A prospective observational study of invasive candidiasis was conducted in the neonatal intensive care unit of Aristotle University in Hippokration Hospital between 1994 and 2000. During this period, 59 neonates developed invasive candidiasis (58 cases of candidemia and 1 case of peritonitis), resulting in an overall incidence of 1.28% that showed a decreasing trend over the study period. Eleven (18.6%) cases developed within the first week of life and the others within a mean (+/-SEM) of 13.4+/-1.7 days after birth. The three most frequent causative species were Candida albicans (65.5%), Candida parapsilosis (15.5%), and Candida tropicalis (7%). C. albicans was the predominant species between 1994 and 1998, whereas, non-albicans Candida spp., particularly C. parapsilosis, were the most frequent species during the period 1999-2000 (P<0.001). While the overall mortality due to candidemia was 29% (17 of 59 cases), mortality associated with C. albicans and C. parapsilosis was 39.5% and 11.1%, respectively (P=0.032), and that observed in the 1999-2000 period was 0% (P=0.011). Virtually all isolates were susceptible to amphotericin B, flucytosine, fluconazole, and itraconazole, and no increases in minimal inhibitory concentrations were observed during these years. With the exception of a limited cluster of cases due to genotypically identical isolates, no clonal relation of C. albicans isolates was found. Moreover, no clonal persistence of C. albicans and no decrease in antifungal drug susceptibility occurred over the 6-year study period. Non-albicans Candida spp., mostly C. parapsilosis, have emerged as important pathogens in neonatal intensive care units, with infected patients having better outcomes as compared to patients infected with C. albicans.

Emergence of multidrug-resistant Gram-negative nosocomial pathogens has led to resurgence of colistin use. Safety and efficacy data regarding colistin use in pediatric patients are sparse, while optimal dosage has not been defined. We present a case series of neonates and children without cystic fibrosis treated with various doses of colistin intravenously. The records of patients who received colistin in a tertiary-care hospital from January 2007 to March 2009 were reviewed. Thirteen patients (median age 5 years, range 22 days to 14 years) received 19 courses of colistin as treatment of pneumonia, central nervous system infection, bacteremia, or complicated soft tissue infection. The isolated pathogens were Acinetobacter baumannii, Enterobacter cloacae, Klebsiella pneumoniae, Pseudomonas aeruginosa, and Stenotrophomonas maltophilia. Daily dose of colistin (colistimethate) ranged between 40,000 and 225,000 IU/kg. Duration of administration ranged from 1 to 133 days. Other antimicrobials were co-administered in 18/19 courses. Increase of serum creatinine in one patient was associated with co-administration of colistin and gentamicin. Sixteen of 19 courses had a favorable outcome, and only two of the three deaths were infection-related. Colistin intravenous administration appears well tolerated even at higher than previously recommended doses and of prolonged duration.

, two episodes of Candida tropicalis fungemia occurred in the Aristotle University neonatal intensive care unit (ICU). To investigate this uncommon event, a prospective study of fungal colonization and infection was conducted. From December 1998 to December 1999, surveillance cultures of the oral cavities and perinea of the 593 of the 781 neonates admitted to the neonatal ICU who were expected to stay for >7 days were performed. Potential environmental reservoirs and possible risk factors for acquisition of C. tropicalis were searched for. Molecular epidemiologic studies by two methods of restriction fragment length polymorphism analysis and two methods of random amplified polymorphic DNA analysis were performed. Seventy-two neonates were colonized by yeasts (12.1%), of which 30 were colonized by Candida albicans, 17 were colonized by C. tropicalis, and 5 were colonized by Candida parapsilosis. From December 1998 to December 1999, 10 cases of fungemia occurred; 6 were due to C. parapsilosis, 2 were due to C. tropicalis, 1 was due to Candida glabrata, and 1 was due to Trichosporon asahii (12.8/1,000 admissions). Fungemia occurred more frequently in colonized than in noncolonized neonates (P < 0.0001). Genetic analysis of 11 colonization isolates and the two late blood isolates of C. tropicalis demonstrated two genotypes. One blood isolate and nine colonization isolates belonged to a single type. The fungemia/colonization ratio of C. parapsilosis (3/5) was greater than that of C. tropicalis (2/17, P ‫؍‬ 0.05), other non-C. albicans Candida spp. (1/11, P ‫؍‬ 0.02), or C. albicans (0/27, P ‫؍‬ 0.05). Extensive environmental cultures revealed no common source of C. tropicalis or C. parapsilosis. There was neither prophylactic use of azoles nor other risk factors found for acquisition of C. tropicalis except for total parenteral nutrition. A substantial risk of colonization by non-C. albicans Candida spp. in the neonatal ICU may lead to a preponderance of C. tropicalis as a significant cause of neonatal fungemia.Candida spp. are common causes of nosocomial invasive infections in neonatal intensive care units (ICUs). Although Candida albicans has historically been the most frequently isolated species, infections caused by non-C. albicans Candida spp. have been diagnosed with increased frequency in recent years (14,17). In particular, Candida parapsilosis has become the predominant fungal pathogen in many neonatal ICUs (11,14,17). Moreover, recent studies have shown that C. parapsilosis is often a cause of clusters and common-source outbreaks (12, 29).In contrast, little is known about the roles of other non-C. albicans Candida spp. in neonatal ICUs (4). To our knowledge, Candida tropicalis fungemia in neonates has not been adequately described, and the significance of mucocutaneous colonization of neonates by this pathogen remains speculative.Two chronologically related unusual cases of C. tropicalis fungemia that occurred in the Aristotle University neonatal ICU prompted us to initiate a prospective study of fungal co...

These data are suggestive of a differential relationship between antimicrobial consumption and the prevalence of antimicrobial resistance among various species and for various antimicrobial agents. These findings may help to optimize antimicrobial prescription policies in the hospital, especially in departments that have both high rates of antimicrobial consumption and a high prevalence of antimicrobial resistance.

, nine nonrepetitive isolates of Klebsiella pneumoniae with reduced susceptibility or resistance to carbapenems were recovered from clinical specimens from separate patients hospitalized in a tertiary care hospital. The imipenem-EDTA synergy test was positive for all isolates. PCR, sequencing, and transferability experiments revealed the novel bla VIM-12 metallo-␤-lactamase gene, which was plasmid mediated and located in a class 1 integron. Pulsed-field gel electrophoresis demonstrated a single macrorestriction pattern, indicating the clonal spread of VIM-12-producing K. pneumoniae.Acquired metallo-␤-lactamases (MBLs) constitute a growing class of ␤-lactamases that readily hydrolyze most ␤-lactam antibiotics, including imipenem and meropenem (20). They are usually embedded in class 1 integron structures carrying various gene cassettes and belong to the group B ␤-lactamases according to the classification scheme proposed by Ambler (1). Five different groups of acquired MBLs have been described (IMP, VIM, SPM, GIM, and SIM enzymes), but the first two of these groups have predominated in gram-negative organisms (8,9,13,20). VIM-type MBLs are commonly encountered among nonfermenters in the Far East and southern Europe (14,15,18,21,22), but during the last few years, the respective bla genes have also spread in members of the family Enterobacteriaceae (11,20,23). Reports of VIM-type MBL-producing K. pneumoniae isolates from Greek hospitals are increasing (5, 7). Recently, a novel VIM-type MBL variant, VIM-12, was identified from a clinical isolate of Klebsiella pneumoniae in Greece (16). In this report, we describe an outbreak caused by K. pneumoniae harboring the bla VIM-12 gene. MATERIALS AND METHODSFrom November 2006 to April 2007, nine nonrepetitive K. pneumoniae isolates exhibiting reduced susceptibility or resistance to imipenem were isolated from clinical specimens collected from separate patients hospitalized in different medical and surgical wards at Hippokration General Hospital, Thessaloniki, Greece. All patients had a long-term hospitalization and had been treated with multiple courses of antimicrobials, including carbapenems. Identification of the isolates to the species level and initial antibiotic susceptibility testing were performed by the Vitek-2 automated system (BioMérieux, Marcy l'Étoile, France), by which they were characterized as imipenem intermediate or resistant.Susceptibilities to a range of antimicrobials (amikacin, amoxicillin-clavulanate, ampicillin, aztreonam, cefepime, cefotaxime, cefoxitin, ceftazidime, ciprofloxacin, cotrimoxazole, ertapenem, imipenem, meropenem, and tetracycline) were also determined by disk diffusion (3). MICs of imipenem, meropenem, ertapenem, and tigecycline were additionally determined by Etest (AB Biodisk, Solna, Sweden) and the broth microdilution method (3). Susceptibilities were interpreted according to CLSI guidelines (3), when available. For tigecycline, the U.S.FDA (Food and Drug Administration) recommendation was used (susceptible, Յ2 g/ml; resistant, Ն8...