INTRODUCTION — Babesiosis is an infectious disease caused by protozoa of the genus Babesia. Babesia spp are transmitted primarily by tick vectors and rarely via blood transfusion, organ transplantation, or congenitally. Babesia protozoa invade and cause lysis of red blood cells in mammalian hosts [1-5].
Babesia microti is the primary agent of human babesiosis in the United States, particularly in the Northeast and upper Midwest where it is endemic. Nearly all cases in Europe have been attributed to Babesia divergens, but the infection is sporadic. Babesia venatorum and Babesia crassa-like infections are endemic in northeastern China.
The treatment and prevention of babesiosis will be reviewed here. The clinical manifestations, diagnosis, microbiology, epidemiology, and pathogenesis of babesiosis are discussed separately. (See "Babesiosis: Clinical manifestations and diagnosis" and "Babesiosis: Microbiology, epidemiology, and pathogenesis".)
TREATMENT OF B. MICROTI INFECTION
Immunocompetent patients
Nonpregnant adults
Asymptomatic infection — In general, individuals with asymptomatic infection do not warrant routine treatment [1]. For patients with persistent parasitemia (≥1 month), we administer treatment.
Mild to moderate disease — Mild to moderate babesiosis typically occurs in immunocompetent patients and is associated with parasitemia <4 percent; it does not require hospital admission. (See "Babesiosis: Clinical manifestations and diagnosis", section on 'Mild to moderate disease'.)
Treatment with antimicrobial therapy is warranted for symptomatic individuals with mild to moderate B. microti infection confirmed by microscopy or polymerase chain reaction (PCR). The preferred regimen consists of azithromycin plus atovaquone given orally; clindamycin plus quinine given orally is an alternative option [1,2,5]. The duration of therapy is 7 to 10 days; dosing is summarized in the table (table 1).
This approach is supported by a randomized trial in which 58 adults with non–life-threatening babesiosis were treated with a seven day course of either atovaquone plus azithromycin (40 patients) or clindamycin plus quinine (18 patients) [6]. Three months after completion of therapy, no parasites were seen by microscopy and no Babesia deoxyribonucleic acid (DNA) was detected by endpoint PCR in any patient. Atovaquone plus azithromycin was associated with less frequent adverse effects than clindamycin plus quinine (15 versus 72 percent, respectively). Adverse effects associated with atovaquone plus azithromycin include diarrhea and rash. Adverse effects associated with clindamycin plus quinine include diarrhea, rash, and symptoms of cinchonism (eg, tinnitus, decreased hearing, and vertigo), prompting dose reduction or drug discontinuation in one-third of cases. Both azithromycin and quinine can produce QT prolongation and cardiac arrhythmias [7].
Symptoms usually begin to abate within 48 hours after initiating antimicrobial therapy and resolve within one to two weeks [4]. Fatigue may persist but generally resolves within three months after initiating therapy. Patients with mild to moderate babesiosis seldom experience complications. Data regarding the timeframe for resolution of anemia and other laboratory parameters are limited. No follow-up is required unless the patient has persistent or recurrent symptoms.
In immunocompetent patients who complete treatment for babesiosis and subsequently undergo splenectomy or become immunocompromised, an unexplained febrile illness should raise suspicion of babesiosis and prompt immediate clinical evaluation.
Severe disease — Severe babesiosis is associated with parasitemia ≥4 percent (although it can occur with parasitemia <4 percent) and may lead to complications and/or persistent or relapsing disease [8,9]. (See "Babesiosis: Clinical manifestations and diagnosis", section on 'Severe disease'.)
Management of severe babesiosis consists of hospitalization, antimicrobial therapy, and, in some cases, red blood cell exchange transfusion.
Antimicrobial therapy — For treatment of severe babesiosis, we favor intravenous (IV) azithromycin plus oral atovaquone; IV clindamycin plus oral quinine is an alternative option (table 1) [1,2,10]. IV therapy can be replaced with oral therapy once symptoms have abated and parasitemia has been reduced.
The usual duration of therapy for immunocompetent patients with severe babesiosis is 7 to 10 days. The duration of therapy should be extended if parasitemia and symptoms, such as fever, persist. Such cases are uncommon in immunocompetent patients. Cessation of therapy should be guided by parasite clearance and clinical improvement. Fatigue may persist for months following completion of a standard course of antibiotic therapy, but fatigue alone does not warrant extension of therapy [11].
There have been no prospective trials to compare the efficacy of antimicrobials in patients with severe babesiosis. In a retrospective study including 40 patients hospitalized for severe babesiosis and treated with a combination of atovaquone plus azithromycin, all but one patient fully recovered [10].
The optimal approach for treatment of severe babesiosis when the above regimens have been ineffective is uncertain. Alternative options (based on case reports) include IV clindamycin plus oral atovaquone or a three-drug regimen consisting of azithromycin, atovaquone, and clindamycin [3,5,12].
Chloroquine is not effective for treatment of human B. microti infection. In animal models, other antimalarials (such as primaquine, quinacrine, pyrimethamine, pyrimethamine-sulfadoxine, and sulfadiazine) are also ineffective [13,14]. Studies in highly immunocompromised mice have described drugs for treatment of B. microti infection including clofazimine, tafenoquine, and the combination of an endochin-like quinolone plus atovaquone [15-19].
Azithromycin and quinine are known to prolong the QT interval; however, a retrospective study including 163 patients hospitalized for babesiosis found no association between use of these antibiotics and QT interval prolongation [20].
Exchange transfusion — Red blood cell exchange transfusion (ie, removing patient red blood cells and replacing with allogeneic red blood cells; either partially or completely) may be warranted for patients with high-grade parasitemia (>10 percent) and/or one or more of the following: severe hemolytic anemia or severe organ (pulmonary, renal or hepatic) compromise [1,3,5,21].
This approach is based on a limited number of case reports and case series [8,22-24]. There have been no prospective systematic studies on this therapeutic modality, nor are there data on the benefit and optimal use of red blood cell exchange versus whole blood or plasma exchange.
Exchange transfusion reduces parasitemia and corrects anemia [22,25].
Use of exchange transfusion early in the course of severe B. microti infection has been advocated on the basis that prompt reduction in parasitemia reduces the risk of complications [8,12,23,24,26-28]. In Europe, mortality from B. divergens infection in immunocompromised patients has markedly decreased with improved adjunctive therapy including prompt use of exchange transfusion [29,30]. Repeat exchange transfusion may be considered when parasitemia remains elevated following initial exchange transfusion [12,31].
Two retrospective studies have examined the relationship between parasitemia and clinical outcome of B. microti infection. In one study including 19 patients who underwent red blood cell exchange, higher baseline parasitemia was associated with a longer hospital stay but had no impact on one-month mortality [23]. In another study including 91 patients hospitalized for babesiosis, a significant association between parasitemia and disease severity was observed [24]. These data support use of parasitemia >10 percent and/or end organ impairment as the criteria for consideration of exchange transfusion in severe babesiosis. Successful management of three patients with parasitemia >10 percent without exchange transfusion has been described [32].
Management of exchange transfusion should be handled in close consultation with experts in hematology and apheresis [8,23,26,27]. The efficacy of plasma exchange compared with red blood cell exchange has not been evaluated. Exchange transfusion can be performed manually or using apheresis equipment [28]. Red blood cell transfusion is indicated for patients who do not warrant exchange transfusion but have hemoglobin level ≤7 g/dL or symptoms attributable to anemia (eg, hemodynamic compromise, dyspnea). (See "Indications and hemoglobin thresholds for RBC transfusion in adults" and "Red blood cell transfusion in infants and children: Indications".)
Monitoring — For immunocompetent patients, we suggest monitoring parasitemia using peripheral blood smears during treatment of acute illness [1]. Monitoring parasitemia once symptoms have resolved is of limited value because immunocompetent patients almost never relapse. (See 'Mild to moderate disease' above and 'Severe disease' below.)
Recurrent infection — Management of reinfection in immunocompetent patients consists of a repeat standard course of atovaquone and azithromycin, unless antimicrobial resistance is documented [33].
Pregnant patients — Treatment of pregnant patients with babesiosis should consist of clindamycin plus quinine rather than azithromycin plus atovaquone. A case of successful treatment of B. microti infection in pregnancy with clindamycin plus quinine has been reported [34].
Patients with splenic rupture — For patients with splenic rupture who are hemodynamically unstable or deteriorate rapidly, emergent splenectomy is warranted. For patients who are hemodynamically stable with persistent hemorrhage, splenic artery embolization may be considered [35,36]. A nonsurgical approach is preferable, because splenectomy may impede parasite clearance and predispose to increased severity of subsequent infections.
Immunocompromised patients
Acute infection
Mild to moderate disease — Immunocompromised patients with mild to moderate B. microti infection may be treated on an outpatient basis with close monitoring. Antimicrobial therapy consists of oral azithromycin (500 to 1000 mg orally per day) plus oral atovaquone (750 mg orally twice daily).
Laboratory parameters (complete blood count and parasitemia) should be monitored every two to three days until the blood count normalizes and parasites are no longer seen on smear.
The duration of antimicrobial therapy is discussed below. (See 'Duration of antimicrobial therapy' below.)
Severe disease — Immunocompromised patients with severe disease should be managed with hospital admission for administration of antimicrobial therapy and monitoring; exchange transfusion is warranted in some circumstances. (See 'Exchange transfusion' above.)
Antimicrobial therapy for immunocompromised patients with severe disease consists of IV azithromycin (500 mg/day) plus oral atovaquone (750 mg twice daily). Once symptoms have abated and parasitemia has diminished, azithromycin can be given orally (500 mg/day), and oral atovaquone (750 mg twice daily) should be continued. Higher doses of oral azithromycin (up to 1000 mg per day) have been used and may accelerate parasite clearance [37-39].
Laboratory parameters (complete blood count and parasitemia) should be monitored daily until parasitemia is <4 percent and symptoms have abated; thereafter, parasitemia should be monitored every two to three days until parasites are no longer seen on smear. Renal function and hepatic function should be closely monitored until they become normal. (See 'Monitoring' below.)
The duration of antimicrobial therapy is discussed below. (See 'Duration of antimicrobial therapy' below.)
An alternative antimicrobial regimen is IV clindamycin (adult dose 600 mg IV every six hours) plus oral quinine (adult dose 650 mg orally every eight hours), although quinine is often poorly tolerated. IV clindamycin can be replaced with oral clindamycin once symptoms have abated and parasitemia has been reduced.
Duration of antimicrobial therapy — The duration of therapy in immunocompromised patients depends upon the risk of relapse [40]:
●Severe acute disease with low risk of relapse typically occurs in patients with one of the following conditions: age >50 years, asplenia, malignancy, and human immunodeficiency virus (HIV) infection without acquired immunodeficiency syndrome (AIDS). (See "Babesiosis: Clinical manifestations and diagnosis", section on 'Severe disease'.)
●Severe acute disease with high risk of relapse typically occurs in patients with impaired Babesia antibody production [40]. These include patients with B cell lymphoma or other conditions treated with rituximab (or other B cell-depleting agents), patients with malignancy who also are asplenic, patients with solid organ or stem cell transplantation, and patients with HIV/AIDS. Relapse usually occurs within a few days or a week after discontinuation of antibiotics, but the interval can be longer. (See "Babesiosis: Clinical manifestations and diagnosis", section on 'Relapse'.)
Low risk of relapse — For patients at low risk of relapse, the duration of therapy is at least 7 to 10 days; in some circumstances, a longer duration of therapy may be needed. The total duration of therapy depends on individual clinical circumstances and should be tailored to resolution of symptoms and laboratory parameters (complete blood count and parasitemia <4 percent). If low-grade parasitemia persists following completion of therapy, patients should be monitored with blood smear twice weekly until Babesia parasites are no longer observed.
High risk of relapse — For patients at high risk of relapse, antibiotics should be administered for at least six consecutive weeks and should be discontinued only after Babesia parasites have no longer been detected on blood smear for two consecutive weeks. This approach is supported by a retrospective case-control study that included 14 case patients in whom parasites persisted on blood smear despite repeated courses of antimicrobial therapy and 46 control patients in whom parasitemia cleared and symptoms resolved within one month following a single course of standard antimicrobial therapy. The case patients required treatment for ≥6 weeks to achieve cure, including 2 weeks during which parasites were no longer detected on blood smear [40]. However, this approach has been unsuccessful in a few cases [37,39].
PCR is more sensitive than blood smear but typically remains positive for months after clinical cure (complete resolution of symptoms with no recurrence) [11]. DNA may persist in the blood as long as 27 months in the setting of immunosuppression [11,41]. Thus, for immunocompromised patients at high risk of relapse, the benefit of administering antimicrobial therapy until PCR becomes negative should be balanced against the risks and costs associated with unnecessarily prolonged antimicrobial therapy. Despite the sensitivity provided by real-time PCR, cases of relapse following apparent parasite clearance (as assessed by both blood smear and PCR) have been described [42-44].
Clinicians should advise immunocompromised patients to seek immediate medical attention if they develop fever or other symptoms consistent with babesiosis following apparent successful antibiotic therapy. If fever and/or other symptoms consistent with babesiosis recur within a few days or weeks of initial treatment, a blood smear should be obtained. (See "Babesiosis: Clinical manifestations and diagnosis", section on 'Microscopy'.)
Monitoring — For immunocompromised patients, we suggest monitoring parasitemia using peripheral blood smears during treatment of acute illness and after resolution of symptoms, until blood smears are negative [1]. Additional details regarding use of monitoring to guide duration of therapy depend on the likelihood of relapse, as discussed above. (See 'Duration of antimicrobial therapy' above.)
Relapse
●Clinical approach – Management of relapse consists of a repeat course of antibiotic therapy. In addition, the level of immunosuppression should be reduced if feasible [37,41].
The antibiotic regimen used for the repeat course can be the same as that used for the initial course (usually azithromycin plus atovaquone). The duration of therapy is as described for immunocompromised patients with high risk of relapse. (See 'High risk of relapse' above.)
Treatment failure has been observed with atovaquone plus azithromycin and with clindamycin plus quinine. Antimicrobial resistance has been documented for atovaquone, azithromycin, and clindamycin in immunocompromised hosts [38-40,42,45,46].
●Alternative regimens – For patients who do not appear to respond well to atovaquone and azithromycin, therapy may be switched to clindamycin plus quinine. Since quinine often is poorly tolerated, an acceptable alternative regimen consists of azithromycin, atovaquone, and clindamycin.
Other antibiotic combinations have been used successfully, but there have been few reports of their use. These include atovaquone plus clindamycin (with or without azithromycin), atovaquone-proguanil plus azithromycin, atovaquone plus azithromycin plus clindamycin plus quinine, and azithromycin plus quinine [1,5,40,47-50].
Successful use of tafenoquine (300 mg on day 1, 150 mg on days 2 and 3, and 300 mg weekly for 9 weeks) for treatment of relapse in an immunocompromised patient has been described in a case report [45]. Blood smears were negative after one week and PCR was negative after three weeks of tafenoquine. G6PD status should be assessed before use of tafenoquine; the drug is contraindicated in the setting of G6PD deficiency. (See "Diagnosis and management of glucose-6-phosphate dehydrogenase (G6PD) deficiency".)
Co-infection with tick-transmitted pathogens — In the United States, Ixodes scapularis ticks transmit three major human pathogens: Borrelia burgdorferi (Lyme disease), Anaplasma phagocytophilum (anaplasmosis), and Babesia microti (babesiosis). They are also capable of transmitting other pathogens including Borrelia mayonii (Lyme disease), Borrelia miyamotoi (hard tick relapsing fever), Powassan virus (Powassan virus disease), and Ehrlichia muris eauclairensis (ehrlichiosis).
Human coinfection rates differ with respect to pathogen and geography, as well as research methods including case definitions. Approximately half of patients with babesiosis are coinfected with Lyme disease, and most of these patients present with an erythema migrans rash [51-56]. The frequency of coinfection with babesiosis and anaplasmosis is much lower [53,55].
Patients with known or suspected babesiosis should be evaluated carefully for erythema migrans rash; in addition, testing for Lyme disease and anaplasmosis is warranted. In addition, in settings where Lyme disease and anaplasmosis are endemic, we suggest empiric treatment with doxycycline (for coinfection with Lyme disease and/or anaplasmosis), pending definitive diagnostic data regarding coinfection. For patients treated for babesiosis whose symptoms worsen or do not resolve within the first 48 hours of therapy, we initiate empiric doxycycline therapy, pending further diagnostic data. (See "Clinical manifestations of Lyme disease in adults" and "Diagnosis of Lyme disease" and "Human ehrlichiosis and anaplasmosis".)
TREATMENT OF INFECTION DUE TO OTHER SPECIES
B. divergens — Clinical information about treatment of B. divergens infections is limited to case reports. Infection due to B. divergens frequently causes fulminant illness; therefore, illness attributed to this species should be considered a medical emergency and treated with a combination of antimicrobial therapy and exchange transfusion.
The antimicrobial regimen of choice has been intravenous (IV) clindamycin (in adults: 600 mg IV every 6 to 8 hours; in children: 7 to 10 mg/kg IV every 6 to 8 hours [maximum 600 mg/dose]) combined with oral quinine (in adults: 650 mg orally every 8 hours; in children: 8 mg/kg orally every 8 hours [maximum 650 mg/dose]). The duration of therapy is at least 7 to 10 days [1,57]. Other regimens have included clindamycin monotherapy and, in one case, IV pentamidine plus oral trimethoprim-sulfamethoxazole [29,58].
Following clearance of B. divergens parasitemia, anemia that is severe enough to warrant transfusion of red blood cells may persist for >1 month [29].
B. divergens-like organisms — Clinical experience with treatment of infection due to B. divergens–like organisms is limited to case reports [59-63]. Oral quinine or quinidine (650 mg three times daily) plus IV clindamycin (650 to 900 mg three times daily or 1200 mg twice daily) have been used. Quinidine is no longer available in the United States.
B. duncani — Clinical experience with treatment of infection due to B. duncani is limited [64-68]. All reported cases of B. duncani infection have been treated with a course of clindamycin (600 mg three to four times per day or 1200 mg twice daily) plus quinine or quinidine (600 to 650 mg three times daily). Quinidine is no longer available in the United States. In one case, symptoms relapsed and were successfully treated with IV clindamycin (1200 mg twice daily). In severe cases, red blood cell exchange transfusion and hemodialysis were instituted.
B. venatorum — Clinical experience with treatment of infection due to B. venatorum is derived from cases in Europe and China [69-73]. The European cases were treated with one or two antibiotic regimens. A mild case was cured with IV clindamycin (600 mg three times daily) [70]. A more severe case was successfully treated with IV clindamycin (600 mg three times daily) plus oral quinine (650 mg three times daily). Hemolytic anemia required the transfusion of 11 units of packed red blood cells [70]. Another severe case complicated by acute renal failure was successfully treated with oral clindamycin (600 mg three times daily) plus oral quinine (500 mg three times daily) [71]. A fourth case had received rituximab prior to the diagnosis of babesiosis and relapsed following a course of oral clindamycin plus oral quinine. Because of intolerance to quinine, the second course consisted of oral atovaquone (750 mg twice daily) plus oral azithromycin (500 mg once daily). Atovaquone was continued for 5 months to treat persistence of parasites in the absence of symptoms [69].
A child from northwestern China experienced severe B. venatorum disease but was cured with a course of oral atovaquone (20 mg/kg twice daily) plus oral azithromycin (12 mg/kg once daily) [72]. In a case series of B. venatorum infection from northeastern China, 4 of 48 patients were treated with clindamycin alone, whereas the other cases resolved despite receiving antibiotics that are not commonly used for babesiosis.
B. crassa-like organisms — A case series noted that B. crassa-like organisms that typically infect sheep can induce a mild to moderate illness in immunocompetent humans [74]. None of the 31 patients were treated with one of the antimicrobial regimens recommended for babesiosis caused by B. microti. Three patients received clindamycin alone. None of the patients died.
PREVENTION — Prevention of babesiosis consists of personal protective measures that minimize exposure to ticks [3,5]. Patients at risk of severe babesiosis (asplenic individuals and other immunocompromised individuals) should avoid Babesia endemic areas during the tick transmission season (late spring, summer, and early fall), particularly those where ticks abound. (See "Prevention of Lyme disease", section on 'Personal protection'.)
If it is not possible to avoid such exposure, the risk of babesiosis can be reduced by wearing long pants and long-sleeved shirts, applying tick repellants to skin (such as N,N-diethyl-metatoluamide [DEET]) and clothing (Permethrin), and performing tick checks after possible exposure. (See "Prevention of arthropod and insect bites: Repellents and other measures".)
Environmental management also may be helpful; interventions include keeping lawns mown, placing stone or wood chip barriers between lawn and woods, spraying property with an acaricide, placing cotton balls impregnated with permethrin in yards, and culling the local deer herd.
There is no antibiotic regimen for prophylaxis of babesiosis. There is no vaccine available for human use.
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Tick-borne infections (Lyme disease, ehrlichiosis, anaplasmosis, babesiosis, and Rocky Mountain spotted fever)".)
SUMMARY AND RECOMMENDATIONS
●Immunocompetent patients
•Mild to moderate illness – For immunocompetent individuals with mild to moderate Babesia microti infection, we suggest treating with oral azithromycin plus oral atovaquone (Grade 2C). Treatment is administered orally for 7 to 10 days; dosing is summarized in the table (table 1). For individuals with asymptomatic B. microti infection, we suggest no antimicrobial therapy (Grade 2C). (See 'Mild to moderate disease' above and 'Asymptomatic infection' above.)
•Severe illness
-Antimicrobial therapy – For immunocompetent individuals with severe B. microti infection, we suggest treatment with intravenous (IV) azithromycin plus oral atovaquone (Grade 2C); IV clindamycin plus oral quinine is an alternative regimen (table 1). (See 'Severe disease' above.)
-Exchange transfusion – Patients with severe B. microti infection may warrant exchange transfusion. We suggest exchange transfusion for patients with high-grade parasitemia (>10 percent), severe hemolysis (hemoglobin <10 g/dL), or organ (pulmonary, renal, or liver) impairment (Grade 2C). (See 'Exchange transfusion' above.)
-Duration of therapy – The usual duration of antimicrobial therapy for immunocompetent patients with severe B. microti infection is 7 to 10 days; in some circumstances, a longer duration of therapy may be needed. IV therapy can be replaced with oral therapy once symptoms have abated and parasitemia has been reduced. (See 'Antimicrobial therapy' above.)
●Immunocompromised patients
•Mild to moderate illness – For immunocompromised patients with mild to moderate B. microti infection, we suggest initial treatment with oral azithromycin plus oral atovaquone (Grade 2C) as well as close monitoring. For patients who do not improve within 48 hours, we hospitalize and treat as for severe illness. (See 'Mild to moderate disease' above.)
•Severe illness – Immunocompromised patients with severe B. microti infection should be managed with hospitalization and IV therapy. We suggest treatment with IV azithromycin plus oral atovaquone (Grade 2C); IV clindamycin plus oral quinine is an alternative regimen. (See 'Severe disease' above.)
•Duration of therapy – The duration of therapy for B. microti infection in immunocompromised patients depends on the risk of relapse (see 'Duration of antimicrobial therapy' above):
-Patients with one of the following conditions typically have low risk of relapse: age >50 years, asplenia, malignancy, and HIV infection without AIDS. In such patients, the duration of therapy is at least 7 to 10 days; it should be tailored to the resolution of symptoms and laboratory parameters. If low-grade parasitemia on blood smear persists following completion of therapy and resolution of symptoms, patients should be monitored with blood smear twice weekly until no Babesia are observed. (See 'Low risk of relapse' above.)
-Patients with impaired Babesia antibody production typically have high risk of relapse. These include patients with B cell lymphoma or other conditions treated with rituximab (or other B cell-depleting agent), patients with malignancy who also are asplenic, patients with solid organ or stem cell transplantation, and patients with HIV/AIDS. In such patients, the duration of therapy is at least six weeks, including two final consecutive weeks during which Babesia parasites are no longer seen on blood smear. (See 'High risk of relapse' above.)
•Relapse – Management of relapsed B. microti infection consists of a repeat course of antibiotic therapy. The antibiotic regimen used for the repeat course can be the same as that used for the initial course (usually azithromycin plus atovaquone). The duration of therapy is the same as the duration for immunocompromised patients with high risk of relapse. (See 'Relapse' above.)
●Coinfection with tick-transmitted pathogens – For patients with known or suspected babesiosis, we suggest empiric treatment with doxycycline (for coinfection with Lyme disease and/or anaplasmosis), pending definitive diagnostic data regarding coinfection (Grade 2C). (See 'Co-infection with tick-transmitted pathogens' above.)
●Babesia divergens – B. divergens frequently causes fulminant illness and should be considered a medical emergency. Management consists of antimicrobial therapy and exchange transfusion. We suggest treatment with IV clindamycin and oral quinine; the duration of therapy is at least 7 to 10 days. (See 'B. divergens' above.)
●Prevention – Prevention of babesiosis consists of personal protective measures that minimize exposure to ticks. (See 'Prevention' above.)
ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Jeffrey A Gelfand, MD, FACP, who contributed to earlier versions of this topic review.
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