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The recovery of DNA and fingermark evidence from the same site can be problematic on account of potential contamination from fingermark visualisation techniques, and/or the destructive capability of the DNA recovery method. Forensic investigators are therefore often required to choose which evidence type to recover, or to recover both evidence types from different sites. Research typically documents the effects of fingermark visualisation techniques on the subsequent recovery of DNA, whereas this research has investigated the effects of DNA recovery on the quality of subsequently recovered latent fingermarks. Eccrine rich, sebaceous rich, and 'normal' latent fingermarks were deposited onto five substrates: glass; aluminium; textured plastic; varnished wood; photocopier paper and aged from 4h to 4 weeks. Approximately half of the control fingermarks were developed without DNA recovery on all substrates. The remaining samples were subjected to one of five DNA recovery methods prior to fingermark development. Pre and post DNA recovered fingermarks were graded for quality, and AFIS correlations scores were obtained and analysed for statistically significant differences using Wilcoxon Signed Rank tests and Friedman tests. All of the DNA recovery methods reduced the quality of latent fingermarks on glass surfaces. Flocked swabs and gel lifts were the least destructive DNA recovery methods on the remaining surfaces, except for aluminium sheet metal. The quality of latent fingermarks deposited onto glossed wood and textured plastic and paper were less affected by dry swabbing. Wet swabbing and tape lifting were very damaging methods of DNA recovery., (Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.)

Febrile neutropenia (FN) remains a potentially life-threatening complication of anticancer chemotherapy. Bacterial translocation via intestinal mucosa is a significant mechanism of FN development. Competitive inhibition of bowel colonization by pathogenic microorganisms by lactic acid bacteria could be a useful prevention of FN. The aim of the study was the evaluation of dose and safety of probiotic strain Enterococcus faecium M-74 enriched with organic selenium in patients with solid and hematological malignancies. Eleven (9 M/2F) patients were included in the study. In the first phase six patients with germ cell tumors treated by chemotherapy were included. They received prophylaxis by nonpathogenic strain E. faecium M-74 during 2 cycles of chemotherapy. The planned daily dose was 6 x 10(9) bacteria. Regarding the insufficient colonization of the gut, the dose was further increased up to 18 x 10(9) tid. After safety evaluation, five patients were included with relapse of acute leukemia. In patients with germ cell cancer, severe neutropenia G3/4 was noted in 10 of 12 cycles of chemotherapy. The febrile episode was not observed in any of the patients. The gut colonization by enterococci reaches 10(6) CFU/g stool. In 5 patients with acute leukemia during 127 days of severe neutropenia 12 febrile episodes occurred. There was not noted any febrile episode or infection provoked by the tested strain. Tolerance of therapy was excellent without significant undesirable effects. Optimal dose was assessed and safety of probiotic strain was evaluated in neutropenic patients with solid, or hematological malignancies. Based on these results we plan phase II study to evaluate the effectiveness of this strain in FN prophylaxis.

60 patients with 60 viridans streptococcal bacteraemic episodes (42 due to penicillin-sensitive and 18 due to penicillin-resistant viridans streptococci) were analysed in a population of 12,185 admissions and 1,380 bacteraemic episodes during a 7-year period in a National Cancer Institute. The incidence of viridans streptococci among bacteraemias decreased from 11.5% in 1989 to 2.5% in 1995 after penicillin was introduced for prophylaxis of febrile neutropenia in acute leukaemia in 1993. However, the proportion of penicillin-resistant viridans streptococcal bacteraemias increased from 0 in 1989 and 1990 before any prophylaxis was given, to 12.9-16.7% after quinolones were used for prophylaxis in 1991 and 1992, and to 44.4-81.8% in 1993-1995 after penicillin was added to the quinolones. Mortality rate was higher in the subgroup of penicillin-resistant viridans streptococcal bacteraemias (p < 0.05). Statistically significant risk factors in patients with penicillin-resistant (compared with penicillin-sensitive) viridans streptococcal bacteraemia were: acute leukaemia (p < 0.03), high doses of cytarabine (p < 0.05), mucocutaneous lesions (p < 0.004), breakthrough bacteraemia during prophylaxis with ofloxacine plus penicillin (p < 0.001). Multiple logistic regression analysis showed that only acute leukaemia (OR 2.05, CI 0.85-1.85, p < 0.00452) and penicillin-resistance (OR 0.71, CI 0.103-4.887, p < 0.0209) were significant independent predictors of inferior outcome. Breakthrough bacteraemia during empiric therapy with vancomycine occurred in 5 of 116 patients treated with vancomycine, and during therapy with ampicillin plus gentamicin in 6 patients of 18 treated.

The aim of this study was to retrospectively compare the incidence, risk factors, and outcome in patients seen over a 7-year period at the National Cancer Institute in the Slovak Republic, with vancomycin-sensitive or vancomycin-resistant enterococcal bacteremia. The total incidence of enterococcal bacteremia at the National Cancer Institute increased from 5.1% in 1991 to 11.1% in 1993 and then decreased to 4.3% in 1995. Analysis of the 77 episodes of enterococcal bacteremia from 66 patients showed that 69 episodes from 60 patients were due to vancomycin-sensitive Enterococcus faecalis (group 1) and 8 episodes from 8 patients were due to vancomycin-resistant Enterococcus faecium (group 2). The features most frequently associated with enterococcal bacteremia were the insertion of a central venous catheter, neutropenia lasting more than 10 days, previous therapy with cephalosporins or vancomycin, previous prophylaxis with quinolones, and the incidence of superinfections. There was no difference in the clinical course or outcome between the 2 study groups. Previous therapy with aminoglycosides, cephalosporins, vancomycin or imipenem, neutropenia less than 10 days in length, malignancies other than leukemia or solid tumors, and the incidence of breakthrough bacteremia significantly correlated with patients with vancomycin-resistant E. faecium rather than patients with vancomycin-sensitive E. faecalis. The overall mortality was similar in both groups and averaged 32.5% for all enterococcal bacteremic patients. In this study, the major risk factors associated with cancer patients for developing vancomycin-resistant enterococcal bacteremia were previous therapy with aminoglycosides, cephalosporins or vancomycin, superinfections with other organisms and the incidence of breakthrough bacteremia., (Copyright © 1996 Japanese Society of Chemotherapy and the Japanese Association for Infectious Diseases. Published by Elsevier Ltd. All rights reserved.)

Ninety-nine patients with 101 bacteraemic episodes due to Pseudomonas aeruginosa (PA) within 6 years were divided into two groups according to their resistance to imipenem; of these 91 episodes were due to imipenem-sensitive (ISPA) and 10 due to imipenem-resistant (IRPA) strains. Risk factors, clinical course and outcome were evaluated and compared in the two groups. Acute leukaemia, long-lasting neutropenia, previous therapy with amikacin, third-generation cephalosporins, imipenem and prophylaxis with quinolones were significantly more frequently associated with IRPA than with ISPA. Imipenem-resistant PA bactereamias were associated with a higher incidence of septic shock (40% vs 19.8%) p. 161 0.02) and death 33.3%) than were ISPA bacteraemias. Since 1992, when first IRPA appeared, the incidence of imipenem-resistance increased tenfold, and in 1994, up to 10% of the PA populations causing bloodstream infections in cancer patients in our centre were imipenem-resistant.