欧洲中毒性休克综合征研讨会概要

欧洲中毒性休克综合征(ＴＳＳ)研讨会于近期在英国的伦敦召开,为了让广大的内科医生对这一综合征有一定的了解,现将会议的主要内容概述如下。一、ＴＳＳ的发现1978年,美国科罗拉多大学儿科流行病学主任ＪａｍｅｓＴｏｄｄ教授向著名的《新英格兰医学杂志》提交了第一篇概述ＴＳＳ病因及后果的论文,10天内论文被拒绝刊登。该杂志的编辑未将论文送交同行评审,因为他认为Ｔｏｄｄ将未适当定性的微生物与该病联系到一起,幸运的是《柳叶刀》杂志的反应却不同,它在1978年11月登出一篇文章,确定了金黄色葡萄球菌与ＴＳＳ之间的联系,并列举了其关键…     

链球菌中毒性休克综合征研究进展

链球菌中毒性休克综合征研究进展卢洪洲，翁心华自１９７８年Ｔｏｄｄ等首次报告噬菌体－１群金黄色葡萄球菌中毒性休克综合征（ＴＳＳ）以后［１］，ＴＳＳ已为人们所熟知。１９８３年Ｗｉｌｌｏｕｇｈｂｙ等报道链球菌也可引起相似的综合征［２］，并称为链球菌中毒性休...     

2例链球菌中毒性休克综合征

链球菌中毒性休克综合征（Streptococcal Toxic Shock syndrome STSS）为与A组溶血性链球菌感染相关的严重疾病。它主要表现为皮疹,高热,休克,急进性的多器官功能障碍,病死率极高,预后不良。现报告2例链球菌中毒性休克综合征患者     

反向被动乳胶凝集法检测葡萄球菌中毒性休克综合征毒素1

反向被动乳胶凝集法检测葡萄球菌中毒性休克综合征毒素１王文风，闻玉梅ＢｅｒｇｄｏｌｌＭＳ中毒性休克综合征（Ｔｏｘｉｃｓｈｏｃｋｓｙｎｄｒｏｍｅ，ＴＳＳ）是一种以高热，低血压、红斑皮疹伴脱屑为主要病征，伴有呕吐、腹泻、腹痛、肌痛、结膜及粘膜充血、肝肾功能...     

与经期污染相关的葡萄球菌中毒性休克综合征1例

患者女性 ,15岁。腹泻、腹痛、呕吐伴头晕 12ｈ ,直立性晕厥 1次入院。腹痛呈阵发性 ,泻稀水样便 4次 ,呕吐胃内容物 1次 ,非喷射状 ,全身酸软无力 ,入院前突然晕倒 ,意识丧失 ,5ｍｉｎ后自行清醒 ,来急诊时血压测不到 ,扩容后入院。无明确不洁饮食史 ,月经史 14( 6～ 7/2 8～ 30 )。入院前 5ｄ月经来潮 ,量中等 ,发病时处于月经期 ,未使用月经栓 ,但使用了不洁卫生纸。体检 :体温 37.5℃ ,血压 85/60ｍｍＨｇ ,神志淡漠 ,皮肤巩膜无黄染及出血点 ,胸腹及四肢皮肤呈花斑样或充血性粟粒大小丘疹 ,压之褪色。双肺呼吸音粗 ,未闻及罗音。脉搏细…     

Streptococcus-induced syndrome of toxic shock (streptococcal toxic shock syndrome)

Report on the first case of streptococcal toxic shock syndrome in the GDR. The patient was a 54-year-old female. One week before admission to the hospital she cut her finger. The day before admission to the hospital she presented with a painful left shoulder. Demarcation followed, and Streptococcus pyogenes (group A streptococci) was isolated from this area. The temperature rose to more than 40 degrees C and she became confused, hypotensive and anuric. There was evidence for disseminated intravascular coagulation. She died 23 h after admission. Clinical course and laboratory parameters resembles staphylococcal toxic shock syndrome, except a diarrhoea. The streptococcal strain produced a large amount of erythrogenic toxin type B (more than 20 ng/ml), but not erythrogenic toxins A or C. Erythrogenic toxins of Streptococcus pyogenes seem to play the same role in the development of streptococcal toxic shock syndrome as the toxic shock syndrome 1 (TSST-1) in staphylococcal toxic shock syndrome.     

Therapeutic approaches to streptococcal toxic shock syndrome

The streptococcal toxic shock syndrome (STSS) is a severe, life-threatening condition characterized by hypotension and multiorgan system dysfunction associated with infection by the group A Streptococcus (GAS) or rarely by streptococci of other Lancefield serogroups. It is associated with a soft tissue infection, such as necrotizing fasciitis, in about half of the cases; the remainder are secondary to a variety of other invasive and noninvasive GAS infections. Although the pathophysiology of STSS is not yet fully understood, there are compelling reasons to believe that the syndrome results at least in part from the action of the streptococcal pyrogenic exotoxins, which act as superantigens. Patients with STSS should be admitted to an intensive care unit for support of cardiovascular, respiratory, and renal function as required. In experimental models of overwhelming GAS infection, clindamycin has greater efficacy than penicillin, and therapy with this agent is recommended. Penicillin, to which GAS are uniformly susceptible, may be used in addition to clindamycin. Limited clinical experience, most of which is anecdotal, suggests marked improvement in some STSS patients after administration of intravenous immunoglobulin. Even in the absence of conclusive data, the potential benefits of intravenous immunoglobulin in this highly lethal disease make its use reasonable in life-threatening cases. Other experimental approaches are also discussed, such as the use of anti-tumor necrosis factor monoclonal antibodies and plasmapheresis.     

Development of serum antibody to toxic shock toxin among individuals with toxic shock syndrome in Wisconsin

The presence of Staphylococcus aureus producing toxic shock toxin (TST) and the absence of antibody to TST (anti-TST) in acute-phase sera are markers for toxic shock syndrome (TSS). We used radioimmunoassay methods to examine 133 acute-phase and 277 convalescent-phase serum specimens from 181 patients with TSS for anti-TST. Among confirmed menstrual cases, nine (9.5%) of 95 patients had demonstrable anti-TST in acute-phase sera obtained during the first seven days of illness; patients with probable or non-menstrual TSS had a higher prevalence of anti-TST in acute-phase sera. Five (33.3%) of 15 individuals with confirmed menstrual TSS developed anti-TST as early as seven to nine days after TSS onset; 32 (62.7%) of 51 patients had demonstrable anti-TST in sera obtained more than one year after their episode of TSS. This study demonstrates a gradual rate and low magnitude of development of anti-TST after TSS and supports the diagnostic usefulness of measuring anti-TST levels in sera from patients suspected of having TSS.     

Evolutionary genomics of Staphylococcus aureus: Insights into the origin of methicillin-resistant strains and the toxic shock syndrome epidemic

An emerging theme in medical microbiology is that extensive variation exists in gene content among strains of many pathogenic bacterial species. However, this topic has not been investigated on a genome scale with strains recovered from patients with well-defined clinical conditions. Staphylococcus aureus is a major human pathogen and also causes economically important infections in cows and sheep. A DNA microarray representing >90% of the S. aureus genome was used to characterize genomic diversity, evolutionary relationships, and virulence gene distribution among 36 strains of divergent clonal lineages, including methicillin-resistant strains and organisms causing toxic shock syndrome. Genetic variation in S. aureus is very extensive, with approximately 22% of the genome comprised of dispensable genetic material. Eighteen large regions of difference were identified, and 10 of these regions have genes that encode putative virulence factors or proteins mediating antibiotic resistance. We find that lateral gene transfer has played a fundamental role in the evolution of S. aureus. The mec gene has been horizontally transferred into distinct S. aureus chromosomal backgrounds at least five times, demonstrating that methicillin-resistant strains have evolved multiple independent times, rather than from a single ancestral strain. This finding resolves a long-standing controversy in S. aureus research. The epidemic of toxic shock syndrome that occurred in the 1970s was caused by a change in the host environment, rather than rapid geographic dissemination of a new hypervirulent strain. DNA microarray analysis of large samples of clinically characterized strains provides broad insights into evolution, pathogenesis, and disease emergence.