- Original article
- Open Access
Bovine Spongiform Encephalopathy (BSE) – Infectious, Contagious, Zoonotic or Production Disease?
- Marcus G. Doherr1
© The Author(s); licensee BioMed Central Ltd. 2003
Published: 31 March 2003
In 1986, a new progressive neurological condition similar to scrapie of sheep and goats was recognised in cattle in the United Kingdom (UK), and was named bovine spongiform encephalopathy (BSE). There is an ongoing discussion whether BSE should be classified as infectious, contagious, or zoonotic, and if it fits the definition of a production disease. The objective of this work is to briefly describe the main characteristics of transmissible spongiform encephalopathies (TSE), to review the epidemiology of BSE, and to address the question of how to classify BSE. TSEs are characterised as chronic wasting diseases with spongiform vacuolation and the accumulation of infectious prion protein (PrPSc) in the central nervous system. TSE infectivity is very difficult to inactivate. Cattle BSE most likely originated from sheep scrapie, although this will remain to be an issue for debate. The disease can be transmitted from cattle to a range of species, and has resulted in smaller TSE epidemics in domestic cats, zoo cats and zoo ruminants, and in humans. Transmission in the field occurred through feed containing ruminant-derived protein, and measures to prevent the recycling of infectivity have proven effective to reduce the number of new infections. Mandatory reporting of clinical suspects combined with targeted screening of risk populations is needed to assess the BSE status of a country. Infection studies and the transmissibility to other species classify BSE as infectious and zoonotic. Absence of excretion of the agent, and therefor of horizontal transmission, categorise BSE as non-contagious. However, BSE is a multifactorial infectious disease that is dependent on management factors (mainly feeding), and therefore fits into the broader definition of production diseases.
In 1986, a new clinical disease in cattle was recognised in the United Kingdom (UK). It was classified as a progressive neurological condition similar to scrapie of sheep and goats, and was named bovine spongiform encephalopathy (BSE) . Other transmissible spongiform encephalopathies (TSE) had been described before the occurrence of BSE, namely scrapie of sheep and goats (first observed/described as a clinical entity around 1730), a transmissible mink encephalopathy (TME, 1947), a chronic wasting disease of North American deer and elk (CWD, 1978), and the human TSEs sporadic Creutzfeldt-Jakob disease (sCJD, 1920), Gerstmann-Sträussler-Scheinker Syndrom (GSS, 1928), Kuru (1957), and fatal familiar insomnia (FFI, 1986). These TSEs can arise spontaneously (sCJD), be inherited (FFI, GSS), or are naturally or accidentally transmitted (scrapie, Kuru, CWD, BSE). Some of them possess several of these properties [16, 9, 22, 59, 57, 20, 41, 31]. There is an ongoing discussion whether BSE should be classified as infectious, contagious, or zoonotic, and if it fits the definition of a production disease. The objective of this work is to briefly describe the main characteristics of TSEs, to review the epidemiology of BSE, and to address the question of how to classify BSE.
Characteristics of prion diseases
All known TSEs are characterised by an accumulation of prions ("proteinacious infectious particles", PrP) and vacuolation of the CNS in the final stages of the disease. PrPC is routinely synthesised by various cells, and is metabolised (digested) by proteinase K (enzymes). The infectious prion protein, denoted PrPSc or PrPres, is partly proteinase K resistant. It forms oligomers, accumulates mainly in the cells of the CNS, and results in the specific histopathological changes observed in the differed TSEs . Both PrPC and PrPSc have the same aminoacid sequence, but they have different three-dimensional structures: PrPC in 42% is composed of structures called alpha helices, and has only a few beta sheets . The infectious PrPSc has only 30% alpha helices, and more than 40% beta sheets. The transition of PrPC to PrPSc, based on the prion dimer theory of Prusiner, occurs by merging of a normal (healthy) and an infectious prion molecule to form a PrPC-PrPSc heterodimer, in which the normal PrPC molecule is restructured into PrPSc. After separation of the 2 molecules, 2 new PrPSc homodimers have been created which again can convert healthy PrPC molecules . It still is debated whether PrPSc and TSE infectivity are one and the same, or if there is an additional factor "X" (protein, virion, virus?) besides exposure to PrPSc required to result in a TSE infection .
TSE infectivity is difficult to destroy (decontaminate). The most efficient method is application of wet heat (autoclaving) after treatment with sodium hydroxide (1–2 M NaOH). Application of dry heat will conserve TSE infectivity, and temperatures up to 600°C have been described as insufficient to fully eliminate it from brain tissue cubes [3, 5]. The commonly used methods to treat MBM during rendering (133°C at 3 bars for 20 minutes) will reduce TSE infectivity by at least 98%, but not always by 100% [43, 45, 38, 44, 46]. TSE infectivity, once excreted, can survive in the environment (soil) for several years, as has been demonstrated with the scrapie agent .
Epidemiology of BSE
The origin of BSE (as a cattle disease) is an issue of controversial debate, but it is unlikely that this controversy will ever be resolved. The most widely accepted hypothesis is that cattle BSE originated from sheep scrapie, i.e. that one of the British sheep scrapie strains was recycled with MBM to cattle, and was (or became during recycling) infectious for cattle. After this adaptation, on-going intra-species recycling caused the BSE epidemic in British cattle [35, 47]. Alternatively, a spontaneous mutation in the genome coding for the PrP gene, similar to sporadic CJD in humans, could have resulted in a TSE strain either in sheep or in cattle that was subsequently infectious for – and recycled to – cattle. The introduction of BSE from a wildlife population seems to be a less realistic hypothesis. Large scale recycling of BSE infectivity in the UK became possible after 1970 when changes in the tallow (fat) extraction during MBM rendering from solvent-based (wet, higher temperatures) to pressure-based (dry, lower temperatures) allowed the infectious agent to survive [54, 22].
Experimental oral inoculation of calves and sequential slaughter done in the UK documented that BSE infectivity was only present in the anatomical region of the Peyers patches of the distal ileum at distinct time points during the incubation period, and in the central nervous system (CNS: brain, spinal cord, dorsal root ganglia) late in incubation (few months before clinical disease) and during clinical disease. In cattle, BSE infectivity has not been documented in meat, milk, blood, urine, lymph nodes or any other tissue besides the CNS and the distal ileum wall [25, 42, 51, 52]. One report in which sternal bone marrow isolated from a clinical BSE case in one of the experimentally exposed mice induced a TSE was never reproduced, and was later speculated to have been cross-contamination. Without excretion of the infectious agent during incubation or clinical disease, direct horizontal transmission (from infected to susceptible cattle) does not occur. BSE infectivity levels of CNS tissue from clinically diseased cattle have been titrated in cattle, and there is evidence that 0.1 gram of brain tissue is sufficient to orally infect calves with BSE. Direct intracerebral inoculation of the infectious agent into susceptible mice strains seems to be 500 to 1000 times more efficient than oral exposure of the mice, and this method is used extensively to study the distribution of BSE infectivity in various tissues of experimentally infected animals or field cases, and to differentiate between BSE and other TSE strains.
BSE spread and surveillance
Implementation of mandatory reporting for bovine spongiform encephalopathy (BSE), year of the first BSE cases, implementation of a targeted screening, total BSE case numbers in 2000 and 2001, and assessment of the overall BSE surveillance system in the European Union Member States and Switzerland as of December 21, 2001.
Adult cattle pop.1
Mandatory reporting since (year)
First reported BSE case (OIE)
Detected BSE cases (OIE)
Surveillance system meets OIE requirements (GBR June 2000)
No data available
Transmission of BSE to other species
Transmission of BSE to other species is possible. This has been documented in experimental infection of several species, but also in the observed FSE epidemic in domestic cats (over 90 cases in the UK reported since 1990), in ruminants and large cats kept in British zoos, and by the epidemic of the new variant of Creutzfeldt-Jakob disease (vCJD) in humans with over 100 cases in the UK and 4 cases reported from France so far [30, 60, 50, 36, 6, 58, 17].
BSE can be orally transmitted to sheep and goats where it results in a TSE very similar to scrapie [14, 15]. No field cases of BSE in sheep have yet been diagnosed, however, differentiation to sheep scrapie is only possible by strain typing in mice bioassays, which takes several years to perform. Attempts to orally infect pigs or poultry with BSE failed so far [7, 13, 24].
BSE is a new disease in cattle. Infectivity can be titrated, and the disease has been transmitted to the same and to other species including cats and humans. This classifies BSE as infectious and zoonotic. However, even cattle in the final stages of (clinical) disease do not actively excrete the infectious agent, and horizontal transmission comparable with that of foot-and-mouth disease (FMD), classical swine fever (CSF) or even sheep scrapie does not occur; the disease therefore is not considered to be contagious. The term "production diseases" traditionally was used exclusively for metabolic diseases that were induced by management practices. More recently, the definition of production diseases has been widened to include other traits such as infertility, and multifactorial diseases such as mastitis and lameness that might involve infectious agents but that are exacerbated by nutritional or management factors . BSE, which is caused by an infectious agent (even though some "infectiologists" might not agree to classify prion diseases as such) and is dependent on management factors, would fit into the broader definition of production diseases. This, however, could be true for the majority of diseases that currently affect our animal production systems.
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