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181.
R. Jory Brinkerhoff Chris Ray Bala Thiagarajan Sharon K. Collinge Jack F. Cully Jr Brian Holmes Kenneth L. Gage 《Ecography》2008,31(5):654-662
Wildlife disease is recognized as a burgeoning threat to imperiled species and aspects of host and vector community ecology have been shown to have significant effects on disease dynamics. The black‐tailed prairie dog is a species of conservation concern that is highly susceptible to plague, a flea‐transmitted disease. Prairie dogs (Cynomys) alter the grassland communities in which they exist and have been shown to affect populations of small rodents, which are purported disease reservoirs. To explore potential ecological effects of black‐tailed prairie dogs on plague dynamics, we quantified flea occurrence patterns on small mammals in the presence and absence of prairie dogs at 8 study areas across their geographic range. Small mammals sampled from prairie dog colonies showed significantly higher flea prevalence, flea abundance, and relative flea species richness than those sampled from off‐colony sites. Successful plague transmission likely is dependent on high prevalence and abundance of fleas that can serve as competent vectors. Prairie dogs may therefore facilitate the maintenance of plague by increasing flea occurrence on potential plague reservoir species. Our data demonstrate the previously unreported ecological influence of prairie dogs on vector species assemblages, which could influence disease dynamics. 相似文献
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There have been remarkably rapid advances in the understanding of prion diseases over the past year. The controversial notion that the transmissible agent may be an abnormal isoform of a host-encoded protein, the prion protein, is now gaining wide acceptance. The conundrum of how a disease can both be inherited as an autosomal dominant condition and also be experimentally transmissible by inoculation is beginning to make sense. 相似文献
185.
O. Windl Maureen Dempster J. Peter Estibeiro Richard Lathe Rajith de Silva Thomas Esmonde Robert Will Anthea Springbett Tracy A. Campbell Katie C. L. Sidle Mark S. Palmer J. Collinge 《Human genetics》1996,98(3):259-264
Creutzfeldt-Jakob disease (CJD) is a transmissible neurodegenerative disorder characterized by the accumulation of aggregates
of a cellular protein, PrP, in the brain. In both human and animals, genetic alterations to the gene encoding PrP (PRNP in human) modulate susceptiblity to CJD. The recent epidemic of bovine spongiform encephalopathy in the UK has raised the
possibility of transmission from animal produce to humans. To provide a baseline against which to assess possible risk factors,
we have determined the frequencies of predisposing mutations and allelic variants in PRNP and their relative contributions to disease. Systematic PRNP genotype analysis was performed on suspected CJD cases referred to the National Surveillance Unit in the UK over the period
1990–1993. Inspection of 120 candidate cases revealed 67 patients with definite and probable CJD, based on clinical and neuropathological
criteria. No PRNP mutations were detected in any of the remaining 53 patients assessed as “non-CJD”. A disease-associated mutation in the PRNP gene was identified in nine (13.4%) definite and probable cases of CJD, a reliable estimate of the incidence of PRNP-related inherited CJD based on a prospective epidemiological series. Within the group of sporadic CJD patients (lacking PRNP mutations), we confirmed that the genotype distribution with respect to the common methionine/valine (Met/Val) polymorphism
at codon 129 within PRNP was significantly different from the normal Caucasian population. The incidence of Met homozygosity at this site was more
than doubled and correlated with increased susceptibility to the development of sporadic CJD. Unlike other recent studies,
Val homozygosity was also confirmed to be a significant risk factor in sporadic CJD, with the relative risks for the three
genotypes Met/Met:Val/Val:Met/Val being 11:4:1.
Received: 18 December 1995 / Revised: 19 January 1996 相似文献