Babesiosis is a parasitic disease caused by intraerythrocytic protozoa of the Babesia genus (Babesia microti and other species). Babesia parasites are transmitted in nature through the bites of infected ticks but can also be acquired through contaminated blood components from asymptomatic parasitemic donors or, more rarely, transplacentally. Babesia infection can range from subclinical to life-threatening. Clinical manifestations, if any, can include hemolytic anemia and nonspecific influenza-like signs and symptoms (e.g., fever, chills, sweats, headache, myalgia, arthralgia, malaise, fatigue, generalized weakness). Splenomegaly, hepatomegaly, or jaundice may be evident. In addition to signs of hemolytic anemia, laboratory findings may include thrombocytopenia, proteinuria, hemoglobinuria, and elevated levels of liver enzymes, blood urea nitrogen, and creatinine. Risk factors for severe babesiosis include asplenia, advanced age, and other causes of impaired immune function (e.g., HIV, malignancy, corticosteroid therapy). Some immunosuppressive therapies or conditions may mask or modulate the clinical manifestations (e.g., the patient may be afebrile). Severe cases can be associated with marked thrombocytopenia, disseminated intravascular coagulation, hemodynamic instability, acute respiratory distress, myocardial infarction, renal failure, hepatic compromise, altered mental status, and death.
Confirmatory Laboratory Evidence:
Confirmed:
Probable:
Suspected:
A new case is one that has not been previously enumerated within the same calendar year (January through December)*.
The validity of the diagnosis of babesiosis is highly dependent on the laboratory that performs the testing. For example, differentiation between Plasmodium and Babesia organisms on peripheral blood smears can be difficult. Confirmation of the diagnosis of babesiosis by a reference laboratory is strongly encouraged, especially for patients without residence in or travel to areas known to be endemic for babesiosis.
A positive Babesia IFA result for immunoglobulin M (IgM) is insufficient for diagnosis and case classification of babesiosis in the absence of a positive IFA result for IgG (or total Ig). If the IgM result is positive but the IgG result is negative, a follow-up blood specimen drawn at least one week after the first should be tested. If the IgG result remains negative in the second specimen, the IgM result likely was a false positive.
When interpreting IFA IgG or total Ig results, it is helpful to consider factors that may influence the relative magnitude of Babesia titers (e.g., timing of specimen collection relative to exposure or illness onset, the patient’s immune status, the presence of clinically manifest versus asymptomatic infection). In immunocompetent persons, active or recent Babesia infections that are symptomatic are generally associated with relatively high titers (although antibody levels may be below the detection threshold early in the course of infection); titers can then persist at lower levels for more than a year. In persons who are immunosuppressed or who have asymptomatic Babesia infections, active infections can be associated with lower titers.
Babesia microti is the most frequently identified agent of human babesiosis in the United States; most reported tick-borne cases have been acquired in parts of northeastern and upper Midwest, but incidence in other parts of the country has also increased as populations of the primary vectors, Ixodes spp. ticks, have expanded into new areas. Sporadic U.S. cases caused by other Babesia agents include B. duncani (formerly the WA1 parasite) and related organisms (CA1-type parasites) in several western states as well as parasites characterized as "B. divergens like" (MO1 and others) in various states. Blood-borne transmission of Babesia is not restricted by geographic region or season.
Additionally, since the addition of babesiosis to the Nationally Notifiable Condition List in 2011, the Food and Drug Administration (FDA) has recommended routine screening of blood donors in jurisdictions with evidence of vectorborne transmission of babesiosis, which has reduced cases of transfusion-associated babesiosis (2)
| Confirmed | Probable | Suspect | ||
|---|---|---|---|---|
| Clinical Evidence | ||||
| Objective Clinical Evidence | ||||
| Fever as reported by patient or healthcare provider | O | O | O | |
| Anemia | O | O | O | |
| Thrombocytopenia | O | O | O | |
| Subjective Clinical Evidence | ||||
| Chills | O | O | ||
| Sweats | O | O | ||
| Headache | O | O | ||
| Myalgia | O | O | ||
| Arthralgia | O | O | ||
| Laboratory Evidence | ||||
| Identification of intraerythrocytic Babesia organisms by light microscopy in a Giemsa, Wright, or Wright-Giemsa–stained blood smear | O | |||
| Detection of Babesia spp. DNA in a whole blood specimen through nucleic acid testing such as polymerase chain reaction (PCR) assay, nucleic acid amplification test (NAAT), or genomic sequencing that amplifies a specific target | N | |||
| Serological evidence of a four-fold change1 in IgG-specific antibody titer to B. microti antigen by indirect immunofluorescence assay (IFA) in paired serum samples (one taken in the first two weeks after illness onset and a second taken two to ten weeks after acute specimen collection)2 | O | |||
| Serologic evidence3 of an elevated IgG4 or total antibody reactive to B. microti antigen by IFA at a titer ≥1:256 | N | |||
| Serologic evidence3 of an elevated IgG4 or total antibody reactive to B. divergens antigen by IFA at a titer ≥1:256 | O | |||
| Serologic evidence3 of an elevated IgG4 or total antibody reactive to B. duncani antigen by IFA at a titer ≥1:512 | O | |||
| Sample taken within 60 days of illness onset | N | N | ||
| Epidemiologic Evidence | ||||
| N/A | ||||
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