A tick-borne illness caused by species of the intraerythrocytic protozoan Babesia microti.

Babesiosis is a disease caused by microscopic parasites that infect red blood cells. 

Most infections occur between May and September, and the caused by the protozoan B. Microt an obligate parasite of human erythrocytes that is transmitted to humans through the bite of the Ixodes scapularis tick, with an incubation period of 1 to 4 weeks.

Babesia microti usually infects white-footed mice and other small mammals—is the main species that has been found in people in the United States. 

As a result of warming temperatures I. Ccapularis is extending north beyond the Canadian border, increasing suburban sprawl in rural areas also increasing scrub habitat and boosts tick populations.

Occasional cases caused by other Babesia species have been detected.



White-tailed deer are the most important food source for the adult stage of the tick.

Deer are not infected with B. microti.


Babesia microti parasite is typically spread by the young nymph stage of the tick. 


Tick nymphs are mostly found during warm months in areas with woods, brush, or grass, and infected people might not recall a tick bite because I. scapularis nymphs are about the size of a poppy seed.


Additional ways of becoming infected with Babesia include:


Contaminated blood transfusion 


Transmission from an infected mother to her baby during pregnancy or delivery.

Solid organ transplantation.


Most cases occur in the Northeast and upper Midwest, including off-shore islands.

Since 2019, the FDA requires nucleic acid testing for B. Microti or the use of pathogen reduction technology for blood donations collected in 14 states and the District of Columbia, locations where it may be endemic.


Many patients infected with Babesia are asymptomatic.


The main way people get infected is through the bite of an infected tick.


Babesia microti is spread by Ixodes scapularis ticks, which are commonly called blacklegged ticks or deer ticks. 


B. microti usually must stay attached to a person for more than 36–48 hours to be able to transmit the parasite.


Humans are opportunistic hosts for Babesia when bitten by ticks.

1-2000 cases reported in the US annually, with most originating in the Northeast and upper Midwest.

Transmitted by various tick vectors in Europe, Asia, and the northwestern and northeastern United States.

A zoonotic infection in which ticks transmit Babesia organisms from a vertebrate reservoir to humans.

The infection is incidental in humans.

The primary Babesia species infect cattle, horses, dogs , cats, and mice.

Most human babesial infections are caused by B microti, found only in the United States, or by B divergens and B bovis found only in Europe.

In endemic areas of New England seroprevalence rates of 2%, mostly for B microti are present.

In Western states B duncanti is the predominant variant.

Deer population increasing in suburban areas of the US increasing the number of donors carrying the parasite and increasing transfusion linked disease.

More than 100 species of Babesia exist, but only a small number of them are known to be responsible for the majority of symptomatic disease.

The causative agent of babesiosis varies according to geographic region.

In the United States, human infection is primarily due to the rodent strain B microti, found mostly in northeastern and midwestern states.

B microti is transmitted mainly by black legged or deer ticks.

In Europe, the causative agent of babesiosis is typically the cattle strain B divergens, though B microti and B microti -like agents have been identified.

Human babesiosis is an infrequent and occurs in limited geographic locations.

The most frequent transmitted parasite via transfusion in the US.

In healthy individuals infection is usually asymptomatic.

Symptomatic disease with significant morbidity and mortality may occur in the elderly, immunocompromised and asplenic patients.

Some people develop flu-like symptoms, such as fever, chills, sweats, headache, body aches, loss of appetite, nausea, or fatigue. 


Babesia parasites infect red blood cells, and babesiosis can cause hemolytic anemia.


may have thrombocytopenia and elevated aminotransferase levels.


It can be a life-threatening disease, particularly in people who.



Do not have a spleen



Have an impaired immune system



Have other serious health 


Are elderly.

Can range in severity from asymptomatic disease observed in 20% of healthy adults to severe illness is complicated by acute respiratory distress syndrome and disseminated intravascular coagulation.

Severe disease is most common among immunocompromise patients and older patients.

generally less 1 to 2 weeks, but fatigue may last several months, and asymptomatic parasitemia ma persist for more than a year without treatment.

Infection can result in flu like symptoms, although most people are asymptomatic and or never diagnosed.

A zoonotic disease maintained by the interaction of tick vectors, transport hosts, and animal reservoirs.

The primary vectors of the parasite are ticks of the genus Ixodes.

The black-legged deer tick, Ixodes scapularis is the primary vector for the parasite in the US.

The Ixodes tick vector for Babesia is the same vector that locally transmits Borrelia burgdorferi, the agent implicated in Lyme disease.

Ioxides scapularis has 3 developmental stages, larva, nymph, and adult, and each of which requires a blood meal for development into the next stage.

As a larva and nymph, the tick feeds on rodents, and  as an adult, the tick feeds on the white-tailed deer.

Female ticks are impregnated while obtaining their blood meal on the deer, with the formation of thousands of eggs.

Increasing deer populations in the NE will increase spread of babesiosis.

The ticks ingest Babesia from the host during feeding.

Babesia protozoa multiply in their gut wall and concentrate them in their salivary glands  and when they feed on a new host, they inoculate the new host with Babesia.

Upon entering the host’s bloodstream during the tick bite, the parasite infects RBCs, and trophozoites are produced.

Mature trophozoites undergo asynchronous asexual budding and divide into 2 or 4 merozoites.

When parasites leave the erythrocyte, the membrane is damaged and hemolysis results.

Babesia species in the host erythrocyte range from 1 to 5 µm in length, and the  organisms are pear-shaped, oval, or round.

Their ring forms and  peripheral location in RBCs  allow them to be mistaken for Plasmodium falciparum.

Because schizogony is asynchronous massive hemolysis does not occur, as in Plasmodium falciparum infections.

Involved RBCs have membrane changes that decrease conformability and increase RBC adherence, which can lead to development of  pulmonary edema and acute respiratory distress syndrome.

Process associated with fever, hemolytic anemia, and hemoglobinuria.

Rash usually not seen and symptomatic disease is unusual in healthy, young adults.

Babesia parasites from rodents, primarily the white-footed deer mouse but also the field mouse, vole, rat, and chipmunk are transmitted to humans during tick bites in endemic areas.

More prevalent during the periods of tick activity, such as spring and summer, and the proximity of deer, mouse, and tick create the conditions for human infection.

Infection is primarily produced by the bite of an infected nymph during a blood meal.

Infection via blood transfusions from donors who lived in or traveled to an endemic area have been documented, with an incubation period in transfusion-associated disease of 6-9 weeks.

The rate of acquiring B microti from a unit of packed RBCs has been estimated to be 1 in 600-1800 in endemic areas.

Transplacental transmission has also occurred rarely.

Infection has a spectrum of severity, which may be divided into 3 distinct parts:as an asymptomatic infection, a mild -to-moderate viral-like syndrome, and severe disease with a fulminant course resulting in death or a persistent relapsing course.

Produces an acute infectious disease that resembles malaria.

Most cases are subclinical or are mildly symptomatic.

Infection may continue for more than 2 months after treatment.

Asymptomatic infections can persist silently for months to years.

Patients with positive smears or positive polymerase chain reaction tests more than 3 months after initial treatment should be retreated.

Rarely a fatal process, but in asplenic patients babasiosis may be a severe illness with death.

Most patients recover spontaneously.

About 25% of adults and 50% of children infected are asymptomatic, and improve spontaneously without treatment.

Fewer than 10% of patients in the US die, and most of these individuals are elderly or asplenic.

In Europe babesiosis is a life-threatening disease.

In Europe the diseases caused primarily by the Babesia divergens, a parasite carried by Ixodes ricinus tick.

In Europe incubation period 21-3 weeks and patients may present with fever, chills, thrombocytopenia, hemolytic anemia, and elevated liver functions.

Approximately 20% of patients with babesiosis are co-infected with Lyme disease, and such individuals have more severe symptoms and prolonged illness.

Patients experience fever and chills and symptoms are related to the degree of red blood cell (RBC) parasitemia.

Bovine babesiosis due to B divergens and B bovis in Europe mostly occurs in patients who are asplenic, and is a severe and often fatal process.

Usually patients report traveling to an endemic area between May and September when Ixodes tick is in its infectious nymph stage.

Most patients do not recall a tick bite and the incubation period after the tick bite is usually 1-3 weeks but as long as 9 weeks.

Initial symptoms are nonspecific and include: Malaise, fatigue, anorexia, fever, diapheresis, chills, headache, myalgias, arthralgias, nausea, vomiting, abdominal pain, depression, photophobia, conjunctival injection, sore throat, or cough.

Symptoms may last for months.

Most patients have few, if any, physical findings.

Symptoms, start within a week or so. 

Diagnosis of a tick borne illness record as a high index of suspicion and familiarity with the local epidemiological factors.


Babesiosis usually is diagnosed by examining blood under a microscope and seeing Babesia parasites inside red blood cells. 

B. microti trophozoites appear as round, oval, or pear-shaped ring forms within erythrocytes that are occasionally arranged in a pathognomonic tetrads.

The sensitivity of microscopy is in the range of 59 to 84%, compared with 95% for PCR testing.

between six and 23% of patients with babesiosis are infected with B burgdorferi and approximately 2 to 19% of patients with Lyme disease are infected B. Microbiome.

Testing for Lyme disease is typically recommended in patients with babesiosis.

Babesiosis is reportable in some states.


Patients who do not have symptoms or signs of babesiosis do not require treatment.



Prevention: areas infested with ticks should be avoided, especially during warm months. 



Use of  protective clothing.



Daily tick checks can prevent transmission of the parasite.


Treatment regimen is atovaquone and azithromycin for 7 to 10 days, with longer treatment reserve the patients who are highly immunocompromised or who have refractory disease.

Clindamycin and quinine sulfate is an alternative regimen, but has high incidence of adverse effects.

Exchange transversion transfusion is reserved for patients with greater than 10% parasitemia, hemolytic, anemia, DIC, respiratory, renal, or hepatic failure.

Doxycycline is not an effective agent.

No vaccine is available to protect people against babesiosis.


Complications are related to the degree of intravascular hemolysis, and include jaundice, hemoglobinuria, and renal failure, shock, relapse, splenic rupture and death.

Splenectomized patients are unable to clear infected RBCs, resulting in higher levels of parasitemia, and subsequent risk of cardiopulmonary arrest.

In severe cases, RBC membrane abnormalities decrease deformability, and increase adherence to capillaries and venules leading to pulmonary edema and respiratory failure.

Respiratory difficulties occur following treatment possibly related to endotoxins, complement activation, immune complex deposition, and DIC initiated by death of parasitic cells.

Severe disease may precipitate congestive heart failure, myocardial infarction, seizures, renal insufficiency and multiple organ failure.

Relative bradycardia is a common finding.

Splenomegaly may be present and may be associated with a normal or slightly decreased peripheral white blood cell count is the characteristic hematologic finding.

Differential diagnosis includes: malaria, typhoid fever, tularemia, infectious mononucleosis, monocytic ehrlichiosis and EBV.

Confirmation of the diagnosis depends on the degree of parasitemia present, and only the demonstration of Babesia in the peripheral smear can confirm the diagnosis.

Peripheral blood smears yield the most useful results.

Buffy-coat smears increase the likelihood of demonstrating Babesia parasites in the peripheral blood.

Multiple peripheral-stained thin smears or stained buffy-coat preparations may be necessary to detect parasitemia.

Liver function tests usually show mild elevation, and the erythrocyte sedimentation rate (ESR) is usually elevated.

The percentage of red blood cells parasitized in clinical cases is usually 1-10% but has ranged from less than 1% to 85%.

Most patients with intact splenic function who are mildly to moderately ill with babesiosis have 10% or less of parasitemia in their peripheral blood, while patients with asplenia usually have greater degrees of parasitemia, up to 85%.

Level of parasitemia does not directly correspond to the severity of disease.

LDH levels reflect the degree of parasitemia, the severity of infection, or both.

Serum protein electrophoresis usually shows a polyclonal gammopathy indicative of B-cell hyp2242eactivity in response to T-cell suppression by parasites.

Indirect immunofluorescent antibody (IFA) assay of immunoglobulin M (IgM) titer of 1:64 or greater for B microti is considered positive for infection, while a titer of 1:32 or less indicates a prior infection.

Immunoglobulin G (IgG) B microti titers that are increased indicate past exposure rather than current infection.

An IgM titer of 1:256 or higher or a greater than 4-fold increase in the titer is considered diagnostic of recent B microti infection.

Serum titters of 1:1024 or higher are reached in most patients with an active infection, within a few weeks, and decline slowly over a period of months to 1:256 or lower.

Cross-reactions may occur in patients with malaria infections.

Immunocompetent patients who acquire the infection by tick bite or transfusion May remain asymptomatic for present with a mild flulike illness.

Asymptomatic patients may remain parasitemic for months or years.

Immunocompromised or a splenic patient’s although available to severe disease characterized by fever, hemolytic anemia, thrombocytopenia DIC, and multi-organ failure.

Immunoblot assay for the diagnosis has sensitivity and specificity comparable to those of IFA testing.

The enzyme-linked immunosorbent assay (ELISA) IgM for Lyme test is used with suspected babesiosis because of the high incidence of coinfection with Lyme disease.

Coinfection with Lyme disease increases the severity of disease.

A polymerase chain reaction (PCR)–based diagnostic assay increases the detection rate of very low-level parasitemia.

Urinalysis should be performed for hemoglobinuria, which is related to the intensity of the Babesia infection.

Bone marrow biopsy is indicated in patients with pancytopenia, hepatosplenomegaly, fever, coagulopathy, or lymphadenopathy.

Suspicion of diagnosis in a patient with a history of exposure in an endemic area, tick bite, fever, chills, and fatigue.

Treatment in an otherwise healthy and asymptomatic patient is not required.

Treatment, however, is recommended for all diagnosed cases to prevent sequelae and potential transmission through blood donation.

In immunocompromised, elderly or asplenic patients treatment regimen of intravenous clindamycin and oral quinine or IV atovaquone and IV azithromycin is recommended.

In asymptomatic patients with positive diagnostic tests, the studies should be repeated and treatment started if parasitemia persists for more than 3 months.

Patients treated initially may require repeat treatment if repeat smears or PCR assays are positive more than 3 months after initial therapy.

Atovaquone and azithromycin is the first-line treatment for mild-to-moderate disease and is effective, if clindamycin and quinine fail.

Atovaquone and azithromycin associated with marked fewer adverse effects than clindamycin and quinine.

With severe symptoms, clindamycin and quinine remain the first line of treatment.

In areas endemic for Lyme disease, it should be treated empirically.

Immunocompromised patients are at risk for persistent relapsing illness, and require treatment for 6 weeks or longer to achieve cure, including 2 weeks after parasites are no longer detected on blood smears.

Exchange transfusion may be used in profoundly ill patients with high levels of parasitemia and hemolysis.

Treated patients should be monitored with serial blood smears to document the degree of parasitemia and effectiveness of therapy.

RBC fragments may cause capillary blockage and microvascular stasis, with liver, splenic, renal, and central nervous system symptoms.

Higher incidence and greater severity of babesiosis in asplenic patients, as the spleen traps the infected erythrocytes, and their ingestion by the macrophages follows.

Decreased complement levels, increased circulating C1q-binding activity, increase tumor necrosis factor, IL-1and decreased C4, C3, and CH50 levels are observed.

Clinical features include: fever, anorexia, arthralgias, myalgias, and shock.

Babesiosis associated with  an increase in T-suppressor lymphocytes, T-cytotoxic lymphocytes, or both.

Infection associated with impaired responses to lymphocyte mitogens.

Difficult to diagnose, without localizing signs to suggest the disease.

Because the parasite reproduces in red blood cells, a marked hemolytic anemia may be present.

Diagnosis is usually made by direct visualization of organisms in thick and thin smears.

Treatment is recommended for all diagnosed cases to prevent sequelae and potential transmission through blood donation.

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