一起由蜡样芽胞杆菌引起的食物中毒

蜡样芽胞菌为条件致病菌,在一定条件下可引起疾病.2003年8月23日,勃利县冷冻厂工地民工食常发生了一起食物中毒,对食堂及患者采样进行实验室检验,从剩余食物及患者呕吐物中检出蜡样芽胞杆菌.通过进一步的毒力试验和血清学试验,根据流行病学调查,认为该起食物中毒是由蜡样芽胞菌污染食物所引起的.现将实验结果报告如下.     

小剂量红霉素在小婴儿功能性呕吐的应用

目的观察小剂量红霉素治疗小婴儿功能性呕吐的疗效。方法随机分为两组,对照组应用源首胶囊(蜡样芽胞杆菌活菌制剂) 维生素B6,治疗组应用源首胶囊(蜡样芽胞杆菌活菌制剂) 小剂量红霉素。结果两组对比观察,治疗组疗效在统计学上有显著差异P<0.005。结论小剂量红霉素治疗小婴儿功能性呕吐疗效确切,无明显毒副作用,值得临床使用。     

抗生素相关性腹泻及结肠炎

绪言抗生素治疗中,腹泻为较常见的并发症。临床及解剖所见可自轻度自限性稀便以至严重危及生命的结肠炎。近来研究确认顽固梭状芽胞杆菌(Clostridiu Dif-ficile)为本并发症的重要原因。本菌产生致细胞病变毒素(Cytopathic Toxin),可用组织培养而测得。顽固梭状芽胞杆菌所致的腹泻或结肠炎患者常对口服应用万古霉素以直接抗菌或应用消胆胺以结合毒素均具良好效应。本文目的在于复习因     

奶粉等四类食品中蜡样芽胞杆菌的污染情况及生物学型别

在1983午的夏秋两季对我省部份地区的市售奶粉、米饭(过夜)、糕点(有馅)、豆腐乳四类食品进行了蜡样芽胞杆菌污染情况和生物学型别的调查。蜡样芽胞杆菌的计数、食品中的菌量测定试验方法按照吴光先报导(《乳品工业》2∶5,1983):蜡样芽胞杆菌生物学分型按     

枯草杆菌二联活菌肠溶胶囊联合地衣芽胞杆菌活菌胶囊治疗老年抗生素相关性腹泻的效果分析

目的探讨枯草杆菌二联活菌肠溶胶囊联合地衣芽胞杆菌活菌胶囊对老年抗生素相关性腹泻的临床疗效。方法收集2013年2月~2014年2月本院老年抗生素相关性腹泻患者120例,根据随机数字表法分为枯草杆菌二联活菌肠溶胶囊组、地衣芽胞杆菌活菌胶囊组、枯草杆菌二联活菌肠溶胶囊和地衣芽胞杆菌活菌胶囊联合组各40例。比较3组的治疗效果。结果联合组1个月内的腹泻治愈率高于枯草杆菌二联活菌肠溶胶囊组及地衣芽胞杆菌活菌胶囊组,差异有统计学意义(χ2=8.26,P=0.02)。联合组未愈患者1个月内的腹泻次数明显低于枯草杆菌二联活菌肠溶胶囊组及地衣芽胞杆菌活菌胶囊组,差异有统计学意义(F=91.03,P=0.00)。结论枯草杆菌二联活菌肠溶胶囊以及地衣芽胞杆菌活菌胶囊均为益生菌类药物,对治疗老年人抗生素相关性腹泻有一定的疗效,但是枯草杆菌二联活菌肠溶胶囊联合地衣芽胞杆菌活菌胶囊对老年抗生素相关性腹泻的疗效更显著,对于临床治疗有一定的协助作用。     

一起蜡样芽胞杆菌引起的食物中毒调查

目的探讨一起食物中毒的流行因素及病原学。方法按流行病学现场调查方法,结合临床表现和实验室细菌学鉴定方法。结果就餐人数为150例,中毒病人108例,罹患率72%;临床表现以呕吐为主;中毒食物为隔夜剩饭,病原学检查为蜡样芽孢杆菌,中毒食物中蜡样芽孢杆菌菌落为1.2×106/g。结论此次食物中毒事件是由蜡样芽胞杆菌引起,此类食物中毒应引起人们的关注。     

116例蜡样芽胞杆菌食物中毒的临床分析

2000年10月31日，佛冈县机关幼儿园发生一起食物中毒事件，经现场流行病学调查、临床症状分析以及实验室检验，确认为一起由蜡样芽胞杆菌引起的食物中毒。近年来，由蜡样芽胞杆菌引起的食物中毒在全国多个省份均有报道。为了掌握本病特点，为防治提供依据，现将我院2000年10月31日收治的116例蜡样芽胞杆菌食物中毒作一临床分析。     

蜡样芽孢杆菌与类似菌鉴别方法研究

目的:验证和完善蜡样芽孢杆菌与类似菌鉴别方法,降低蜡样芽孢杆菌检验结果假阳性率。方法:按照国标GB/T4789.14-2003对蜡样芽孢杆菌标准菌株与类似菌(苏云金芽孢杆菌,蕈状芽孢杆菌)参考菌株以及我们从食品中分离出的蜡样芽孢杆菌可疑菌株从菌体和菌落形态、生化性状、根状试验、蛋白质毒素晶体试验等几个方面进行鉴别。结果:10株可疑菌中只有1号株菌为蜡样芽孢杆菌。结论:补充和完善后的"蜡样芽孢杆菌与类似菌鉴别方法"能有效地鉴别蜡样芽孢杆菌与类似菌,根状试验和蛋白质毒素晶体试验是最关键的鉴别手段,能明显地降低蜡样芽孢杆菌检验结果假阳性率。     

乙醇对常见病原菌最低杀菌浓度的试验研究

目的：探讨乙醇对常见病原菌的最低杀菌浓度。方法：采用试管稀释法检测乙醇对15种病原菌的最低杀菌浓度。结果：10％乙醇对革兰氏阴性杆菌和某些革兰氏阳性菌有杀灭作用，25％乙醇对14无芽胞菌均有杀灭,而5％－95％乙醇对蜡样芽胞杆菌均无杀灭作用。结论：乙醇对无芽胞菌的最低杀菌浓度为10％－25。     

核黄素对双歧杆菌和蜡样芽孢杆菌增殖的影响

目的　探讨不同浓度核黄素对双歧杆菌、蜡样芽孢杆菌生长的影响。方法　应用常规细菌定量培养及革兰染色镜检技术 ,观察 1、0 5、0 2 5 g·L-1的核黄素对双歧杆菌和蜡样芽孢杆菌增殖生长的影响。结果　① 1g·L-1核黄素组 ,在 4 8h后双歧杆菌活菌数增加约 10～ 10 0倍 ;0 5和 0 2 5g·L-1核黄素组 ,在 72h内活菌数增加约 10～ 390倍 ,镜检示双歧杆菌链的长度亦增加。② 0 5g·L-1核黄素组 ,36h后蜡样芽孢杆菌活菌数增加 ;0 2 5 g·L-1核黄素组 ,在 72h内活菌数均增加 ,约 0 5～ 315倍 ,链长度增加 ,芽胞形成时间延迟。 (3) 4℃存放 ,悬液加核黄素 (0 5g·L-1)可提高双歧杆菌和蜡样芽孢杆菌 6mon内的存活率。结论　核黄素可促进双歧杆菌、蜡样芽孢杆菌的增殖 ,在一定范围内存在剂量依赖关系 ,并可提高悬液中双歧杆菌和蜡样芽孢杆菌的长期存活率     

Production, Secretion and Biological Activity of Bacillus cereus Enterotoxins

Bacillus cereus behaves as an opportunistic pathogen frequently causing gastrointestinal diseases, and it is increasingly recognized to be responsible for severe local or systemic infections. Pathogenicity of B. cereus mainly relies on the secretion of a wide array of toxins and enzymes and also on the ability to undergo swarming differentiation in response to surface-sensing. In this report, the pathogenicity exerted by B. cereus toxins is described with particular attention to the regulatory mechanisms of production and secretion of HBL, Nhe and CytK enterotoxins.     

Bacterial toxins and the nervous system: neurotoxins and multipotential toxins interacting with neuronal cells

Toxins are potent molecules used by various bacteria to interact with a host organism. Some of them specifically act on neuronal cells (clostridial neurotoxins) leading to characteristics neurological affections. But many other toxins are multifunctional and recognize a wider range of cell types including neuronal cells. Various enterotoxins interact with the enteric nervous system, for example by stimulating afferent neurons or inducing neurotransmitter release from enterochromaffin cells which result either in vomiting, in amplification of the diarrhea, or in intestinal inflammation process. Other toxins can pass the blood brain barrier and directly act on specific neurons.     

Multifaceted toxin profile,an approach toward a better understanding of probiotic Bacillus cereus

Abstract

Strains of the Bacillus cereus group have been widely used as probiotics for human beings, food animals, plants, and environmental remediation. Paradoxically, B. cereus is responsible for both gastrointestinal and nongastrointestinal syndromes and represents an important opportunistic food-borne pathogen. Toxicity assessment is a fundamental issue to evaluate safety of probiotics. Here, we summarize the state of our current knowledge about the toxins of B. cereus sensu lato to be considered for safety assessment of probiotic candidates. Surfactin-like emetic toxin (cereulide) and various enterotoxins including nonhemolytic enterotoxin, hemolysin BL, and cytotoxin K are responsible for food poisoning outbreaks characterized by emesis and diarrhea. In addition, other factors, such as hemolysin II, Certhrax, immune inhibitor A1, and sphingomyelinase, contribute to toxicity and overall virulence of B. cereus.     

Bt Toxin Modification for Enhanced Efficacy

Insect-specific toxins derived from Bacillus thuringiensis (Bt) provide a valuable resource for pest suppression. Here we review the different strategies that have been employed to enhance toxicity against specific target species including those that have evolved resistance to Bt, or to modify the host range of Bt crystal (Cry) and cytolytic (Cyt) toxins. These strategies include toxin truncation, modification of protease cleavage sites, domain swapping, site-directed mutagenesis, peptide addition, and phage display screens for mutated toxins with enhanced activity. Toxin optimization provides a useful approach to extend the utility of these proteins for suppression of pests that exhibit low susceptibility to native Bt toxins, and to overcome field resistance.     

The role of bacterial and non-bacterial toxins in the induction of changes in membrane transport: implications for diarrhea.

Bacterial toxins induce changes in membrane transport which underlie the loss of electrolyte homeostasis associated with diarrhea. Bacterial- and their secreted toxin-types which have been linked with diarrhea include: (a) Vibrio cholerae (cholera toxin, E1 Tor hemolysin and accessory cholera enterotoxin); (b) Escherichia coli (heat stable enterotoxin, heat-labile enterotoxin and colicins); (c) Shigella dysenteriae (shiga-toxin); (d) Clostridium perfringens (C. perfringens enterotoxin, alpha-toxin, beta-toxin and theta-toxin); (e) Clostridium difficile (toxins A and B); (f) Staphylococcus aureus (alpha-haemolysin); (g) Bacillus cereus (cytotoxin K and haemolysin BL); and (h) Aeromonas hydrophila (aerolysin, heat labile cytotoxins and heat stable cytotoxins). The mechanisms of toxin-induced diarrhea include: (a) direct effects on ion transport in intestinal epithelial cells, i.e. direct toxin interaction with intrinsic ion channels in the membrane and (b) indirect interaction with ion transport in intestinal epithelial cells mediated by toxin binding to a membrane receptor. These effects consequently cause the release of second messengers, e.g. the release of adenosine 3',5'-cyclic monophosphate/guanosine 3',5'-monophosphate, IP(3), Ca2+ and/or changes in second messengers that are the result of toxin-formed Ca2+ and K+ permeable channels, which increase Ca2+ flux and augment changes in Ca2+ homeostasis and cause depolarisation of the membrane potential. Consequently, many voltage-dependent ion transport systems, e.g. voltage-dependent Ca2+ influx, are affected. The toxin-formed ion channels may act as a pathway for loss of fluid and electrolytes. Although most of the diarrhea-causing toxins have been reported to act via cation and anion channel formation, the properties of these channels have not been well studied, and the available biophysical properties that are needed for the characterization of these channels are inadequate.     

Toxicological profile of cereulide, the Bacillus cereus emetic toxin, in functional assays with human, animal and bacterial cells.

Some strains of the endospore-forming bacterium Bacillus cereus produce a heat-stable ionophoric peptide, cereulide, of high human toxicity. We assessed cell toxicity of cereulide by measuring the toxicities of crude extracts of cereulide producing and non-producing strains of B. cereus, and of pure cereulide, using cells of human, animal and bacterial origins. Hepatic cell lines and boar sperm, with cytotoxicity and sperm motility, respectively, as the end points, were inhibited by 1 nM of cereulide present as B. cereus extract. RNA synthesis and cell proliferation in HepG2 cells was inhibited by 2 nM of cereulide. These toxic effects were explainable by the action of cereulide as a high-affinity mobile K+ carrier. Exposure to cereulide containing extracts of B. cereus caused neither activation of CYP1A1 nor genotoxicity (comet assay, micronucleus test) at concentrations below those that were cytotoxic (0.6 nM cereulide). Salmonella typhimurium reverse mutation (Ames) test was negative. Exposure of Vibrio fischeri to extracts of B. cereus caused stimulated luminescence up to 600%, independent on the presence of cereulide, but purified cereulide inhibited the luminescence with an IC(50% (30 min)) of 170 nM. Thus the luminescence-stimulating B. cereus substance(s) masked the toxicity of cereulide in B. cereus extracts to V. fischeri.     

The Role of Rho GTPases in Toxicity of Clostridium difficile Toxins

Clostridium difficile (C. difficile) is the main cause of antibiotic-associated diarrhea prevailing in hospital settings. In the past decade, the morbidity and mortality of C. difficile infection (CDI) has increased significantly due to the emergence of hypervirulent strains. Toxin A (TcdA) and toxin B (TcdB), the two exotoxins of C. difficile, are the major virulence factors of CDI. The common mode of action of TcdA and TcdB is elicited by specific glucosylation of Rho-GTPase proteins in the host cytosol using UDP-glucose as a co-substrate, resulting in the inactivation of Rho proteins. Rho proteins are the key members in many biological processes and signaling pathways, inactivation of which leads to cytopathic and cytotoxic effects and immune responses of the host cells. It is supposed that Rho GTPases play an important role in the toxicity of C. difficile toxins. This review focuses on recent progresses in the understanding of functional consequences of Rho GTPases glucosylation induced by C. difficile toxins and the role of Rho GTPases in the toxicity of TcdA and TcdB.     

Antimicrobial activities of human beta-defensins against Bacillus species

Natural defences in the human body function to protect us from numerous environmental toxins and exposure to potential harmful biological agents. An important frontline defence is antimicrobial peptides. These peptides occur at environmental interfaces and serve to limit bacterial invasion. There has been little work comparing specific peptides as potential antimicrobial compounds. In this study, we evaluated the antimicrobial activity of peptides from the human beta-defensin (HBD) family against four species of Bacillus, chosen as models for Bacillus anthracis, a potential bioweapon. The impact of peptide concentration, sequence and protein binding was evaluated on their biological activity. The results indicated that HBD-3 was the most biologically active against Bacillus subtilis and Bacillus licheniformis, whilst HBD-2 was found to be most active against Bacillus cereus and Bacillus thuringiensis. Moreover, the antimicrobial activity of the peptides was directly related to peptide concentration and indirectly related to albumin concentration (i.e. protein binding).     

Prokaryotic toxins provoke different types of cell deaths in the eukaryotic cells

Bacterial toxins play major roles in developing infections and can cause diverse morphological and physiological changes via certain biochemical mechanisms leading to cell death. Most of the bacterial toxins induce apoptosis in host cell by intrinsic and extrinsic apoptosis pathways that are caused by intracellular organelle dysfunction and caspase cascade activation. Some of bacterial toxins encourage the programmed necrosis (necroptosis) in mature RBCs. In addition, pore-forming toxins can induce autophagy. Another kind of cell death, the pyroptosis, is induced by Salmonella typhimurium and Pseudomonas aeruginosa and Shigella flexneri and the lethal toxin of Bacillus anthracis. Therefore, recently scientists utilize cytotoxic properties of bacterial toxins for designing novel anti-tumor drugs.     

Mode of action of beta-barrel pore-forming toxins of the staphylococcal alpha-hemolysin family.

Staphylococcal alpha-hemolysin is the prototype of a family of bacterial exotoxins with membrane-damaging function, which share sequence and structure homology. These toxins are secreted in a soluble form which finally converts into a transmembrane pore by assembling an oligomeric beta-barrel, with hydrophobic residues facing the lipids and hydrophilic residues facing the lumen of the channel. Besides alpha-hemolysin the family includes other single chain toxins forming homo-oligomers, e.g. beta-toxin of Clostridium perfringens, hemolysin II and cytotoxin K of Bacillus cereus, but also the staphylococcal bi-component toxins, like gamma-hemolysins and leucocidins, which are only active as the combination of two similar proteins which form hetero-oligomers. The molecular basis of membrane insertion has become clearer after the determination of the crystal structure of both the oligomeric pore and the soluble monomer. Studies on this family of beta-barrel pore-forming toxins are important for many aspects: (i) they are involved in serious pathologies of humans and farmed animals, (ii) they are a good model system to investigate protein-membrane interaction and (iii) they are the basic elements for the construction of nanopores with biotechnological applications in various fields.