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The appearance of Foot and Mouth Disease Type 0 (Asian types) in the United Kingdom shortly after the occurrence of Classical Swine Fever has been a very great threat to the United Kingdom livestock industry. The occurrence of the two so soon after one another, and both supposedly originating from the same part of the world suggests that there have been changes in the patterns of food importation into the UK that have allowed these strains to enter. Recent observations by television journalists have even shown that “bush meat” including monkeys is freely available but at very high prices in the ethnic markets of North London. This material is basically brought in by returning foreign nationals in small quantities and by professional smugglers in larger quantities. Who knows what disease agents are coming in with these specimens. We must have increased numbers of staff and improved techniques for the detection of illegally imported materials. A wider use of sniffer dogs at airports in the UK would be a start. The appearance of blue tongue in the UK can reasonably be expected from dairy and milk products carried in by holidaymakers returning from Sardinia (in ever-increasing numbers).
The fact the present outbreak is probably as a result of swill feeding of pigs obviously containing infected material that was not known to be contained in restaurants, schools, catering or retail outlet material has, in fact, led to the banning of swill feeding in the United Kingdom.
This outbreak (2001) is very different from the last big UK outbreak in 1967. This one is a single primary with secondary spread to abattoir (transport of pigs) and by local contact to sheep and thence to markets across a large part of the country. Probably two million sheep were moved through dangerous contact points prior to the detection of the disease and a movement ban initiated so what has been happening is that “catch-up” has been played ever since the original diagnosis.
So here we have a multicentric sheep-based epidemic via markets and dealers, nationwide, including exports (France and Netherlands) in which clinical diagnosis has often been very difficult. This is particularly so in sheep where the occurrence of typical lesions appears rare. There have been few occasions where foot lesions, mouth lesions and pyrexia have been reported. This has often resulted in animals not diagnosed on clinical grounds but being slaughtered on suspicion and subsequently being converted to infected premises on the basis of confirmatory laboratory tests.
In cattle almost all cases have been diagnosed on clinical grounds because the clinical signs have been much more obvious (serious fall in milk yield, lameness, very painful feet, sores on udders, slavering [slobbering or excessive salivation], mouth lesions [including blisters, vesicles, erosions, ulcers] on hard palate, dental pad, gums and tongue and foot lesions, principally vesicles in the interdigital cleft and along the coronary band).
For us pig farmers and veterinarians the most amazing thing has been although the index case was in pigs in an abattoir and the source of this infection was a swill feeder several hundred miles away there has been little further involvement with pigs. Two other pig premises were affected early on by lateral spread from the abattoir but since then perhaps only three other groups of pigs in close proximity to sheep have been culled on clinical grounds, but in each case confirmation tests were negative. There has only been one other incident in pigs and that was also early on in an abattoir where positive pigs were taken in from one of the original infected premises but the other cases taken on clinical grounds have been negative. Because of the possibility of high virus release by infected pigs (40 times+ compared to cattle and sheep) pigs have often been culled as dangerous contacts to present the formation of virus plumes but in no instance have these pigs proved positive as in-contacts and no demonstration of a virus plume (i.e. airborne infection) has, as yet, been demonstrated.
