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9.1 The possibility of endemic infection
9.2
The worst-case scenario
There are two scenarios for the future course of BSE. The first is that BSE, like TME and kuru, is a dead-end disease. If this is true, and if meat and bone meal was the sole source of the infection, then removing this source would be sufficient for the eventual eradication of BSE from the United Kingdom.
In July 1988, the United Kingdom Government introduced a ban on the feeding of all ruminant-derived protein to ruminants (HMSO, 1988a; for subsequent modifications see HMSO, 1988e; 1989a; 1990b). However, the incubation period of BSE in cattle averages about four to five years. This means that no reduction in the current incidence can be expected until 1992 at the earliest.
9.1 The possibility of endemic infection
The alternative scenario is that there are natural routes of transmission of BSE and that the outbreak could turn into an endemic infection of cattle in the way that scrapie is in sheep.
As of July 1991 the ongoing epidemiological survey had not revealed any firm evidence of maternal transmission of BSE, as would be expected from the analogy with scrapie. Only one putative case of maternal transmission in cattle has been reported (Anon., 1991b).
A major experiment was set up in 1989 in order to investigate this question. Carefully matched groups of test and control animals are being observed to see if the incidence of BSE is higher in calves born to BSE-affected dams. A high level of maternal transmission of infection could be manifest after 1992. A much longer observation period (up to a maximum of seven years) will be necessary to prove a low incidence of maternal transmission or to show that it does not occur.
To sustain BSE infection in the cattle population requires that each breeding cow is replaced by at least one infected female calf, which then transmits infection to at least one of her offspring. The current breeding regimes in the United Kingdom dairy herds, with an annual herd replacement rate of 20 to 25 percent, would not enable this to occur for a prolonged period of time, even with a 100 percent maternal transmission of infection to calves. Therefore, the worst that could happen in this situation is that the rate of decline in the incidence of BSE would be somewhat slower than if BSE were a dead-end infection (Wilesmith and Wells, 1991).
For BSE to become endemic, the number of infected cattle would need to increase by horizontal spread. In scrapie, this can occur particularly at lambing as a by-product of the postnatal component of maternal transmission. For example, an infected placenta can be a source of infection to unrelated ewes.
Cattle management is sufficiently different from sheep management for the chances of horizontal spread of BSE to be lower, especially in dairy herds where cows often calve in isolation and the calves are separated after a few days.
The same is not true of beef suckler herds in which cows and calves run together. This would increase the chances of postnatal maternal transmission and it might also create opportunities for the horizontal spread of infection. However, BSE is much rarer in beef than in dairy herds (see Table 4 and Wilesmith et al., 1988; 1992a).
In conclusion, BSE is unlikely to become an endemic infection of cattle unless a high level of maternal transmission enables the epidemic to be amplified by the horizontal spread of infection. It is too soon to assess this possibility but it seems improbable that BSE is highly contagious because the average incidence within affected herds is only about 2 percent. There is little point in imposing additional control measures until there is a demonstrable need for them. However, common sense urges two simple precautionary steps. The first is that calves born to cows which are or which become confirmed cases of BSE should not be selected as replacement heifers within the herd. The existence in the United Kingdom of a specified offals ban means that such calves could, for example, be fattened for beef without risk to public health.
The second recommendation is to minimize the risk of horizontal spread of infection at calving by good hygiene and the early disposal of the placenta (by incineration or burial). This is a legal requirement on those rare occasions when a suspect BSE case is calving (HMSO, 1988b), but it is good practice for reducing the spread of other infections as well.
Although unlikely, the worst possible situation would be if BSE became established as an endemic infection in exactly the same manner as scrapie. The difficulties of eradication would then be similar.
Scrapie can be controlled quite effectively by selective culling in the female line and by husbandry measures to limit the horizontal spread of infection at lambing. But two problems make this a difficult task.
The first is the need for accurate breeding records, which rarely exist when most needed, at the start of the outbreak. Selective culling cannot begin without them and it takes several years to build up sufficient records.
The second problem is that infected ewe lines can only be identified when the clinical disease appears. The spread of infection from a ewe to several successive lamb crops can easily go unnoticed for a generation if the anima dies or is culled before developing the clinical disease. Since only a small proportion of ewe lambs may be retained for breeding, another infected generation could be missed if the few lambs that survive as breeding ewes happen to be of a sip genotype which can be infected but never develops the disease.
It therefore requires many years of patient application to bring scrapie under control. Much of the work can easily be undone if bought-in flock replacements reintroduce the infection. This is why the eradication of scrapie is so difficult. The same problems could attend the eradication of BSE, with one important difference, described below.
In sheep, the sip gene has a major effect in controlling the susceptibility and incubation period of scrapie. Sip and PrP genes in sheep are almost certainly the same. The PrP gene is also present in cattle and allelic variants have been found which have either five or six copies of an octapeptide repeat sequence in the coding region (Goldmann et al., 1991).
However, studies of a large herd affected with multiple cases showed no association of BSE with this polymorphism of the PrP gene (Dawson and Martin, personal communication). These findings are consistent with the biological evidence (particularly from transmission studies as mentioned in Chapter 4, suggesting that there may be little or no allelic variation at the PrP or any other genetic locus that affects BSE. If true, the occurrence of infected carriers may be far less common in BSE than in scrapie, making BSE easier to eradicate.
If further steps to eradicate BSE become necessary, they would not be worth applying on less than a national scale. The essential prerequisite is good breeding and movement records which are currently being compiled in the United Kingdom following recent legislation (HMSO, 1990c; 1990d). By the time they are sufficient for the task, the necessity (or otherwise) for further action to eradicate BSE will be known. Meanwhile, the precautionary measures to safeguard other species, including human beings, are already in place.