Babesiosis Prior to 1969 Babesia infections were rare and limited to B. divergens (a cattle parasite) and some others species that were parasitic in rodents. It was only seen in splenectomized patients who had disabled immune systems as a result of the splenectomy. 1969, Nantucket Island, Mass: 1 st human Babesia infection in a non-splenectomized patient. Hundreds of cases have been reported since.
Morphology Easily misdiagnosed as Plasmodium in areas high in Malaria prevalence due to its “ring shape” Variation in shape and size Do not produce pigment Intraerythrocytic Babesia microti
Geographic Distribution Worldwide –Europe: B. divergens, most common –United States: B. microti, most common in NE and MW portions WA-1 strain recently found on west coast * May not be as prevalent in malaria-endemic countries*
Hosts Definitive host: Humans or Deer tick Vector: Ixodes scapularis (Deer tick) Intermediate host: White-footed mouse and other rodents and Deer –When the deer or mouse pop. increases, the tick pop. does too.
Life Cycle 1.Babesia infected tick introduces sporozoites into the mouse host. 2.Sporozoites enter erythrocytes and undergo asexual reproduction (budding). 3.In the blood, parasites undergo male and female differentiation (micro- and macrogametes are formed). 4.The deer tick (definitive host) takes a blood meal ingesting gametes, which can now undergo fertilization within the gut, 5. resulting in sporozoite formation. Spread to salivary glands.
Life Cycle Cont’d… 6. During a blood meal, the tick infects the human host. Inoculation occurs by a tick larva, nymph or adult. 7.Sporozoites invade erythrocytes and a trophozoite differentiates, replicating asexually by budding: responsible for the clinical manifestations. This forms 2-4 merozoites which eventually reinvade other RBCs. 8.Humans are for all practical purposes “dead- end” hosts, because subsequent transmission after the tick feeds on a human is unlikely. Human to human transmission is well recognized to occur through blood transfusions. Babesia can be transmitted in utero.
Pathogenesis (Signs & Symptoms) 1-4 weeks (can last several weeks): fever, chills, headache, nausea, vomiting, and/or muscle aches (myalgia), hemolytic anemia, jaundice and splenomegaly. May be mild in otherwise healthy people May be asymptomatic Severe form of Babesiosis may be life- threatening if untreated (usually people who have been splenectomized, the elderly, or who have impaired immune systems).
Host Immune Response Mice develop immunity –CD4 T cells are partially responsible for resolution of primary infection and protection against re-infection. Influx in IgG due to the infection being in the blood
Diagnosis Microscopic examination: thick and thin blood smears stained with Giesma Antibody detection: detects even low levels of parasitic invasion –Indirect fluorescent antibody test (IFA) detects antibodies (IgM & IgG) of patients with B. microti infection –Recommended only if low levels of parasitemia or blood smear is inconclusive Diagnosis can be derived from molecular techniques, such as PCR –Valuable in investigations of new Babesia species
Treatment Clindamycin*: antibiotic with little or no side effects Quinine or Atovaquone*: antiparasitic Azithromycin*: antibiotic, some side effects Clindamycin combined with Quinine is treatment of choice * FDA approved, but considered investigational
Public Health Concerns Avoidance of endemic areas May-September Clothing that covers lower body and light colored Tuck pants into boots/shoes Repellent that contains Diethyltoluamide (DEET) should be applied regularly Inspect pets Avoid tall grass and brush Examine skin thoroughly and carefully remove ticks if found Avoid accepting blood donations from those with a history of tick bites
In conclusion, be aware of your surroundings, especially in areas with high deer tick populations.