Human Borrelia Miyamotoi Infection In The United States

New England Journal of Medicine

Borrelia miyamotoi

Borrelia miyamotoi, a spirochete that is genetically related to the species of borrelia that cause relapsing fever, has been detected in all tick species that are vectors of Lyme disease.1,2 It was detected in Ixodes scapularis ticks from Connecticut in 2001 and subsequently has been detected in all areas of the United States where Lyme disease is endemic. The first human cases of B. miyamotoi infection were reported in Russia in 2011.3 We now provide evidence of B. miyamotoi infection and the prevalence of this infection among people in the United States.

Enzyme-linked immunosorbent assays and confirmatory Western blot assays of archived serum samples obtained from three groups of patients who were living in areas where Lyme disease was endemic between 1990 and 2010 were used to detect antibody against B. miyamotoi GlpQ protein (an antigen that is nonreactive to B. burgdorferi antibody).4 Group 1 consisted of 584 patients who participated in serologic surveys for tickborne infections on Block Island and Prudence Island, Rhode Island, and Brimfield, Massachusetts. Patients in the serologic survey were healthy at the time of blood sampling and were enrolled during the spring and autumn of each year. Group 2 included 277 patients from southern New England who were evaluated for suspected Lyme disease. Group 3 consisted of 14 patients from southern New York who were evaluated at a Lyme disease clinic with a viral-like illness in the late spring or summer; these patients did not have symptoms or signs suggestive of an upper respiratory tract infection or gastroenteritis.

The seroprevalence was 1.0% in group 1, 3.2% in group 2, and 21.0% in group 3 (P<0.001 for comparisons among the three groups). In one patient in group 2 and two patients in group 3, the antibody titer was at least four times as high in the convalescent serum samples as in the acute serum samples; these findings suggest that these patients were recently infected with B. miyamotoi (Table 1). All symptomatic patients presented with a viral-like illness and were treated with doxycycline or amoxicillin. Unlike the patient with well-documented B. miyamotoi infection described by Gugliotta et al.5 elsewhere in this issue of the Journal, none of the three patients with evidence of recent B. miyamotoi infection in our study were immunocompromised. One patient had B. miyamotoi seroconversion and no erythema migrans skin lesion or laboratory evidence of human granulocytic anaplasmosis coinfection (Patient 17). This patient had a temperature of 39.4°C, chills, sweats, a headache, neck stiffness, fatigue, myalgias, arthralgias, abdominal pain, a cough, a sore throat, and right inguinal lymphadenopathy. He was treated successfully with 14 days of doxycycline. The identification of B. miyamotoi antibody in 18 of our study patients, including seroconversion associated with symptoms in 3 patients, suggests that B. miyamotoi infection may be prevalent in areas where Lyme disease is endemic in the United States.

This article was first published at The New England Journal of Medicine.

Peter J. Krause, M.D.
Yale School of Public Health, New Haven, CT

Sukanya Narasimhan, Ph.D.
Yale School of Medicine, New Haven, CT

Gary P. Wormser, M.D.
New York Medical College, Valhalla, NY

Lindsay Rollend, M.P.H.
Yale School of Public Health, New Haven, CT

Erol Fikrig, M.D.
Yale School of Medicine, New Haven, CT

Timothy Lepore, M.D.
Nantucket Cottage Hospital, Nantucket, MA

Alan Barbour, M.D.
University of California, Irvine, Irvine, CA

Durland Fish, Ph.D.
Yale School of Public Health, New Haven, CT

The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institute of Allergy and Infectious Diseases or the National Institutes of Health. Supported by grants from the National Institute of Allergy and Infectious Diseases at the National Institutes of Health (R21AI088079, to Drs. Krause and Fish), the Gordon and Llura Gund Foundation (to Drs. Krause and Lepore), the G. Harold and Leila Y. Mathers Foundation (to Dr. Fish), and the Howard Hughes Medical Institute (to Dr. Fikrig). Disclosure forms provided by the authors are available with the full text of this letter at