Rodent-associated Bartonella febrile illness, Southwestern United States.

Serum specimens from 114 patients hospitalized with a febrile illness were tested with an indirect immunofluorescence assay (IFA) using Bartonella antigens prepared from 6 species of sigmodontine rodents and 3 known human Bartonella pathogens: B. henselae, B. quintana, and B. elizabethae. Acute- and convalescent-phase serum samples from 5 of these patients showed seroconversion with an IFA titer >512 to rodent-associated Bartonella antigens. The highest titer was against antigen derived from the white-throated woodrat (Neotoma albigula), although this rodent is not necessarily implicated as the source of infection. Three of the 5 who seroconverted showed no cross-reaction to the 3 Bartonella human pathogens. Common clinical characteristics were fever, chills, myalgias, leukopenia, thrombocytopenia, and transaminasemia. Although antibodies to Bartonella are cross-reactive, high-titer seroconversions to rodent-associated Bartonella antigens in adults with common clinical characteristics should stimulate the search for additional Bartonella human pathogens.

Hantavirus pulmonary syndrome: a zebra worth knowing.

Hantavirus pulmonary syndrome (HPS) is a severe cardiopulmonary illness most often caused by the Sin Nombre virus, which is transmitted to humans by inhalation of aerosolized particles of rodent excreta or direct rodent contact. Although HPS is more common in the western United States, cases have been identified in 31 states. The illness begins as a nonspecific febrile prodrome, sharing many of its initial symptoms with other more common viral infections. Patients then quickly develop noncardiogenic pulmonary edema, respiratory failure, and shock. Characteristic laboratory findings include thrombocytopenia, a left-shifted leukocytosis, hemoconcentration, and presence of immunoblasts. The overall case fatality rate of HPS is approximately 40 percent. Diagnosis is confirmed by serologic identification of IgM and IgG antibodies to Sin Nombre virus. There is no specific therapy, but early recognition of HPS during the prodromal phase can expedite initiating cardiopulmonary support in an intensive care unit, which is associated with improved survival rates. Prevention of HPS involves avoiding contact with rodents and rodent habitats.