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A large outbreak caused by expanded-spectrum cephalosporin-resistant Klebsiella pneumoniae (ESCRKP) was observed in a neonatal intensive care unit (NICU) in central Italy. The outbreak involved 127 neonates (99 colonizations and 28 infections, with seven cases of sepsis and two deaths) over a period of more than 2 years (February 2008 to April 2010). Characterization of the 92 nonredundant isolates that were available for further investigation revealed that all of them except one produced the FOX-7 AmpC-type β-lactamase and belonged to either sequence type 14 (ST14) or ST26. All of the FOX-7-positive isolates were resistant to cefotaxime, ceftazidime, and piperacillin-tazobactam, while 76% were susceptible to cefepime, 98% to ertapenem, 99% to meropenem, and 100% to imipenem. The two carbapenem-nonsusceptible isolates had alterations in the genes encoding outer membrane proteins K35 and K36, which resulted in truncated and likely nonfunctional proteins. The outbreak was eventually controlled by the reinforcement of infection control measures based on a multitiered interventional approach. This is the first report of a large NICU outbreak caused by ESCRKP producing an AmpC-type enzyme. This study demonstrates that AmpC-type enzyme-producing strains can cause large outbreaks with significant morbidity and mortality effects (the mortality rate at 14 days was 28.5% for episodes of sepsis), and it underscores the role of laboratory-based surveillance and infection control measures to contain similar episodes.

Twelve isolates of Enterobacteriaceae (1 of Klebsiella pneumoniae , 8 of Escherichia coli , 1 of Proteus mirabilis , and 2 of Proteus vulgaris ) classified as extended-spectrum β-lactamase (ESBL) producers according to the ESBL screen flow application of the BD-Phoenix automatic system and for which the cefotaxime MICs were higher than those of ceftazidime were collected between January 2001 and July 2002 at the Laboratory of Clinical Microbiology of the San Matteo University Hospital of Pavia (northern Italy). By PCR and sequencing, a CTX-M-type determinant was detected in six isolates, including three of E. coli (carrying bla CTX-M-1 ), two of P. vulgaris (carrying bla CTX-M-2 ), and one of K. pneumoniae (carrying bla CTX-M-15 ). The three CTX-M-1-producing E. coli isolates were from different wards, and genotyping by pulsed-field gel electrophoresis (PFGE) revealed that they were clonally unrelated to each other. The two CTX-M-2-producing P. vulgaris isolates were from the same ward (although isolated several months apart), and PFGE analysis revealed probable clonal relatedness. The bla CTX-M-1 and bla CTX-M-2 determinants were transferable to E. coli by conjugation, while conjugative transfer of the bla CTX-M-15 determinant from K. pneumoniae was not detectable. Present findings indicate that CTX-M enzymes of various types are present also in Italy and underscore that different CTX-M determinants can be found in a single hospital and can show different dissemination patterns. This is also the first report of CTX-M-2 in P. vulgaris .

We describe two cases of bacteremic infections caused by a multidrug-resistant Klebsiella pneumoniae isolate producing the OXA-48 carbapenemase that occurred in two solid organ transplant (liver and kidney) recipients, which was apparently transmitted with the allografts. This finding underscores the risk of donor-derived infections by multidrug-resistant Gram-negative pathogens in solid organ transplant recipients and emphasizes the need for rapid screening of organ donors for carriage of similar pathogens.

KPC-type carbapenemases are emerging resistance determinants in Klebsiella pneumoniae and other gram-negative pathogens, being an increasingly important mechanism of acquired resistance to carbapenems and other β-lactams ([9][1], [10][2]). KPC producers have recently undergone an important