Imported Fatal Hantavirus Pulmonary Syndrome

To the Editor: Hantavirus pulmonary syndrome (HPS) is characterized by fever, gastrointestinal symptoms, respiratory distress, elevated hematocrit, hypoalbuminemia, and thrombocytopenia. Most cases in North America are acquired from rodent vectors and are caused by the Sin Nombre virus. Person-to-person transmission has been reported for Andes virus (1,2) but not for Sin Nombre virus (3). We describe a patient with fatal hantavirus pulmonary syndrome.

were given as intravenous drips. Arrangements were made for the patient to be transferred to a tertiary pediatric care center for possible extracorporeal membrane oxygenation. During air transport, she had an asystolic cardiac arrest. While administering cardiopulmonary resuscitation, members of the healthcare team were exposed to a considerable volume of pulmonary edema fl uid expelled from the patient's endotracheal tube. Few, if any, were able to maintain adequate protection with face shields or protective eyewear. Resuscitation efforts were unsuccessful, and the patient was pronounced dead on arrival at the tertiary care center at 7:26 PM. Postmortem examination showed evidence of marked pulmonary edema, diffuse alveolar damage, and lymphoid infl ammation in the pulmonary interstitium.
Serologic examination of an acute blood sample was immunoglobulin M (IgM) positive for Sin Nombre virus, but low optical densities indicated potential for an infection with a related hantavirus rather than Sin Nombre virus. Subsequently, reverse transcription-PCR (RT-PCR) on blood in EDTA and lung tissue followed by sequence analysis confi rmed an Andeslike hantavirus infection. None of the 40 household and healthcare contacts of the patient had symptoms compatible with HPS during an 8-week monitoring period. Two contacts with nonspecifi c symptoms were tested and found to be negative for hantavirusspecifi c IgM and IgG and negative by RT-PCR.
Additonally, a seroprevalence survey of close contacts and assessment of level of contact was conducted. Close contacts were defi ned as persons who lived in the same household as the patient, were in the same enclosed space for >2 hours, or provided healthcare to her while she was symptomatic. Twenty-eight (62%) of 45 close contacts provided serum over the next 5 months. All serum samples were negative for Sin Nombre and Andes IgG and Sin Nombre IgM by ELISA. Fourteen (50%) of the 28 completed a self-administered questionnaire which assessed the type and intensity of contact. Of these, 12 were healthcare workers and 2 were friends. One friend had contact with the patient 3 days before she died, a friend and a healthcare worker had contact with her on the day before her death, and the rest of the healthcare workers had contact with the patient on the day she died.
To our knowledge, this is the fi rst imported case and the tenth case of HPS reported in British Columbia, Canada, since 1994 (2006 BC Annual Summary of Reportable Diseases, available from www.bccdc.org/content.php?item=33) (4). Six of these 10 cases were fatal. All cases except the 1 described here have been locally acquired Sin Nombre infections. Sin Nombre virus is endemic in the Peromyscus maniculatus (deer mice) population in most of British Columbia (5).
Worldwide, imported cases of HPS are unusual, although HPS has been reported in countries that are in close geographic proximity or in travelers to disease-endemic areas (6)(7)(8). Fortunately, none of the persons exposed to the patient reported symptoms consistent with HPS during the incubation period, and none who were tested seroconverted. Seroprevalence surveys in Chile among healthcare worker contacts of patients with HPS caused by the Andes virus showed a prevalence of 0% (9). A report from Argentina showed that cases due to secondary transmission occurred mostly in nonhealthcare workers after prolonged close contact in the prodromal period (10). In conclusion, we describe an imported case of fatal HPS due to an Andes-like hantavirus with no evidence of secondary transmission.

Disseminated Bocavirus Infection after Stem Cell Transplant
To the Editor: Human bocavirus (HBoV) (1) is increasingly recognized as a cause of respiratory infections worldwide. Children and infants appear to be most at risk (2-7), although HBoV's role in immunocompromised patients remains unclear. We report on a child with disseminated HBoV infection after hematopoietic stem cell transplantation (HSCT). HBoV DNA was detected at high levels in nasopharyngeal aspirates (NPAs) and in blood and stool samples.