comparative genomic hybridization analysis shows different epidemiology of chromosomal and plasmid-borne cpe-carrying clostridium perfringens type a比较基因组杂交分析显示不同流行病学的染色体和plasmid-borne cpe-carrying perfringens梭状芽胞杆菌类型.pdfVIP

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comparative genomic hybridization analysis shows different epidemiology of chromosomal and plasmid-borne cpe-carrying clostridium perfringens type a比较基因组杂交分析显示不同流行病学的染色体和plasmid-borne cpe-carrying perfringens梭状芽胞杆菌类型.pdf

comparative genomic hybridization analysis shows different epidemiology of chromosomal and plasmid-borne cpe-carrying clostridium perfringens type a比较基因组杂交分析显示不同流行病学的染色体和plasmid-borne cpe-carrying perfringens梭状芽胞杆菌类型

Comparative Genomic Hybridization Analysis Shows Different Epidemiology of Chromosomal and Plasmid- Borne cpe-Carrying Clostridium perfringens Type A ¨ ¨ Paivi Lahti*, Miia Lindstrom, Panu Somervuo, Annamari Heikinheimo, Hannu Korkeala Department of Food Hygiene and Environmental Health, Faculty of Veterinary Medicine, University of Helsinki, Helsinki, Finland Abstract Clostridium perfringens, one of the most common causes of food poisonings, can carry the enterotoxin gene, cpe, in its chromosome or on a plasmid. C. perfringens food poisonings are more frequently caused by the chromosomal cpe-carrying strains, while the plasmid-borne cpe-positive genotypes are more commonly found in the human feces and environmental samples. Different tolerance to food processing conditions by the plasmid-borne and chromosomal cpe-carrying strains has been reported, but the reservoirs and contamination routes of enterotoxin-producing C. perfringens remain unknown. A comparative genomic hybridization (CGH) analysis with a DNA microarray based on three C. perfringens type A genomes was conducted to shed light on the epidemiology of C. perfringens food poisonings caused by plasmid-borne and chromosomal cpe-carrying strains by comparing chromosomal and plasmid-borne cpe-positive and cpe-negative C. perfringens isolates from human, animal, environmental, and food samples. The chromosomal and plasmid-borne cpe- positive C. perfringens genotypes formed two distinct clusters. Variable genes were involved with myo-inositol, ethanolamine and cellobiose metabolism, suggesting a new epidemiological model for C. perfringens food poisonings. The CGH results were complemented with growth studies, which demo

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