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Animal Waste, Water Quality and Human Health

Animal Waste, Water Quality and Human Health

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38<strong>Animal</strong> <strong>Waste</strong>, <strong>Water</strong> <strong>Quality</strong> <strong>and</strong> <strong>Human</strong> <strong>Health</strong>associated with intestinal <strong>and</strong> extra-intestinal diseases in both humans <strong>and</strong> animals(Donnenberg & Whittam 2001). Most E. coli pathogroups that cause entericdisease in humans are host species-specific <strong>and</strong> are important agents ofwaterborne disease in children <strong>and</strong> adults in parts of the world where theinfrastructure <strong>and</strong> services necessary for adequate treatment of drinking-water<strong>and</strong> sewage are rudimentary. In contrast to these human-restricted E. colipathogroups, members of the enterohemorrhagic E. coli (EHEC) pathogroup arezoonotic pathogens. Although E. coli O157:H7 has been isolated from a widevariety of other animals sources, including feral <strong>and</strong> domestic pigs, dogs, horses,raccoons, starlings, gulls, geese <strong>and</strong> flies (Renter & Sargeant 2002, Pedersen &Clark 2007), most outbreaks of infection have been linked to ruminants. Itremains unclear whether other animal species are significant pathogen sources orsimply act as passive carriers.EHEC produce one or more antigenic type of potent bipartite protein toxinstermed Shiga toxins (Stxs) (Gyles 2007; Karch et al. 2009; Karmali et al. 2010;Mohawk & O’Brien 2011; Tam et al. 2008b). The toxins are thought to bind tospecific glycolipid receptors on host cells <strong>and</strong> become internalised. Once in thecytoplasm, the toxin A subunit cleaves the host ribosomal RNA at a specificsite. As this ribosomal RNA is essential for protein synthesis this actioneventually leads to cell death. During EHEC infection, Stxs are absorbed intothe blood stream <strong>and</strong> damage endothelial cells lining the small vessels of organssuch as the intestine, kidney, pancreas <strong>and</strong> brain. Stxs not only cause cell deathbut also the release of mediators of inflammation from endothelial cells whichpromote clot formation in the small blood vessels. This formation ofmicrothrombi causes platelet depletion, haemolysis <strong>and</strong> prevents blood flow,resulting in ischemic damage to vital organs. Damage to the colon is manifest ashaemorrhagic colitis <strong>and</strong> to the kidney as the sometimes fatal haemolytic uremicsyndrome (HUS).In addition to Stx production, EHEC typically possess a large plasmid whichencodes a number of virulence-related genes including a special haemolysin (Limet al. 2010) <strong>and</strong> also specific chromosomal regions known as pathogenicityisl<strong>and</strong>s that are thought to contribute to bacterial virulence (Hayashi et al. 2001,Perna et al. 2001). One of the best characterized of these is the locus ofenterocyte attachment <strong>and</strong> effacement which encodes for a specific bacterialattachment factor called intimin <strong>and</strong> proteins which form a so-called type IIIsecretion system which acts like a molecular syringe <strong>and</strong> injects effectorproteins from a number of different pathogenicity isl<strong>and</strong>s into the eukaryotic cell(Coombes et al. 2008, Kaper et al. 1997, Ogura et al. 2007, Tobe et al. 2006).These effector proteins participate in bacterial binding to the microvilli ofentocytes <strong>and</strong> also change the cell’s morphology <strong>and</strong> physiology.

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