- Infectious Diseases of Livestock
- Part 2
- GENERAL INTRODUCTION: PRION DISEASES
- Enteric caliciviruses of pigs and cattle
- Porcine epidemic diarrhoea
- Porcine haemagglutinating encephalomyelitis virus infection
- Caprine arthritis-encephalitis
- Papillomavirus infection of ruminants
- Hendra virus infection
- Swine influenza
- Porcine deltacoronavirus infection
- Enzootic bovine leukosis
- Jaagsiekte
- Bovine coronavirus infection
- Papillomavirus infection of equids
- Porcine respiratory coronavirus infection
- Visna-maedi
- Pseudorabies
- Ovine coronavirus infection
- Equid gammaherpesvirus 2 and equid gammaherpesvirus 5 infections
- Suid herpesvirus 2 infection
- Adenovirus infections
- Bovine parvovirus infection
- Equid herpesvirus 1 and equid herpesvirus 4 infections
- Malignant catarrhal fever
- Porcine parvovirus infection
- Old World alphavirus infections in animals
- Equine coronavirus infection
- Equine coital exanthema
- Infectious bovine rhinotracheitis/infectious pustular vulvovaginitis and infectious pustular balanoposthitis
- Bovine alphaherpesvirus 2 infections
- Sheeppox and goatpox
- Pseudocowpox
- Bovine spongiform encephalopathy
- Buffalopox
- Ulcerative dermatosis
- Foot-and-mouth disease
- Scrapie
- Transmissible spongiform encephalopathies related to bovine spongiform encephalopathy in other domestic and captive wild species
- Borna disease
- Cowpox
- Encephalomyocarditis virus infection
- Orf
- Post-weaning multi-systemic wasting syndrome in swine
- Bovine rhinovirus infection
- Swine vesicular disease
- Camelpox
- Equine picornavirus infection
- Swinepox
- Teschen, Talfan and reproductive diseases caused by porcine enteroviruses
- Bovine papular stomatitis
- Horsepox
- GENERAL INTRODUCTION: CIRCOVIRIDAE AND ANELLOVIRIDAE
- Rift Valley fever
- Getah virus infection
- Equine encephalosis
- Border disease
- Diseases caused by Akabane and related Simbu-group viruses
- Louping ill
- West nile virus infection
- Crimean-Congo haemorrhagic fever
- Porcine reproductive and respiratory syndrome
- Bovine viral diarrhoea and mucosal disease
- Equine encephalitides caused by alphaviruses in the Western Hemisphere
- Rotavirus infections
- Ibaraki disease in cattle
- African horse sickness
- Rabies
- Hog cholera
- African swine fever
- Bovine ephemeral fever
- Epizootic haemorrhagic disease
- Palyam serogroup orbivirus infections
- Nairobi sheep disease
- Wesselsbron disease
- Equine viral arteritis
- Vesicular stomatitis and other vesiculovirus infections
- Lumpy skin disease
- Bluetongue
- GENERAL INTRODUCTION: ORTHOMYXOVIRIDAE
- GENERAL INTRODUCTION: RHABDOVIRIDAE
- GENERAL INTRODUCTION: PARAMYXOVIRIDAE AND PNEUMOVIRIDAE
- GENERAL INTRODUCTION: PRION DISEASES
- GENERAL INTRODUCTION: ARTERIVIRIDAE
- GENERAL INTRODUCTION: RETROVIRIDAE
- GENERAL INTRODUCTION: HERPESVIRIDAE
- GENERAL INTRODUCTION: BUNYAVIRIDAE
- GENERAL INTRODUCTION: CORONAVIRIDAE
- GENERAL INTRODUCTION: POXVIRIDAE
- Peste des petits ruminants
- GENERAL INTRODUCTION: TOGAVIRIDAE
- GENERAL INTRODUCTION: PICORNAVIRIDAE
- GENERAL INTRODUCTION: PARVOVIRIDAE
- GENERAL INTRODUCTION: BORNAVIRIDAE
- GENERAL INTRODUCTION: ASFARVIRIDAE
- GENERAL INTRODUCTION: PAPILLOMAVIRIDAE
- GENERAL INTRODUCTION: FLAVIVIRIDAE
- GENERAL INTRODUCTION: CALICIVIRIDAE AND ASTROVIRIDAE
- GENERAL INTRODUCTION: REOVIRIDAE
- GENERAL INTRODUCTION: ADENOVIRIDAE
- Rinderpest
- Vesicular exanthema
- Porcine transmissible gastroenteritis
- Bovine respiratory syncytial virus infection
- Equine influenza
- Paramyxovirus-induced reproductive failure and congenital defects in pigs
- Nipah virus disease
- Parainfluenza type 3 infection
- Equine infectious anaemia
GENERAL INTRODUCTION: PRION DISEASES
PRION DISEASES
A General Introduction has been added to each disease chapter in an attempt to give a brief updated overview of the taxonomic, biological and other characteristics of the virus family or group of bacteria/protozoa that cause disease in livestock and, where relevant, involve wildlife. As the text of the three-volume book Infectious Diseases of Livestock is currently under revision the Editors are aware that there are inconsistencies between the updated introductions to chapters and the content of the chapters themselves. Once the chapters have been updated – a process that is currently underway – these inconsistencies will be removed.
There is strong scientific evidence that a group of infectious neurodegenerative diseases of humans and some other mammals – known collectively as the transmissible spongiform encephalopathies (TSEs; Table 1) – are caused by prions, i.e. transmissible mis-folded variants (PrPSc) of the normal cell-membrane protein designated PrPC. PrPSc, after a long incubation period, accumulates in the brains of infected individuals as microscopic fibrils, disturbing the architecture through characteristic vacuole and plaque formation, accompanied by neuronal loss. The resulting is an invariably fatal illness. Prions have no associated nucleic acid as is the case with other infectious agents.3
Transmission usually occurs horizontally, mostly by the oral route but in some TSEs transmission can also be vertical. The epidemiology of TSEs is often complicated by genetic predisposition. Furthermore, because prions are not recognised as foreign by the adaptive immune system of the host, PrPSc does not induce immunological responses. That probably contributes to the pathogenicity of TSEs and renders laboratory diagnosis more difficult than for most other infectious diseases.
Despite the fact that scrapie in sheep was recognised as long ago as the 1732, why and how the mis-folding of PrPC occurs is still a subject of fundamental research.
Prior to the 1980s TSEs were of limited practical importance. However, the so-called mad-cow disease (bovine spongiform encephalopathy - BSE) pandemic, centred on the United Kingdom (UK) from about 1985 caused the most complex, financially costly and frightening zoonotic crises in the modern era. At the height of the pandemic in 1992, more than 36 000 cases of BSE occurred in cattle in the UK; that, together which demonstration of the zoonotic potential of the disease in 1996,1 resulted in widespread consternation. However, the recorded human death toll worldwide due to variant Creutzfeldt-Jakob (vCJD) disease currently stands at only 228. Of those, 77 per cent occurred in the UK (www.cjd.ed.ac.uk/sites/default/files/worldfigs_0.pdf). The effort and expense required to eliminate the pandemic – for all practical purposes now achieved – was unprecedented in recent times. It has been estimated that the eventual cost to the European Union for managing the pandemic will reach € 92 billion.2 Ironically, the threat of BSE will probably never be finally eliminated because sporadic, atypical cases of most TSEs, BSE and scrapie included, occur at extremely low prevalence rates. Therefore, if in future, the same set of circumstances that precipitated the 1985 BSE pandemic were to recur, the pandemic would likely be repeated.
Table 1 Known transmissible spongiform encephalopathies
Disease | Host species (unusual hosts) | Mechanism of transmission |
Classical scrapie | Sheep, goats | Mostly via oral exposure to excretions/ secretions from infected animals |
Bovine spongiform encephalopathy | Cattle (some African antelope & various domestic & wild felids, goats) | Consumption of tissues from infected cattle – usually in the form of meat and bone meal in feed concentrates (cattle and antelope) or beef carcass material (felids) |
Atypical scrapie | Sheep, goats | Uncertain (sporadic disease?) |
Atypical bovine spongiform encephalopathy | Cattle | Uncertain (sporadic disease?) |
Chronic wasting disease | Deer, elk, moose | Mostly via oral exposure to excretions/ secretions from infected animals |
Kuru | Human | Ritual cannibalism |
Transmissible mink encephalopathy | Mink | Consumption of contaminated feedstuffs but source uncertain (cattle, sheep?) |
Creutzfeldt-Jakob Disease | Human | Iatrogenic & genetic andsporadic forms |
Variant Creutzfeldt-Jakob Disease | Human | Consumption of contaminated beef or beef products |
Gerstmann-Sträussler- Scheinker Syndrome | Human | Genetic |
Fatal familial insomnia | Human | Genetic and sporadic |
Proteinase-sensitive prionopathy | Human | Sporadic |
References
- COLLINGE, J., SIDLE, K. C., MEADS, J., IRONSIDE, J. & HILL, A. F., 1996. Molecular analysis of prion strain variation and the aetiology of 'new variant' CJD. Nature, 383(6602), 685-90.
- CUNNINGHAM, E. P., 2003. After BSE: A future for the European Livestock Sector, pp 90. Wageningen Academic Pub., Netherlands.
- MACLACHLAN, N. J. & DUBOVI, E. J., (eds.) 2016. Veterinary Virology, 5th edition, Academic Press.
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