Human babesiosis in Europe

Brasseur, Philippe; Gorenflot, A.

doi:10.1590/s0074-02761992000700019

Cited by 32 publications

(14 citation statements)

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“…The reticulocyte count is elevated, the white count is normal or low, and thrombocytopenia is common. Parasitemia ranges from 1 to 10% but can reach as high as 80% in asplenic patients (45,66). Liver enzymes (alkaline phosphatase, lactate dehydrogenase, and aspartate and alanine aminotransferases) and bilirubin are elevated.…”

Section: Babesiosismentioning

confidence: 99%

Infections of People with Complement Deficiencies and Patients Who Have Undergone Splenectomy

2010

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SUMMARY The complement system comprises several fluid-phase and membrane-associated proteins. Under physiological conditions, activation of the fluid-phase components of complement is maintained under tight control and complement activation occurs primarily on surfaces recognized as “nonself” in an attempt to minimize damage to bystander host cells. Membrane complement components act to limit complement activation on host cells or to facilitate uptake of antigens or microbes “tagged” with complement fragments. While this review focuses on the role of complement in infectious diseases, work over the past couple of decades has defined several important functions of complement distinct from that of combating infections. Activation of complement in the fluid phase can occur through the classical, lectin, or alternative pathway. Deficiencies of components of the classical pathway lead to the development of autoimmune disorders and predispose individuals to recurrent respiratory infections and infections caused by encapsulated organisms, including Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae. While no individual with complete mannan-binding lectin (MBL) deficiency has been identified, low MBL levels have been linked to predisposition to, or severity of, several diseases. It appears that MBL may play an important role in children, who have a relatively immature adaptive immune response. C3 is the point at which all complement pathways converge, and complete deficiency of C3 invariably leads to severe infections, including those caused by meningococci and pneumococci. Deficiencies of the alternative and terminal complement pathways result in an almost exclusive predisposition to invasive meningococcal disease. The spleen plays an important role in antigen processing and the production of antibodies. Splenic macrophages are critical in clearing opsonized encapsulated bacteria (such as pneumococci, meningococci, and Escherichia coli) and intraerythrocytic parasites such as those causing malaria and babesiosis, which explains the fulminant nature of these infections in persons with anatomic or functional asplenia. Paramount to the management of patients with complement deficiencies and asplenia is educating patients about their predisposition to infection and the importance of preventive immunizations and seeking prompt medical attention.

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Section: Babesiosismentioning

confidence: 99%

Infections of People with Complement Deficiencies and Patients Who Have Undergone Splenectomy

2010

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“…Human infections with the bovine pathogen B. divergens should also be regarded as a medical emergency, and prompt therapy is indicated. Exchange transfusions in combination with intravenous clindamycin and intravenous or oral quinine have been successful in treating B. divergens in Europe (26,27).…”

Section: Treatment Of Babesiosismentioning

confidence: 99%

Coinfections Acquired from Ixodes Ticks

et al. 2006

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SUMMARY The pathogens that cause Lyme disease (LD), human anaplasmosis, and babesiosis can coexist in Ixodes ticks and cause human coinfections. Although the risk of human coinfection differs by geographic location, the true prevalence of coinfecting pathogens among Ixodes ticks remains largely unknown for the majority of geographic locations. The prevalence of dually infected Ixodes ticks appears highest among ticks from regions of North America and Europe where LD is endemic, with reported prevalences of ≤28%. In North America and Europe, the majority of tick-borne coinfections occur among humans with diagnosed LD. Humans coinfected with LD and babesiosis appear to have more intense, prolonged symptoms than those with LD alone. Coinfected persons can also manifest diverse, influenza-like symptoms, and abnormal laboratory test results are frequently observed. Coinfecting pathogens might alter the efficiency of transmission, cause cooperative or competitive pathogen interactions, and alter disease severity among hosts. No prospective studies to assess the immunologic effects of coinfection among humans have been conducted, but animal models demonstrate that certain coinfections can modulate the immune response. Clinicians should consider the likelihood of coinfection when pursuing laboratory testing or selecting therapy for patients with tick-borne illness.

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“…In the eastern and upper Midwestern United States, Babesia microti is the most common zoonotic agent (8,9,20,26,32), whereas other species and types of Babesia (WA1, CA1, and MO1) predominate in Europe and areas of the United States where B. microti is not endemic (2,11,14,29,33). B. microti is transmitted to humans by the same tick (Ixodes scapularis) that is responsible for the transmission of Lyme disease (Borrelia burgdorferi infection) and human granulocytic ehrlichiosis (HGE) (31).…”

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confidence: 99%

Serological Expression Cloning of Novel Immunoreactive Antigens of Babesia microti

et al. 2000

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Increased recognition of the prevalence of human babesiosis in the United States, together with rising concern about the potential for transmission of this infection by blood transfusion, has provided motivation to develop definitive serologic and molecular tests for the causative agent, Babesia microti. To develop more sensitive and specific assays for B. microti, we screened a genomic expression library with patient serum pools. This screening resulted in the identification of three classes of novel genes and an additional two novel, unrelated genes, which together encode a total of 17 unique B. microti antigens. The first class (BMN1-2 family) of genes encodes seven closely related antigens with a degenerate six-amino-acid repeat that shows limited homology to Plasmodium sp. merozoite and sporozoite surface antigens. A second class (BMN1-8 family) of genes encodes six related antigens, and the third class (BMN1-17 family) of genes encodes two related antigens. The two remaining genes code for novel and unrelated sequences. Among the three classes of antigens and remaining novel sequences, five were chosen to code for the most immunodominant antigens (BMN1-2, -9, -15, and -17 and MN-10). Western blot analysis with the resulting recombinant proteins indicated that these antigens were targets of humoral immune responses during B. microti infection in humans.

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Human babesiosis in Europe

Cited by 32 publications

References 0 publications

Infections of People with Complement Deficiencies and Patients Who Have Undergone Splenectomy

Infections of People with Complement Deficiencies and Patients Who Have Undergone Splenectomy

Coinfections Acquired from Ixodes Ticks

Serological Expression Cloning of Novel Immunoreactive Antigens of Babesia microti

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