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posted Jul 17, 2013, 7:36 AM by Eliany Mejia   [ updated Jul 17, 2013, 11:42 AM by Purnema Madahar ]

Here is another good case! This is a 55 yo female presenting with headaches and fevers, found to have pancytopenia, elevated AST/ALT, low haptaglobin and elevated LDH, consistent with hemolytic anemia. Peripheral smear shows spherocytes and parasites in the erythrocytes suggestive of babesiosis. Pt probably acquired at a picnic in Connecticut - from tick bite. So let’s talk about Babesia

-          Etiology and Natural Cycle

-          Epidemiology

-          What is the clinical presentation?

-          How it is diagnosed?

-          What is the treatment?

Babesiosis is an emerging infection transmitted by ticks and caused by intraerythrocytic protozoa of the genus Babesia. Wild and domestic animals are the natural reservoirs of Babesia species.  Only in the past 50 years has Babesia been appreciated to be a pathogen in humans. 

The disease was first documented by the Romanian scientist Victor Babes in 1888. He described symptoms of a severe hemolytic illness seen uniquely in cattle and sheep. Although he identified the causative agent in 1888, he incorrectly believed it to be due to the bacterium he named Haematococcus bovis. Later in 1893, Theobald Smith and Fred Kilborne identified the parasite as the cause of Texas cattle fever, the same disease described by Babeş. They also identified the tick as the agent of transmission, a discovery that first introduced the concept of arthropods functioning as disease vectors.  Long believed to be a disease that only affected nonhuman mammals, the first case of babesiosis was seen in humans in 1957.

Etiology and Natural Cycle

In the northeastern United States, Babesia microti is transmitted to humans by the tick Ixodes scapularis (same vector tick species as Lyme disease and Anaplasma).  Other babesia species cause clinically similar infections but are endemic to the northwestern and Midwestern United States.

The life cycle of Ixodes scapularis spans over two years and includes deer and mice. Mice are the primary reservoir for B. microti; deer are not competent reservoirs. Adult ticks feed on white-tailed deer, whereas tick larvae and nymphs feed on white-footed mice. In the fall, adult ticks feed primarily on white-tailed deer. The deer are incomplete reservoirs for B. microti but are essential for the maintenance of the I. scapularis.  As the tick feed, babesia-infected RBCs accumulate in their gut.  Once in the blood, sporozoites invade the erythrocytes to become trophozoites. Trophozoites undergo asynchronous schizogony, resulting in the budding of two or four merozoites. Tetrads (“Maltese Crosses”) are pathognomonic of B. microti and other small Babesia species.

Person- to-person transmission may occur after transfusion of infected asymptomatic donor. As of 2003, though, the Centers for Disease Control and Prevention (CDC) acknowledged more than 40 cases of babesiosis contracted from PRBC transfusions and two infections documented from organ transplantation.


Human babesiosis is caused by one of several babesial species that have distinct geographic distribution. In North America, babesiosis is caused predominantly by Babesia microti, a rodent-borne piroplasm, and also occasionally by a newly recognized species, the so-called WA1 piroplasm. In Europe, babesiosis is considerably rarer but more lethal; it is caused by the bovine pathogen Babesia divergens. Endemic areas are regions of tick habitat, including the forest regions of the northeastern United States and temperate regions of Europe. The tick vectors of B. microti, may also be co-infected with Lyme Disease and Anaplasma. For reasons that remain unclear, in areas endemic to both Lyme disease and babesiosis, Lyme disease transmission prevails and is more predominant in the region. 

As the disease results in a high number of asympomatic individuals, many populations can possess high seroprevalence without much documentation of illness. For example, in Rhode Island and Nantucket, seroprevalence has been measured to be 20-25%. Prevalence of babesiosis is mostly documented during the months of May to September when tick activity in endemic regions is high.

The spectrum of disease is broad, ranging from an apparently silent infection to a fulminant, malaria-like disease resulting occasionally in death. Various determinants are involved in the severity of disease manifestation; among those identified are age, immunocompetence, asplenic patients and coinfection with other pathogenic agents. 

What is the clinical presentation?

Asymptomatic infection or self-limiting flulike illness occurs in 25% of adults and 50% of children. The incubation period last 1-6 weeks. Onset is gradual and the most common manifestation is fever , fatigue, malaise, chills, myalgias and artharlgias.

Other findings such as hemolytic anemia, splenomegaly and hepatomegaly may be noted. Jaundice is rare.

The parasitemia levels are usually 1-10% in immunocompetent host but can reach 85% in asplenic patients. Reticulocytes are elevated, WBCs are normal or slightly low, and thrombocytopenia is common.  Levels of AST and ALT, and Bilis are usually elevated. With hemolysis, the serum haptaglobin concentration is low and urianalysis may show hemobinuria and proteinuria.

Asplenic patients tend to have high levels of parasitemia and more severe disease. 

The clinical presentation in patients with severe babesiosis may include profound anemia, acute kidney injury, DIC, high output heart failure, respiratory failure, and circulatory collapse.

B. microti infection may be fatal in 5-10% of cases in hospitalized patients. Severe anemia with Hgb < 10 and high level of parasitemia (> 10%) are risk factors for complications. Alkaline phosphatase > 125, WBC > 5,000, and male gender are strong predictors of severe disease, defined by death, hospitalization > 2 weeks, or admission to the ICU for > 2 days.

How it is diagnosed?

Check the smear! "Maltese cross formations" on the blood film are essentially diagnostic of babesiosis. Careful examination of multiple smears may be necessary, since Babesia may infect less than 1% of circulating RBCs and thus be easily overlooked. Visualization of this intraerythrocytoc ring forms on thin-preparation blood smear is suggestive of babesiosis, but differentiation from falciparum malaria may be difficult if the patient has a compatible travel history for both infections. Even with much study of babesiosis and malaria, misdiagnosis with blood smear can be frequent and problematic. The preferred method for low levels parasitemia,when the smear is negative,  is PCR using whole blood specimens, which is more sensitive than direct microscopy, but also more expensive. 

Serology with indirect fluorescent antibody (IFA) testing has a much higher specificity than stained blood smears with antibody detection in 88-96% of infected patients. However, serology testing is no recommended because seroconversion may lag behind onset of clinical symptoms, or conversely, detectable antibodies may reflect a previous symptomatic infection. Serology is most useful when parasites are not visualized by microscopy and DNA is not detected by PCR. Such cases include asymptomatic blood donors implicated in transfusion-acquired babesiosis, and asymptomatic individuals who were infected but cleared the parasites with or without treatment.

What is the treatment?

Treatment is indicated for all symptomatic patients with laboratory confirmation of infection as well for asymptomatic patients with documented persistence of parasites for more than 3 months.

Treatment regimens for patients with mild disease include the combination of Atovaquone and Azithromycin or quinine and clindamycin. Quinine combined with clindamycin is the treatment of choice for severe disease, and exchange transfusion is recommended for patients with greater than 10% parasitemia.

Symptoms typically respond rapidly to therapy but may recur in immunocompromised patients. Administration of antimicrobial therapy for 7 to 10 days is usually sufficient for curative treatment of mild disease. Longer duration of antimicrobial therapy may be needed in cases of persistent and relapsing babesiosis. Immunocompromised patients should be treated for at least six weeks, including two weeks after parasites are no longer detectable on blood smear. In some patients with suspected co-infection or severe illness adjunctive therapy with Doxycycline may be indicated. 

Our patients had 1% parasitemia with mild symptoms. She was treated with Atovaquone and Azrithomycin. ID also recommended doxycycline to cover for possible co-infection with lyme/anaplasma. (Lyme serology is still in lab). 

I have attached a really good review article by one of the guru in the field and the latest guidelines for the diagnosis, treatment and management of Lyme disease, Anaplasma and Babesia by the IDSA. Till next time...

Purnema Madahar,
Jul 17, 2013, 7:46 AM
Purnema Madahar,
Jul 17, 2013, 7:39 AM