THE JOURNAL OF INFECTIOUS DISEASES. VOL. 152, NO.3· SEPTEMBER 1985 © 1985 by The University of Chicago. All rights reserved. 0022-1899/85/5203-0006$01.00

Serological Evidence for Simultaneous Occurrences of Lyme Disease and Babesiosis Jorge L. Benach, James L. Coleman, Gail S. Habicht, Alan MacDonald, Edgar Grunwaldt, and Jose A. Giron

From the State of New York Department of Health, Health Sciences Center and the Department of Pathology, The School of Medicine, SUNY at Stony Brook, Stony Brook; the Southhampton Hospital Laboratory, Southhampton; the Flushing Hospital and Medical Center, Flushing; and Shelter Island, New York

patients with babesiosis tested have IgG and IgM antibodies to the spirochete causing Lyme disease. Likewise, 66% of randomly selected patients with Lyme disease from geographic areas endemic for both diseases, but not from areas where babesiosis does not occur, also have IgM and IgG antibodies to B. microti. Antigenic cross-reactivity is not the reason for these findings, as laboratory animals experimentally infected with B. microti do not develop antibodies to B. burgdorferi, and laboratory animals immunized with organisms derived from pure cultures of spirochetes do not develop antibodies to B. microti. We suggest that these patients are concurrently exposed to both organisms by doubly infected tick vectors.

ent evidence to show that a significant number of patients with Lyme disease also have antibodies to

Babesiosis in humans was first reported in New York State in 1976 [1]. It became apparent over the next few years that this disease had a unique geographic distribution, restricted to the offshore islands and seashore of New York and Massachusetts [2]. Babesia microti is transmitted by Ixodes dammini ticks [3]. Circumstantial evidence for the involvement of ticks in the cycle of Lyme disease was provided shortly after this disease was clinically defined [4]. The discovery of a spirochete, now known as Borrelia burgdorjeri [5], carried in ticks from New York [6] and the demonstration of antibodies in the serum of patients with Lyme disease [6] followed with isolations of the organism from patients [7, 8], as well as the demonstration of its presence in skin lesions [9], clearly established the etiologic role of the spirochete in Lyme disease. Evidence for an erythema chronicum migrans (ECM)-like lesion in the early stages of clinical babesiosis was noted as early as 1979[10], and a case report of simultaneous occurrences of babesiosis and Lymedisease has been presented [11]. Wepresent here retrospective, serological evidence for babesiosis and Lyme disease in patients who werediagnosed as having babesiosis in the past several years. We also pres-

B. microti. Materials and Methods

Sera. All sera used in this retrospective study had been sent to our laboratory for the diagnosis of antibodies to B. microtior B. burgdorferi; aliquots had been kept frozen at -70 C since their arrival. Criteria for selection of sera from patients with babesiosis. Forty-one single serum specimens (all of the sera available to us) from patients who were diagnosed as having babesiosis after direct observation of intraerythrocytic parasites in peripheral blood smears and who also had titers of IgG antibodies to antigens of B. microti ~1 :512 were selected for study. Of these specimens, 39 were from patients in the endemic areas of eastern Long Island and Shelter and Fire Islands (New York), one was from Nantucket (Massachusetts), and one was a patient who acquired disease by transfusion [12]. In addition, serial serum specimens from nine patients with babesiosis who met the above criteria wereincluded. The sera from all of these patients were collected from 1978 through 1984.

Criteria for selection of sera from patients with Lymedisease. Sera submitted to our laboratory for

Received for publication31 December 1984, and in revised form 26 March 1985. Please address requests for reprints to Dr. Jorge L. Benach, Departmentof Pathology, HealthSciences Center, StateUniversity of New York at Stony Brook, Stony Brook, New York 11794.

detection of antibodies to B. burgdorferi during 1983 and 1984 were selected on the basis of an IgG antibody titer ~1 :512 from patients with one or more

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Babesia microtiand Borrelia burgdorferi, the spirochetal agent of Lyme disease, are both transmitted by the tick Ixodes dammini. Serological evidence has shown that 54070 of the

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