Zoonoses

Infectious Diseases Transmissible Between Animals and Humans

Zoonoses

Infectious Diseases Transmissible Between Animals and Humans

Rolf Bauerfeind

Institute for Hygiene and Infectious Diseases of Animals

Justus Liebig University Giessen

Giessen, Germany

Alexander von Graevenitz

Department of Medical Microbiology University of Zurich

Zurich, Switzerland

Peter Kimmig

Department of Parasitology

University of Hohenheim

Stuttgart, Germany

Hans Gerd Schiefer

Medical Microbiology

Justus Liebig University Giessen

Giessen, Germany

Tino Schwarz

Central Laboratory and Vaccination Center

Stiftung Juliusspital,

University of Wuerzburg,

Wuerzburg, Germany

Werner Slenczka

Institute for Virology

University Hospital of Marburg and Giessen

Marburg/Lahn, Germany

Horst Zahner

Institute for Parasitology

Justus Liebig University Giessen

Giessen, Germany

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Copyright © 2013 by Deutscher Ärzte-Verlag GmbH, Käln. English language edition published in arrangement with Deutscher Ärzte-Verlag GmbH through ASM Press.

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Library of Congress Cataloging-in-Publication Data

Names: Bauerfeind, R. (Rolf), editor. | Von Graevenitz, Alexander, editor. | Kimmig, Peter, editor. | Schiefer, H. G. (Hans Gerd), 1935-editor. | Schwarz, Tino F., editor. | Slenczka, Werner, editor. | Zahner, Horst, editor.

Title: Zoonoses: infectious diseases transmissible between animals and humans/editors, Rolf Bauerfeind, Justus Liebig University Giessen, Giessen, Germany; Alexander von Graevenitz, University of Zurich, Zurich, Switzerland; Peter Kimmig, University of Hohenheim, Stuttgart, Germany; Hans Gerd Schiefer, Justus Liebig University Giessen, Giessen, Germany; Tino Schwarz, University of Wuerzburg, Wuerzburg, Germany; Werner Slenczka, University Hospital Giessen and Margurg, Marburg/Lahn, Germany; Horst Zahner, Justus Liebig University Giessen, Giessen, Germany.

Other titles: Zoonosen. English

Description: Fourth edition. | Washington, DC: ASM Press, [2016] | ?2016 | Includes bibliographical references and index.

Identifiers: LCCN 2015037193 | ISBN 9781555819255 (alk. paper) | ISBN 9781683673323 (ebook)

Subjects: LCSH: Zoonoses.

Classification: LCC RC113.5.Z6813 2016 | DDC 616.95/9–dc23 LC record available at http://lccn.loc.gov/2015037193

ISBN 978-1-55581-925-5

e-ISBN 978-1-68367-332-3

doi:10.1128/9781555819262

Printed in Canada

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Contents

Preface

Introduction

Abbreviations

1 Viral Zoonoses

1.1 Introduction

1.1.1 Classification Principles

1.1.2 Zoonotic viruses

1.1.2.1 Bat-borne viruses

1.1.2.2 Zoonotic viruses as B-weapons

1.1.2.3 Global distribution of zoonotic agents

1.1.3 Cycles of Arbovirus Infections

1.2 Zoonoses Caused by Alphaviruses

1.2.1 Agents

1.2.2 Alphaviral Zoonoses

1.2.3 Eastern Equine Encephalitis

1.2.4 Western Equine Encephalitis

1.2.5 Venezuelan Equine Encephalitis

1.2.6 Semliki Forest Fever

1.2.7 Sindbis Fever

1.2.8 Epidemic Polyarthritis (Ross River Fever) and Barmah Forest Fever

1.2.9 Chikungunya Fever

1.2.10 O’Nyong-Nyong Fever

1.2.11 Mayaro Fever

1.3 Zoonoses Caused by Flaviviruses

1.3.1 Agents

1.3.2 Complexes of the Flaviviridae with Clinical Importance

1.3.2.1 Virus Complex Transmitted by Ticks

1.3.2.2 Virus Complex Transmitted by Mosquitoes: Japanese Encephalitis Virus and Related Encephalitis Viruses

1.3.2.3 Agents Causing Yellow Fever and Dengue, Forming Two Closely Related Virus Complexes

1.3.3 Zoonoses Caused by Tick-Borne Flaviviruses

1.3.3.1 Tick-Borne Encephalitis (TBE) European Subtype (Central European Encephalitis) and TBE Eastern Subtype (Russian Spring-Summer Meningoencephalitis)

1.3.3.2 Louping Ill

1.3.3.3 Powassan Virus Encephalitis

1.3.3.4 Kyasanur Forest Disease and Alkhurma Virus Hemorrhagic Fever

1.3.3.5 Omsk Hemorrhagic Fever

1.3.4 Zoonoses Caused by Mosquito-Borne Flaviviruses

1.3.4.1 Japanese Encephalitis

1.3.4.2 Murray Valley Encephalitis and Kunjin Virus Disease

1.3.4.3 St. Louis Encephalitis

1.3.4.4 Rocio Encephalitis

1.3.4.5 West Nile Fever

1.3.4.6 Usutu Virus

1.3.4.7 Wesselsbron Fever

1.3.4.8 Yellow Fever

1.3.4.9 Dengue Fever (Dengue Hemorrhagic Fever and Dengue Shock Syndrome)

1.4 Zoonoses Caused by Bunyaviruses

1.4.1 La Crosse (California Encephalitis) Virus, Snowshoe Hare Virus, and Tahyna Virus

1.4.2 Oropouche Fever

1.4.3 Crimean-Congo Hemorrhagic Fever

1.4.4 Rift Valley Fever

1.4.5 Sandfly Fever

1.4.6 Zoonoses Caused by Hantaviruses

1.4.6.1 Hemorrhagic Fever with Renal Syndrome (Old World Hantaviruses) and Hantavirus Pulmonary Syndrome (New World Hantaviruses)

1.5 Zoonoses Caused by Reoviruses (Coltiviridae and Orbiviridae)

1.5.1 Genus Coltivirus

1.5.1.1 Colorado Tick Fever

1.5.2 Genus Orbivirus (Kemerovo Complex)

1.5.3 Genus Rotavirus

1.6 Zoonoses Caused by Arenaviruses

1.6.1 Lymphocytic Choriomeningitis

1.6.2 Lassa Fever

1.6.3 Zoonoses Caused by New World Arenaviruses (Agents of Hemorrhagic Fever)

1.7 Zoonoses Caused by Filoviruses

1.7.1 Marburg Virus Hemorrhagic Fever

1.7.2 Ebola Virus Hemorrhagic Fever

1.8 Zoonoses Caused by Rhabdoviruses

1.8.1 Rabies

1.8.2 Vesicular Stomatitis

1.9 Zoonoses Caused by Paramyxoviruses

1.9.1 Newcastle Disease

1.9.2 Zoonoses Caused by Hendra Virus

1.9.3 Nipah Virus Encephalitis

1.10 Zoonoses Caused by Orthomyxoviruses

1.10.1 Influenza-Viruses

1.10.1.1 Swine Influenza Virus H1N1

1.10.1.2 Avian Influenza Viruses H5N1, H7N7, H7N9, and H9N2

1.10.2 Thogotoviruses

1.11 Zoonoses Caused by Picornaviruses

1.11.1 Swine Vesicular Disease

1.11.2 Foot-and-Mouth Disease

1.11.3 Encephalomyocarditis

1.12 Hepatitis E

1.13 Coronaviruses

1.13.1 SARS: Severe Acute Respiratory Syndrome

1.13.2 Middle East Respiratory Syndrome Coronavirus (MERS-CoV)

1.14 Retroviruses

1.14.1 Primate T-cell-Lymphotropic Viruses: PTLV 1 and PTLV 2 (HTLV 1 and 2)

1.14.2 Lentiviruses: HIV 1 and HIV 2

1.14.3 Endogenous Retroviruses

1.15 Zoonoses Caused by Herpesviruses

1.15.1 Herpes B Virus: Simian Herpes Infection

1.16 Zoonoses Caused by Poxviruses

1.16.1 Zoonoses Caused by Orthopoxviruses

1.16.2 Individual Orthopoxvirus Infections

1.16.2.1 Monkeypox

1.16.2.2 Vaccinia Virus

1.16.2.3 Buffalopox

1.16.2.4 Camelpox

1.16.2.5 Cowpox

1.16.2.6 Elephantpox

1.16.3 Parapoxvirus Infections

1.16.3.1 Contagious Ecthyma of Sheep (Orf)

1.16.3.2 Milker’s Nodules (Pseudocowpox)

1.16.3.3 Papular Stomatitis

1.16.4 Zoonoses Caused by Yabapoxviruses

1.16.4.1 Tanapox Virus

1.16.4.2 Yaba Monkey Tumor Virus

1.17 Zoonoses Associated with Prions

1.17.1 Bovine Spongiform Encephalopathy and the New Variant of Creutzfeldt - Jakob disease

2 Bacterial Zoonoses

2.1 Introduction

2.2 Anthrax

2.3 Bartonelloses

2.3.1 Cat Scratch Disease

2.3.2 Endocarditis due to Bartonella Species

2.3.3 Bartonella Infections in Immunocompromised Patients

2.4 Borrelioses

2.4.1 Lyme Borreliosis

2.4.2 Relapsing Fever

2.5 Brucelloses

2.6 Campylobacterioses

2.7 Chlamydioses

2.7.1 Psittacosis/Ornithosis

2.7.2 Chlamydioses Transmitted from Mammals

2.8 Ehrlichioses/Anaplasmosis

2.9 Enterohemorrhagic Escherichia coli (EHEC) Infections

2.10 Erysipeloid

2.11 Glanders

2.12 Leptospiroses

2.13 Listeriosis

2.14 Mycobacterioses

2.14.1 Infections with the Mycobacterium tuberculosis Complex

2.14.2 Infections with Mycobacterium marinum

2.14.3 Possible Zoonotic Mycobacterioses

2.14.3.1 Infections with M. avium subsp. avium

2.14.3.2 Infections with M. avium subsp. hominissuis

2.14.3.3 Infections with M. avium subsp. paratuberculosis

2.14.3.4 Infections with M. genavense

2.15 Pasteurelloses

2.16 Plague

2.17 Q Fever

2.18 Rat Bite Fever

2.19 Rickettsioses

2.19.1 General Features

2.19.2 Rocky Mountain Spotted Fever

2.19.3 Mediterranean Spotted Fever

2.19.4 African Tick Bite Fever and Other Spotted Fever Diseases

2.19.5 Rickettsioses in Central Europe

2.19.6 Rickettsialpox

2.19.7 Epidemic Typhus

2.19.8 Murine Typhus

2.19.9 Tsutsugamushi Fever (Scrub Typhus)

2.20 Salmonelloses

2.21 Staphylococcal Infections

2.22 Streptococcal Infections

2.22.1 General Features

2.22.2 Streptococcus equi infections (Group C)

2.22.3 Streptococcus suis Infections (groups R, S, and T)

2.22.4 Streptococcus pyogenes (serogroup A) Infections

2.22.5 Streptococcus agalactiae (serogroup B) Infections

2.22.6 Infections with other Streptococcus spp

2.23 Tularemia

2.24 Vibrioses

2.24.1 Cholera

2.24.2 Disease due to other Vibrio spp. and closely related species

2.25 Yersinioses (Enteric Infections due to Yersinia enterocolitica and Y. pseudotuberculosis)

2.26 Rare and Potential Agents of Bacterial Zoonoses

2.26.1 Actinobacillus Infections

2.26.2 Aeromonas Infections

2.26.3 Arcobacter Infections

2.26.4 Bordetella Infections

2.26.5 Capnocytophaga Infections

2.26.6 Corynebacterium pseudotuberculosis Infections

2.26.7 Corynebacterium ulcerans Infections

2.26.8 Dermatophilus congolensis Infections

2.26.9 Helicobacter Infections

2.26.10 Melioidosis (Burkholderia pseudomallei Infections)

2.26.11 Rhodococcus equi Infections

2.26.12 Trueperella pyogenes Infections

3 Fungal Zoonoses

3.1 Introduction

3.2 Dermatophytoses Caused by Microsporum spp

3.3 Dermatophytoses Caused by Trichophyton spp

3.4 Sporotrichosis

3.5 Pneumocystosis (Pneumocystis Pneumonia) as a Potential Zoonotic Mycosis

4 Parasitic Zoonoses

4.1 Introduction

4.2 Zoonoses Caused by Protozoa

4.2.1 Amebiasis

4.2.2 Babesiosis

4.2.3 Balantidiasis

4.2.4 Chagas’ Disease (American Trypanosomiasis)

4.2.5 Cryptosporidiosis

4.2.6 Giardiasis (Lambliasis)

4.2.7 Leishmaniasis

4.2.7.1 Visceral Leishmaniasis (Kala-Azar)

4.2.7.2 Old World Cutaneous Leishmaniasis

4.2.7.3 American Cutaneous and Mucocutaneous Leishmaniases (Espundia and Related Forms)

4.2.8 Microsporoses

4.2.9 Monkey Malaria (Simian Malaria)

4.2.10 Sarcosporidiosis

4.2.11 Sleeping Sickness (African Trypanosomiasis)

4.2.12 Toxoplasmosis

4.2.13 Other Zoonotic Protozoal Infections

4.3 Zoonoses Caused by Trematodes

4.3.1 Cercarial Dermatitis

4.3.2 Clonorchiasis

4.3.3 Dicrocoeliais (Distomatosis)

4.3.4 Dwarf Fluke Infections (Intestinal Dwarf Fluke Infections)

4.3.5 Fascioliasis

4.3.6 Fasciolopsiasis

4.3.7 Opisthorchiasis

4.3.8 Paragonimiasis (Pulmonary Distomatosis)

4.3.9 Schistosomiasis (Bilharziosis)

4.3.10 Other Zoonotic Trematode Infections

4.4 Zoonoses Caused by Cestodes

4.4.1 Coenurosis

4.4.2 Diphyllobothriasis (Broad Tapeworm infection)

4.4.3 Dipylidiosis

4.4.4 Echinococcosis

4.4.4.1 Alveolar echinococcosis

4.4.4.2 Cystic Echinococcosis (Hydatidosis)

4.4.5 Hymenolepiasis (Dwarf Tapeworm Infection)

4.4.6 Sparganosis

4.4.7 Taeniasis saginata (including Taeniasis asiatica)

4.4.8 Taeniasis solium and Cysticercosis

4.4.9 Other Zoonotic Cestode Infections

4.4.9.1 Intestinal Infestation: Etiology, Occurrence, and Transmission

4.4.9.2 Extraintestinal Infestation: Infection with Taenia crassiceps

4.5 Zoonoses Caused by Nematodes

4.5.1 Angiostrongyliasis

4.5.1.1 Cerebral Angiostrongyliasis (Eosinophilic Meningoencephalitis or Eosinophilic Meningitis)

4.5.1.2 Intestinal Angiostrongyliasis

4.5.2 Anisakiasis (Herring Worm Disease)

4.5.3 Capillariases

4.5.3.1 Hepatic Capillariasis

4.5.3.2 Intestinal Capillariasis

4.5.3.3 Pulmonary Capillariasis

4.5.4 Dioctophymiasis

4.5.5 Dracunculiasis (Guinea Worm Infection)

4.5.6 Eosinophilic Enteritis

4.5.7 Filariases

4.5.7.1 Brugia Filariasis (Lymphatic Filariasis)

4.5.7.2 Dirofilariasis

4.5.8 Gnathostomiasis

4.5.9 Gongylonemiasis

4.5.10 Hookworm Infection (Infection with Ancylostoma ceylanicum)

4.5.11 Lagochilascariasis

4.5.12 Larva Migrans Cutanea (Creeping Eruption)

4.5.13 Larva Migrans Visceralis

4.5.14 Oesophagostomiasis

4.5.15 Strongyloidiasis

4.5.16 Syngamiasis

4.5.17 Thelaziasis

4.5.18 Trichinellosis (Trichinosis)

4.5.19 Trichostrongylidiasis

4.5.20 Other Zoonotic Infections by Nematodes

4.6 Zoonoses Caused by Acanthocephala

4.6.1 Acanthocephaliosis

4.7 Zoonoses Caused by Arthropods

4.7.1 Zoonoses Caused by Ticks

4.7.1.1 Tick Bites

4.7.1.2 Tick Toxicoses (Tick Paralyses)

4.7.2 Zoonoses Caused by Mites

4.7.3 Zoonoses Caused by Diptera

4.7.3.1 Dipteran Bites

4.7.3.2 Myiasis

4.7.4 Zoonoses Caused by Fleas (Siphonaptera)

4.7.4.1 Flea bites

4.7.4.2 Tungiasis (Chigoe Flea infestation)

4.7.5 Infestations by Heteroptera (Bed Bugs and Triatomine Bugs)

4.8 Zoonoses Caused by Pentastomids

4.8.1 Pentastomidosis, Linguatulosis (Halzoun, Marrara Syndrome)

Appendix A

A.1 Animal Bite Infections

A.1.1 Dog Bites and Bites by Foxes, Skunks, and Raccoons

A.1.2 Cat Bites

A.1.3 Simian Bites

A.1.4 Alligator Bites

A.1.5 Squirrel Bites

A.1.6 Lizard Bites

A.1.7 Fish Bites

A.1.8 Bat Bites

A.1.9 Shark Bites

A.1.10 Hamster/Guinea Pig/Ferret Bites

A.1.11 Camel Bites

A.1.12 Opossum Bites

A.1.13 Horse Bites

A.1.14 Rat and Mouse Bites

A.1.15 Sheep Bites

A.1.16 Snake Bites

A.1.17 Pig Bites

A.1.18 Seal Bites

A.1.19 Bird Bites

A.1.20 Bear Bites

Appendix B: Infections and Intoxications Transmissible by Foodstuffs of Animal Origin

B.1 Viruses

B.2 Bacteria

B.3 Fungi (Mycotoxins)

B.4 Parasites

B.5 Fish Poisoning

B.6 Shellfish Poisoning

B.7 Phytotoxins Transmitted by Bats

Appendix C: Iatrogenic Transmission of Zoonotic Agents

Appendix D: Zoonotic Diseases Notifiable at the National Level

Index

Preface

Zoonoses are infectious diseases transmissible from vertebrate animals to humans and vice versa under natural conditions. They comprise a complex spectrum of diseases due to the diversity of pathogenic agents involved. They may confront veterinarians as well as general practitioners, pediatricians, infectious disease specialists, and microbiologists with special diagnostic and therapeutic problems. While we did not intend to write a handbook of zoonoses, we wanted to cover not only well-known diseases but also rare ones that may be of importance to physicians active in developing countries and to travelers going to distant or rarely visited areas.

Our book is based on the 4th German edition of Zoonosen: Zwischen Tier und Mensch übertragbare Infektionskrankheiten which was published in 2013 by Deutscher Ärzte-Verlag, Cologne, Germany. It has been thoroughly revised, updated, and amended.

We have tried to present the most significant aspects of the great variety of zoonotic diseases in a concise manner. However, in some cases readers may even need more detailed information.

We express our appreciation to Christine Charlip, Director, and Larry Klein, Production Manager of ASM Press for their constant encouragement, assistance and advice. We are indebted to Professor Gaby Pfyffer von Altishofen, Lucerne, for helpful suggestions and constructive criticism of the chapter on mycobacterioses, and Dr Tanja Matt, Zürich, for technical help with the figures on transmission chains. We also want to thank Prof. Peter Mayser, Giessen, for valuable advice on the chapter on fungal zoonoses and Prof. Brigitte Frank, Hohenheim, for her support in the translation. And all of us, particularly those involved in translating the German text into English, are deeply grateful to our families for their patience, tolerance, and support.

Finally it is the particular concern of the authors to commemorate our co-author Hans Gerd Schiefer who unfortunately died shortly before completion of this edition. His work and participation had been extremely important for this book.

Introduction

Numerous human infectious diseases are caused by agents that are directly or indirectly transmissible from various animal species to humans. Today, more than 200 diseases occurring in humans and animals are known to be mutually transmitted. They are caused by prions, viruses, bacteria (including rickettsiae and chlamydiae), fungi, protozoa, and helminths, as well as arthropods. An Expert Committee of the World Health Organization defined zoonoses in 1958 as “diseases and infections which are naturally transmitted between vertebrates and humans.” This definition is still valid.

Originally, zoonoses were regarded as animal diseases (in Greek zoon means “animal”). In the 19th century, the meaning of the word changed. Thus, in 1855, R. Virchow included in his book, Handbuch der Speciellen Pathologie und Therapie, the chapter “Infectionen durch contagiöse Thiergifte” (“Infections Caused by Animal Contagious Poisons”) with the subtitle “Zoonosen” (“Zoonoses”). Shortly after this, the word “zoonoses” received a double meaning for the first time. W. Probstmayer (1863) stated in the Etymologisches Wörterbuch der Veterinärmedizin und ihrer Hilfswissenschaften (Etymological Dictionary of Veterinary Medicine and its Auxilliary Sciences) “zoonoses are (i) animal diseases and (ii) diseases of humans transmitted from animals by means of a vector or contact.” Today, no difference is made with regard to the direction of transmission, that is, animal to human or human to animal, although attempts exist to describe precisely the direction of transmission. The term “zooanthroponoses” referred to diseases transmitted from animals to humans, and the term “anthropozoonoses” referred to diseases transmitted from humans to animals. However, the latter play only a minor role in the epidemiology of zoonoses. The term “zoonosis” still underlies conceptual changes. For instance, increasing epidemiological knowledge has put into doubt the traditional associations of some infectious diseases with zoonoses. Diseases that do not require a vertebrate reservoir because of their occurrence in water, in soil, on plants, or in food or fodder, whence they are transmitted to vertebrates (including humans), are also called sapronoses, saprozoonoses, or geonoses.

Zoonoses are a persisting threat to the human society. Classical infectious diseases, such as rabies, plague, and yellow fever, well known for centuries, are zoonoses that have not been eradicated despite major efforts. And the importance of zoonoses still increases. In recent years, new zoonotic entities, for example, Lyme borreliosis, ehrlichiosis, infections with enterohemorrhagic Escherichia coli, cryptosporidiosis, and hantavirus pulmonary syndrome, have been detected.

The steadily increasing threat that zoonoses pose to humans have many causes that differ from country to country. Overpopulation, wars, and progressive deterioration of living conditions may cause migration of countless people into slums of large cities, with a subsequent breakdown of hygiene and public health care. The proximity of their dwellings to huge garbage dumping grounds and their dependence on water contaminated with sewage facilitate contact with rodents, stray animals, and their parasites.

Scarcity of food forces millions of humans to clear woodlands for cultivation and to produce new settlements in areas where animal populations and their pathogenic agents were formerly separated from humans. Humans may participate unwittingly in unknown parasite-host cycles and become a new link in an infectious chain. In many of these cases, humans, as accidental hosts, are in no way adapted to the new pathogenic species, which may result in high mortality.

Artificial irrigation changes the ecology of whole countries. Artificial lakes and ponds attract animals and their parasites over vast distances and provide optimal breeding grounds, especially for mosquitoes. Increasingly warm and moist winters in the Northern Hemisphere favor the propagation of parasites, especially ticks. Stray animals, usually infected with various pathogens, are reservoirs for infectious agents, not only in developing countries, but also in developed countries.

Worldwide tourism, especially trekking tours to remote areas and so-called adventure challenges (e.g., “survival training” with camping in open areas and consumption of raw or insufficiently cooked food) has encouraged contact of humans from industrialized countries who grew up under nearly aseptic conditions and agents and vectors that they have never encountered before.

Zoonotic agents of low virulence may cause fatal infections in immunosuppressed humans (e.g., patients infected with HIV).

A further potential source of infection is transport of breeding and slaughter animals over vast distances and across borders, often with insufficient inspection for disease control. New disease agents may be introduced to a country by legal, or, even worse, illegal importation of exotic animals for zoos, research purposes, or private homes. Isolated animal organs (xenotransplants) and cultures of animal cells may contain dangerous zoonotic agents. Furthermore, several zoonotic pathogens, for example, Francisella tularensis, Yersinia pestis, Brucella spp., Bacillus anthracis, Coxiella burnetii, and hemorragic fever viruses, are considered possible bioterrorism weapons.

The problem of diseases transmitted between animals and humans has many aspects, especially as it is not uncommon for animals serving as reservoir or intermediate hosts to be clinically inapparent carriers and/or excreters of an agent. Undoubtedly, currently unknown zoonoses will emerge in future. New methods for direct or indirect detection of microorganisms contribute to the detection of new zoonoses. When human invasion of hitherto uninhabited areas results in voluntary or involuntary environmental changes, new and potentially dangerous zoonoses may become evident. Severe acute respiratory syndrome, caused by a newly emerged coronavirus, is one of the latest examples of the threat of dangerous infections, although its possible zoonotic background has not yet been clarified.

In the study of zoonoses, medical experts and veterinarians should cooperate closely to study the etiology, epidemiology, and frequently complex developmental cycles and modes of transmission of pathogens and their vectors, as well as the clinical presentation, diagnosis, differential diagnosis, therapy, and prophylaxis of the attendant diseases. Our book is based on such cooperation, which since recently, is also postulated under the concept “One World – One Health.”

Abbreviations

Viral Zoonoses 1

1.1 Introduction

1.1.1 CLASSIFICATION PRINCIPLES

Viruses are usually classified according to structural principles and genetic homology. Agents causing zoonoses exist in various virus groups that have similarities in the disease patterns that they induce. There may also be similarities involved in hosts and vectors. In this chapter, we have chosen a sequential arrangement following viral classifications for the most part. This sequence makes it possible to point out similarities within individual virus groups. Tables include the geographical distribution and clinical signs that are important for differential diagnosis. Viral zoonoses are also compared with nonviral zoonotic diseases.

1.1.2 ZOONOTIC VIRUSES

Among the agents causing zoonotic disease, zoonotic viruses are the most abundant and the majority of zoonotic viruses have RNA as genetic material. DNA viruses, due to effective proofreading mechanisms of the DNA polymerases, have greater genetic stability, restricting their host range to a spectrum of closely interrelated host animals. Only poxviruses and some representatives of the herpes virus family are able to cross species barriers and cause zoonotic infections.

RNA viruses on the other hand do not have proofreading mechanisms; consequently, every reproductive cycle will produce a great number of genetic variants, which may often be unable to reproduce in their original host cells. By chance, new variants may be produced with the ability to extend the host range to other hosts. Of course, all these variants will have to overcome a selection process that will, in most cases, restrict, or in some cases, even improve their reproductive success.

Single point mutation is not the only mechanism that is responsible for the variability of RNA viruses. In addition, some groups of RNA viruses have powerful mechanisms to use genetic recombination or genetic reassortment to extend their genetic variability enabling them to change or enlarge their host range, an ideal preposition for the life cycle of a zoonotic virus. Regarding the genetic variability of RNA-bacteriophages, von Eigen has coined the term “quasispecies,” which offers an ideal understanding of the variability of zoonotic RNA viruses. In consequence of these developments, it has become more difficult to explain and to understand the relative stability that is observed in some none zoonotic RNA virus species, for example, in measles, mumps or rubella.

In some cases, viruses have established themselves in the human host so successfully that epidemics and epizootics can proceed independently of each other. In such cases, the classification as a zoonosis is justified if a host change from an animal to a human host can be proven. Examples are the influenza A viruses and the rotaviruses. Both viruses are widespread in animal hosts and cause epizootics that do not necessarily lead to epidemic spread. Influenza A viruses and rotaviruses have segmented genomes that allow genetic exchange by re-assortment. New variants, differing from the original virus in respect to host range, pathogenicity, and contagiosity may result from genetic recombination. In hepatitis E, there is also coexistence of epidemic and epizootic spread. In this case, it has been shown that among the four viral subtypes, strains 1 and 2 cause epidemics that are spread via the fecal-oral route. Strains 3 and 4 are causing zoonotic infections that are not transmitted by human-to-human contacts.

The causal agents of AIDS, the human immunodeficiency (HI) viruses, have switched to epidemic spread in a short period of time. However, even in this case, the zoonotic origin is indisputable as HIV I and HIV II exhibit a close relationship with immunodeficiency viruses occurring in monkeys and sporadic transmission of the simian viruses to humans happens. HIV I is closely related to SIV-cpz, a chimpanzee virus (from Pan troglodytes), HIV II is most probably derived from a virus that persists in mangabeys (Cercocebus torquatus). Genetic analyses have shown that HIV I was transferred at a minimum of four different occasions from chimpanzees or gorillas to humans.

Narrow relatives exist in the animal kingdom of TT virus, a newly discovered parvovirus, which is transferred between humans via blood transfusions. As human infections result from contact with infected people, and not from animal contacts, we do not speak of a zoonosis. Foamy agent is a simian retrovirus that is transmitted to people working or living in close contact with monkeys but apparently does not cause disease. This virus does not meet the definition of a zoonotic virus. Borna-virus, a horse virus belonging to the Negavirales, is highly pathogenic for horses. Antibodies against Borna are also found in the human population, mainly in psychiatric patients. The meaning is unclear. As all viral isolates obtained from human specimens agree in their genomic base sequence and do not differ from the laboratory strain, there is no convincing proof that these viruses are transferred from animals to humans. Newer findings about a murine retrovirus, XMRV, which is supposed to be transferred with blood donations, are based on serological evidence that has not been confirmed by other investigators.

This book does not include virus infections primarily affecting humans that are normally transmitted from human-to-human and only under special circumstances are transmitted to animals. Herpes simplex virus and hepatitis A virus are examples, both of which can be transmitted to monkeys.

Clams have long been known to pick up and concentrate viruses pathogenic for humans from sewage. In particular, enteroviruses, calicivirus, reoviruses, and hepatitis A and B viruses can be found in clams. Hepatitis A virus and several agents causing gastroenteritis, such as the “Norwalk agent,” have caused epidemics in humans after eating clams. These infections caused by food-borne viruses are, according to present knowledge, not considered to be zoonoses. They are mentioned only in the context of food-borne infections in this book.

Virus infections, such as Russian spring-summer encephalitis and Kyasanur Forest disease, which are spread by ticks but may be transmitted from milk of infected animals, are included as zoonoses.

New arboviruses (arthropod-borne viruses) with a potential for human and animal infection without causing disease (see “Cycles of Arbovirus Infections” below) are constantly being isolated. Any listing of these agents with doubtful pathogenicity for humans would be incomplete and would reach beyond the purpose of this book.

Zoonotic viruses have in some cases been transmitted to humans deliberately, for example, for the purpose of vaccination against smallpox, or inadvertently, as in the early poliomyelitis vaccines (before 1960), which are suspected to have introduced simian virus 40 (SV40) from cercopithecine monkeys to humans. This virus, a polyomavirus, is known to be oncogenic in unrelated hosts. There is, however, debate about whether a virus closely related to SV40 might have existed in humans before poliomyelitis vaccination was begun. Nevertheless, sequences of the gene coding for SV40 T antigen are found in 40% of non-Hodgkin’s lymphomas but not in any other malignancies. At present, it cannot be determined whether non-Hodgkin’s lymphomas constitute an example of an iatrogenic zoonosis. The intended usage of xenotransplantation, for example, the transplantation of porcine organs to humans, is criticized for the possible transmission of porcine viruses into humans. The immune suppressive therapy of the acceptor might enable a change of host species.

Some of the viruses covered in this section reflect the modern concept of emerging and reemerging infections. This concept gives the appearance of a secret, perhaps active role of the viruses when they reemerge. Mutations and changes in the host spectrum are supposed to play a role here. There are examples of the surprising and miraculous appearance of new diseases and new agents, which cannot be denied. The Rocio encephalitis virus and the equine morbillivirus (Hendra virus) should be mentioned here. The emergence of new influenza viruses pathogenic for humans has appeared as a puzzle. Nowadays, analysis of the basic molecular mechanisms of these viruses has offered a better understanding. In most instances, however, it is not the virus itself that plays the active part in its spread, but rather, it is humans, who advance into areas from which humans were formerly excluded. Oropouche virus and Kyasanur Forest virus are classical examples of this type of spreading. The violation of well-known rules in hygiene is often responsible in other cases (e.g., Lassa virus and Ebola virus) when the circumstances for the spreading of “new” viruses are clarified. The talk about “emerging and reemerging” in these cases covers up the facts and is not useful for avoiding the causes of the spread. An important causative factor, often neglected in discussions on the spectacular reemergence of arboviral diseases that we see at this time, is the interruption in the use of dichlorodiphenyltrichloroethane (DDT) as a pesticide. This effect is intensified by overpopulation in areas of endemicity and an increase in diagnostic facilities and public awareness.

1.1.2.1 Bat-borne viruses

In addition to arboviruses transmitted by arthropods and roboviruses transmitted from rodents to humans, viruses that are transmitted from bats to animals and humans have recently been identified. They include known and newly recognized strains of rabies virus and paramyxoviruses, which are transmitted by flying foxes (suborder Megachiroptera) to horses (Hendra virus) and pigs (Nipah virus and Menangle virus). With the exception of Menangle virus, these agents can cause fatal infections in humans. Flying foxes are also believed to be the host species of filoviruses and of newly detected coronaviruses, severe acute respiratory syndrome associated coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV). Analogous to tick-borne viruses, which are transmitted by ticks, one could describe those transmitted by bats as “bat-borne viruses.” Transmission of Hendra virus is facilitated by pregnancy in the bat, and pregnant horses are highly susceptible to the disease.

The connection between varying population densities of reservoir animals or vectors of some viruses and the frequency of their manifestation is interesting and often poorly understood. Changes in climatic conditions can explain the frequency of ticks and the spreading of tick-transmitted infections. The relationship is unknown between the changing population density of some rodents, which serve as reservoirs for viruses (e.g. Arena- and Hantaviruses), and the frequency of human infections. The weather phenomenon El Niño has been held responsible for the fluctuation in the mouse populations. Arena- and Hantaviruses do not seem to influence the survival chances of their reservoir animals because they are not pathogenic for them. It remains a possibility, however, that the virus infection itself could influence the population density of its host animals. If only one part, but not another, of the host population is resistant to the virus, it is easy to speculate that viruses themselves control the population density by eliminating sick individuals. Any animal surviving an epizootic will be protected. In this way, the chances for a new epizootic will be reduced, until a new generation of susceptible individuals is born or there is a variation in the viral agent.

It is important to know whether a person or an animal grew up in an area of endemicity in order to assess their susceptibility to zoonotic viral infections. Children living in areas of endemicity are often protected by maternal antibodies and are latently infected, or they are less susceptible at an early age. Based on serological studies, the relative frequency of clinically apparent diseases may be underestimated. The potential danger of contracting tick-borne meningoencephalitis or Japanese encephalitis is much greater for people who have not lived in an area of endemicity. This should be taken into consideration, for example, when giving vaccination advice for travelers.

1.1.2.2 Zoonotic viruses as B-weapons

Some of the most dangerous pathogens for humans must be discussed in this chapter. It seems to be inevitable that specialists who are interested in biological warfare are attracted by pathogens that have an extremely high case fatality rate, such as the Ebola virus. Yet, by way of compensation, the contagiousness of these pathogens is low as a rule, rendering them less suitable for military use. Influenza A viruses of human origin are feared for their pandemic potential. However, influenza virus strains of avian origin, which may cause fatal infections in humans, lack the ability to spread in the human population. Nevertheless, by way of genetic engineering, viruses of low pathogenicity could be transformed into dangerous pathogens, as has been experienced in the case of the ectromelia virus, an orthopoxvirus pathogenic for mice.

1.1.2.3 Global distribution of zoonotic agents

A potential risk of spreading zoonotic infections results from deliberate or inadvertent liberation of imported animals. Importation of exotic animals can be connected with the introduction of zoonotic viruses and should be controlled. The foot-and-mouth disease (FMD) virus can be imported with frozen meat or with latently infected sheep. Crimean Congo virus and Rift Valley virus were imported to Yemen, to Saudi Arabia, and to the United Emirates with fat stock. Raccoons, which were transported from Florida to the State of New York, have introduced raccoon rabies. Raccoon dogs imported from Iran have reintroduced rabies to Scandinavia. The most probable explanation for the introduction of West Nile Virus to North America is the importation of exotic birds. Giant rats, imported from Ghana have introduced monkey pox virus into the United States, where the virus was transmitted to prairie dogs, which were kept as pets.

For survival and transmission, arboviruses are dependent on the availability of competent arthropod vectors; the global distribution of arthropods is facilitated by climatic change and international traffic. The global migration of the Asian “tiger mosquito” (Stegomyia albopicta) is especially alarming. This vector is competent for the propagation of the Dengue virus, yellow fever, Chikungunya, and other arboviruses. Eggs of this mosquito were detected in used automobile tires that were shipped from South East Asia to the USA. The tires contained pools of rainwater sufficient for development and survival of the mosquito larvae. Since that time, the vector has settled in the south of the USA and in southern Europe.

Diagnostic Procedures. Approved diagnostic procedures for virus infections that are rare are not easily available. As a rule, ELISA techniques and PCR techniques are displacing older approaches for detection of viruses, e.g. virus-specific antigens, nucleic acids and antibodies.

The advantage of this displacement is that specialization is losing its importance. Anybody who is trained to do an ELISA or a PCR can learn to do it for any purpose. However, compared to those for non-zoonotic virus infections, the diagnostic reagents for many zoonotic infections are not commercially available. References to the literature are included, and it is stressed that the original papers must be consulted for the correct conditions to perform the tests. Most of these PCR techniques have not been evaluated in large numbers of diagnostic cases.

1.1.3 CYCLES OF ARBOVIRUS INFECTIONS

Arboviruses (arthropod-borne viruses) exist in maintenance cycles between vertebrate hosts and primary vectors (Fig. 1.1). Mosquitoes are the most important vectors. Ticks, sand flies (Phlebotomus spp.), and gnats (Culicoides spp.) play a role as vectors of certain arboviruses. There is a close dependence between the virus and the vector. However, different mosquitoes may act as vectors for the same virus in different vertebrates depending on different geographical or ecological situations. Besides a few exceptions, humans are usually the dead-end host and not important as intermediate hosts in the maintenance cycle. Infection of humans by means other than vectors (e.g., via aerosols) is possible, especially in laboratories or as nosocomial infections if the level of viremia is sufficiently high.

Figure 1.1(a, b, c) Arboviral Transmission cycles (a) Urban infectious cycles where humans are the source of infection for mosquitoes have been demonstrated, or are possible, if the level of viremia is sufficient. Infected people have to be protected from mosquito bites. This type of infection cycle has been found for yellow fever, dengue, St. Louis encephalitis, Venezuelan equine encephalitis, and Chikungunya fever. It is possible for O’nyong-nyong, Mayaro, Ross River, Oropouche, Rift Valley, and Wesselsbron fevers. (b) Humans are the dead-end hosts in the infection chain and do not serve for amplification. This type of infection chain exists for eastern and western equine encephalitides and Rocio, West Nile, and Sindbis fevers. (c) A vertical transmission (transovarial and transstadial) exists in arthropods and is of importance epidemiologically. This type of transmission is found in the following tick-transmitted virus infections: spring-summer meningoencephalitis, Russian spring-summer meningoencephalitis, louping ill, Kyasanur Forest fever, Omsk hemorrhagic fever, Crimean-Congo hemorrhagic fever, and Colorado tick encephalitis. It is found in the following mosquito-transmitted infections: California and Japanese encephalitides and Murray Valley fever.

The epidemiology of arbovirus infections is regulated by a number of independent factors. They include the number and immune status of the vertebrates that represent the agent reservoir, as well as climatic conditions under which the vector population can reproduce with changing efficiency. Different kinds of mosquitoes with changing host specificity are involved in the complex maintenance cycles with multiple host changes. The seasonal increase in frequency of virus infections is regulated by breeding conditions and the survival rate of the vectors.

In areas with temperate climatic conditions, the question has to be resolved whether arboviruses survive the winter or if they are reintroduced. It is important to know whether a vector maintains its role as reservoir by transovarial and transstadial virus transmission.

La Crosse virus is the most important virus among the agents causing California encephalitis. It is transmitted by its main vector, Aedes (Stegomyia) triseriatus, not only by transovarial and transstadial routes but also sexually. Bunyaviruses, similar to influenza viruses, are directly dependent on the viral gene expression and the metabolic activity of the host. Replication of bunyaviruses is controlled by a transnucleotidase, which transcribes the 5′ cap of the mRNA to the viral message (5′-end scavenging). Blood meals activate the cellular gene activity in the ovaries of the mosquitoes and simultaneously stimulate virus replication. Two different cap sequences, CS1 and CS2, are available for the activation of the viral messenger. Viral gene expression can be demonstrated during the hibernation of the eggs (diapause). However, 5′- end structures with CS2 sequences are used almost exclusively for the viral mRNA. After completion of the diapause, 100% of CS1-carrying viral messengers are used.

This special kind of viral gene expression of a gene recombination with intermolecular and intramolecular reassortment is facilitated if an egg is infected with two different bunyaviruses. This could contribute to the genetic multiplicity of the Bunyaviruses.

For viruses transmitted by ticks, it is important to remember that the tick development from egg to larva to nymph to the adult stage takes at least 2 years in a temperate climate. The tick needs a blood meal during each stage, which can cause transmission of an agent. The population density of ticks is influenced not only by atmospheric conditions of the present year but also by the climate of previous years.

Sometimes, entirely different viruses use the same maintenance cycles between virus reservoir and vector. A close epidemiological connection can be the result; for example, the western equine encephalitis virus, an alphavirus, and the St. Louis encephalitis virus, a flavivirus, are spread by the same cycle between wild birds and the mosquito species Culex tarsalisCulexCulex univittatusCulex annulirostrisAedes (Stegomyia) aegypti. Anopheles gambiae