BSE in the Netherlands: an update

Up to 2006, there have been 82 cases of BSE in cattle born in the Netherlands. This article reviews the current situation regarding BSE in the Netherlands and summarizes the clinical symptoms of the disease. Data from the Netherlands show that a passive surveillance system, by which farmers and veterinarians have to report suspect clinical cases, has a low sensitivity. The epidemiology of, and risk factors for, BSE are discussed. All the Dutch cases of BSE can be attributed to cross-contamination of feed with meat-and-bone meal. On the basis of information about the epidemic and the cases reported to date, it is anticipated that the number of cases of BSE will continue to decline in the Netherlands and Europe. The European Commission has presented a road map that describes how the European BSE policy can be changed in the short and long term if the current favourable trend in BSE cases continues. It is time for a new phase in the management of BSE but with continued protection of the public's health and eradication of BSE.     

Pathogenesis of BSE

Before the emergence of bovine spongiform encephalopathy (BSE) and recognition of its zoonotic potential, the major example of the transmissible spongiform encephalopathies (TSEs) of animals was scrapie of sheep. But there is no evidence that scrapie transmits naturally to any species other than sheep and goats. The pathogenesis of scrapie has been studied most in experimental laboratory rodent species. In most experimental models of scrapie, after peripheral non-neural routes of infection, replication of the agent can first be detected in lymphoreticular system (LRS) tissue. When the route of introduction of agent into the body is localized, initial involvement will be in LRS tissue draining the infection site. Thereafter, there is a striking amplification of the agent in the LRS and spread by lymphatic/haematogenous routes, giving widespread dissemination in the LRS. This precedes replication in the CNS, but is not the means by which infection reaches the CNS. There is now substantial evidence from experimental models of scrapie that involvement of the CNS is by peripheral nervous system (PNS) pathways. In some models employing oral exposure the earliest localized LRS replication is in the gut-associated lymphoid tissue (GALT) and autonomic PNS routing to the CNS has been implicated. However, the relative importance of different routes of spread of TSEs within the body is determined by a number of host- and agent-dependent factors and, therefore, generalizations from an experimental model to a natural disease across a species barrier may not be appropriate. With the occurrence of BSE and recognition of its food-borne route of transmission via meat and bone meal, has come greater awareness of the probable importance of the oral route of infection in ruminant species affected by TSEs. In consequence, studies have increasingly focused on the natural host species to examine pathogenetic events.     

Pathogenesis of BSE

Before the emergence of bovine spongiform encephalopathy (BSE) and recognition of its zoonotic potential, the major example of the transmissible spongiform encephalopathies (TSEs) of animals was scrapie of sheep. But there is no evidence that scrapie transmits naturally to any species other than sheep and goats. The pathogenesis of scrapie has been studied most in experimental laboratory rodent species. In most experimental models of scrapie, after peripheral non-neural routes of infection, replication of the agent can first be detected in lymphoreticular system (LRS) tissue. When the route of introduction of agent into the body is localized, initial involvement will be in LRS tissue draining the infection site. Thereafter, there is a striking amplification of the agent in the LRS and spread by lymphatic/haematogenous routes, giving widespread dissemination in the LRS. This precedes replication in the CNS, but is not the means by which infection reaches the CNS. There is now substantial evidence from experimental models of scrapie that involvement of the CNS is by peripheral nervous system (PNS) pathways. In some models employing oral exposure the earliest localized LRS replication is in the gut-associated lymphoid tissue (GALT) and autonomic PNS routing to the CNS has been implicated. However, the relative importance of different routes of spread of TSEs within the body is determined by a number of host- and agent-dependent factors and, therefore, generalizations from an experimental model to a natural disease across a species barrier may not be appropriate. With the occurrence of BSE and recognition of its food-borne route of transmission via meat and bone meal, has come greater awareness of the probable importance of the oral route of infection in ruminant species affected by TSEs. In consequence, studies have increasingly focused on the natural host species to examine pathogenetic events.     

BSE: clinical diagnosis and field experience

The clinical diagnosis 'suspected of having BSE' is difficult. Cows older than 2.5 years, presented to the private veterinary practitioner with disturbed locomotion present for more than 14 days and with no detectable cause, should be investigated with suspicion. Questions on changes in behaviour of the animal and during the examination attention on exaggerated responses to handling and sound can give additional information. Notification of suspected cases and gained field experiences are discussed.