UNC Water and Health Conference 2011: Professor Glenn Morris, University of Florida

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UNC Water and Health Conference 2011: Professor Glenn Morris, University of Florida

  1. 1. New Frontiers, Old Obstacles<br />Pathogens, Genetics, Models, and Public Health<br />J. Glenn Morris, Jr., MD, MPH&TM<br />Emerging Pathogens Institute<br />University of Florida<br />
  2. 2. UF Emerging Pathogens Institute<br />Created with $60 million appropriation from Florida state legislature, focusing on human, animal, and plant pathogens<br />Over 200 faculty members, from 9 UF colleges (including medicine, public health, veterinary medicine, and agriculture)<br />Strong global emphasis, reflecting Florida’s sub-tropical location<br />
  3. 3. How do you guide optimal allocation of limited public health resources for prevention of diarrheal disease? <br />
  4. 4. Why do kids in the developing world get symptomatic diarrhea?<br />Driven by specific pathogens, but with occurrence of illness dependent on a complex set of interactions that include:<br />Prior exposure to the pathogen /vaccination (immunity)<br />Inoculum size<br />Nutritional status<br />Intestinal microenvironment, driven by local exposures<br />
  5. 5. Lindsey et al, EID 2011;17:608-611<br />Sample of 2,748 patients with diarrheal disease in Kolkata; samples screened for 26 pathogens using standard microbiological techniques<br />Approximately 1/3 had multiple pathogens<br />Likelihood of infection with another specific pathogen among patients culture-positive for V. cholerae<br />
  6. 6. Global Enterics Multi-Center Study (GEMS)(Levine et al, funded by Gates Foundation)<br />3609 samples from children with and without diarrhea, collected at 7 sites in Africa and Southern Asia<br />Samples screened for pathogens using standard microbiological techniques<br />Sub-Study: Comprehensive genetic analysis/ identification of all microorganisms in samples<br />Data to date: analysis of 16S sequence data from samples from 1007 cases (514 children with diarrhea, 493 control children)<br />Average of 3,900 sequences per sample<br />
  7. 7. Bacterial Identification and Classification by 16S rRNA<br />Permits screening of “total community DNA,” and identification of all “OTU” in sample<br />Stool samples<br />Environmental samples<br />
  8. 8. Percentage of Case and Control Samples with Specific Pathogens, as Identified by Genetic vs. Microbiologic Techniques<br />
  9. 9. Underlying intestinal flora did not differ by case/control status (although further analysis does suggest that risk can be influenced by flora composition) <br />Patterns of intestinal flora (and pathogen distribution) did differ by country<br />RedControl<br />BlackCase<br />Blue – Bangladesh<br />Green -Kenya<br />Black - Gambia<br />
  10. 10. So does pathogen really matter?<br />Yes: may be striking differences in public health impact, depending on pathogen<br />Report released: April 28, 2011<br />Funded by: Robert Wood Johnson Foundation<br />Available: epi.ufl.edu<br />
  11. 11. U.S. Foodborne Pathogen Incidence* <br />*Scallan et al, EID 2011;17:7-15<br />
  12. 12.
  13. 13. So does pathogen really matter?<br />Yes: may be striking differences in public health impact, depending on pathogen<br />Yes: transmission pathways (and optimal prevention strategies) may differ dramatically, depending on pathogen<br />
  14. 14. Environmental Parameters<br />V. cholerae in environment<br />including plankton<br />Cholera infections in humans<br />Cholera Transmission Pathways<br />“Slow” transmission: through fecal contamination of environment/water sources<br />“Fast” transmission: driven by genetically-induced hyperinfectious state, occurring within a time window of a few hours after passage of stool. Transmission generally occurs within household or immediate environment of patient<br />
  15. 15. Zimbabwe<br />Spatial Models<br />SIR model<br />Calculation of R0<br />Average number of secondary infections that occur when one infective is introduced into a completely susceptible host population<br />Estimation of relative contributions of:<br />human/human transmission (short cycle, increased infectivity) vs.<br />human/environment/human (long cycle, decreased infectivity)<br />Use of these estimates to assess utility of intervention strategies such as vaccination<br />
  16. 16. R0 by ProvinceZimbabwe Cholera Epidemic, 2008-9<br />Mukandavire et al, PNAS 2011;108:8767-72 <br />
  17. 17. Mapping ℛ0 values: Haiti Cholera Epidemic, 2010<br />
  18. 18. Relative Contribution of “Slow” (Environmental) vs. “Fast” (Human) Sources to Cholera Transmission<br />Zimbabwe<br />RE (slow cycle) = 0.20 (17%)<br />RH (fast cycle) = 0.95 (83%<br />R0 = 1.15 <br />Vaccine coverage to stop epidemic: 17%<br />Haiti<br />RE(slow cycle) = 0.84 (54%)<br />RH (fast cycle) = 0.70 (46%)<br />R0 = 1.54<br />Vaccination coverage to stop epidemic: 45%<br />
  19. 19. How do you guide optimal allocation of limited public health resources for prevention of diarrheal disease? <br />Systems are complex<br />Mix of pathogens<br />Mix of factors driving occurrence of symptomatic infection (disease) in individual patients<br />Varying outcomes dependent on pathogen<br />Mix of transmission routes, varying by pathogen, country, and region<br />Variety of potential interventions, including water systems, sanitation, improved protection of water and food in households, vaccination…..<br />
  20. 20. How do you guide optimal allocation of limited public health resources for prevention of diarrheal disease? <br />Need for geographically-targeted, data-driven risk analysis, to define optimal approaches to disease prevention<br />

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