少动鞘氨醇单胞菌引起小儿败血症合并脑膜炎1例

本文报道1例罕见的由少动鞘氨醇单胞菌引起的小儿败血症合并脑膜炎。该患儿突发高热起病,伴有皮肤散在瘀点。根据实验室微生物分离和鉴定,确诊为少动鞘氨醇单胞菌引起的败血症;同时根据脑脊液生化常规结果,诊断为合并细菌性脑膜炎。少动鞘氨醇单胞菌引起的小儿败血症合并脑膜炎属罕见病例,且该患儿有类似流行性脑脊髓膜炎的症状,易被误诊为春季小儿流行性脑脊髓膜炎,需引起临床及实验室工作人员的重视。     

合成生物聚合物的重要微生物资源-鞘氨醇单胞菌

摘要：鞘氨醇单胞菌属的许多菌株能够合成结冷胶、沃仑胶、迪特胶等多种结构相似,物理性能多样的生物聚合物,统称为鞘氨醇胶。目前,结冷胶已经大规模的生产和应用,由于鞘氨醇单胞菌属的提出仅有十几年的历史,其他种类鞘氨醇胶的研究和开发才刚刚起步。本文综述了鞘氨醇单胞菌属分类研究的最新进展,以及鞘氨醇胶的结构、特性、生物合成途径、分子遗传学和基因工程的研究现状,并对今后的研究重点和方向进行了展望。     

鞘氨醇单胞菌的研究进展

鞘氨醇单胞菌(Sphingomonas)不仅细胞膜含有比脂多糖更疏水的鞘糖脂,而且具有高效的代谢调控机制和基因调控能力,使其在威兰胶合成、环境修复和促进植物生长等方面具有巨大的应用潜力。目前国内在鞘氨醇单胞菌代谢机制方面的研究尚无新突破。本文主要综述了鞘氨醇单胞菌的系统分类、基因组学、基因调控机制及其应用等方面的研究,从基因层面分析鞘氨醇单胞菌产威兰胶的合成机制,为后续鞘氨醇单胞菌高密度发酵、工业化生产等研究提供理论基础,以便进一步发掘其在生物技术上的应用潜力。     

水环境中微囊藻毒素的生物降解

微囊藻毒素在水环境中的生物降解是决定其环境归趋和影响其毒性的重要因素。本文综述了水细菌、鱼类、水生植物、水生无脊椎动物、浮游动物等水生生物对微囊藻毒素生物降解方面的研究进展。目前报道的微囊藻毒素降解菌有鞘氨醇单胞菌、铜绿假单胞菌和青枯菌。鞘氨醇单胞菌和铜绿假单胞菌分别以微囊藻毒素酶和碱性蛋白酶降解毒素,青枯菌降解机理未明;而鱼类、水生植物、水生无脊椎动物、浮游动物等水生生物主要通过谷胱甘肽S-转移酶催化形成低毒性的微囊藻毒素-谷胱甘肽结合物进行转化。本文还对水环境微囊藻毒素的生物修复方式进行了初步的探讨。     

大莲湖池杉林湿地土壤可培养细菌的分离与鉴定

采用牛肉膏蛋白胨培养基培养,从大莲湖池杉林土壤中共分离得到20个菌落形态不同的菌株。通过对这些菌株的形态、培养特征、生理生化特征的研究以及16S rDNA序列分析,初步确定这些菌株分别属于假单胞菌属(Pseudomonas)、芽胞杆菌属(Bacillus)、红球菌属(Rhodococcus)、北里孢菌属(Kitasatosporia)、金黄杆菌属(Chryseobacterium)、不动杆菌属(Acinetobacter)、黄杆菌属(Flavobacterium)、鞘氨醇杆菌属(Sphingobacte-rium)和丛毛单胞菌属(Comamonas)等9个属细菌。其中芽胞杆菌属和不动杆菌属细菌是优势菌,分离到的红球菌属、北里孢菌属、鞘氨醇杆菌属和丛毛单胞菌属细菌在国内湿地土壤中报道较少。     

石油污染土壤强化修复前后细菌多样性变化研究

采用高通量测序技术,对石油污染土壤及石油降解菌强化修复土壤的细菌群落多样性进行了分析。发现污染前后各组间在门水平和属水平上变化显著,污染前细菌多样性丰富,包括34门675属,主要优势菌群依次为变形菌门(Proteobacteria)、放线菌门(Actinobacteria)、酸杆菌门(Acidobacteria)、拟杆菌门(Bacteroidetes)、芽单胞菌门(Gemmatimonadetes)等。优势菌属依次为芽单胞菌属(Gemmatimonas)、鞘氨醇单胞菌属(Sphingomonas)、节杆菌属(Arthrobacter)等。石油污染110 d后土壤细菌类群多样性降低,分布在29门507属,细菌优势门变化不显著等,优势菌属依次为鞘氨醇单胞菌属、假单胞菌属(Pseudomonas)、GP6、芽单胞菌属、GP4、微小杆菌属(Exiguobacterium)、寡养单胞菌(Stenotrophomonas)和类诺卡氏菌属(Nocardioides)。添加铜绿假单胞菌1217、红平红球菌KB1和混合菌剂的三个强化修复组细菌分别分布在31门471属、32门474属和29门473属,在细菌组成上差异不显著,在丰度上差异显著。鞘氨醇单胞菌属、假单胞菌属、芽单胞菌属和类诺卡氏菌属细菌是主要的石油污染物降解菌。     

鞘磷脂代谢与脑缺血

鞘磷脂特别是鞘脂是髓鞘的主要成分,高度集中在中枢神经系统。在生理和病理生理条件下,具有生物活性的鞘磷脂及其代谢产物以及信号传导过程的重要性正在逐步被人们所认识。鞘脂代谢产物鞘氨醇及其前体物质神经酰胺与细胞生长停滞和凋亡有关,而1-磷酸鞘氨醇与增强细胞增殖、分化和细胞生存以及调节细胞的生理和病理过程有关,具有细胞外第一信使和细胞内第二信使的双重功能。这三者之间的相互转换、鞘脂代谢物的相对水平以及细胞的命运,受到鞘氨醇激酶的活性的强烈影响。鞘氨醇激酶可催化磷酸鞘氨醇产生1-磷酸鞘氨醇。1-磷酸鞘氨醇在中枢神经系统中与G蛋白偶联受体家族结合对中枢神经系统发挥作用。本文对鞘磷脂代谢过程中的鞘氨醇激酶、1-磷酸鞘氨醇及其受体与脑缺血之间的关系进行概述。     

狗小肠鞘氨醇糖脂中长链碱组成的研究

 利用气相色谱、气相色谱-质谱联用等方法测定了狗小肠鞘氨醇糖脂中的长链碱组成。其主要的长链碱为鞘氨醇(Sphingosine)、异鞘氨醇(isosphingosine)、二氢鞘氨醇(Sphinganine)和植物鞘氨酸(Phyto-sphingosine)。一共分离出十三个鞘氨醇糖脂。在唯一的五糖基神经酰胺中异鞘氨醇是主要成份。在一个一糖基神经酰胺中植物鞘氨醇是主要成份。植植物鞘氨酸也是两个二糖基神经酰胺和一个三糖基神酰胺的主要长链碱。说明它不仅存于植物体内。     

溶微囊藻细菌的富集筛选及其菌群结构特征

利用铜绿微囊藻(Microcystis aeruginosa)作为溶藻对象富集、筛选, 获得一个稳定的溶藻菌群。采用叶绿素、PCR和变性梯度凝胶电泳(DGGE)方法研究溶藻过程及其细菌种群结构的变化。结果显示, 富集的溶藻菌经1×10-5稀释后仍有显著溶藻效果。Rubritepida菌C1、假单胞菌C2和鞘氨醇单胞菌C3是存在于铜绿微囊藻中的3种伴生细菌。加入富集的溶藻菌群后, 菌群结构发生明显的变化, Rubritepida菌C1、假单胞菌C2消失, 混合菌群包含未培养黄杆菌A2、鞘氨醇单胞菌C3和噬氢     

四乙酰基植物鞘氨醇生物合成的研究进展

四乙酰基植物鞘氨醇(tetraacetyl phytosphingosine, TAPS)是一种性能卓越的天然护肤品原料,经去乙酰化后生成的植物鞘氨醇可作为前体合成保湿护肤品神经酰胺,因此广泛应用于护肤化妆品行业。非常规酵母威克汉姆西弗酵母(Wickerhamomyces ciferrii)是已知的唯一可天然分泌四乙酰基植物鞘氨醇的微生物,目前已成为四乙酰基植物鞘氨醇工业生产的宿主。本文介绍了四乙酰基植物鞘氨醇的发现、功能及其生物合成途径,综述了近年来利用单倍体筛选、诱变育种和代谢工程改造威克汉姆西弗酵母高产四乙酰基植物鞘氨醇的研究进展,并展望了实现四乙酰基植物鞘氨醇工业生产的未来发展方向。     

Role of echocardiography in the diagnosis and management of infective endocarditis

Infective endocarditis is one of the most common causes of serious infection and carries a high risk of morbidity and mortality. It represents the fourth leading cause of life-threatening infections after urosepsis, pneumonia, and intra-abdominal sepsis. There is still a continuous rise in the incidence of infective endocarditis, with a rate of about 20,000 new cases in the United States alone. This rise in incidence of infective endocarditis is mainly caused by increasing numbers of intravenous drug abusers, patients with artificial valves and elderly patients. In this paper, we will briefly review the crucial role of echocardiography in the diagnosis and management of infective endocarditis.     

Amplification reaction to bacterial DNA for diagnosing infective endocarditis

The aim of this study was to evaluate the usefulness of broad-range bacterial PCR in infective endocarditis of bacterial etiology, and to determine its specificity and sensitivity. Twenty five blood samples were taken for analysis from patients with infective endocarditis and acquired valvular heart disease. Infective endocarditis was diagnosed according to Duke criteria. There were two control groups consisting of patients with acquired valvular heart disease: 10 patients with urinary tract infection and 15 patients without. Three different primer pairs for the region of the gene coding for 16S rRNA were tested, to find the most specific one. The highest specificity was found for F/R primers, as the relevant amplified PCR product was present in every blood sample with infective endocarditis, and also in 4 out of 10 patients with urinary tract infection. Broad-range PCR in bacterial endocarditis is a fast, sensitive and inexpensive tool for the detection of bacteria, but it is far more prone to contamination than species specific-PCR. However, in controlled conditions it may be valuable in the identification of non-specific infection allowing for a more rapid clinical diagnosis of endocarditis.     

Infective endocarditis due to Leptotrichia buccalis: a case report.

A patient with Down''s syndrome presented with infective endocarditis due to Leptotrichia buccalis. The source of the infection was not detected, but the predisposing factor was a complex cardiac malformation. The disease followed a subacute course, had a number of immunologic manifestations and was successfully treated with a 28-day course of penicillin G, given intravenously. L. buccalis has never been reported before as a cause of endocarditis.     

Platelet aggregation by oral streptococci

One proposed mechanism in the pathogenesis of infective endocarditis is the direct aggregation of platelets by the bacteria causing the disease. Some, but not all, strains of Streptococcus sanguis have been reported to aggregate platelets but the taxonomy of this and related taxa has changed recently. The ability to aggregate platelets by 24 genetically grouped laboratory stock strains was studied along with 8 recent isolates from cases of endocarditis. Strains belonging to S. sanguis could aggregate platelets, but not S. gordonii, "S. parasanguis", S. mitis, S. oralis or related taxa. Also, preliminary data indicate that certain biotypes of S. sanguis lack the ability to aggregate platelets. Of the recent clinical isolates, only 4 aggregated platelets and each of these showed phenotypes typical of S. sanguis. These data suggest that the ability to aggregate platelets is not essential for an organism to be able to cause endocarditis, although it may be a significant virulence factor.     

Development of a mouse model of induced Staphylococcus aureus infective endocarditis

We developed a mouse model of Staphylococcus aureus infective endocarditis to evaluate the efficacy of experimental antibacterial compounds for this disease. Experimental infective endocarditis was produced in CD1 mice by intravenous challenge with approximately 6 log10 colony-forming units (CFU) of methicillin-sensitive (MSSA) SA-3529 or -resistant (MRSA) SA-2015 S. aureus 1 d after aortic valve trauma. Valve trauma was produced by introduction of an indwelling 32-gauge polyurethane catheter into the aortic valve via the left carotid artery. Histologic examination of MSSA- and MRSA-infected and catheterized aortic valve sections revealed neutrophilic inflammation and vegetative bacterial colonies encapsulated within fibrin along the aortic valves 1 d after infection. The MSSA or MRSA endocarditis was determined to be catheter-dependent based on catheterized mice exhibiting heart bacterial counts 4 orders of magnitude greater than those seen for noncatheterized mice. The model was validated by using a 3-d regimen of vancomycin at exposures comparable to human dosing (500 microg x h/ml). Vancomycin treatment produced statistically significant reductions of 3.4 and 3.1 log10 CFU/heart for MSSA and MRSA, respectively, relative to controls. This mouse model of endocarditis shows promise in evaluating the predictive efficacy of antibiotics for S. aureus infective endocarditis.     

Platelet receptor polymorphisms do not influence Staphylococcus aureus-platelet interactions or infective endocarditis

Cardiac vegetations result from bacterium-platelet adherence, activation and aggregation, and are associated with increased morbidity and mortality in infective endocarditis. The GPIIb/IIIa and FcγRIIa platelet receptors play a central role in platelet adhesion, activation and aggregation induced by endocarditis pathogens such as Staphylococcus aureus, but the influence of known polymorphisms of these receptors on the pathogenesis of infective endocarditis is unknown. We determined the GPIIIa platelet antigen Pl(A1/A2) and FcγRIIa H131R genotype of healthy volunteers (n?=?160) and patients with infective endocarditis (n?=?40), and investigated the influence of these polymorphisms on clinical outcome in infective endocarditis and S. aureus-platelet interactions in vitro. Platelet receptor genotype did not correlate with development of infective endocarditis, vegetation characteristics on echocardiogram or the composite clinical end-point of embolism, heart failure, need for surgery or mortality (P?>?0.05 for all), even though patients with the GPIIIa Pl(A1/A1) genotype had increased in vivo platelet activation (P?=?0.001). Furthermore, neither GPIIIa Pl(A1/A2) nor FcγRIIa H131R genotype influenced S. aureus-induced platelet adhesion, activation or aggregation in vitro (P?>?0.05). Taken together, our data suggest that the GPIIIa and FcγRIIa platelet receptor polymorphisms do not influence S. aureus-platelet interactions in vitro or the clinical course of infective endocarditis.     

The role of endothelial cell biology in endocarditis

The treatment of endocarditis remains a challenge for physicians, even in times of modern antibiotic treatment. Depending on its cause, endocarditis can either be of infectious or non-infectious origin. Infective endocarditis is caused by bacterial (or fungal) pathogens, and the clinical course is critically dependent on the virulence factors of the specific microorganisms involved. Therefore, the clinical type of endocarditis can be divided into an acute and more aggressive form and a subacute form (endocarditis lenta). Much of our knowledge regarding the pathogenesis of infective endocarditis is based on studies of the virulence of Staphylococcus aureus, which has become the most frequent cause of infective endocarditis nowadays. However, independently of the underlying cause of endocarditis (infectious or noninfectious), the pathogenesis involves the damage and disturbance of endothelial function and the formation of associated “vegetation”. Surprisingly little is known about the specific role of the endothelium in the pathogenesis of endocarditis. This review will thus give insights into current knowledge of the pathogenesis of endocarditis with a focus on the role of the endothelium.     

How does Staphylococcus aureus escape the bloodstream?

Staphylococcus aureus is a major cause of bacteraemia, which frequently leads to infective endocarditis, osteomyelitis, septic arthritis and metastatic abscess formation. The development of these secondary infections is due to bacterial dissemination from the blood into surrounding tissues and is associated with significantly increased morbidity and mortality. Despite the importance of S. aureus extravasation in disease progression, there is relatively little understanding of the molecular mechanisms by which this pathogen crosses the endothelial barrier and establishes new sites of infection. Recent work has identified a number of putative routes by which S. aureus can escape the bloodstream. In this article we review these new developments and set them in the context of strategies used by other established pathogens to traverse cellular barriers.     

Identification of soil micro-habitats for growth, death and survival of a bacterium, γ-1,2,3,4,5,6-hexachlorocyclohexane-assimilating Sphingomonas paucimobilis, by fractionation of soil

Abstract A soil bacterium, Sphingomonas paucimobilis , is known to be the only bacterium which can aerobically assimilate γ-1,2,3,4,5,6-hexachlorocyclohexane (γ-HCH). Indigenous γ-HCH-assimilating S. paucimobilis survives in the soil where γ-HCH has been annually applied since 1973. In contrast, γ-HCH-assimilating S. paucimobilis strain SS86 cannot survive when inoculated into the control soil, although it can multiply in the presence of γ-HCH. Micro-habitats of γ-HCH-assimilating S. paucimobilis indigenous or inoculated into the soils were identified by fractionation of the soils. When γ-HCH was added to the soil, indigenous γ-HCH-assimilating S. paucimobilis grew. Most of the growing indigenous bacteria were found in fractions smaller than 0.025 mm which corresponded to soil inter-aggregate pores, and died afterwards. However, the indegenous bacteria which survived for a long period were found mainly in fractions larger than 0.025 mm which contained soil aggregates. When γ-HCH-assimilating strain SS86 was inoculated, the bacteria were located in inter-aggregate pores and died quickly. Consequently, association of the bacteria with soil aggregates was suggested to be related to the long-term survival of γ-HCH-assimilating S. paucimobilis .     

The heterogeneity of Streptococcus viridans: therapeutic considerations in infective endocarditis

A 24-year-old woman with Marfan''s syndrome and mitral regurgitation had clinical features suggestive of infective endocarditis. The causative organism was Streptococcus viridans. Initial therapy with penicillin G, in a dose that should have been bactericidal and hence curative according to the results of the initial quantitative antimicrobial studies, became inadequate. The strain of S. viridans displayed considerable variation in both growth properties and antimicrobial sensitivity during the course of therapy. In addition, a different strain of S. viridans was cultured 1 month after treatment had begun. It is therefore important to repeat cultures and antimicrobial sensitivity testing during treatment of infective endocarditis.