Mobile contingency locus controlling Escherichia coli K1 polysialic acid capsule acetylation.
Mobile contingency locus controlling Escherichia coli K1 polysialic acid capsule acetylation.
复制标题
控制大肠杆菌K1聚唾液酸胶囊乙酰化的移动应急位点。
DOI:
10.1111/j.1365-2958.2006.05158.x
复制
发表时间:
2006
期刊:
影响因子:
--
通讯作者:
Steenbergen,SusanM
中科院分区:
文献类型:
--
作者:
Vimr,EricR;Steenbergen,SusanM
Escherichia coliK1 is part of a reservoir of adherent, invasive facultative pathogens responsible for a wide range of human and animal disease including sepsis, meningitis, urinary tract infection and inflammatory bowel syndrome. A prominent virulence factor in these diseases is the polysialic acid capsular polysaccharide (K1 antigen), which is encoded by thekps/neuaccretion domain inserted nearpheVat 67 map units. SomeE. coliK1 strains undergo form (phase) variation involving loss or gain of O‐acetyl esters at carbon positions 7 or 9 of the individual sialic acid residues of the polysialic acid chains. Acetylation is catalysed by the receptor‐modifying acetyl coenzyme‐A‐dependent O‐acetyltransferase encoded byneuO, a phase variable locus mapping near the integrase gene of the K1‐specific prophage, CUS‐3, which is inserted inargWat 53.1 map units. As the firstE. colicontingency locus shown to operate by a translational switch, further investigation ofneuOshould provide a better understanding of the invasive K1 pathotype. Minimal estimates of morbidity and economic costs associated with human infections caused by extraintestinal pathogenicE. colistrains such as K1 indicate at least 6.5 million cases with attendant medical costs exceeding $2.5 billion annually in the United States alone.