OVERVIEW: What every practitioner needs to know

Are you sure your patient has babesiosis? What are the typical findings for this disease?

Babesiosis should be suspected if a patient has typical symptoms and lives in or has recently traveled to an endemic area or has had a blood transfusion within the previous 3 months.

The most common symptoms are fever, fatigue, chills, and sweating in more than half of patients. Headache, myalgia, anorexia, cough, arthralgia, or nausea also may occur. Physical examination may reveal fever, splenomegaly, hepatomegaly, and pallor or jaundice.

The diagnosis is confirmed with laboratory testing (see below).

What other disease/condition shares some of these symptoms?

Other diseases that share some of these symptoms include Lyme disease, anaplasmosis, and infection by a variety of viruses.

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What caused this disease to develop at this time?

Babesiosis is primarily transmitted by tick bite, but most people who are infected do not recall a tick bite. Babesiosis is most commonly caused by Babesia microti and is endemic in the northeastern and northern midwestern United States. B. duncani causes babesiosis in the far West. Cases have been described in Africa, Asia, and Europe.

Rarely, babesiosis may be transmitted through blood transfusion or perinatally.

About half of infected children are asymptomatic. Severe disease that may end in death occurs in immunocompromised hosts. These patients may include newborn infants; children who lack a spleen; those who have malignancy, HIV infection, sickle cell disease, or thalassemia; or those who are taking immunosuppressive drugs.

Epidemiologic risk factors for infection include living or traveling in an endemic region, history of recent tick bite or blood transfusion, and onset of illness in the late spring, summer, or early fall.

What laboratory studies should you request to help confirm the diagnosis? How should you interpret the results?

A complete blood count may be ordered to check for anemia and thrombocytopenia. In more severe cases, hemoglobinuria, elevation of aspartate aminotransferase, alanine aminotransferase, or lactate dehydrogenase levels, and elevated blood urea nitrogen or creatinine levels may occur.

Thick and thin blood smears should be obtained in all suspected cases. Identification of the causitive pathogen in red blood cells using Giemsa or Wright stain may be difficult early in the course of infection when parasitemia may be low. Multiple blood fields may need to be examined microscopically. If the blood smear results are negative, a Babesia polymerase chain reaction and immunofluorescent antibody test should be performed.

Identification of organisms on blood smear, amplification of Babesia DNA, or a fourfold rise in specific antibody in acute and convalescent sera confirms the diagnosis. Detection of B. microti IgM antibody or an IgG titer of 1:1024 or greater is suggestive of acute infection.

Would imaging studies be helpful? If so, which ones?

Imaging studies generally are of little help in establishing a specific diagnosis. Splenomegaly may be observed on ultrasonography or with other imaging methods but it is a nonspecific finding. A chest roentgenogram wouild help diagnose adult respiratory distress syndrome, the most common complication of babesiosis, but this finding is uncommon except in severe disease.

If you are able to confirm that the patient has babesiosis, what treatment should be initiated?

For mild to moderate disease, give atovaquone: 20 mg/kg (maximum 750 mg/dose) by mouth every 12 hours plus azithromycin: 10 mg/kg (maximum 500 mg/dose on day 1 and then 5 mg/kg, maximum 250 mg/dose on subsequent days) by mouth. Treat for 7 to 10 days.

For severe disease, give clindamycin: 7-10 mg/kg (maximum 600 mg/dose) by mouth or by intravenous infusion every 6 to 8 hours plus quinine: 8 mg/kg (maximum 650 mg) by mouth every 8 hours.

Treat for 7 to 10 days. Antibiotic treatment for 6 weeks should be given to highly immunocompromised hosts who do not respond to a single 7- to 10-day course of therapy.

Exchange transfusion or partial exchange transfusion may be life saving in severe disease.

What are the adverse effects associated with each treatment option?

The atovaquone and azithromycin combination generally is well tolerated, but adverse effects include headache, gastrointestinal upset, difficulty sleeping, dizziness, and cough.

The combination of clindamycin and quinine frequently is associated with side effects, especially in adults. These include decreased hearing, tinnitus, vertigo, and diarreha.

What are the possible outcomes of babesiosis?

The prognosis for babesiosis in children usually is very good. Symptoms resolve after appropriate antibiotic therapy, and there are no reported long-term complications in previously healthy children.

Immunocompromised children may have more severe disease that may end in death. These patients include newborn infants; children who lack a spleen; those who have malignancy, HIV infection, sickle cell disease, or thalassemia; those who are taking immunosuppressive drugs; or those who acquire infection through transfusion.

The benefits of the standard treatment outweigh the risks, even for apparently mild disease.

What causes this disease and how frequent is it?

Currently about 700 cases a year are reported to state health departments in endemic regions, but the actual number of cases is likely to be much greater and is increasing.

Babesiosis was named a nationally notifiable disease in 2011 by the Centers for Disease Control and Prevention.

The most common species causing human disease is B. microti, which is found in the Northeast and the northern Midwest and in Asia and Europe.

A few cases of B. duncani have been described in the far West of the United States.

Babesiosis is primarily transmitted by hard-bodied ticks, and most cases occur in the summertime but occasionally occur in the late spring and early autumn.

Children are as frequently infected as adults but generally have a milder clinical course. Children who lack a spleen; have cancer, HIV infection, sickle cell disease, or thalassemia; or who are taking immunosuppressive drugs experience more severe disease.

Rarely, babesiosis may be acquired through blood transfusion or perinatally.

How do these pathogens/genes/exposures cause the disease?

Babesia infects red blood cells and causes them to lyse, resulting in anemia and hemoglobinuria. Pathogenesis of severe disease is thought to include either excessive proinflammatory cytokine production or increased erythrocyte cytoadherence to vascular endothelium, or both.

What complications might you expect from the disease or treatment of the disease?

Complications are unusual in children but may include acute respiratory failure, disseminated intravascular coagulopathy, congestive heart failure, renal or liver failure, or splenic infarction.

Mortality rates range from 3% to 5% in previously healthy adults to 10% to 28% in immunocompromised adults and in people who acquire babesiosis through blood transfusion.

How can babesiosis be prevented?

Personal protective measures include avoiding areas where ticks, mice, and deer are known to thrive, especially wooded and tall grassy areas, from May through October. It is especially important for immunocompromised individuals to avoid tick-infested areas.

When in tick-infested areas in endemic regions, wear long sleeve shirts and long pants. Consider use of tick repellants. DEET-containing sprays or lotion should be used with caution in young children. Tick checks and removal of ticks with tweezers are recommended.

Property management should include keeping lawns mowed, using acaricidal spays, sealing stone walls where mice build nests, and plantings and fencing to keep deer away.

No vaccine or antimicrobial prophylaxis is available.

What is the evidence?

Gubernot, DM, Nakhasi, HL, Mied, P. “Transfusion-transmitted babesiosis in the United States: summary of a workshop”. Transfusion. vol. 49. 2009. pp. 2759-27. (A review of transfusion-transmitted babesiosis.)

Krause, PJ, Telford, SR, Pollack, RJ. “Babesiosis: an underdiagnosed disease of children”. Pediatrics. vol. 89. 1992. pp. 1045-48. (A study of the prevalence and clinical manifestations of babesiosis in children.)

Vannier, E, Gewurtz, B, Krause, PJ. “Human babesiosis”. Infect Dis Clin N Am. vol. 22. 2008. pp. 469-88. (A general review of human babesiosis.)

Krause, PJ, McKay, K, Thompson, CA. “Disease-specific diagnosis of coinfecting tick-borne zoonoses: babesiosis, human granulocytic ehrlichiosis, and Lyme disease”. Clin Infect Dis. vol. 34. 2002. pp. 1184-91. (A review of the diagnosis of babesiosis, human granulocytic ehrlichiosis, and Lyme disease.)

Krause, PJ, Lepore, T, Sikand, VK. “Atovaquone and azithromycin for the treatment of human babesiosis”. N Engl J Med. vol. 343. 2000. pp. 1454-8. (Report of the first clinical trial of antibiotic therapy for human babesiosis.)

Wormser, GP, Dattwyler, RJ, Shapiro, ED. “The clinical assessment, treatment, and prevention of Lyme disease, human granulocytic anaplasmosis, and babesiosis: clinical practice guidelines by the Infectious Diseases Society of America”. Clin Infect Dis. vol. 43. 2006. pp. 1089-134. (Treatment guidelines for babesiosis, human granulocytic ehrlichiosis, and Lyme disease.)