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Livros sobre o tema "Zoonosis Virales"

Autor: Grafiati

Publicado: 29 de julho de 2024

Última modificação: 31 de julho de 2024

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1

Elba Regina Sampaio de Lemos, Livia Melo Villar, Luciane Almeida Amado Leon, Monick Lindenmeyer Guimarães, Sylvia Lopes Maia Teixeira e Vanessa Salete de Paula, eds. Tópicos em Virologia. Rio de Janeiro, Brasil: Coleção Bio | Editora FIOCRUZ, 2023.

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2

W, Beran George, ed. Viral [zoonoses]. 2^a ed. Boca Raton, Fla: CRC Press, 1994.

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3

Malik, Yashpal Singh, Raj Kumar Singh e Kuldeep Dhama, eds. Animal-Origin Viral Zoonoses. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-2651-0.

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4

Kaaden, Oskar-Rüger, Claus-Peter Czerny e Werner Eichhorn, eds. Viral Zoonoses and Food of Animal Origin. Vienna: Springer Vienna, 1997. http://dx.doi.org/10.1007/978-3-7091-6534-8.

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5

Calisher, Charles H., e Diane E. Griffin, eds. Emergence and Control of Zoonotic Viral Encephalitides. Vienna: Springer Vienna, 2004. http://dx.doi.org/10.1007/978-3-7091-0572-6.

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6

Evermann, James F. Laboratory diagnosis of zoonotic infections: Viral, rickettsial, and parasitic agents obtained from food animals and wildlife. Editado por Garcia Lynne Shore, Stone Diana M e Inzana Thomas J. Washington, D.C: American Society for Microbiology, 1999.

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7

-R, Kaaden O., Czerny C. -P, Eichhorn W e Munich Symposium on Microbiology (9th : 1997 : Ludwig-Maximilians-University of Munich), eds. Viral zoonoses and food of animal origin: A re-evaluation of possible hazards for human health. Wien: Springer, 1997.

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8

Beran, George W. Handbook of Zoonoses, Section B: Viral Zoonoses. Taylor & Francis Group, 2017.

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9

Beran, George W. Handbook of Zoonoses, Section B: Viral Zoonoses. Taylor & Francis Group, 2017.

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10

Beran, George W. Handbook of Zoonoses, Section B: Viral Zoonoses. Taylor & Francis Group, 2017.

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11

Beran, George W. Handbook of Zoonoses, Section B: Viral Zoonoses. Taylor & Francis Group, 2017.

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12

Singh, Raj Kumar, Kuldeep Dhama e Yashpal Singh Malik. Animal-Origin Viral Zoonoses. Springer Singapore Pte. Limited, 2021.

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13

Singh, Raj Kumar, e Yashpal Singh Malik. Animal-Origin Viral Zoonoses. Springer Singapore Pte. Limited, 2020.

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14

Beran, George W. Handbook of Zoonoses, Second Edition, Section B: Viral Zoonoses (Handbook of Zoonoses). 2^a ed. CRC, 1994.

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15

Palmer, Stephen. Deliberate release of zoonotic agents. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0002.

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Since 9/11 2001, international attention has once again focused on the risks to human and animal health from the deliberate release of infectious or toxic chemical agents. In theory any agent could be used by terrorists and disaffected people, but the most serious risk for infectious agents are mainly zoonotic (Franz et al. 1997). Three modes of exposure may be anticipated, inhalation of powder or spray or dust from explosives, direct contact or inoculation from an explosion, and ingestion. Centers for Disease Control (CDC) list 19 bioterrorism agents or groups of agents of which 14 are zoonotic. In Category A are 6 agents which can be easily disseminated or transmitted from person to person, that result in high mortality rates and have the potential for major public health impact, which might cause public panic and social disruption and which require special action from public health preparedness. Of these 6, four are zoonoses — Anthrax, Plague, Tularaemia and Viral Haemorrhagic Fevers. In Category B, are 12 groups of agents, which are moderately easy to disseminate and cause moderate morbidity. Of these 12 groups, 8 contain zoonoses: Brucellosis, Food Safety threats (e.g. Salmonella, E.coli 0157, Campylobacter), Meliodiosis, Psittacoccosis, Q Fever, Typhus, Viral encephalitis, Water safety threats (e.g. Cryptosporidium).

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16

Viral Zoonoses and Food of Animal Origin. Island Press, 1997.

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17

Calisher, Charles H., e Diane E. Griffin. Emergence and Control of Zoonotic Viral Encephalitides. Springer London, Limited, 2013.

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18

Ermonval, Myriam, e Serge Morand, eds. Viral Zoonoses: Interactions and Factors Driving Virus Transmission. MDPI, 2024. http://dx.doi.org/10.3390/books978-3-0365-9899-4.

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19

(Editor), C. H. Calisher, e D. E. Griffin (Editor), eds. Emergence and Control of Zoonotic Viral Encephalitides (Archives of Virology. Supplementa). Springer, 2004.

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20

Lamarque, Carole. Zoonotic: The Formula for an Extremely Successful Viral Business Strategy. Lannoo N. V., Uitgeverij, 2022.

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21

(Editor), C. H. Calisher, e D. Griffin (Editor), eds. Emergence and Control of Zoonotic Viral Encephalitides (Archives of Virology Supplement). Springer, 2004.

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22

Role of Animals in Emerging Viral Diseases. Elsevier Science & Technology Books, 2013.

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23

Johnson, Nicholas. Role of Animals in Emerging Viral Diseases. Elsevier Science & Technology Books, 2013.

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24

Nandi, Jayashree Seema. Global Perspectives of the Transmission of Zoonotic RNA Viruses from Wild Animal Species to Humans: Zoonotic, Epizootic, and Anthropogenic Transmission Viral Pathogens. Elsevier Science & Technology Books, 2023.

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25

Global Perspectives of the Transmission of Zoonotic RNA Viruses from Wild Animal Species to Humans: Zoonotic, Epizootic, and Anthropogenic Transmission Viral Pathogens. Elsevier Science & Technology, 2023.

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26

Kaaden, Oskar-Rüger, Claus-Peter Czerny e Werner Eichhorn. Viral Zoonoses and Food of Animal Origin: A Re-Evaluation of Possible Hazards for Human Health. Springer London, Limited, 2012.

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27

Kurkela, Satu, e David W. G. Brown. Foot-and-mouth disease, Vesicular stomatitis, Newcastle disease, and Swine vesicular disease. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0034.

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In this chapter we review four viral zoonoses that are an important cause of a vesicular disease in animals, but only occasionally cause human infections. These viruses represent three different taxonomical families (Picornaviridae, Rhabdoviridae, Paramyxoviridae). Their clinical manifestations in animals resemble each another, characterised by vesicular eruptions in skin and mucous membranes, while human manifestations are generally mild and range from skin lesions and conjunctivitis to influenza-like illness and rarely encephalitis.

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28

Clement, Jan, e Piet Maes. Hantaviral infections. Editado por Vivekanand Jha. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0188_update_001.

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Hantavirus disease is a viral zoonosis, caused by inhalation of infectious aerosolized excreta from chronically infected rodents, which are both the reservoir and the vector of different hantavirus species. Hantavirus infections manifest mainly as haemorrhagic fever with renal syndrome and hantavirus pulmonary syndrome, which traditionally but incorrectly were thought to be caused by exclusively Old World hantaviruses and New World hantaviruses, respectively.Hantavirus diseases are characterized by non-specific flu-like symptoms, followed by a sometimes lethal capillary leak syndrome, haemorrhage, and rarely by shock. Infection is accompanied by augmented release of pro-inflammatory cytokines which indirectly causes organ damage. Diagnosis can be made by serology or plaque reduction neutralization tests, detection of viral proteins by Western blot assay, or detection of hantavirus genome by reverse transcription-polymerase chain reaction. Treatment is mainly supportive.Together with leptospirosis, haemorrhagic fever with renal syndrome is the only form of acute kidney injury against which vaccines are in use, but a World Health Organization-licensed vaccine is still lacking.

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29

Vinod, Nikhra. COVID-19: Perspective, Patterns and Evolving strategies. Heighten Science Publications Inc., 2020. http://dx.doi.org/10.29328/ebook1003.

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The Global Virome: The viruses have a global distribution, phylogenetic diversity, and host specificity. They are obligate intracellular parasites with single- or double-stranded DNA or RNA genomes, and afflict bacteria, plants, animals, and human population. The infecting virus binds to receptor proteins on the host cell surface, followed by internalisation, replication, and cell lysis. Further, trans-species interactions of viruses with bacteria, small eukaryotes and host are linked with various zoonotic viral diseases and disease progression.

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30

(Editor), Oskar-Rüger Kaaden, Claus-Peter Czerny (Editor) e Werner Eichhorn (Editor), eds. Viral Zoonoses and Food of Animal Origin: A Re-Evaluation of Possible Hazards for Human Health (Archives of Virology Supplement). Springer, 2001.

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31

(Editor), Oskar-Rüger Kaaden, Claus-Peter Czerny (Editor) e Werner Eichhorn (Editor), eds. Viral Zoonoses and Food of Animal Origin: A Re-Evaluation of Possible Hazards for Human Health (Archives of Virology. Supplementa). Springer, 2001.

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32

Clement, Jan. Acute kidney injury and hantavirus disease. Editado por Norbert Lameire. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0242_update_001.

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Hantavirus disease or at least its renal form, the so-called haemorrhagic fever with renal syndrome is the only globally emerging acute kidney injury (AKI) form, and currently without doubt the most underestimated form of community-acquired AKI. Hantavirus disease is a viral zoonosis, caused by inhalation of infectious aerosolized excreta from chronically infected rodents, which are both the reservoir and the vector of different hantavirus species. Clinical presentation consists of sudden flu-like symptoms (fever, headache, myalgia), followed by gastrointestinal discomfort and AKI, often with anuria or oliguria. More rarely, acute myopia and/or non-cardiogenic acute lung oedema or injury is the presenting or complicating symptom. Laboratory hallmarks are initial thrombocytopenia and proteinuria, raised C-reactive protein and lactate dehydrogenase, left-shift leucocytosis, and typical but transient serum lipid disturbances. Spontaneous remission occurs within 2–3 weeks without sequelae. Case fatality rate is between 0.1% and 15% according to the infecting hantavirus species, but most infections show in fact an asymptomatic or paucisymptomatic presentation. Treatment is only supportive, but may necessitate life-saving intensive care techniques. Together with leptospirosis, haemorrhagic fever with renal syndrome is the only form of AKI against which different vaccines are in use, but a World Health Organization-licensed hantavirus vaccine is still lacking.

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33

Howard, Colin R. Arenaviruses. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0032.

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There are few groups of viral zoonoses that have attracted such widespread publicity as the arenaviruses, particularly during the 1960’s and 1970’s when Lassa emerged as a major cause of haemorrhagic disease in West Africa. More than any other zoonoses, members of the family are used extensively for the study of virus-host relationships. Thus the study of this unique group of enveloped, single-stranded RNA viruses has been pursued for two quite separate reasons. First, lymphocytic choriomeningitis virus (LCM) has been used as a model of persistent virus infections for over half a century; its study has contributed, and continues to contribute, a number of cardinal concepts to our present understanding of immunology. LCM virus remains the prototype of the Arenaviridae and is a common infection of laboratory mice, rats and hamsters. Once thought rare in humans there is now increasing evidence of LCM virus being implicated in renal disease and as a complication in organ transplantation. Second, certain arenaviruses cause severe haemorrhagic diseases in man, notably Lassa fever in Africa, Argentine and Bolivian haemorrhagic fevers in South America, Guaranito infection in Venezuela and Chaparé virus in Bolivia. The latter is a prime example for the need of ever-continuing vigilance for the emergence of new viral diseases; over the past few years several new arenaviruses have been reported as implicated with severe human disease and indeed the number of new arenaviruses discovered since the last edition of this book have increased the size of this virus family significantly.In common with LCM, the natural reservoir of these infections is a limited number of rodent species (Howard, 1986). Although the initial isolates from South America were at first erroneously designated as newly defined arboviruses, there is no evidence to implicate arthropod transmission for any arenavirus. However, similar methods of isolation and the necessity of trapping small animals have meant that the majority of arenaviruses have been isolated by workers in the arbovirus field. A good example of this is Guaranito virus that emerged during investigation of a dengue virus outbreak in Venezuela (Salas et al. 1991).There is an interesting spectrum of pathological processes among these viruses. All the evidence so far available suggests that the morbidity of Lassa fever and South American haemorrhagic fevers due to arenavirus infection results from the direct cytopathic action of these agents. This is in sharp contrast to the immunopathological basis of ‘classic’ lymphocytic choriomeningitis disease seen in adult mice infected with LCM virus and the use of this system for elucidating the phenomenon of H2-restriction of the host cytotoxic T cell response (Zinkernagel and Doherty 1979). Despite the utility of this experimental model for dissecting the nature of the immune response to virus infection and the growing interest in arenaviruses of rodents, there remains much to be done to elucidate the pathogenesis of these infections in humans.

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34

Vaheri, Antti, James N. Mills, Christina F. Spiropoulou e Brian Hjelle. Hantaviruses. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0035.

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Hantaviruses (genus Hantavirus, family Bunyaviridae) are rodent- and insectivore-borne zoonotic viruses. Several hantaviruses are human pathogens, some with 10-35% mortality, and cause two diseases: hemorrhagic fever with renal syndrome (HFRS) in Eurasia, and hantavirus cardiopulmonary syndrome (HCPS) in the Americas. Hantaviruses are enveloped and have a three-segmented, single-stranded, negative-sense RNA genome. The L gene encodes an RNA-dependent RNA polymerase, the M gene encodes two glycoproteins (Gn and Gc), and the S gene encodes a nucleocapsid protein. In addition, the S genes of some hantaviruses have an NSs open reading frame that can act as an interferon antagonist. Similarities between phylogenies have suggested ancient codivergence of the viruses and their hosts to many authors, but increasing evidence for frequent, recent host switching and local adaptation has led to questioning of this model. Infected rodents establish persistent infections with little or no effect on the host. Humans are infected from aerosols of rodent excreta, direct contact of broken skin or mucous membranes with infectious virus, or rodent bite. One hantavirus, Andes virus, is unique in that it is known to be transmitted from person-to-person. HFRS and HCPS, although primarily affecting kidneys and lungs, respectively, share a number of clinical features, such as capillary leakage, TNF-, and thrombocytopenia; notably, hemorrhages and alterations in renal function also occur in HCPS and cardiac and pulmonary involvement are not rare in HFRS. Of the four structural proteins, both in humoral and cellular immunity, the nucleocapsid protein appears to be the principal immunogen. Cytotoxic T-lymphocyte responses are seen in both HFRS and HCPS and may be important for both protective immunity and pathogenesis. Diagnosis is mainly based on detection of IgM antibodies although viral RNA (vRNA) may be readily, although not invariably, detected in blood, urine and saliva. For sero/genotyping neutralization tests/RNA sequencing are required. Formalin-inactivated vaccines have been widely used in China and Korea but not outside Asia. Hantaviruses are prime examples of emerging and re-emerging infections and, given the limited number of rodents and insectivores thus far studied, it is likely that many new hantaviruses will be detected in the near future.

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35

Simpson, A., E. Aarons e R. Hewson. Marburg and Ebola viruses. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0038.

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Infection with Marburg and Ebola viruses cause haemorrhagic fevers that are characterized by organ malfunction, bleeding complications, and high mortality. The viruses are members of the family Filoviridae, a group of membrane-enveloped filamentous RNA viruses. Five distinct species of the genus Ebolavirus have been reported; the genus Marburgvirus contains only one species. Both Marburg and Ebola virus diseases are zoonotic infections whose primary hosts are thought to be bats. The initial human infection is acquired from wildlife and subsequent person-to-person spread propagates the outbreak until it is brought under control. Ebola and Marburg viruses are classified as hazard or risk group 4 pathogens because of the very high case fatality rates observed for Ebola and Marburg virus diseases, the frequency of person-to-person transmission and community spread, and the lack of an approved vaccine or antiviral therapy. This mandates that infectious materials are handled and studied in maximum containment laboratory facilities. Epidemics have occurred sporadically since the discovery of Marburg in 1967 and Ebola virus in 1976. While some of these outbreaks have been relatively large, infecting a few hundreds of individuals, they have generally occurred in rural settings and have been controlled relatively easily. However, the 2013–2016 epidemic of Ebola virus disease in West Africa was different, representing the first emergence of the Zaire species of Ebola in a high-density urban location. Consequently, this has been the largest recorded filovirus outbreak in both the number of people infected and the range of geographical spread. Many of the reported and confirmed cases were among people living in high-density and impoverished urban environments. The chapter summarizes the most up-to-date taxonomic status of the family Filoviridae. It focuses on Marburg and Ebola viruses in a historical context, culminating in the 2013–2016 outbreak of Ebola virus in West Africa. Virus biology of the most well-studied member is described, with details of the viral genome and the protein machinery necessary to propagate viruses at the molecular and cellular level. This information is used to build a wider-scale virus–host perspective with detail on the pathology and pathogenesis of Ebola virus disease. The consequences of cell infection are examined, together with our current understanding of the immune response to Ebola virus, leading to a broader description of the clinical features of disease. The chapter closes by drawing information together in a section on diagnosis, ecology, prevention, and control.

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