徐州地区感染性腹泻病人中致病性弧菌的分布研究

目的了解徐州地区感染性腹泻中致病性弧菌的分布情况,掌握其流行规律,为致病性弧菌引起的感染性腹泻提供科学的控制和防治依据。方法用常规分离培养方法检测感染性腹泻粪便或肛拭子标本2674例。结果共检出致病性弧菌10个种类,518株,总检出率为19.37%。结论致病性弧菌是引起本地区感染性腹泻的主要病原菌之一,种类分布繁多。应加强对致病性弧菌的动态监测。     

小鼠动物毒性试验、神奈川溶血试验以及tdh试验对副溶血性弧菌致病性检测有效性的研究

目的比较小鼠动物腹腔注射、灌胃、神奈川溶血实验以及荧光tdh基因PCR反应对副溶血性弧菌致病性检测的有效性。方法采用四种方法,对分离自腹泻者、水产品及自然水体中的菌株测定阳性率,以精确卡方统计比较结果。结果tdh反应可区分腹泻者来源菌株阳性率为90.0%,水产品来源阳性率为9.62%,自然水体来源阳性率为7.32%, P<0.001。结论荧光tdh 基因PCR反应可有效应用于致病性菌株检测。     

首次从北京市腹泻病人粪便中检出致病性弧菌

本文报告1986年夏季从北京市腹泻病例中首次检出致病性弧菌。经形态、生长表现和生物学性状检查,确定一株为弗尼斯弧菌,它具有与河弧菌极为相似的特性,主要通过对葡萄糖产酸产气加以区别。另一株为麦契尼可夫弧菌,它对氧化酶和硝酸盐还原反应均阴性。两菌都不产生肠毒素,豚鼠眼角膜试验阴性,但对乳鼠有较强的致死作用,并对L929小鼠成纤维细胞有明显的粘附表现。对常用的抗菌药物均较敏感。     

食品与临床分离的致病性副溶血性弧菌耐药性比较

目的比较食品与临床分离的致病性副溶血性弧菌耐药性差异,为该菌耐药机制研究提供基础。方法运用K-B纸片法,对上海市28株临床菌株、18株食品源菌株的副溶血性弧菌进行耐药性监测,以PCR分析菌株的耐药基因。再用多位点测序技术揭示46株副溶血性弧菌的遗传多样性,针对相同进化分支中不同来源的分离株进行耐药性比较。结果28株临床菌株的耐药率(100%)明显高于18株食品源分离株(88.9%),而且临床菌株全部为多重耐药性菌株(n=28),而食品源中仅有2株具有多重耐药性。临床菌株所携带的耐药基因数量比食品源分离菌株更多、种类更为丰富。多位点测序分型结果也显示相同的趋势,在同一进化分支中,临床菌株的耐药性也显著高于食品分离株。结论本研究系统地比较食品与临床分离的致病性副溶血性弧菌耐药表型与耐药基因型的差异,分析了耐药性形成的原因,为副溶血性弧菌耐药性的起源、传播与控制提供依据。     

2015-2018年贵阳市水产品中致泻性弧菌监测

目的分析2015—2018年贵州省贵阳市水产品中致泻性弧菌污染情况,为贵阳市制定针对性的公共卫生防控措施提供依据。方法随机采集贵阳市水产品市场和餐馆的水产品检测致泻性弧菌,分析致泻性弧菌在贵阳市的污染和流行状况。结果 2015—2018年共采集960份样品,检出致泻性弧菌17株,各年检出率分别为2.50%,0.42%,2.92%和1.25%,差异无统计学意义(χ2=5.450,P0.05);不同种类水产品阳性检出率两两比较,甲鱼与贝类之间(χ2=11.301)和甲鱼与鱼类之间(χ2=6.490)阳性检出率差异有统计学意义(P0.05),其他几种水产品之间两两比较,差异无统计学意义(P0.05)。结论贵阳市水产品中存在致泻性弧菌污染,检出率低于其他地区;建议有关部门加强对水产品批发和销售市场环境的消毒及监测。     

2014—2019年福建省市售淡水产品寄生虫感染情况调查

目的 了解福建省市售淡水产品寄生虫感染情况,为制定食源性寄生虫病的防控策略提供依据.方法 按照《福建省卫生健康委系统食品污染及有害因素监测方案》,采用分层整群随机抽样的方法进行抽样,将全省分为闽东、闽南、闽西、闽北和闽中5个地区,采集超市或农贸市场售卖的淡水鱼和淡水螺,采用消化法、压片法和剖检法检测寄生虫囊蚴或幼虫.结...     

中、高海拔地区高血压患者肠道菌群的特点

目的 分析中、高海拔地区高血压患者其肠道菌群是否存在各自特征性的分布,探究是否可以肠道菌群为靶点进行预防、治疗高血压。方法 分别收集世居于中海拔地区（1500～2500 m）及高海拔地区（2500～4500 m）的高血压患者粪便样本各20例,中、高海拔地区健康者粪便样本分别为21、20例,四组分别为：中海拔地区高血压患者组、中海拔地区健康者组、高海拔地区高血压患组、高海拔地区健康者组。提取样本DNA,利用16S rRNA高通量测序技术,研究肠道菌群分布特点。使用SPSS 26.0统计软件及生物信息学数据分析方法进行统计分析。探讨中、高海拔地区高血压患者肠道菌群结构是否存在其各自的特点及差异。结果 与MA-HTN相比,HA-HTN组肠道高表达Akkermansia、Catenibacterium、Slackia和Senegalimassilia(P<0.05);与HA-HTN相比,MA-HTN组肠道高表达Candidatus＿Saccharibacteria、Clostridium＿ⅩⅧ和Lachnospiracea＿incertae＿sedis(P<0.05)。结论 HA-...     

厦门地区低致病性禽流感病毒流行病学调查与分析

目的 了解厦门地区家禽低致病性禽流感病毒的流行情况。方法 本研究选取禽流感病毒检出率最高的冬春季节,从厦门市几家主要活禽交易市场采集家禽棉拭子及环境样品,用荧光定量PCR方法进行低致病性禽流感病毒的检测和分型鉴定。结果 从534份样品中,检测出低致病性禽流感病毒阳性216份,检出率为40.4%。本地低致病禽流感病毒的HA亚型至少6种,检出率由高到低依次为H9、H6、H11、H12、H1、H3;NA亚型至少5种,检出率由高到低依次为N2、N6、N3、N8、N9。结论 活禽交易市场家禽中存在不同亚型混合感染情况,尤其以水禽最明显,可同时检出多种亚型。提示今后厦门的疫病防控须加大对水禽的监测及交易市场的管理和消毒。     

甘肃武威地区2005～2007年痢疾杆菌菌群及药敏特点分析

细菌性痢疾是夏秋季节常见的感染性疾病.由于抗生素的广泛应用,痢疾杆菌的耐药性不断增加,及时检测痢疾杆菌及对抗生素的敏感性,为临床医生合理选用抗菌药物十分必要.我们对甘肃省武威市人民医院2005～2007年痢疾杆菌的菌群分布特点及耐药状况进行分析.     

上海市市售水产品中副溶血性弧菌的分离、鉴定及耐药性研究

目的了解上海市市售水产品中副溶血性弧菌(Vibrio parahaemolyticus,Vp)污染状况和耐药性,为防治Vp引起的食源性疾病提供依据。方法采集上海市各大农贸市场3类水产品共273份检测Vp,用统计学处理分析结果;K-B法进行药敏试验。结果水产品中Vp平均检出率为38.46%,其中甲壳类的检出率为50.96%,贝类为27.12%,鱼类为15.79%,三者间有极显著差异(P<0.01)。药敏试验结果显示,105株分离菌株对头孢曲松、萘啶酸和诺氟沙星100%敏感,对氨苄西林的耐药率达69.52%,有20株对多种抗生素耐药。结论上海市售水产品中Vp污染比较严重,药敏结果对多种抗生素耐药。     

丽水市贝类产品中副溶血性弧菌的血清分型及耐药性研究

目的了解丽水市贝类产品中副溶血性弧菌的血清型分布及耐药性,为防治副溶血性弧菌引起的食源性疾病提供依据。方法从丽水市区农贸市场等采集贝壳类水产品,常规方法分离副溶血性弧菌,参照GB/T 4789.7—2003方法,用标准血清进行分型,用纸片扩散法进行药敏试验。结果检出阳性标本28份,检出率为26.67%(28/105)。分离得到的28株副溶血性弧菌分属于7个血清群,分别为O:4群占39.29%(11/28)、O:3群占14.29%(4/28)、O:2群占14.29%(4/28)、O:11群占14.29%(4/28)、O:1群占7.14%(2/28)、O:7群占7.14%(2/28)、O:10群占3.57%(1/28)。28株副溶血性弧菌中有25株对氨苄西林耐药,1株对四环素耐药。结论从丽水市贝类产品分离的副溶血性弧菌具有血清分群多样化和耐药性简单的特点。     

河南省某一淡水养殖环节中非O1/O139群霍乱弧菌毒力基因及分子分型分析

目的 了解河南省淡水养殖环节中非O1/O139群霍乱弧菌毒力基因分布及分子分型情况.方法 对河南省淡水养殖环节中50株非O1/O139群霍乱弧菌和3株病人来源菌株进行全基因测序,利用PubMLST-Vc数据库分析其序列分型(ST),利用最小生成树关系图分析进化关系,通过VFDB数据库获得其毒力基因分布.结果 来源于淡水...     

Ecological diversification reveals routes of pathogen emergence in endemic Vibrio vulnificus populations

Pathogen emergence is a complex phenomenon that, despite its public health relevance, remains poorly understood. Vibrio vulnificus, an emergent human pathogen, can cause a deadly septicaemia with over 50% mortality rate. To date, the ecological drivers that lead to the emergence of clinical strains and the unique genetic traits that allow these clones to colonize the human host remain mostly unknown. We recently surveyed a large estuary in eastern Florida, where outbreaks of the disease frequently occur, and found endemic populations of the bacterium. We established two sampling sites and observed strong correlations between location and pathogenic potential. One site is significantly enriched with strains that belong to one phylogenomic cluster (C1) in which the majority of clinical strains belong. Interestingly, strains isolated from this site exhibit phenotypic traits associated with clinical outcomes, whereas strains from the second site belong to a cluster that rarely causes disease in humans (C2). Analyses of C1 genomes indicate unique genetic markers in the form of clinical-associated alleles with a potential role in virulence. Finally, metagenomic and physicochemical analyses of the sampling sites indicate that this marked cluster distribution and genetic traits are strongly associated with distinct biotic and abiotic factors (e.g., salinity, nutrients, or biodiversity), revealing how ecosystems generate selective pressures that facilitate the emergence of specific strains with pathogenic potential in a population. This knowledge can be applied to assess the risk of pathogen emergence from environmental sources and integrated toward the development of novel strategies for the prevention of future outbreaks.

The emergence of human pathogens is one of the most concerning public health topics of modern times (1–4). According to the World Health Organization, over 300 emerging infectious diseases have been reported in the 1940 to 2004 period, a trend that has continued steadily with recent outbreaks of Ebola in West Africa, Cholera in Yemen, and the global pandemic caused by COVID-19 (3–5). Even though classical molecular approaches have advanced our understanding of bacterial pathogenesis, to date, the genetic adaptations and ecological drivers that facilitate selected strains within a species to emerge as pathogens and successfully colonize the human host remain poorly understood. Given the magnitude and complexity of this urgent threat, it is critical to develop tractable organismal model systems and theoretical frameworks that allow us to dissect the molecular adaptations and environmental factors that lead to the emergence of such human pathogens.Vibrio vulnificus, an emergent human pathogen, is one of the leading causes of non-Cholera, Vibrio-associated deaths globally (6). Despite being a natural inhabitant of estuarine, coastal, and brackish waters (7), this flesh-eating bacterium has gained particular notoriety as one of the fastest killing pathogens (8, 9). Humans are typically infected with V. vulnificus through ingestion of contaminated raw seafood or by direct exposure of open wounds to seawater (6). V. vulnificus infections often result in fulminant septicaemia with an alarming mortality rate exceeding 50% (6, 10–13). The bacterium is particularly lethal in some susceptible hosts, such as immunocompromised patients or those with alcohol-associated liver cirrhosis, diabetes mellitus, or hemochromatosis (14). The annual case counts of V. vulnificus infections have steadily increased over the past 20 y in the United States (15). An upsurge in its worldwide distribution over the past three decades, in correlation with climate change, has led to disease outbreaks in regions with no history of V. vulnificus infections (16–18). Furthermore, models predict this trend to continue resulting in a steady expansion of its geographical range and the subsequent increased risk of human infections (16, 19–21).Based on a series of biochemical and phenotypic traits, V. vulnificus strains have been historically classified into three Biotypes (BT): BT1, which is mostly associated with human infections (22, 23), BT2, which is primarily pathogenic to eels (24, 25), and BT3, which is geographically restricted to Israel and possesses hybrid characteristics from BT1 and BT2 (26, 27). In contrast to Vibrio cholerae, in which all strains capable of causing cholera belong to a single clade, genomic comparisons of V. vulnificus reveal a more complex pattern in the distribution of its clinical strains (28–30). Phylogenomic analyses indicate that the population of V. vulnificus is composed of four distinct groups or clusters (Cluster 1 to 4), which largely overlap with the classical BT classification system (23, 26, 28, 31, 32). Our analyses indicate that the two largest clusters, C1 and C2, exhibit high genomic divergence and appear to be speciating (28), with clinical strains from BT1 predominantly belonging to C1 (22, 23), whereas strains from C2 are primarily associated with BT2 (6, 24, 25). C3 is highly clonal and fully overlaps with BT3, and the rare C4 contains only four nonclonal strains and belongs to BT1 (28, 31). Interestingly, despite patients showing conserved clinical symptoms, C1 clinical strains arise from different clades within the cluster, suggesting independent emergence events of this deadly pathogen (28, 31, 32). To date, the unique genetic traits that allow certain C1 strains to cause severe septicemia remain mostly unknown, posing a daunting public health risk as it hinders our ability to detect potentially pathogenic V. vulnificus (33).Recently, using a combination of bioinformatic and phenotypic analyses that surveyed more than 100 strains of V. vulnificus, we determined that V. vulnificus C1 appears to be associated with a unique ecological lifestyle or ecotype (28). Nonetheless, to date, the ecological drivers that lead to the emergence of clinical V. vulnificus C1 and their pathogenic traits remain poorly understood. In order to start untangling the complex in-situ interactions between genotypes and the environment that underlie the emergence of clinical strains, in this study, we recently surveyed a large estuary in eastern Florida, the Indian River Lagoon (IRL), where outbreaks of the disease frequently occur (7, 34). We found endemic populations of V. vulnificus in the estuary and established two sampling locations to study the environmental dynamics of this bacterium in several natural reservoirs such as water, sediment, oysters, and cyanobacteria. Interestingly, the two sampling sites show major differences in the distribution of V. vulnificus clusters. One of them, Feller’s house (Site A), appears to be significantly enriched with C1 strains, whereas in the second sampling site, Shepard Park (Site B), we mostly recovered strains from C2. Genomic analyses of these strains indicate that, despite these major differences in distribution, high recombination rates as well as frequent exchange of mobile genetic elements and virulence factors between these V. vulnificus populations occur. Microdiversity analyses of these genomes revealed unique genomic markers among C1 strains in the form of clinical-associated alleles (CAAs) with a potential direct role in virulence. The isolated V. vulnificus strains are resistant to numerous commonly used antibiotics irrespective of cluster or site of isolation. However, phenotypic analyses indicate that strains from Site A exhibit traits associated with clinical outcomes, including the ability to resist serum and catabolize sialic acid, unlike those from Site B. Finally, metagenomic and physicochemical analyses of the sampling sites indicate that this marked cluster distribution is strongly associated with distinct biotic and abiotic factors (e.g., salinity, nutrients, or biodiversity) revealing how ecosystems might generate selective pressures that facilitate the emergence of specific strains in a population with pathogenic potential.     

猪轮状病毒的分离鉴定及致病性的研究

<正> 1983～1984年在江苏省的沿长江南北57个养猪场采集了205窝仔猪白痢粪样进行了病原学调查,用电子显微镜及核酸电泳技术检测出轮状病毒89窝份,占43.3％,其中以15～35日龄的病猪粪样感染最高。检测25日龄仔猪粪样     

云南省昆明地区高危人群HIV-1二重感染的研究

目的了解云南省昆明地区高危人群艾滋病病毒I型（HIV-1）二重感染的发生情况与特征。方法筛选昆明地区高危人群出现HIV-1二重感染的病例。通过不同的PCR／测序引物得到不同的测序结果,或直接测序时碱基模糊不清而确定的可疑二重感染病例,然后采用TA克隆的方法对单个PCR克隆进行测序,找到血浆标本中的HIV-1准种,并分析其系统发生和重组结构。结果昆明地区的高危人群中,HIV-1二重感染的发生率为7．7％（2／26）。2名具有高危异性性接触史的HIV-1感染者,分别为CRF01_AE和CRF08-BC或CRF07-BC的二重感染。结论昆明地区高危人群HIV-1的二重感染较为常见,这为快速产生新的重组病毒株提供了基础。该研究提示,该地区高危人群经常暴露于新的病毒株,将加速基因型内重组的发生。     

宁波地区海产品及环境中副溶血弧菌主要毒力及耐药性分析

目的了解浙江省宁波地区海产品和环境中副溶血弧菌主要毒力和耐药性。方法采用生化反应、抗菌药物敏感性试验及PCR方法对分离的宁波地方副溶血弧菌进行毒力及耐药性测定。结果 90株分离株中,耐热直接溶血素基因（tdh）阳性率为2.2%,与神奈川溶血表型（KP,Kanagawa phenomenon）一致,但在tdh＋和KP阳性的分离株中未检测到Ⅲ型分泌系统2（T3SS2）;trh与ureC基因携带率分别为20.0%和12.2%,而在11株trh＋-ureC＋菌株中未显示尿素酶表型阳性,2株尿素酶阳性的菌株未携trh或ureC基因;Ⅵ型分泌系统的携带率为17.8%。所有的分离株对氟喹诺酮类、氯霉素类、四环素类药物敏感;72%以上分离株对青霉素类、磺胺类及氨基糖苷类中链霉素和卡那霉素耐药;分离株中至少耐2种药物,最多耐10种药物,超过82%的分离株对6种以上药物耐药。耐药基因tetB的检出率为0,bla TEM、sul2和strB的携带率分别为91.7%、16.7%和43.3%。结论宁波地区相当比例的菌株携带毒力,并呈现不同程度耐药。     

广东省2003～2008年副溶血性弧菌血清学分型研究

目的了解广东省副溶血性弧菌食物中毒患者和水产品分离株的血清型分布。方法采用血清玻片凝集试验对365株从食物中毒患者和水产品中分离的副溶血性弧菌进行血清分型。结果365株副溶血性弧菌中,205株食物中毒患者分离株以O3：K6型为主,血清型中排前3位的是O3：K6（71.71%）、O4：K8（10.24%）、O2：K3（4.39%）;160株水产品分离株共分50个血清型,排前3位的是O5：K17（8.13%）、O2：K28（6.25%）、O2：K3（5.63%）,无优势菌型。结论2003～2008年广东省副溶血性弧菌食物中毒分离株血清型以O3：K6型为主,水产品分离株血清型呈多样性。