摘要
Background: Urinary tract infection caused by Escherichia coli is a frequently observed condition both in humans and animals. Uropathogenic E. coli (UPEC) has been shown to have a pathogenicity island that enables them to infect the urinary tract. Because there is little information about the presence of UPEC-associated virulent genes in animal isolates this work was carried out with the intent to enhance the understanding about the strains of E.coli that cause infections in animals. Results: We screened 21 E. coli strains isolated causing urinary tract infection in domestic animals. Primers were designed to amplify urinary infection-associated genes. Nine genes, papA, tcpC, fyuA, tpbA, Lma, hylA, picU, tonB, and flicC were then amplified and sequenced. Different from the human isolate CFT073, all the animals E. coli lack some of the pathogenesis-associated genes. Genes encoding for proteins used to scavenge iron appear not to be so necessary during animal infections as they are in human infection. In further investigation of phenotypic properties, it was observed that animal UPECs have significantly more impaired ability to form biofilms than human UPEC strain. Conclusions: This study identified significant differences between human and animal UPECs. This may have its roots in the fact that it is difficult to determine if an animal has symptoms. Future studies will focus on some of the observations.
Background: Urinary tract infection caused by Escherichia coli is a frequently observed condition both in humans and animals. Uropathogenic E. coli (UPEC) has been shown to have a pathogenicity island that enables them to infect the urinary tract. Because there is little information about the presence of UPEC-associated virulent genes in animal isolates this work was carried out with the intent to enhance the understanding about the strains of E.coli that cause infections in animals. Results: We screened 21 E. coli strains isolated causing urinary tract infection in domestic animals. Primers were designed to amplify urinary infection-associated genes. Nine genes, papA, tcpC, fyuA, tpbA, Lma, hylA, picU, tonB, and flicC were then amplified and sequenced. Different from the human isolate CFT073, all the animals E. coli lack some of the pathogenesis-associated genes. Genes encoding for proteins used to scavenge iron appear not to be so necessary during animal infections as they are in human infection. In further investigation of phenotypic properties, it was observed that animal UPECs have significantly more impaired ability to form biofilms than human UPEC strain. Conclusions: This study identified significant differences between human and animal UPECs. This may have its roots in the fact that it is difficult to determine if an animal has symptoms. Future studies will focus on some of the observations.
