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Babesiosis

  • Author: Burke A Cunha, MD; Chief Editor: Michael Stuart Bronze, MD  more...
 
Updated: Mar 17, 2016
 

Background

Babesiosis is a tick-borne malaria-like illness caused by species of the intraerythrocytic protozoan Babesia. Humans are opportunistic hosts for Babesia when bitten by nymph or adult ticks. Currently, Babesia infection is transmitted by various tick vectors in Europe, Asia, and the northwestern and northeastern United States.

Human babesiosis is a zoonotic infection in which ticks transmit Babesia organisms from a vertebrate reservoir to humans[1, 2] ; 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 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.

Babesia species and organisms of the closely related genus Theileria have worldwide distribution, parasitizing the erythrocytes of wild and domestic animals. These parasites are commonly called piroplasms because of the pear-shaped forms found within infected red blood cells (RBCs). 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).

Human babesiosis is infrequent and occurs in limited geographic locations. In the United States, it 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.

Babesiosis is difficult to diagnose. Although the index of suspicion should be high in areas endemic for Babesia infection, patients with babesiosis have few, if any, localizing signs to suggest the disease. Confirmation of the diagnosis depends on the degree of parasitemia and the expertise and experience of the laboratory personnel.

Most patients infected by B microti who are otherwise healthy appear to have a mild illness and typically recover without specific chemotherapy; however, treatment is recommended for all diagnosed cases to prevent sequelae and potential transmission through blood donation. In addition, patients should be advised to take precautions against tick exposure and to refrain from donating blood until completely cured of babesiosis.

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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 deer tick, Ixodes scapularis (also known as Ixodes dammini; see the image below), 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. Im Ixodes scapularis, tick vector for babesiosis. Image courtesy of Centers for Disease Control and Prevention.

I scapularis has 3 developmental stages—larva, nymph, and adult—each of which requires a blood meal for development into the next stage. As a larva and nymph, the tick feeds on rodents (eg, the white-footed mouse, Peromyscus leucopus); however, as an adult, the tick prefers to feed on the white-tailed deer. Female ticks are impregnated while obtaining their blood meal on the deer, with the formation of up to 20,000 eggs. (In Europe, by way of contrast, cattle constitute the primary animal reservoir).

The clinical signs and symptoms of babesiosis are related to the parasitism of RBCs by Babesia. The ticks ingest Babesia from the host during feeding; they then multiply the protozoa in their gut wall and concentrate them in their salivary glands. When they feed again on a new host, they inoculate the new host with Babesia.

Entering the host’s bloodstream during the tick bite, the parasite infects RBCs, and differentiated and undifferentiated trophozoites are produced. Upon infection of the host erythrocyte, mature B microti trophozoites undergo asynchronous asexual budding and divide into 2 or 4 merozoites. As parasites leave the erythrocyte, the membrane is damaged. The precise mechanism of hemolysis is unknown.

Babesia species in the host erythrocyte range from 1 to 5 µm in length. B microti measures 2 × 1.5 µm, B divergens measures 4 × 1.5 µm, and B bovis measures 2.4 × 1.5 µm. As noted, the organisms are pear-shaped, oval, or round. Their ring form and peripheral location in the erythrocyte frequently lead to their being mistaken for Plasmodium falciparum. However, they differ from P falciparum in that the schizogony is asynchronous and massive hemolysis does not occur.

Alterations in RBC membranes cause decreased conformability and increased RBC adherence, which can lead to development of noncardiac pulmonary edema and acute respiratory distress syndrome (ARDS) among those severely affected.[1]

Fever, hemolytic anemia, and hemoglobinuria may result from Babesia infection. As with malaria, RBC fragments may cause capillary blockage or microvascular stasis, which explains liver, splenic, renal, and central nervous system (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.

The spleen offers a critical host defense against babesiosis, as suggested by the higher incidence and greater severity of babesiosis in asplenic patients. The spleen traps the infected erythrocytes, and their ingestion by the macrophages follows.

Complement activation by Babesia may lead to the generation of tumor necrosis factor (TNF) and interleukin-1 (IL-1). Decreased complement levels, increased circulating C1q-binding activity, and decreased C4, C3, and CH50 levels are observed in patients with babesiosis. The generation of these primarily macrophage-produced mediators may explain many of the clinical features, such as fever, anorexia, arthralgias, myalgias, and the fulminant shock syndrome of bovine babesiosis.

Babesiosis elicits a B-cell response and a T-cell response. Patients with acute babesiosis have an increase in T-suppressor lymphocytes, T-cytotoxic lymphocytes, or both and decreased responses to lymphocyte mitogens with a polyclonal hypergammaglobulinemia.

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Etiology

Babesiosis is an infection caused by parasites of the Babesia genus. It is a zoonosis that is transmitted from vertebrates to humans through the bite of a tick from the Ixodidae family (I scapularis in the United States, I ricinus in Europe). Ixodes ticks are small and differ from the large Dermacentor ticks that transmit Rocky Mountain spotted fever (RMSF) and ehrlichiosis.

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 with Babesia is primarily due to the rodent strain B 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: MO-1 (Missouri; closely related to B divergens), CA-1 (California), and WA-1 (Washington; also known as CA5 and Babesia duncani).

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. Another cattle strain found in Europe, B bovis, also causes disease in humans on occasion.

Tick life cycle

The I scapularis life cycle requires 2 years for completion, beginning from egg deposition in the spring. 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. This development takes 1 year (ie, until the next spring).

Nymphs infected with B microti may transmit the Babesia organisms to other mice or rodents or to a human host. Nymphs feed for 3-4 days on white-footed mice or rodents and mature into adults the following fall.

Adult Ixodes tick populations are maintained in white-tailed deer. The adults mate and feed on the deer during the spring; they 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.

Larvae, nymphs, and adult ticks all may infect humans, but the nymph is the primary vector of B microti infection in humans.

Risk factors

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. Babesiosis is understandably more prevalent during the periods of tick activity, such as spring and summer.

Although rodents are infected with Babesia, the white-tailed deer does not carry the organism. B microti is transmitted from the larval phase of I scapularis to the nymphal phase (transstadial transmission) but not transovarially. Human infection is primarily produced by the bite of an infected nymph during a blood meal. Restocking of deer populations and curtailment of hunting has increased deer herds in certain areas. The proximity of deer, mouse, and tick create the conditions for human infection.

Several reported cases of infection via blood transfusions from donors who lived in or traveled to an endemic area have been documented.[3, 4] All of these cases have occurred in the United States, with the exception of 1 patient in Canada (acquired from a donor who became infected while in the United States) and 1 in Japan. The incubation period in transfusion-associated disease appears to be 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.

Case reports of transplacental or perinatal transmission have been documented. Transplacental transmission has also occurred rarely.

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Epidemiology

United States statistics

Human babesiosis is endemic in the northeastern coastal region of the United States, particularly Nantucket Island, Martha’s Vineyard, and Cape Cod (Massachusetts); Block Island (Rhode Island); and eastern Long Island,[5] Shelter Island, and Fire Island (New York). Disease prevalence in Cape Cod, as suggested by antibody to B microti, has been reported as 3.7%, whereas on Shelter Island in individuals with a high risk of exposure to ticks, it was 4.4% in June and reached 6.9% by October.

Cases have also been reported from the Connecticut mainland and Washington State. In addition, infections with Babesia species have been reported in New Jersey, Maryland, Virginia, California, Wisconsin, Minnesota, Missouri, Georgia, and Mexico.

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.

In endemic areas, the organism may also be transmitted by blood transfusion.[6, 7, 8, 9, 10, 11]

International statistics

Babesiosis occurs in areas of Europe and Asia, where the tick vector and vertebrate host reside, and it occurs in healthy as well as asplenic persons.[12] On the whole, however, it is rare in Europe. Since 1957, when the first case of human babesiosis was reported in an asplenic farmer from the former Yugoslavia, approximately 40 cases have been reported, mostly in Ireland, the United Kingdom, and France. All of the cases involved bovine Babesia and occurred in individuals who were splenectomized.

Sporadic case reports of babesiosis in Japan, Korea, China, Mexico, South Africa, and Egypt have also been documented. One report describes human Babesia infection in Columbia.

Age-, sex-, and race-related demographics

Although persons of any age can be affected by babesiosis, clinically ill patients with intact spleens are usually aged 50 years or older, which suggests that age plays a factor in the severity of the clinical response. Patients with babesiosis who were previously healthy individuals are generally older (mean, >60 years) than those who had previous medical problems (mean, 48 years). Vannier et al suggested that the age-associated decline in resistance to B microti is genetically determined.[1, 2]

Babesiosis has no predilection for sex or race.

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Prognosis

Babesiosis has a spectrum of severity, which may be divided into 3 distinct parts as follows[1] :

  • Asymptomatic infection
  • A mild-to-moderate viral-like syndrome
  • Severe disease with a fulminant course resulting in death or a persistent relapsing course

Babesiosis in otherwise healthy hosts produces an acute infectious disease that resembles malaria. Most cases of babesiosis are subclinical or are mildly symptomatic. Babesiosis 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 (PCR) test results more than 3 months after initial treatment should be treated again, regardless of the presence or absence of seizures.

In healthy individuals with intact spleens, babesiosis is rarely fatal; however, in patients who are asplenic, babesiosis is generally quite severe and is associated with substantial mortality. Asplenic patients have a more fulminant and prolonged clinical course and may have overwhelming infection that results in death.[13] In a 1998 review by White et al, 9 of 139 (6.5%) patients who were hospitalized with babesiosis in New York State from 1982-1983 died.[14]

In the United States, the prognosis for babesiosis is excellent; most patients recover spontaneously. About 25% of adults and 50% of children infected with Babesia are asymptomatic, improve spontaneously without treatment, or both. Fewer than 10% of US patients with babesiosis have died, and most of these have been elderly or asplenic.

In Europe, however, babesiosis is a life-threatening disease. Most symptomatic European patients are asplenic, which contributes to a poor prognosis. More than 50% of patients with babesiosis in Europe become comatose and die. About 83% of infected patients are asplenic.

Deaths have been reported from transfusion-transmitted babesiosis within the immunocompromised population in areas where Babesia infection is not endemic.[15]

Approximately 20% of patients with babesiosis are co-infected with Lyme disease. The symptoms experienced by these patients are more severe symptoms and last longer than those experienced by patients who have either disease alone.

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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, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Chief Editor

Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American Medical Association, Oklahoma State Medical Association, Southern Society for Clinical Investigation, Association of Professors of Medicine, American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Acknowledgements

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.

Itzhak Brook, MD, MSc Professor, Department of Pediatrics, Georgetown University School of Medicine

Itzhak Brook, MD, MSc is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians-American Society of Internal Medicine, American Federation for Clinical Research, American Medical Association, American Society for Microbiology, Armed Forces Infectious Diseases Society, Association of Military Surgeons of the US, Infectious Diseases Society of America, International Immunocompromised Host Society, International Society for Infectious Diseases,Medical Society of the District of Columbia, New York Academy of Sciences, Pediatric Infectious Diseases Society, Society for Ear, Nose and Throat Advances in Children, Society for Experimental Biology and Medicine, Society for Pediatric Research, Southern Medical Association, and Surgical Infection Society

Disclosure: Nothing to disclose.

Vinod K Dhawan, MD, FACP, FRCP(C) Professor, Department of Clinical Medicine, University of California, Los Angeles, David Geffen School of Medicine; Chief, Division of Infectious Diseases, Rancho Los Amigos National Rehabilitation Center, Downey, California.

Vinod K Dhawan, MD, FACP, FRCP(C) is a member of the following medical societies: American College of Physicians, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, and Royal College of Physicians and Surgeons of Canada

Disclosure: Pfizer Inc Honoraria Speaking and teaching

Allan D Friedman, MD, MPH Chairman, Division of General Pediatrics, Dept of Pediatrics, Professor of Pediatrics, Virginia Commonwealth University, VCUH Health System

Allan D Friedman, MD, MPH is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Tarlan Hedayati, MD Assistant Professor of Emergency Medicine, Rush Medical College, John H Stroger Hospital of Cook County

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.

Rick Kulkarni, MD Attending Physician, Department of Emergency Medicine, Cambridge Health Alliance, Division of Emergency Medicine, Harvard Medical School

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

Cameron Nima Nourani, MD Resident Physician, Department of Emergency Medicine, John H Stroger Hospital of Cook County

Cameron Nima Nourani, MD is a member of the following medical societies: Emergency Medicine Residents Association

Disclosure: Nothing to disclose.

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: Nothing to disclose.

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.

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.

Russell W Steele, MD Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Reference Salary Employment

Martin Weisse, MD Program Director, Associate Professor, Department of Pediatrics, West Virginia University

Martin Weisse, MD is a member of the following medical societies: Ambulatory Pediatric Association, American Academy of Pediatrics, and Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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Peripheral smear showing babesiosis.
Ixodes scapularis, tick vector for babesiosis. Image courtesy of Centers for Disease Control and Prevention.
Blood smear showing Babesia species in erythrocytes. Image courtesy of Centers for Disease Control and Prevention.
Babesia species, tetrad formation. Image courtesy of Centers for Disease Control and Prevention.
 
 
 
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