3. BSE IN IRELAND

3.1 Overview

The first case of Bovine Spongiform Encephalopathy (BSE) in the Republic of Ireland was recorded in 1989, 3 years after the disease was first identified in the United Kingdom.　For the next seven years the number of cases remained at a fairly constant low level of between 14 and 19 per year. In 1996 the numbers started to increase reaching 145 in 2000 giving a cumulative total of 580 cases at 31^st December 2000. The incidence of BSE is summarised in Figure 3.1. The increasing numbers of cases is clearly a cause for concern, but the numbers are still far less than in the United Kingdom which still had some 1270 cases last year (a reduction from 2274 in 1999) and a cumulative total of 177,611 to the end of 2000.

Figure 3.1: BSE Cases in Ireland

3.2 Infectivity in Animals Slaughtered

In order to assess the risk from DRG, it is necessary to have an estimate of the numbers of animals that are slaughtered for human consumption with a significant level of infectivity. In order to define when an animal would have “significant” infectivity it is necessary to understand how the BSE agent builds up over time following infection. MAFF in the UK have carried out a pathogenesis experiment to provide data on this.

The BSE Pathogenesis Experiment. Preliminary results of the BSE Pathogenesis Experiment have been given in the paper by Wells et al (1998). The purpose of the experiment is to determine the spatial and temporal development of infectivity and pathological change in cattle exposed to BSE.　In the experiment a group of 40 calves were selected from farms with no history of BSE and 30 were fed 100 grams of brain collected from BSE infected cattle at four months of age. Ten calves received no treatment and were kept as controls.　At two months post infection 3 infected calves plus one control were killed and a range of tissues collected for analysis.　This was then repeated at about four monthly intervals until clinical signs of the disease appeared. Tissues from the three infected animals were pooled, with a total of some 44 different tissues tested.　Tissues were tested by preparing an homogenate of the tissue and injecting this directly into the brains of a group of 20 R111 laboratory mice.　These mice are used because they have a known and repeatable response to BSE infectivity.

As far as this study is concerned the main results of this experiment are:

In summary, the pathogenesis experiment has shown that there is significant infectivity present in the CNS at 3 months before clinical onset but not at 9 months. In previous risk assessments it has been assumed that there may be “significant” levels of infectivity up to one year before clinical onset, and it is proposed to use the same assumption here. It is also assumed that the infectivity in an animal within one year of onset is the same as that of a clinical case. In practice, the infectivity would be increasing over time so that this assumption is clearly cautious.

Model of the BSE Epidemic in Ireland. The Department of Agriculture Food and Rural Development (DAFRD) has commissioned a model of the BSE epidemic in Ireland from the Department of Statistics at University College Cork (UCC), National University of Ireland, Cork. The model uses data on the progression of the epidemic to predict the numbers of infected animals, and the numbers of infected animals slaughtered. Results for the year 2000 are given in Table 3.1.

The model has been set up to work on a calendar year basis so it cannot provide estimates of animals slaughtered within one year of clinical onset. Instead it estimates the numbers slaughtered in the same calendar year as clinical onset (BSE-0), in the year before onset (BSE-1) or two years before (BSE-2). Thus an animal slaughtered in December 2000 and predicted to have clinical onset of the disease in January 2001 would be classed as BSE-1. An animal classed as BSE-0 could be between 0 and 12 months of clinical onset, whilst an animal classed as BSE-1 could be between 1 month and 24 months of clinical onset. For this assessment it is proposed to use BSE-1 as the basis for animals with significant infectivity. BSE-1 includes the numbers for BSE-0.

The total number of animals slaughtered used in this model is slightly different to the total numbers notified to the CMMS as shown in Table 2.1. The model uses numbers of cattle population data estimated from the Central Statistical Office livestock surveys which breaks the available population over different age groups at each calendar year from which the numbers slaughtered (and disposed of) can be calculated. The numbers slaughtered are thus estimated in a totally different way and the fact that the totals are similar (6% difference) is a good validation of the data.

On advice from the author of the model the 95% range for the results will be taken to x/2 to 2^*x where the mean value is x. Where the result is 0 the 95% range can be assumed to be 0 to 3.

An important result from this model is that it is predicted that there would be no animals slaughtered in the calendar year before clinical onset at less than 36 months of age. The vast majority of animals slaughtered for domestic consumption, and certainly those normally used for prime beef cuts such as rib of beef and T-bone steaks, will be less than 36 months. The UCC model predictions suggest that there is no infectivity associated with animals slaughtered at less than 36 months. Whilst the expected value from the model is zero, the probabilistic assessment will include the possibility that up to 3 animals with significant infectivity could have been slaughtered at less than 36 months but at a low probability.

The model results also show that the numbers of animals slaughtered within one year of onset (BSE-1) will reduce from 79 in 2000 to 38 in 2001 and 20 in 2002. The associated risk levels would therefore also reduce. It will be important to monitor the actual situation to check that these results remain valid.

3.3 Source Term

The estimate of infected animals slaughtered can now be combined with the data on numbers slaughtered given in Section 2.1 to estimate the number of animals in the calendar year before clinical onset that would have been slaughtered for domestic consumption in 2000.　This is summarised in Table 3.2. This shows that it is predicted that less than one bovine would have been slaughtered for domestic consumption in the calendar year before clinical onset of BSE in 2000.