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Correspondence

More on Hantavirus in New England and New York

N Engl J Med 1995; 332:337-338February 2, 1995

Article

To the Editor:

The report of a fatal case of hantavirus pulmonary syndrome in a Rhode Island resident (Aug. 25 issue)1 prompted us to examine whether hantaviruses are enzootic in New England. Because deer mice (Peromyscus maniculatus) serve as the main reservoir of the agent of hantavirus pulmonary syndrome in the western states,2 we reasoned that the closely related white-footed mouse (P. leucopus) might fill this role in New England.

We studied two sites2 with a high prevalence of the Lyme disease spirochete and Babesia microti, which are tick-borne pathogens carried by the white-footed mouse. Both sites are densely inhabited by this mouse (median annual maximal density, 25 per hectare over a 10-year period), which invades virtually all homes there during the winter and spring, thus exposing residents. We analyzed serum samples from 142 P. leucopus and 41 Microtus pennsylvanicus (meadow voles) trapped at these sites during 1992 and 1993 as part of a long-term ecologic study. To determine whether humans were at risk of acquiring hantaviral infection, we examined serum samples from 248 persons with homes near our trap sites, as well as from 10 laboratory personnel engaged in research on tick-borne zoonoses, 5 of whom had examined about 15,000 live rodents without using gloves or masks.

All serum samples were tested by the indirect immunofluorescent-antibody technique for IgG antibodies against Prospect Hill virus, a hantavirus that served as the surrogate antigen in studies of hantavirus pulmonary syndrome in the Four Corners region of New Mexico, Arizona, Colorado, and Utah.3 All serum samples from the mice and the humans were nonreactive, whereas 27 percent of the serum samples from the meadow voles had antibodies against Prospect Hill virus (geometric mean antibody titer, 136; range, 64 to 1024).

We conclude that hantaviruses are not maintained in white-footed mice in two coastal New England sites where Prospect Hill virus frequently infects meadow voles. Although these two types of rodents were trapped in the same area, this virus appears to infect just the voles. Accordingly, the absence of serologic evidence of hantaviral infection in humans may reflect either the behavior of voles, which rarely invade homes, or the low transmissibility of Prospect Hill virus, even among persons with frequent exposure to rodents.4 Because hantaviruses may exist in microfoci, however, rodents from other areas should be studied to determine their importance to public health in the region.

Sam R. Telford, III, D.Sc.
Harvard School of Public Health, Boston, MA 02115

Jin-Won Song, M.D., Ph.D.
Richard Yanagihara, M.D.
National Institutes of Health, Bethesda, MD 20892

4 References
  1. 1

    Brackett LE, Rotenberg J, Sherman CB. Hantavirus pulmonary syndrome in New England and Europe. N Engl J Med 1994;331:545-545
    Full Text | Web of Science | Medline

  2. 2

    Wilson ML, Telford SR III, Piesman J, Spielman A. Reduced abundance of immature Ixodes dammini (Acari: Ixodidae) following elimination of deer. J Med Entomol 1988;25:224-228
    Web of Science | Medline

  3. 3

    Childs JE, Ksiazek TG, Spiropoulou CF, et al. Serologic and genetic identification of Peromyscus maniculatus as the primary rodent reservoir for a new hantavirus in the Southwestern United States. J Infect Dis 1994;169:1271-1280
    CrossRef | Web of Science | Medline

  4. 4

    Yanagihara R, Gajdusek DC, Gibbs CJ Jr, Traub R. Prospect Hill virus: serologic evidence for infection in mammalogists. N Engl J Med 1984;310:1325-1326
    Full Text | Web of Science | Medline

To the Editor:

New hantaviruses are the cause of an often fatal respiratory disease called hantavirus pulmonary syndrome.1-3 One death due to hantavirus has been reported in the northeastern United States, in Rhode Island.4 In that case the infection was probably contracted in Shelter Island, New York, which is just off Long Island.5 We analyzed the seroprevalence of hantaviruses in the Long Island and Shelter Island areas and found that the G2 neutralization antigen of the Shelter Island hantavirus is virtually identical to that of pathogenic hantaviruses responsible for hantavirus pulmonary syndrome.

In 782 residents of Long Island who were screened for Lyme disease, we detected a 2.6 percent rate of seroprevalence for hantavirus, which indicates substantial exposure of humans to hantaviruses on Long Island. The white-footed mouse, P. leucopus, is the predominant woodland mouse species in northeastern coastal areas and has been associated with nonpathogenic hantavirus infections.6 The seroprevalence of hantavirus in P. leucopus was determined to be 15 to 41 percent (n = 293) in three locations on Long Island between 1984 and 1994, with an overall seroprevalence rate of 26 percent. As early as 1984 28 percent of serum samples from peromyscus on Shelter Island (47 of 169 mice) were seropositive for hantavirus. In the fall of 1994 we found a similar seroprevalence rate of 25 percent (4 of 16 mice) in P. leucopus on Shelter Island.

A 220-base-pair fragment of the hantavirus M segment carried by seropositive mice on Shelter Island was cloned and sequenced. These hantavirus clones (termed “NY- 3”) are distantly related to the nonpathogenic Prospect Hill virus, with 84 percent of amino acids identical in the two viruses and another 5 percent similar. In contrast, amino acid sequences obtained from NY-3 clones are virtually identical to the strains causing hantavirus pulmonary syndrome in humans (with 95 percent of amino acids identical and another 5 percent similar).1,3 The unique genetic structure of these hantaviruses was verified by the finding that the nucleic acid sequence differed by 21 percent from that of other strains causing hantavirus pulmonary syndrome and by the failure of standard oligonucleotides from strains causing hantavirus pulmonary syndrome to amplify M-segment sequences by means of the polymerase chain reaction.

These results indicate that genetically unique hantaviruses resembling those causing hantavirus pulmonary syndrome are carried by P. leucopus on Shelter Island and further implicate these mice as the source of infection in the patient who died of hantavirus pulmonary syndrome in Rhode Island. The seroprevalence of hantaviruses in the New York area and the presence on Shelter Island of hantaviruses resembling those causing hantavirus pulmonary syndrome warrant further surveillance and suggest that greater clinical awareness of hantaviruses is appropriate in northeastern states.

Erich R. Mackow, Ph.D.
Benjamin J. Luft, M.D
University Hospital, SUNY, Stony Brook, NY 11794

Ed Bosler, Ph.D.
New York State Department of Health, Northport, NY 11733

Dmitry Goldgaber, Ph.D.
Irina N. Gavrilovskaya, M.D.
University Hospital, SUNY, Stony Brook, NY 11794

6 References
  1. 1

    Nichol ST, Spiropoulou CF, Morzunov S, et al. Genetic identification of a hantavirus associated with an outbreak of acute respiratory illness. Science 1993;262:914-917
    CrossRef | Web of Science | Medline

  2. 2

    Duchin JS, Koster FT, Peters CJ, et al. Hantavirus pulmonary syndrome: a clinical description of 17 patients with a newly recognized disease. N Engl J Med 1994;330:949-955
    Full Text | Web of Science | Medline

  3. 3

    Spiropoulou CF, Morzunov S, Feldmann H, Sanchez A, Peters CJ, Nichol ST. Genome structure and variability of a virus causing hantavirus pulmonary syndrome. Virology 1994;200:715-723
    CrossRef | Web of Science | Medline

  4. 4

    Brackett LE, Rotenberg J, Sherman CB. Hantavirus pulmonary syndrome in New England and Europe. N Engl J Med 1994;331:545-545
    Full Text | Web of Science | Medline

  5. 5

    Song JW, Baek LJ, Gajdusek DC, et al. Isolation of pathogenic hantavirus from white-footed mouse (Peromyscus leucopus). Lancet 1994;344:1637-1637
    CrossRef | Web of Science | Medline

  6. 6

    Lee P-W, Amyx HL, Yanagihara R, Gajdusek DC, Goldgaber D, Gibbs CJ Jr. Partial characterization of Prospect Hill virus isolated from meadow voles in the United States. J Infect Dis 1985;152:826-829
    CrossRef | Web of Science | Medline