Bruggemann Holger, Baumer Sebastian, Fricke Wolfgang Florian, Wiezer Arnim, Liesegang Heiko, Decker Iwona, Herzberg Christina, Martinez-Arias Rosa, Merkl Rainer, Henne Anke, Gottschalk Gerhard
Göttingen Genomics Laboratory and Department of General Microbiology, Institute of Microbiology and Genetics, Georg-August-University, Grisebachstrasse 8, D-37077 Göttingen, Germany.
Proc Natl Acad Sci U S A. 2003 Feb 4;100(3):1316-21. doi: 10.1073/pnas.0335853100. Epub 2003 Jan 27.
Tetanus disease is one of the most dramatic and globally prevalent diseases of humans and vertebrate animals, and has been reported for over 24 centuries. The manifestation of the disease, spastic paralysis, is caused by the second most poisonous substance known, the tetanus toxin, with a human lethal dose of approximately 1 ng/kg. Fortunately, this disease is successfully controlled through immunization with tetanus toxoid; nevertheless, according to the World Health Organization, an estimated 400,000 cases still occur each year, mainly of neonatal tetanus. The causative agent of tetanus disease is Clostridium tetani, an anaerobic spore-forming bacterium, whose natural habitat is soil, dust, and intestinal tracts of various animals. Here we report the complete genome sequence of toxigenic C. tetani E88, a variant of strain Massachusetts. The genome consists of a 2,799,250-bp chromosome encoding 2,372 ORFs. The tetanus toxin and a collagenase are encoded on a 74,082-bp plasmid, containing 61 ORFs. Additional virulence-related factors could be identified, such as an array of surface-layer and adhesion proteins (35 ORFs), some of them unique to C. tetani. Comparative genomics with the genomes of Clostridium perfringens, the causative agent of gas gangrene, and Clostridium acetobutylicum, a nonpathogenic solvent producer, revealed a remarkable capacity of C. tetani: The organism can rely on an extensive sodium ion bioenergetics. Additional candidate genes involved in the establishment and maintenance of a pathogenic lifestyle of C. tetani are presented.
破伤风是人类和脊椎动物中最严重且全球流行的疾病之一,据报道已有2400多年的历史。该病的表现形式——痉挛性麻痹,是由已知毒性第二大的物质破伤风毒素引起的,人类致死剂量约为1纳克/千克。幸运的是,通过接种破伤风类毒素可成功控制这种疾病;然而,据世界卫生组织估计,每年仍有大约40万例病例发生,主要是新生儿破伤风。破伤风的病原体是破伤风梭菌,一种厌氧的产芽孢细菌,其自然栖息地是土壤、灰尘和各种动物的肠道。在此,我们报告了产毒破伤风梭菌E88(马萨诸塞菌株的一个变体)的完整基因组序列。该基因组由一条2799250碱基对的染色体组成,编码2372个开放阅读框(ORF)。破伤风毒素和一种胶原酶编码在一个74082碱基对的质粒上,该质粒含有61个ORF。还可鉴定出其他与毒力相关的因子,如一系列表层和粘附蛋白(35个ORF),其中一些是破伤风梭菌特有的。与气性坏疽病原体产气荚膜梭菌和非致病性溶剂产生菌丙酮丁醇梭菌的基因组进行比较基因组学研究,揭示了破伤风梭菌的显著能力:该生物体可以依赖广泛的钠离子生物能学。文中还介绍了参与破伤风梭菌致病生活方式建立和维持的其他候选基因。