no recurrance of the babesial infection after the discontinuation of the treatment.
It is important to control rodents around human habitation and to use tick repellents. It is helpful to wear light colored clothing and to tuck pants into socks when walking through tick-infested areas.
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