eMedicine Specialties > Emergency Medicine > Infectious Diseases

Babesiosis

Tarlan Hedayati, MD, Instructor of Clinical Emergency Medicine, Director of Observation Unit, Director of Chest Pain Unit, Department of Emergency Medicine, Los Angeles County/University of Southern California Medical Center
Joseph Choi, MD, Resident Physician, Department of Emergency Medicine, LAC+USC Medical Center, Keck School of Medicine, University of Southern California

Updated: Apr 28, 2009

Introduction

Background

Babesiosis is an intraerythrocytic parasitic infection caused by protozoa of the genus Babesia and transmitted through the bite of the Ixodes tick, the same vector responsible for transmission of Lyme disease. While most cases are tick-borne, transfusion and transplacental transmission have been reported. In the United States, babesiosis is usually an asymptomatic infection in healthy individuals. Several groups of patients become symptomatic, and, within these subpopulations, significant morbidity and mortality occur. The disease most severely affects patients who are elderly, immunocompromised, or asplenic. Among those symptomatically infected, the mortality rate is 10% in the United States and 50% in Europe.

Pathophysiology

Babesiosis is 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. In the United States, the black-legged tick, Ixodes scapularis (also known as Ixodes dammini) is the primary vector for the parasite; in Europe, Ixodes ricinus appears to be the primary tick vector. In each location, the Ixodes tick vector for Babesia is the same vector that locally transmits Borrelia burgdorferi, the agent implicated in Lyme disease.

Ixodes scapularis, tick vector for babesiosis. Courtesy of the Centers for Disease Control and Prevention.

Peripheral smear showing babesiosis.

Frequency

United States

The first US case of babesiosis was reported on Nantucket Island in 1966. An increasing trend over the past 30 years may be the result of restocking of the deer population, curtailment of hunting, and an increase in outdoor recreational activities. Between 1968 and 1993, more than 450 cases of Babesia infections were confirmed in the United States. However, the actual prevalence of this disease is unknown because most infected patients are asymptomatic.

International

The first case of human babesiosis was reported in 1957 from the former Yugoslavia in an asplenic farmer. Approximately 40 cases have been reported since then, mostly in Ireland, the United Kingdom, and France. Sporadic case reports of babesiosis in Japan, Korea, China, Mexico, South Africa, and Egypt have also been documented.

Mortality/Morbidity

Babesiosis exists as a spectrum of disease in 3 distinct groups: (1) asymptomatic infection, (2) a mild/moderate viral-like syndrome, and (3) severe disease with a fulminant course resulting in death or persistent relapsing course.¹

The US mortality rate is significant.

• Twenty-five percent of adults and 50% of children infected with babesiosis are asymptomatic and/or improve spontaneously without treatment.
• Fewer than 10% of patients with babesiosis have died in the United States, mostly composed of elderly or asplenic patients.
• Deaths have been reported from transfusion-transmitted babesiosis within the immunocompromised population in areas where Babesia infection is not endemic.²
• Approximately 20% of patients with babesiosis are co-infected with Lyme disease. These patients experience more severe symptoms for a longer duration than those with either disease alone.

In Europe, babesiosis is a life-threatening disease.

• Fifty-three percent of infected patients become comatose and die.
• Eighty-three percent of infected patients are asplenic.

Race

Babesiosis has no predilection for race.

Sex

The male-to-female ratio is about 1:1.

Age

Babesiosis affects all age groups with similar frequency; however, patients older than 50 years are at increased risk for severe infection and death.

Clinical

History

Patients report a history of travel to an endemic area between the months of May and September. This is the period during which the Ixodes tick is in its infectious nymph stage; however, most do not recall the tick bite. The incubation period is between 1 and 4 weeks. The signs and symptoms mimic malaria and range in severity from asymptomatic to septic shock.

• Symptoms
  
  
  • Generalized weakness
  • Fatigue
  • Depression
  • Fever
  • Anorexia and weight loss
  • CNS - Headache, photophobia, neck stiffness, altered sensorium
  • Pulmonary - Cough, shortness of breath
  • GI - Nausea, vomiting, abdominal pain
  • Musculoskeletal - Arthralgia and myalgia
  • Renal - Dark urine

Physical

Physical examination findings of babesiosis can include the following:

• Fever
• Rigors
• Diaphoresis
• Altered mental status
• Renal insufficiency/failure
• Pulmonary edema
• Hepatosplenomegaly
• Spontaneous splenic rupture³
• Jaundice
• Shock

Causes

More than 100 species of Babesia exist, but only a small number of species 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 with Babesia species is primarily due to Babesia microti, found mostly in northeastern and midwestern states. A few cases have been reported in Missouri, California, and Washington and are found to be caused by Babesia -like agents named after their geographic location, MO1 (Missouri), CA-1 (California), and WA-1 (Washington).
• In Europe, the causative agent of babesiosis is typically Babesia divergens, though B microti and B microti -like agents have been identified.
• Several reported cases of infection via blood transfusions from donors who lived in or traveled to an endemic area have been documented. All of these cases have occurred in the United States with the exception of one patient in Canada (acquired from a donor who became infected while in the United States) and one in Japan. The rate of acquiring B microti from a unit of packed red cells has been estimated to be 1 in 600-1800 in endemic areas.
• Case reports of transplacental/perinatal transmission have been documented.

Differential Diagnoses

Workup

Laboratory Studies

• In individuals who are asymptomatic, laboratory studies may be unremarkable.
• Wright- or Giemsa-stained peripheral blood smear
  • This test reveals intraerythrocytic parasites (ring forms with a central pallor) and, rarely, pathognomonic tetrads of budding trophozoites, the so-called Maltese cross.
  • The smear result may be negative in individuals with asymptomatic infection.
  • Level of parasitemia does not correspond to severity of disease, although patients who are mildly ill may have less than 1% parasitemia and patients who are severely ill may have greater than 85% parasitemia. High parasite levels are especially seen in asplenic patients.
• Complete blood count (CBC) with differential may demonstrate mild-to-severe hemolytic anemia, thrombocytopenia, atypical lymphocytes, and leukopenia.
• Haptoglobin will be decreased.¹
• Liver function test results often reveal mildly elevated hepatic transaminase levels, erythrocyte sedimentation rate (ESR), lactic dehydrogenase (LDH) level, alkaline phosphatase level, and serum bilirubin level.
• Urinalysis may reveal hemoglobinuria, proteinuria, and a dark color may be present.
• Direct Coombs test result may or may not be positive.
• Pulse oximetry results will be low in hypoxic patients with severe disease.

Imaging Studies

• Chest radiography may be indicated for patients with respiratory complications including suspected pneumonia or ARDS.

Other Tests

• Further testing specific for babesiosis takes place outside of the ED.
• Inoculation of a golden hamster or mouse with B microti- infected patient blood or a gerbil with B divergens- infected blood and subsequent antibody analysis of the animal's blood is used to confirm diagnosis when peripheral blood smear and laboratory results are equivocal. However, this test requires checking the animal periodically over 6-8 weeks, making the test time- and labor-intensive and impractical for rapid diagnosis.
• Polymerase chain reaction
  • Polymerase chain reaction (PCR) is more sensitive and equally specific when compared with peripheral smear evaluation and hamster inoculation.
  • PCR may be useful in monitoring the infection, although it cannot differentiate between acute/active forms and chronic forms of the disease.
• Immunofluorescence antibody testing
  • Immunofluorescence antibody test (IFA) is considered the criterion standard for serologic detection of B microti infection.
  • This test is used to confirm the diagnosis when the peripheral blood smear result is negative.
  • A titer of greater than 1:64 is considered positive.
  • A greater than 4-fold rise in titer or a single titer greater than 1:256 is suggestive of acute infection, with a gradual decline seen over weeks to months
  • Correlation between severity of symptoms and titer levels is poor.
• Enzyme-linked immunosorbent assay immunoglobulin M Lyme titer
  • Enzyme-linked immunosorbent assay (ELISA) immunoglobulin M (IgM) Lyme test is used because of the high percentage (25%) of patients co-infected with Lyme disease.
  • Co-infection increases the severity of disease; therefore, diagnosing and treating both infections is important.
• Immunoblot antibody test
  • This test has similar sensitivity and specificity for diagnosing babesiosis as that of IFA.
  • Potential advantages over IFA include the lack of need for concentrated serum samples and ease of use, as immunoblot assays can be performed by generalist technicians versus trained microscopists.

Procedures

• Because of the possibility of hemophagocytic syndrome, bone marrow biopsy is indicated in patients whose laboratory studies reveal pancytopenia and whose physical examination reveals hepatosplenomegaly, fever, coagulopathy, or lymphadenopathy.

Treatment

Emergency Department Care

• Suspicion of babesiosis in a patient with a history of exposure in an endemic area, tick bite, fever, chills, and fatigue is crucial.
• Peripheral blood smear or immunologic testing (see Workup) is necessary to make the diagnosis.
• If the patient is otherwise healthy and asymptomatic, no treatment is required.
• CBC with differential is important to determine the severity of infection.
• Immediately start elderly, immunocompromised, or asplenic patients on a combination treatment regimen of intravenous clindamycin and oral quinine or intravenous atovaquone and intravenous azithromycin to avoid acute renal failure.
• Intubation and mechanical ventilation may be required for patients who develop respiratory distress or failure.

Consultations

• Consult an infectious disease specialist on all babesiosis-infected patients who require hospital admission.
• Consult a hematologist for whole-blood exchange transfusion in severe cases.

Medication

Antibiotic and antimalarial therapy should begin immediately after diagnosis in symptomatic patients to reduce the level of parasitemia. The standard treatment has been clindamycin and quinine, but this regimen occasionally fails and patients report frequent side effects including tinnitus, decreased hearing, and diarrhea. Because of this, the drug regimen consisting of atovaquone and azithromycin is now the first line of treatment for mild/moderate disease and has been shown to be effective especially when clindamycin and quinine fail. For patients with severe symptoms, clindamycin and quinine are the first line of treatment.¹ Parasitemia may persist despite treatment with either of the described drug regimens. In areas endemic for Lyme disease, physicians should consider treating for Lyme disease empirically.

Asymptomatic patients with positive smears and/or PCR results should have these studies repeated and a course of treatment started if parasitemia persists more than 3 months. Additionally, patients initially treated may require re-treatment if repeat smears or PCR are positive more than 3 months after initial therapy.

Partial or whole-blood exchange transfusion is indicated for patients with severe babesiosis, as demonstrated by high parasitemia (>10%); significant hemolysis; and/or renal, hepatic, or pulmonary dysfunction.

Antibiotics

Therapy should cover all likely pathogens in the context of this clinical setting.

Clindamycin (Cleocin)

Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Administer in combination with quinine.

Dosing

Adult

300-600 mg IV qid or 600 mg PO tid for 7-10 d

Pediatric

7-10 mg/kg/d IV or PO tid/qid for 7-10 d; maximum of 600 mg/dose

Interactions

Increases duration of neuromuscular blockade induced by tubocurarine and pancuronium; erythromycin may antagonize effects of clindamycin; antidiarrheals may delay absorption of clindamycin

Contraindications

Documented hypersensitivity; regional enteritis; ulcerative colitis; hepatic impairment; antibiotic-associated colitis

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in severe hepatic dysfunction; no adjustment necessary in renal insufficiency; associated with severe and possibly fatal colitis

Azithromycin (Zithromax)

Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Treats mild-to-moderate microbial infections. Administer in combination with atovaquone.

Dosing

Adult

Day 1: 500 mg PO
Days 2-10: 250 mg PO
Immunocompromised patients: Higher doses of 600-1000 mg/d may be used

Pediatric

Day 1: 10 mg/kg/d PO; maximum of 500 mg/dose
Days 2-10: 5 mg/kg/d PO; maximum of 250 mg/dose

Interactions

May increase toxicity of theophylline, warfarin, and digoxin; effects are reduced with coadministration of aluminum and/or magnesium antacids; nephrotoxicity and neurotoxicity may occur when coadministered with cyclosporine

Contraindications

Documented hypersensitivity; hepatic impairment; do not administer with pimozide

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Site reactions can occur with IV route; bacterial or fungal overgrowth may result from prolonged antibiotic use; may increase hepatic enzyme levels and cholestatic jaundice; caution in patients with impaired hepatic function, prolonged QT intervals, or pneumonia; caution in hospitalized patients, geriatric patients, or debilitated patients

Antiprotozoals

These agents may contribute to the eradication of the parasite.

Atovaquone (Mepron)

May inhibit metabolic enzymes, which, in turn, inhibit growth of microorganisms. Administer in combination with azithromycin.

Dosing

Adult

750 mg PO q12h for 7 d

Pediatric

20 mg/kg q12h; maximum of 750 mg/dose

Interactions

May increase zidovudine serum levels; coadministration with rifampin or rifabutin may decrease atovaquone levels; atovaquone may decrease levels of TMP-SMZ

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Caution in elderly patients and in hepatic and renal impairment

Anti-malarials

These agents are effective in eradicating the parasite.

Quinine sulfate (Formula Q)

Inhibits growth of parasite by increasing the pH within intracellular organelles and possibly by intercalating into DNA of the parasites. Administer in combination with clindamycin.

Dosing

Adult

650 mg PO tid/qid for 7-10 d

Pediatric

8 mg/kg PO tid for 7 d; maximum of 650 mg/dose

Interactions

Aluminum-containing antacids may delay or decrease quinine bioavailability when administered concurrently; cimetidine increases quinine blood levels and creates the potential for toxicity; rifamycins decrease quinine concentrations by increasing hepatic clearance of quinine (effect can persist for several days after discontinuing rifamycins); concurrent administration of acetazolamide or sodium bicarbonate may increase toxicity by increasing quinine blood levels; quinine may enhance action of warfarin and other oral anticoagulants by decreasing synthesis of vitamin K–dependent clotting factors; digoxin serum concentrations may increase when digoxin administered concurrently with quinine; important to monitor digoxin levels periodically; quinidine may decrease plasma cholinesterase activity, causing a decrease in the metabolism of succinylcholine

Contraindications

Documented hypersensitivity; optic neuritis; tinnitus; G-6-PD deficiency; history of black water fever

Precautions

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Caution in G-6-PD deficiency and tendency to develop granulocytopenia; prolonged treatment or overdosing with quinine may cause cinchonism; quinine has quinidinelike activity, and thus can cause cardiac arrhythmias

Follow-up

Further Inpatient Care

• Monitor level of oxygenation and watch for development of respiratory complications after initiation of treatment in patients who present with respiratory complaints. Respiratory distress may be due to endotoxin sensitivity; endotoxin release often results from medication-induced intraerythrocytic death of the parasites.
• In severe cases of babesiosis, exchange transfusion may be the only means of reducing the level of parasitemia.
• Mechanical ventilation may be necessary in patients with severe disease.
• Monitor CBC for development of hemophagocytic syndrome.
• If the patient does not respond to or cannot tolerate treatment with clindamycin and quinine, commence alternative treatment with atovaquone and azithromycin.

Deterrence/Prevention

• Exposure to endemic areas
  
  
  • Persons at risk of severe infection should avoid endemic areas between the months of May and September.
  • Skin should be covered with appropriate clothing, including tucking long pants inside socks.
  • Early removal of ticks from humans and pets should prevent transmission of disease; a tick must remain attached for at least 24 hours for transmission of the parasite.
  • Tick repellent, such as products with 10-35% diethyltoluamide (DEET), should be applied on skin and clothes.
  • People from endemic areas who report a fever within the last 2 months or a history of tick bite are not allowed to donate blood.

Complications

• Respiratory
  • Patients who have undergone splenectomy are unable to clear infected RBCs, thereby leading to higher levels of parasitemia, eventually leading to hypoxemia and subsequent risk of cardiopulmonary arrest.
  • In severe cases, damage to RBC membranes, decreased deformability, and cytoadherence to capillaries and venules lead to pulmonary edema and respiratory failure.
  • These respiratory problems begin after treatment has been initiated when intraerythrocytic death of parasites has been postulated to cause sensitivity to endotoxin.
  • ARDS may be due to mechanisms such as endotoxemia, complement activation, immune complex deposition, cytoadherence, microemboli, and disseminated intravascular coagulation.
• Cardiac
  • Myocardial infarction
  • Congestive heart failure
• Renal
  • Renal insufficiency
  • Renal failure
• Postsplenectomy patients may develop hemophagocytic syndrome, acute renal failure, and generalized seizure.
• Coma can occur, possibly due to severe sepsis, ARDS, or multisystem organ failure.
• Co-infection with Lyme disease is a possible complication.

Prognosis

• In the United States, the prognosis for babesiosis is excellent; most patients recover spontaneously. Patients who have had their spleen removed are at the greatest risk for severe complications and death.
• In Europe, most symptomatic patients are asplenic, which contributes to a poor prognosis. More than 50% of patients become comatose and die.
  
• Babesiosis may continue for more than 2 months after treatment; asymptomatic infections can persist silently for months to years. Patients with positive smears or PCR more than 3 months after initial treatment should be re-treated, regardless of the presence or absence of seizures.

Patient Education

• For excellent patient education resources, visit eMedicine's Bites and Stings Center. Also, see eMedicine's patient education article Ticks.

Miscellaneous

Medicolegal Pitfalls

• Failure to consider diagnosis in children
• Failure to initiate immediate therapy in individuals considered at high risk (ie, asplenic, elderly, immunocompromised)
• Administration of quinine therapy to a patient who is pregnant

Special Concerns

• Pregnancy
  • Do not give quinine to pregnant patients.
  • If the infection is subclinical, drug therapy is not indicated.
  • Combination therapy with clindamycin and quinine or atovaquone and azithromycin is more effective than either atovaquone or azithromycin alone.
• Geriatric patients: Initiate therapy with clindamycin and quinine immediately.
• In patients with fever of unknown origin (FUO), consider babesiosis as a diagnosis if the patient lives in or has traveled to an endemic area or received a blood transfusion in the past.⁴

Multimedia

Media file 1: Peripheral smear showing babesiosis.

Media file 2: Ixodes scapularis, tick vector for babesiosis. Courtesy of the Centers for Disease Control and Prevention.

References

1. Vannier E, Gewurz BE, Krause PJ. Human babesiosis. Infect Dis Clin North Am. Sep 2008;22(3):469-88, viii-ix. [Medline].

2. Gubernot DM, Lucey CT, Lee KC, Conley GB, Holness LG, Wise RP. Babesia infection through blood transfusions: reports received by the US Food and Drug Administration, 1997-2007. Clin Infect Dis. Jan 1 2009;48(1):25-30. [Medline].

3. Froberg MK, Dannen D, Bernier N, Shieh WJ, Guarner J, Zaki S. Case report: spontaneous splenic rupture during acute parasitemia of Babesia microti. Ann Clin Lab Sci. Autumn 2008;38(4):390-2. [Medline].

4. Cunha BA, Cohen YZ, McDermott B. Fever of unknown origin (FUO) due to babesiosis in a immunocompetent host. Heart Lung. Nov-Dec 2008;37(6):481-4. [Medline].

5. Berry A, Morassin B, Kamar N, Magnaval JF. Clinical picture: human babesiosis. Lancet. Feb 3 2001;357(9253):341. [Medline].

6. Boustani MR, Gelfand JA. Babesiosis. Clin Infect Dis. Apr 1996;22(4):611-5. [Medline].

7. Boustani MR, Lepore TJ, Gelfand JA, Lazarus DS. Acute respiratory failure in patients treated for babesiosis. Am J Respir Crit Care Med. Jun 1994;149(6):1689-91. [Medline].

8. Brasseur P, Lecoublet S, Kapel N, Favennec L, Ballet JJ. Quinine in the treatment of Babesia divergens infections in humans. Eur J Clin Microbiol Infect Dis. Oct 1996;15:840-841. [Medline].

9. Dobroszycki J, Herwaldt BL, Boctor F, et al. A cluster of transfusion-associated babesiosis cases traced to a single asymptomatic donor. JAMA. Mar 10 1999;281(10):927-30. [Medline].

10. Feder HM, Lawlor M, Krause PJ. Babesiosis in pregnancy. N Engl J Med. Jul 10 2003;349(2):195-6. [Medline].

11. Froberg MK, Dannen D, Bakken JS. Babesiosis and HIV. Lancet. Feb 28 2004;363(9410):704. [Medline].

12. Gorenflot A, Moubri K, Precigout E, Carcy B, Schetters TP. Human babesiosis. Ann Trop Med Parasitol. Jun 1998;92(4):489-501. [Medline].

13. Gratz NG. The vector-borne human infections of Europe: their distribution and burden on human health. WHO; 2004. 1-154. [Full Text].

14. Gupta P, Hurley RW, Helseth PH, Goodman JL, Hammerschmidt DE. Pancytopenia due to hemophagocytic syndrome as the presenting manifestation of babesiosis. Am J Hematol. Sep 1995;50(1):60-2. [Medline].

15. Gutman JD, Kotton CN, Kratz A. Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 29-2003. A 60-year-old man with fever, rigors, and sweats. N Engl J Med. Sep 18 2003;349(12):1168-75. [Medline].

16. Horowitz ML, Coletta F, Fein AM. Delayed onset adult respiratory distress syndrome in babesiosis. Chest. Oct 1994;106(4):1299-301. [Medline].

17. Krause PJ. Babesiosis. Med Clin North Am. Mar 2002;86(2):361-73. [Medline].

18. Krause PJ, Lepore T, Sikand VK, et al. Atovaquone and azithromycin for the treatment of babesiosis. N Engl J Med. Nov 16 2000;343(20):1454-8. [Medline].

19. Krause PJ, Telford SR 3rd, Pollack RJ, et al. Babesiosis: an underdiagnosed disease of children. Pediatrics. Jun 1992;89(6 Pt 1):1045-8. [Medline].

20. Krause PJ, Telford SR, Spielman A, et al. Concurrent Lyme disease and babesiosis. Evidence for increased severity and duration of illness. JAMA. Jun 5 1996;275(21):1657-60. [Medline].

21. Leiby DA. Babesiosis and blood transfusion: flying under the radar. Vox Sang. Feb 2006;90(3):157-165. [Medline].

22. Leiby DA, Chung APS, Gill JE, et al. Demonstrable parasitemia among Connecticut blood donors with antibodies to Babesia microti. Transfusion. Nov 2005;45:1804-1810. [Medline].

23. Mylonakis E. When to suspect and how to monitor babesiosis. Am Fam Physician. May 15 2001;63(10):1969-74. [Medline].

24. Perdrizet GA, Olson NH, Krause PJ, Banever GT, Spielman A, Cable RG. Babesiosis in a renal transplant recipient acquired through blood transfusion. Transplantation. Jul 15 2000;70(1):205-8. [Medline].

25. Persing DH, Herwaldt BL, Glaser C, et al. Infection with a babesia-like organism in northern California. N Engl J Med. Feb 2 1995;332(5):298-303. [Medline].

26. Pruthi RK, Marshall WF, Wiltsie JC, Persing DH. Human babesiosis. Mayo Clin Proc. Sep 1995;70(9):853-62. [Medline].

27. Ryan R, Krause PJ, Radolf J, et al. Diagnosis of babesiosis using an immunoblot serologic test. Clin Diagn Lab Immunol. Nov 2001;8(6):1177-80. [Medline].

28. Shoemaker RC, Hudnell HK, House DE, Van Kempen A, Pakes GE, COL40155 Study Team. Atovaquone plus cholestyramine in patients coinfected with Babesia microti and Borrelia burgdorferi refractory to other treatment. Adv Ther. Jan-Feb 2006;23(1):1-11. [Medline].

29. Slovut DP, Benedetti E, Matas AJ. Babesiosis and hemophagocytic syndrome in an asplenic renal transplant recipient. Transplantation. Aug 27 1996;62(4):537-9. [Medline].

30. Spach DH, Liles WC, Campbell GL, Quick RE, Anderson DE Jr, Fritsche TR. Tick-borne diseases in the United States. N Engl J Med. Sep 23 1993;329(13):936-47. [Medline].

31. Weinberg GA. Laboratory diagnosis of ehrlichiosis and babesiosis. Pediatr Infect Dis J. Apr 2001;20(4):435-7. [Medline].

32. Weiss LM, Wittner M, Tanowitz HB. The treatment of babesiosis. N Engl J Med. Mar 8 2001;344(10):773. [Medline].

33. Wittner M, Lederman J, Tanowitz HB, Rosenbaum GS, Weiss LM. Atovaquone in the treatment of Babesia microti infections in hamsters. Am J Trop Med Hyg. Aug 1996;55(2):219-22. [Medline].

34. Wormser GP, Dattwyler RJ, Shapiro ED, et al. 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. Nov 1 2006;43(9):1089-134. Epub 2006 Oct 2. [Medline].

Keywords

babesiosis, Babesia species, Ixodes tick, parasitic infection, intraerythrocytic parasitic infection, tick bite, hemolytic anemia, thrombocytopenia, atypical lymphocyte formation, acute respiratory distress syndrome, ARDS, Lyme disease, Ixodes scapularis, white-tailed deer, white-footed mouse, Peromyscus leucopus, adult tick vector

Contributor Information and Disclosures

Author

Tarlan Hedayati, MD, Instructor of Clinical Emergency Medicine, Director of Observation Unit, Director of Chest Pain Unit, Department of Emergency Medicine, Los Angeles County/University of Southern California Medical Center
Tarlan Hedayati, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Joseph Choi, MD, Resident Physician, Department of Emergency Medicine, LAC+USC Medical Center, Keck School of Medicine, University of Southern California
Joseph Choi, MD is a member of the following medical societies: American Academy of Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Edward Bessman, MD, Chairman, Department of Emergency Medicine, John Hopkins Bayview Medical Center; Assistant Professor, Department of Emergency Medicine, Johns Hopkins University
Edward Bessman, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Barry J Sheridan, DO, Chief, Department of Emergency Medical Services, Brooke Army Medical Center
Barry J Sheridan, DO is a member of the following medical societies: American Academy of Emergency Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Rick Kulkarni, MD, Assistant Professor of Surgery, Section of Emergency Medicine, Yale-New Haven Hospital
Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: WebMD Salary Employment

Clinical guidelines

Infectious Diseases Society of America practice guidelines for clinical assessment, treatment and prevention of Lyme disease, human granulocytic anaplasmosis, and babesiosis. Wormser GP, Dattwyler RJ, Shapiro ED, Halperin JJ, Steere AC, Klempner MS, Krause PJ, Bakken JS, Strle F, Stanek G, Bockenstedt L, Fish D, Dumler JS, Nadelman RB. 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 2006 Nov 1;43(9):1089-134. PubMed

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