OBJECTIVE: To characterize the etiologic agents (MO1) of the first reported case of babesiosis acquired in Missouri. DESIGN: Case report, serologic testing, animal inoculations, and molecular studies. SETTING: Southeastern Missouri. PATIENT: A 73-year-old man who had had a splenectomy and had a fatal case of babesiosis. MEASUREMENTS: Serum specimens from the patient were assayed by indirect immunofluorescent antibody testing and immunoprecipitation for reactivity with antigens from various Babesia species. Whole blood obtained from the patient before treatment was inoculated into hamsters and jirds and into calves and bighorn sheep that had had splenectomy and were immunosuppressed with dexamethasone. Piroplasm-specific nuclear small-subunit ribosomal DNA was recovered from the patient's blood by using broad-range amplification with the polymerase chain reaction; a 144 base-pair region of the amplification product was sequenced; and phylogenetic analysis was done to compare MO1 with various Babesia species. RESULTS: Indirect immunofluorescent antibody testing showed that the patient's serum had strong reactivity with Babesia divergens, which causes babesiosis in cattle and humans in Europe, but that it had minimal reactivity with B. microti and WA1, which are the piroplasms previously known to cause zoonotic babesiosis in the United States. Immunoprecipitations showed that MO1 is more closely related to B. divergens than to B. canis (a canine parasite). None of the experimentally inoculated animals became demonstrably parasitemic. Phylogenetic analyses, after DNA sequencing, showed that MO1 is most closely related to B. divergens (100% similarity). CONCLUSIONS: Although MO1 is probably distinct from B. divergens, the two share morphologic, antigenic, and genetic characteristics; MO1 probably represents a Babesia species not previously recognized to have infected humans. Medical personnel should be aware that patients in the United States can have life-threatening babesiosis even though they are seronegative to B. microti and WA1 antigen.
OBJECTIVE: To characterize the etiologic agents (MO1) of the first reported case of babesiosis acquired in Missouri. DESIGN: Case report, serologic testing, animal inoculations, and molecular studies. SETTING: Southeastern Missouri. PATIENT: A 73-year-old man who had had a splenectomy and had a fatal case of babesiosis. MEASUREMENTS: Serum specimens from the patient were assayed by indirect immunofluorescent antibody testing and immunoprecipitation for reactivity with antigens from various Babesia species. Whole blood obtained from the patient before treatment was inoculated into hamsters and jirds and into calves and bighorn sheep that had had splenectomy and were immunosuppressed with dexamethasone. Piroplasm-specific nuclear small-subunit ribosomal DNA was recovered from the patient's blood by using broad-range amplification with the polymerase chain reaction; a 144 base-pair region of the amplification product was sequenced; and phylogenetic analysis was done to compare MO1 with various Babesia species. RESULTS: Indirect immunofluorescent antibody testing showed that the patient's serum had strong reactivity with Babesia divergens, which causes babesiosis in cattle and humans in Europe, but that it had minimal reactivity with B. microti and WA1, which are the piroplasms previously known to cause zoonotic babesiosis in the United States. Immunoprecipitations showed that MO1 is more closely related to B. divergens than to B. canis (a canine parasite). None of the experimentally inoculated animals became demonstrably parasitemic. Phylogenetic analyses, after DNA sequencing, showed that MO1 is most closely related to B. divergens (100% similarity). CONCLUSIONS: Although MO1 is probably distinct from B. divergens, the two share morphologic, antigenic, and genetic characteristics; MO1 probably represents a Babesia species not previously recognized to have infected humans. Medical personnel should be aware that patients in the United States can have life-threatening babesiosis even though they are seronegative to B. microti and WA1 antigen.
Authors: P Martín-Dávila; J Fortún; R López-Vélez; F Norman; M Montes de Oca; P Zamarrón; M I González; A Moreno; T Pumarola; G Garrido; A Candela; S Moreno Journal: Clin Microbiol Rev Date: 2008-01 Impact factor: 26.132
Authors: A Saito-Ito; M Tsuji; Q Wei; S He; T Matsui; M Kohsaki; S Arai; T Kamiyama; K Hioki; C Ishihara Journal: J Clin Microbiol Date: 2000-12 Impact factor: 5.948
Authors: Patricia J Holman; Angela M Spencer; Robert E Droleskey; Heidi K Goethert; Samuel R Telford Journal: J Clin Microbiol Date: 2005-08 Impact factor: 5.948
Authors: Annetta Zintl; Grace Mulcahy; Helen E Skerrett; Stuart M Taylor; Jeremy S Gray Journal: Clin Microbiol Rev Date: 2003-10 Impact factor: 26.132
Authors: Joseph Z Lux; Don Weiss; Jeanne V Linden; Debra Kessler; Barbara L Herwaldt; Susan J Wong; Jan Keithly; Phyllis Della-Latta; Brian E Scully Journal: Emerg Infect Dis Date: 2003-01 Impact factor: 6.883