Using geographic information systems and spatial and space-time scan statistics for a population-based risk analysis of the 2002 equine West Nile epidemic in six contiguous regions of Texas.

BACKGROUND: In 2002, West Nile virus (WNV) first appeared in Texas. Surveillance data were retrospectively examined to explore the temporal and spatial characteristics of the Texas equine WNV epidemic in 2002. Using Geographic Information Systems (GIS) and the Spatial and Space-Time Scan (SaTScan) statistics, we analyzed 1421 of the reported equine WNV cases from six contiguous state Health Service Regions (HSRs), comprising 158 counties, in western, northern, central and eastern Texas. RESULTS: Two primary epidemic peaks occurred in Epidemiological (Epi) week 35 (August 25 to 31) and Epi week 42 (October 13 to 19) of 2002 in the western and eastern part of the study area, respectively. The SaTScan statistics detected nine non-random spatio-temporal equine case aggregations (mini-outbreaks) and five unique high-risk areas imbedded within the overall epidemic. CONCLUSION: The 2002 Texas equine WNV epidemic occurred in a bi-modal pattern. Some "local hot spots" of the WNV epidemic developed in Texas. The use of GIS and SaTScan can be valuable tools in analyzing on-going surveillance data to identify high-risk areas and shifts in disease clustering within a large geographic area. Such techniques should become increasingly useful and important in future epidemics, as decisions must be made to effectively allocate limited resources.

Hepatitis B virus x gene and cyanobacterial toxins promote aflatoxin B1-induced hepatotumorigenesis in mice.

AIM: To assess the combinative role of aflatoxin B1(AFB1), cyanobacterial toxins (cyanotoxins), and hepatitis B virus (HBV) x gene in hepatotumorigenicity. METHODS: One-week-old animals carrying HBV x gene and their wild-type littermates were intraperitoneally (ip) injected with either single-dose AFB1 [6 mg/kg body weight (bw)], repeated-dose cyanotoxins (microcystin-LR or nodularin, 10 microg/kg bw once a week for 15 wk), DMSO (vehicle control) alone, or AFB1 followed by cyanotoxins a week later, and were sacrificed at 24 and 52 wk post-treatment. RESULTS: AFB1 induced liver tumors in 13 of 29 (44.8%) transgenic mice at 52 wk post-treatment, significantly more frequent than in wild-type mice (13.3%). This significant difference was not shown in the 24-wk study. Compared with AFB1 exposure alone, MC-LR and nodularin yielded approximately 3-fold and 6-fold increases in the incidence of AFB(1)-induced liver tumors in wild-type animals at 24 wk, respectively. HBV x gene did not further elevate the risk associated with co-exposure to AFB1 and cyanotoxins. With the exception of an MC-LR-dosed wild-type mouse, no liver tumor was observed in mice treated with cyanotoxins alone at 24 wk. Neither DMSO-treated transgenic mice nor their wild-type littermates had pathologic alterations relevant to hepatotumorigenesis in even up to 52 wk. CONCLUSION: HBV x gene and nodularin promote the development of AFB(1)-induced liver tumors. Co-exposure to AFB1 and MC-LR tends to elevate the risk of liver tumors at 24 wk relative to exposure to one of them. The combinative effect of AFB1, cyanotoxins and HBVx on hepatotumorigenesis is weak at 24 wk.