We determined the frequency of isolation of staphylococcal small-colony variants (SCVs) from 31 culture-positive patients undergoing revision of total hip prosthesis for aseptic loosening or presumed prosthetic-joint infection (PJI). We analysed auxotrophy of cultured SCVs, their antimicrobial susceptibility profiles and their biofilm-forming capacity. Eight SCV strains were cultivated from six (19 %) patients. All SCVs were coagulase-negative staphylococci (CNS) with Staphylococcus epidermidis as the predominant species; there was also one Staphylococcus warneri SCV. The SCVs were auxotrophic for haemin, with one strain additionally auxotrophic for menadione. We noted the presence of two phenotypically (differences concerning antimicrobial susceptibility) and genetically distinct SCV strains in one patient, as well as the growth of two genetically related SCVs that differed in terms of their morphology and the type of auxotrophy in another. Seven out of eight SCVs were resistant to meticillin and gentamicin. In addition, antibiotic sensitivity testing revealed three multidrug-resistant SCV-normal-morphology isolate pairs. One S. epidermidis SCV harboured icaADBC genes and was found to be a proficient biofilm producer. This paper highlights the involvement of CNS SCVs in the aetiology of PJIs, including what is believed to be the first report of a S. warneri SCV. These subpopulations must be actively sought in the routine diagnosis of implant-associated infections. Moreover, in view of the phenotypic and genetic diversity of some SCV pairs, particular attention should be paid to the investigation of all types of observed colony morphologies, and isolates should be subjected to antimicrobial susceptibility testing.

No abstract

BackgroundThe etiology of osteonecrosis of femoral head (ONFH) has not been fully elucidated. Increased intravascular coagulation and/or hypofibrinolysis have been proposed as pathogenic mechanisms. Previous reports demonstrated significant association between incidence of ONFH and polymorphisms of genes related with thrombophilia especially in Caucasian subjects. The aim of our study was to evaluate the relationship between genetic mutations leading to coagulation disorders and ONFH in Polish patients.MethodsWe have investigated the frequencies of four markers among 68 unrelated individuals with clinically and radiographically documented ONFH and among 100 healthy unrelated blood donors in Eastern part of Poland. The three genes were involved in thrombophilia: factor V Leiden (G1691A), prothrombin (G20210A), Methylenetetrahydrofolate Reductase (MTHFR C677T) and one in hypofibrinolysis: Tissue Plasminogen Activator (PLAT TPA25 I/D). The samples were genotyped with polymerase chain reaction followed by restriction enzyme analysis for the restriction fragment length polymorphisms. The allele and genotype frequencies were analyzed in the relation to ONFH etiology (idiopathic and secondary), gender, age (patients younger or older than 50 years) and the number of affected joints (unilateral or bilateral ONFH).ResultsNo significant difference in allele frequencies between patients and control groups were observed in genes involved in thrombophilia. We have found a statistically significant increased frequency of D allele of PLAT TPA 25 I/D polymorphism between the entire group of patients with ONFH and controls (p=0,026, OR=1,54, CI 0,99-2,4). D allele frequency was also significantly increased in patients with primary ONFH (p=0,009, OR=1,81 CI 1,1-3,01), in males (p= 0,013; OR 1,74; 95% CIs 1,08-2,78), patients older than 50 years (p= 0,018, OR= 2,04; 95% CIs 1,09-3,82) and in cases with bilateral ONFH (p= 0,01; OR= 1,92; 95% CIs 1,13-3,27) (Table 9). The differences in DD homozygous genotype frequency were statistically significant for patients with idiopathic ONFH compared with control group (p=0,023, OR=2,75, CI 0,99-7,9) and in cases of bilateral ONFH (p=0,034; OR 3,12; 95% CIs 1,06-9,18) (Table 10). The frequencies of ID heterozygous genotype were statistically significantly higher in entire group of patients with ONFH (p=0,004 OR 2,71; 95% CIs 1,32-5,57), idiopathic ONFH (p= 0,01; OR 2,91; 95% CIs 1,24-6,87), males (p=0,0007; OR 3,75; 95% CIs 1,67-8,42), patients older than 50 years (p=0,001; OR 6,89; 95% CIs 1,87-25,84) and in cases with bilateral ONFH (p=0,009; OR 3,19; 95% CIs 1,26-8,03).ConclusionThe results suggest that inherited hypofibrinolysis is a risk factor of idiopathic ONFH in Polish population.

Poor prognosis of lung adenocarcinoma is associated with early occurrence of distant metastases. This type of non-small-cell lung carcinoma more frequently involves EGFR gene abnormalities, which determine the efficacy of EGFR tyrosine kinase inhibitor therapies (EGFR TKIs). It is probable that genetic abnormalities present in primary tumor will also be present in metastases. Unfortunately little is known about the incidence of these mutations in the metastases and about the effectiveness of molecularly targeted therapy in such patients. Formalin-fixed, paraffin-embedded tumor tissue was prepared from 431 samples of primary adenocarcinoma, 61 of adenocarcinoma central nervous system (CNS) metastases and 8 of adenocarcinoma bone metastases. The presence of exon 19 deletions was examined using the PCR technique and amplified PCR product fragment length analysis. The ASP-PCR technique was used to evaluate the L858R substitutions in exon 21, and the results were analyzed using ALF Express II sequencer. In the adenocarcinoma metastases to bone obtained from 8 patients, deletions in exon 19 of the EGFR gene were revealed in 3 smoking men and one non-smoking woman, while L858R substitution in exon 21 was found in one smoking woman and one man of unknown smoking status. The incidence of EGFR gene mutations in the bone metastases was 75 %, in the primary adenocarcinoma - 12.8 %, and in the adenocarcinoma metastases to CNS - 14.75 %. Five patients with EGFR gene mutation revealed in bone metastases were treated with EGFR TKIs; the majority of them had a satisfactory response to therapy.

MP4OX significantly reduced the incidence of hypotensive episodes in patients undergoing hip arthroplasty, but the adverse event profile does not support use in routine low-risk surgical patients for the indication evaluated in this study.