المؤلفون: Tripodi, M.-F.^1,2, Fortunato, R.¹, Utili, R.^2,3 riccardo.utili@ospedalemonaldi.it, Triassi, M.⁴, Zarrilli, R.⁴

المصدر: Clinical Microbiology & Infection. Oct2005, Vol. 11 Issue 10, p814-819. 6p.

مصطلحات موضوعية: *STREPTOCOCCUS, *ENDOCARDITIS, *MOLECULAR epidemiology, *BACTEREMIA, *BACTERIAL diseases

مستخلص: Streptococcus bovis is being recognised increasingly as a cause of infective endocarditis, and has also been associated with underlying gastrointestinal malignancy. This study evaluated the molecular epidemiology of S. bovis isolates responsible for endocarditis or bacteraemia in Italian patients between January 1990 and August 2003. S. bovis isolates were classified on the basis of their biochemical profiles, antimicrobial susceptibilities and genotypes. Of 25 isolates studied, 20 were S. bovis I and five were S. bovis II. Seven biochemical profiles were identified. Pulsed-field gel electrophoresis (PFGE) analysis identified 22 profiles that differed by at least two DNA fragments and showed a similarity of < 87%. Most PFGE patterns represented single isolates that differed in antimicrobial susceptibility, but three PFGE types were observed, with identical profiles and antibiotypes, in isolates from two different patients. S. bovis I and II isolates grouped into two distinct genetic clusters (I and II) with a similarity coefficient of 38%. Two sub-clusters (Ia and Ib), with a similarity coefficient of 47%, included 17 S. bovis I isolates with similar biochemical profiles (15 with biotype A, and two with biotype B), but different resistance phenotypes. Based on the phenotypic and genotypic heterogeneity of the isolates, it is postulated that the increase in S. bovis endocarditis in this geographical area might have been caused by the selection of sporadic endemic clones from the endogenous intestinal flora. [ABSTRACT FROM AUTHOR]

المؤلفون: Durante-Mangoni, E.¹, Andini, R.¹, Signoriello, S.², Cavezza, G.¹, Murino, P.³, Buono, S.³, De Cristofaro, M.⁴, Taglialatela, C.⁴, Bassetti, M.⁵, Malacarne, P.⁶, Petrosillo, N.⁷, Corcione, A.³, Viscoli, C.⁸, Utili, R.¹ riccardo.utili@unina2.it, Gallo, C.²

المصدر: Clinical Microbiology & Infection. Dec2016, Vol. 22 Issue 12, p984-989. 6p.

مصطلحات موضوعية: *KIDNEY injuries, *COLISTIN, *ACINETOBACTER baumannii, *NEPHROTOXICOLOGY, *DRUG side effects, *DRUG resistance in bacteria, *SURVIVAL analysis (Biometry), *INJURY risk factors, *THERAPEUTICS, RISK factors

مستخلص: The study aimed to prospectively assess incidence and risk factors for colistin-associated nephrotoxicity. This is a secondary analysis of a multicentre, randomized clinical trial, comparing efficacy and safety of colistin versus the combination of colistin plus rifampicin in severe infections due to extensively drug-resistant (XDR) Acinetobacter baumannii . The primary end point was acute kidney injury (AKI) during colistin treatment, assessed using the AKI Network Criteria, and considering death as a competing risk. A total of 166 adult patients without baseline kidney disease on renal replacement therapy were studied. All had life-threatening infections due to colistin-susceptible XDR A. baumannii . Patients received colistin intravenously at the same initial dose (2 million international units (MIU) every 8 h) with predefined dose adjustments according to the actual renal function. Serum creatinine was measured at baseline and at days 4, 7, 11, 14 and 21 (or last day of therapy when discontinued earlier). Outcomes assessed were ‘time to any kidney injury’ (AKI stages 1–3) and ‘time to severe kidney injury’ (considering only AKI stages 2–3 as events). When evaluating overall mortality, AKI occurrence was modelled as a time-dependent variable. AKI was observed in 84 patients (50.6%, stage 1 in 40.4%), with an incidence rate of 5/100 person-days (95% CI 4–6.2). Risk estimates of AKI at 7 and 14 days were 30.6% and 58.8%. Age and previous chronic kidney disease were significantly associated with any AKI in multivariable analysis. Neither ‘any’ nor ‘severe AKI’ were associated with on-treatment mortality (p 0.32 and p 0.54, respectively). AKI occurs in one-third to one-half of colistin-treated patients and is more likely in elderly patients and in patients with kidney disease. As no impact of colistin-associated AKI on mortality was found, this adverse event should not represent a reason for withholding colistin therapy, whenever indicated. [ABSTRACT FROM AUTHOR]

المؤلفون: Zarrilli, R.^1,2 rafzarri@unina.it, Casillo, R.³, Di Popolo, A.¹, Tripodi, M.-F.⁴, Bagattini, M.¹, Cuccurullo, S.⁵, Crivaro, V.¹, Ragone, E.³, Mattei, A.⁶, Galdieri, N.⁷, Triassi, M.¹, Utili, R.³

المصدر: Clinical Microbiology & Infection. May2007, Vol. 13 Issue 5, p481-489. 9p. 2 Charts, 2 Graphs.

مصطلحات موضوعية: *ACINETOBACTER, *MOLECULAR epidemiology, *NOSOCOMIAL infections, *PNEUMONIA, *DISEASE outbreaks

مصطلحات جغرافية: NAPLES (Italy), ITALY

مستخلص: This study investigated the molecular epidemiology of a clonal outbreak of multidrug-resistant Acinetobacter baumannii that occurred between June 2003 and June 2004 in a tertiary-care hospital in Naples, Italy. A. baumannii was isolated from 74 patients, of whom 38 were infected and 36 were colonised. Thirty-three patients had ventilator-associated pneumonia, three had hospital-acquired pneumonia, and two had sepsis. Genotypic analysis of 45 available A. baumannii isolates revealed two distinct pulsed-field gel electrophoresis (PFGE) patterns. Of these, PFGE pattern 1 was represented by isolates from 44 patients and was identical to that of an epidemic A. baumannii clone isolated in another hospital of Naples during 2002. All A. baumannii isolates of PFGE type 1 showed identical multiresistant antibiotypes, characterised by resistance to all antimicrobial agents tested, including carbapenems, with the exception of colistin. In these isolates, inhibition of OXA enzymes by 200 mM NaCl reduced the imipenem MIC by up to four-fold. Molecular analysis of antimicrobial resistance genes showed that all A. baumannii isolates of PFGE type 1 harboured a class 1 integron containing the aacA4, orfX and blaOXA-20 gene cassettes, an ampC gene and a blaOXA-51-like allele. Moreover, a blaOXA-58-like gene surrounded by the regulatory elements IS Aba2 and IS Aba3 was identified in a 30-kb plasmid from A. baumannii isolates of PFGE type 1, but not PFGE type 2. Thus, selection of a single A. baumannii clone producing an OXA-58-type carbapenem-hydrolysing oxacillinase was responsible for the increase in the number of A. baumannii infections that occurred in this hospital. [ABSTRACT FROM AUTHOR]

المؤلفون: MARRONE, A.¹ (AUTHOR), ZAMPINO, R.¹ (AUTHOR), KARAYANNIS, P.² (AUTHOR), CIRILLO, G.³ (AUTHOR), CESARO, G.¹ (AUTHOR), GUERRERA, B.¹ (AUTHOR), RICCIOTTI, R.¹ (AUTHOR), MIRAGLIA DEL GIUDICE, E.³ (AUTHOR), UTILI, R.⁴ (AUTHOR), ADINOLFI, L. E.¹ (AUTHOR), RUGGIERO, G.¹ (AUTHOR)

المصدر: Alimentary Pharmacology & Therapeutics. Oct2005, Vol. 22 Issue 8, p707-714. 8p. 3 Charts.

مصطلحات موضوعية: *HEPATITIS B virus, *DRUG resistance, *VIRUS inhibitors, *ANTIVIRAL agents, *LIVER diseases, *VIRAL hepatitis, *GENETIC mutation, *THERAPEUTICS

مستخلص: Background : Drug-resistant mutants may emerge in patients with chronic hepatitis B receiving lamivudine therapy. Aim : To evaluate whether different viral mutational patterns may be associated with clinical reactivation during lamivudine treatment in patients with chronic B hepatitis. Methods : Eight anti-hepatitis B e-positive patients with (group A) and 14 patients without clinical exacerbation (five anti-hepatitis B e-positive, group B1; nine hepatitis B e antigen-positive, group B2) during lamivudine treatment were investigated. Results : ‘Polymerase region’: M204V/I variants were found in all group A patients, but in none of group B1 ( P = 0.0007) and in four of nine of group B2 (44%; P = 0.02) patients. The L180M substitution was detected in four of eight (50%) of group A and in none of groups B1 and B2. ‘Core promoter’: the double basic core promoter (A1762T/G1764A) variant was detected in seven of eight (87%) of group A and in one of five (20%; P = 0.03) of group B1 and one of nine (11%; P = 0.002) of group B2 patients. ‘Precore’: the G1896A stop codon mutation was present in seven of eight (87%) of group A and in zero of five ( P = 0.004) of group B1 and one of nine (11%; P = 0.002) of group B2. Conclusions : Different mutational patterns were observed in the lamivudine-treated patients with and without exacerbation. There was an association of the basic core promoter and stop codon mutations with lamivudine resistance in patients with disease exacerbation. [ABSTRACT FROM AUTHOR]