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EFSA and ECDC review scientific evidence on possible links between TSEs in animals and humans

The European Food Safety Authority (EFSA) and the European Centre for Disease Prevention and Control (ECDC) have published a joint opinion reviewing the latest available scientific information on possible links between Transmissible Spongiform Encephalopathies (TSEs)[1] in animals and humans. Current epidemiological and laboratory tools and methods for the evaluation of possible association of animal and human TSEs were also critically evaluated.

In the opinion, EFSA and ECDC have undertaken the first comprehensive review of epidemiological and laboratory studies on possible links between TSEs in animals and humans at EU level. The opinion builds on previous work carried out by EFSA on the zoonotic potential of single TSE agents, as well as a considerable number of other scientific studies on prion diseases.

The findings in the opinion confirm that at present the only TSE proven to be zoonotic (i.e. transmissible from animals to humans), remains Classical Bovine Spongiform Encephalopathy (BSE), known in humans as variant Creutzfeldt-Jakob disease (vCJD)[2].

Epidemiological evidence shows that the most common form of TSE in humans is sporadic Creutzfeldt-Jakob disease (sCJD). The cause of sporadic CJD remains uncertain[3]. While scientific research to date has not identified an environmental source of infection[4], the Panel could not exclude the possibility that a small number of cases could be zoonotic.

Regarding Classical scrapie in goats and sheep, no epidemiological evidence suggests it is zoonotic; whereas for Atypical scrapie in sheep and goats, the scientific data currently available are too limited to conclude whether it has the potential to be zoonotic or not.

For other TSEs, a number of uncertainties make it impossible at present to draw definite conclusions on possible links between animals and humans. One of the reasons for this is that data on the monitoring of TSEs in animals are too recent to be compared to the respective human data. The opinion therefore recommends that systematic monitoring of TSE diseases be continued in both humans and animals.

In addition to epidemiological data, the scientists also evaluated evidence obtained from experimental transmission of TSEs in laboratory studies. The opinion states that the results of some of these studies suggest there might be a possibility of animal-to-human transfer for other TSEs, in addition to Classical BSE in cattle. In particular, some data indicate that one of the new atypical BSE agents[5], the L-BSE or BASE agent, may have a similar or higher zoonotic potential than the Classical BSE agent. The opinion however points out that at present it is not possible to define how informative these laboratory studies are for measuring the transfer of TSEs between animals and humans under real exposure conditions.

This joint opinion of EFSA and ECDC provides an overview of the situation in relation to the zoonotic potential of TSEs and may support risk managers in their work on those TSEs which are of major concern for human health.

[1] TSEs or so-called prion diseases are a family of diseases that affect the brain and nervous system of humans and animals. These include Classical BSE and Atypical (L-type and H-type) BSE, Classical and Atypical scrapie, Chronic Wasting Disease and Transmissible Mink Encephalopathy.

[2] Creutzfeld-Jakob disease (CJD) is a transmissible spongiform encephalopathy in humans. Various forms of CJD are recognised: of these, sporadic CJD is the most common and its origin is uncertain; variant CJD was identified in the 1990s and is closely linked to exposure – probably through food – to the cattle disease bovine spongiform encephalopathy (BSE).

[3] See also World Health Organization

[4] For example, direct/indirect transmission of the infective agent from animals, micro-organisms, food, water, objects, body fluids or through air inhalation.

[5] Atypical H-type BSE (H-BSE) and Atypical L-type BSE (L-BSE or BASE) agents are two distinct Atypical BSE agents, discovered after 2004.

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