An infant with meningococcal arthritis of the hip

Meningococcus is a well known cause of meningitis and septicaemia. It is less well known as a cause of arthritis. This case report describes an infant with meningococcal arthritis and with further discussion of the role of meningococcal serogroup W135 in disease, as well as current and future immunisation strategies.     

Twenty-three neutrophil granulocytes in 10 high-power fields is the best histopathological threshold to differentiate between aseptic and septic endoprosthesis loosening

Aims:  The histopathological diagnosis of infection in periprosthetic tissue from loose total joint endoprosthesis has been the subject of controversy. The aim was to define a histological criterion that would best differentiate between aseptic and septic endoprosthesis loosening.
Methods and results:  Neutrophilic granulocytes (NG) were enumerated histopathologically in 147 periprosthetic membranes obtained from aseptic and septic revision surgery, using periodic acid–Schiff (PAS) stains and CD15 immunohistochemistry. Cell numbers were correlated with the results of microbiological culture and the clinical diagnoses. Using receiver–operating characteristics, an optimized threshold was found at 23 NG in 10 high-power fields (HPF). Using this threshold, histopathological examination had a sensitivity of 73% and specificity of 95% when compared with microbiological diagnosis (area under the curve 0.881), and a sensitivity of 77% and specificity of 97% when compared with clinical diagnosis (area under the curve 0.891).
Conclusions:  We therefore recommend a counting algorithm with a threshold of ≥23 NG in 10 HPF (visual field diameter 0.625 mm) for the histopathological diagnosis of septic endoprosthesis loosening. If the enumeration of NG is difficult in conventional haematoxylin and eosin-stained slides, CD15 immunohistochemistry should be performed, whereas the PAS stain has not proven to be helpful .     

An audit of the use of granulocyte colony-stimulating factor in septic shock

Background: Granulocyte colony‐stimulating factor (G‐CSF) stimulates the production of neutrophils and modulates the function and activity of developing and mature neutrophils. In septic shock, the immune system can be considered one of the failing organ systems.G‐CSF improves immune function and may be a useful adjunctive therapy in patients with septic shock. Aim: To evaluate the introduction of G‐CSF as an adjunct to our standard treatment for community‐acquired septic shock. Methods: We performed a prospective data collection and analysis to determine whether the addition of G‐CSF to our standard treatment for community‐acquired septic shock was associated with improved hospital outcome, compared with an historical cohort ofsimilar patients. We included all patients admitted to the Intensive Care Unit (ICU) with community‐acquired septic shock between December 1998 and March 2000. Patients received 300 µg G‐CSF intravenously daily for 10 days in addition to ourstandard treatment for community‐acquired septic shock. G‐CSF was discontinued early if the patient was discharged from ICU before10 days or if the absolute neutrophil count exceeded 75 × 10⁶/mL. Results: A total of 36 patients with community‐acquired septic shock, an average Apache 2 score of 26.7, and a predictedmortality of 0.79, were treated with G‐CSF from December 1998 to March 2000. Hospital mortality was 31% compared with an historical cohort of 11 similar patients with a hospital mortality of 73% (P = 0.018). In the subgroup of patients with melioidosis septic shock, the hospital survival improved from 5% to 100% (P < 0.0001).No significant adverse events occurred as a result of the administration of G‐CSF. Conclusion: G‐CSF is a safe adjunctive therapy in community‐acquired septic shock and may be associated with improved outcome. The use of G‐CSF in septic shock should undergo further investigation to define subgroups of patients who may benefit from G‐CSF. The use of G‐CSF in patients with septic shock due to Burkholderia pseudomallei is recommended. (Intern Med J 2002; 32: 143?148)     

严重感染患者发生感染性休克的危险因素分析

目的研究严重感染患者发生感染性休克的危险因素。方法选取北京协和医院加强医疗病房中5个月内连续收治的49例严重感染患者，记录其人口统计学资料、临床信息、血单核细胞人白细胞抗原DR（HLA-DR）、血二胺氧化酶（DAO）等指标，主要研究终点为住院病死率，对上述资料先进行单因素分析，在此基础上选择有统计学差异的变量进行多因素非条件Logistic回归分析。结果共有23例（46．9％）严重感染患者发生感染性休克。统计结果显示血培养阳性、HLA—DR降低、血小板计数下降和血DAO升高与感染性休克的发生有关；其中血培养阳性（OR=6．524，95％CI：1．364—31．206，P：0．019）、HLA—DR降低（OR=0．956，95％CI：0．920—0．993，P=0．020）和血DAO活性升高（OR=2．312，95％CI：1．162～4．600，P=0．017）是发生感染性休克的独立危险因素。结论伴有血培养阳性、HLA—DR降低和外周血DAO活性升高的严重感染患者发生感染性休克的风险较高。     

Citrobacter freundii septic arthritis

Septic arthritis in an 8 month old infant due to Citrobacter freundii was treated successfully with a third generation cephalosporin. Infections due to Citrobacter are uncommon in this age group and are almost unknown as a cause of septic arthritis.     

Gene therapy in surgery

Summary Background With the increasing body of knowledge in molecular biology, gene transfer respectively gene therapy becomes more and more a valid therapeutic option. Methods This is a critical review of gene therapy protocols for treatment of different types of cancer. Furthermore, the pathophysiological mechanism, therapeutically strategies as well as experimental approaches toward gene transfer in septic shock and organ transplantation are critically elucidated. Results Gene transfer as a therapeutic option was first successfully applied in children with severe combined immunodeficiency (SCID) in 1990. The majority of gene marking or gene therapy protocols approved for human clinical trials to date are related to the treatment of cancer. Besides viral vectors for brain tumors, non-viral vectors, liposomes particularly, with almost no side effects are increasingly used. Conclusions Different approaches of gene transfer in cancer patients are under investigation. Experimental data of septic shock treatment and rejection therapy of the allograft in organ recipients with gene transfer are encouraging for future applications in clinical trials. Part II: “Application to septic shock and to organ transplantation” will be published in Acta Chir Austriaca 1997; 29: Issue 1. References are listed at the end of part. II.     

FcgammaRIIb balances efficient pathogen clearance and the cytokine-mediated consequences of sepsis

The immune response to infection must be controlled to ensure it is optimal for defense while avoiding the consequences of excessive inflammation, which include fatal septic shock. Mice deficient in FcgammaRIIb, an inhibitory immunoglobulin G Fc receptor, have enhanced immune responses. Therefore, we examined whether FcgammaRIIb controls the response to Streptococcus pneumoniae. Macrophages from FcgammaRIIb-deficient mice showed increased antibody-dependent phagocytosis of pneumococci in vitro, and consistent with this infected FcgammaRIIb-deficient mice demonstrated increased bacterial clearance and survival. In contrast, previously immunized FcgammaRIIb-deficient mice challenged with large inocula showed reduced survival. This correlated with increased production of the sepsis-associated cytokines tumor necrosis factor alpha and interleukin 6. We propose that FcgammaRIIb controls the balance between efficient pathogen clearance and the cytokine-mediated consequences of sepsis, with potential therapeutic implications.     

蛋白激酶对内毒素休克后内皮细胞骨架的作用

目的　探讨内毒素休克发病机制中蛋白激酶G(PKG)的作用。　方法　用脂多糖 (LPS)刺激培养的内皮细胞 ,通过细胞裂解和离心获得细胞裂解液 ,用放射性同位素法标记法检测PKG的活性。同时采用特异性荧光染色法检测LPS刺激后细胞内肌动蛋白微丝 (F actin)的结构和分布变化。用PKG特异性抑制剂KT5 82 3预处理细胞后 ,再检测LPS介导的细胞内PKG活性和F actin的变化。以空白组为阴性对照 ,以PKG激动剂 8 Br cGMP刺激细胞作为阳性对照组。　结果　LPS分别刺激 5、10、30和 6 0min后细胞内PKG活力呈时间依赖性的增高 (与空白组相比P <0 .0 1) ,细胞内的F actin出现极性分布 ;而KT5 82 3预刺激 2 0min后再用LPS刺激没有出现上述变化。PKG的激动剂 8 Br cGMP刺激细胞后的变化与LPS的刺激相似。　结论　LPS可以介导血管内皮细胞PKG的激活和F actin的应力性变化 ;内毒素休克后内皮细胞通透性增高与cGMP PKG通路的激活有关。