eMedicine Specialties > Infectious Diseases > Parasitic Infections

Babesiosis

Author: Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Contributor Information and Disclosures

Updated: Jul 28, 2008

Introduction

Background

Babesiosis is a tick-borne malarialike illness caused by species of the intraerythrocytic protozoan Babesia. Humans are opportunistic hosts for Babesia when bitten by nymph or adult ticks.

Babesiosis is named for Victor Babes, who first identified the RBC protozoan in 1888. Babes noticed intraerythrocytic protozoa in cattle with febrile hemoglobinuria. In 1893, Smith and Kilbourne discovered that the protozoa was transmitted by ticks and was the cause of Texas cattle fever. In 1957, the first human case of babesiosis, in a Yugoslavian cattle farmer, was described. The first case in the United States case was reported in Nantucket, Massachusetts, in 1969.

Currently, Babesia infection is transmitted by various tick vectors in Europe, Asia, and the northwestern and northeastern United States.

Babesiosis is 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 that infect cattle include Babesia divergens, Babesia bigemina, Babesia bovis, and Babesia major. In horses, the main species of Babesia is Babesia equi. Babesia canis is the primary species in dogs, and Babesia felis is the main species in cats. Babesia microti is the species found in mice.

Pathophysiology

The clinical signs and symptoms of babesiosis are related to the parasitism of RBCs by Babesia. Fever, hemolytic anemia, and hemoglobinuria may result from Babesia infection. As with malaria, RBC fragments may cause capillary blockage and/or microvascular stasis, explaining liver, splenic, renal, and CNS involvement. As with malaria, cells of the reticuloendothelial system (RES) in the spleen remove damaged RBC fragments from the circulation. RBC destruction results in hemolytic anemia.

Babesiosis elicits a B-lymphocyte response and a T-lymphocyte response. As with malaria, the primary immune response is a T-cell–mediated cellular immunity, and a secondary reactive polyclonal hypergammaglobulinemia occurs because of excessive B-lymphocyte reactivity.

Frequency

United States

Babesiosis is common in endemic areas of the northeastern and northwestern United States, particularly Long Island, New York, and Nantucket and Martha's Vineyard, Massachusetts. Infections have also been reported in the upper Midwest. In endemic areas, the organism may also be transmitted by blood transfusion.1,2,3,4,5,6

International

Babesiosis occurs in areas of Europe and Asia, where the tick vector and vertebrate host reside.

Mortality/Morbidity

  • Babesiosis in otherwise healthy hosts produces an acute infectious disease that resembles malaria. Mortality due to babesiosis is uncommon in patients with normal splenic function.
  • Patients who are asplenic have a more fulminant and prolonged clinical course and may have overwhelming infection and a fatal outcome.

Race

  • Babesiosis has no predilection for race.

Sex

  • Babesiosis has no predilection for sex.

Age

  • Persons of any age can be affected with babesiosis.

Clinical

History

The history of babesiosis includes fever and chills. Patients with babesiosis have symptoms similar to those of malaria. Symptoms are related to the degree of RBC parasitemia.

Physical

Most patients with babesiosis have few, if any, physical findings. A minority of patients have jaundice and splenomegaly.

Causes

  • Babesia organisms may be transmitted in utero.
  • Persons who come into contact with nymphs or adult Ixodidae ticks are at risk for acquiring babesiosis.
  • Large populations of field mice and white-tailed deer are likely to support a large Ixodidae tick population, which perpetuates areas endemic for babesiosis.
  • Babesiosis is caused by Babesia species, and the main species in the United States is B microti. B divergens is the main species in Europe.
  • Other Babesia species, namely B divergens and B bovis, occasionally cause disease in humans. B divergens and B bovis primarily infect cattle. Another strain, WA-1, has been implicated in human babesiosis on the west coast of the United States.
  • Babesiosis is a zoonosis that requires Babesia to be present in vertebrate vectors, such as white-tailed deer, white-footed mouse, and Ixodes ticks.
    • The main tick vectors of babesiosis include Ixodes scapularis and Ixodes dammini. Ixodes ticks are small and differ from the large Dermacentor ticks that transmit Rocky Mountain spotted fever (RMSF) and ehrlichiosis.
    • The white-footed mouse is the primary enzootic reservoir. After feeding on infected white-footed mice, the tick larvae become infected with B microti. The tick larvae are maintained as the tick develops from the larval phase to the nymphal phase. Nymphs infected with B microti may transmit the Babesia organisms to other mice or rodents or to a human host.
    • Adult Ixodes tick populations are maintained in white-tailed deer. Larvae, nymphs, and adult ticks all may infect humans, but the nymph is the primary vector of B microti infection in humans.
    • The I scapularis life cycle requires 2 years for completion, beginning from egg deposition in the spring. Larvae take 1 year, until the next spring, to develop to the nymph stage. Nymphs feed for 3-4 days on white-footed mice or rodents and mature into adults the following fall. Adults mate and feed on white-tailed deer during the spring; the adults then deposit their eggs and die. The white-footed mouse is necessary to perpetuate the Babesia organisms, and the deer is needed to perpetuate the Ixodes tick population.
    • Humans acquire babesiosis when in close proximity to large populations of white-footed mice infected with Babesia and white-tailed deer infested with I scapularis or I dammini ticks.
  • Babesiosis may also be transmitted via blood transfusion.

More on Babesiosis

Overview: Babesiosis
Differential Diagnoses & Workup: Babesiosis
Treatment & Medication: Babesiosis
Follow-up: Babesiosis
Multimedia: Babesiosis
References
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References

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Further Reading

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Keywords

babesiosis, Babesia, Babesia infection, Babesia microti, B microti, Babesia divergens, B divergens, Ixodes, Ixodes scapularis, I scapularis, Ixodes dammini, I dammini, Babesia bigemina, B bigemina, Babesia bovis, B bovis, Babesia major, B major, Babesia equi, B equi, Babesia canis, B canis, Babesia felis, B felis, Babesia microti, B microti, tick-borne infection, tick disease, tickborne illness, tick-borne illness, tick infection, malaria, Lyme disease, protozoan infection, Ixodidae, Texas cattle fever

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Contributor Information and Disclosures

Author

Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Medical Editor

Sat Sharma, MD, FRCPC, Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St. Boniface General Hospital
Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Om Prakash Sharma, MD, FRCP, FCCP, DTM&H, Professor, Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of Southern California Keck School of Medicine
Om Prakash Sharma, MD, FRCP, FCCP, DTM&H is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, American Osler Society, American Thoracic Society, New York Academy of Medicine, and Royal Society of Medicine
Disclosure: Keck School of Medicine, USC None None

CME Editor

Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Chief Editor

Michael Stuart Bronze, MD, Professor, Stewart G Wolf Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center
Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physician Executives, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Federation for Clinical Research, American Medical Association, American Society for Microbiology, Association of Professors of Medicine, Association of Program Directors in Internal Medicine, Infectious Diseases Society of America, Oklahoma State Medical Association, and Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.

 
 
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