肉鸡源多重耐药空肠、结肠弯曲菌的耐药分子特征

目的了解肉鸡源空肠和结肠弯曲菌的耐药谱特征,检测多重耐药菌株Ⅰ类整合子/基因盒、gyrA基因突变位点、tetO基因、23S rRNA突变位点的分子特征。方法利用PCR检测弯曲菌Ⅰ类整合子/基因盒的存在情况;利用MAMA PCR技术检测弯曲菌gyrA基因第257位碱基的突变情况;针对弯曲菌23S rRNA的V区2075突变位点检测突变菌株。结果多重耐药菌株占分离株的94.5%。146株多重耐药空肠和结肠弯曲菌中Ⅰ类整合子检出率为98.6%,有78株菌株检出3种基因盒,1 000 bp+750 bp+500 bp+250 bp为主要谱型,所占比例为92.3%;有131株在gyrA喹诺酮类耐药决定区发生突变,突变率为92.9%。127株四环素耐药弯曲菌tetO基因的检出率为95.3%。81株红霉素耐药菌株中,23S rRNA的V区2075处突变发生率为96.3%。结论空肠和结肠弯曲菌分离株携带aadA2耐药基因盒,与氨基糖苷类药物的耐药性相关;gyrA基因突变、tetO基因的携带以及23S rRNA突变,与弯曲菌对喹诺酮、四环素和大环内酯类耐药密切相关。     

鸡肉生产链中空肠弯曲杆菌的污染分析及PFGE分型研究

目的 了解鸡肉生产链中空肠弯曲杆菌的分布和传播情况。方法 参考GB/T4789.9-2008、SN0175-2010、ISO10272-1:2006、FDA/BAM:2001、USDA/FSIS:1998等方法组合出分离鸡源疑似空肠弯曲杆菌（Campylobcrter jejun,Cj）的方法,采用16S rDNA和hipO基因的二重PCR方法对其准确鉴定;采用SmaⅠ对83株空肠弯曲杆菌进行PFGE分型。结果 从鸡肉生产链中采集样品519份,分离鉴定出空肠弯曲杆菌 180株,分离率为34.87%。其中养鸡场和屠宰场鸡粪样空肠弯曲杆菌分离率分别为74.29%和66.38%,屠宰场和市场的鸡肉样中空肠弯曲杆菌的分离率分别为17.33%和13.66%。83株空肠弯曲杆菌通过PFGE分型结果产生了45种不同的谱型。结论 四川省部分地区鸡肉生产链中空肠弯曲杆菌的污染较严重,空肠弯曲杆菌在鸡肉生产链中可能存在水平传播现象。     

空肠弯曲菌喹诺酮类抗生素敏感性检测及其耐药机理分析

目的 了解我国不同宿主来源空肠弯曲菌对喹诺酮及氟喹诺酮类抗生素的耐药现状,分析耐药菌株的耐药机制。方法 利用96孔琼脂稀释法分析不同来源空肠弯曲菌对萘啶酸、环丙沙星两种抗生素的最小抑菌浓度(MIC)。对102株检测耐药的菌株和27株敏感菌株通过基因测序的方法分析其耐药机制。结果 234株空肠弯曲菌中共筛查到218株(93.16%)萘啶酸耐药菌株,其中鸡粪和鸭粪来源菌株耐药率均为100.00%,腹泻病人粪便来源菌株耐药率是97.96%,食品动物来源菌株耐药率是97.83%,牛粪来源菌株耐药率是77.97%,耐药率差异有统计学意义(P<0.05),鸡粪和鸭粪来源菌株耐药率最高;211株(90.17%)环丙沙星耐药菌株,其中鸡粪和鸭粪来源菌株耐药率均为100%,腹泻病人粪便来源菌株耐药率是91.84%,食品动物来源菌株耐药率是95.65%,牛粪来源菌株耐药率是77.97%,耐药率差异有统计学意义(P<0.05),鸡粪和鸭粪来源菌株耐药率最高。所有的耐药菌株gyrA基因的喹诺酮类耐药决定区(QRDR)都存在Thr-86-Ile点突变。gyrB基因相关区域测序显示不存在有意义突变。结论 我国分离空肠弯曲菌菌株对萘啶酸、环丙沙星耐药严重,gyrA基因QRDR内的Thr-86-Ile突变能引起空肠弯曲菌对喹诺酮类及氟喹诺酮类抗生素高水平耐药。     

颅脑外伤病人痰液中鲍曼不动杆菌gyrA基因突变与环丙沙星耐药关系研究

目的了解分离自颅脑外伤病人痰液中鲍曼不动杆菌gyrA基因突变与环丙沙星耐药性的关系。方法用ATB药敏试验条板微量肉汤法测定27株鲍曼不动杆菌对14种抗菌药物的敏感性,采用聚合酶链反应(PCR)及序列分析的方法分析gyrA基因序列。结果27株菌中除HZ16号菌株对环丙沙星敏感外,其余26株均耐药。序列分析表明HZ16号菌株gyrA基因无突变,其序列已登录GenBank(accessionAY642140),其余26株耐药菌均存在gryA基因突变,导致耐喹诺酮决定区(QRDR)第83位的丝氨酸被亮氨酸取代。其中HZ28号菌株gyrA基因序列也已登录(GenBankAY642141)。结论gyrA基因突变是导致分离自颅脑外伤病人痰液中鲍曼不动杆菌对环丙沙星耐药的主要原因。     

鲍曼不动杆菌喹诺酮类耐药基因突变分析

目的调查鲍曼不动杆菌对喹诺酮类药物的耐药情况,并对喹诺酮类耐药基因突变进行分析。方法对中南大学湘雅附二医院2002~2008年间鲍曼不动杆菌临床分离株的耐药情况进行统计。同时于2008年7~12月随机收集50株鲍曼不动杆菌,PCR扩增gyrA基因和parC基因,并对扩增产物进行限制性片段长度多态性分析(PCR-RFLP),选取部分PCR扩增产物进行测序和分析。结果鲍曼不动杆菌对喹诺酮类药物的耐药率呈逐年上升的趋势。50株鲍曼不动杆菌对环丙沙星耐药率为62%,对左氧氟沙星耐药率为46%。gyrA基因及parC基因扩增分别获得305 bp和400 bp的基因产物。PCR-RFLP结果显示,对gyrA基因,耐药株100%不能被HinfⅠ酶切,敏感株53%能被HinfⅠ酶切;对parC基因,耐药株29%能被HinfⅠ酶切,敏感株有63%能被HinfⅠ酶切。分析测序结果,耐药株中的gyrA基因和parC基因存在突变,未被酶切的敏感株也存在突变,使HinfⅠ的识别序列GACTC变为GACTT,酶切位点GANTC消失。被酶切耐药株中发现parC基因新的突变点,第89碱基密码子GAA中的A突变成G,被酶切敏感株的parC基因出现多个位点的同义突变。结论鲍曼不动杆菌临床分离株对喹诺酮类药物耐药情况严重,呈逐年上升的趋势。鲍曼不动杆菌对喹诺酮类药物产生耐药与gyrA基因突变和parC基因突变有关。     

肉鸡屠宰加工生产链中弯曲菌污染状况及耐药性分析

目的 了解江苏某肉鸡屠宰加工厂不同环节弯曲菌的污染状况及耐药现状。方法 采集屠宰前肉鸡泄殖腔、不同环节鸡酮体以及环境等样品,运用无血弯曲杆菌选择性培养基(modified charcoal-cefoperazone-deoxycholate agar,CCDA)平板法进行分离纯化,PCR鉴定后,采用K-B法测定6大类14种抗生素耐药情况。PCR检测弯曲菌Ⅰ型整合子、四环素耐药基因tet(O)、氨基糖苷类耐药基因簇aadE-sat4-aphA-3以及弯曲菌gyrA基因第257位碱基的突变情况。结果 细菌分离结果显示170份样品分离到124株弯曲菌(72.95%)。分离株对链霉素、妥布霉素、卡那霉素、环丙沙星、氧氟沙星、萘啶酸、红霉素和四环素耐药率为100%,多重耐药现象普遍,多重耐药率高达100%,其优势耐药谱主要为CTX-CRO-cDA-K-NOR-S-AZM-CIP-TE-NA-E-LEV-ENR-TOB。分离株经PCR扩增未检测到Ⅰ型整合子,所有菌株在gyrA喹诺酮类耐药决定区发生了C-257-T点突变,tet(O)基因和aadE-sat4-aphA-3检出率分别为100%和90.23%。结论 江苏某肉鸡屠宰加工生产链中弯曲菌污染及耐药情况比较严重,gyrA基因突变、tet(O)基因及aadE-sat4-aphA-3耐药基因簇的携带,与弯曲菌对喹诺酮类、四环素类和氨基糖苷类耐药密切相关。     

鸡肉空肠弯曲杆菌的分离鉴定及耐药性分析

目的 分离和收集食源性空肠弯曲杆菌的优势流行株,了解市场上鸡肉中空肠弯曲杆菌的污染和药物敏感性情况。方法 根据GB/T4789.9-2003、SN0175-2010、ISO10272-1:2006、FDA/BAM:2001、USDA/FSIS:1998等方法优化组合出一套对动物性食品源空肠弯曲杆菌有效的分离鉴定方法,从市场上鸡肉中分离疑似空肠弯曲杆菌,并进一步用生化试验及PCR方法进行准确鉴定。采用微量肉汤稀释法测定了所分离的空肠弯曲杆菌对22种常见抗菌药物（组合）的最低抑菌浓度值（MIC）。结论 根据培养特征、形态特征、生化试验和PCR结果准确鉴定出21株空肠弯曲杆菌,其污染率为11.5%。86%生化试验阳性的菌株经PCR鉴定为阳性。将空肠弯曲杆菌标准菌株和随机选出的分离株的16S rDNA扩增序列进行比对,二者同源率为100%。药敏试验表明,14.3%的分离菌株对氨苄西林具有耐药性;大多数菌株对头孢类抗生素MIC值相对较高;42.9%的菌株对萘啶酸具有耐药性;所有分离株对环丙沙星、四环素、红霉素、氯霉素、庆大霉素、链霉素不耐药。     

福建地区鼠伤寒沙门菌喹诺酮耐药基因特征及MLVA分子分型

目的了解福建地区鼠伤寒沙门菌喹诺酮耐药状况及其分子分型机制。方法采用微量肉汤稀释法测定萘啶酸、环丙沙星和左氧氟沙星对83株鼠伤寒沙门菌的最小抑菌浓度(MIC);PCR扩增沙门菌的喹诺酮耐药区(QRDR)基因(gyrA,parC)和质粒介导的喹诺酮耐药基因(PMQR)(aac(6’)-Ib-cr,oqxA,oqxB);采用多位点可变数目串联重复序列分析(MLVA)比较菌株间的遗传相似性。结果 83株鼠伤寒沙门菌对萘啶酸、环丙沙星和左氧氟沙星的耐药率分别为27.7%(23/83),13.2%(11/83)和4.8%(4/83),QRDR基因突变率为25.3%(21/83)。21株基因突变株存在gyrA和parC两个突变类型,突变氨基酸类型分别为Ser83Tyr、Ser83Phe、Asp87Tyr和Asp87Asn,其中以第87位氨基酸突变为主,占总突变数的52.4%(11/21)。parC基因突变菌1株,为第80位氨基酸突变Ser80Arg,该菌株同时为gyrA:Ser83Phe突变。PMQR基因(aac(6’)-Ib-cr,oqxA,oqxB)在83株鼠伤寒沙门菌中的检出率分别为20.5%(17/83)、15.7%(13/83)和16.9%(14/83)。72株鼠伤寒沙门菌经MLVA分型后遗传关联度介于42.3%～100%之间,按照100%的相似度可分为18个型别,其中次优势型MT5菌株耐药基因与MLVA分型表现出一定的关联性。结论福建地区鼠伤寒沙门菌对喹诺酮类药物的耐药率不高,但环丙沙星和左氧氟沙星中度敏感菌中存在耐药基因突变,并具有一定的聚集性,需继续加强检测。     

福建地区鼠伤寒沙门菌喹诺酮耐药基因特征及MLVA分子分型北大核心CSCD

目的了解福建地区鼠伤寒沙门菌喹诺酮耐药状况及其分子分型机制。方法采用微量肉汤稀释法测定萘啶酸、环丙沙星和左氧氟沙星对83株鼠伤寒沙门菌的最小抑菌浓度(MIC);PCR扩增沙门菌的喹诺酮耐药区(QRDR)基因(gyrA,parC)和质粒介导的喹诺酮耐药基因(PMQR)(aac(6’)-Ib-cr,oqxA,oqxB);采用多位点可变数目串联重复序列分析(MLVA)比较菌株间的遗传相似性。结果 83株鼠伤寒沙门菌对萘啶酸、环丙沙星和左氧氟沙星的耐药率分别为27.7%(23/83),13.2%(11/83)和4.8%(4/83),QRDR基因突变率为25.3%(21/83)。21株基因突变株存在gyrA和parC两个突变类型,突变氨基酸类型分别为Ser83Tyr、Ser83Phe、Asp87Tyr和Asp87Asn,其中以第87位氨基酸突变为主,占总突变数的52.4%(11/21)。parC基因突变菌1株,为第80位氨基酸突变Ser80Arg,该菌株同时为gyrA:Ser83Phe突变。PMQR基因(aac(6’)-Ib-cr,oqxA,oqxB)在83株鼠伤寒沙门菌中的检出率分别为20.5%(17/83)、15.7%(13/83)和16.9%(14/83)。72株鼠伤寒沙门菌经MLVA分型后遗传关联度介于42.3%~100%之间,按照100%的相似度可分为18个型别,其中次优势型MT5菌株耐药基因与MLVA分型表现出一定的关联性。结论福建地区鼠伤寒沙门菌对喹诺酮类药物的耐药率不高,但环丙沙星和左氧氟沙星中度敏感菌中存在耐药基因突变,并具有一定的聚集性,需继续加强检测。     

鸭源弯曲菌的分离鉴定及其耐药性、毒力基因分析

目的了解鸭肉生产链中弯曲菌的污染情况及其耐药性和毒力基因分布情况。方法根据GB 4789.9-2014,从肉鸭屠宰链中分离疑似弯曲菌,采用三重PCR方法,对疑似菌株进行准确鉴定;采用微量肉汤稀释法,对弯曲菌分离菌株进行8种抗菌药物敏感性试验,参考NARMS标准判定药敏试验结果;利用PCR检测与弯曲菌致病相关的4个毒力基因。结果根据形态特征、生化指标及PCR鉴定结果,从489份样品中,鉴定出空肠弯曲菌100株、结肠弯曲菌79株,其他弯曲菌8株,弯曲菌的总体分离率为38.24%,肉鸭屠宰前、脱毛环节、掏膛环节、屠宰后样品弯曲菌分离率分别为76.33%、5.62%、24.00%、0%;药敏试验结果表明弯曲菌对TET(95.72%)、CLI(90.91%)的耐药率较高,对AZI(63.64%)耐药率居中,对CIP(31.02%)、GEN(34.76%)、NAL(37.43%)、ERY(41.18%)、CHL(41.18%)的耐药率相对较低,所分离菌株多重耐药现象较为普遍,多重耐药率达72.19%。弯曲菌分离株对黏附相关基因cadF、鞭毛基因flaA、侵袭蛋白基因iamA、毒素调节基因cdtB的携带率分别为100%、80.75%、71.12%、94.65%。结论肉鸭屠宰过程中存在不同程度的弯曲菌污染,且其耐药情况较为严重,毒力相关基因广泛存在于弯曲菌中,应该加强卫生管理和抗菌药物使用监督。     

gyrA mutations in ciprofloxacin-resistant, methicillin-resistant Staphylococcus aureus from Indiana, Minnesota, and Tennessee.

Mutational changes occurring at amino acid codons 84 and 85 located in the gyrA gene of methicillin-resistant Staphylococcus aureus (MRSA) were studied using radiolabeled oligonucleotide probes to examine the incidence of these ciprofloxacin resistance determinants in 30 MRSA isolates from Indiana, Minnesota, and Tennessee. Four separate oligonucleotide probes, one each corresponding to the wild-type sequence, a mutation at codon 84 (nucleotide 251), a mutation at codon 85 (nucleotide 253), and mutations at both, were used to examine the total genomic DNA from each of the 30 isolates, which had been restricted, electrophoresed, and Southern blotted. The probes indicated that 15 of the 28 ciprofloxacin-resistant isolates gave results consistent with a single mutation at codon 84. Four of the 28 ciprofloxacin-resistant strains had results consistent with a mutation at codon 84 and possibly at codon 85. The two ciprofloxacin-sensitive isolates from Tennessee showed homology with the wild-type probe sequence. Five isolates (4, Minnesota; 1, Tennessee) had no homology with any probe. By oligonucleotide probes, ciprofloxacin-resistant MRSA from diverse geographic regions contained similar gyrA mutations at codons 84 or 85 in 19 of 28 ciprofloxacin-resistant isolates.     

重庆市耐多药结核分枝杆菌gyrA与rrs基因突变特征分析

目的分析重庆市耐多药结核分枝杆菌gyrA、rrs基因突变特征及其与氧氟沙星(ofloxacin,Ofx)、卡那霉素耐药(kanamycin,Km)的关系。方法对89株耐多药结核分枝杆菌的Ofx耐药相关基因gyrA和Km耐药相关基因rrs进行序列测定,分析其基因突变特征。结果89株MDR结核分枝杆菌中有50株对Ofx耐药,其中46株(92.00%,46/50)gyrA基因发生突变,突变位点包括74、89、90、91和94位密码子;22株耐Km菌株中,19株(86.36%,19/22)发生rrs基因突变,突变类型均为A1401G。Ofx、Km耐药株的gyrA、rrs基因突变率明显高于相应敏感株的基因突变率,两者之间的差异有统计学意义(χ²=62.937,P<0.001;Fisher双侧P<0.001)。结论gyrA基因90、91、94位密码子突变是重庆市耐多药结核分枝杆菌Ofx耐药的主要机制;rrs基因A1401G突变则是Km耐药的主要原因。     

结核分枝杆菌DNA促旋酶基因突变与耐氟喹诺酮类药物的相关性研究

目的 分析MDR TB结核分枝杆菌临床分离株的DNA促旋酶（gyr）基因突变特点,初步探究MDR-TB对氟喹诺酮类药物耐药与gyr基因突变的相关性.方法 采用最低抑菌浓度（MIC）法筛选MDR-TB,对17株临床MDRTB菌株应用DNA直接测序法检测gyr基因的突变情况,分析细菌基因突变与耐药产生的相关性.结果 Mtb 1株标准菌株（H37Rv）未见gyr A亚单位基因（gyrA）和gyr B亚单位基因（gyrB）基因突变,所有17株临床菌株gyrA均存在95位AGC→ACC.12株耐环丙沙星和左氧氟沙星菌株中,10株gyrA产生了错义突变,突变率为83.3％;突变位点位于89位、90位、91位和94位;1株发生了gyrB突变,突变位点位于500位.耐莫西沙星的9株耐药株中,8株gyrA发生突变,占88.9％.结论 gyrA基因突变是Mtb对氟喹诺酮类药物产生耐药的机制之一;gyrA的错义突变主要发生在第89位、90位、91位、94位密码子上.     

Genetic defect responsible for the dysfunctional protein: factor IXLong Beach

DNA sequence analysis of the gene coding for the variant protein, factor IXLong Beach (FIXLB), has identified a transition mutation in an otherwise normal factor IX (FIX) gene. Genomic DNA clones spanning 35 kilobase (kb) pairs of the FIXLB gene were isolated. A gene analysis strategy that specifically characterized exons and their flanking intron sequences predicted the entire amino acid sequence of FIXLB. A thymine to cytosine transition causes the substitution of a threonine codon (ACA) for an isoleucine codon (ATA) in exon VIII of the FIXLB gene. This mutation results in an amino acid substitution at residue 397 of the FIX zymogen and the phenotypic display of hemophilia-B. Previous studies revealed that activated purified FIXLB (FIXaLB) had normal Ca2+, phospholipid, and factor VIIIa binding characteristics. However, FIXaLB activated factor X or factor VII (with their cofactors Ca2+ and phospholipid) at significantly reduced rates, suggesting that the defect in FIXaLB lies near or within the catalytic triad of the FIX heavy chain. Identification of an amino acid substitution near the carboxy-terminus of the FIXaLB heavy chain supports the earlier characterization of this variant protein. Moreover, our data identify a residue in the catalytic domain of FIXa essential for normal function.     

Prolonged diarrhea due to ciprofloxacin-resistant campylobacter infection

BACKGROUND: Campylobacter causes >1 million infections annually in the United States. Fluoroquinolones (e.g., ciprofloxacin) are used to treat Campylobacter infections in adults. Although human infections with ciprofloxacin-resistant Campylobacter have become increasingly common, the human health consequences of such infections are not well described. METHODS: A case-control study of persons with sporadic Campylobacter infection was conducted within 7 FoodNet sites during 1998-1999. The E-test system (AB Biodisk) was used to test for antimicrobial susceptibility to ciprofloxacin; ciprofloxacin resistance was defined as a ciprofloxacin minimum inhibitory concentration of > or =4 microg/mL. We conducted a case-comparison study of interviewed persons who had an isolate tested. RESULTS: Of 858 isolates tested, 94 (11%) were ciprofloxacin resistant. Among 290 persons with Campylobacter infection who did not take antidiarrheal medications, persons with ciprofloxacin-resistant infection had a longer mean duration of diarrhea than did persons with ciprofloxacin-susceptible infection (9 vs. 7 days [P=.04]). This difference was even more pronounced among the 63 persons who did not take antidiarrheal medications or antimicrobial agents (12 vs. 6 days [P=.04]). In a multivariable analysis-of-variance model, the persons with ciprofloxacin-resistant infection had a longer mean duration of diarrhea than did the persons with ciprofloxacin-susceptible infection (P=.01); this effect was independent of foreign travel. The association between ciprofloxacin resistance and prolonged diarrhea is consistent across a variety of analytical approaches. CONCLUSIONS: Persons with ciprofloxacin-resistant Campylobacter infection have a longer duration of diarrhea than do persons with ciprofloxacin-susceptible Campylobacter infection. Additional efforts are needed to preserve the efficacy of fluoroquinolones.     

Emergence and properties of fluoroquinolone resistant Salmonella enterica serovar Typhi strains isolated from Nepal in 2002 and 2003

A total of 171 Salmonella enterica serovar Typhi strains isolated from Nepal, mostly from patients with typhoid fever in 2002-2003, were tested for antimicrobial susceptibility by disk diffusion assay. Selected S. enterica serovar Typhi isolates were tested for MICs by E-test for ceftriaxone, ciprofloxacin and ofloxacin. Mutations of DNA gyrase gyrA and gyrB and topoisomerase IV parC and parE were identified by sequencing of PCR amplicons. By disk diffusion assay, 75/171 S. enterica serovar Typhi isolates were resistant to nalidixic acid, ampicillin, choramphenicol, streptomycin, tetracycline, sulfisoxazole, and trimethroprim/sulfamethoxazoles. Multiple drug resistance to the 7 antimicrobials was most predominant among S. enterica serovar Typhi isolates in this study. Resistance to nalidixic acid was detected in 76/111 and 56/60 of total isolates collected in 2002 and 2003, respectively. Nalidixic acid-resistant isolates in 2002 and 2003 showed MIC range for ciprofloxacin of 0.125-0.250 mg/l. Nalidixic acid-resistant isolates contained point mutations in gyrA and parC but not gyrB and parE. The gyrA mutation of nalidixic acid-resistant isolates obtained in 2002 and 2003 had amino acid substitution at position 83 of Serine-->Tyrosine and Serine-->Phenylalanine, respectively. Two different mutations of gyrA were detected among nalidixic acid-resistant isolates. Thus it is necessary to monitor mutation in DNA topoisomerase associated with increases in quinolones resistance.     

Enhanced in vivo fitness of fluoroquinolone-resistant Campylobacter jejuni in the absence of antibiotic selection pressure

Campylobacter jejuni, a major foodborne human pathogen, has become increasingly resistant to fluoroquinolone (FQ) antimicrobials. By using clonally related isolates and genetically defined mutants, we determined the fitness of FQ-resistant Campylobacter in chicken (a natural host and a major reservoir for C. jejuni) in the absence of antibiotic selection pressure. When monoinoculated into the host, FQ-resistant and FQ-susceptible Campylobacter displayed similar levels of colonization and persistence in the absence of FQ antimicrobials. The prolonged colonization in chickens did not result in loss of the FQ resistance and the resistance-conferring point mutation (C257 --> T) in the gyrA gene. Strikingly, when coinoculated into chickens, the FQ-resistant Campylobacter isolates outcompeted the majority of the FQ-susceptible strains, indicating that the resistant Campylobacter was biologically fit in the chicken host. The fitness advantage was not due to compensatory mutations in the genes targeted by FQ and was linked directly to the single point mutation in gyrA, which confers on Campylobacter a high-level resistance to FQ antimicrobials. In certain genetic backgrounds, the same point mutation entailed a biological cost on Campylobacter, as evidenced by its inability to compete with the FQ-susceptible Campylobacter. These findings provide a previously undescribed demonstration of the profound effect of a resistance-conferring point mutation in gyrA on the fitness of a major foodborne pathogen in its natural host and suggest that the rapid emergence of FQ-resistant Campylobacter on a worldwide scale may be attributable partly to the enhanced fitness of the FQ-resistant isolates.     

Campylobacter antimicrobial resistance in Peru: a ten-year observational study

ABSTRACT: BACKGROUND: : Campylobacter jejuni and Campylobacter coli are food-borne pathogens of great importance and feature prominently in the etiology of developing world enteritis and travellers' diarrhoea. Increasing antimicrobial resistant Campylobacter prevalence has been described globally, yet data from Peru is limited. Our objective was to describe the prevalence trends of fluoroquinolone and macrolide-resistant C. jejuni and C. coli stool isolates from three regions in Peru over a ten-year period. METHOD: S: Surveillance for enteric pathogens was conducted in Lima, Iquitos and Cusco between 2001 and 2010. Campylobacter stool isolates were tested for susceptibilities to ciprofloxacin, azithromycin and erythromycin. Susceptibilities were reviewed for 4652 isolates from Lima (n = 3419), Iquitos (n = 625) and Cusco (n=608). RESULTS: : Comparing the study periods of 2001-2005 and 2006-2010, prevalence of ciprofloxacin-resistant C.jejuni isolates rose in the study areas of Lima (73.1% to 89.8%, p < 0.001) and Iquitos (24.1% to 48.9%, p < 0.001). Ciprofloxacin-resistant C.coli rates also increased in Lima (48.1% to 87.4%, p < 0.001) and Cusco (10.0% to 65.9%, p = 0.005). Small but significant increases in azithromycin-resistant and erythromycin-resistant C. jejuni prevalence were noted in Iquitos (2.2% to 14.9%, p < 0.001; 3.2% to 14.9%, p = 0.002), and erythromycin-resistant C.coli rates increased in Lima (0.0% to 5.3%, p = 0.038). The prevalence of C.jejuni isolates resistant to both ciprofloxacin and azithromycin increased in Iquitos (0.3% to 14.9%, p < 0.001) and Lima (0.3% to 1.6%, p = 0.011), and prevalence of C.jejuni isolates resistant to both ciprofloxacin and erythromycin rose in Iquitos (0.0% to 14.9%, p < 0.001). Ciprofloxacin and erythromycin resistant C.coli prevalence increased in Lima (0.0% to 5.3%, p = 0.034). CONCLUSIONS: : These results have implications for the empirical management of enterocolitis in Peru. Ongoing surveillance is essential to guide appropriate antimicrobial use in this setting. Local epidemiological studies to explore the relationship between increasing antimicrobial resistance and agricultural or human antibiotic use may be valuable.