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Tackling One Health from a multi-disciplinary perspective, this book offers in-depth insight into how our health and the health of every living creature and our ecosystem are all inextricably connected. * Presents critical population health topics, written by an international group of experts * Addresses the technical aspects of the subject * Offers potential policy solutions to help mitigate current threats and prevent additional threats from occurring
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Cover
Title Page
List of Contributors
Foreword
Foreword
Preface
Reference
Section 1: The Science of One Health
1 Epidemiology
1.1 Introduction
1.2 Enhancing Our Understanding of Health and Disease
1.3 From Understanding Epidemiology to Public Policy
1.4 Examples of the Benefits of Using a One Health Approach
References
2 Health Impacts in a Changing Climate
2.1 Introduction
2.2 Our Changing Climate
2.3 The Basis for a Human Cause for Climate Change
2.4 Twenty‐first Century Projections of Climate Change
2.5 Climate and Health
2.6 Summary and a Look Forward
References
3 Food Safety and Security
3.1 Evolution of Food Production
3.2 Foodborne Illness
3.3 A One Health Approach to Foodborne Illness Detection and Response
3.4 Antibiotic Resistance and Food Safety
3.5 Zoonotic Disease and Foodborne Pathogens
3.6 Outbreak Response Communication
References
4 Water Security in a Changing World
4.1 Introduction
4.2 Waterborne Pathogens and Contaminants: Technologies for Drinking Water Treatment and Management of Water Safety
4.3 The Water/Energy/Food Nexus: Mitigating Global Risks
Acknowledgments
References
5 One Toxicology, One Health, One Planet
5.1 Introduction
5.2 Key Concepts
5.3 Ecotoxicology and Human Exposures
5.4 Toxicological Risk Assessment and One Health
5.5 Conclusions
References
6 Biodiversity and Health
6.1 Introduction
6.2 Connectivity
6.3 Grand Challenges, Development Goals, Global Health Security, and Ecosystem Health
6.4 Conclusions and a Way Forward
References
7 Emerging Infectious Diseases
7.1 Introduction
7.2 Rabies
7.3 Avian Influenza
7.4 Zika Virus
7.5 Ebola Virus Disease (EVD)
7.6 Summary
Acknowledgments
References
8 Reigning Cats and Dogs
8.1 Introduction
8.2 Benefits and Hazards of Human‐Pet Relationships
8.3 Interactions Among Humans, Pets, and the Environment
8.4 Conclusion
Disclaimer
References
9 Zoological Institutions and One Health
9.1 Introduction
9.2 Zoos, Aquariums, and Field Conservation
9.3 Zoos, Aquariums, and the Care of Animals
9.4 Social Aspects of Zoos and Aquariums
9.5 Zoonotic Disease Challenges: Protecting Visitors, Staff, and Animals
9.6 Case Studies in One Health from Zoological Institutions
9.7 Conclusion
References
Section 2: Four Perspectives on One Health Policy
10 One Health Leadership and Policy
10.1 Introduction and Definitions
10.2 Grand Challenges in Health (aka “Wicked Problems”)
10.3 Implications of Grand Challenges for One Health Leadership
10.4 Critical Competencies for One Health Leadership
10.5 Policy‐Making with One Health in Mind
10.6 Integrating One Health Leadership Approaches in Hierarchical Organizations
10.7 Demonstrating One Health Leadership and Policy in Action
10.8 Case Study 1: National One Health Policy Development in Cameroon and Rwanda
10.9 Case Study 2: The Campaign for Global Elimination of Dog‐Mediated Human Rabies
10.10 Case Study 3: Antimicrobial Resistance – USA
References
11 Implementing One Health
11.1 Financing One Health Initiatives
11.2 Conclusion
References
12 The Social Cost of Carbon
12.1 Introduction
12.2 Some Context on Cost‐Benefit Analyses
12.3 The Social Cost of Carbon (SCC)
12.4 Current Challenges to Reducing and Mitigating the Effects of Climate Change
References
13 Complex Problems, Progressive Policy Solutions, and One Health
13.1 One Health as Prevention
13.2 Translating Science: Risk Communication and Science Literacy
13.3 The Economics of One Health
13.4 From Here to There
References
Section 3: Conclusion
14 The Long and Winding Road
14.1 One Health: Many Facets, All Interrelated
14.2 One Health Policy Development
References
Index
End User License Agreement
Chapter 01
Table 1.1 Incubation periods of selected exposures and diseases.
Table 1.2 Important anthroponoses, zoonoses, and sapronoses.
Table 1.3 Illustration of savings in US dollars as a result of applying a One Health approach to a brucellosis outbreak investigation and response in Western Uganda 2013.
Chapter 04
Table 4.1 Selected waterborne pathogens and their characteristics.
Table 4.2 Water usage per electricity generation method.
Chapter 06
Table 6.1 Millennium and Sustainable Development Goals compared.
Chapter 08
Table 8.1 Epidemiologic characteristics of various infectious organisms with established potential for transmission from dogs, cats, birds, and rabbits to humans.
Table 8.2 Centers for Disease Control and Prevention (CDC) rabies post‐exposure prophylaxis (PEP) guidelines for various animal bites.
Table 8.3 World Health Organization (WHO) rabies post‐exposure prophylaxis (PEP) guidelines.
Table 8.4 Reported cases of infectious diseases in companion animals with molecular or other strong evidence to support humans as the source.
Chapter 09
Table 9.1 Summary of serologic and clinical data from animals sampled during the 1999 West Nile virus (WNV) outbreak at the Bronx Zoo, New York.
Table 9.2 West Nile virus disease cases reported to ArboNET, USA, 2000.
Chapter 14
Table 14.1 Timeline of environmental milestones – USA.
Table 14.2 Summary of international environmental legislation.
Chapter 01
Figure 1.1 The One Health triad.
Figure 1.2 The “epidemiologic triad” of infectious disease summarizes the factors that influence an infection, and the measures you might take to combat the infection.
Figure 1.3 Infection modeling: the SIR model.
Susceptible
nodes – have not been infected yet and are therefore available for infection. They do not infect other nodes.
Infectious
nodes – have been infected and infect other nodes with a certain probability.
Removed
(recovered) nodes – have gone through an infectious period and cannot take part in further infection (neither actively nor passively).
Figure 1.4 Necessary, sufficient, and component causes. The individual factors are called component causes. The complete pie (or causal pathway) is called a sufficient cause. A disease may have more than one sufficient cause. A component that appears in every pie or pathway is called a necessary cause, because without it, disease does not occur.
Figure 1.5 Natural history of disease timeline.
Figure 1.6 The steps for confirming that a pathogen is the cause of a particular disease using Koch’s postulates.
Figure 1.7 Ecosocial framework. An heuristic framework for the social epidemiology of human immunodeficiency virus (HIV)/acquired immunodeficiency syndrome (AIDS). The dotted lines separating the levels illustrate the porous nature of the distinctions made between levels of analysis. In reality, there are extensive linkages between factors at all levels that give rise to observed epidemic patterns. STI, sexually transmitted infection.
Figure 1.8 Economic impact of disease.
Figure 1.9 Leptospirosis reservoirs and transmission to humans.
Figure 1.10 A Nenets herder in a malitsa with his reindeer‐drawn sledge on the Yamal Peninsula in the Siberian Arctic in winter. Yamal Peninsula, Yamalo‐Nenets, Russia (2014).
Figure 1.11 Role of epidemiology research in prevention and control of infectious disease. The black arrows illustrate a generalized infectious cycle; the shaded arrows indicate points where infectious diseases can be prevented. (1) A host is infected by the reservoir or a vector for the pathogen. This individual may infect (2) other hosts in a population or (3) new vectors. (4) The pathogen also may cycle between the vector and a reservoir.
Figure 1.12 Districts in Western Uganda where brucellosis outbreak investigations were conducted 2013.
Figure 1.13 County map of the lower peninsula of Michigan depicting locations where
Mycobacterium bovis
‐infected deer and
M. bovis
‐affected beef and dairy herds have been identified between 1975 and 2016.
Chapter 02
Figure 2.1 Changes in observed globally averaged temperature since 1880. Red bars show temperatures above the long‐term average, and blue bars indicate temperatures below the long‐term average. The black line shows the changes in atmospheric carbon dioxide (CO
2
) concentration in parts per million (ppm) over the same time period (Melillo et al., 2014; temperature data from NOAA National Climate Data Center).
Figure 2.2 Surface temperature trends for the period 1901–2012 (top) and 1979–2012 (bottom) from NOAA National Climate Data Center’s surface temperature product. Updated from Vose et al. (2012).
Figure 2.3 Observed changes, as analyzed by many independent groups in different ways, of a range of climate indicators. All of these are in fact changing as expected in a warming world. This diagram is from http://nca2014.globalchange.gov/report/appendices/climate‐science‐supplement.
Figure 2.4 Global precipitation trends for the period 1901–2012 (top) and 1979–2012 (bottom). Based on data from NOAA NCDC.
Figure 2.5 The number of severe loss events from natural catastrophes per year since 1980 through 2015 as evaluated by Munich Re. Overall losses totaled $90 billion dollars (2015 was not a high year in terms of total costs; the previous year was $110 billion), of which roughly $27 billion was insured. In 2015, natural catastrophes claimed 23 000 lives (average over the last 30 years was 54 000).
Figure 2.6 Percent increases in the amount of precipitation falling in very heavy events (defined as the heaviest 1% of all daily events) from 1958 to 2012 for each region of the continental USA. These trends are larger than natural variations for the Northeast, Midwest, Puerto Rico, Southeast, Great Plains, and Alaska. The trends are not larger than natural variations for the Southwest, Hawaii, and the Northwest. The changes shown in this figure are calculated from the beginning and end points of the trends for 1958 to 2012.
Figure 2.7 Observed global average changes (black line), and model simulations using only changes in natural factors (solar and volcanic) in green, and with the addition of human‐induced emissions (blue). Climate changes since 1950 cannot be explained by natural factors or variability, and can only be explained by human factors.
Figure 2.8 Multi‐model simulated time series from 1950 to 2100 for the change in global annual mean surface temperature relative to 1986–2005 for a range of future emissions scenarios that account for the uncertainty in future emissions from human activities – as analyzed with the 20+ models from around the world used in the most recent international assessment (IPCC, 2013). The mean and associated uncertainties (1.64 standard deviations (5–95%) across the distribution of individual models (shading)) based on the averaged over 2081−2100 are given for all of the RCP scenarios as colored vertical bars. The numbers of models used to calculate the multi‐model mean is indicated.
Figure 2.9 Projected change in average annual temperature over the period 2071–2099 (compared to the period 1971–2000) under a low scenario that assumes rapid reductions in emissions and concentrations of heat‐trapping gases (RCP 2.6), and a higher scenario that assumes continued increases in emissions (RCP 8.5).
Figure 2.10 Projected change in average annual precipitation over the period 2071–2099 (compared to the period 1971–2000) under a low scenario that assumes rapid reductions in emissions and concentrations of heat‐trapping gasses (RCP 2.6), and a higher scenario that assumes continued increases in emissions (RCP 8.5). Hatched areas indicate confidence that the projected changes are significant and consistent among models. White areas indicate that the changes are not projected to be larger than could be expected from natural variability. In general, northern parts of the USA (especially the Northeast and Alaska) are projected to receive more precipitation, while southern parts (especially the Southwest) are projected to receive less.
Figure 2.11 Estimated, observed, and projected amounts of global sea level rise from 1800 to 2100, relative to the year 2000. Estimates from proxy data (e.g., based on sediment records) are shown in red (1800–1890, pink band shows uncertainty), tide gauge data in blue for 1880–2009 (Church and White, 2011; Church et al., 2011), and satellite observations are shown in green from 1993 to 2012 (Nerem et al., 2010). The future scenarios range from 0.66 feet (0.20 m) to 6.6 feet (2 m) in 2100 (Parris et al., 2012). These scenarios are not based on climate model simulations, but rather reflect the range of possible scenarios based on scientific studies. The orange line at right shows the currently projected range of sea level rise of 1 to 4 feet (0.3–1.22 m) by 2100, which falls within the larger risk‐based scenario range. The large projected range reflects uncertainty about how glaciers and ice sheets will react to the warming ocean, the warming atmosphere, and changing winds and currents. As seen in the observations, there are year‐to‐year variations in the trend.
Figure 2.12 The inner circle represents the physical environment. The first ring represents the four primary manifestations of climate change in the physical environment (climate drivers): increasing carbon dioxide concentrations in the atmosphere (yellow), rising temperatures (red), rising sea levels (blue), and more extreme weather (green). The four climate drivers can act through natural and human systems to cause conditions listed in the second ring, such as changes in vector ecology, extreme heat, and changes in water and food supply. Surrounding the second ring are the types of health effects that may result from the conditions listed in the ring.
Figure 2.13 Ragweed pollen season length has increased in central North America between 1995 and 2011 by as much as 11 to 27 days in parts of the USA and Canada in response to rising temperatures. Increases in the length of this allergenic pollen season are correlated with increases in the number of days before the first frost. As shown in the figure, the largest increases have been observed in northern cities.
Figure 2.14 Heavy downpours, which are increasing in much of the USA, have contributed to increases in heavy flood events. The figure illustrates how humans can become exposed to waterborne diseases, which typically arise in the weeks following inundation. Human exposures to waterborne diseases can occur via drinking water, as well as recreational waters.
Chapter 03
Figure 3.1 A brief depiction of the global food production chain.
Figure 3.2 Food production chain with potential points for food safety interventions.
Figure 3.3 Burden of illness pyramid: A model for understanding foodborne disease reporting.
Figure 3.4 Examples of how consumers can practice good food safety techniques.
Figure 3.5 Three legs of evidence used in outbreak investigations to determine food vehicles.
Figure 3.6 PulseNet timeline.
Figure 3.7 Pulsed‐field gel electrophoresis (PFGE) workflow.
Figure 3.8 Whole genome sequencing (WGS) workflow.
Figure 3.9 Some examples of how antibiotic resistance can spread.
Figure 3.10 Antibiotic resistance from farm to fork.
Chapter 04
Figure 4.1 Pore size (dashed lines) and range of removal capacity (solid lines) of various filtration methods and general size range of microbial particles (dotted lines).
Figure 4.2 Schematic illustration of the water supply system from raw water source to water consumer (in the middle) combined with the hazards and risk factors (arrow boxes downwards) and risk management options (arrow boxes upwards). Hazards and risk factors may have direct or indirect impacts on drinking water safety and increase the risk consequences and severity. Risk management includes actions that intend to reduce and manage the hazards and risk factors. Steps 0–4 of the Water Safety Plan (WSP) represent fundamental parts of the WSP taking into account the whole water supply system from the raw water to the water consumer.
Figure 4.3 Incidence of drought within the state of Illinois.
Figure 4.4 Recharge and withdrawals from aquifers across the western USA. HPA, High Plains aquifers.
Figure 4.5 Annual growth in electricity consumption (GEC) and nominal gross domestic product (GDP) for India.
Figure 4.6 Relationship between energy consumption and gross domestic product (GDP) for the USA.
Figure 4.7 Renewable infrastructure trends across Europe. (a) Proportion of electricity generated from renewable sources, 2014 (% of gross electricity consumption). (b) Electricity generated from renewable energy sources, EU‐28, 2004–14 YB16.
Chapter 05
Figure 5.1 Rachel Carson and the jacket of her most famous and impactful book.
Figure 5.2 Theo Colborn and the jacket of
Our Stolen Future
.
Figure 5.3 Toxicology in the context of One Health.
Figure 5.4 Different types of dose‐response relationships.
Figure 5.5 Developmental periods: pre‐organogenesis, embryonic, and fetal.
Figure 5.6 Mercury biogeochemical cycle.
Figure 5.7 A radiographic image of a bald eagle showing the presence of two radio‐opaque lead bullet fragments in the gastrointestinal tract of the bird.
Figure 5.8 Lesions in the hippocampus of a domoic acid‐poisoned sea lion (left) as compared to a normal sea lion (right).
Figure 5.9
Anabaena
, a commonly encountered toxigenic genus of cyanobacteria. Upper right, left, and middle: Photos of bloom materials in ponds where swine died after drinking the contaminated water. Lower left and right: Microscopic views of chains of
Anabaena
cells; the lower right image is of chains of
Anabaena
with nitrogen‐fixing heterocyst (clear cell with two “dots”) and spore (large cell).
Figure 5.10 Top right: A wind‐concentrated bloom of
Microcystis
along the shoreline of a pond in a heavily farmed area of central Illinois. Lower right: Microscopic view of thousands of cells of
Microcystis
. The colonies of cells are often surrounded by a clear coating. Upper middle: Histological section of liver showing early changes due to microcystin poisoning (initial separation of hepatocytes from one another). Lower middle: Histological section of liver showing massive separation of hepatocytes and intrahepatic hemorrhage. Upper left: hepatocytes lost from the damaged liver in capillaries of the lung. Lower left: Transmission electron photomicrograph of liver altered by microcystin poisoning, including damage to hepatocytes and endothelial cells, and red blood cells that have escaped from the damaged sinusoids.
Figure 5.11 Life cycle of
Schistosoma mansoni
in humans and potential changes in the environment that may increase the extent of harm experienced.
Chapter 06
Figure 6.1 Ecosystem services.
Figure 6.2 Synergistic effects of ecosystem stressors.
Chapter 08
Figure 8.1 Examples of the relationships among humans, companion animals, and the environment. Humans can share close contact with pets in much the same way they do with their fellows, supporting each other (e,j,k), eating together (c), sleeping together (g), and sharing kisses (a). When appropriate pet care is provided and hygiene is practiced, human and pet health can thrive. However, this close contact provides opportunities for contamination of indoor and outdoor environments and pathogen sharing (b,d,f). In the presence of negligence (i) or animal or interpersonal violence (h), humans and pets can also share suffering.
Figure 8.2 Elderly man hugging black dog.: A dog was suspected to have acquired a fatal MRSA infection through licking the hand of her elderly owner, who had been previously hospitalized for MRSA cellulitis.
Figure 8.3 Child kissing cat. A cat was suspected of having acquired a fatal H1N1 influenza A infection following close contact with an infected child.
Figure 8.4 Younger man with collared dog. Prison dog‐training programs offer inmates unconditional love, skills, and a sense of compassion and purpose. In return, hard‐to‐adopt shelter dogs get a new shot at finding a forever home and enriching the lives of others.
Chapter 09
Figure 9.1 Timeline of West Nile virus (WNV) outbreak in New York, 1999.
Figure 9.2 West Nile virus neuroinvasive disease incidence reported to ArboNET, by state, USA, 2002.
Chapter 10
Figure 10.1 Examples of how antibiotic resistance spreads.
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Edited by John A. Herrmann and Yvette J. Johnson‐Walker
University of Illinois, IL, USA
This edition first published 2018© 2018 John Wiley & Sons, Inc.
Chapter 3 is from public domain.
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Limit of Liability/Disclaimer of WarrantyThe contents of this work are intended to further general scientific research, understanding, and discussion only and are not intended and should not be relied upon as recommending or promoting scientific method, diagnosis, or treatment by physicians for any particular patient. In view of ongoing research, equipment modifications, changes in governmental regulations, and the constant flow of information relating to the use of medicines, equipment, and devices, the reader is urged to review and evaluate the information provided in the package insert or instructions for each medicine, equipment, or device for, among other things, any changes in the instructions or indication of usage and for added warnings and precautions. While the publisher and authors have used their best efforts in preparing this work, they make no representations or warranties with respect to the accuracy or completeness of the contents of this work and specifically disclaim all warranties, including without limitation any implied warranties of merchantability or fitness for a particular purpose. No warranty may be created or extended by sales representatives, written sales materials or promotional statements for this work. The fact that an organization, website, or product is referred to in this work as a citation and/or potential source of further information does not mean that the publisher and authors endorse the information or services the organization, website, or product may provide or recommendations it may make. This work is sold with the understanding that the publisher is not engaged in rendering professional services. The advice and strategies contained herein may not be suitable for your situation. You should consult with a specialist where appropriate. Further, readers should be aware that websites listed in this work may have changed or disappeared between when this work was written and when it is read. Neither the publisher nor authors shall be liable for any loss of profit or any other commercial damages, including but not limited to special, incidental, consequential, or other damages.
Library of Congress Cataloging‐in‐Publication Data
9781119194491 [paperback]
Cover design: WileyCover image: Courtesy of John Herrmann
For Wanda, who always knew the way; and for Anne and Kate, who are my guideposts.
J.A. Herrmann
For Mom, Lauren, and Lamar – my shelter from the storm; and for Ikenna, Ndidi, and Amaya – my windows of hope.
Y.J. Johnson‐Walker
Jonathan D. Alpern, MDInfectious Disease FellowDepartment of Medicine, Division of Infectious Diseases & International MedicineSchool of MedicineUniversity of MinnesotaMinneapolis, Minnesota, USA
Casey Barton Behravesh, MS, DVM, DrPH, DACVPMCaptain, US Public Health ServiceDirector, One Health OfficeNational Center for Emerging and Zoonotic Infectious DiseasesCenters for Disease Control and PreventionAtlanta, Georgia, USA
Val R. Beasley, DVM, PhD, Diplomate ABVTProfessor of Veterinary, Wildlife, and Ecological ToxicologyDepartment of Veterinary and Biomedical SciencesCollege of Agricultural SciencesThe Pennsylvania State UniversityUniversity Park, Pennsylvania, USA
Matteo Convertino, PhD, PEAssistant ProfessorDivision of Environmental Health Sciences & PH InformaticsSchool of Public HealthUniversity of MinnesotaMinneapolis, Minnesota, USA
Meggan Craft, PhDAssistant Professor of Disease EcologyDepartment of Veterinary Population MedicineCollege of Veterinary MedicineUniversity of MinnesotaMinneapolis, Minnesota, USA
William J. Craven, JDChief ConsultantCalifornia State SenateSacramento, California, USA
Timur Durrani, MD, MPH, MBACo‐Director of the Western States Pediatric Environmental Health Specialty UnitAssistant Clinical ProfessorUniversity of California at San Francisco School of MedicineSan Francisco, California, USA
Robert V. Ellis, MD, FAAFPAssociate ProfessorUniversity of Cincinnati College of MedicineCincinnati, Ohio, USA
Thomas R. Gillespie, PhDAssociate ProfessorDepartments of Environmental Sciences & Environmental HealthEmory University & Rollins School of Public HealthMath and Science CenterGeorgia, USA
Marja‐Liisa Hänninen, DVMProfessor EmeritusDepartment of Food Hygiene and Environmental HealthUniversity of HelsinkiHelsinki, Finland
John A. Herrmann, DVM, MPH, DACTClinical Associate ProfessorDirector, DVM/MPH Joint Degree ProgramCenter for One Health IllinoisCollege of Veterinary MedicineUniversity of Illinois at Urbana‐ChampaignUrbana, Illinois, USA;Division AffiliateEpidemiology and BiostatisticsSchool of Public HealthUniversity of Illinois at ChicagoChicago, Illinois, USA
Ronald C. Hershow, MDDirector, Division of Epidemiology and BiostatisticsSchool of Public HealthUniversity of Illinois at ChicagoChicago, Illinois, USA
Ari Hörman, DVM, PhD, MPHDepartment of Food Hygiene and Environmental HealthUniversity of HelsinkiHelsinki, Finland
Daniel Hryhorczuk, MD, MPH, FACMTClinical Professor of Medical ToxicologyDirector, Environmental Health, Center for Global HealthCollege of MedicineUniversity of Illinois at ChicagoChicago, Illinois, USA;Professor EmeritusEnvironmental and Occupational Health Sciences and EpidemiologySchool of Public HealthUniversity of Illinois at ChicagoChicago, Illinois, USA
William D. Hueston, DVM, PhD, Diplomate ACVPM, Epidemiology SpecialtyProfessor EmeritusCollege of Veterinary Medicine and School of Public HealthGlobal Leadership ProgramsCenter for Animal Health and Food SafetyUniversity of MinnesotaMinneapolis, Minnesota, USA
Yvette J. Johnson‐Walker DVM, MS, PhDClinical EpidemiologistCenter for One Health IllinoisUniversity of Illinois Urbana‐ChampaignCollege of Veterinary MedicineUrbana, Illinois, USA
Laura H. Kahn, MD, MPH, MPPResearch ScholarProgram on Science and Global SecurityWoodrow Wilson School of Public and International Affairs Princeton UniversityPrinceton, New Jersey, USA;Co‐Founder, One Health Initiative
John B. Kaneene DVM, MPH, PhD, FAES, FAVESUniversity Distinguished Professor of Epidemiology and Public HealthDirector, Center for Comparative EpidemiologyMichigan State UniversityEast Lansing, Michigan, USA
Shaun Kennedy, PhDPresident and CEOFood Systems InstituteSt Paul, Minnesota;Adjunct Associate ProfessorCollege of Veterinary Medicine, University of MinnesotaMinneapolis, Minnesota, USA
Sandra L. Lefebvre, BA, BSc (Hons Neuroscience), DVM, PhDAssistant Editor, JAVMA and AJVRAmerican Veterinary Medical AssociationSchaumburg, Illinois, USA
Jeffrey M. Levengood, PhDIllinois Natural History Survey, Prairie Research InstituteUniversity of Illinois at Urbana‐ChampaignUrbana, Illinois, USA
Thomas P. Meehan, DVMVice‐President of Veterinary ServicesChicago Zoological SocietyAdjunct Clinical Assistant ProfessorVeterinary Clinical MedicineCollege of Veterinary MedicineBrookfield ZooUniversity of Illinois at Urbana‐ChampaignBrookfield, Illinois, USA
Yvonne Nadler, DVM, MPHProgram ManagerZoo and Aquarium All Hazards Preparedness, Response, and Recovery Fusion CenterSilver Spring, Maryland, USA
Megin Nichols, DVM, MPH, DACVPMLead, Enteric Zoonoses ActivityDivision of Foodborne, Waterborne, and Environmental DiseasesNational Center for Emerging and Zoonotic Infectious Diseases (NCEZID)Centers for Disease Control and PreventionAtlanta, Georgia, USA
Kenneth E. Nusbaum, DVM, PhDProfessor EmeritusCollege of Veterinary MedicineAuburn UniversityAuburn, Alabama, USA
Kevin O’Brien, PhDDirectorIllinois Sustainable Technology Center Prairie Research InstituteUniversity of Illinois at Urbana‐ChampaignUrbana, Illinois, USA
Robert H. Poppenga, DVM, PhD, DABVTProfessorCAHFS Toxicology LaboratorySchool of Veterinary MedicineUniversity of CaliforniaWest Health Sciences DriveDavis, California, USA
Cheryl Robertson, PhD, MPH, RN, FAANAssociate ProfessorChair, Population Health and Systems Cooperative UnitSchool of NursingUniversity of MinnesotaMinneapolis, Minnesota, USA
Innocent B. Rwego, BVM, MSc, PhDAssistant ProfessorDepartment of Veterinary Population MedicineCollege of Veterinary MedicineUniversity of MinnesotaMinneapolis, Minnesota, USA;Senior Technical Lead for AfricaUSAID One Health Workforce ProjectUniversity of Minnesota‐Makerere University Uganda HubKampala, Uganda
Christopher A. Shaffer, PhDAssistant ProfessorDepartment of AnthropologyGrand Valley State UniversityAllendale, Michigan, USA
William Stauffer, MD, MSPH, FASTMHProfessorDepartment of Medicine, Division of Infectious Diseases & International MedicineDepartment of Pediatrics, Infectious DiseasesSchool of Medicine and Public HealthUniversity of MinnesotaMinneapolis, Minnesota, USA
Lauren Stevenson, MHSAssessment EpidemiologistDivision of Foodborne, Waterborne, and Environmental DiseasesNational Center for Emerging and Zoonotic Infectious DiseasesCenters for Disease Control and Prevention,Atlanta, Georgia, USA
Robert V. Tauxe, MD, MPHDirectorDivision of Foodborne, Waterborne, and Environmental DiseasesNational Center for Emerging and Zoonotic Infectious DiseasesCenters for Disease Control and PreventionAtlanta, Georgia, USA
Dominic A. Travis, DVM, MSAssociate ProfessorDivision of Ecosystem HealthDepartment of Veterinary Population MedicineCollege of Veterinary MedicineUniversity of MinnesotaMinneapolis, Minnesota, USA
Ed G.M. van Klink, DVM, PhD, Dipl. ECVPH, MRCVSSenior Lecturer in Veterinary Public HealthSchool of Veterinary ScienceUniversity of BristolLower LangfordBristol, United Kingdom;Wageningen Bioveterinary ResearchLelystad, The Netherlands
Donald J. Wuebbles, PhDHarry E. Preble Endowed Professor of Atmospheric SciencesDepartment of Atmospheric SciencesUniversity of IllinoisUrbana, Illinois, USA
We encourage you to set aside time to read Beyond One Health: From Recognition to Results. We hope that you will be as inspired by its contents as we are.
One Health is one of the great innovations of our time. It is an idea, a concept, a way of thinking and working, and a means to organize action. One Health starts from a recognition that 75% of the new infections affecting humans come from animals. The risks of animal diseases can be decreased through proper attention to livestock health in livestock production: the One Health approach guides efforts to intensify production. It recognizes the benefits of food systems that are sensitive to nutrition and the threats posed by infections that are resistant to antimicrobial therapies.
The One Health idea came to life in 2004 as scientists considered how best to tackle diseases that move between human, domestic animal, and wildlife populations. It reflected experiences with the Ebola virus disease, avian influenza, and chronic wasting disease. It is set out as the Manhattan principles (https://www.cdc.gov/onehealth/pdfs/manhattan/twelve_manhattan_principles.pdf) for One World, One Health.1 It is an international, interdisciplinary approach for tackling threats to the health of life on Earth. It has practical application for reducing risks of unsafe foods and diseases that move from animals to humans.
One Health connects science and systems to the needs of society. It has matured into a new way of thinking and working and contributes to the health of both humans and animals. It links several disciplines that focus on health. It helps professionals to see their work differently and to do it with new purpose. It stimulates integration when remaining separate is less effective. One Health frames how we speak and act: it encourages us to focus on the interfaces between human, animal, and environmental systems. It helps us make sense of multiple interacting determinants of illness. It helps us to better reduce risk and prepare for threats.
Many of us with coordination responsibilities have found that One Health makes our joint working more effective and efficient. It makes sense on the farm, in the factory, and at home, encouraging us to prevent costly outbreaks.
More recently, One Health has helped with restructuring institutions and transforming education. It helped drive collaboration between the World Health Organization (WHO), the World Organisation for Animal Health (OIE), and the Food and Agriculture Organization of the United Nations (FAO). It stimulated new academic departments and degree programmes. It provided a basis for local and national governments to combine animal, human, and environmental health programs, and to reap economic benefits.
Beyond One Health: from Recognition to Results offers us an update on One Health topics from the perspectives of different professional and academic disciplines. It includes an analysis of different threats to people and planet (including zoonoses and climate change), the epidemiology that underlies One Health, as well as the evidence base for different One Health policies and their benefits. It shows how One Health is best approached from a systems perspective and explains the importance of good leadership in making One Health a reality.
If we want to learn how One Health can best be applied in practice, we should study its use in different situations. In this book, we can see how One Health approaches help when analyzing risk and devising prevention, preparedness, and response strategies; when monitoring the evolution of threats and establishing early warning systems; or when prioritizing actions and coordinating actors during implementation. We can understand how One Health has been used in responses to avian influenza, yellow fever, Zika, Middle East respiratory syndrome (MERS), and Ebola.
When combining animal and environmental health practice, we must be sensitive to variations in motivations, responsibilities, and accountability of practitioners in these disciplines. In our experience, the One Health approach is especially useful when coalitions of actors are being established and a consensus is being built. It should be applied in ways that are sensitive to context, adapted to capabilities of systems (for public, veterinary, and environmental health), and adjusted to ecosystem, economic, and societal realities of interfaces between humans, animals, and nature.
We are starting to see One Health approaches being used to frame analyses of costs, benefits, acceptability, and scalability of different interventions. Academic groups are often asked to provide the evidence base for One Health policies and interventions. Their inputs are most helpful when interdisciplinary research methods are used. This is especially necessary when exploring links among environmental dynamics, disease vectors, pathogens, and human susceptibility.
Enlightened approaches like One Health – which focus on prevention and response from the perspectives of multiple disciplines – are vital to success in achieving the 2030 Agenda for Sustainable Development and in building a common future for all. This book will help you move along that path.
Chadia WannousDavid Nabarro
Chadia Wannous, PhD, is a Public Health professional and expert in prevention, emergency preparedness, and risk reduction for health threats. She previously served in several senior policy advisory positions with the UN.
David Nabarro, MD, is a medical doctor and Adviser on Sustainable Development. He previously served as Special Adviser to the United Nations Secretary‐General.
1
Organized by the Wildlife Conservation Society and hosted by The Rockefeller University (
http://www.oneworldonehealth.org
).
The naturalist and conservationist, John Muir, once stated, “When one tugs at a single thing in nature, he finds that it is attached to the rest of the world.” The interconnectedness that Muir described in the early twentieth century is much more profound today, and much more consequential, regarding our health. The globalization of trade, travel, information, and investments, integrated and consolidated global food systems, urbanization, and a group of anthropogenic drivers that negatively impact our ecosystems, have created a new dynamic and an unprecedented interdependence among the health and well‐being of people, animals, and our environment. The complex construct that describes these three domains of health is termed “One Health” and, indeed, tugging on any one of these domains demonstrates their significant attachments to one another. As a corollary to this axiom, we can no longer focus on health through a single lens or discipline.
Our new twenty‐first century interdependence, including social, economic, political, and biological factors, has created new threats and risks to our health and has produced ecological changes that have fractured our planet. Several decades ago, the concept of One Health re‐emerged from past medical thinking and gained important traction and acceptance. Recently, there have been many articles and books published focusing on One Health but, fortunately and very timely, this book has added special insights and brought together diverse disciplines and thinking to give us a better understanding of One Health in our contemporary lives, with an important and unique emphasis on operationalizing the concept. The book’s authors have substantially improved our understanding of the key themes of One Health, added to our knowledge base, and stressed that new skills and competencies need to be acquired to successfully address the threats to human, animal, and ecosystem health.
The factors and drivers of our interdependent world, and increasingly risky lives, show no signs of abating; rather, they are accelerating. These drivers are leading to the intensification of the human‐animal‐ecosystem interface and causing further ecological damage. One consequence of this reality has been the dramatic increase in zoonotic diseases worldwide over the last few decades, which is thoroughly detailed in several chapters. This book also discusses the serious consequences of the degradation of our water resources and ecosystems, as well as threats to biodiversity and food security, all underpinned by climate change. The authors present evidence that our complex and interconnected world has generated a group of “wicked problems” that demand our attention and resources to resolve. A key feature of “wicked problems” is the recognition that past solutions and practices are not likely to be relevant or effective when applied to today’s unparalleled challenges. A One Health mindset and an ability to work holistically across disciplines need to become the new norm to address complex problems and to take appropriate actions. In addition, we must champion new partnerships and innovations, and learn to effectively lead and manage change.
However, our medical fields continue to become progressively more specialized and, at the same time, progressively more isolated and siloed. While we appreciate the impressive advances in medicine, our health systems are increasingly disease‐oriented and reactive. One Health, on the other hand, stresses disease prevention, shifting interventions closer to the origins of the problem, often in our animals and environment. Beyond One Health:From Recognition to Results argues that improving animal and environmental health can be a very effective and cost‐beneficial public health strategy. As this text points out so well, maintaining and improving health must go beyond a strictly disease‐oriented approach to consider the impact of the environment, social‐economic status, genetics and human behavior, and other social determinants of health, which is truly a One Health perspective. This timely book makes the case that we need to normalize good health through this larger and more comprehensive context.
In differentiating Beyond One Health: From Recognition to Results from past One Health books, this book emphasizes the need to translate new knowledge into practice. We know that this transformation is a difficult and dynamic process that involves synthesis, dissemination, exchange, and finally application of One Health knowledge to the maintenance and improvement of health in all of its domains and dimensions. The book’s authors acknowledge and present compelling evidence that critical gaps exist today between the promise of good health and actual results. The book reiterates that developing and implementing new strategies and polices represent the tactics necessary to support a One Health framework and plan of action. In addition, the authors argue in favor of the growing evidence that One Health thinking can offer a favorable value proposition, demonstrating that maintaining the status quo for our current healthcare delivery and disease response system is no longer acceptable, cost‐effective, or scientifically valid.
While we remember John Muir as an outstanding ecological thinker, we also recognize that he was a very effective political spokesperson who understood the importance of translating science and knowledge into policies in support of conservation. Likewise, we need to move One Health from an abstract concept to a catalyst for new policies and interventions that can change the existing dynamic and improve health outcomes across all the domains of health. We understand that there are three stages of translating knowledge into practice, and this book discusses all three throughout its chapters. Awareness, acceptance, and adoption comprise the sectors of translation and all are integrated throughout the text. The authors also stress an important lesson: as we develop and adopt new strategies and policies, we also must design and carry out processes for outcome measurement and evaluation and continuous improvement for them to remain relevant and effective.
We are indebted to the editors and authors who have successfully built momentum toward a more universal acceptance of One Health and, perhaps even more importantly, have been especially instructive in helping us appreciate the need to enact new policies and shift One Health from theory to effective field implementation. They have reminded us, throughout this text, that One Health is likely just to be relegated to an academic exercise if it is not accompanied by a new value proposition, new policies, and more efficient interventions in the rapidly changing human, animal, and environmental health dynamic. Finally, we are grateful for both the intellectual and practical contributions of the book’s editors and authors and are well advised to use their ideas and examples to better address the threats to our health, in all its dimensions.
Lonnie King, DVM, MS, MPA, DACVPMProfessor and Dean EmeritusCollege of Veterinary MedicineOhio State University
“One Health” has caught on, some 140 years after Virchow coined the term “zoonoses” and said, “between animal and human medicine there are no dividing lines – nor should there be” (Schultz, 2008). The principles of One Health are often assigned singular ownership of that conceptual triad. However, other models, such as the Ecological Model in public health, eco‐social theory, EcoHealth, conservation medicine, ecological medicine, and others, also take the holistic view that individual or population health outcomes are the result of many interrelated exposures, determinants, and contributing factors, and that an understanding of them, and their relatedness to each other, is required to formulate effective public policy designed to improve health.
Much has been written about One Health, its history and importance, especially in the context of emerging infectious diseases. One cannot minimize previous essays and textbooks focused on the need for viewing modern challenges to population health through a One Health lens, or the many peer reviewed journal articles that framed their research findings as examples of the demand for One Health thinking. We also must appreciate the excellent efforts of various national and international groups devoted to promoting One Health concepts and spreading awareness of their importance. However, we are at an inflection point in world events at which it has never been more critical that policy‐makers set aside their ideologies and prejudices and promote science and technology policies that affect health, broadly defined. Those policies must be based on scientific consensus drawn from independent, well‐constructed, repeatable research that is published for all to read and analyzed in well‐respected, peer reviewed journals. We need to get beyond the abstract and actually do. Centuries ago, the German writer and statesman, Johann Wolfgang von Goethe, counseled that knowing and willing to do something is all well and good but eventually we must actually do it.
When we received a request from our publisher to edit a textbook about One Health, we initially declined. There were already four or five excellent books that describe One Health thinking and the challenges associated with it. It was only after we discussed our interest in public policy, and our experiences in the policy formation process, that we came up with the idea to edit a One Health book that is directed at policy solutions. The title of this textbook should be instructive. Our book is intended to serve as a reference for students and professionals in many disciplines, from architecture through urban planning, and not just for those working in traditional healthcare and health‐related fields. The concept of One Health, that human, animal, and ecosystem health are inextricably linked, is an idea that is, at its core, about prevention. One Health may be easy to describe but it is a challenge to operationalize as policy. One Health thinking recognizes the interrelatedness of determinants of health and uses the scientific method to discover how strongly exposures are related to outcomes. Data are tested until they are accepted as fact; those facts can, gradually, after the iterative process of the scientific method, be translated into policy that should be designed to prevent the adverse effects of natural and human‐derived phenomena on an ecosystem and to improve health.
Population growth, climate change, environmental degradation, inconsistent food production and distribution, water resource management, nonparticipatory governance, lack of civil society – all of the many determinants of global health – indicate that we are at a critical point in world history. To make significant improvements in global health, to improve the lives of global societies, we must engage thinkers from virtually all academic and professional fields and develop solutions, in public policy and in individual behaviors, that are effective, efficient, and sustainable. This is true One Health.
So, it is in this context that we offer this collection of critical population health topics, written by an international group of experts, that addresses not only the technical aspects of their topics but also offers potential policy solutions to help mitigate current threats and to prevent additional threats from occurring. Too often, public policy is based on the short‐term benefit for the few at the long‐term cost to the many. Too often, short‐sighted policies defer current costs to future generations.
Schultz, M. (2008). Rudolf Virchow.
Emerging Infectious Diseases
14(9), 1480–1481.
John A. HerrmannYvette J. Johnson‐Walker
Yvette J. Johnson‐Walker1 and John B. Kaneene2
1 University of Illinois Urbana‐Champaign, Urbana, IL, USA
2 Michigan State University, East Lansing, MI, USA
Epidemiology is the study of disease dynamics in populations. It seeks to understand patterns of disease as a means of identifying potential prevention and control measures. It has been described as “an interesting and unique example of cross‐fertilization between social and natural sciences” (Vineis, 2003). The basic principle of epidemiology is that disease is not a random event. Each individual in a population has a unique set of characteristics and exposures (risk factors) that determine his or her probability of disease. Clinical medicine is focused on the health of the individual while epidemiology and public health seek to apply assessment of risk factors at the community level. Understanding how those risk factors impact a community provides public health officials with the tools to develop policies and interventions for disease control and prevention in the community as a whole.
The One Health concept is coherent with the principles of epidemiology because risk factors for many diseases occur at the interface between humans, animals, and the environment. Failure to consider the interactions between them may result in public health policies that fail to effectively control disease and protect the environment. The One Health triad (Figure 1.1) of humans, animals, and the environment is analogous with the other triads that epidemiologists use to describe disease dynamics within a population:
The host, agent, environment triad (
Figure 1.2
) is used to describe the interplay between these three key components of infectious disease transmission. Changes in any of these components alters the probability of disease.
The three states of infectious disease status are illustrated by the susceptible, infected, removed (SIR) triad (
Figure 1.3
).
Outbreaks of disease are characterized in terms of person or animal, place, and time as the first step of identifying the population at risk.
Risk factors for disease causation are categorized as: necessary, sufficient, and component causes (
Figure 1.4
).
Figure 1.1 The One Health triad.
Source: Thompson, 2013. Reproduced with permission of Elsevier.
Figure 1.2 The “epidemiologic triad” of infectious disease summarizes the factors that influence an infection, and the measures you might take to combat the infection.
Source: Used with permission from Ian McDowell (http://www.med.uottawa.ca/SIM/data/Pub_Infectious_e.htm#epi_triad).
Figure 1.3 Infection modeling: the SIR model. Susceptible nodes – have not been infected yet and are therefore available for infection. They do not infect other nodes. Infectious nodes – have been infected and infect other nodes with a certain probability. Removed (recovered) nodes – have gone through an infectious period and cannot take part in further infection (neither actively nor passively).
Source: Used with permission from Michael Jaros (http://mj1.at/articles/infection‐modelling‐the‐sir‐model/).
Figure 1.4 Necessary, sufficient, and component causes. The individual factors are called component causes. The complete pie (or causal pathway) is called a sufficient cause. A disease may have more than one sufficient cause. A component that appears in every pie or pathway is called a necessary cause, because without it, disease does not occur.
Source: Rothman, 1976. Reproduced with permission of Oxford University Press.
The goal of public health policy is to prevent transmission of disease agents to the susceptible segment of the population by controlling and treating disease among the infected and increasing the segment of the population that is removed (recovered or resistant). Identification and isolation of cases, quarantine of the exposed, and vaccination of the susceptible are the primary tools employed by public health practitioners for infectious disease control. Development of effective programs to accomplish these goals requires an understanding of the:
Causes of disease (etiologic agent, pathophysiology, and risk factors.
Impact of the disease on the population (number of cases, ease of transmission, economic and social impact).
Natural course of the disease (reservoirs for the agents of disease, means of introduction of the agent into the population, period of infectivity, severity of disability, length of immunity, and potential for long‐term sequelae) (
Figure 1.5
).
Figure 1.5 Natural history of disease timeline.
Source: CDC, 1992.
The goals of this chapter are to elucidate how epidemiology can 1) provide a tool for understanding the causes, impacts, and course of disease in human and animal populations within various ecosystems, and 2) form the basis for evidence‐based health and environmental policy development.
Epidemiology is unique among biomedical investigative approaches because of the observational nature of many of the study designs. Unlike laboratory studies, the epidemiologist often studies a naturally occurring disease within a free‐living population in which study subjects are not assigned to intervention groups (except in the case of clinical trials). Individuals may have a variety of independent exposures during the study period. Whether studying human or animal populations, the epidemiologist seeks to identify exposures that are associated with the probability of disease using statistical analysis of data from carefully documented exposures and outcomes. However, even if a statistically significant association between an exposure and disease outcome has been identified, that does not necessarily mean that a cause and effect relationship has been established. Much more rigorous standards have been set for establishing a causal relationship between a risk factor and the probability of disease.
Criteria for establishing causation for infectious disease have been described since the nineteenth century. Research by Robert Koch, Friedrich Loeffler, and Jakob Henle resulted in the Koch–Henle postulates published in 1882 (Sakula, 1983; Gradmann, 2014) (Figure 1.6). While this approach is useful when seeking to identify the etiologic agent responsible for an infectious disease, it has many limitations. The simplistic approach of a deterministic model for establishing disease causation is insufficient for identifying risk factors for chronic noninfectious diseases (such as type II diabetes) or even infectious diseases with a multifactorial etiology (such as new variant Creutzfeldt–Jakob disease, or CJD). In more recent years more complex models have been used to establish a causal relationship between a putative risk factor and disease.
Figure 1.6 The steps for confirming that a pathogen is the cause of a particular disease using Koch’s postulates.
Austin Bradford Hill published “The environment and disease: association or causation?” in 1965 (Hill, 1965). The manuscript describes nine criteria necessary for establishing a causal relationship between a risk factor and a disease:
Strength of association:
the greater the magnitude of the association between the risk factor and the outcome, the more likely the relationship is to be causal.
Temporality:
the risk factor must precede the onset of the disease.
Consistency:
the same association should be observed in multiple studies with different populations.
Theoretical plausibility:
the association should be biologically plausible and consistent with the pathophysiology of the disease.
Coherence:
the association should be consistent with what is known about the disease.
Specificity in the causes:
a risk factor should be associated with a single disease or outcome.
Dose‐response relationship:
as the dose of the risk factor is increased the probability and severity of the disease should increase in a linear fashion.
Experimental evidence:
data from
in vitro
studies and animal models should support the causal association between the risk factor and the disease.
Analogy:
similar causal relationships should be known.
The nature of these criteria makes it impossible for a single observational study to establish a causal relationship between an exposure and a disease outcome. The criterion of consistency requires that multiple studies, in different populations, show the same association. The criterion of temporality also requires that the association be demonstrated in prospective studies. Prospective study designs monitor the study population prior to the onset of disease and follow their exposures over time until the disease of interest occurs. However, as we learn more about the complexity of the interactions between hosts and their exposures, limitations of the Bradford Hill Causal Criteria have also been described (Rothman, 2012). Some of Hill’s Causal Criteria have been challenged by known causal associations that are contradictory. Specificity of effect, dose‐response gradient, and coherence are all criteria whose validity has been challenged.
The criterion of specificity fails to acknowledge the potential for a single exposure to cause a multiplicity of pathologic effects. One well‐known example of this is seen with exposure to tobacco smoke, which is associated with lung cancer, chronic obstructive pulmonary disease, heart disease, stroke, asthma, impaired fertility, diabetes, premature/low birthweight babies, blindness, cataracts, age‐related macular degeneration, and cancers of the colon, cervix, liver, stomach, and pancreas (American Lung Association, 2017).
Many disease‐causing exposures fail to produce a linear dose‐response gradient. Goldsmith and Kordysh (1993) reviewed the literature for examples of nonlinear dose‐response relationships and concluded that nonlinear causal relationships are equally as common as linear associations. Their analysis of the literature concluded that dose‐response relationships are often nonlinear when countervailing outcomes are likely. They cautioned against linear extrapolation of dose‐response data to develop policies and regulations for the protection of human populations. Exposures such as ionizing radiation and vitamin toxicity have been reported to produce U‐ or J‐shaped dose‐response curves (May and Bigelow, 2005). Inadequate sample size in the research study, insufficient range in the exposure dosages, and variability in individual susceptibility are all factors that impede the identification of these nonlinear dose‐response causal relationships.
The criterion of coherence doesn’t allow for paradigm shifts in models of disease causation. Identification of new mechanisms of disease pathogenesis may require elucidation of relationships that are not coherent with the current body of knowledge about the disease process. This is illustrated by the work of Marshall and Warren (1984) and their discovery of the role of Helicobacter pylori in the etiology of gastritis and peptic ulcers. Prior to their research, acid production was believed to be the key risk factor for the development of gastritis and peptic ulcers. Gastritis was thought to be a chronic inflammatory disease; the concept that it was actually due to a bacterial infection, was not coherent with the theory of the disease at the time of the findings by Marshall and Warren.
Krieger (1994) describes the transition in epidemiology from a focus on acute and infectious diseases to research focused on chronic disease. These more complex disease etiologies were first described as a “web of causation” in 1960. Multifactorial causes of disease have been framed as host‐agent‐environment models and social determinants of health. The public health application of these models is manifested as identification of the necessary component causes of disease and directing policies and interventions at those causes that are most amenable to alteration (see Figure 1.4).
In summary, epidemiology has evolved from a monocausal (deterministic) model to the multicausal concept of the “web of causation” (Vineis, 2003). The models that seek to describe disease causation continue to evolve. More recently, an “ecosocial framework” has been proposed as a more holistic, comprehensive approach to describing the how and why of disease occurrence (Krieger, 1994) (Figure 1.7
