Assessment of the risk of Ebola virus transmission from bodily fluids and fomites.

Although Ebola virus (EBOV) is transmitted by unprotected physical contact with infected persons, few data exist on which specific bodily fluids are infected or on the risk of fomite transmission. Therefore, we tested various clinical specimens from 26 laboratory-confirmed cases of Ebola hemorrhagic fever, as well as environmental specimens collected from an isolation ward, for the presence of EBOV. Virus was detected by culture and/or reverse-transcription polymerase chain reaction in 16 of 54 clinical specimens (including saliva, stool, semen, breast milk, tears, nasal blood, and a skin swab) and in 2 of 33 environmental specimens. We conclude that EBOV is shed in a wide variety of bodily fluids during the acute period of illness but that the risk of transmission from fomites in an isolation ward and from convalescent patients is low when currently recommended infection control guidelines for the viral hemorrhagic fevers are followed.

Rapid diagnosis of Ebola hemorrhagic fever by reverse transcription-PCR in an outbreak setting and assessment of patient viral load as a predictor of outcome.

The largest outbreak on record of Ebola hemorrhagic fever (EHF) occurred in Uganda from August 2000 to January 2001. The outbreak was centered in the Gulu district of northern Uganda, with secondary transmission to other districts. After the initial diagnosis of Sudan ebolavirus by the National Institute for Virology in Johannesburg, South Africa, a temporary diagnostic laboratory was established within the Gulu district at St. Mary's Lacor Hospital. The laboratory used antigen capture and reverse transcription-PCR (RT-PCR) to diagnose Sudan ebolavirus infection in suspect patients. The RT-PCR and antigen-capture diagnostic assays proved very effective for detecting ebolavirus in patient serum, plasma, and whole blood. In samples collected very early in the course of infection, the RT-PCR assay could detect ebolavirus 24 to 48 h prior to detection by antigen capture. More than 1,000 blood samples were collected, with multiple samples obtained from many patients throughout the course of infection. Real-time quantitative RT-PCR was used to determine the viral load in multiple samples from patients with fatal and nonfatal cases, and these data were correlated with the disease outcome. RNA copy levels in patients who died averaged 2 log(10) higher than those in patients who survived. Using clinical material from multiple EHF patients, we sequenced the variable region of the glycoprotein. This Sudan ebolavirus strain was not derived from either the earlier Boniface (1976) or Maleo (1979) strain, but it shares a common ancestor with both. Furthermore, both sequence and epidemiologic data are consistent with the outbreak having originated from a single introduction into the human population.

Experimental evaluation of rodent exclusion methods to reduce hantavirus transmission to residents in a Native American community in New Mexico.

We conducted a pilot study to evaluate the efficacy of rodent proofing continuously occupied homes as a method for lowering the risk for hantavirus pulmonary syndrome (HPS) among residents of a Native American community in northwestern New Mexico. Rodent proofing of dwellings was paired with culturally appropriate health education. Seventy homes were randomly assigned to treatment or control categories. Treatment homes were rodent-proofed by sealing openings around foundations, doors, roofs, and pipes and repairing screens and windows. Repairs to each dwelling were limited to $500 US. After repairs were completed, 15-20 snap traps were placed in each treatment and control home and checked approximately every 2 days for an average of 3-4 weeks. During 23,373 trap nights, one house mouse (Mus musculus) was captured in one treatment home, and 20 mice (16 deer mice, Peromyscus maniculatus, two Pinyon mice, Peromyscus truei, and two unidentified mice) were captured in five control homes (one house had 14 captures, two had two captures, and two had one capture). Trap success was 0.01% in treatment homes and 0.15% in controls. Intensity of infestation (mean number of mice captured per infested home) was 1 in treatment homes and 4 in controls. Observations of evidence of infestation (feces, nesting material, gnaw marks, or reports of infestation by occupant) per 100 days of observation were 1.2 in treatment homes and 3.1 in controls. Statistical power of the experiment was limited because it coincided with a period of low rodent abundance (August-November 2000). Nevertheless, these results suggest that inexpensive rodent proofing of occupied rural homes can decrease the frequency and intensity of rodent intrusion, thereby reducing the risk of HPS among rural residents in the southwestern United States.