Facts about babesiosis


Babesiosis is an illness caused by a parasite of the Babesia spp., which infects and destroys the red blood cells. The disease is transmitted mainly by ticks which become infected by feeding on infected cattle, roe deer and rodents, which are the main reservoirs for this parasite.

While most infections pass by without symptoms, some people may become sick and present with flu-like symptoms like fever, chills, muscle ache, fatigue, as well as jaundice (yellowing of the skin due to a bile disorder). Severe cases, affecting the kidneys or the lungs, may occur and lead to death.

Human babesiosis infection is treated with antibiotics and quinine. There is no vaccine available.

1. Name and nature of infecting organism

Five Babesia species have been described as zoonotic in the world. Generally, the epidemiology of human babesiosis is complex and uncertain due to the diversity of these Babesia species.

Human transmission of Babesia species in Europe is mainly due to Ixodes ricinus. Thedistribution and frequency of this tick implies that human babesiosis could occur in any part of Europe. The 39 published human cases in Europe were clinically severe and were attributed to B. divergens, B. venatorum (EU1) and B. microti. However, formal identification of the Babesia species is not undertaken for all cases.

Bovine B. divergens babesiosis is widely distributed on the European continent and human cases have been reported in different countries. Among EU overseas territories, one human case has been attributed to B. divergens,which occurred in the Canary Islands. Outside Europe, human babesiosis occurs mainly in the USA. Pathogenic agents are B. microti, B. duncani n sp. and MO1-type B. sp. Other cases have been reported from Africa, Mexico, Japan, Taiwan and India (B. microti or unindentified Babesia).

2. Clinical features

Most infections seem to remain asymptomatic. For clinical cases, the incubation period varies between one and eight weeks, but delayed appearance of symptoms after a prolonged asymptomatic infection may occur after several months. The intensity of clinical signs of babesiosis in humans varies from mild to severe. Beginning with non-specific flu-like symptoms, the acute illness generally presents with intravascular haemolysis causing haemoglobinuria and mild to severe symptoms, including jaundice due to haemolysis, non-periodic high fever, headaches, chills, myalgia. This may last from several days to a few months. Shock-like syndrome with renal failure and pulmonary oedema can occur and may be fatal.

3. Transmission

3.1 Reservoir

Cattle, roe deer and rodents are reservoirs of B. divergens, B. venatorum and B. microti respectively. The Ixodes ricinus tick is also the reservoir of B. divergens and B. venatorum because of the transovarial and transstadial transmission of the protozoa in the tick host.

3.2 Transmission mode

In Europe, human transmission occurs mainly by an Ixodes ricinus tick bite. Human infection by blood transfusion has also been documented. Rare cases of transplacental or perinatal transmission have been described.

3.3 Risk groups

Human cases occur mostly in splenectomised or immunocompromised patients.
Exposure to ticks represents the main risk factor for infection. The geographical distribution of I. ricinus covers the temperate broadleaf and mixed forests biome; small populations of this tick can be observed at altitude in the Mediterranean forest biome. Specific factors for increased human risk of exposure to the reservoir ticks include landscape modifications affecting tick populations, the increase in cervid populations (particularly roe deer, which could disseminate both B. venatorum and I. ricinus), different leisure activities in I. ricinus infested woodland or agro-ecosystems, and the movement of cattle by bovine trade or repopulation processes, which may disseminate new pathogens or new pathogen strains.

4. Prevention measures

Prevention is limited to avoiding tick bites and promoting personal measures of protection against ticks, with particular attention to splenectomised and immunologically compromised patients.

Possible risk of infection through blood transfusion needs to be controlled in particular for splenectomised or immunologically compromised patients. Human babesiosis in Europe is of potentially high severity, thus rapid diagnosis is essential to initiate treatment following clinical suspicion of infection.

5. Diagnosis

During the acute phase, diagnosis of Babesia sp. infection can be assessed by microscopic examination of stained blood smears, which show the typical piriform merozoites associated by twos and fours, and round forms without parasitic pigment. Xenodiagnosis or in vitro culture allows the isolation of the parasite. Species identification is possible by PCR. Serology does not allow species identification, but used in epidemiological studies it can assist in evaluating exposure to Babesia spp.

6. Management and treatment

The course of the treatment depends on the severity of the symptoms. Criteria associated with high morbidity and mortality are parasitaemia >10%; haemoglobin <10 g/dl; previous splenectomy; adult respiratory distress syndrome and acute renal failure.

Typical treatment of human babesiosis in Europe is based on clindamycine and quinine, associated with blood exchange transfusion. Clindamycine could sometimes be used alone and in mild cases exchange transfusion could be avoided. Atovaquone associated with azithromycin is also effective.

7. Key areas of uncertainty

Many biological and epidemiological data on human pathogenic Babesia species are lacking. Missing key data are the formal characterisation of the identity of the Babesia species and genotypes involved in each human case, better characterisation of the epidemiology of the infection in animal reservoirs and vectors, and the development of accurate diagnosis for the management of human risk (rapid diagnosis in clinical cases, control of the risk of transfusional transmission in splenectomised or immunocompromised patients).

8. References

Duh D, Jelovsek M, Avsic-Zupanc T. Evaluation of an indirect fluorescence immunoassay for the detection of serum antibodies against Babesia divergens in humans. Parasitology 2007;134:179-185.

Gorenflot A, Moubri K, Précigout E, Carcy B, Schetters TP. Human babesiosis. Ann Trop Med Parasitol 1998;92:489-501. Gray JS. Identity of the causal agents of human babesiosis in Europe. Int J Med Microbiol 2006;296 Suppl 40:131-136.

Herwaldt BL, Cacciò S, Gherlinzoni F, Aspöck H, Slemenda SB et al. Molecular characterization of a non-Babesia divergens organism causing zoonotic babesiosis in Europe. Emerg Infect Dis 2003;9:942-948.

Hildebrandt A, Tenter AM, Straube E, Hunfeld KP. Human babesiosis in Germany: Just overlooked or truly new? Int J Med Microbiol 2007.

Kjemtrup AM, Conrad PA. Human babesiosis: an emerging tick-borne disease. Int J Parasitol 2000;30:1323-1337.

Uilenberg G. Babesia--a historical overview. Veterinary Parasitology 2006;138:3-10.
Vial HJ, Gorenflot A. Chemotherapy against babesiosis. Vet Parasitol 2006;138:147-160.
Zintl A, Mulcahy G, Skerrett HE, Taylor SM, Gray JS. Babesia divergens, a bovine blood parasite of veterinary and zoonotic importance. Clin Microbiol Rev 2003;16: 622-636.