Staphylococcus aureus can exemplify better than any other human pathogen the adaptive evolution of bacteria in the antibiotic era, as it has demonstrated a unique ability to quickly respond to each new antibiotic with the development of a resistance mechanism, starting with penicillin and methicillin, until the most recent, linezolid and daptomycin. Resistance mechanisms include enzymatic inactivation of the antibiotic (penicillinase and aminoglycoside-modification enzymes), alteration of the target with decreased affinity for the antibiotic (notable examples being penicillin-binding protein 2a of methicillin-resistant S. aureus and D-Ala-D-Lac of peptidoglycan precursors of vancomycin-resistant strains), trapping of the antibiotic (for vancomycin and possibly daptomycin) and efflux pumps (fluoroquinolones and tetracycline). Complex genetic arrays (staphylococcal chromosomal cassette mec elements or the vanA operon) have been acquired by S. aureus through horizontal gene transfer, while resistance to other antibiotics, including some of the most recent ones (e.g., fluoroquinolones, linezolid and daptomycin) have developed through spontaneous mutations and positive selection. Detection of the resistance mechanisms and their genetic basis is an important support to antibiotic susceptibility surveillance in S. aureus.

Consecutive non-replicate clinical isolates (n=191) of carbapenem non-susceptible Enterobacteriaceae were collected from 21 hospital laboratories across Italy from November 2013 to April 2014 as part of the European Survey on Carbapenemase-producing Enterobacteriaceae (EuSCAPE) project. Klebsiella pneumoniae carbapenemase-producing K. pneumoniae (KPC-KP) represented 178 (93%) isolates with 76 (43%) respectively resistant to colistin, a key drug for treating carbapenamase-producing Enterobacteriaceae. KPC-KP colistin-resistant isolates were detected in all participating laboratories. This underscores a concerning evolution of colistin resistance in a setting of high KPC-KP endemicity.

Predisposing factors, clinical characteristics, and antimicrobial treatment of 37 hematology patients with Stenotrophomonas maltophilia bacteremia wh

Over the years 1983–1994, Candida parapsilosis caused 35 of 138 fungemic episodes (24 of 69 candidemias in the last quadriennium) in patients with hematologic malignancies who were being treated at a large university hospital in Italy. The central venous catheter was usually the source of bloodstream invasion; in most cases, the resolution of fungemia in patients receiving antifungal therapy required catheter removal. In seven cases, C. parapsilosis fungemia evolved to five proven (two cases with endocarditis) and two probable deep-seated infections; three of these seven patients died of deep-seated infections. Deep-seated infection was associated with the detection of a circulating mannoprotein antigen of C. parapsilosis but not with in vitro resistance to antifungal agents. Almost all fungal isolates produced slime in vitro, but only 34%were pathogenic in a model of bloodstream infection in neutropenic mice. The four isolates associated with endocarditis or persistent fungemia with multiorgan failure were among the most virulent in the model of infection. Overall, our findings highlight the role of C. parapsilosis as an agent of fungemia in patients with malignant hemopathies.