Viral Infections and Global Change E-Book
140,99 €
Mehr erfahren.
- Herausgeber: John Wiley & Sons
- Kategorie: Wissenschaft und neue Technologien
- Sprache: Englisch
A timely exploration of the impact of global change on the emergence, reemergence, and control of vector-borne and zoonotic viral infections From massively destructive "superstorms" to rapidly rising sea levels, the world media is abuzz with talk of the threats to civilization posed by global warming. But one hazard that is rarely discussed is the dramatic rise in the number and magnitude of tropical virus outbreaks among human populations. One need only consider recent developments, such as the spread of chikungunya across southern Europe and dengue in Singapore, Brazil, and the southern United States, to appreciate the seriousness of that threat. Representing a major addition to the world literature on the subject, Viral Infections and Global Change explores trends of paramount concern globally, regarding the emergence and reemergence of vector-borne and zoonotic viruses. It also provides up-to-date coverage of both the clinical aspects and basic science behind an array of specific emerging and reemerging infections, including everything from West Nile fever and Rift Valley fever to zoonotic hepatitis E and human bunyavirus. Important topics covered include: style="line-height: 25px; margin-left: 15px; margin-top: 0px; font-family: Arial; font-size: 13.333333969116211px;"> * Epidemiology, molecular pathogenesis, and evolutionary mechanisms * Host-pathogen interactions in an array of viral infections * The impact of climate change on historical viral outbreaks * The roles of socioeconomics, human behavior, and animal and human migrations * The growing prevalence of drug and pesticide resistance * The introduction of microbes and vectors through increased transboundary travel * Spillover transmissions and the emergence of viral outbreaks * Detecting and responding to threats from bioterrorism and emerging viral infections * Predictive modeling for emerging viral infections Viral Infections and Global Change is an indispensable resource for research scientists, epidemiologists, and medical and veterinary students working in ecology, environmental management, climatology, neurovirology, virology, and infectious disease.
Sie lesen das E-Book in den Legimi-Apps auf:
Seitenzahl: 1543
Veröffentlichungsjahr: 2013
Ähnliche
CONTENTS
FOREWORD
PREFACE
CONTRIBUTORS
ABOUT THE EDITOR
I GENERAL ASPECTS
1 CLIMATE CHANGE AND VECTOR-BORNE VIRAL DISEASES
1.1 INTRODUCTION
1.2 EPIDEMIOLOGY OF VVD
1.3 ASSOCIATION BETWEEN CLIMATIC VARIABLES AND EMERGING VVD
1.4 INVASION OF NONZOONOTIC VVD TO HUMANS
1.5 IMPLICATIONS AND RECOMMENDATIONS FOR PREVENTION AND CONTROL
REFERENCES
2 IMPACT OF CLIMATE CHANGE ON VECTOR-BORNE ARBOVIRAL EPISYSTEMS
2.1 INTRODUCTION
2.2 THE COMPLEX FACTORS INFLUENCING MOSQUITO-BORNE ARBOVIRUS EPISYSTEMS
2.3 WEST NILE VIRUS
2.4 DENGUE IN FLORIDA
2.5 BLUETONGUE
2.6 CONCLUSIONS
ACKNOWLEDGEMENT
REFERENCES
3 INFLUENCE OF CLIMATE CHANGE ON MOSQUITO DEVELOPMENT AND BLOOD-FEEDING PATTERNS
3.1 INTRODUCTION
3.2 MOSQUITO DEVELOPMENT
3.3 BLOOD-FEEDING PATTERNS
REFERENCES
4 ENVIRONMENTAL PERTURBATIONS THAT INFLUENCE ARBOVIRAL HOST RANGE: INSIGHTS INTO EMERGENCE MECHANISMS
4.1 INTRODUCTION
4.2 THE CHANGING ENVIRONMENT
4.3 DEFORESTATION AND THE EPIZOOTIC EMERGENCE OF VENEZUELAN EQUINE ENCEPHALITIS VIRUS
4.4 RICE, MOSQUITOES, PIGS, AND JAPANESE ENCEPHALITIS VIRUS
4.5 CULEX PIPIENSCOMPLEX, HOUSE SPARROWS, URBANIZATION, AND WEST NILE VIRUS
4.6 URBANIZATION, GLOBAL TRADE, AND THE REEMERGENCE OF CHIKUNGUNYA VIRUS
4.7 CONCLUSIONS
REFERENCES
5 THE SOCIO-ECOLOGY OF VIRAL ZOONOTIC TRANSFER
5.1 INTRODUCTION
5.2 HISTORICAL PERSPECTIVE
5.3 HUMAN–ANIMAL INTERFACE
5.4 SURVEILLANCE
5.5 DEFORESTATION AND FRAGMENTATION
5.6 URBANIZATION
5.7 EXAMPLES
5.8 CONCLUSION
REFERENCES
6 HUMAN BEHAVIOR AND THE EPIDEMIOLOGY OF VIRAL ZOONOSES
6.1 INTRODUCTION
6.2 SOCIETAL CHANGES AND THE EPIDEMIOLOGY OF VIRAL ZOONOSES
6.3 VIRAL ZOONOSES AND HUMAN SOCIETAL VALUES
6.4 HUMAN BEHAVIOR AND THE EPIDEMIOLOGY OF VECTOR-BORNE VIRAL ZOONOSES
6.5 HUMAN BEHAVIOR AND THE EPIDEMIOLOGY OF RESPIRATORY VIRAL ZOONOSES
6.6 HUMAN BEHAVIOR AND THE EPIDEMIOLOGY OF WATERBORNE VIRAL ZOONOSES
6.7 HUMAN BEHAVIOR AND THE EPIDEMIOLOGY OF WILDLIFE-ASSOCIATED VIRAL ZOONOSES
6.8 THE ROLE OF HUMAN BEHAVIOR IN THE CONTROL OF VIRAL ZOONOSES
REFERENCES
7 GLOBAL TRAVEL, TRADE, AND THE SPREAD OF VIRAL INFECTIONS
7.1 INTRODUCTION
7.2 BASIC PRINCIPLES
7.3 AN OVERVIEW OF POPULATION MOBILITY
7.4 THE DYNAMICS OF MODERN POPULATION MOBILITY
7.5 HUMAN POPULATION MOBILITY AND THE SPREAD OF VIRUSES
7.6 THE BIOLOGICAL ASPECTS OF POPULATION MOBILITY AND THE SPREAD OF VIRUSES
7.7 THE DEMOGRAPHIC ASPECTS OF POPULATION MOBILITY AND THE SPREAD OF VIRUSES
7.8 POTENTIAL IMPACT OF CLIMATE CHANGE
7.9 CONCLUSION
REFERENCES
8 EFFECTS OF LAND-USE CHANGES AND AGRICULTURAL PRACTICES ON THE EMERGENCE AND REEMERGENCE OF HUMAN VIRAL DISEASES
8.1 INTRODUCTION
8.2 ECOLOGICAL AND ENVIRONMENTAL CHANGES
8.3 AGRICULTURAL CHANGE
8.4 DEMOGRAPHIC CHANGES
8.5 LAND USE, DISEASE EMERGENCE, AND MULTIFACTORIAL CAUSATION
8.6 CONCLUSION
REFERENCES
9 ANIMAL MIGRATION AND RISK OF SPREAD OF VIRAL INFECTIONS
9.1 INTRODUCTION
9.2 DOES ANIMAL MIGRATION INCREASE RISK OF VIRAL SPREAD?
9.3 EXAMPLES OF MIGRATORY ANIMALS AND SPREAD OF VIRAL DISEASE
9.4 CLIMATE CHANGE EFFECTS ON ANIMAL MIGRATION AND VIRAL ZOONOSES
9.5 SHIFTS IN TIMING OF MIGRATION AND RANGE EXTENTS
9.6 COMBINED EFFECTS OF CLIMATE CHANGE, DISEASE, AND MIGRATION
9.7 CONCLUSIONS AND FUTURE DIRECTIONS
ACKNOWLEDGEMENTS
REFERENCES
10 ILLEGAL ANIMAL AND (BUSH) MEAT TRADE ASSOCIATED RISK OF SPREAD OF VIRAL INFECTIONS
10.1 INTRODUCTION
10.2 SEARCH STRATEGY AND SELECTION CRITERIA
10.3 THE BUSHMEAT TRADE
10.4 BUSHMEAT HUNTING AND EMERGING INFECTIOUS DISEASES
10.5 RISK FACTORS AND MODES OF TRANSMISSION
10.6 CONSERVATION AND WILDLIFE SUSTAINABILITY
10.7 CASE STUDY: THE ROLE OF THE BUSHMEAT TRADE IN THE EVOLUTION OF HIV
10.8 ILLEGAL TRADE OF DOMESTIC ANIMALS AND EXOTIC PETS
10.9 DISCUSSION AND FUTURE DIRECTIONS
10.10 PREVENTION AND CONTROL: FROM SUPPLY AND DEMAND TO HEALTH EDUCATION TECHNIQUES
10.11 NEW TECHNOLOGIES
10.12 COLLABORATION: MULTIDISCIPLINARY ADVANCES AND NEXT STEPS
10.13 CONCLUSION
CONFLICTS OF INTEREST
REFERENCES
11 BIOLOGICAL SIGNIFICANCE OF BATS AS A NATURAL RESERVOIR OF EMERGING VIRUSES
11.1 INTRODUCTION
11.2 BATS AS EXEMPLARS OF BIODIVERSITY
11.3 BATS ARE RESERVOIR HOSTS FOR ZOONOTIC AND EMERGING PATHOGENS
11.4 CONTACT RATE AS A DRIVER FOR EMERGENCE OF BAT-ASSOCIATED ZOONOSES
11.5 POTENTIAL IMPACT OF CLIMATE CHANGE ON VIRUSES TRANSMITTED BY BATS
11.6 CONCLUSIONS
REFERENCES
12 ROLE AND STRATEGIES OF SURVEILLANCE NETWORKS IN HANDLING EMERGING AND REEMERGING VIRAL INFECTIONS
12.1 INTRODUCTION
12.2 GLOBAL TREND OF VIRAL INFECTIOUS AGENTS AND DISEASES
12.3 RECOGNIZED IMPORTANCE OF PUBLIC HEALTH SURVEILLANCE
12.4 DEFINITION AND SCOPE OF PUBLIC HEALTH SURVEILLANCE
12.5 KEY FUNCTIONS AND USES OF DISEASE SURVEILLANCE
12.6 NEW EXPANSION OF SURVEILLANCE BY THE IHR-2005
12.7 EMERGENCE OF NEW GLOBAL SURVEILLANCE NETWORKS
12.8 GLOBAL INFLUENZA SURVEILLANCE AND WHO’S PANDEMIC INFLUENZA PREPAREDNESS FRAMEWORK
12.9 EARLY WARNING SURVEILLANCE SYSTEMS
12.10 INNOVATIVE APPROACHES FOR SURVEILLANCE
12.11 ELECTRONIC AND WEB-BASED INFORMATION PLATFORMS FOR INFORMATION REPORTING, SHARING, AND DISSEMINATION
12.12 REAL-TIME AND NEAR REAL-TIME INFORMATION
12.13 NEW UPDATED STATISTICAL METHODS FOR TRACKING VIRAL AND INFECTIOUS DISEASE OUTBREAKS
12.14 USING PROXY AND COMPILED WEB-BASED INFORMATION FROM DIFFERENT SOURCES
12.15 INCORPORATION OF PUBLIC–PRIVATE PARTNERSHIPS IN SURVEILLANCE ACTIVITIES
12.16 USE OF VOLUNTEER SENTINEL PHYSICIANS
12.17 IMPROVING GUIDELINES AND PROTOCOLS FOR VIRAL SURVEILLANCE
12.18 INCORPORATING HEALTH SITUATION ROOMS OR STRATEGIC COMMAND CENTERS FOR MONITORING, ANALYSIS, AND RESPONSE IN SURVEILLANCE EFFORTS
12.19 CHALLENGES OF VIRAL AND PUBLIC HEALTH SURVEILLANCE
REFERENCES
13 PREDICTIVE MODELING OF EMERGING INFECTIONS
13.1 INTRODUCTION
13.2 TYPES OF MODELS
13.3 REMOTE SENSING AND ITS USE IN DISEASE OUTBREAK PREDICTION
13.4 APPROACHES TO MODELING AND THEIR EVALUATION
13.5 EXAMPLES OF PREDICTION MODELS
13.6 CONCLUSION
REFERENCES
14 DEVELOPMENTS AND CHALLENGES IN DIAGNOSTIC VIROLOGY
14.1 INTRODUCTION
14.2 PREPAREDNESS
14.3 CHALLENGES IN DIAGNOSIS OF EMERGING VIRAL INFECTIONS
14.4 APPROACHES TO THE DIAGNOSIS OF EMERGING VIRAL INFECTIONS
14.5 CONCLUSIONS
ACKNOWLEDGEMENT
REFERENCES
15 ADVANCES IN DETECTING AND RESPONDING TO THREATS FROM BIOTERRORISM AND EMERGING VIRAL INFECTIONS
15.1 INTRODUCTION
15.2 EMERGING, REEMERGING, AND INTENTIONALLY EMERGING DISEASES
15.3 BIOTERRORISM
15.4 VIRUSES AS BIOWEAPONS
15.5 IMPACT OF BIOTECHNOLOGY
15.6 DETERRENCE, RECOGNITION, AND RESPONSE
15.7 PUBLIC HEALTH SURVEILLANCE
15.8 CONCLUSION
REFERENCES
16 MOLECULAR AND EVOLUTIONARY MECHANISMS OF VIRAL EMERGENCE
16.1 INTRODUCTION: BIOSPHERE AND VIROSPHERE DIVERSITIES
16.2 VIRUS VARIATION AS A FACTOR IN VIRAL EMERGENCE: A ROLE OF COMPLEXITY
16.3 HIGH ERROR RATES ORIGINATE QUASISPECIES SWARMS
16.4 EVOLUTIONARY MECHANISMS THAT MAY PARTICIPATE IN VIRAL DISEASE EMERGENCE
16.5 AMPLE GENETIC AND HOST RANGE VARIATIONS OF FMDV: A HUMAN EPIDEMIC TO BE?
16.6 THE ARBOVIRUS HOST ALTERNATIONS: HIGH EXPOSURE TO ENVIRONMENTAL MODIFICATIONS
16.7 ARENAVIRUSES AS AN EMERGING THREAT
16.8 CONCLUSION
ACKNOWLEDGEMENT
REFERENCES
17 DRIVERS OF EMERGENCE AND SOURCES OF FUTURE EMERGING AND REEMERGING VIRAL INFECTIONS
17.1 INTRODUCTION
17.2 PREHISTORIC AND HISTORIC UNFOLDING OF THE DRIVERS OF DISEASE EMERGENCE
17.3 PROXIMAL DRIVERS OF DISEASE EMERGENCE AND SOURCES OF FUTURE EMERGING AND REEMERGING VIRAL INFECTIONS
17.4 FURTHER INSIGHTS FROM THE THEORY OF ISLAND BIOGEOGRAPHY
REFERENCES
18 SPILLOVER TRANSMISSION AND EMERGENCE OF VIRAL OUTBREAKS IN HUMANS
18.1 INTRODUCTION
18.2 MAJOR ANTHROPOGENIC FACTORS RESPONSIBLE FOR SPILLOVER
18.3 MAJOR VIRAL FACTORS PLAYING A ROLE IN SPILLOVER
18.4 INTERMEDIATE HOSTS AND SPECIES BARRIERS IN VIRAL TRANSMISSION
18.5 CONCLUSION
REFERENCES
II SPECIFIC INFECTIONS
19 NEW, EMERGING, AND REEMERGING RESPIRATORY VIRUSES
19.1 INTRODUCTION
19.2 INFLUENZA VIRUSES
19.3 HUMAN METAPNEUMOVIRUS
19.4 HUMAN CORONAVIRUSES: SARS AND NON-SARS
19.5 HUMAN BOCAVIRUS
19.6 KI AND WU POLYOMAVIRUSES
19.7 NIPAH AND HENDRA VIRUSES
19.8 CONCLUSION
19.9 LIST OF ABBREVIATIONS
REFERENCES
20 EMERGENCE OF ZOONOTIC ORTHOPOX VIRUS INFECTIONS
20.1 SMALLPOX, A REPRESENTATIVE ORTHOPOXVIRUS INFECTION: THE ERADICATED NON-ZOONOTIC ORTHOPOXVIRUS
20.2 ZOONOTIC ORTHOPOXVIRUSES
ACKNOWLEDGEMENT
REFERENCES
21 BIOLOGICAL ASPECTS OF THE INTERSPECIES TRANSMISSION OF SELECTED CORONAVIRUSES
21.1 INTRODUCTION
21.2 CORONAVIRUS CLASSIFICATION AND PATHOGENESIS
21.3 NATURAL RESERVOIRS AND EMERGENCE OF NEW CORONAVIRUSES
21.4 ALPHA-, BETA- AND GAMMA CORONAVIRUSES: CROSS-SPECIES TRANSMISSION
21.5 ANTHROPOGENIC FACTORS AND CLIMATE INFLUENCE ON CORONAVIRUS DIVERSITY AND OUTBREAKS
21.6 CONCLUSION
REFERENCES
22 IMPACT OF ENVIRONMENTAL AND SOCIAL FACTORS ON ROSS RIVER VIRUS OUTBREAKS
22.1 INTRODUCTION
22.2 HISTORY OF MOSQUITO-BORNE EPIDEMIC POLYARTHRITIS OUTBREAKS IN AUSTRALIA AND THE PACIFIC
22.3 RRV TRANSMISSION CYCLES HAVE A VARIETY OF ECOLOGIES
22.4 TYPICAL ENVIRONMENTAL DETERMINANTS OF RRV ACTIVITY
22.5 SOCIAL DETERMINANTS OF RRV DISEASE ACTIVITY
22.6 A CONCEPTUAL FRAMEWORK FOR UNDERSTANDING THE INFLUENCE OF ENVIRONMENTAL AND SOCIAL FACTORS ON RRV DISEASE ACTIVITY
22.7 CLIMATE CHANGE AND RRV
22.8 CONCLUSION
ACKNOWLEDGEMENT
REFERENCES
23 INFECTION PATTERNS AND EMERGENCE OF O’NYONG-NYONG VIRUS
23.1 INTRODUCTION
23.2 HISTORY OF OUTBREAKS
23.3 CLINICAL MANIFESTATIONS
23.4 EPIDEMIOLOGY
23.5 FACTORS AFFECTING EMERGENCE
23.6 CONCLUSION
REFERENCES
24 ZOONOTIC HEPATITIS E:
24.1 INTRODUCTION
24.2 HEV BIOLOGY AND CLASSIFICATION
24.3 PATHOGENESIS IN HUMANS
24.4 ANIMAL RESERVOIRS
24.5 ZOONOTIC AND INTERSPECIES TRANSMISSION OF HEV AND HEV-LIKE VIRUSES
24.6 HEV IN THE ENVIRONMENT
24.7 CLIMATE CHANGE AND IMPACT ON HEV EXPOSURE
24.8 PREVENTION
24.9 CONCLUSION
ACKNOWLEDGEMENT
REFERENCES
25 IMPACT OF CLIMATE CHANGE ON OUTBREAKS OF ARENAVIRAL INFECTIONS
25.1 INTRODUCTION
25.2 NATURAL HISTORY OF ARENAVIRUSES
25.3 PREDICTED CLIMATE CHANGES
25.4 ARENAVIRAL DISEASES AND CLIMATE CHANGE
REFERENCES
26 EMERGING AND REEMERGING HUMAN BUNYAVIRUS INFECTIONS AND CLIMATE CHANGE
26.1 INTRODUCTION
26.2 BUNYAVIRIDAEFAMILY
26.3 CLIMATE CHANGE AND BUNYAVIRIDAE: CLIMATIC INFLUENCES ON TRANSMISSION CYCLES AND SUBSEQUENT RISK FOR TRANSMISSION OF BUNYAVIRUSES
26.4 DISEASE SPREAD DUE TO GROWING GEOGRAPHIC DISTRIBUTION OF COMPETENT VECTORS
26.5 USING CLIMATE AS A MEANS FOR OUTBREAK PREDICTION
26.6 FUTURE PROBLEMS
REFERENCES
27 EMERGING TREND OF ASTROVIRUSES, ENTERIC ADENOVIRUSES, AND ROTAVIRUSES IN HUMAN VIRAL GASTROENTERITIS
27.1 INTRODUCTION
27.2 EMERGING TRENDS IN ROTAVIRUSES
27.3 EMERGING TRENDS IN ENTERIC ADENOVIRUSES
27.4 EMERGING TRENDS IN ASTROVIRUSES
REFERENCES
28 EMERGING HUMAN NOROVIRUS INFECTIONS
28.1 INTRODUCTION
28.2 NOROVIRUS EPIDEMIOLOGY
28.3 FEATURES OF NOROVIRUS OUTBREAKS
28.4 CLINICAL FEATURES OF NOROVIRUS INFECTION
28.5 HOST SUSCEPTIBILITY
28.6 EFFECT OF INCREASED SIZE OF IMMUNOCOMPROMISED POPULATION
28.7 EFFECT OF GLOBALIZATION OF THE FOOD MARKET ON NOROVIRUS SPREAD
28.8 EFFECT OF CLIMATE CHANGE
REFERENCES
29 EMERGENCE OF NOVEL VIRUSES (TOSCANA, USUTU) IN POPULATION AND CLIMATE CHANGE
29.1 INTRODUCTION
29.2 TOSV
29.3 USUV
29.4 CONCLUSIONS
ACKNOWLEDGEMENT
REFERENCES
30 BORNA DISEASE VIRUS AND THE SEARCH FOR HUMAN INFECTION
30.1 INTRODUCTION
30.2 LONG-STANDING CONTROVERSY AROUND BDV AS A HUMAN PATHOGEN
30.3 A NEGATIVE IS IMPOSSIBLE TO PROVE, BUT DO WE HAVE ENOUGH EVIDENCE TO STOP LOOKING?
30.4 RECENT IMPROVEMENTS IN TESTING FOR EVIDENCE OF BDV IN HUMAN SAMPLES
30.5 THE POSSIBILITIES FOR CLINICAL EXPRESSION OF HUMAN BDV INFECTION ARE MYRIAD AND ALMOST IMPOSSIBLE TO PREDICT
30.6 EPIDEMIOLOGY: THE “NEW” FRONTIER OF HUMAN BDV STUDIES?
30.7 WHERE DO WE GO FROM HERE?
ACKNOWLEDGEMENT
REFERENCES
31 TICK-TRANSMITTED VIRUSES AND CLIMATE CHANGE
31.1 INTRODUCTION
31.2 TICKS IN NATURE
31.3 FAMILYFLAVIVIRIDAE
31.4 FAMILY BUNYAVIRIDAE
31.5 FAMILY REOVIRIDAE
31.6 FAMILY ORTHOMYXOVIRIDAE
31.7 OTHER TICK-TRANSMITTED VIRUSES
31.8 CONCLUSIONS
ACKNOWLEDGEMENTS
REFERENCES
32 THE TICK–VIRUS INTERFACE
32.1 INTRODUCTION
32.2 VIRUSES WITHIN THE TICK VECTOR
32.3 SALIVA-ASSISTED TRANSMISSION
32.4 SUMMARY AND FUTURE DIRECTIONS
ACKNOWLEDGEMENTS
REFERENCES
SUPPLEMENTAL IMAGES
INDEX
Cover Design: WileyCover Images: Vitruvian man, © iStockphoto.com/Mads Abildgaard; virus image, © iStockphoto.com/Baris Simsek; mosquito, © iStockphoto.com/Antagain; globe, © iStockphoto.com/Anton Balazh
Copyright © 2014 by John Wiley & Sons, Inc. All rights reserved.
Published by John Wiley & Sons, Inc., Hoboken, New Jersey.
Published simultaneously in Canada.
No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, scanning, or otherwise, except as permitted under Section 107 or 108 of the 1976 United States Copyright Act, without either the prior written permission of the Publisher, or authorization through payment of the appropriate per-copy fee to the Copyright Clearance Center, Inc., 222 Rosewood Drive, Danvers, MA 01923, (978) 750–8400, fax (978) 750–4470, or on the web at www.copyright.com. Requests to the Publisher for permission should be addressed to the Permissions Department, John Wiley & Sons, Inc., 111 River Street, Hoboken, NJ 07030, (201) 748–6011, fax (201) 748–6008, or online at http://www.wiley.com/go/permission.
Limit of Liability/Disclaimer of Warranty: While the publisher and author have used their best efforts in preparing this book, they make no representations or warranties with respect to the accuracy or completeness of the contents of this book and specifically disclaim any implied warranties of merchantability or fitness for a particular purpose. No warranty may be created or extended by sales representatives or written sales materials. The advice and strategies contained herein may not be suitable for your situation. You should consult with a professional where appropriate. Neither the publisher nor author shall be liable for any loss of profit or any other commercial damages, including but not limited to special, incidental, consequential, or other damages.
For general information on our other products and services or for technical support, please contact our Customer Care Department within the United States at (800) 762–2974, outside the United States at (317) 572–3993 or fax (317) 572–4002.
Wiley also publishes its books in a variety of electronic formats. Some content that appears in print may not be available in electronic formats. For more information about Wiley products, visit our web site at www.wiley.com.
Library of Congress Cataloging-in-Publication data is available.
ISBN: 978-1-118-29787-2
Printed in Singapore.
10 9 8 7 6 5 4 3 2 1
Dedicated to my Parents
FOREWORD
Tropical viruses, especially vector-borne and zoonotic viruses, contribute a huge although often hidden proportion of the world’s burden of human infectious diseases. Yet despite their importance, these viruses are often severely neglected by the scientific community and global health policy makers. For instance, in the recently released Global Burden of Disease 2010 Study (Murray et al., 2012), only two vector-borne viral diseases (i.e., yellow fever and dengue) and one zoonotic viral infection (i.e., rabies) are listed by name. Together, dengue, yellow fever, and rabies cause roughly 40,000 deaths annually (Lozano et al., 2012), but the actual number of deaths and disability resulting from vector-borne and zoonotic viruses is undoubtedly much greater if we also consider other flaviviruses such as Japanese encephalitis and West Nile virus, as well as important alpha viruses such as Ross River, Chikungunya, and O’nyong-nyong virus, among others.
Dr. Sunit Singh’s edited volume on these and related viral infections are a welcome addition to the biomedical literature. He and his colleagues have focused on the tropical viral infections that seldom get adequate attention relative to HIV/AIDS, hepatitis, and influenza, yet these are infections that in many respects may be almost as important. His book emphasizes unique aspects of these viral diseases and their etiologies including the important influence of climate change, as well as nonintuitive elements including socioeconomics, human behavior, travel, and animal and human migrations. The book really gets to the key elements of what helps to promote the emergence of vector-borne and zoonotic viruses and then perpetuate them in an endemic area.
While the viruses and their diseases emphasized in “Viral Infections and Global Change” are typically thought of as the major purview of low- and middle-income countries, we are seeing increasingly their emergence in wealthy countries. Important examples include Chikungunya in southern Europe, dengue in Singapore and coastal Brazil, and most recently a potentially serious dengue threat to the southern United States. Dengue type 2 has emerged in Texas, while dengue type 1 is now in Florida, setting up a possible scenario for dengue hemorrhagic fever one day appearing on the Gulf Coast of the United States (Hotez and Ryan, 2010). These viruses will receive increasing attention in the coming decade and in this sense, the current volume is ahead of the curve!
I wish to congratulate Dr. Singh and his colleagues for this important and timely volume on vector-borne and zoonotic viral infections. It will benefit both medical and graduate students interested in medical virology, as well as senior investigators working in this important but often neglected area!
REFERENCES
1. MurrayCJL, VosT, LozanoR, et al. 2012. Disability-adjusted life years (DALYs) for 291 diseases and injuries in 21 regions, 1990–2010: a systematic analysis for the Global Burden of Disease Study 2010. Lancet380: 2197–2223.
2. LozanoR, NaghaviM, ForemanK, et al. 2012. Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: a systematic analysis for the Global Burden of Disease Study 2010. Lancet380: 2095–2128.
3. HotezPJ, RyanET. 2010. Gulf Coast must remain vigilant for new health threat. Houston Chronicle, July 17, 2010.
PETER HOTEZ, MD, PHD, FASTMH, FAAP Dean, National School of Tropical MedicineProfessor, Pediatrics and Molecular Virology & MicrobiologyHead, Section of Pediatric Tropical MedicineBaylor College of Medicine, Houston, TX, USATexas Children’s Hospital Endowed Chair of Tropical Pediatrics, Houston, TX, USADirector, Sabin Vaccine Institute Texas Children’s Hospital Center for Vaccine Development, Houston, TX, USAPresident, Sabin Vaccine Institute, Washington, DC, USABaker Institute Fellow in Disease and Poverty, Rice University, Houston, TX, USACo-Editor-in-Chief, PLoS Neglected Tropical Diseases
PREFACE
Global changes have important health-related consequences. The emergence and reemergence of viral infections depend on the interaction between global changes and viruses and/or their reservoirs. Increased morbidity and mortality from emerging and reemerging viral outbreaks affect the growth of nations adversely in terms of economy and medical costs. Global changes may affect the health of human beings through the direct impact of changing environment, which may alter the geographic distribution and/or transmission dynamics of viruses. It is important to recognize complex factors that play a role in the distribution and transmission of viruses. Climate change as well as other factors that contribute to the emergence and reemergence of viral outbreaks such as social and demographic factors, geographical variables, global trade and transportation, land-use patterns, animal and human migration, and public health interventions affect the transmission and geographical distribution of viral infections. Population growth, changes in human behavior, livestock and agricultural farming practices, disturb the ecosystem and increase the risk of outbreak of viral infections.
It is important to study the effect of global changes on viral infections, including the ecological and environmental factors and influences of extreme weather fluctuations on viral outbreaks. The ease of international travel facilitates further the spread of viral infections globally. Systematic increases in mean temperature and precipitation, resulting in greater humidity, have facilitated the spread of many vector-borne viral diseases. Most vector-borne viral infections exhibit a distinct seasonal pattern, which suggests their relation with changes in weather conditions. Rainfall, temperature, and other climatic variables affect both the vectors and the viruses in several ways. High temperature can affect (increase or decrease) vector survival rate, depending on the vector, its behavior, ecology, and many other factors. However, viral infections that may be transmitted to humans from animals (zoonoses) continue to circulate in nature. Zoonotic viruses spread from animals to humans by broadening their host range, which increases their speed of transmission. The growing need to feed an increasing population has led to the adoption of intensive farming practices, which has led to close contact between farmworkers and animals. Animals contained in small areas/cages enable viruses to infect large numbers of animals at a single site, which might result into the generation of virulent forms through mutation or recombination processes.
In order to understand the mechanisms of the spread of viruses and strategies to deal with such outbreaks, we must understand the whole ecosystem in which diverse species such as humans, bats, and livestock coexist.
This book has been divided into two parts. Part I focuses on the general aspects of viral infections and global change. Part II deals with specific viral infections and their interrelationships with global change. This book is primarily targeted toward virologists, environmentalists, ecologists, health-care workers, clinicians, microbiologists, and students and research scholars of veterinary medicine, human medicine, or biology wishing to have an overview of the role of global changes and viral infections. I hope that this book will serve as a useful resource for all those who are interested in the field of viral infections. I am honored to have had a large panel of international experts as chapter contributors, whose detailed knowledge has greatly enriched this book.
We have so far conducted our studies related to wildlife, animal, and human viral infections separately. We should focus on a “one-health” approach to understand the complex interactions of the system (humans, wild animals, livestock production, and the environment) as a whole. The influence of global changes on the emergence and reemergence of vector- and non-vector-borne viral infections, the challenges associated with disease surveillance strategies, early detection of viral outbreaks, and international policy implications on human health are all major areas of investigation for infectious disease experts in the future.
SUNIT K. SINGH
CONTRIBUTORS
Assaf Anyamba Universities Space Research Association and Biospheric Science Laboratory, NASA Goddard Space Flight Center, Greenbelt, MD, USA
Steven M. Babin Johns Hopkins University Applied Physics Laboratory, Laurel, MD, USA
Luisa Barzon Department of Molecular Medicine, University of Padova, Padova, Italy
Microbiology and Virology Unit, Padova University Hospital, Padova, Italy
Peng Bi Discipline of Public Health, The University of Adelaide, Adelaide, Australia
Satesh Bidaisee Department of Public Health and Preventive Medicine, School of Medicine, St. George’s University, Grenada, West Indies
Marshall E. Bloom Laboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rocky Mountain Laboratories, Hamilton, MT, USA
Angela M. Bosco-Lauth Colorado State University, Fort Collins, CO, USA
Jérôme Bouquet UMR 1161 Virology, ANSES, Laboratoire de Santé Animale, Maisons-Alfort, France
UMR 1161 Virology, INRA, 94706 Maisons-Alfort, France
UMR 1161 Virology, Ecole Nationale Vétérinaire d’Alfort, Maisons-Alfort, France
Richard A. Bowen Colorado State University, Fort Collins, CO, USA
Aaron C. Brault Division of Vector-Borne Diseases, Centers for Disease Control and Prevention, Fort Collins, CO, USA
Anna L. Buczak Johns Hopkins University Applied Physics Laboratory, Laurel, MD, USA
Kathryn M. Carbone Division of Intramural Research, NIDCR/NIH, Bethesda, MD, USA
Carlos Castillo-Salgado Department of Epidemiology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, USA
Bruno Chomel Department of Population Health and Reproduction, School of Veterinary Medicine, University of California, Davis, CA, USA
James Christopher Clegg Les Mandinaux, Le Grand Madieu, France
Richard Coker Communicable Diseases Policy Research Group (CDPRG), Department of Global Health and Development, London School of Hygiene and Tropical Medicine, London, UK
Faculty of Public Health, Mahidol University, Bangkok, Thailand
Saw Swee Hock School of Public Health, National University of Singapore, Singapore
Daniel Cowley Enteric Virus Group, Murdoch Childrens Research Institute, Royal Children’s Hospital, Parkville, VIC, Australia
Jonathan F. Day Florida Medical Entomology Laboratory, Department of Entomology and Nematology, University of Florida, Vero Beach, FL, USA
Esteban Domingo Centro de Biología Molecular “Severo Ochoa” (CSIC-UAM), Consejo Superior de Investigaciones Científicas (CSIC), Campus de Cantoblanco, Madrid, Spain
Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Barcelon, Spain
Celeste Donato Enteric Virus Group, Murdoch Childrens Research Institute, Royal Children’s Hospital, Parkville, VIC, Australia
Department of Microbiology, La Trobe University, Bundoora, VIC, Australia
Agustín Estrada-Peña Department of Parasitology, Faculty of Veterinary Medicine, Miguel Servet, Zaragoza, Spain
Mari Paz Sánchez-Seco Fariñas Laboratory of Arbovirus and Imported Viral Diseases, Virology Department, National Center of Microbiology, Institute of Health “Carlos III”, Ctra Pozuelo-Majadahonda, Madrid, Spain
Brian H. Feighner Johns Hopkins University Applied Physics Laboratory, Laurel, MD, USA
Kimberly Fornace Veterinary Epidemiology and Public Health Group, Royal Veterinary College, Hatfield, Hertfordshire, UK
Pieter L.A. Fraaij Department of Viroscience, Erasmus Medical Center, Rotterdam, The Netherlands
Brian D. Gushulak Migration Health Consultants, Inc., Qualicum Beach, BC, Canada
Alana Hansen Discipline of Public Health, The University of Adelaide, Adelaide, Australia
David O. Harley National Centre for Epidemiology and Population Health, The Australian National University, Canberra, ACT, Australia
Zdenek Hubálek Institute of Vertebrate Biology, v.v.i., Academy of Sciences of the Czech Republic, and Masaryk University, Faculty of Science, Department of Experimental Biology, Brno, Czech Republic
Melissa K. Jones Department of Molecular Genetics and Microbiology, University of Florida College of Medicine, Gainesville, FL, USA
Stephanie M. Karst Department of Molecular Genetics and Microbiology, University of Florida College of Medicine, Gainesville, FL, USA
Christopher Kilonzo Department of Population Health and Reproduction, School of Veterinary Medicine, University of California, Davis, CA, USA
Carl D. Kirkwood Enteric Virus Group, Murdoch Childrens Research Institute, Royal Children’s Hospital, Parkville, VIC, Australia
Department of Microbiology, La Trobe University, Bundoora, VIC, Australia
Phillip T. Koshute Johns Hopkins University Applied Physics Laboratory, Laurel, MD, USA
A. Desiree LaBeaud Children’s Hospital Oakland Research Institute, Center for Immunobiology and Vaccine Development, Oakland, CA, USA
Sheri H. Lewis Johns Hopkins University Applied Physics Laboratory, Laurel, MD, USA
Marco Liverani Department of Global Health and Development, London School of Hygiene and Tropical Medicine, London, UK
Calum N.L. Macpherson Department of Microbiology, School of Medicine, St George’s University, Grenada, West Indies
Windward Islands Research and Education Foundation, Grenada, West Indies
Cheryl Cox Macpherson Bioethics Department, School of Medicine, St. George’s University, Grenada, West Indies
Douglas W. MacPherson Migration Health Consultants, Inc., Qualicum Beach, BC, Canada
Verónica Martín Centro de Investigación en Sanidad Animal, Instituto Nacional de Investigación Agraria y Alimentaria, Valdeolmos, Madrid, Spain
Jonathan D. Mayer Department of Epidemiology, Geography, and Global Health, University of Washington, Washington, DC, USA
Kristin L. McNally Laboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rocky Mountain Laboratories, Hamilton, MT, USA
Fleur M. Moesker Department of Viroscience, Erasmus Medical Center, Rotterdam, The Netherlands
Shigeru Morikawa Department of veterinary science, National Institute of Infectious Diseases, Tokyo, Japan
Stephen A. Morse Division of Foodborne, Waterborne, and Environmental Diseases, National Center for Emerging and Zoonotic Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA, USA
Jessica Nagel U.S. Geological Survey, Patuxent Wildlife Research Center, Beltsville, MD, USA
Albert D.M.E. Osterhaus Department of Viroscience, Erasmus Medical Center, Rotterdam, The Netherlands
Monia Pacenti Microbiology and Virology Unit, Padova University Hospital, Padova, Italy
Sarah Paige University of Wisconsin, Madison, WI, USA
Giorgio Palù Department of Molecular Medicine, University of Padova, Padova, Italy
Microbiology and Virology Unit, Padova University Hospital, Padova, Italy
Nicole Pavio UMR 1161 Virology, ANSES, Laboratoire de Santé Animale, Maisons-Alfort, France
UMR 1161 Virology, INRA, Maisons-Alfort, France
UMR 1161 Virology, Ecole Nationale Vétérinaire d’Alfort, Maisons-Alfort, France
Celia Perales Centro de Biología Molecular “Severo Ochoa” (CSIC-UAM), Consejo Superior de Investigaciones Científicas (CSIC), Campus de Cantoblanco, Madrid, Spain
Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Barcelon, Spain
Ann M. Powers Centers for Disease Control and Prevention, Fort Collins, CO, USA
Diann J. Prosser U.S. Geological Survey, Patuxent Wildlife Research Center, Beltsville, MD, USA
William K. Reisen Center for Vectorborne Diseases and Department of Pathology, Microbiology and Immunology, School of Veterinary Medicine, University of California, Davis, CA, USA
Leslie A. Reperant Department of Viroscience, Erasmus Medical Centre, Rotterdam, The Netherlands
Ivo Rudolf Institute of Vertebrate Biology, v.v.i., Academy of Sciences of the Czech Republic, and Masaryk University, Faculty of Science, Department of Experimental Biology, Brno, Czech Republic
Jonathan Rushton Veterinary Epidemiology and Public Health Group, Royal Veterinary College, Hatfield, Hertfordshire, UK
Linda J. Saif Food Animal Health Research Program, The Ohio State University, Wooster, OH, USA
Masayuki Saijo Department of Virology I, National Institute of Infectious Diseases, Tokyo, Japan
Juan Carlos Saiz Departamento de Biotecnología, INIA, Ctra. Coruña, Madrid, Spain
Noemí Sevilla Centro de Investigación en Sanidad Animal, Instituto Nacional de Investigación Agraria y Alimentaria, Valdeolmos, Madrid, Spain
Sunit K. Singh Laboratory of Neurovirology and Inflammation Biology, Centre for Cellular and Molecular Biology (CCMB), Hyderabad, India
Francisco Sobrino Centro de Biología Molecular “Severo Ochoa” (CSIC-UAM), Consejo Superior de Investigaciones Científicas (CSIC), Campus de Cantoblanco, Madrid, Spain
Laura Squarzon Department of Molecular Medicine, University of Padova, Padova, Italy
Thomas J. Stopka Department of Public Health and Community Medicine, Tufts University School of Medicine, Boston, MA, USA
Laura J. Sutherland Case Western Reserve University, Cleveland, Ohio, USA
Walter J. Tabachnick Florida Medical Entomology Laboratory, Department of Entomology and Nematology, University of Florida, Vero Beach, FL, USA
John Y. Takekawa U.S. Geological Survey, Western Ecological Research Center, Vallejo, CA, USA
Juan Carlos de la Torre IMM-6 The Scripps Research Institute, La Jolla, CA, USA
Ana Vazquez Laboratory of Arbovirus and Imported Viral Diseases, Virology Department, National Center of Microbiology, Institute of Health “Carlos III”, Ctra Pozuelo-Majadahonda, Madrid, Spain
Anastasia N. Vlasova Food Animal Health Research Program, The Ohio State University, Wooster, OH, USA
William E. Walton Department of Entomology and the Center for Disease Vector Research, University of California, Riverside, CA, USA
Angela Weber Division of Foodborne, Waterborne, and Environmental Diseases, National Center for Emerging and Zoonotic Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA, USA
Craig R. Williams Sansom Institute for Health Research, University of South Australia, Adelaide, SA, Australia
National Centre for Epidemiology and Population Health, The Australian National University, Canberra, ACT, Australia
Tomoki Yoshikawa Department of Virology I, National Institute of Infectious Diseases, Tokyo, Japan
Ying Zhang Discipline of Public Health, The University of Adelaide, Adelaide, Australia
School of Public Health, China Studies Centre, University of Sydney, Sydney, Australia
Shu Zhu Department of Molecular Genetics and Microbiology, University of Florida College of Medicine, Gainesville, FL, USA
ABOUT THE EDITOR
Dr. Sunit K. Singh completed his bachelor’s degree program from GB Pant University of Agriculture and Technology, Pantnagar, India, and his master’s degree program from the CIFE, Mumbai, India. He then joined the Department of Pediatric Rheumatology, Immunology, and Infectious Diseases, Children’s Hospital, University of Wuerzburg, Wuerzburg, Germany, as a biologist. He completed his PhD degree from the University of Wuerzburg in the area of molecular infection biology.
Dr. Singh completed his postdoctoral training in the Department of Internal Medicine, Yale University, School of Medicine, New Haven, CT, United States, and the Department of Neurology, University of California Davis Medical Center, Sacramento, CA, United States, in the areas of vector-borne infectious diseases and neuroinflammation, respectively. He also worked as a visiting scientist in the Department of Pathology, Albert Einstein College of Medicine, New York, United States, the Department of Microbiology, College of Veterinary Medicine, Chonbuk National University, Republic of Korea, the Department of Arbovirology, Institute of Parasitology, Ceske Budejovice, Czech Republic, and the Department of Genetics and Laboratory Medicine, University of Geneva, Switzerland. Presently, he serves as a scientist and leads a research group in the area of neurovirology and inflammation biology at the prestigious Centre for Cellular and Molecular Biology, Hyderabad, India. His main areas of research interest are neurovirology and immunology. Dr. Singh has several awards to his credit, including the Skinner Memorial Award, Travel Grant Award, NIH-Fogarty Fellowship, and Young Scientist Award. He is also associated with several international journals of repute as associate editor and editorial board member.
I
GENERAL ASPECTS
1
CLIMATE CHANGE AND VECTOR-BORNE VIRAL DISEASES
Ying Zhang
Discipline of Public Health, The University of Adelaide, Adelaide, Australia School of Public Health, China Studies Centre, University of Sydney, Sydney, Australia
Alana Hansen
Discipline of Public Health, The University of Adelaide, Adelaide, Australia
Peng Bi
Discipline of Public Health, The University of Adelaide, Adelaide, Australia
TABLE OF CONTENTS
1.1 INTRODUCTION
There is an increasing threat of infectious disease due to globalization and climate change. It is now widely accepted in the scientific community that the Earth’s climate system is changing, which has brought great public health challenges around the world. The impact of climate change on the transmission of infectious diseases, particularly on vector-borne diseases (VVD), has been examined in both developing and developed countries (Lafferty, 2009; Weaver and Reisen, 2010). In particular, emerging and reemerging VVD are expected to increase due to climate change and variability (Zell et al., 2008). For the first time, in the last decades, several VVD, such as West Nile virus infection, chikungunya virus infection, and viral hemorrhagic fevers, have been spreading geographically and recorded in areas outside their original ranges. However, the lack of knowledge and effective, safe vaccines and diagnosis for some VVD makes it challenging to prevent and reduce the burden of disease associated with the changing environment.
This chapter aims to present a synthetic view of the health impact of climate change and variability on VVD in order to assist evidence-based decision and policy making for disease prevention and control. We have divided this chapter into three parts. The first part will discuss the epidemiological background of VVD, including the scope; the temporal–spatial distribution around the world; a summary of the factors that affect their transmission, including the causal relationship between climatic factors and VVD; and its prevention and control. The second part will focus on the association between climatic variables and some emerging VVD, such as dengue fever (DF), Rift Valley fever (RVF), viral encephalitis, yellow fever (YF), and others. Implications and recommendations are provided in the third part of this chapter to inform decision and policy making for a range of stakeholders, for example, public health practitioners, doctors, and other health service providers at medical clinics, governments, researcher centers, and local communities.
1.2 EPIDEMIOLOGY OF VVD
1.2.1What are VVD?
Vector-borne viral diseases are virus infections transmitted via vectors. To clarify the scope of the discussion in this chapter, we adopted epidemiological and biological definitions of vector and virus to select eligible VVD for discussion. Vectors are organisms that transmit infections from one host to another (Last, 2001). Vectors of human disease are typically arthropods (e.g., species of mosquitoes and ticks) that are able to transmit pathogens. A virus is a small infectious agent, consisting of nucleic acid in a protein coat, that can replicate only inside the living cells of organisms with a wide diversity of shapes and sizes (Koonin et al., 2006). There are more than 500 “vector-borne viruses” and about 100 of them are of veterinary and/or human importance, which can cause major epidemics (Moormann, 2012). Some selected emerging VVD have been listed in Table 1.1. Some other important infectious diseases that are sensitive to climate variations, for example, malaria (not viral) and hemorrhagic fever with renal syndrome (not vector borne), are not included in our discussion.
TABLE 1.1 Summary of Selected Emerging VVD and Their Vectors
Source: Modified from WHO (2012a, b).
1.2.2 Temporal–spatial distribution of VVD around the world
Most VVD are restricted to the tropics and are often seen in temperate regions only as imported diseases, because of the required living environment for certain arthropod vectors like the Anopheles or Aedes mosquitoes. The majority of the mortality and morbidity burden of VVD occurs in Africa, South America, South Asia, and the Pacific Islands (WHO, 2004). However, geographical expanding of VVD has been reported around the world recently. This includes the emergence of West Nile virus in the Americas and Japanese encephalitis (JE) in Australasia, the spread of dengue, and the reemergence of YF virus in South America (Mackenzie and Williams, 2009; Mackenzie et al., 2004).
Due to the development of effective public health preventions and control measures targeted for VVD during the last century, many VVD, particularly mosquito-borne diseases, were controlled in many areas. However, over the last 20 years, some VVD, such as DF and West Nile virus infections, have reemerged in some areas, for example, Asia and the Americas (DeCarlo et al., 2011; Phillips, 2008; Rezza, 2012). Potential invasion of non-zoonotic VVD (only affect animals, not human beings) is of concern. For example, the world has recently witnessed the emergence and spread of a tick-borne VVD, that is, the outbreak of bluetongue, which currently affects sheep, goats, and cattle (Institute of Medicine of the National Academies, 2008).
1.2.3Factors that affect the transmission
The epidemiology of VVD is influenced by the probability of contact between the vectors, the human population, and, for many viruses, the amplifying hosts, whether birds (most arboviral encephalitis), monkeys (YF virus), or rodents (hemorrhagic fever), which serve as reservoirs for the viruses. Like other infectious diseases, the transmission of VVD is influenced by social, economic, and environmental factors (Figure 1.1).
It is well established that climate is an important determinant of the spatial and temporal distribution of vectors and viruses (Bezirtzoglou et al., 2011; Slenning, 2010). The interplay of climate, vector, and host significantly influences the transmission of VVD (Sellers, 1980). Climate conditions affect the transmission of VVD mainly in three ways: altering the distribution of vector species and their reproductive cycles; influencing the reproduction of the virus within the vector organism, known as the external incubation period (EIP); and affecting human behaviors and activity that may increase the chance of contact with infected vectors (Zhang et al., 2008).
Figure 1.1. The VVD episystem showing interactions with influencing factors. For color detail, please see color plate section.
1.3 ASSOCIATION BETWEEN CLIMATIC VARIABLES AND EMERGING VVD
Some emerging and reemerging VVD have been selected for discussion in this chapter with a focus on their epidemiology and the association with climatic variability and climate change. These are DF, YF, several types of viral encephalitis, Ross River fever, Barmah Forest virus (BFV) disease, chikungunya fever, RVF, Omsk hemorrhagic fever (OHF), and Crimean–Congo hemorrhagic fever (CCHF). Findings from both historical data analyses and projective modelings indicate an increasing number of cases and expanding epidemic areas with projected climate change scenarios.
1.3.1Dengue fever
Dengue is the most common arboviral infection in the world (Rezza, 2012). The disease, caused by the four dengue virus serotypes, ranges from asymptomatic infection, undifferentiated fever, and DF to severe dengue hemorrhagic fever (DHF) with or without shock. Symptoms may include fever, chills, and joint pain. It can be diagnosed by laboratory testing for virus isolation, viral antigen detection, or specific antibodies (serology). During the last 25 years, there have been increasing reports of dengue infection with unusual manifestations (Pancharoen et al., 2002). Great efforts are being made to understand the pathogenesis of this disease in order to develop a safe and effective dengue vaccine.
Dengue is transmitted by several species of mosquitoes within the genus Aedes, principally Aedes aegypti. Ae. aegypti has adapted well to urban environmental conditions such as poor housing, overcrowding, and inadequate sanitation, indicating the persistence of this species in regions with lower socioeconomic status, due to the close association between Ae. aegypti, humans, and the environment (Jansen and Beebe, 2010). The resilient vector may be a reason for the observed reemerging of dengue around the world (Bangs et al., 2007; Phillips, 2008; Rezza, 2012). Figure 1.2 shows the reemerging of dengue in the Americas following a successful hemispheric eradication campaign during the 1950s and 1960s (CDC).
Figure 1.2. Reemergence of Ae. aegypti and dengue in the Americas. For color detail, please see color plate section. Source: Image from CDC.
The association between climatic variables and DF has been documented worldwide, indicating a positive relationship between notified cases and increasing temperature (Banu et al., 2011; Johansson et al., 2009; Patz et al., 1998; Russell et al., 2009; Vezzani and Carbajo, 2008). Climate change, in particular a warming climate, along with globalization and international traveling, may broaden the transmission range for Ae. aegypti. Accordingly, a slight increase in temperatures could result in epidemics of dengue in the world. But the vector population may develop independently from rainfall (Pontes et al., 2000), which could be due to the characteristics of the vector, Ae. aegypti, in the urban environment. Using logistic regression analysis, Hales et al. (2002) found that the annual vapor pressure (humidity) was the most important indicator of DF outbreak globally. This study was the only one to point out the very important effect of vapor pressure on dengue transmission, which indicated that the incidence of DF for the people living in humid areas could be 30% higher than people living in areas with less humidity (odds ratio 1.3). Recently, a series of papers studying the association between climatic factors and dengue have been published, which suggest a nonstationary influence (not with a single trend or a stable pattern) of climatic situation on dengue epidemics in Thailand (Nagao et al., 2012).
Projective modelings also provide evidence of potential expanding of DF to nonendemic areas. Globally, it is suggested that climate change could increase the number of people living in areas of higher dengue risk, from 1.5 billion in 1990 to about 50–60% of the global population by 2085 (Hales et al., 2002). It is estimated that there might be a dengue threat for southern parts of Australia where there have been no previous outbreaks, which may lead to 1.6 million people living in northern Australia at risk of dengue infection by 2050, due to the southwest expanding of suitable conditions for the transmission (Russell et al., 2005) (Figure 1.3).
Figure 1.3. Areas at risk of dengue transmission. Source: Image from WHO. For color detail, please see color plate section.
1.3.2 Yellow fever
Yellow fever is a viral disease transmitted by infected mosquitoes from, principally, Aedes and Haemagogus mosquito species. Yellow fever varies in severity with some mild symptoms as fever, headache, chills, and back pain. Severe patients may have yellow coloring of the skin and kidney and liver function failure (Bell, 2007). Although safe and effective vaccination is available, there are an estimated 200 000 cases of YF, causing 30 000 deaths worldwide each year. When epidemics occur in unvaccinated populations, case-fatality rates may exceed 50% (WHO, 2011). The true number of cases is estimated to be 10–250 times what is now being reported due to underreporting.
Yellow fever is endemic in tropical and subtropical regions in African and Central/South American countries. The World Health Organization (WHO) has highlighted a greater risk of international spread of YF than in previous years (WHO, 2011). Historically, YF was once common in the United States but is no longer present mainly due to quarantine and mosquito control and improvements in living standards. However, the virus has the potential to spread to Asia and the Pacific, and the United States and Europe could expect a dramatic increase in imported YF cases for the same reasons as those applying to DF (Gubler et al., 2001). The tremendous growth in international travel as well as increasing temperature and rainfall will increase the risk of importation of YF in the United States (Monath and Cetron, 2002). The invasive YF mosquito species in Europe raised the concern of the potential risk of YF (Scholte et al., 2010). Although the disease has never been reported in Asia, the region is at risk due to the presence of the conditions required for transmission.
The number of YF cases has increased over the past two decades due to declining population immunity to infection, deforestation, urbanization, population movements, and climate change. Climate change will likely further exacerbate inequality in global health due to the potential to exacerbate endemic YF in developing countries, for example, India, where there is poor environmental sanitation, malnutrition, and a shortage of drinking water (Bush et al., 2011). Increasing temperature and rainfall were associated with the outbreak of YF in Brazil in 2000 (Vasconcelos et al., 2001). Concern regarding the reemergence of YF has risen in Brazil because of the large susceptible human population; high prevalence of vectors and primary hosts (monkeys); favorable climate conditions, especially increased rainfall; emergence of a new genetic lineage; and circulation of people and/or monkeys infected with the virus (Vasconcelos, 2010).
1.3.3Viral encephalitis: Japanese encephalitis, Murray Valley encephalitis, and West Nile encephalitis
Like dengue virus, JE virus (endemic throughout Asia and the Pacific), Murray Valley encephalitis virus (mainly in northern Australia), and West Nile virus (spread in Africa, Europe, the Middle East, west and central Asia, Oceania, and, most recently, North America) are of the family Flaviviridae (Endy and Nisalak, 2002). Encephalitis (inflammation of the brain) is the most severe neurological symptom of these virus infections, although many may be asymptomatic. The viral encephalitis diseases are transmitted by mosquitoes, but the infected mosquito species vary according to geographical area, for examples, Culex pipiens in East United States and Culex tritaeniorhynchus in Asia. Birds are the main reservoir of these viruses. In recent years, these diseases have extended beyond their traditionally recognized boundaries. For example, outbreaks of JE occurred in the Torres Strait and north Queensland (Australia) in 1995 and 1998, and West Nile virus epidemics recently occurred in America and Europe (Monaco et al., 2011; Reisen et al., 2008; van den Hurk et al., 2010).
The threats posed by the importation of exotic arboviruses, the introduction of exotic mosquitoes and reservoirs, and the potential geographic expansion of key local vectors are of great concern to public health. Climate change and anthropogenic influences provide additional uncertainty regarding the future health burden of viral encephalitis. Studies on JE indicate that increasing rainfall and temperature may bring more cases and high humidity may reduce the health burden in India (Murty et al., 2010). In China, it is suggested that the transmission of JE in both rural and urban areas may be affected by temperatures, rainfall, humidity, and air pressure with a threshold temperature of 21.0–25.2 °C and a lagged effect of 1–2 months (Bi et al., 2003, 2007). Incorporating variables for mosquito density, seasonal factors, and density of pigs (which are reservoir for the virus) can be of assistance in forecasting JE epidemics in Taiwan (Hsu et al., 2008).
There are very limited studies on the impact of climate variation on Murray Valley encephalitis virus in Australia, necessitating the need for analysis to prevent future potential risks relevant to climate change. Retrospective analysis of the epidemics of Murray Valley encephalitis in southern Australia during 1951 and 1974 indicated that mosquito longevity, extrinsic incubation period, and duration of the feeding cycle were the most important variables predisposing rapid amplification (Kay et al., 1987). Evidence also suggests that an early warning system for Murray Valley encephalitis could be effective when considering patterns of the Southern Oscillation, a synthetic indicator of climate change (Nicholls, 1986).
The relationship between climate variables and West Nile infection is not well understood. However, recent outbreaks with severe cases of West Nile encephalitis in America and European countries have led to more studies in this field. In New York, specific favorable weather conditions, for example, wet winter, warm and wet spring conditions, and dry summer, are associated with the increased local prevalence of West Nile virus among Culex mosquitoes (Shaman et al., 2011). Studies in other U.S. states have suggested that temperature and low precipitation alone are strong predictors of Culex vector population growth and more effective early warning systems can be achieved by including climate variables (Deichmeister and Telang, 2011; Liu et al., 2009; Ruiz et al., 2010). In 2009, an expansion of West Nile virus into the Canadian province of British Columbia was detected, and analysis shows that the establishment and amplification of West Nile virus in this region was likely facilitated by above-average nightly temperatures and a rapid accumulation of hot days in late summer (Roth et al., 2010). Expert opinions are consistent that climate change is predicted to increase the risk of incursion of vectors for West Nile virus infections in Canada (Gale et al., 2010). Analysis of the reemerging of West Nile infection in Russia in 2007 revealed the climate conditions favorable for the epidemic in mild winters and hot summers (Platonov et al., 2008). In addition, great concern of the potential risk of West Nile encephalitis for other countries has risen due to the changing climate and environment that are conducive to the vectors and reservoirs (van den Hurk et al., 2010).
1.3.4Ross River fever and Barmah Forest fever
Ross River fever, caused by infection with Ross River virus (RRV), is the most common mosquito-borne disease in Australia. There have been more than 41 000 notified cases during the last decade with the most serious situation occurring in 1996. The RRV causes a flu-like illness with joint pains, rash, and fever in approximately 30% of infected people 3–11 days after being infected. The vertebrate reservoir hosts of RRV could include marsupials, placental mammals and birds, kangaroos, horses, and rats. There are over 40 species of mosquito vectors, with Aedes vigilax, Aedes camptorhynchus (saltmarsh along coastline), and Culex annulirostris (inland) being the most important (McMichael et al., 2003). Peak incidence of the disease is through the summer and autumn months, when the mosquito vectors are most abundant. Most affected people are middle aged and there seems to be no gender difference.
Barmah Forest virus and RRV demonstrate many similarities in disease symptoms and seasonal distribution (Flexman et al., 1998). They are both characterized by arthralgia, arthritis, and myalgia, often accompanied by fever and rash. Arthritis is more common and more prominent in RRV infection, and rash is more common and florid with BFV infection. These symptoms may continue for at least 6 months in up to 50% of patients with RRV, but in only about 10% of patients with BFV. Both diseases can be confirmed by serological tests. However, BFV infection has not yet been as intensively studied as RRV (Jacups et al., 2008a, b).
Studies suggest that climate variables, for example, temperature, rainfall, level of river flow, and sea level, are related to the transmission of Ross River fever, but associations vary in different regions due to different vector species and ecological situations (Bi et al., 2009; Tong et al., 2002, 2005, 2008). It has been suggested that climate variability might be a contributor to the spatial change of the disease in Queensland, Australia, over the period from 1985 to 1996 (Tong et al., 2001). The response of RRV to climate variability between coastline and inland regions is also different (Tong and Hu, 2002). A recent study in Queensland confirmed the various associations, depending on different environmental conditions (Gatton et al., 2005). Kelly-Hope et al. found that the environmental risks of RRV outbreaks varied among different regions throughout Australia and that the Southern Oscillation Index (SOI) could be a predictor only for the southeast temperate region (Kelly-Hope et al., 2004). Projections of RRV epidemics from regional weather data were conducted in different areas in Australia, demonstrating high accuracy of early warning models that combined data on local patterns of climate change and mosquitoes (Woodruff et al., 2002). In Western Australia, predicted climatic changes, especially rising sea level and greater rainfall and flooding, might significantly increase RRV activity (Lindsay et al., 1996). In Darwin, a model that included rainfall, minimum temperature, and three mosquito species was proven to have the best accuracy of disease prediction that could explain 63.5% model fit (Jacups et al., 2008a, b).
Projected various ecological scenarios could result in the transmission of RRV infection being different across Australia. Recent outbreaks of RRV in the state of Victoria suggest an increasing risk in southern Australia due to increasing global temperatures. Therefore, it would be useful to generate a complete map of the vulnerability of RRV infection by systematic ecological studies across the whole of Australia, noting the relationship between environmental factors and RRV, which will lead to a better understanding of RRV transmission and control strategies.
1.3.5Chikungunya fever
Similar to RRV and BFV, chikungunya virus is an alphavirus, first identified in an outbreak in southern Tanzania in 1952. Characterized by sudden onset of fever and severe joint pain, symptoms are very similar to those of dengue but, unlike dengue, there is no hemorrhagic or shock syndrome form (Kamath et al., 2006). There is currently no specific treatment and no vaccine available for this disease. Both Ae. aegypti and Aedes albopictus mosquitoes have been implicated in large outbreaks of chikungunya. Whereas Ae. aegypti is confined within the tropics and subtropics, Ae. albopictus spreads in temperature areas. Ae. albopictus is generally considered to have a low vectorial capacity because of its lack of host specificity. Nevertheless, Ae. albopictus is abundant in rural and urban areas due to the diversity of the habitats (Delatte et al., 2008).
Chikungunya fever cases once occurred only in Africa, Asia, and the Indian subcontinent. However, there has recently been emergence of chikungunya globally, with thousands of people affected in Singapore, Malaysia, Thailand, and the Republic of the Congo (Kelvin, 2011; Pulmanausahakul et al., 2011). The major outbreak in 2005 in India resulted in a large number of imported cases in 2006 in Europe, and local transmission was first identified in Italy in 2007 (WHO, 2008).
In addition to the result of viral genetic mutations leading to the adaptation of new vector hosts and insecticide resistance, the rapid global spread may also be attributed to climate change. The relationship between climate change and reemerging of chikungunya has been reviewed in India, indicating potential risk of increased disease burden associated with changed patterns of temperature and rainfall (Dhiman et al., 2010). Using geographic information system (GIS) techniques, the investigation of the 2008/2009 incidence of chikungunya suggested that the direction of the outbreaks moved from south to north with a median speed of 7.5 km per week and the number of cases increased after 6 weeks of increasing cumulative rainfall with variation of average daily temperatures (23.7–30.7 °C) (Ditsuwan et al., 2011). Climate change that shortens the extrinsic incubation period was also considered as one of the drivers for an outbreak in Italy in 2007, the first large outbreak documented in a temperate climate country (Bezirtzoglou et al., 2011; Poletti et al., 2011). Hence, there is an increasing risk of tropical VVD in temperate climate countries, as a consequence of globalization and a changing climate.
1.3.6Rift Valley fever
Rift Valley fever is caused by Rift Valley virus affecting humans and a wide range of animals. Infected patients usually suffer from only a mild illness with fever, headache, myalgia, and liver abnormalities. Outbreaks of RVF have occurred across Africa. Since the outbreak in Kenya/Tanzania in 1997–1998 when the Rift Valley virus claimed over 400 deaths, outbreaks in 2000 in Yemen and Saudi Arabia, 2007 in Kenya/Tanzania/Somalia, and 2008 in Sudan/Madagascar and South Africa have caused nearly 1000 deaths (WHO, 2010). The outbreak in 2000 marked the first reported occurrence of the disease outside the African continent and raised concerns that it could extend to other parts of Asia and Europe (Gale et al., 2010). With Aedes and Culex mosquitoes as major vectors, RVF virus has the potential to infect a wide range of vectors, for example, ticks and flies, unlike the majority of arboviruses that tend to be adapted to a narrow range of vectors (Pepin et al., 2010). Different species of vectors can play different roles in sustaining the transmission of the virus.
Although research on the association between climate change and RVF is limited, it is likely that the geography of RVF and the vectors will be altered by climate change and extreme weather events that will create the necessary conditions for RVF to expand its geographical range northward and cross the Mediterranean and Arabian seas (Martin et al., 2008). Consistent findings indicate that increasing rainfall, especially heavy rainfall events, is closely related to the outbreaks of RVF in Africa, Saudi Arabia, and Yemen (Andriamandimby et al., 2010; Hightower et al., 2012). A study in Senegal using remote-sensing techniques that simply relied upon rainfall distribution provided a new approach to enhance early warning systems for RVF based on both natural and anthropogenic climatic and environmental changes (Tourre et al., 2009). These findings will assist the development of forecasting models and early warning systems for RVF using climate forecasting data so as to better predict and respond to RVF outbreaks in Africa and other regions.
1.3.7Omsk hemorrhagic fever and Crimean–Congo hemorrhagic fever
Omsk hemorrhagic fever (OHF) and Crimean–Congo hemorrhagic fever (CCHF) are tick-borne viral diseases. Omsk hemorrhagic fever virus is a member of the family Bunyaviridae, while CCHF virus is of the family Flaviviridae (Bajpai and Nadkar, 2011; Ruzek et al., 2010). They have symptoms of viral hemorrhagic fever but CCHF has a shorter incubation period (1–3 days) after tick bite than OHF (3–7 days). Specific symptoms for viral hemorrhagic fever vary, but initial signs often include marked fever, fatigue, dizziness, muscle aches, loss of strength, and exhaustion. Severe cases often show symptoms of bleeding under the skin, in internal organs, or from body orifices, for example, the mouth, eyes, or ears.
Omsk hemorrhagic fever has only been notified in Russia so far. Since the first description of OHF in the 1940s in Siberia, the clinical course, pathology, and epidemiology of the disease, as well as the ecology of the virus, vectors, and natural hosts (rodents), have been studied extensively, although English studies are scarce (Ruzek et al., 2010). Given the lack of a specific treatment or vaccine against OHF virus, elimination of wild rodents is a basic approach to reduce the disease burden. The morbidity from OHF has two seasonal peaks (autumn and winter, being the hunting seasons of muskrats) that correlate with activity of muskrats. There were outbreaks of OHF in the early 1990s after remarkably decreased incidence in 1970s and severe and fatal cases in 1998. As a family of tick-borne flaviviral disease, the transmission of OHF virus, like other vector-borne agents, is affected by a range of factors, including changes in climate and ecology. Climate conditions that favor the activities of muskrats and OHF ticks have not been studied. The reemergence of OHF in Russia is, nevertheless, an example of a human disease that emerged owing to human-mediated disturbance of an ecological function. Therefore, further research is necessary for a better understanding of the climatic factors that may contribute to the reemergence of OHF in Russia and other regions.
Crimean–Congo hemorrhagic fever is a severe disease in humans, with a high mortality rate. Treatment can be with antiviral agents such as ribavirin. However, review of ribavirin for patients with CCHF found that data are inadequate to support its efficacy in CCHF (Ascioglu et al., 2011). Crimean–Congo hemorrhagic fever is now endemic in many countries in Africa, Asia, and Europe and continues to emerge. The geographical distribution of the CCHF virus is widespread around the world (Leblebicioglu, 2010). Since the first disease was described in the Crimea in 1944 and later in 1956 in the Congo, the disease incidence has dropped significantly due to increasing living standards. However, reports of sporadic cases and outbreaks have recently increased significantly since 2000. In Turkey, the annual number of reported CCHF cases increased dramatically from 17 in 2002 to 1315 cases in 2008 and 1318 in 2009 (Yilmaz et al., 2009). In 2010/2011, outbreaks with severe and fatal cases were reported in Pakistan and India.
There is a strong need to better understand the underlying reasons of the reemergence of CCHF in different regions. Potential reasons for the emergence or reemergence of CCHF include climate changes, which may have a significant impact on the reproduction rate of the vector (Hyalomma ticks), as well as anthropogenic factors (Maltezou and Papa, 2010). A possible picture of the interaction among the potential factors for the emergence of CCHF may include climate and other environmental change, migratory birds, increase in tick density, livestock movement, and increase in host animals (Leblebicioglu, 2010). Nevertheless, the association between climate change and CCHF, the virus, and its reservoir is not clear at all. Tick-borne disease has already been labeled as a “clear and present danger in Europe,” and the probability of CCHF extending to other countries around the Mediterranean basin suggests that veterinarian and human surveillance should be enhanced (Chinikar et al., 2010; Heyman et al., 2010).
1.4 INVASION OF NONZOONOTIC VVD TO HUMANS
There are some nonzoonotic VVD, such as bluetongue, currently only affecting animals (e.g., sheep, goats, cattle) but not human beings. Recent emergence of bluetongue, an arthropod-borne viral disease of both domestic and wild ruminants in Europe, has raised concerns for the increasing risk to livestock and potential threats to humans. Bluetongue is widely distributed in Australia, the United States, Africa, the Middle East, Asia, and Europe, and the virulence of different strains of the virus varies considerably across countries (Maclachlan, 2011). However, disease invasion, that is, the emergence of a pathogen into a new host species, may happen in the future because of increased contact between humans and wildlife and potential unexpected impacts of a changing environment/climate on genetic mutations of the serotypes of these viruses (Daszak et al., 2001). Reasons for the spread are complex and the role changes in climate patterns and landscapes play is unclear, although increasing temperature and other meteorological variables may extend existing spatial and vector transmission models (Maclachlan, 2010). Surveillance for the vectors and vulnerable animals should be strengthened to ensure closer monitoring and better prediction of these diseases. This may avoid any unexpected transmission to humans within a changing world (Tabachnick, 2010).
