ABSTRACT
Previously, we reported the development of a Hazard Prediction and Assessment Capability plume dispersion model of the 2005 Graniteville, South Carolina, USA accidental release of chlorine. Here, we assess this model by spatial and statistical comparison with post-incident observed environmental indicators of exposure and other types of observations. Spatial agreement was found when the model was compared to phytotoxic bleaching and corrosion events observed in 2 km radius around the release site. When spatially compared to locations of injured or killed animals, model predictions of the plume footprint were in relatively good agreement. Model-predicted human casualties differed from observed casualty counts primarily due to the shielding effect of buildings. A statistical comparison of observed dog health outcome-derived exposure vs. model predicted exposure showed relatively good agreement, particularly when a subcohort of indoor dogs was excluded. Evaluation and assessment of the building infiltration effect would further improve the model prior to application in epidemiologic study.
Subject(s)
Air Pollutants/analysis , Chlorine/analysis , Environmental Exposure , Environmental Monitoring/methods , Irritants/analysis , Epidemiologic Studies , Humans , Models, Theoretical , South CarolinaABSTRACT
The present study demonstrates that multiple NoV genotypes belonging to genogroup II contributed to an acute gastroenteritis outbreak at a US military facility in Turkey that was associated with significant negative operational impact. Norovirus (NoV) is an important pathogen associated with acute gastroenteritis among military populations. We describe the genotypes of NoV outbreak occurred at a United States military facility in Turkey. Stool samples were collected from 37 out of 97 patients presenting to the clinic on base with acute gastroenteritis and evaluated for bacterial and viral pathogens. NoV genogroup II (GII) was identified by RT-PCR in 43% (16/37) stool samples. Phylogenetic analysis of a 260 base pair fragment of the NoV capsid gene from ten stool samples indicated the circulation of multiple and rare genotypes of GII NoV during the outbreak. We detected four GII.8 isolates, three GII.15, two GII.9 and a sole GII.10 NoV. Viral sequences could be grouped into four clusters, three of which have not been previously reported in Turkey. The fact that current NoV outbreak was caused by rare genotypes highlights the importance of norovirus strain typing. While NoV genogroup II is recognized as causative agent of outbreak, circulation of current genotypes has been rarely observed in large number of outbreaks.
