Division of Dermatology, Department of Medicine, University of Toronto, Toronto, ON, Canada; Mycology Section, Mediprobe Research Inc., 645 Windermere Road, London, ON, N5X 2P1, Canada.
Br J Dermatol. 2015 Jan;172(1):74-80. doi: 10.1111/bjd.13165. Epub 2014 Nov 30.
The dermatophyte Trichophyton rubrum is responsible for approximately 80% of onychomycosis cases. Genetic strain typing was developed to help elucidate its epidemiology and pathogenicity.
To determine T. rubrum DNA strain types in North American patients with onychomycosis and to track the patients before and after their course of treatments.
T. rubrum DNA strain types were determined by restriction fragment length polymorphisms in ribosomal DNA and Southern blotting from toenails that were cultured from 50 North American patients with onychomycosis prior to treatment. Some of the patients were subsequently typed from oral terbinafine (n = 6), laser (n = 9) or placebo (n = 8) treatment groups. Three European DNA strains were obtained for comparison. DNA strains from the terbinafine group were tested for in vitro susceptibility to terbinafine.
Six DNA strain types (A-F) accounted for 94% of T. rubrum DNA strains and corresponded to European isolates. Three DNA strains (6%) novel to North America were detected. DNA strain type switching occurred in all treatment groups: terbinafine (83%), laser (56%) and placebo (25%). Most of the switches (50%) observed in the terbinafine group coincided with mycological cures followed by relapse. Patients treated with laser therapy or placebo exhibited no intermittent cures. DNA strains from the terbinafine group were all susceptible to terbinafine in vitro.
Nine T. rubrum DNA strains were identified in a North American population: three novel and six predominant to a European population. Although DNA strain type switching in onychomycosis is a natural phenomenon, with presence in the placebo group, increases following the course of failed onychomycosis treatment suggest an antifungal-induced response.
亲表皮癣菌红色毛癣菌是导致 80%甲真菌病的原因。遗传株型分析用于阐明其流行病学和致病性。
确定北美甲真菌病患者的红色毛癣菌 DNA 株型,并在治疗前后对患者进行跟踪。
对 50 例北美甲真菌病患者的趾甲进行培养,采用核糖体 DNA 限制片段长度多态性和 Southern 印迹法确定红色毛癣菌 DNA 株型。部分患者随后接受特比萘芬(n=6)、激光(n=9)或安慰剂(n=8)治疗组的分型。同时获得了 3 株欧洲 DNA 株进行比较。对特比萘芬组的 DNA 株进行体外药敏试验。
6 种 DNA 株型(A-F)占红色毛癣菌 DNA 株的 94%,与欧洲分离株相对应。检测到 3 种新型北美 DNA 株型(6%)。所有治疗组均发生 DNA 株型转换:特比萘芬组(83%)、激光组(56%)和安慰剂组(25%)。特比萘芬组观察到的大部分转换(50%)与真菌学治愈后复发有关。接受激光治疗或安慰剂治疗的患者没有间歇性治愈。特比萘芬组的 DNA 株在体外均对特比萘芬敏感。
在北美人群中发现了 9 种红色毛癣菌 DNA 株型:3 种新型和 6 种主要型与欧洲人群相对应。虽然甲真菌病中 DNA 株型转换是一种自然现象,但在安慰剂组中也存在,并且在失败的甲真菌病治疗后增加,提示抗真菌药物诱导反应。