title: Dose response models for infectious gastroenteritis.
abstract: When pathogenic microorganisms enter the human body via ingestion with food or drinking water, they encounter a system of barriers mounted by the host. In order to reach parts of the intestinal tract that are suitable for growth and attachment, each of the barriers must be overcome successfully. The present view on infection states that at least one of the ingested pathogens must survive to start colonization. This is the basis for dose response models, used for quantitative risk assessment. In this paper, the usefulness of the Beta Poisson model for multiple barriers is corroborated. Infection is associated with the presence of elevated numbers of reproducing pathogens in the intestinal tract. This does not necessarily imply illness symptoms: when intestinal microorganisms engage in damaging activities, this may lead to illness symptoms. At the same time, these activities probably elicit defensive measures from the host, promoting the removal of pathogens and terminating infection. The duration of the period of colonization reflects the balance between the colonization potential of pathogens and the strength of host defenses. Starting from the assumption that during infection the host has a certain hazard of becoming ill, a simple dose response relation for acute gastroenteritis is developed. With the use of literature data from volunteer experiments, we show that examples can be found for three possible alternatives: an increase in the probability of illness with increasing dose, a decrease with higher doses, and a probability of illness (given infection) independent of the ingested dose. These alternatives may reflect different modes of interaction between pathogens and host.
authors.affiliation: National Institute for Public Health and the Environment, Bilthoven, The Netherlands.
authors.forename: P F
authors.initials: PF
authors.lastname: Teunis
authors.forename: N J
authors.initials: NJ
authors.lastname: Nagelkerke
authors.forename: C N
authors.initials: CN
authors.lastname: Haas
mesh_terms: D000818:Animals; D002169:Campylobacter Infections / Q000209:etiology; D003457:Cryptosporidiosis / Q000209:etiology; D005516:Food Microbiology; D016266:Food Parasitology; D005517:Foodborne Diseases / Q000209:etiology* / Q000382:microbiology / Q000469:parasitology; D005759:Gastroenteritis / Q000209:etiology* / Q000382:microbiology / Q000469:parasitology; D006801:Humans; D008954:Models, Biological; D016012:Poisson Distribution; D018570:Risk Assessment; D012478:Salmonella Food Poisoning / Q000209:etiology; D014867:Water / Q000469:parasitology; D014871:Water Microbiology
chemical_list: D014867:Water