Erythromycin resistance rates were found to be increased, from 7.1 in 1993 to 32.8% in 1997, among community-acquired Streptococcus pneumoniae isolates from the Siena area of central Italy. Most of the erythromycin-resistant isolates carried ermAM determinants and were also resistant to josamycin and clindamycin, whereas a minority (5.8%) carried mefA determinants and remained susceptible to the latter drugs.

Recently, concern has increased regarding the spread of methicillin-resistant Staphylococcus aureus (MRSA) in the community. We studied 812 subjects from central Italy to establish the rates of nasal carriage of S. aureus, and antibiotic susceptibility patterns, in the community. The prevalence of S. aureus nasal carriage was 30.5%. Only one subject, with predisposing risk factors for acquisition, was identified as carrier of MRSA (prevalence of 0.12%). The presence of MRSA in the community of our area still appears to be a rare event. Among methicillin-susceptible S. aureus (MSSA) isolates, a surprisingly high rate (18%) of resistance to rifampin was observed.

The prevalence of the cphA gene or related carbapenemase-encoding genes was investigated in 114 Aeromonas strains belonging to the six species of major clinical interest. A species-related distribution of cphA-related sequences was observed. Similar sequences were found in A. hydrophila, A. veronii bv. sobria, A. veronii bv. veronii, and A. jandaei, but not in A. caviae, A. trota, or A. schubertii. However, a single A. caviae strain (of 62 tested) was found carrying cphA-related sequences, suggesting the possibility of the horizontal transfer of this gene to species which normally do not carry it. Production of carbapenemase activity was detectable in 83% of the hybridization-positive strains but in none of the hybridization-negative ones. When it was present, carbapenemase activity was always inhibitable by EDTA. Either carbapenemase-producing or not, Aeromonas strains appeared to be susceptible to imipenem when in vitro susceptibility testing was performed with inocula of conventional size (10 5 CFU), for which MICs were always Յ1 g/ml. With a larger inoculum (10 8 CFU), the MICs for carbapenemase-negative strains always remained Յ1 g/ml, while those for carbapenemase-producing strains were always Ն4 g/ml, being usually higher than the breakpoint for susceptibility. The present results indicate that the production of metallocarbapenemase activity, apparently encoded by cphA homologs, is widespread among some of the Aeromonas species of clinical interest (A. hydrophila, A. veronii bv. sobria, A. veronii bv. veronii, and A. jandaei) and that imipenem MICs for carbapenemase-producing strains are subjected to a relevant inoculum size effect.Carbapenem compounds are ␤-lactam antibiotics of great therapeutic potential owing to their broad spectra of activity and resistance to most bacterial ␤-lactamases. However, enzymes able to inactivate the carbapenem molecule by hydrolysis of the ␤-lactam ring (carbapenemases) are produced by some microbial species and can cause microbial resistance to these compounds (11,12,18). Most of the carbapenemases thus far described are metalloenzymes which use a zinc ioncontaining active site (11), and all of the metallocarbapenemases thus far characterized at the sequence level belong to the same molecular class (class B), suggesting a common phylogeny (6,7,14,17,25).Members of the genus Aeromonas, which in the last decade have been the objects of increasing interest as human and animal pathogens (9), are among the few microorganisms that can produce metallocarbapenemase activities (1, 8, 24). The CphA metallo-␤-lactamase of A. hydrophila is one of the most active carbapenemases known, showing also, in comparison with other class B enzymes, a very specific substrate profile (5, 6, 23). The production of carbapenemase activity has previously been investigated in Aeromonas strains belonging to different species (1,8,24). However, recent developments in the field of Aeromonas taxonomy have led to a redefinition of some of the old species and to the description of new species (9) in which...

Susceptibility to macrolides and lincosamides was investigated with 299 consecutive nonduplicate Streptococcus pyogenes clinical isolates collected over a 6-year period (1992 to 1997) from an area of central Italy. During this period, macrolide resistance rates steadily increased (from 9% in 1992 to 53% in 1997; P < 0.001). The increase was caused by isolates with a macrolide-lincosamide-streptogramin B resistance phenotype, carrying mostly erm(B) but also erm(TR) genes, that were not detected in the first 2 years and were detected with increasing prevalence (8, 5, 26, and 37%, respectively) during the following 4 years. During the same period, the prevalence of isolates with a macrolide resistance phenotype, carrying mef(A) determinants, did not vary significantly; on average it was 13%, with modest rate fluctuations in different years and no definite trend. Molecular typing revealed a remarkable clonal diversity among susceptible and resistant isolates and a notable heterogeneity of the genetic environment of the resistance genes. The analysis of clonal diversity in relation with resistance phenotypes and genotypes revealed that increased macrolide resistance rates were due to a complex interplay of different mechanisms, with a relevant contribution played by an "epidemic" spread of genetic elements carrying the erm(B) gene among the circulating streptococcal population.Streptococcus pyogenes (group A streptococcus) remains one of the leading bacterial pathogens worldwide. Superficial infections caused by group A streptococci, such as pharyngitis and impetigo, are usually mild and self-limiting but ubiquitous and extremely common. On the other hand, the occurrence of severe invasive infections and of nonsuppurative sequelae, although less common, make of S. pyogenes a major public health concern (see reference 3 and references therein).Macrolide antibiotics are among the preferred drugs for the treatment of group A streptococcal pharyngitis and are largely used in community medicine for empirical chemotherapy of respiratory tract infections, due to their clinical efficacy, good compliance, and low toxicity (34). Resistance to macrolides in S. pyogenes can be caused by two different mechanisms: (i) active drug efflux via a transmembrane pump encoded by horizontally acquired mef genes (7, 35) and (ii) modification of the 23S rRNA target by rRNA adenine methylases encoded by horizontally acquired erm genes (see references 19 and 38 and references therein). The Mef efflux system operates only with 14-and 15-membered ring macrolides (M resistance phenotype) (7), while ribosomal modification by Erm methylases prevents the binding of macrolides, lincosamides, and streptogramins B, leading to resistance to all these compounds (MLS resistance phenotype) (19 (19,38,39).Since the first report in the 1950s (20), a large number of epidemiological surveys on macrolide resistance in S. pyogenes have been carried out. Results of these studies overall revealed a remarkable variability of resistance rates at different times and...

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 ␤-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 AmpCtype 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.