Water and Infectious Disease - Waterborne Disease Global distribution of infectious disease Transmission cycles Water and infectious disease Enteric disease.

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<ul><li> Slide 1 </li> <li> Water and Infectious Disease - Waterborne Disease Global distribution of infectious disease Transmission cycles Water and infectious disease Enteric disease in children Case studies E.coli Cholera (Vibrio cholerae) Cryptosporidium parvum </li> <li> Slide 2 </li> <li> Slide 3 </li> <li> Slide 4 </li> <li> Slide 5 </li> <li> Slide 6 </li> <li> Slide 7 </li> <li> Slide 8 </li> <li> Slide 9 </li> <li> Slide 10 </li> <li> Slide 11 </li> <li> Slide 12 </li> <li> Slide 13 </li> <li> Slide 14 </li> <li> Slide 15 </li> <li> Slide 16 </li> <li> Slide 17 </li> <li> Slide 18 </li> <li> Slide 19 </li> <li> Slide 20 </li> <li> Slide 21 </li> <li> Slide 22 </li> <li> What is needed to control water-borne disease? Reduce exposure to excrement Water- quantity Water- quality Sanitation - proper disposal of feces </li> <li> Slide 23 </li> <li> Slide 24 </li> <li> Slide 25 </li> <li> Slide 26 </li> <li> Slide 27 </li> <li> Slide 28 </li> <li> Microbial Pathogenicity Entry into host Find a unique niche Evasion, subversion or circumvention of initial host defense mechanisms Multiplication or persistence Cause overt disease (optional) Exit the host - transmissibility Stanley Falkows lecture at Columbia University 4/17/97; Falkow, S. American Society of Microbiology News, 63: 539-365. A key distinction is that a pathogen has an inherent capacity to breach host cell barriers, whereas a commensal species and opportunistic pathogens do not. </li> <li> Slide 29 </li> <li> Not all E.coli are created equally Escherichia coli commensal part of normal gut microflora Enterohemorrhagic E. coli pathogen, causes GI disease Enterotoxigenic E. coli Enteropathogenic E. coli Enteroaggregative E. coli Enteroinvasive E. coli </li> <li> Slide 30 </li> <li> Slide 31 </li> <li> Slide 32 </li> <li> Slide 33 </li> <li> Virulence of Vibrio cholerae [Classical Inaba strain] Inoculum 10 4 10 6 10 8 Subjects 13522 Symptoms None 4 (30%)10 (19%)0 Mild diarrhea 9 (70%)28 (54%)1 Severe diarrhea 014 (27%)1 </li> <li> Slide 34 </li> <li> Vibrio cholerae cholera contr ol transmission control phytoplankton zooplankton VNC physical &amp; chemical characteristics of water - temperature - sunlight - rainfall - pH - dissolved oxygen tension - salinity &amp; other chemical nutrients transmission of V. cholerae to humans via ingested water containing colonized copepods or other vectors classic fecal-oral transmission from human to human via ingestion of fecal V. cholerae in water &amp;/ food The intersection of V. cholerae ecology and cholera </li> <li> Slide 35 </li> <li> Slide 36 </li> <li> Slide 37 </li> <li> Slide 38 </li> <li> Slide 39 </li> <li> Slide 40 </li> <li> Slide 41 </li> <li> Domestically-acquired cholera cases in the United States 1992-1994 2 exposure: eating shellfish harvested off Gulf Coast caused by endemic Gulf Coast Vibrio cholerae 01 4 exposure: unusual foods of non-US origin No evidence of secondary transmission in the US From: Mahon et al. 1996, JAMA, 276: 307-312 </li> <li> Slide 42 </li> <li> Slide 43 </li> <li> Slide 44 </li> <li> Slide 45 </li> <li> Features favoring transmissibility of Cryptosporidium parvum Broad host ranges Life cycle in single host / autoinfective Highly infectious Oocysts fully infective upon excretion Large numbers of oocysts may be shed Ubiquitous distribution in environment Highly resistant to disinfection and environmental pressures No effective therapy </li> <li> Slide 46 </li> <li> Slide 47 </li> <li> Slide 48 </li> <li> Slide 49 </li> <li> Slide 50 </li> <li> Exposure Reported Case Infection RISK ASSESSMENT EPIDEMIOLOGY </li> <li> Slide 51 </li> <li> Slide 52 </li> <li> Conclusions the distribution of cases is consistent with common source exposure tapwater may contribute to endemic cryptosporidiosis </li> <li> Slide 53 </li> <li> Slide 54 </li> <li> Slide 55 </li> </ul>


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