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Timely surveillance of enteric diseases is necessary to identify and control cases and outbreaks. Our objective was to evaluate the timeliness of enteric disease surveillance in British Columbia, Canada, compare these results to other settings, and recommend improvements. In 2012 and 2013, information was collected from case report forms and laboratory information systems on 2615Salmonella, shigatoxin-producingE. coli,Shigella, andListeriainfections. Twelve date variables representing the surveillance process from onset of symptoms to case interview and final laboratory results were collected, and intervals were measured. The median time from onset of symptoms to reporting subtyping results to BC epidemiologists was 26–36 days and from onset of symptoms to case interview was 12–14 days. Our findings were comparable to the international literature except for a longer time (up to 29 day difference) to reporting of PFGE results to epidemiologists in BC. Such a delay may impact our ability to identify and solve outbreaks. Several process and system changes were implemented which should improve the timeliness of enteric disease surveillance.

Background: Approximately one third of the hereditary diffuse gastric cancer (HDGC) families carry germline mutations in the E-cadherin gene (CDH1). Risk prediction in members of families with this rare but deadly cancer could be improved by the identification of additional HDGC genes in non-CDH1 families. Methods: Affected individuals from 22 CDH1 mutation-negative families were screened for germline mutations in four catenin genes: CTNNA1, CTNNB1, JUP, and CTNND1. Catenins interact closely with E-cadherin molecules in cells, and are therefore logical candidate genes for mutation screening in HDGC families. Results: No nonsynonymous variants were seen in CTNNA1, CTNNB1, or CTNND1; only JUP contained nonsynonymous variants, of which only two rare variants were predicted to be deleterious. Conclusion: Catenin genes are not commonly mutated in non-CDH1 HDGC families. Impact: Germline mutations in CTNNA1, CTNNB1, JUP, or CTNND1 are unlikely to play a major role in HDGC. Cancer Epidemiol Biomarkers Prev; 21(12); 2272–4. ©2012 AACR.