Chapter X. Pathogenic Escherichia coli Kyle S. Enger, MPH

Similar documents
Risk Assessment of Staphylococcus aureus and Clostridium perfringens in ready to eat Egg Products

CONTROL OF SUBSTRATE UTILIZATION BY O-ISLANDS AND S- LOOPS IN ESCHERICHIA COLI O157:H7

FOR RUMINANTS. kemin.com/guthealth

In vitro the effect of intestinal normal flora on some pathogenic bacteria.

Gram negative bacilli

Bacteria Outline. 1. Overview. 2. Structural & Functional Features. 3. Taxonomy. 4. Communities

Indicator Organisms SCI5508

Cairo University Faculty of Veterinary Medicine Department of Microbiology. Thesis Presented By

Year 09 Science Learning Cycle 5 Overview

THE IDENTIFICATION OF TWO UNKNOWN BACTERIA AFUA WILLIAMS BIO 3302 TEST TUBE 3 PROF. N. HAQUE 5/14/18

The Evolution of Infectious Disease

NIH Public Access Author Manuscript Ann N Y Acad Sci. Author manuscript; available in PMC 2012 April 13.

Two-sample inference: Continuous Data

An introduction to the Serotypes, Pathotypes and Phylotypes of Escherichia coli

The Bacterial Causes of Camel-calf (Camelus dromedarius) Diarrhea in Eastern Sudan.

The Pangenome Structure of Escherichia coli: Comparative Genomic Analysis of E. coli Commensal and Pathogenic Isolates

1 Disease Spread Model

PHENOTYPIC AND GENOTYPIC CHARACTERIZATION OF Escherichia. coli ISOLATES RECOVERED FROM TREATED WASTEWATER

Introduction to Microbiology. CLS 212: Medical Microbiology Miss Zeina Alkudmani

The Scope of Food Microbiology p. 1 Micro-organisms and Food p. 2 Food Spoilage/Preservation p. 2 Food Safety p. 4 Fermentation p.

Contents. The Trajectory of Food Microbiology 3. Spores and heir Significance 39. Factors That Influence Microbes infoods 11

Typhoid Fever Dr. KHALID ALJARALLAH

INVESTIGATING BACTERIAL LIPOPOLYSACCHARIDES AND INTERACTIONS WITH ANTIMICROBIAL PEPTIDES

BACTERIAL PHYSIOLOGY SMALL GROUP. Monday, August 25, :00pm. Faculty: Adam Driks, Ph.D. Alan Wolfe, Ph.D.

Seminar 2 : Good Bugs

Thursday. Threshold and Sensitivity Analysis

Analysis of Longitudinal Data. Patrick J. Heagerty PhD Department of Biostatistics University of Washington

Molecular Evolution of Large Virulence Plasmid in Shigella Clones and Enteroinvasive Escherichia coli

A mathematical and computational model of necrotizing enterocolitis

COMMISSION REGULATION (EU)

This is a repository copy of Evidence for antibiotic induced Clostridium perfringens diarrhoea.

PDF // IS BACTERIA A PROKARYOTE OR EUKARYOTE

Salmonella enteritidis Identification and Isolation

Natural Genetic Resistance to Infection

Epithelial cell signaling responses to enterohemorrhagic Escherichia coli infection

Horizontal transfer and pathogenicity

By Eliza Bielak Bacterial Genomics and Epidemiology, DTU-Food Supervised by Henrik Hasman, PhD

CRISPR-SeroSeq: A Developing Technique for Salmonella Subtyping

KEY CONCEPTS AND PROCESS SKILLS. 2. Most infectious diseases are caused by microbes.

Microbiota: Its Evolution and Essence. Hsin-Jung Joyce Wu "Microbiota and man: the story about us

Introductory Microbiology Dr. Hala Al Daghistani

VIRULENCE. Vibrio cholerae Yersinia Shigella

no.1 Raya Ayman Anas Abu-Humaidan

Role of GIS in Tracking and Controlling Spread of Disease

Immunization of mice with live oral vaccine based on a Salmonella enterica (sv Typhimurium) aroa strain expressing the Escherichia coli O111 O antigen

Asymptotic Confidence Ellipses of Parameters for the Beta-Poisson Dose-Response Model

Interactions between symbiotic microbes, their mammalian host, and invading pathogens

A broad spectrum vaccine to prevent invasive Salmonella Infections for sub- Saharan Africa

Chapter 11 Survival strategies of pathogens in the host. a.a

VPM 201: Veterinary Bacteriology and Mycology 6-7/10/2010. LABORATORY 5a - ENTEROBACTERIACEAE

Bayesian inference and model selection for stochastic epidemics and other coupled hidden Markov models

Vocabulary- Bacteria (34 words)

IN VIETNAM. Benjamin Robert Sobkowiak. A thesis submitted for the degree of Doctorate of Philosophy. Department of Genetics, Evolution and Environment

Explain your answer:

Hypothesis testing for µ:

Displacement of bacterial pathogens from mucus and Caco-2 cell surface by lactobacilli

Quantitative Risk Assessment of Salmonella spp. in Fermented Pork Sausage (Nham)

Genetic Variation: The genetic substrate for natural selection. Horizontal Gene Transfer. General Principles 10/2/17.

Department of Mathematics. Mathematical study of competition between Staphylococcus strains within the host and at the host population level

Brief history of life on Earth

Comparing two independent samples

Modeling the Spread of Epidemic Cholera: an Age-Structured Model

The outer membrane of Borrelia 7/3/2014. LDA Conference Richard Bingham 1. The Outer Membrane of Borrelia; The Interface Between Them and Us

Studies on Pathogenesis and Immunity to Turkey Clostridial Dermatitis. K.V. Nagaraja and Anil Thachil

Introduction to microbiology

LESSON 1.3 WORKBOOK. Bacterial structures. Workbook Lesson 1.3

Fernando Leite, Connie Gebhart, Randall Singer, Richard Isaacson. University of Minnesota, St. Paul, MN

Prokaryotes & Viruses. Multiple Choice Review. Slide 1 / 47. Slide 2 / 47. Slide 3 / 47

Supplementary materials Quantitative assessment of ribosome drop-off in E. coli

HACCP: INTRODUCTION AND HAZARD ANALYSIS

Fimbriae, Fibrils, Sex and Fuzzy Coats

Clinical Trials. Olli Saarela. September 18, Dalla Lana School of Public Health University of Toronto.

Water Microbiology. Bacterial Pathogens and Water

C. elegans as an in vivo model to decipher microbial virulence. Centre d Immunologie de Marseille-Luminy

Dr. habil. Anna Salek. Mikrobiologist Biotechnologist Research Associate

Phylogenetic background of enterotoxigenic and enteroinvasive Escherichia coli from patients with diarrhea in Sirjan, Iran

Bacterial Virulence Strategies That Utilize Rho GTPases

Genes Related to Long Polar Fimbriae of Pathogenic Escherichia coli Strains as Reliable Markers To Identify Virulent Isolates

Bacterial Morphology and Structure م.م رنا مشعل

WHY IS THIS IMPORTANT?

Introduction to Microbiology BIOL 220 Summer Session I, 1996 Exam # 1

OCR Biology Checklist

OCR Biology Checklist

World Journal of Pharmaceutical Research SJIF Impact Factor 8.074

3 S. Heidelberg ESBL Extended spectrum lactamase

Contains ribosomes attached to the endoplasmic reticulum. Genetic material consists of linear chromosomes. Diameter of the cell is 1 m

(A) Exotoxin (B) Endotoxin (C) Cilia (D) Flagella (E) Capsule. A. Incorrect! Only gram-positive bacteria secrete exotoxin.

Supporting information

B1 REVISION CHAPTER 1 KEEPING HEALTHY

Introduction to Bacteria

MICROBIOLOGY (MICRO) Microbiology (MICRO) 1. MICRO 310: Medical Microbiology

Natalie C. Marshall Finlay Lab University of British Columbia. How EPEC and EHEC modulate human cells via their type III secretion system

Virulence of Enteropathogenic Escherichia coli, a Global Pathogen

Advanced Herd Management Probabilities and distributions

chapter one: the history of microbiology

Fate of Enterohemorrhagic Escherichia coli 0157:H7 in Apple Cider with and without Preservatives

Prokaryotes & Viruses. Multiple Choice Review. Slide 1 / 47. Slide 2 / 47. Slide 3 / 47

Prokaryotes & Viruses. Multiple Choice Review. Slide 2 / 47. Slide 1 / 47. Slide 3 (Answer) / 47. Slide 3 / 47. Slide 4 / 47. Slide 4 (Answer) / 47

ANALYSIS OF MICROBIAL COMPETITION

E. coli ETEC ETEC EPEC (AAEC) normal ETEC

Transcription:

Chapter X. Pathogenic Escherichia coli Kyle S. Enger, MPH X.1 Overview Escherichia coli usually exists as a commensal bacterium in the mammalian large intestine, benefiting itself as well as the host. However, there are several well-established pathotypes of disease-causing E. coli (Kaper 2004, Nataro 1998): Enteropathogenic () o Attaches to small intestinal wall and produces attaching and effacing lesions, in which microvilli are destroyed and the bacteria become perched on pedestals on the surface of the epithelial cell. This ability is encoded on the locus of enterocyte effacement (LEE) pathogenicity island. o Causes an inflammatory response and diarrhea, but seldom in persons older than 2y; it can also be isolated from healthy older persons. o Primarily found in developing countries. Enterohemorrhagic (EHEC) o This is discussed in more detail in its own chapter. Enterotoxigenic () o Attaches to small intestinal wall. o Produces a heat-labile (LT) and/or heat-stable (ST) toxins, both of which cause secretion from the small intestinal wall, leading to mild to severe watery diarrhea. LT is an immunogenic multisubunit protein similar to cholera enterotoxin. ST is a nonimmunogenic polypeptide containing 18-19 amino acids. o Primarily found in developing countries and is a major cause of diarrhea in weaned infants, as well as traveler s diarrhea. o Can be shed even by immune asymptomatic individuals. Enteroaggregative (EAEC) o Loosely classified group, some of which may be nonpathogenic. o Produces a thick biofilm ( stacked brick configuration) in the small or large intestines. o Thought to cause persistent diarrhea (lasting >14d). o Can produce many different secretory toxins and cytotoxins, but not ST or LT. Enteroinvasive (EIEC) o Actually invades the epithelial cells of the large intestine, where it multiplies. o Usually produces watery diarrhea similar to that of and, sometimes inflammatory colitis or dysentery. o Particularly closely related to Shigella sp. (which are now thought to be subgroups of E. coli); much pathogenesis from EIEC and Shigella sp. is mediated by the pwr100 virulence plasmid. Diffusely adherent (DAEC) o Attaches to the small intestinal wall and induces formation of projections which wrap around the bacterium.

Enterotoxigenic Escherichia coli () is the most common type of diarrheagenic E. coli (Qadri 2005). It may also be the most common cause of childhood diarrhea in the developing world, responsible for approximately 1/7 of diarrheal episodes in children aged less than 1y and almost ¼ of diarrheal episodes in 1-4 year olds (Wenneras 2004). It can also cause severe dehydrating cholera-like disease in adults (Qadri 2005). Diagnosis is complicated since many other Gram-negative bacteria produce similar toxins, so toxins as well as the E. coli bacterium must be tested for in order to yield accurate results (Wenneras 2004). can often be detected in apparently healthy people. In developing countries among healthy 0-11 month olds, and 1-4 year olds, 11.7% and 7.1%, respectively, are estimated to be colonized (Wenneras 2004). Feeding studies of or in healthy volunteers typically give 2-3g of, which neutralizes stomach acid and reduces the infectious dose (Levine et al. 1977). However, it has been suggested that food as a vehicle would have a similar acid-neutralizing effect, so feeding studies given may better represent natural foodborne infection.(levine et al. 1977) and generally have high ID 50, and partly as a consequence of this, they do not appear to be transmitted person-to-person; a study of -infected volunteers co-housed uninfected volunteers did not result in any transmission of infection.(levine 1980) Food was all served individually to the volunteers over the course of the experiment, so there was no opportunity for to spread via that route.(levine 1980) X.2 Summary of data and models There are many feeding studies of various E. coli types and strains, which can be pooled in various ways to yield different dose response models. Many of these have small sample sizes and cannot be used on their own to reliably fit a dose response model. In general, data exist spanning a wide range of doses and responses for disease. This is not the case for infection; most datasets describe high levels of infection resulting from high doses. Lower doses remain to be investigated, and dose response models for infection are therefore uncertain. Another important factor is whether the dose was given bicarbonate, which would neutralize some stomach acid and possibly increase infectivity. Haas, Rose, and Gerba (1999) fitted beta-poisson models to strains O111 (Ferguson et al. 1952) and O55 (June et al. 1953), as well as EIEC strains 4608 and 1624 (DuPont et al. 1971). Diarrhea was the response. However, it mixed data from experiments in which bacteria were given and out bicarbonate. The best available dataset using infection as a response comes from an experiment 3 dose levels, feeding EIEC to adult s (DuPont et al. 1971). Haas, Rose, and Gerba (1999) fitted a beta-poisson model to several pooled datasets describing the disease response from,, and EIEC. One strain ( O111) was found to differ from the rest, and was excluded. Powell et al. (2000) pooled 3 trial datasets (Levine et al. 1978, Beiber et al. 1998) for

to produce a beta-poisson model and a Weibull-gamma model. Additional pooling analyses for this chapter were conducted on the basis of pathotype ( or ), whether the dose was given bicarbonate, and the nature of the response (disease or infection), incorporating more data from the literature than the previous two published models. Since some combinations of these factors lacked data, analyses could only be done for disease (buffered or unbuffered), disease (buffered), infection (unbuffered), and infection (buffered). The pooled datasets for infection contained mostly positive responses, and therefore their behavior at low doses is very uncertain. For the pooled analyses describing disease, datasets were excluded if they contributed significantly (P < 0.05) to the -2 log likelihood of the model given the data (Haas, Rose, and Gerba 1999). Two experiments (DuPont et al. 1971) examining diarrhea from EIEC were also pooled. Table X.X: Summary of dose response data and models Experiment Reference Route Host Pathogen type type number Respons e of disease 38 39 40 99 42 43 142 DuPont et al. 1971 DuPont et al. 1971 DuPont et al. 1971 DuPont et al. 1971 June et al. 1953 Ferguson et al. 1952 Coster et al. 2007 143.. 144 Graham et al. 1983 145 Levine et al. 1979 B7A EIEC 4608 EIEC 1624 B2C O55 O111 B7A H10407 H10407 B7A milk milk milk milk Dose units cells Respon se diarrhea Best fit model None (2 doses) Optimized parameters ID 50 cells diarrhea Exponential k = 9.70E-09 7.14E+07 cells diarrhea Exponential k = 1.22E-08 5.70E+07 cells diarrhea cells diarrhea None (2 doses) Beta-Poisson (no significant trend) cells diarrhea Beta-Poisson CFU diarrhea CFU diarrhea CFU diarrhea None (2 doses) None (2 doses) cells diarrhea None (2 doses) α = 8.69E-02 N 50 = 1.94E+05 α = 2.61E-01 N 50 = 3.39E+06 1.94E+05 3.39E+06

147.. 151.. 153 155 Tacket et al. 2000 Donnenbe rg et al. 1998 157.. 159.. 161 Clements et al. 1981 162.. 163.. 164.. 165 168 Levine et al. 1977 Levine et al. 1982 169.. 170 Levine et al. 1980 B7A E2528- C1 2348/69 2362-75 2348/69 2348/69 214-4 TD225- C4 H10407 B7A 214-4 H10407 B7A H10407 cells diarrhea cells diarrhea CFU diarrhea CFU diarrhea CFU diarrhea CFU diarrhea CFU diarrhea CFU diarrhea CFU diarrhea CFU diarrhea milk cells diarrhea or vomitin g cells diarrhea cells diarrhea None (2 doses) None (2 doses) Beta-Poisson None (2 doses) cells diarrhea α = 2.50E-01 N 50 = 9.10E+07 9.10E+07

172.. 214 216 Bieber et al. 1998 Levine et al. 1978 217.. 218.. Respons e of infection 96 97 98 100 146 148 150 152 DuPont et al. 1971 DuPont et al. 1971 DuPont et al. 1971 DuPont et al. 1971 Levine et al. 1979 Levine et al. 1979 Levine et al. 1979 Levine et al. 1979 154 Tacket et al. 2000 214-4 B171-8 2348/69 E851/17 1 E74/68 B7A EIEC 4608 EIEC 1624 B2C B7A B7A B7A E2528- C1 2348/69 cells diarrhea CFU diarrhea Exponential k = 1.97E-09 3.51E+08 CFU diarrhea CFU diarrhea CFU diarrhea milk milk milk milk cells cells cells cells cells cells cells cells CFU positive isolation positive isolation positive isolation positive isolation positive isolation positive isolation positive isolation positive isolation sheddin g in None (2 doses) None (poor fit) None (all responses negative) None (2 doses) No dose response trend Beta-Poisson None (2 doses) None (2 doses) α = 1.55E-01 N 50 = 2.11E+06 2.11E+006

156 158 160 166 219 220 221 Donnenbe rg et al. 1993 Donnenbe rg et al. 1993 Donnenbe rg et al. 1993 Levine et al. 1977 Levine et al. 1978 Levine et al. 1978 Levine et al. 1978 2362-75 2348/69 2348/69 214-4 2348/69 E851/71 E74/68 milk CFU CFU CFU cells CFU CFU CFU sheddin g in sheddin g in sheddin g in positive isolation positive isolation positive isolation positive isolation None (2 doses) All but 1 subject positive None (2 doses) All subjects positive All but 1 subject positive Pooled models 38, 39, 40, 42, 99, 144 214, 216, 217 142, 143, 144, 145, 147, 151, 161, 162, 163, 164, 168, 169, 170, 172 38, 42, 99, 165 96, 100, 166 See above; fit by Haas, Rose, and Gerba 1999 See above; fit by Powell 2000,, EIEC See above milk or See above (no ) See above (no CFU diarrhea Beta-Poisson CFU diarrhea Beta-Poisson CFU diarrhea Beta-Poisson CFU diarrhea Beta-Poisson CFU infectio n Beta-Poisson α = 1.78E-01 N 50 = 8.60E+07 α = 2.21E-01 N 50 = 6.85E+07 α = 7.54E-02 N 50 = 1.70E+06 α = 2.06E-01 N 50 = 1.28E+08 α = 3.75E-01 N 50 = 1.78E+05 8.60E+07 6.85E+07 1.70E+006 1.28E+008 1.78E+005

153, 157, 159, 214, 216, 217 154, 156, 158, 160, 219, 220, 221 39, 40 See above See above DuPont et al. 1971 EIEC ) CFU diarrhea Beta-Poisson Exponential infectio CFU (no low dose n data) milk α = 1.62E-01 N 50 = 9.98E+07 k = 1.95E-06 9.98E+007 3.56E+005 cells diarrhea Exponential k = 1.07E-08 6.50E+007

X.3. Optimized models and fitting analysis X.3.1. Data and optimization output for experiment 39. Table 2. Model data for Escherichia coli (EIEC 4608) in the Dose Positive Negative Total Model Table 3. Best fitting model determination Devianc e Δ Degrees of freedom χ 2 0.95,1 χ 2 0.95,m-k 1 (10 4 ) 0 5 5 1 (10 6 ) 0 5 5 1 (10 8 ) 5 3 8 DuPont et al. (1971) Exponential 0.0 0.1 Beta-Poisson 0.1 1 2 1.000 6.0 0.952 0.751 Exponential fits better than beta-poisson; cannot reject good fit for exponential. Table 4. Optimized parameter(k) and ID 50 for best fitting model (exponential); percentiles from 10 4 bootstrap iterations Parameter MLE estimate Percentiles 0.5% 2.5% 5% 95% 97.5% 99.5% k 9.70E-09 1.33E-09 2.86E-09 4.66E-09 2.04E-08 5.07E-08 5.07E-08 ID 50 7.14E+07 1.37E+07 1.37E+07 3.40E+07 1.49E+08 2.43E+08 5.23E+08 Figure 1. Histogram of k parameter for exponential model. Figure 2. Exponential model plot, confidence bounds around the optimized model.

X.3. Optimized models and fitting analysis X.3.1. Data and optimization output for experiment 40. Table 2. Model data for Escherichia coli (EIEC 1624) in the Dose Positive Negative Total Model Table 3. Best fitting model determination Devianc e Δ Degrees of freedom χ 2 0.95,1 χ 2 0.95,m-k 1 (10 4 ) 0 5 5 1 (10 6 ) 1 8 9 1 (10 8 ) 3 2 5 DuPont et al. (1971) Exponential 0.9 0.9 Beta-Poisson 0.02 1 2 0.085 6.0 0.224 0.901 Exponential fits better than beta-poisson; cannot reject good fit for exponential. Table 4. Optimized parameter(k) and ID 50 for best fitting model (exponential); percentiles from 10 4 bootstrap iterations Parameter MLE estimate Percentiles 0.5% 2.5% 5% 95% 97.5% 99.5% k 1.22E-08 1.97E-09 2.19E-09 4.40E-09 4.03E-08 1.17E-07 4.03E-07 ID 50 5.70E+07 1.72E+06 5.92E+06 1.72E+07 1.58E+08 3.17E+08 3.52E+08 Figure 1. Histogram of k parameter for exponential model. Figure 2. Exponential model plot, confidence bounds around the optimized model.

X.3. Optimized models and fitting analysis X.3.1. Data and optimization output for experiment 42. Table 2. Model data for Escherichia coli ( O55 (in paper as type 55, B5 )) in the Dose Positive Negative Total 1.4 (10 8 ) 6 2 8 1.7 (10 9 ) 5 2 7 5.3 (10 9 ) 6 2 8 1.6 (10 10 ) 7 1 8 June et al. (1953) Model Table 3. Best fitting model determination Devianc e Exponential 53.3 Δ 48.7 Degrees of freedom Beta-Poisson 4.6 2 3 χ 2 0.95,1 χ 2 0.95,m-k 7.8 6.0 0.780 Beta-Poisson fits better than exponential; cannot reject good fit for beta-poisson. Table 4. Optimized parameters and LD 50 for best fitting model (beta-poisson); percentiles from 10 4 bootstrap iterations Parameter MLE estimate Percentiles 0.5% 2.5% 5% 95% 97.5% 99.5% α 7.23E-02 9.87E-04 1.02E-03 1.66E-02 3.55E-01 4.54E-01 8.24E-01 N 50 2.38E+04 3.96E-09 3.38E-06 2.08E-04 1.39E+08 2.08E+08 5.44E+008 Figure 1. Parameter scatter plot for beta-poisson model. Ellipses signify the 0.90, 0.95 and 0.99 confidence intervals. Figure 2. Beta-Poisson model plot, confidence bounds around the optimized model.

X.3. Optimized models and fitting analysis X.3.1. Data and optimization output for experiment 43. Table 2. Model data for Escherichia coli ( O111 (in paper as E. coli 111, B4 )) in the Dose Positive Negative Total 7 (10 6 ) 7 4 11 5.3 (10 8 ) 8 4 12 6.5 (10 9 ) 11 0 11 9 (10 9 ) 12 0 12 Ferguson et al. (1952) Model Table 3. Best fitting model determination Devianc e Exponential 51.4 Δ 45.0 Degrees of freedom Beta-Poisson 6.4 2 3 χ 2 0.95,1 χ 2 0.95,m-k 7.8 6.0 0.041 Neither the exponential nor beta-poisson fits well; beta-poisson is less bad. Table 4. Optimized parameters and LD 50 for best fitting model (beta-poisson); percentiles from 10 4 bootstrap iterations Parameter MLE estimate Percentiles 0.5% 2.5% 5% 95% 97.5% 99.5% α 2.61E-01-6.92E+00-2.58E+00-2.32E+00-7.51E-01-5.81E-01 3.16E+00 N 50 3.39E+06 9.65E-02 1.12E+03 2.21E+03 1.84E+07 2.52E+07 5.03E+007 Figure 1. Parameter scatter plot for beta-poisson model. Ellipses signify the 0.90, 0.95 and 0.99 confidence intervals. Figure 2. Beta-Poisson model plot, confidence bounds around the optimized model.

X.3. Optimized models and fitting analysis X.3.1. Data and optimization output for experiment 165. Table 2. Model data for Escherichia coli ( 214-4 (ST)) in the Dose Positive Negative Total Model Table 3. Best fitting model determination Devianc e Δ Degrees of freedom χ 2 0.95,1 χ 2 0.95,m-k 1 (10 6 ) 0 4 4 1 (10 8 ) 3 2 5 1 (10 10 ) 4 1 5 Levine et al. (1977) Exponential 0.5 1.3 Beta-Poisson 1.7 1 2 6.0 0.466 Beta-Poisson fits better than exponential; cannot reject good fit for beta-poisson. Table 4. Optimized parameters and LD 50 for best fitting model (beta-poisson); percentiles from 10 4 bootstrap iterations Parameter MLE estimate Percentiles 0.5% 2.5% 5% 95% 97.5% 99.5% α 2.50E-01-6.91E+00-6.91E+00-6.91E+00 5.17E+00 6.60E+00 6.60E+00 N 50 9.10E+07 3.00E+04 4.09E+04 5.00E+04 3.20E+08 6.91E+08 6.91E+008 Figure 1. Parameter scatter plot for beta-poisson model. Ellipses signify the 0.90, 0.95 and 0.99 confidence intervals. Figure 2. Beta-Poisson model plot, confidence bounds around the optimized model.

X.3. Optimized models and fitting analysis X.3.1. Data and optimization output for experiment 214. Table 2. Model data for Escherichia coli ( B171-8 (serotype O11:NM)) in the Dose Positive Negative Total 5 (10 8 ) 3 2 5 2.5 (10 9 ) 6 0 6 2 (10 10 ) 2 0 2 Bieber et al. (1998) Model Table 3. Best fitting model determination Devianc e Exponential 0.6 Δ NA Degrees of freedom Beta-Poisson NA 1 2 χ 2 0.95,1 1.000 χ 2 0.95,m-k 6.0 0.950 NA 0.747 Exponential fits better than beta-poisson; cannot reject good fit for exponential. Table 4. Optimized parameter(k) and ID 50 for best fitting model (exponential); percentiles from 10 4 bootstrap iterations Parameter MLE estimate Percentiles 0.5% 2.5% 5% 95% 97.5% 99.5% k 1.97E-09 7.78E-10 1.02E-09 1.03E-09 3.23E-09 3.23E-09 5.67E-08 ID 50 3.51E+08 1.22E+07 2.14E+08 2.14E+08 6.76E+08 6.76E+08 8.90E+08 Figure 1. Histogram of k parameter for exponential model. Figure 2. Exponential model plot, confidence bounds around the optimized model.

X.3. Optimized models and fitting analysis X.3.1. Data and optimization output for experiment 98. Table 2. Model data for Escherichia coli (EIEC 1624) in the Dose Positive Negative Total Model Table 3. Best fitting model determination Devianc e Δ Degrees of freedom χ 2 0.95,1 χ 2 0.95,m-k 1 (10 4 ) 0 5 5 1 (10 6 ) 5 4 9 1 (10 8 ) 3 2 5 DuPont et al. (1971) Exponential 37.5 36.4 Beta-Poisson 1.1 1 2 6.0 0.240 Beta-Poisson fits better than exponential; cannot reject good fit for beta-poisson. Table 4. Optimized parameters and ID 50 for best fitting model (beta-poisson); percentiles from 10 4 bootstrap iterations Parameter MLE estimate Percentiles 0.5% 2.5% 5% 95% 97.5% 99.5% α 1.55E-01 1.26E-03 1.26E-03 2.87E-02 2.01E+01 1.29E+02 1.90E+02 N 50 2.11E+06 1.53E+05 2.67E+05 2.95E+05 7.85E+08 1.81E+21 9.24E+140 Figure 1. Parameter scatter plot for beta-poisson model. Ellipses signify the 0.90, 0.95 and 0.99 confidence intervals. Figure 2. Beta-Poisson model plot, confidence bounds around the optimized model.

X.3. Optimized models and fitting analysis X.3.1. Data and optimization output, pooled experiments 38, 39, 40, 42, 99, 144. Table 2. Model data for E. coli disease (,, EIEC) in the Dose Positive Negative Total Model Table 3. Best fitting model determination Devianc e Δ Degrees of freedom χ 2 0.95,1 χ 2 0.95,m-k 1 (10 4 ) 0 5 5 1 (10 4 ) 0 5 5 1 (10 6 ) 0 5 5 1 (10 6 ) 1 8 9 1 (10 8 ) 5 3 8 Exponential 80.1 58.3 14 Beta-Poisson 21.9 13 23.7 22.4 0.924 Beta-Poisson fits better than exponential; cannot reject good fit for beta-poisson. 1 (10 8 ) 1 4 5 1 (10 8 ) 3 2 5 1 (10 8 ) 2 3 5 1.4 (10 8 ) 6 2 8 2.7 (10 8 ) 9 7 16 1.7 (10 9 ) 5 2 7 5.3 (10 9 ) 6 2 8 1 (10 10 ) 4 1 5 1 (10 10 ) 3 2 5 1.6 (10 10 ) 7 1 8 DuPont et al. (1971), June et al. (1953), Graham et al. (1983) Table 4. Optimized parameters for best fitting model (beta-poisson); percentiles from 10 4 bootstrap iterations Parameter MLE estimate Percentiles 0.5% 2.5% 5% 95% 97.5% 99.5% α 1.78E-01-2.37E+00-2.21E+00-2.13E+00-1.12E+00-1.00E+00-7.37E-01 N 50 8.60E+07 1.77E+07 2.63E+07 3.26E+07 2.69E+08 3.22E+08 5.52E+008

Figure 1. Parameter scatter plot for beta-poisson model. Ellipses signify the 0.90, 0.95 and 0.99 confidence intervals. Figure 2. Beta-Poisson model plot, confidence bounds around the optimized model.

X.3. Optimized models and fitting analysis X.3.1. Data and optimization output for pooled experiments 214 and 216 and 217. Table 2. Model data for disease in the Dose Positive Negative Total Model Table 3. Best fitting model determination Devianc e Δ Degrees of freedom χ 2 0.95,1 χ 2 0.95,m-k 1 (10 6 ) 0 4 4 1 (10 6 ) 1 4 5 1 (10 8 ) 1 4 5 5 (10 8 ) 3 2 5 2.5 (10 9 ) 6 0 6 Exponential 31.0 14.5 Beta-Poisson 16.5 6 7 14.1 12.6 0.081 Beta-Poisson fits better than exponential; cannot reject good fit for beta-poisson. 2 (10 10 ) 2 0 2 1 (10 10 ) 3 2 5 Levine et al. (1978), Bieber et al. (1998) Table 4. Optimized parameters for best fitting model (beta-poisson); percentiles from 10 4 bootstrap iterations Parameter MLE estimate Percentiles 0.5% 2.5% 5% 95% 97.5% 99.5% α 2.21E-01 8.88E-02 1.12E-01 1.26E-01 1.25E+00 7.07E+02 9.29E+03 N 50 6.85E+07 5.79E+06 1.08E+07 1.48E+07 6.83E+08 7.69E+08 1.09E+009

Figure 1. Parameter scatter plot for beta-poisson model. Ellipses signify the 0.90, 0.95 and 0.99 confidence intervals. Figure 2. Beta-Poisson model plot, confidence bounds around the optimized model.

X.3. Optimized models and fitting analysis X.3.1. Data and optimization output for pooled experiments 142, 143, 144, 145, 147, 151, 161, 162, 163, 164, 168, 169, 170, 172. Table 2. Model data for disease, buffered, in the Dose Positive Negative Total Model Table 3. Best fitting model determination Deviance Δ Degrees of freedom χ 2 0.95,1 χ 2 0.95,m-k 1 (10 6 ) 3 3 6 1 (10 7 ) 6 9 15 1 (10 8 ) 6 1 7 1 (10 8 ) 7 4 11 1 (10 8 ) 7 5 12 Exponential 432.7 393.5 18 Beta-Poisson 39.2 17 28.9 27.6 0.322 Beta-Poisson fits better than exponential; cannot reject good fit for beta-poisson. 1 (10 8 ) 9 3 12 1 (10 8 ) 6 3 9 1 (10 8 ) 4 2 6 1 (10 8 ) 3 1 4 1 (10 8 ) 4 0 4 2.7 (10 8 ) 9 7 16 5 (10 8 ) 19 8 27 1 (10 9 ) 5 3 8 1 (10 9 ) 7 1 8 1 (10 9 ) 5 5 10 1 (10 10 ) 8 0 8 1 (10 10 ) 5 4 9 1 (10 10 ) 9 3 12 1 (10 10 ) 9 5 14 Coster et al. (2007), Graham et al. (1983), Levine et al. (1979), Levine et al. (1980), Clements et al. (1981), Levine et al. (1982) Table 4. Optimized parameters & ID 50 for best fitting model (beta-poisson); percentiles from 10 4 bootstrap iterations Parameter MLE estimate Percentiles 0.5% 2.5% 5% 95% 97.5% 99.5% α 7.54E-02 8.29E-03 1.10E-02 1.52E-02 1.46E-01 1.60E-01 1.92E-01 N 50 1.70E+06 6.62E-11 4.33E-06 3.57E-03 2.35E+07 3.18E+07 4.95E+007

Figure 1. Parameter scatter plot for beta-poisson model. Ellipses signify the 0.90, 0.95 and 0.99 confidence intervals. Figure 2. Beta-Poisson model plot, confidence bounds around the optimized model.

X.3. Optimized models and fitting analysis X.3.1. Data and optimization output for pooled experiments 38, 42, 99, 165. Table 2. Model data for disease, unbuffered, in the Dose Positive Negative Total Model Table 3. Best fitting model determination Devianc e Δ Degrees of freedom χ 2 0.95,1 χ 2 0.95,m-k 1 (10 6 ) 0 4 4 1 (10 8 ) 1 4 5 1 (10 8 ) 2 3 5 1 (10 8 ) 3 2 5 1.4 (10 8 ) 6 2 8 Exponential 79.5 50.2 Beta-Poisson 29.3 9 10 18.3 16.9 0.786 Beta-Poisson fits better than exponential; cannot reject good fit for beta-poisson. 1.7 (10 9 ) 5 2 7 5.3 (10 9 ) 6 2 8 1 (10 10 ) 4 1 5 1 (10 10 ) 3 2 5 1 (10 10 ) 4 1 5 1.6 (10 10 ) 7 1 8 DuPont et al. (1971), June et al. (1953), Levine et al. (1977) Table 4. Optimized parameters and ID 50 for best fitting model (beta-poisson); percentiles from 10 4 bootstrap iterations Parameter MLE estimate Percentiles 0.5% 2.5% 5% 95% 97.5% 99.5% α 2.06E-01 2.02E-02 1.20E-01 1.33E-01 3.77E-01 4.26E-01 5.33E-01 N 50 1.28E+08 8.82E+05 3.23E+07 4.22E+07 2E+08 4.68E+08 6.55E+008

Figure 1. Parameter scatter plot for beta-poisson model. Ellipses signify the 0.90, 0.95 and 0.99 confidence intervals. Figure 2. Beta-Poisson model plot, confidence bounds around the optimized model.

X.3. Optimized models and fitting analysis X.3.1. Data and optimization output for pooled experiments 96, 100, 166. Table 2. Model data for infection, unbuffered, in the Dose Positive Negative Total Model Table 3. Best fitting model determination Devianc e Δ Degrees of freedom χ 2 0.95,1 χ 2 0.95,m-k 1 (10 6 ) 3 1 4 1 (10 8 ) 5 0 5 1 (10 8 ) 4 1 5 1 (10 8 ) 5 0 5 1 (10 10 ) 5 0 5 Exponential 200.5 190.7 Beta-Poisson 9.8 5 6 12.6 11.1 0.745 Beta-Poisson fits better than exponential; cannot reject good fit for beta-poisson. 1 (10 10 ) 5 0 5 1 (10 10 ) 5 0 5 DuPont et al. (1971), Levine et al. (1977) Table 4. Optimized parameters and ID 50 for best fitting model (beta-poisson); percentiles from 10 4 bootstrap iterations Parameter MLE estimate Percentiles 0.5% 2.5% 5% 95% 97.5% 99.5% α 3.75E-01 1.29E-01 1.34E-01 1.34E-01 9.97E+00 9.97E+00 1.07E+01 N 50 1.78E+05 3.63E-01 3.63E-01 3.63E-01 2.46E+06 3.48E+06 6.09E+006

Figure 1. Parameter scatter plot for beta-poisson model. Ellipses signify the 0.90, 0.95 and 0.99 confidence intervals. Figure 2. Beta-Poisson model plot, confidence bounds around the optimized model.

X.3. Optimized models and fitting analysis X.3.1. Data and optimization output for pooled experiments 153, 157, 159, 214, 216, 217. Table 2. Model data for disease, buffered, in the Dose Positive Negative Total Model Table 3. Best fitting model determination Devianc e Δ Degrees of freedom χ 2 0.95,1 χ 2 0.95,m-k 1 (10 6 ) 0 4 4 1 (10 6 ) 1 4 5 1 (10 8 ) 1 4 5 5 (10 8 ) 3 2 5 2.5 (10 9 ) 6 0 6 Exponential 58.0 41.5 Beta-Poisson 16.5 9 10 18.3 16.9 0.108 Beta-Poisson fits better than exponential; cannot reject good fit for beta-poisson. 1 (10 10 ) 9 1 10 1 (10 10 ) 9 5 14 1 (10 10 ) 3 2 5 1 (10 10 ) 5 0 5 2 (10 10 ) 2 0 2 2.3 (10 10 ) 14 5 19 Tacket et al. (2000), Donnenberg et al. (1998), Bieber et al. (1998), Levine et al. (1978) Table 4. Optimized parameters and ID 50 for best fitting model (beta-poisson); percentiles from 10 4 bootstrap iterations Parameter MLE estimate Percentiles 0.5% 2.5% 5% 95% 97.5% 99.5% α 1.62E-01 8.38E-02 9.98E-02 1.09E-01 3.67E-01 4.14E-01 5.13E-01 N 50 9.98E+07 8.96E+06 1.59E+07 2.22E+07 8.72E+08 1.07E+09 1.53E+009

Figure 1. Parameter scatter plot for beta-poisson model. Ellipses signify the 0.90, 0.95 and 0.99 confidence intervals. Figure 2. Beta-Poisson model plot, confidence bounds around the optimized model.

X.3. Optimized models and fitting analysis X.3.1. Data and optimization output for pooled experiments 154, 156, 158, 160, 219, 220, 221. Table 2. Model data for, infection, buffered, in the Dose Positive Negative Total Model Table 3. Best fitting model determination Devianc e Δ Degrees of freedom χ 2 0.95,1 χ 2 0.95,m-k 1 (10 6 ) 3 1 4 1 (10 6 ) 5 0 5 1 (10 6 ) 4 1 5 1 (10 8 ) 5 0 5 1 (10 8 ) 5 0 5 Exponential 2.0 2 12 Beta-Poisson 0 11 0.999 21.0 0.999 19.7 0.999 Exponential fits better than beta-poisson; cannot reject good fit for exponential. 9 (10 8 ) 8 0 8 1 (10 10 ) 10 0 10 1 (10 10 ) 9 0 9 1 (10 10 ) 14 0 14 1 (10 10 ) 5 0 5 1 (10 10 ) 5 0 5 1 (10 10 ) 5 0 5 2.3 (10 10 ) 19 0 19 Tacket et al. (2000), Donnenberg et al. (1993), Levine et al. (1978) Table 4. Optimized parameter(k) and ID 50 for best fitting model (exponential); percentiles from 10 4 bootstrap iterations Parameter MLE estimate Percentiles 0.5% 2.5% 5% 95% 97.5% 99.5% k 1.95E-06 8.47E-07 1.03E-06 1.25E-06 2.64E-06 2.64E-06 2.64E-06 ID 50 3.56E+05 2.63E+05 2.63E+05 2.63E+05 5.53E+05 6.73E+05 8.18E+05

Figure 1. Histogram of k parameter for exponential model. Figure 2. Exponential model plot, confidence bounds around the optimized model.

X.3. Optimized models and fitting analysis X.3.1. Data and optimization output for pooled experiments 39 and 40. Table 2. Model data for EIEC disease, unbuffered, in the Dose Positive Negative Total Model Table 3. Best fitting model determination Devianc e Δ Degrees of freedom χ 2 0.95,1 χ 2 0.95,m-k 1 (10 4 ) 0 5 5 1 (10 4 ) 0 5 5 1 (10 6 ) 0 5 5 1 (10 6 ) 1 8 9 1 (10 8 ) 5 3 8 Exponential 10.3 9.5 Beta-Poisson 0.8 4 5 0.134 11.1 0.670 9.5 0.917 Exponential fits better than beta-poisson; cannot reject good fit for exponential. 1 (10 8 ) 3 2 5 DuPont et al. (1971) Table 4. Optimized parameter(k) and ID 50 for best fitting model (exponential); percentiles from 10 4 bootstrap iterations Parameter MLE estimate Percentiles 0.5% 2.5% 5% 95% 97.5% 99.5% k 1.07E-08 3.46E-09 4.79E-09 5.77E-09 2.04E-08 2.28E-08 3.21E-08 ID 50 6.50E+07 2.16E+07 3.04E+07 3.40E+07 1.20E+08 1.45E+08 2.00E+08 Figure 1. Histogram of k parameter for exponential model. Figure 2. Exponential model plot, confidence bounds around the optimized model.

References Bieber, D. et al., 1998. Type IV pili, transient bacterial aggregates, and virulence of enteropathogenic Escherichia coli. Science (New York, N.Y.), 280(5372), pp.2114-2118. Clements, M.L. et al., 1981. Lactobacillus prophylaxis for diarrhea due to enterotoxigenic Escherichia coli. Antimicrobial Agents and Chemotherapy, 20(1), pp.104-108. Coster, T.S. et al., 2007. Immune response, ciprofloxacin activity, and gender differences after experimental challenge by two strains of enterotoxigenic Escherichia coli. Infection and Immunity, 75(1), pp.252-259. Donnenberg, M.S. et al., 1993. Role of the eaea gene in experimental enteropathogenic Escherichia coli infection. The Journal of Clinical Investigation, 92(3), pp.1412-1417. Donnenberg, M.S. et al., 1998. Effect of prior experimental enteropathogenic Escherichia coli infection on illness following homologous and heterologous rechallenge. Infection and Immunity, 66(1), pp.52-58. DuPont, H.L. et al., 1971. Pathogenesis of Escherichia coli diarrhea. The New England Journal of Medicine, 285(1), pp.1-9. Ferguson, W.W. & June, R.C., 1952. Experiments on feeding adult volunteers Escherichia coli 111, B4, a coliform organism associated infant diarrhea. American Journal of Hygiene, 55(2), pp.155-169. Graham, D.Y., Estes, M.K. & Gentry, L.O., 1983. Double-blind comparison of bismuth subsalicylate and placebo in the prevention and treatment of enterotoxigenic Escherichia coli-induced diarrhea in volunteers. Gastroenterology, 85(5), pp.1017-1022. Haas, C.N., Rose, J.B. & Gerba, C.P., 1999. Quantitative Microbial Risk Assessment, John Wiley & Sons, Inc. June, R.C., Ferguson, W.W. & Worfel, M.T., 1953. Experiments in feeding adult volunteers Escherichia coli 55, B5, a coliform organism associated infant diarrhea. American Journal of Hygiene, 57(2), pp.222-236. Kaper, J.B., Nataro, J.P. & Mobley, H.L., 2004. Pathogenic Escherichia coli. Nature Reviews. Microbiology, 2(2), pp.123-140. Levine, M.M. et al., 1978. Escherichia coli strains that cause diarrhoea but do not produce heatlabile or heat-stable enterotoxins and are non-invasive. Lancet, 1(8074), pp.1119-1122. Levine, M.M. et al., 1982. Reactogenicity, immunogenicity and efficacy studies of Escherichia coli type-1 somatic pili parenteral vaccine in man. Scandinavian Journal of Infectious Diseases, Suppl. 33, pp.83-95. Levine, M.M. et al., 1977. Diarrhea caused by Escherichia coli that produce only heat-stable enterotoxin. Infection and Immunity, 17(1), pp.78-82. Levine, M.M. et al., 1979. Immunity to enterotoxigenic Escherichia coli. Infection and Immunity, 23(3), pp.729-736. Levine, M.M. et al., 1980. Lack of person-to-person transmission of enterotoxigenic Escherichia coli despite close contact. American Journal of Epidemiology, 111(3), pp.347-355.

Nataro, J.P. & Kaper, J.B., 1998. Diarrheagenic Escherichia coli. Clinical Microbiology Reviews, 11(1), pp.142-201. Powell, M.R., 2000. Dose-response envelope for Escherichia coli O157:H7. Quantitative Microbiology, 2, pp.141-163. Qadri, F. et al., 2005. Enterotoxigenic Escherichia coli in developing countries: epidemiology, microbiology, clinical features, treatment, and prevention. Clinical Microbiology Reviews, 18(3), pp.465-483. Tacket, C.O. et al., 2000. Role of EspB in experimental enteropathogenic Escherichia coli infection. Infection and Immunity, 68(6), pp.3689-3695. Wennerås, C. & Erling, V., 2004. Prevalence of enterotoxigenic Escherichia coli-associated diarrhoea and carrier state in the developing world. Journal of Health, Population, and Nutrition, 22(4), pp.370-382.