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1 April 1996 | Volume 124 Issue 7 | Pages 643-650
Objective: To characterize the etiologic agent (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.
Author and Article Information
From the Centers for Disease Control and Prevention, Atlanta, Georgia; Mayo Clinic and Foundation, Rochester, Minnesota; Universite Montpellier, Montpellier, France; U.S. Department of Agriculture, Pullman, Washington; and Cape Girardeau Physician Associates, Cape Girardeau, Missouri.
ARTICLE
A Fatal Case of Babesiosis in Missouri: Identification of Another Piroplasm That Infects Humans
Acknowledgments: The authors thank the patient and his family and Patricia A. Conrad, DVM, PhD, Jennifer W. Dickerson, BA, K. Friedhoff, DMV (for provision of B. divergens in vitro antigen), Theodore J. Grieshop, MD, W. Carl Johnson, MS, Donald O. Miles, PhD, Stanley D. Sides, MD, John W. Thomford, PhD, Essie M. Walker, Doris A. Ware, and Marianna Wilson, MS, for their contributions.
Grant Support: Dr. Persing is supported by Public Health Service grants AI32403, AR41497, and AI30548.
Requests for Reprints: Barbara L. Herwaldt, MD, MPH, Centers for Disease Control and Prevention, Division of Parasitic Diseases, Mailstop F-22, 4770 Buford Highway NE, Atlanta, GA 30341-3724.
Current Author Addresses: Drs. Herwaldt and Eberhard: Centers for Disease Control and Prevention, Division of Parasitic Diseases, Mailstop F-22, 4770 Buford Highway NE, Atlanta, GA 30341-3724.
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