犬隻泌尿道病原性大腸桿菌毒力特徵的調查與分析

Abstract

泌尿道病原性大腸桿菌為犬隻泌尿道感染最常見的病原之一，當其演變為持續性泌尿道感染時，將增加治療的困難度。為了能在泌尿道成功入侵與定殖，大腸桿菌會攜帶許多毒力因子與致病島嶼。本研究目的為：調查持續性與非持續性泌尿道感染大腸桿菌分離株，其所攜帶的毒力因子、致病島嶼與親緣族群分佈，以及抗藥性的表現，是否有差異。 本實驗由2010年7月到2011年11月，自臺灣大學附屬動物醫院收集36個犬隻大腸桿菌泌尿道感染病例，其中14個為持續性泌尿道感染病例。持續性泌尿道感染多發生在已結紮的母犬，而非持續性泌尿道感染則多發生在未結紮的公犬。絕大多數的泌尿道感染病患有其他潛在的病因，而持續性泌尿道感染的潛在病因多為不容易治癒的疾病，如：後肢癱瘓與膀胱腫瘤。而非持續性泌尿道感染病畜，則較多為可使用外科手術治癒之疾病，如泌尿道結石與赫尼亞。持續性泌尿道感染的分離株，攜帶P型纖毛、S型纖毛與α溶血素的比率，低於非持續性泌尿道感染。其致病島嶼Ⅱ的攜帶率亦較低。在抗藥性表現中，持續性與非持續性泌尿道感染的分離株，其抗藥性比率並沒有顯著的差異。 綜合以上實驗結果，可以發現於持續性泌尿道感染所分離之大腸桿菌，其致病性較低。此情況可能源自持續性泌尿道感染病患多有未治癒的潛在疾病，使致病性較弱的大腸桿菌，有機會造成持續的感染。另一個可能原因為，感染成立後，許多毒力因子並非大腸桿菌生存所必須，而經由致病島嶼或質體的刪除機制移除。此外，抗藥性的提升，並非造成持續性泌尿道感染治療無效的原因。是否能成功的治癒或良好的控制潛在的病因，更是持續性泌尿道感染治療的關鍵。

Uropathogenic Escherichia coli (UPEC) is one of the important pathogens of canine urine tract infections (UTIs). It becomes a frustrating clinical problem when it developed into persistent urine tract infection (PUTI). To successfully colonize the harsh environment of the host urinary tract, UPEC strains express an array of diverse virulence factors and pathogenicity islands. The aims of the study were to determine the difference of antimicrobial sensitivities, distribution of virulence factors and pathogenicity islands between UPEC from canine persistent and non-persistent urine tract infections (NPUTIs). There were 36 canine E. coli UTI cases collected from National Taiwan University veterinary hospital since July, 2010 to November, 2011. Fourteen cases belonged with PUTIs. The results showed that neutered females were more common in the UTI population, and NPUTIs were most prevalent in intact male dogs. Most UTI patients had potentially predisposing disorders. Many PUTIs patients had diseases that couldn’t get cure easily such as hindlimbs paresis or bladder masses. On the other hand, a lot of NPUTI patients had diseases that could be corrected with surgery like urolithiasis or hernias. Virulence factors S fimbriae, P fimbriae and α-hemolysin were detected less significantly frequent for UPEC strains isolated from patient with PUTIs than for those from patients without PUTIs. Pathogenicity islands II536 were also detected less frequently from persistent UPEC isolates. The resistance rates of antimicrobial had no significant difference between PUTIs and NPUTIs isolates.In summary, UPEC isolated form PUTIs had lower pathogenicity. The possible explanations were: predisposing disorders would weaken host defense mechanism, and that made UPEC with lower pathogenicity could cause persistent infections. The other explanation is that virulence factors won’t be necessary for UPEC after the infection. UPEC may lose its virulence factors by pathogenicity islands or plasmids deletions. The causes for failed treatments in PUTI patients were not due to increased resistance to antibiotics. Successfully removing or appropriately managing the predisposing disorder is the key to PUTI therapies.