Babesiosis, is an infection with the malaria-like protozoan Babesia that parasitizes and reproduces within mammalian red blood cells. It has been recognized as a disease in both wild and domestic animals such as cattle, horses, and sheep for many years however, it wasn’t until the late 1960s, that the first North American human cases appeared on Nantucket Island. The CDC reports growing incidence, and the disease is now recognized as an emerging and occasionally serious zoonotic infection in the United States. Over 100 distinct species have since been identified within the Babesia genus, though only a few of these are currently known to be human pathogens including, but not limited to, B. microti, B. divergens, and B. duncani. Babesiosis has also been reported in North and South America, Europe, and southern and eastern Asia. Some species of Babesia, such as B. divergens, appear to be more virulent than others. Babesia have a complex life cycle involving several different stages and physical forms and are maintained in nature primarily through exchange between Ixodes ticks and various mammals.
Most human cases of Babesiosis in the U.S. are caused by Babesia microti which is transmitted by the bite of the black legged tick, Ixodes scapularis and Ixodes pacificus, usually at the nymphal stage. Because the size of these ticks are so small, “poppy seed”, many people that contract Babesia do not recall a tick bite. These are the same ticks that transmit Lyme disease and co-infection with Lyme or Anaplasmosis is possible. Co-infection may complicate both diagnosis and treatment. Because of the similarity in hosts (primarily mice) and vectors, Babesiosis is reported in the same geographic areas as Lyme disease including the Northeast, upper Midwest states and West coast. Although primarily transmitted by a tick bite, Babesiosis can also be acquired via blood transfusion and maternal-fetal transmission (congenital Babesiosis) during pregnancy or at birth. Blood banks across the US are not currently screening for this disease and it is a growing concern in areas where this disease is highly endemic.
Though Babesiosis is a nationally notifiable condition it is not a reportable disease in Colorado. The primary vectors for this disease in the US are the ticks I. scapularis and I. pacificus, which are not documented to occur in Colorado. However, Ixodes spinipalpis, was discovered to be part of an endemic transmission cycle of Babesia microti in the foothills of the Rocky Mountains in Colorado. B. microti were found in both Ixodes spinipalpis and the reservoir host Microtus ochrogaster (the prairie vole) in this 2001 study. This tick is documented as an occasional human biter. Though, I. spinipalpis has demonstrated questing behavior (outside of host nests) in other parts of the country where humidity is greater, risk for human disease transmission from these ticks is considered low in Colorado based on the nidicolous behavior(remaining within the host species nest) observed in the semi-arid environment of the foothills. No human cases of Babesiosis have been reported from the bite of a Colorado tick. More research is needed on the status of Babesiosis and risk to human health in Colorado and throughout the US.
As blood banks do not currently screen for Babesia in the blood supply, Coloradans may acquire this disease through blood transfusion. Disease may also be acquired through maternal-fetal (congenital Babesiosis) transmission.
Babesiosis manifests in a wide spectrum of disease severity. In people with intact immune systems, symptoms of Babesiosis are non-specific and usually begin 1-6 weeks after an infected tick bite or through an infected blood transfusion. Some people that are infected are entirely asymptomatic. When symptoms do occur, they are often similar to symptoms of the flu and include:
- Joint and muscle aches
- Loss of appetite
- Nausea or Vomiting
- Shortness of breath
Most patients experience a viral-like illness. The course of the disease may last lasts weeks to several months, but some patients take even longer to recover. In patients with a complicating condition, such as underlying immunosuppression, the disease course can be severe and potentially fatal. Coinfection with Lyme disease or Anaplasmosis may also complicate the clinical presentation and severity of the disease.
Some patients may develop enlarged livers or spleens. The most common serious complication of Babesiosis is acute respiratory failure, but heart failure, liver and renal failure, disseminated intravascular coagulation and coma are also well-recognized severe manifestations of Babesiosis.
Early symptoms of Babesiosis are largely non-specific, making diagnosis difficult. A patient with recent travel to an endemic area, especially in the summer months, presenting with fever and viral-like illness may be suspect for this disease. Conventional blood tests can produce a pattern that suggests the diagnosis of Babesisois.
Babesia organisms cause lysis of red blood cells. For patients that are acutely ill, findings on routine laboratory testing frequently include hemolytic anemia, lymphopenia and thrombocytopenia. Additional findings may also include proteinuria, hemoglobinuria, and elevated levels of liver enzymes, blood urea nitrogen, creatinine, serum lactate dehydrogenase, and erythrocyte sedimentation rate. For some adults, as well as children that contract Babesia congentially, neutropenia has also been a finding.
In symptomatic people, Babesiosis is diagnosed by examining blood specimens under a microscope and visualizing Babesia parasites inside red blood cells. A specialized reference laboratory (such as at CDC or a health department) may be used to confirm the diagnosis by blood-smear examination. Antibody detection tests may be useful for detecting infected individuals with very low levels of parasitemia (such as asymptomatic blood donors in transfusion-associated cases), for diagnosis after infection is cleared by therapy, and for discrimination between, Malaria, (Plasmodium falciparum) and Babesia infection in patients whose blood smear examinations are inconclusive and whose travel histories cannot exclude either parasite.
Blood smears are used to visualize the Babesia parasite within the red cells of a patient’s blood. Giemsa or Wright stains are typically used in this process. In early illness, the infection rate of erythrocytes can be less than 1%, so multiple smears over a period of days may be needed to confirm the diagnosis. Babesial DNA can also be detected by polymerase chain reaction (PCR) in cases where smears are negative but the diagnosis is still suspected.
Immunofluorescence (IFA) of IgM and IgG antibodies testing may be used to confirm a Babesiosis diagnosis. However, antibodies to Babesia organisms can remain high for months or years after clinical resolution of illness, so the test is not a reliable indicator of active infection.
A combination therapy with atovaquone (Mepron) and azithromycin is most commonly used for treatment of mild to moderate Babesiosis. A combination therapy of oral clindamycin and quinine has also been proven effective, but the rate of adverse reactions is significantly higher.
For patients with severe Babesiosis, intravenous clindamycin and (oral) quinine may be used. In patients with underlying immunosuppression and persistent signs and symptoms, studies have shown an association between longer treatment duration and a positive outcome.
For those patients co-infected with Lyme disease and/or Anaplasmosis treatment may be more complex.