Community environmental health assessment in Peru's desert hills and rainforest.

Peru's expanding population and rapid urbanization--a result of migration to its largest cities--have stressed the country's public services infrastructure and the provision of public health and environmental health services. In response, the Ministry of Health established the General Directorate of Environmental Health (DIGESA), the branch charged with assuring adequate environmental health services to populations in rural and urban areas. The magnitude of the environmental health problems in peri-urban settlements, however, has exceeded the capacity of DIGESA to respond. The Urban Environmental Health Project is an effort to develop the ability of local communities to address these problems

Epidemiologic linkage of rodent and human hantavirus genomic sequences in case investigations of hantavirus pulmonary syndrome.

Sin Nombre virus (SNV) causes the zoonotic disease hantavirus pulmonary syndrome (HPS). Its mechanisms of transmission from rodent to human are poorly understood. It is possible that specific genetic signature sequences could be used to determine the probable site of each case-patient's exposure. Environmental assessments suggested 12 possible sites of rodent exposure for 6 HPS patients. Rodents were captured at 11 of the 12 sites and screened for SNV infection within 2 weeks of the patient's diagnosis. Viral sequences amplified from tissues of rodents at each site were compared with those from case-patients' tissues. Rodents bearing viruses with genetic sequence identity to case-patients' viruses across 2 genomic segments were identified in 4 investigations but never at >1 site. Indoor exposures to rodents were especially common at implicated sites. By distinguishing among multiple possible sites of exposure, viral genotyping studies can enhance understanding of the conditions associated with infection by SNV.

A household-based, case-control study of environmental factors associated with hantavirus pulmonary syndrome in the southwestern United States.

During an outbreak of hantavirus pulmonary syndrome (HPS) in the southwestern United States, trained environmental assessment teams conducted surveys at 17 case-patient homes and matched controls from June through August 1993. Variables related to rodent abundance were quantified and standardized rodent trapping was conducted around and within households. The majority of households were located in pinon-juniper vegetation zones, and there were no significant differences in the type of house in which cases and controls lived. The only environmental factor that distinguished case households from controls was significantly higher small rodent densities (median trap success for case sites = 17.3%, 12.7% for near controls, and 8.3% for far controls). Frequency of hantaviral infection in deer mice (Peromyscus maniculatus) did not vary significantly among households of cases and controls, with a range of 27.5-32.5% antibody-positive. Indices of rodent fecal contamination were slightly higher in case houses. The data indicate that higher rodent densities were associated with households in which HPS cases occurred. Strategies that control rodent numbers and decrease rodent access to dwellings may reduce risk of human infection.

A case-control study of hantavirus pulmonary syndrome during an outbreak in the southwestern United States.

In May 1993, an outbreak of hantavirus pulmonary syndrome (HPS) occurred in the southwestern United States. A case-control study determined risk factors for HPS. Seventeen case-patients were compared with 3 groups of controls: members of case-patient households (household controls), members of neighboring households (near controls), and members of randomly selected households > or = 24 km away (far controls). Investigators trapped more small rodents at case households than at near (P = .03) or far control households (P = .02). After the number of small rodents was controlled for, case-patients were more likely than household controls to hand plow (odds ratio [OR], 12.3; 95% confidence interval [CI], 1.1-143.0) or to clean feed storage areas (OR, 33.4; 95% CI, 1.7-666.0). Case-patients were more likely than near controls to plant (OR, 6.2; 95% CI, 1.1-34.0) and more likely than far controls to clean animal sheds (OR, 11.9; 95% CI, 1.4-103.0). Peridomestic cleaning, agricultural activities, and an increased number of small rodents at the household were associated with HPS.

Dominant glycoprotein epitope of four corners hantavirus is conserved across a wide geographical area.

A newly identified hantavirus, tentatively called Four Corners virus (FCV), was found to be the aetiological agent of a 1993 outbreak of hantavirus pulmonary syndrome (HPS) in the southwestern United States. Immunodominant epitopes of 43 and 31 amino acids were identified in the nucleocapsid protein and G1 glycoprotein, respectively. The G1 genes of different hantaviruses are highly divergent, suggesting that geographically diverse FCVs might fail to cross-react owing to antigenic drift. We now show that the immunodominant epitope of G1 is conserved among 18 FCVs from a broad geographical area, despite extensive nucleotide sequence heterogeneity. Antibodies from all 45 HPS patients, separated by more than 3000 km were shown to be reactive with the dominant G1 epitope. Evidence for limited cross-reactivity between the G1 antigen of a novel hantavirus of the cotton rat and that of FCV is presented.

Genetic identification of a novel hantavirus of the harvest mouse Reithrodontomys megalotis.

We have cloned the S genomic segment of a novel hantavirus of the harvest mouse Reithrodontomys megalotis. The virus is phylogenetically distinct from other hantaviruses. The new hantavirus was identified in harvest mice separated by approximately 1,000 km. A wood rat (Neotoma mexicana) was found to be infected with the harvest mouse hantavirus.

Serologic and genetic identification of Peromyscus maniculatus as the primary rodent reservoir for a new hantavirus in the southwestern United States.

An outbreak of hantavirus pulmonary syndrome (HPS) in the southwestern United States was etiologically linked to a newly recognized hantavirus. Knowledge that hantaviruses are maintained in rodent reservoirs stimulated a field and laboratory investigation of 1696 small mammals of 31 species. The most commonly captured rodent, the deer mouse (Peromyscus maniculatus), had the highest antibody prevalence (30%) to four hantavirus antigens. Antibody also was detected in 10 other species of rodent and in 1 species of rabbit. Reverse transcriptase-polymerase chain reaction (RT-PCR) products of hantavirus from rodent tissues were indistinguishable from those from human HPS patients. More than 96% of the seropositive P. maniculatus were positive by RT-PCR, suggesting chronic infection. Antibody prevalences were similar among P. maniculatus trapped from Arizona (33%), New Mexico (29%), and Colorado (29%). The numeric dominance of P. maniculatus, the high prevalence of antibody, and the RT-PCR findings implicate this species as the primary rodent reservoir for a new hantavirus in the southwestern United States.