重复序列引物聚合酶链反应追踪金黄色葡萄球菌所致医院感染

目的 利用重复序列引物聚合酶链反应（rep-PCR）追踪我院一起由金葡菌所致的医院感染。方法 分离得到的50株金葡菌用PHOENIX-100微生物自动鉴定系统鉴定，苯唑西林-盐琼脂筛选MRSA表型；PCR检测其耐药基因mecA；rep-PCR作金葡菌基因分型。结果 50株金葡菌中，22株mecA阳性，其中19株分离自患者标本。采用rep-PCR，50株金葡菌均出现9～11条带的电泳图谱，从而可分成11个不同的基因型。结论 rep-PCR是一种快速、简便、可靠的基因分型方法，是在分子水平追踪医院感染病原菌较理想的工具。     

76例金黄色葡萄球菌医院感染患者的临床分析

目的：探讨2006年本院金黄色葡萄球菌（金葡菌）医院感染患者的临床影响因素及耐药情况。方法：回顾本院被确诊为医院感染的住院患者，分析其中金葡菌医院感染患者的临床特点、病原菌分布及耐药情况；并将非金葡菌医院感染患者作为对照组．采用Kirbv—Bauer琼脂扩散测定病原菌对抗菌药物的敏感度，并对患者的性别、年龄构成、原发疾病、所在病区、诊疗经过、诱发因素等资料进行回顾性调查，并进行统计分析。结果：2006年本院共有金葡菌培养阳性标本495例次．确诊为医院感染者96例次，其中91例次（76例患者）病史资料完整，非金葡菌医院感染354例次。76例中死亡20例．占2006年本院金葡菌医院感染者的26.32％。性别、年龄对金葡菌医院感染的发生无显著影响，而金葡菌医院感染发病最多的病区为神经外科，占30．77％（28例次／91例次）。下呼吸道标本培养金葡萄阳性者占所有金葡菌医院感染者的79．16％。诱发金葡菌医院感染的因素为手术、留置导尿、深静脉穿刺等侵入性操作。金葡菌对万古霉素敏感率为98.90％。结论：2006年本院金葡菌医院感染以神经系统疾病住院患者高发，可能与其原发病重、一般情况差有关.金葡菌感染以呼吸道为主，最主要的诱发因素为手术.     

金黄色葡萄球菌肺炎的防治

金黄色葡萄球菌(简称金葡菌)肺炎系金葡菌所致的急性肺部感染。病情较严重,病死率较高。常伴有化脓性并发症。金葡菌肺炎的感染途径有两条,一是呼吸道感染,多继发于麻疹、流感等病毒感染后,或肺结核和肺癌患者。二是血源性感染,如皮肤毛囊炎、蜂窝织炎、痈、疖、伤口或手术感染等。20多年来,产生青霉素酶的金葡菌感染的治疗比较困难,成     

英国社区MRSA感染的诊断与处理指南

金葡菌是引起皮肤软组织及骨感染的主要病原菌，也是引起卫生保健相关血流感染的最常见病原菌之一。正常人中约25％携带该菌，体内的定植菌常可引起感染。金葡菌感染的基本治疗为应用抗菌药和外科引流，但由于对青霉素、甲氧西林和其他药物多重耐药菌株的出现，使药物疗效减弱。甲氧西林应用于临床后不久，1961年首次检测出对其耐药的金葡菌（MRSA），随后的40年里MRSA在全球范围内流行，引起各种卫生保健相关感染。     

金黄色葡萄球菌烫伤样皮肤综合征治疗

金黄色葡萄球菌烫伤样皮肤综合征（staphylococcal scalded skin syndrome，SSSS）又称新生儿剥脱性皮炎或金葡菌型中毒性表皮坏死松解症。是由凝固酶阳性、噬菌体Ⅱ组71型金黄色葡萄球菌所致的一种严重皮肤感染，该型金葡菌可产生表皮松解毒素。临床上因其起病急、进展快，重症者可导致死亡，日益受到临床医师的注意。我总结了2005年7月-2006年2月12例SSSS治疗的疗效，现报告如下。     

鼻腔携带金黄色葡萄球菌与腹膜透析相关感染的观察性和干预性研究现状

腹膜透析相关感染是腹膜透析患者主要并发症,而金黄色葡萄球菌(以下简称金葡菌)是常见的致病菌。鼻腔金葡菌携带在该细菌的内源性感染中发挥重要作用。本文总结金葡菌鼻腔携带与腹膜透析相关感染发生率的关系,并分析去金葡菌鼻腔携带在预防腹膜透析相关感染的效果,以期为后续研究开展提供参考。     

多种金葡菌分型法间的关系

金黄色葡萄球菌引起人类多种严重感染,多重耐药的金葡菌导致院内感染逐年增加,流行病学调查需要将金葡菌分型.常用的金葡菌分型方法有:噬菌体分型、荚膜多糖血清型及酶分型、核酸分型和质粒分型.作者等利用SmaI消化金葡菌染色体DNA然后进行脉冲场凝胶电泳,依酶切图形对流行病学无关的两个来源的69株金葡菌分型(36株来自法国.33株来自德国的囊性纤维化病人的4周夏令营地),并与噬菌体、荚膜和酶分型法比较.     

耐甲氧西林金黄色葡萄球菌耐药基因及致病毒素基因的研究进展

金葡菌是临床最常见的病原菌之一，在临床分离菌中分离率位居前列，其中以MRSA临床意义尤为重要。由于其多重耐药性和易造成医院感染的暴发流行，已成为临床抗感染治疗的一大难题。金葡菌可引起一系列的化脓性感染、食物中毒及中毒性休克综合征等，其化脓性感染从小的皮肤感染病变如疖、痈到严重的感染如组织坏死、坏死性肺炎、骨髓炎和心内膜炎等。     

金黄色葡萄球菌L型致间质性肺炎的实验动物模型的建立

目的观察各实验动物感染金黄色葡萄球菌(金葡菌)L型后肺脏和其它重要脏器的病理变化.方法高渗培育金葡菌L型,经静脉和腹腔人工感染小白鼠、大白鼠等动物,光镜观察其相应脏器变化.结果发现主要脏器实质细胞发生变性、慢性炎细胞浸润和间质细胞增生性改变.结论细菌L型具有侵入和破坏组织脏器实质细胞的能力,引起相应脏器发生间质性炎症改变.     

金黄色葡萄球菌耐药性分析

目的了解金葡菌对常用抗菌药物的耐药情况，指导临床合理用药。方法对2002-2005年各类感染标本分离出的159株金葡菌使用纸片扩散法进行药敏试验和克林霉素诱导试验，并对结果进行分析。结果129株（81．1％）金葡菌为MRSA，敏感度最高的5种抗菌药物依次为万古霉素（100％）、氯霉素（92．5％）、复方磺胺甲嗯唑（88．7％）、利福平（30．8％）和阿米卡星（26．4％）。D试验阳性率为63．6％。结论临床分离的金葡菌对常用抗菌药物产生多重耐药性，应根据分离株耐药特点选用不同的治疗方案。     

Natural history of impetigo: II. Etiologic agents and bacterial interactions

Intensive observations on 37 children in a population with endemic skin infections provided an opportunity to study the interrelationships between and the significance of the bacterial genera commonly associated with impetigo. Cultures of the respiratory tract, three normal skin sites, and lesions, when present, were taken three times weekly from July to October 1969. Impetigo developed in all 37 children. Group A streptococci alone were recovered from 21% of 361 lesions, Staphylococcus aureus alone from 8%, Staphylococcus epidermidis alone from 5% and mixtures of streptococci and staphylococci from 61%.Vesicular or pustular lesions were more often pure streptococcal than pure staphylococcal. Streptococci alone were more often recovered from early stage lesions rather than from later ones. The pure staphylococcal lesions characteristically occurred early in the season whereas streptococcal or mixed lesions had later peaks.Serial observations on 74 lesions revealed longer persistence of streptococci than staphylococci in mixed lesions. In 85% of the instances the same streptococcal serotype was recovered repeatedly from an individual lesion, whereas staphylococcal types changed in 57% of instances.Phage type 75 accounted for the majority of staphylococcal isolates from all sites, whereas phage type 54 was recovered only from skin lesions.In contrast to streptococci, the site sequence of staphylococcal spread was from the nose to normal skin to skin lesions.These studies reveal important differences in the migration of staphylococci (as compared with streptococci) to various body sites and suggest a subsidiary role for staphylococci in nonbullous impetiginous lesions yielding both organisms.     

Treatment of bullous impetigo and the staphylococcal scalded skin syndrome in infants

Impetigo is a common, superficial, bacterial infection of the skin characterized by an inflamed and infected epidermis. The rarer variant, bullous impetigo, is characterized by fragile fluid-filled vesicles and flaccid blisters and is invariably caused by pathogenic strains of Staphylococcus aureus. Bullous impetigo is at the mild end of a spectrum of blistering skin diseases caused by a staphylococcal exfoliative toxin that, at the other extreme, is represented by widespread painful blistering and superficial denudation (the staphylococcal scalded skin syndrome). In bullous impetigo, the exfoliative toxins are restricted to the area of infection, and bacteria can be cultured from the blister contents. In staphylococcal scalded skin syndrome the exfoliative toxins are spread hematogenously from a localized source causing widespread epidermal damage at distant sites. Both occur more commonly in children under 5 years of age and particularly in neonates. It is important to swab the skin for bacteriological confirmation and antibiotic sensitivities and, in the case of staphylococcal scalded skin syndrome, to identify the primary focus of infection. Topical therapy should constitute either fusidic acid (Fucidin, Leo Pharma Ltd) as a first-line treatment, or mupirocin (Bactroban, GlaxoSmithKline) in proven cases of bacterial resistance. First-line systemic therapy is oral or intravenous flucloxacillin (Floxapen, GlaxoSmithKline). Nasal swabs from the patient and immediate relatives should be performed to identify asymptomatic nasal carriers of Staphylococcus aureus. In the case of outbreaks on wards and in nurseries, healthcare professionals should also be swabbed.     

Treatment of bullous impetigo and the staphylococcal scalded skin syndrome in infants

Impetigo is a common, superficial, bacterial infection of the skin characterized by an inflamed and infected epidermis. The rarer variant, bullous impetigo, is characterized by fragile fluid-filled vesicles and flaccid blisters and is invariably caused by pathogenic strains of Staphylococcus aureus. Bullous impetigo is at the mild end of a spectrum of blistering skin diseases caused by a staphylococcal exfoliative toxin that, at the other extreme, is represented by widespread painful blistering and superficial denudation (the staphylococcal scalded skin syndrome). In bullous impetigo, the exfoliative toxins are restricted to the area of infection, and bacteria can be cultured from the blister contents. In staphylococcal scalded skin syndrome the exfoliative toxins are spread hematogenously from a localized source causing widespread epidermal damage at distant sites. Both occur more commonly in children under 5 years of age and particularly in neonates. It is important to swab the skin for bacteriological confirmation and antibiotic sensitivities and, in the case of staphylococcal scalded skin syndrome, to identify the primary focus of infection. Topical therapy should constitute either fusidic acid (Fucidin^®, Leo Pharma Ltd) as a first-line treatment, or mupirocin (Bactroban^®, GlaxoSmithKline) in proven cases of bacterial resistance. First-line systemic therapy is oral or intravenous flucloxacillin (Floxapen^®, GlaxoSmithKline). Nasal swabs from the patient and immediate relatives should be performed to identify asymptomatic nasal carriers of Staphylococcus aureus. In the case of outbreaks on wards and in nurseries, healthcare professionals should also be swabbed.     

Staphylococcal food poisonings in Tokyo, with special reference to the coagulase types of the isolates

Staphylococcus aureus strains isolated from the 391 confirmed cases of staphylococcal food poisonings in Tokyo, in the period 1967-1986, were studied for their coagulase types. Consequently, it was found that all the isolates could be classified into the coagulase types II, III, VI and VII. Namely, the isolates from 54 (13.8%) of 391 outbreaks were typed as type II, 72 (18.4%) as type III, 38 (9.7%) as type VI, and 227 (58.1%) as type VII, respectively. Throughout the investigation, it was found that the outbreaks of staphylococcal food poisonings due to coagulase type VII organisms were remarkably increased since 1975.     

Type V staphylococcal cassette chromosome mec in community staphylococci from Australia

Twenty Australian community staphylococci harboring the type V staphylococcal cassette chromosome mec (SCCmec) were found to belong to eight multilocus sequence types. Five were previously unreported novel type V SCCmec elements. The mec complexes were of two types, based on the polymorphisms in the IS431 transposase genes. Five isolates were multiresistant.     

Skin carriage of antibiotic-resistant coagulase-negative staphylococci in untreated subjects

A detailed microbiological analysis was made of the antibiotic resistant coagulase-negative staphylococcal flora of facial skin of 64 untreated individuals. The flora was quantified at primary isolation using both non-selective and selective media (each containing one of seven different antibiotics). The isolates obtained were tested against 18 antibiotics for multiple resistance and biotyped to species level. The incidence of the seven primary antibiotic resistance markers among the staphylococcal flora of 64 untreated subjects was: tetracycline 87.5%, erythromycin 68.8%, fusidic acid 56.3%, trimethoprim 42.4%, chloramphenicol 25%, clindamycin 9.4% and gentamicin 4.7%. In addition, penicillin resistant staphylococci were isolated from 98% of subjects. Multiply resistant strains were carried by 62.5% of individuals, with 27.9% carrying more than 100 multiply resistant staphylococci/cm2 skin. Analysis of the frequency distributions of the size of resistant staphylococcal populations revealed considerable individual variation, with many individuals carrying greater than 10(3) resistant staphylococci/cm2 skin. Multiply resistant staphylococci usually comprised less than 10% of the total staphylococcal flora, although this often represented a large number of multiply resistant organisms. Three people carried greater than 10(4) multiply resistant staphylococci/cm2 skin. Most of the singly and multiply resistant isolates were identified as strains of Staphylococcus epidermidis, which was found to carry up to eight resistances per isolate. In contrast, S. capitis, a common resident of human facial skin, was never found to carry more than two resistances per isolate. S. aureus was rarely detected on intact facial skin and the strains were not multiply resistant. Resistance to the major antistaphylococcal antibiotics was infrequent (gentamicin, methicillin) or absent (rifampicin, vancomycin, cephalothin). It was concluded that untreated individuals carry a significant pool of singly and multiply resistant staphylococci of sufficient size to be readily disseminated by direct contact and desquamation.     

STUDIES ON THE PATHOGENESIS OF STAPHYLOCOCCAL INFECTION : IV. THE EFFECT OF BACTERIAL ENDOTOXIN

Intracutaneous and intravenous injection of pyrogenic, non-lethal doses of bacterial endotoxin were found to increase the infectivity of pathogenic but not non-pathogenic staphylococci in rabbit skin. The increased infectivity of the microorganism was characterized by accelerated multiplication at the site of inoculation and by the production of necrosis and hemorrhage locally. Histologically, the infection of skin in endotoxin-prepared animals was characterized by necrosis, masses of bacteria, but absence of leukocytic infiltration into the area of bacterial growth. The infectivity of staphylococci in skin of endotoxin-prepared rabbits could be controlled by antibody to the alpha hemolysin of the microorganism. The effect of endotoxin upon staphylococcal infection was demonstrable only within 4 hours after injection of the endotoxin. It could not be prevented with chlorpromazine or dibenamine and was closely related to the effect of endotoxin upon leukocytes. It was suggested that the effect of endotoxin upon leukocytes was probably responsible for its influence upon staphylococcal infection. The implications of these findings in the pathogenesis of staphylococcal infection are discussed.     

Epidermal HLA-DR and the enhancement of cutaneous reactivity to superantigenic toxins in psoriasis

Streptococcal and staphylococcal superantigens (SAg's) have been implicated in the pathogenesis of inflammatory skin diseases, but the mechanisms by which these toxins act are unknown. The present study assessed the ability of nanogram quantities of topically applied purified toxic shock syndrome toxin-1 (TSST-1), staphylococcal enterotoxin type B, and streptococcal pyrogenic enterotoxin types A and C to induce inflammatory reactions in clinically uninvolved skin of normal controls and subjects with psoriasis, atopic dermatitis, and lichen planus. These SAg's triggered a significantly greater inflammatory skin response in psoriatics than in normal control subjects or in subjects with atopic dermatitis or lichen planus. Surprisingly, skin biopsies did not exhibit the T-cell receptor Vbeta stimulatory properties predicted for SAg-induced skin reactions. By 6 hours after patch testing with SAg's, TNF-alpha mRNA had increased in the epidermis (but not the dermis) in biopsies from psoriatics, compared with controls. Immunohistochemical studies revealed significantly higher HLA-DR expression in keratinocytes from psoriatics than from controls. However, a mutant TSST-1 protein that fails to bind HLA-DR did not elicit an inflammatory skin reaction. These results indicate that keratinocyte expression of HLA-DR enhances inflammatory skin responses to SAg's. They may also account for previous studies failing to demonstrate selective expansion of T-cell receptor Vbetas in psoriatics colonized with SAg-producing Staphylococcus aureus, and they identify a novel T cell-independent mechanism by which SAg's contribute to the pathogenesis of inflammatory skin diseases.     

Carriage of gentamicin-resistant coagulase-negative staphylococci in patients on continuous ambulatory peritoneal dialysis

Gentamicin-resistant coagulase-negative staphylococci were found on various sites of the skin of 20 of 27 patients on continuous ambulatory peritoneal dialysis (CAPD). In 12 cases isolates with identical susceptibility patterns could be recovered from the same patients at intervals of 2-8 weeks. In seven of these cases isolates from individuals repeatedly had the same phage type, biotype and plasmid profile and three patients shared such identical strains. The use of plasmid profiles proved to be most satisfactory for epidemiological purposes. It was concluded that out-patients on CAPD may persistently harbour their own gentamicin-resistant coagulase-negative staphylococcal strain and that cross-colonization may also occur.     

Community-acquired methicillin-resistant Staphylococcus aureus infections

Staphylococcus aureus causes a variety of minor diseases but also is responsible for staphylococcal pneumonia and sepsis, both of which can be fatal. It is thought to be responsible for many of the pneumonia deaths associated with the influenza pandemics of the 20th century. The introduction of penicillin in the 1940s greatly improved the prognosis for patients with severe staphylococcal infections. However, after a few years of clinical use, most staphylococcal strains were able to hydrolyze penicillin by producing b-lactamases, making penicillin a useless antibiotic to treat staphylococcal infections caused by b-lactamase-producing S aureus. Methicillin, a semisynthetic penicillin introduced in 1959, was specifically designed to be resistant to b-lactamase degradation, but resistance developed soon after its introduction into clinical practice. Methicillin-resistant S aureus (MRSA) was first reported in the United Kingdom in 1961, followed by reports from other European countries, Japan, and Australia. The first reported case of MRSA in the United States was in 1968. Currently, MRSA is an important pathogen in nosocomial infections and is a problem in hospitals worldwide, and it is increasingly recovered from nursing home residents with established risk factors. More recently, community acquired MRSA infections have been documented among healthy individuals with no recognizable risk factors, and it seems clear that community-acquired MRSA (CA-MRSA) strains are epidemiologically and clonally unrelated to hospital-acquired strains. This review focuses on the epidemiology, clinical significance, and virulence markers of CA-MRSA infections.