Aedes aegypti female mosquitoes are capable of the mechanical transmission of lumpy skin disease virus (LSDV) from infected to susceptible cattle. Mosquitoes that had fed upon lesions of LSDV-infected cattle were able to transmit virus to susceptible cattle over a period of 2-6 days post-infective feeding. Virus was isolated from the recipient animals in 5 out of 7 cases. The clinical disease recorded in the animals exposed to infected mosquitoes was generally of a mild nature, with only one case being moderate. LSDV has long been suspected to be insect transmitted, but these findings are the first to demonstrate this unequivocally, and they suggest that mosquito species are competent vectors.
The mosquitoes Anopheles stephensi Liston and Culex quinquefasciatus Say (Diptera: Culicidae), the stable fly Stomoxys calcitrans Linnaeus (Diptera: Muscidae) and the biting midge Culicoides nubeculosus Meigen (Diptera: Ceratopogonidae) were allowed to feed on either lumpy skin disease (LSD) infected animals or through a membrane on a bloodmeal containing lumpy skin disease virus (LSDV). These arthropods were then allowed to refeed on susceptible cattle at various intervals after the infective feed. Virus was detected in the insects by polymerase chain reaction immediately after feeding and at sufficiently high titre to enable transmission to occur. However, no transmission of virus from infected to susceptible animals by An. stephensi, S. calcitrans, C. nubeculosus and Cx. quinquefasciatus was observed.
There is a well-established association between sheep prion protein (PrP) genotype and the risk of death from scrapie. Certain genotypes are clearly associated with susceptibility to the disease and others to resistance. However, there have been no attempts to quantify the disease risk for all 15 PrP genotypes. Here, datasets of the PrP genotypes of nearly 14 000 British sheep and of more than 1500 confirmed scrapie cases were combined to yield an estimate of scrapie risk (reported cases per annum per million sheep of the genotype, or RCAM) for British sheep. The greatest scrapie risk by far, ranging from 225 to 545 RCAM, was for the VRQ-encoding genotypes ARQ/VRQ, ARH/VRQ and VRQ/VRQ. The next greatest risk (37 RCAM) was for the ARQ/ARQ genotype. The ARR/ARR genotype was the only numerically significant genotype for which no scrapie cases have been reported. The AHQ allele conferred resistance and the risk of scrapie in AHQ/VRQ sheep was very low (0?7 RCAM), although there was a higher and moderate risk for the AHQ homozygote (5 RCAM). The ARH allele appeared to confer susceptibility when encoded with VRQ, but possible resistance when encoded with other alleles. Scrapie risk varied with age: for VRQ/VRQ and ARH/VRQ the risk peaked at 2 years of age; that for ARQ/VRQ peaked at 3 years. There was some evidence that, following the lower risk at 4 and 5 years, a second rise occurred from about 6 years. Comparison with other published data indicated that the scrapie risk of certain PrP genotypes may differ between Great Britain and other countries.
Aims: To analyse the frequencies of prion (PrP) gene haplotypes in UK sheep flocks and evaluate their relevance to transmissible spongiform encephalopathies (TSEs) and TSE resistance breeding programmes in sheep. Methods and Results: Genomic DNA isolated from sheep blood was PCR amplified for the coding region of the PrP gene and then sequenced. This study has analysed the sequence of PrP between codons 110 and 245 in 6287 ARQ haplotypes revealing a total of eight variant sequences, which represent a higher than expected 41% of all ARQ haplotypes. The additional PrP gene dimorphisms were M112T, L141F, M137T, H143R, H151C, P168L, Q175E and P241S. Conclusion: The results do not suggest a correlation between the occurrence of a specific ARQ haplotype and the scrapie disease status of a flock. The ARQ haplotype variability appears to be different in the UK sheep flocks compared with sheep flocks from outside the UK. Significance and Impact of the Study: Additional PrP dimorphisms may impact on the methodologies used for standard PrP genotyping in sheep breeding programmes. Some of these polymorphisms were found with significant frequencies in the UK sheep flocks and should therefore be considered in breeding programmes.
Because there is a theoretical possibility that the British national sheep flock is infected with bovine spongiform encephalopathy (BSE), we examined the extent of a putative epidemic. An age cohort analysis based on numbers of infected cattle, dose responses of cattle and sheep to BSE, levels of exposure to infected feed, and number of BSE-susceptible sheep in the United Kingdom showed that at the putative epidemic peak in 1990, the number of cases of BSE-infected sheep would have ranged from fewer than 10 to about 1500. The model predicts that fewer than 20 clinical cases of BSE in sheep would be expected in 2001 if maternal transmission occurred at a rate of 10%. Although there are large uncertainties in the parameter estimates, all indications are that current prevalence is low; however, a simple model of flock-to-flock BSE transmission shows that horizontal transmission, if it has occurred, could eventually cause a large epidemic.
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