NR ASMY
AU Neilson,S.
TI Is bovine spongiform encephalopathy solely food-borne?
QU BSE-L 18.4.1997
PT LETTER
VT
The recently reported excess of bovine spongiform encephalopathy amongst the calves of cattle with the disease is just as easily explained by inherited susceptibility combined with post-natal exposure as it is by any putative maternal transmission. The highly significant risk ratio (2.9:1, X2 = 17, p < 0.001) is compatible with autosomal recessive inheritance of a trait with an allelic frequency of 0.2 in the cattle population. Thus 20% of the offspring of selected cattle with bovine spongiform encephalopathy mated with unselected bulls could be expected to inherit the recessive trait, as compared with only 4% of the offspring of unselected cattle mated with the same bulls.
A second estimate of allelic frequency is possible from rates of bovine spongiform encephalopathy in well-documented, affected herds of British cattle [1]. The lifetime risk of the disease (the proportion of animals which ultimately develop the disease) is limited to between 12 and 18% of the herd. This might initially suggest an allelic frequency of between 0.34 and 0.42, although there is considerable upward bias resulting from the exclusion of unaffected herds. It is notable in this respect that 50% of British herds number less than 50 animals [2].
The odds ratio of about 1.3:1 in the original case-control study (not significant) [2] and an odds ratio of about 1.9:1 suggested by data graphed in 1995 Progress Report [1] (no significance reported), combined with the latest results, are compelling evidence that maternal status is important. However, the unexpectedly low numbers of (reported) cases of bovine spongiform encephalopathy in exported British cattle suggest that maternal status alone is not sufficient to cause disease in offspring and that continued or subsequent exposure is a necessary condition for disease.
Significant genetic differences between cattle with bovine spongiform encephalopathy, related cattle and unaffected cattle [3] have been reported in only one study, although an abundance of familial relatedness amongst diseased animals does suggest autosomal recessive inheritance [4]. Maternal transmission of bovine spongiform encephalopathy, as for maternal transmission of scrapie [5], is best explained by inherited susceptibilty.
References
1. MAFF (1995) Bovine spongiform encephalopathy in the United Kingdom: A progress report.
2. Hoinville et al (1995) A case-control study of calf feeding practices. Veterinary Record 136(13):312-318
3. Neibergs HL, Ryan et al (1994) Polymerase analysis of the prion gene in BSE-affected and unaffected cattle. Animal Genetics 1994;25(5):313-317
4. Wijeratne WVS and Curnow RN (1990) A study of the inheritance of susceptibility to bovine spongiform encephalopathy. Veterinary Record 1990;126(1):5-8
5. RM Ridley and HF Baker (1995) The myth of maternal transmission of spongiform encephalopathy. BMJ 1995; 311 (7024): 1071-1075
1. Hunter, Goldmann, Smith and Hope (1994) Frequencies of PrP gene variants in healthy cattle and cattle with BSE in Scotland. Vet Rec, 135(17):400-403.
See also:
Brown DR, Zhang et al (1993) Bovine gene allele frequencies determined by AMFLP and RFLP analysis. Animal Biotechnology 1993;4(1):47-51
Grobet L, Vandevenne et al (1994) Polymorphism of the prion protein gene in Belgian cattle. Annales de Medecin Veterinaire 1994;138(8):581-586
AD Dr. Stuart Neilson, CSHSD, Brunel University
SP englisch
PO Deutschland