ETEC_transcriptomics. ETEC_transcriptomics

BACKGROUND Acute infectious diarrhoeal disease is considered to be the second most common cause of childhood death, accounting for one fifth of all childhood deaths among children below five years of age (Bryce et al., 2005). Enterotoxigenic Escherichia coli (ETEC) is one of the most common causes of diarrhoea in low-and middle-income countries and causes up to 400 million childhood diarrhoeal episodes and up to 380,000 deaths each year (Qadri et al., 2000). ETEC is also known to be the most common cause of traveller’s diarrhoea in those who travel to endemic areas (von Sonnenburg et al., 2000). ETEC produce two toxins, heat-labile (LT) and heat-stable (ST), which are secreted by the bacteria in the small intestine. The toxins affect ion channels in the epithelial cells, which subsequently results in the efflux of negatively charged ions and water, i.e. diarrhoea. ETEC bacteria can express one or both toxins. In order get into close contact with intestinal epithelial cells, to allow toxin secretion, outer membrane structures are expressed, so called colonisation factors (CFs). There are more than 25 known CFs which bind to receptors expressed on the surface of the intestinal epithelial cells and are tightly regulated in response to temperature. The permissive temperature being that of the mammalian host ~37oC. ETEC are known to carry and/or co-express one, two or three CFs together with one or both toxins in certain combinations, e.g. CS1+CS3 with LT+STh, CS5+CS6 with LT+STh. It has been shown that clonal groups with specific and common virulence profiles are stable over long periods of time, decades, and globally spread. Aim is to identify novel virulence related genes in ETEC. 1 This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/