caused by hemoprotozoan parasites of the genus Babesia. While
more than 100 species have been reported, only a few have been
identified as causing human infections. Babesia microti and
Babesia divergens have been identified in most human cases, but
variants (considered different species) have been recently identified.
Little is known about the occurrence of Babesia species in
malaria-endemic areas where Babesia can easily be misdiagnosed as
microti life cycle involves two hosts, which includes a rodent,
primarily the white-footed mouse, Peromyscus leucopus. During a
blood meal, a Babesia-infected tick introduces sporozoites into
the mouse host
Sporozoites enter erythrocytes and undergo asexual reproduction
In the blood, some parasites differentiate into male and female gametes
although these cannot be distinguished at the light microscope level
The definitive host is a tick, in this case the deer tick, Ixodes
Once ingested by an appropriate tick
gametes unite and undergo a sporogonic cycle resulting in sporozoites
Transovarial transmission (also known as vertical, or hereditary,
transmission) has been documented for “large” Babesia spp. but
not for the “small” babesiae, such as B. microti
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
undergo asexual replication (budding)
Multiplication of the blood stage parasites is responsible for the
clinical manifestations of the disease. Humans are, for all practical
purposes, dead-end hosts and there is probably little, if any,
subsequent transmission that occurs from ticks feeding on infected
persons. However, human to human transmission is well recognized to
occur through blood transfusions
Deer are the hosts upon which the adult ticks feed and are indirectly
part of the Babesia cycle as they influence the tick population.
When deer populations increase, the tick population also increases, thus
heightening the potential for transmission.
little is known about the prevalence of Babesia in
malaria-endemic countries, where misidentification as Plasmodium
probably occurs. In Europe, most reported cases are due to B.
divergens and occur in splenectomized patients. In the United
States, B. microti is the agent most frequently identified
(Northeast and Midwest), and can occur in non-splenectomized
individuals. Two variants, arguably different species, have been
reported in the U.S. states of Washington and California (WA1- type and
related parasites) and Missouri (MO1).
are probably asymptomatic, as indicated by serologic surveys.
Manifestations of disease include fever, chills, sweating, myalgias,
fatigue, hepatosplenomegaly, and hemolytic anemia. Symptoms typically
occur after an incubation period of 1 to 4 weeks, and can last several
weeks. The disease is more severe in patients who are immunosuppressed,
splenectomized, and/or elderly. Infections caused by B. divergens
tend to be more severe (frequently fatal if not appropriately treated)
than those due to B. microti, where clinical recovery usually
Diagnosis can be
made by microscopic examination of thick and thin blood smears stained
with Giemsa. Repeated smears may be needed.
detection by indirect fluorescent antibody (IFA) test is a
complementary diagnostic test.
Isolation of the
organisms by inoculation of patient blood into hamsters or gerbils may
also assist in diagnosis. Animals inoculated with infective blood
typically develop parasitemia within 1 to 4 weeks.
clindamycin* plus quinine or atovaquone* plus azithromycin* are the
options. The Medical Letter notes that exchange transfusion has been
used in severely ill patients with high parasitemias.
* These drugs are
approved by the FDA, but considered investigational for this purpose.