性传播疾病性尿道炎后慢性前列腺炎病原学分析

目的：了解性传播疾病(sexually transmitted disease,STD)性尿道炎后慢性前列腺炎患者前列腺液(expressed prostatic secretion,EPS)标本中病原体的感染状况及对常用抗菌药物的敏感性。方法：对性传播疾病后慢性前列腺患者的EPS进行病原体检测和药敏试验。结果：126例患者中96例分离出病原体115株,阳性率为76．2％。主要病原体为金黄色葡萄球菌(20．0％)、解脲支原体(18．3％)、表皮葡萄球菌(14．8％)和淋球菌(13．9％),混合感染率达15．1％。药敏试验显示解脲支原体对四环素、红霉素和氧氟沙星耐药,而对原始霉素、强力霉素和交沙霉素敏感。葡萄球菌属对万古霉素、呋喃妥因和头孢唑啉最为敏感。结论,提示EPS的病原体检测对临床诊断和治疗性传播疾病后慢性前列腺炎具有重要意义。     

三重聚合酶链反应检测STD病原体

本文对100例性罪错人员应用三重聚合酶链反应（PCR）一次扩增快速检测淋球菌、沙眼衣原体、解脲支原体混合感染,三种病原体的检出率分别为24％、38％、37％,混合感染率为22．22％,提示在STD诊治中必须重视多种病原体混合感染．另外,对三重PCR法与常规方法和经典PCR进行比较有良好的符合率,显示其在临床检测方面的优势。     

1281例泌尿生殖道感染患者的病原体分析

目的了解汕头地区泌尿生殖道炎患者病原体感染情况。方法应用培养、衣原体快速免疫测定法及镜检,对性病科和妇科门诊1281例泌尿生殖道感染患者进行淋球菌(NG)、沙眼衣原体(Ct)、解脲支原体(Uu)、人型支原体(Mh)、念珠菌(Cd)和滴虫检测。结果男577例．检出262株病原体,女704例．检出656株病原体。6种病原体阳性率男女性分别为(括号内为女性)：NG3．5％(3．1％)、Ct11．6％(10．9％)、Uu24．1％(50．6％)、Mh1．5％(6．3％)、Cd4．5％(20．2％)和滴虫17％(2．0％),感染率为37．3％(65．2％),混合感染占19．1％(37．3％)。结论汕头地区非淋球菌性和条件致病性病原体Ct、Uu和Cd占主导,混合感染普遍．男、女性感染情况除NG、Ct外,女性明显高于男性。     

98年2194份呼吸道标本病原体分析

目的 了解本地区呼吸道感染的病原体。方法 采用回顾性调查方法对我院１９９８年１月～１２月呼吸道标本规培养结果进行全面分析。结果 病原体阳性培养率为３２．３６％,其中Ｇ－杆菌占７３．５２％,Ｇ＋菌占１２．６８％,霉菌占１３．８０％;在病原体种类中前五位依次为,绿脓杆菌占２５．０７％,肺炎克雷伯杆菌占１７．０４％,霉菌占１３．８０％,葡萄球菌占８．１７％,鲍鳗不动杆菌占６．２０％。结论 本地区呼吸道感     

临时多性伴接触者病原体感染分析

目的了解临时多性伴接触者病原体的感染情况。方法对2005年5月至2008年5月于我科门诊就诊的临时多性伴接触者进行病原体检测并分析病种特点。结果临时多性伴接触者病原体感染的阳性率为65．3％,2种以上病原体混合感染阳性率为31．4％,病原体以解脲脲原体为最高,人型支原体阳性率最低;病种以非淋菌性尿道炎、尖锐湿疣及梅毒为主。结论临时多性伴接触者容易感染病原体,混合性感染增多,病种以非淋菌性尿道炎、尖锐湿疣及梅毒为主。     

用复合PCR检测淋球菌、沙眼衣原体和解脲支原体的感染研究

在性传播疾病中,泌尿生殖道感染的主要病原体是淋球菌、沙眼衣原体和解脲支原体,目前临床上常有多种病原体混合感染[1],其临床症状相似或无明显症状,给确诊和治疗带来不便。因此我们应用多重引物ＰＣＲ(ｍｕｌｔｉｐｌｅｘＰＣＲ),一次实验能从临床标本中检测出三种病原体…     

用复合PCR检测淋球菌、沙眼衣原体和解脲支原体的感染研究

在性传播疾病中,泌尿生殖道感染的主要病原体是淋球菌、沙眼衣原体和解脲支原体,目前临床上常有多种病原体混合感染[1],其临床症状相似或无明显症状,给确诊和治疗带来不便。因此我们应用多重引物ＰＣＲ(ｍｕｌｔｉｐｌｅｘＰＣＲ),一次实验能从临床标本中检测出三种病原体...     

PCR技术检测性病病原体在男性泌尿生殖系感染中的意义

用ＰＣＲ技术对我院５８８例男性生殖泌尿系感染患者进行淋病Ｋ球菌（ＮＧＦ）沙眼衣原体（ＣＴ）及解脲支原体（ＵＵ）检测,结果淋球菌感染者７５例（１２．７６％）;沙眼衣原体感染者８４例（１４．２９％）;解脲支原体感染者５１例（８．６７％）。淋球菌与沙眼衣原体混和感染者２５例（４．２５％）;淋球菌与解脲支原体混合感染者９例（１．５３％）;沙眼支原体与解脲支原体混合感染者１２例（２．０４％）;未发现有三种病原体同时感染者,并对ＰＣＲ检测性病病原体的意义及性病病原体传播趋势进行讨论。     

沿海地区淋球菌,沙眼衣原体及解脲支原休流行病帝分析

目的 了解中山市性传播疾病（ＳＴＤ）高危人群中淋球菌（ＮＧ）、沙眼衣原体（ＣＴ）及解脲支原体（ＵＵ）的感染状况,采用聚合酶链反应（ＰＣＲ）检测１４５２例ＳＴＤ患者的尿道（宫颈）拭子标本。结果３种病原体的总检出率为２５．９２,其中ＮＧ１３．７０％、ＣＴ３１．３４％、ＵＵ３２．７１％,混合感染率以ＣＴ最高（８２．８１％）,ＵＵ次之（７５．７８％）,ＮＧ为４９．２２％。非淋病性尿道炎（ＮＧＵ）、淋病性尿     

下呼吸道感染不动杆菌属流行和药敏变迁分析

目的：分析近年来南京医科大学第一附属医院不动杆菌属的流行情况及耐药现状,为临床合理应用抗菌药物提供指导依据。方法：收集2004年-2008年南京医科大学第一附属医院下呼吸道感染住院病人痰培养结果为不动杆菌的数据,用WHONET5.3软件统计分析。结果：2004年-2008年该院下呼吸道感染住院病人痰培养为不动杆菌属占所有病原体比例为7．0％．9．2％,占革兰阴性菌比例为13．9％-17．5％。革兰阴性菌中,不动杆菌始终排在前三位。不动杆菌对亚胺培南、美罗培南和头孢哌酮／舒巴坦较敏感。结论：下呼吸道感染病原体中不动杆菌占据越来越大的比例,减少医源性感染、合理选择的抗菌药物对于降低死亡率、提高医疗资源利用率至关重要。     

Blood vessel occlusion by Cryptococcus neoformans is a mechanism for haemorrhagic dissemination of infection

Meningitis caused by infectious pathogens is associated with vessel damage and infarct formation, however the physiological cause is often unknown. Cryptococcus neoformans is a human fungal pathogen and causative agent of cryptococcal meningitis, where vascular events are observed in up to 30% of patients, predominantly in severe infection. Therefore, we aimed to investigate how infection may lead to vessel damage and associated pathogen dissemination using a zebrafish model that permitted noninvasive in vivo imaging. We find that cryptococcal cells become trapped within the vasculature (dependent on their size) and proliferate there resulting in vasodilation. Localised cryptococcal growth, originating from a small number of cryptococcal cells in the vasculature was associated with sites of dissemination and simultaneously with loss of blood vessel integrity. Using a cell-cell junction tension reporter we identified dissemination from intact blood vessels and where vessel rupture occurred. Finally, we manipulated blood vessel tension via cell junctions and found increased tension resulted in increased dissemination. Our data suggest that global vascular vasodilation occurs following infection, resulting in increased vessel tension which subsequently increases dissemination events, representing a positive feedback loop. Thus, we identify a mechanism for blood vessel damage during cryptococcal infection that may represent a cause of vascular damage and cortical infarction during cryptococcal meningitis.     

Monitoring Spongospora subterranea Development in Potato Roots Reveals Distinct Infection Patterns and Enables Efficient Assessment of Disease Control Methods

Spongospora subterranea is responsible for significant potato root and tuber disease globally. Study of this obligate (non-culturable) pathogen that infects below-ground plant parts is technically difficult. The capacity to measure the dynamics and patterns of root infections can greatly assist in determining the efficacy of control treatments on disease progression. This study used qPCR and histological analysis in time-course experiments to measure temporal patterns of pathogen multiplication and disease development in potato (and tomato) roots and tubers. Effects of delayed initiation of infection and fungicidal seed tuber and soil treatments were assessed. This study found roots at all plant developmental ages were susceptible to infection but that delaying infection significantly reduced pathogen content and resultant disease at final harvest. The pathogen was first detected in roots 15–20 days after inoculation (DAI) and the presence of zoosporangia noted 15–45 DAI. Following initial infection pathogen content in roots increased at a similar rate regardless of plant age at inoculation. All fungicide treatments (except soil-applied mancozeb which had a variable response) suppressed pathogen multiplication and root and tuber disease. In contrast to delayed inoculation, the fungicide treatments slowed disease progress (rate) rather than delaying onset of infection. Trials under suboptimal temperatures for disease expression provided valuable data on root infection rate, demonstrating the robustness of monitoring root infection. These results provide an early measure of the efficacy of control treatments and indicate two possible patterns of disease suppression by either delayed initiation of infection which then proceeds at a similar rate or diminished epidemic rate.     

The Status of Cassava Bacterial Blight Caused by Xanthomonas campestris pv. manihotis in Trinidad

Disease surveys conducted in Trinidad between 1985—1987 showed that Cassava Bacterial Blight (CBB) is present in all but one county of the country with disease severity ratings varying from 1—5 depending on day/night temperatures. Field and greenhouse screening identified varieties such as Point Fortin fine leaf and CMC 40 as being resistant whereas M col 22 was moderately resistant to susceptible. Using a combination of antiserum produced to whole cells of Xanthomonas campestris pv. manibotis and a broth enrichment technique, dissemination of the pathogen by flood water was confirmed. The pathogen was detected at distances of up to 300 meters from infected fields. The significance of this mode of pathogen dissemination in initiating primary infection in Trinidad is discussed.     

COCCIDIOIDOMYCOSIS AS A COMPLICATION OF PREGNANCY

Records of 33 cases of coccidioidomycosis occurring during pregnancy were reviewed. In this group the incidence of dissemination of the disease was considerably greater than the reported incidence of dissemination in all cases of coccidioidomycosis.The incidence of dissemination was higher in the patients who contracted coccidioidomycosis late in pregnancy than it was in those in whom onset of the disease occurred earlier in gestation; but dissemination occurred in all Negro patients in the group, regardless of the time of onset during pregnancy.The chief complicating effect when onset was in the first trimester of pregnancy was a tendency to abortion. In cases in which onset was in the third trimester, the incidence of premature labor was extremely high.There was no evidence of congenital infection in any of the babies, but in one case invasion of the placenta by coccidioidal spherules was observed.     

Dissemination of a Highly Virulent Pathogen: Tracking The Early Events That Define Infection

The series of events that occurs immediately after pathogen entrance into the body is largely speculative. Key aspects of these events are pathogen dissemination and pathogen interactions with the immune response as the invader moves into deeper tissues. We sought to define major events that occur early during infection of a highly virulent pathogen. To this end, we tracked early dissemination of Yersinia pestis, a highly pathogenic bacterium that causes bubonic plague in mammals. Specifically, we addressed two fundamental questions: (1) do the bacteria encounter barriers in disseminating to draining lymph nodes (LN), and (2) what mechanism does this nonmotile bacterium use to reach the LN compartment, as the prevailing model predicts trafficking in association with host cells. Infection was followed through microscopy imaging in addition to assessing bacterial population dynamics during dissemination from the skin. We found and characterized an unexpected bottleneck that severely restricts bacterial dissemination to LNs. The bacteria that do not pass through this bottleneck are confined to the skin, where large numbers of neutrophils arrive and efficiently control bacterial proliferation. Notably, bottleneck formation is route dependent, as it is abrogated after subcutaneous inoculation. Using a combination of approaches, including microscopy imaging, we tested the prevailing model of bacterial dissemination from the skin into LNs and found no evidence of involvement of migrating phagocytes in dissemination. Thus, early stages of infection are defined by a bottleneck that restricts bacterial dissemination and by neutrophil-dependent control of bacterial proliferation in the skin. Furthermore, and as opposed to current models, our data indicate an intracellular stage is not required by Y. pestis to disseminate from the skin to draining LNs. Because our findings address events that occur during early encounters of pathogen with the immune response, this work can inform efforts to prevent or control infection.     

Bacterial adhesion and entry into host cells

Successful establishment of infection by bacterial pathogens requires adhesion to host cells, colonization of tissues, and in certain cases, cellular invasion-followed by intracellular multiplication, dissemination to other tissues, or persistence. Bacteria use monomeric adhesins/invasins or highly sophisticated macromolecular machines such as type III secretion systems and retractile type IV pili to establish a complex host/pathogen molecular crosstalk that leads to subversion of cellular functions and establishment of disease.     

Immunomodulation by cytomegaloviruses: manipulative strategies beyond evasion

Human cytomegalovirus (CMV) remains the major infectious cause of birth defects as well as an important opportunistic pathogen. Individuals infected with CMV mount a strong immune response that suppresses persistent viral replication and maintains life-long latency. Loss of immune control opens the way to virus reactivation and disease. The large number of immunomodulatory functions encoded by CMV increases the efficiency of infection, dissemination, reactivation and persistent infection in hosts with intact immune systems and could contribute to virulence in immunocompromised hosts. These functions modulate both the innate and adaptive arms of the immune response and appear to target cellular rather than humoral responses preferentially. CMV encodes a diverse arsenal of proteins focused on altering and/or mimicking: (1) classical and non-classical major histocompatibility complex (MHC) protein function; (2) leukocyte migration, activation and cytokine responses; and (3) host cell susceptibility to apoptosis. Evidence that the host evolves mechanisms to counteract virus immune modulation is also accumulating. Although immune evasion is certainly one clear goal of the virus, the pro-inflammatory impact of certain viral functions suggests that increased inflammation benefits viral dissemination. The ability of such viral functions to successfully 'face off' against the host immune system ensures the success of this pathogen in the human population and could provide key insights into disease mechanisms.     

Molecular mechanisms involved in vascular interactions of the Lyme disease pathogen in a living host

Hematogenous dissemination is important for infection by many bacterial pathogens, but is poorly understood because of the inability to directly observe this process in living hosts at the single cell level. All disseminating pathogens must tether to the host endothelium despite significant shear forces caused by blood flow. However, the molecules that mediate tethering interactions have not been identified for any bacterial pathogen except E. coli, which tethers to host cells via a specialized pillus structure that is not found in many pathogens. Furthermore, the mechanisms underlying tethering have never been examined in living hosts. We recently engineered a fluorescent strain of Borrelia burgdorferi, the Lyme disease pathogen, and visualized its dissemination from the microvasculature of living mice using intravital microscopy. We found that dissemination was a multistage process that included tethering, dragging, stationary adhesion and extravasation. In the study described here, we used quantitative real-time intravital microscopy to investigate the mechanistic features of the vascular interaction stage of B. burgdorferi dissemination. We found that tethering and dragging interactions were mechanistically distinct from stationary adhesion, and constituted the rate-limiting initiation step of microvascular interactions. Surprisingly, initiation was mediated by host Fn and GAGs, and the Fn- and GAG-interacting B. burgdorferi protein BBK32. Initiation was also strongly inhibited by the low molecular weight clinical heparin dalteparin. These findings indicate that the initiation of spirochete microvascular interactions is dependent on host ligands known to interact in vitro with numerous other bacterial pathogens. This conclusion raises the intriguing possibility that fibronectin and GAG interactions might be a general feature of hematogenous dissemination by other pathogens.