Summary. DNA hybridisation of 309 consecutive Staphylococcus aureus clinical isolates with oligonucleotide probes specific for genes encoding Panton-Valentine leucocidin (luk-PV) and y-haemolysin (hlg) revealed that 99% of randomly selected strains carried the hlg locus whereas only 2 YO harboured the luk-PV as well as the hlg loci. Only 1 YO of the strains did not possess either gene. In a clinical prospective study of independent S . aureus strains, 58 Panton-Valentine leucocidin (PVL)-producing isolates were shown to be responsible for primary skin infections, mainly furuncles (86 YO). Phage susceptibility patterns and pulsed field gel electrophoresis (PFGE) profiles of DNA were shown to be polymorphic epidemiological markers of PVL-producing strains. In eight patients with recurrent furuncles, the PVL-producing strains isolated either from furuncles or from the anterior nares were considered to be identical in each based upon phage sensitivity profiles or PFGE patterns.

Two clinical strains of Enterobacter aerogenes that exhibited phenotypes of multiresistance to ␤-lactam antibiotics, fluoroquinolones, chloramphenicol, tetracycline, and kanamycin were investigated. Both strains showed a porin pattern different from that of a susceptible strain, with a drastic reduction in the amount of the major porin but with an apparently conserved normal structure (size and immunogenicity), together with overproduction of two known outer membrane proteins, OmpX and LamB. In addition, the full-length Opolysaccharide phenotype was replaced by a semirough Ra phenotype. Moreover, in one isolate the intracellular accumulation of chloramphenicol was increased in the presence of the energy uncoupler carbonyl cyanide m-chlorophenylhydrazone, suggesting an energy-dependent efflux of chloramphenicol in this strain. The resistance strategies used by these isolates appear to be similar to that induced by stress in Escherichia coli cells.Bacteria have developed various regulatory systems which coordinate their adaptive responses with the different environmental stresses to which they are exposed. Recently, the wholegenome transcriptional profiles, or "transcriptomes," were determined in vitro for an Escherichia coli strain exposed to an inducer of the soxRS or marRAB system and an E. coli strain constitutively expressing MarA (7,39). Under these conditions, the expression of several genes appeared to be significantly activated or down-regulated. These modulations of gene expression alter the sensitivities of the bacteria to a broad range of antibiotics (1, 2).Enterobacter aerogenes is one of the more frequently described gram-negative bacteria responsible for nosocomial respiratory tract infections (5, 17). In the last 5 years, it has been shown that clinical isolates of this species, which are naturally resistant to aminopenicillins through their production of a chromosomal cephalosporinase, often express an extendedspectrum ␤-lactamase, TEM-24, which gives rise to resistance to ␤-lactam antibiotics (5,17,19,31). Moreover, E. aerogenes exhibits acquired resistance to other families of antimicrobial agents. Previous studies have reported that clinical strains exhibiting an efflux process are resistant to ␤-lactam antibiotics, quinolones, tetracycline, and chloramphenicol (12, 29). Drug efflux can be coincident with a drastic reduction in drug uptake due to the loss of porin content (16,22,23,29).Two E. aerogenes clinical isolates, isolates 117 and 119, were selected from up to 100 strains isolated in our laboratory (12). These two strains exhibited a phenotype of multiresistance to ␤-lactam antibiotics, fluoroquinolones, chloramphenicol, tetracycline, and kanamycin comparable to that of E. aerogenes strains lacking nonspecific porins or expressing mutated porins (12, 29).The aim of this work was to examine some factors that may contribute to the resistance to antimicrobial agents in these two E. aerogenes clinical strains. MATERIALS AND METHODSBacterial strains, growth conditions, and antibiotic suscepti...

Acquired angioedema (AAE) due to C1-inhibitor (C1INH) deficiency is rare. Treatment options for acute attacks are variable and used off-label. Successful treatment of the associated lymphoma with rituximab seems to prevent acute attacks in subjects with AAE. The aim of this study was to describe AAE manifestations, its associated diseases, and patients’ responses to treatments in a representative cohort.A retrospective nationwide study was conducted in France. The inclusion criteria were recurrent angioedema attacks and an acquired decrease in functional C1INH <50% of the reference value.A total of 92 cases were included, with a median age at onset of 62 years. Facial edema and abdominal pain were the most frequent symptoms. Fifteen patients were hospitalized in the intensive care unit because of laryngeal edema, and 1 patient died. Anti-C1INH antibodies were present in 43 patients. The associated diseases were primarily non-Hodgkin lymphoma (n = 44, with 24 splenic marginal zone lymphomas) and monoclonal gammopathy of undetermined significance (n = 24). Three patients had myeloma, 1 had amyloid light-chain (of immunoglobulin) (AL) amyloidosis, 1 patient had a bronchial adenocarcinoma, and 19 patients had no associated disease. Icatibant relieved the symptoms in all treated patients (n = 26), and plasma-derived C1INH concentrate in 19 of 21 treated patients. Six patients experienced thromboembolic events under tranexamic acid prophylaxis. Rituximab prevented angioedema in 27 of 34 patients as a monotherapy or in association with chemotherapy. Splenectomy controlled AAE in 7 patients treated for splenic marginal zone lymphoma. After a median follow-up of 4.2 years, angioedema was on remission in 52 patients.AAE cases are primarily associated with indolent lymphoma—especially splenic marginal zone lymphoma—and monoclonal gammopathy of undetermined significance but not with autoimmune diseases or other conditions. Icatibant and plasma-derived C1INH concentrate control attacks; splenectomy and immunochemotherapy prevent angioedema in lymphoma setting.

Background: Schnitzler syndrome is characterized by an urticarial rash, a monoclonal gammopathy, and clinical, histological, and biological signs of neutrophilmediated inflammation. The aim of this study was to assess the applicability and validity of the existing diagnostic criteria in real-life patients. Methods: This multicentric study was conducted between 2009 and 2014 in 14 hospitals in which patients with Schnitzler syndrome or controls with related disorders were followed up. We compared the sensitivities and specificities and calculated the positive and negative predictive values of the Lipsker and of the Strasbourg criteria for the patients with Schnitzler syndrome and for the controls. We included 42 patients with Schnitzler syndrome, 12 with adult-onset Still's disease, 7 with cryopyrin-associated periodic disease, 9 with Waldenstr€ om disease, and 10 with chronic spontaneous urticaria. Results: All patients with Schnitzler syndrome met the Lipsker criteria. According to the Strasbourg criteria, 34 patients had definite Schnitzler syndrome, five had probable Schnitzler syndrome, and three did not meet the criteria. One control met the Lipsker criteria and had probable Schnitzler syndrome according to the Strasbourg criteria. Sensitivity and specificity of the Lipsker criteria were 100% and 97%, respectively. For the Strasbourg criteria, sensitivity for definite and probable diagnosis was 81% and 93%, respectively, with a corresponding specificity of 100% and 97%. Conclusion: Diagnostic criteria currently in use to diagnose Schnitzler syndrome are reliable. More investigations must be done to attest their efficiency in patients with recent-onset manifestations.

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