面颈部坏死性筋膜炎15例报告

目的探讨面颈部坏死性筋膜炎的早期诊断及有效治疗措施。方法对1970年1月-2009年3月收治的15例面颈部坏死性筋膜炎临床资料进行回顾性分析。结果经切开扩创引流、抗炎、营养支持等综合治疗，10例治愈，5例死亡。结论面颈部坏死性筋膜炎起病急、进展迅速早期临床表现不典型易误诊，诊断处理不当死亡率较高，治疗成功的关键是早期诊断、及早切开扩创引流抗炎支持等综合治疗。     

小儿躯干严重坏死性筋膜炎一例

患儿女,6岁,于2012年7月5日因全身多处出现红色斑丘疹伴有发热,在当地医院诊断为水痘,给予抗病毒治疗,治疗期间因发热间断应用了糖皮质激素,7月11日发现腰背部出现小片状红肿,且逐渐加重,局部皮肤变黑、坏死,且范围逐渐扩大,同时伴有高热,最高体温39.5℃,精神欠佳,因病情变化快,症状逐渐加重,于7月13日转入北京朝阳急诊抢救中心。入院查体:体温:39.3℃,脉搏:110次/min,呼吸:     

乳腺结节性筋膜炎七例临床病理及遗传学分析

目的:探讨乳腺结节性筋膜炎（nodular fasciitis of the breast,NFB）临床病理及分子遗传学特征。方法:回顾性分析7例NFB病例的临床特征及组织学特点,并行免疫组织化学、荧光原位杂交（FISH）及逆转录-聚合酶链反应（RT-PCR）检测。结果:7例患者均为女性,年龄15~51岁,平均年龄36...     

Two cases of fatal necrotizing fasciitis caused by Photobacterium damsela in Japan

We encountered two cases of fatal necrotizing fasciitis caused by Photobacterium damsela in Japan. Both cases occurred in fishermen who became sick after fishing. They developed multiple organ failure within 20 to 36 h from the onset of initial symptoms despite intensive chemotherapy and surgical treatments.     

Two cases of necrotizing fasciitis due to Acinetobacter baumannii

Necrotizing fasciitis has conventionally been associated with the streptococci, and when it is caused by other organisms, it is most often the result of a polymicrobial infection. We report on two cases of fatal monomicrobial necrotizing fasciitis due to Acinetobacter baumannii, an unusual finding that may be an indication of enhanced virulence of the organism.     

Unusual case of necrotizing fasciitis caused by Vibrio cholerae O137

We report a case of necrotizing fasciitis caused by Vibrio cholerae O137 in an immunocompromised 49-year-old man. The infection was acquired following a minor traumatic injury and exposure to seawater during the summer of 2009 in Italy. Although highly immunocompromised, the patient survived. The strain was cytotoxic, invasive, and adhesive and contained a fragment of the El Tor-like hemolysin (El Tor hlyA) gene.     

Culture independent and rapid identification of bacterial pathogens in necrotising fasciitis and streptococcal toxic shock syndrome by fluorescence in situ hybridisation

Fluorescence in situ hybridisation (FISH) targeted to ribosomal RNA is well established for studies in environmental microbiology. Initial applications of this technique in the field of medical microbiology showed that FISH is also a suitable means for the rapid, reliable and cultivation-independent identification of bacterial pathogens. In particular, for infectious diseases that follow a fulminant live-threatening course, such as sepsis or necrotising fasciitis (NF), a fast and reliable detection technique is of great importance. This study describes the development of an rRNA-targeted oligonucleotide set covering more than 95% of the pathogens associated with NF. These probes were tested with a broad collection of target and non-target organisms and found to be highly specific. Subsequently, the FISH approach was applied for the direct detection of bacterial pathogens in clinical samples. Two cases of NF and one case of streptococcal toxic shock syndrome (STSS) were analysed. FISH correctly identified almost all pathogens present in the samples examined within 2–3 h. However, Proteus mirabilis, which was identified in one sample by conventional methods was detected as a rod-shaped bacteria but could not be identified by FISH, since no specific probe was available for this particular organism. In contrast, identification of pathogens in these samples by conventional laboratory methods took 48–72 h. Furthermore, in one patient with pre-sampling antimicrobial therapy bacteria could not be grown from any of the samples. FISH unequivocally revealed the presence of Streptococcus pyogenes in affected tissue samples from this patient. In an experimental setting we demonstrated that FISH readily identifies S. pyogenes cells rendered non-cultivable by antibiotic treatment. Thus, FISH holds great promise for rapid identification of pathogens in fulminant infections such as NF, particularly in cases when pre-sampling antimicrobial therapy hampers culture of the causative agent. Received: 16 December 1999     

Four cases of necrotizing fasciitis caused by <Emphasis Type="Italic">Klebsiella</Emphasis> species

Presented here are four cases of necrotizing fasciitis caused by Klebsiella spp. that were treated at one hospital over a 2-year period. Klebsiella necrotizing fasciitis can occur via direct inoculation, local trauma or, more commonly, hematogenous spread from other septic foci. Early, aggressive, surgical debridement and appropriate antimicrobial treatment are the cornerstones of treatment for this condition. Necrotizing fasciitis due to Klebsiella spp. is unique in that it is commonly associated with multiple septic foci. While liver abscesses and endogenous endophthalmitis are better-known associations of disseminated Klebsiella infection, necrotizing fasciitis is increasingly recognized as one of the manifestations of this syndrome. When treating Klebsiella necrotizing fasciitis, awareness of the potential for multiorgan involvement should prompt a thorough search for associated foci of infection.     

Prognostic factor of mortality and its clinical implications in patients with necrotizing fasciitis caused by Vibrio vulnificus

In Taiwan, the aquatic environment and endemic hepatitis contribute to the high susceptibility of Vibrio vulnificus infection. A multidisciplinary treatment protocol for necrotizing fasciitis caused by V. vulnificus was developed in our institute, namely, ceftriaxone or ceftazidime combined with doxycycline or minocycline followed by an emergency fasciotomy and intensive care unit admission. We retrospectively reviewed 100 cases to evaluate the effectiveness of our treatment protocol and identify independent predictors of mortality to improve clinical outcomes. Cases of culture-confirmed V. vulnificus infection between January 1996 and December 2011 were reviewed. Necrotizing fasciitis was surgically diagnosed if these criteria were met: necrotic fascia, “dishwater discharge”, and loss of resistance while doing finger dissection along the fascia plane. One hundred cases met these criteria and were included for analysis. Eighteen patients died (18 % mortality). Unknown injury events, presence of multiple skin lesions, leukocytes?<?10,000 cells/mm³, platelets?<?100,000/mm³, serum creatinine ≥1.3 mg/dL, serum albumin?<?2.5 mg/dL, and delayed treatment beyond 3 days post-injury or symptom onset were associated with significantly higher mortality. Multivariate analysis showed that treatment delayed beyond 3 days is an independent factor indicating a poor prognosis (OR 10.75, 95 % CI 1.02–113.39, p?=?0.048). Early diagnosis and prompt treatment within 3 days post-injury or symptom onset should be the goal for treating patients with necrotizing fasciitis caused by V. vulnificus. Additional investigations to rescue patients with a prolonged disease course of necrotizing fasciitis (≥3 days) may be important.     

Characterization of group C and G streptococcal strains that cause streptococcal toxic shock syndrome

Twelve strains (the largest number ever reported) of group C and G(1) streptococci (GCS and GGS, respectively) that caused streptococcal toxic shock syndrome (STSS) were collected and characterized. Eleven strains were identified as Streptococcus dysgalactiae subsp. equisimilis, and one strain was identified as Streptococcus equi subsp. zooepidemicus. We found that it was the first reported case of STSS caused by S. equi subsp. zooepidemicus. Cluster analysis according to the 16S rRNA gene (rDNA) sequences revealed that the S. dysgalactiae strains belonged to clusters I and II, both of which were closely related. The emm types and the restriction patterns of chromosomal DNA measured by pulsed-field gel electrophoresis were highly variable in these strains except BL2719 and N1434. The 16S rDNA sequences and other characteristics of these two strains were indistinguishable, suggesting the clonal dissemination of this particular S. dysgalactiae strain in Japan. As the involvement of superantigens in the pathogenesis of group A streptococcus-related STSS has been suggested, we tried to detect known streptococcal superantigens in GCS and GGS strains. However, only the spegg gene was detected in seven S. dysgalactiae strains, with none of the other superantigen genes being detected in any of the strains. However, the sagA gene was detected in all of the strains except Tokyo1291. In the present study no apparent factor(s) responsible for the pathogenesis of STSS was identified, although close genetic relationships of GCS and GGS strains involved in this disease were suggested.