Drinkovic Dragana, Morris Arthur J, Dyet Kristin, Bakker Sarah, Heffernan Helen
Microbiology Laboratory, Labtests, PO Box 12049, Penrose, Auckland 1642, New Zealand.
N Z Med J. 2015 Mar 13;128(1410):50-9.
To estimate the prevalence and characterise plasmid-mediated AmpC beta-lactamase (PMACBL)- producing Escherichia coli in the Auckland community.
All cefoxitin non-susceptible (NS) E. coli identified at the two Auckland community laboratories between 1 January and 31 August 2011 were referred to ESR for boronic acid double-disc synergy testing, to detect the production of AmpC beta-lactamase, and polymerase chain reaction (PCR) to identify the presence of PMACBL genes. PMACBL-producing isolates were typed using pulsed-field gel electrophoresis (PFGE), and PCR was used to determine their phylogenetic group and to identify multilocus sequence type (ST)131. Antimicrobial susceptibility testing and detection of extended-spectrum beta-lactamases (ESBLs) were performed according to the Clinical and Laboratory Standards Institute recommendations.
101 (51%) and 74 (37%) of 200 non-duplicate cefoxitin-NS E. coli were PMACBL producers or assumed hyper-producers of chromosomal AmpC beta-lactamase, respectively. The prevalence of PMACBL-producing E. coli was 0.4%. PMACBL-producing E. coli were significantly less susceptible to norfloxacin, trimethoprim and nitrofurantoin than E. coli that produced neither a PMACBL nor an ESBL. Very few (4%) PMACBL-producing E. coli co-produced an ESBL. Most (88%) of the PMACBL-producing isolates had a CMY-2-like PMACBL. The PMACBL-producing E. coli isolates were diverse based on their PFGE profiles, 44% belonged to phylogenetic group D, and only four were ST131. 100 of the 101 PMACBL-producing E. coli were cultured from urine, and were causing urinary tract infection (UTI) in the majority of patients. The median patient age was 56 years and most (94%) of the patients were women. A greater proportion of patients with community-acquired UTI caused by PMACBL-producing E. coli received a beta-lactam antimicrobial than patients with community-acquired UTI caused by other non-AmpC, non-ESBL-producing E. coli. Thirty-six (43%) patients with community-acquired UTI due to PMACBL-producing E. coli were neither hospitalised nor had any antimicrobial treatment in the previous 6 months.
The prevalence of PMACBL-producing E. coli was relatively low in the Auckland community, but has increased in recent years. Typing revealed that the majority of the PMACBL-producing E. coli in the Auckland region were genetically unrelated meaning that a point source or direct person to person transmission are not drivers of local community spread currently. The isolates were more resistant to non-beta-lactam antimicrobials than other non-AmpC, non-ESBL-producing E. coli, leaving few treatment options. The majority of the PMACBL-producing E. coli isolates seemed to be acquired in the community and were most frequently isolated from women with UTI. A large proportion of patients with community-acquired UTI had not been hospitalised nor had any antimicrobial treatment in the previous 6 months.
评估奥克兰社区中产生质粒介导的AmpCβ-内酰胺酶(PMACBL)的大肠杆菌的流行情况并进行特征分析。
2011年1月1日至8月31日期间在奥克兰两个社区实验室鉴定出的所有对头孢西丁不敏感(NS)的大肠杆菌均被送至环境科学与研究机构(ESR)进行硼酸双纸片协同试验,以检测AmpCβ-内酰胺酶的产生,并通过聚合酶链反应(PCR)鉴定PMACBL基因的存在。对产生PMACBL的分离株进行脉冲场凝胶电泳(PFGE)分型,并用PCR确定其系统发育群并鉴定多位点序列类型(ST)131。根据临床和实验室标准协会的建议进行抗菌药物敏感性试验和超广谱β-内酰胺酶(ESBLs)检测。
200株非重复的头孢西丁NS大肠杆菌中,101株(51%)为PMACBL产生菌,74株(37%)分别为染色体AmpCβ-内酰胺酶的假定高产菌。产生PMACBL的大肠杆菌的流行率为0.4%。与既不产生PMACBL也不产生ESBL的大肠杆菌相比,产生PMACBL的大肠杆菌对诺氟沙星、甲氧苄啶和呋喃妥因的敏感性显著降低。很少(4%)产生PMACBL的大肠杆菌同时产生ESBL。大多数(88%)产生PMACBL的分离株具有CMY-2样PMACBL。根据PFGE图谱,产生PMACBL的大肠杆菌分离株具有多样性,44%属于系统发育群D,只有4株为ST131。101株产生PMACBL的大肠杆菌中有100株从尿液中培养得到,且在大多数患者中引起尿路感染(UTI)。患者年龄中位数为56岁,大多数(94%)患者为女性。与由其他非AmpC、非ESBL产生的大肠杆菌引起的社区获得性UTI患者相比,由产生PMACBL的大肠杆菌引起的社区获得性UTI患者接受β-内酰胺类抗菌药物治疗的比例更高。36例(43%)由产生PMACBL的大肠杆菌引起社区获得性UTI的患者在过去6个月内既未住院也未接受任何抗菌治疗。
在奥克兰社区,产生PMACBL的大肠杆菌的流行率相对较低,但近年来有所上升。分型显示,奥克兰地区大多数产生PMACBL的大肠杆菌在基因上不相关,这意味着目前点源传播或直接人际传播不是当地社区传播的驱动因素。与其他非AmpC、非ESBL产生的大肠杆菌相比,这些分离株对非β-内酰胺类抗菌药物的耐药性更强,治疗选择有限。大多数产生PMACBL的大肠杆菌分离株似乎是在社区中获得的,最常见于患有UTI的女性。很大一部分社区获得性UTI患者在过去6个月内既未住院也未接受任何抗菌治疗。