§ Mr. Hinchliffe
To ask the Minister of Agriculture, Fisheries and Food, pursuant to his answer of 6 November,Official Report, column 581, for what reasons 24.9 per cent. of the BSE cases reported between January and March were not subsequently confirmed; what changes in the procedure used have been introduced since then; and what percentage of reported cases were subsequently conformed. 
§ Mrs. Browning
The hon. Member for Wakefield who is familiar with the way BSE statistics are compiled will of course be aware that the figure given for BSE reported cases necessarily includes cases which recover are alternatively diagnosed and which are still under restriction.473W
As at 18 November for the period January to March 1996, 4,065 BSE suspect cases were reported in the United Kingdom. Of this figure 2,969 or 73 per cent. cases have been confirmed and 764 or 19 per cent. have proved negative. The difference is accounted for by inconclusive results, alternative diagnosis, animals which have recovered, animals still under restriction and pending results.
For 1993 to 1995, BSE was confirmed in approximately 83 per cent. of the suspects compulsorily slaughtered—average figure for 1993 to 1995. Details of the 1996 confirmation rate will be provided in the November progress report, a copy of which should be placed in the Library of the House in December. This will include details provided in previous reports which indicate seasonal and age related variations in diagnostic rate. The period in question represents the period of each year when diagnostic rate is lowest.
§ Mr. Hinchliffe
To ask the Minister of Agriculture, Fisheries and Food, pursuant to his answer to the hon. Member for Wakefield of 6 November,Official Report, columns 581–82, on experiments on BSE infectivity, what assessment he has made of the susceptibility of the mice challenged with BSE, relative to the susceptibility of other animals to comparable diseases. 
§ Mrs. Browning
It is accepted among specialists in this field that there is a likely 3 log difference in sensitivity between the mouse model used for bioassay and assay directly in calves. A specific experiment intended to quantify that difference is still in progress, and while final interpretation is therefore not possible the evidence so far does appear to support the assumption of a 3 log difference.
The same experiment also highlights the compromises that have to be made by using laboratory models in that mouse assays provide results sooner than cattle assays when testing tissues which contain low levels of infectivity, if any at all. Cattle inoculated intracerebrally with pooled lymph nodes or spleen are still clinically healthy 45 months later, but a negative end point will take a further 39 months to achieve. Mouse models currently in use are capable of detecting scrapie in sheep tissues outside the central nervous system. Furthermore, BSE transmits more effectively from central nervous tissue to mice than do known strains of scrapie. It therefore seems logical that the failure to produce a spongiform encephalopathy in mice by the inoculation of bovine tissue indicates at the very least that the level of infectivity in the source tissue is extremely low, and lower than seen with scrapie. It is not simply a reflection of an inefficient model.