Double- and multi-carbapenemase-producers: the excessively armored bacilli of the current decade.

Multidrug-resistant (MDR) and extensively drug-resistant (XDR) Gram-negative nosocomial pathogens commonly carry one carbapenemase gene conferring resistance to carbapenems and other beta-lactam antibiotics. However, increasing reports show that double-carbapenemase-producing (DCP) and even multi-carbapenemase-producing (MCP) bacteria are emerging in some parts of the world, diminishing further, in some cases, the already limited treatment options. In the present review, the up-to-date reports of DCP and MCP isolates are summarized and concerns regarding their emergence are discussed.

Accumulation of carbapenem resistance mechanisms in VIM-2-producing Pseudomonas aeruginosa under selective pressure.

Pseudomonas aeruginosa has the potential to achieve resistance to carbapenems via the acquisition of carbapenemase-encoding genes, the downregulation of the OprD porin, the overexpression of efflux systems and the overproduction of cephalosporinases. One hundred and fifty carbapenem-non-susceptible isolates from 2008 to 2010 were screened for carbapenemase production, OprD porin loss, efflux pumps overexpression and inducible AmpC beta-lactamase production. For comparison reasons, the presence of the same mechanisms was also assessed in a previous collection of 30 carbapenem-non-susceptible P. aeruginosa isolated between 2003 and 2005. Results showed the accumulation of various resistance mechanisms among VIM-2 producers isolated between 2008 and 2010 with a parallel considerable increase in imipenem MIC90 and the geometric mean of the MIC values of imipenem and meropenem between the two study groups. The accumulation of carbapenem resistance mechanisms highlights the potential of this formidable pathogen for evolutionary success under antibiotic selective pressure.

Mechanisms responsible for the emergence of carbapenem resistance in Pseudomonas aeruginosa.

Pseudomonas aeruginosa (P. aeruginosa) is an opportunistic pathogen associated with a range of nosocomial infections. This microorganism is noted for its intrinsic resistance to antibiotics and for its ability to acquire genes encoding resistance determinants. Among the beta-lactam antibiotics, carbapenems with antipseudomonal activity are important agents for the therapy of infections due to P. aeruginosa. The development of carbapenem resistance among P. aeruginosa strains is multifactorial. Plasmid or integron-mediated carbapenemases, increased expression of efflux systems, reduced porin expression and increased chromosomal cephalosporinase activity have all been defined as contributory factors. Phenotypic tests and molecular techniques are used for the characterization of the resistance determinants. The isolation of carbapenem resistant strains is alarming and requires the implementation of strict infection control measures in order to prevent the spread of carbapenemase encoding genes to unrelated clones or to other bacterial species.

Trimebutine as a potential antimicrobial agent: a preliminary in vitro approach.

AIM: The aim of this preliminary study was to investigate the in vitro effect of "non-antibiotic" trimebutine against reference strains Staphylococcus aureus ATCC 29213, ATCC 25923, Escherichia coli ATCC 25922, ATCC 35218, Pseudomonas aeruginosa ATCC 27853 and Enterococcus faecalis ATCC 29212; microbiota that are potentially involved in the pathophysiology of post-infectious functional gastrointestinal disorders. METHODS: Trimebutine activity was assessed by the broth microdilution method according to Clinical and Laboratory Standards Institute recommendations against reference strains S. aureus ATCC 29213 and ATCC 25923, E. coli ATCC 25922 and ATCC 35218, P. aeruginosa ATCC 27853 and E. faecalis ATCC 29212. Bactericidal activity of the compound was determined by spreading a 10 µL aliquot on Mueller-Hinton agar from each dilution showing non-visible growth. All tests were carried out in triplicate. RESULTS: Trimebutine was active against all strains tested presenting with MIC ranging from 1024 to 4000 mg/L. MIC and MBC were similar for E. coli ATCC 25922 and P. aeruginosa ATCC 27853 whereas for Gram-positive isolates and E. coli ATCC 35218 the MBC was higher. CONCLUSIONS: We demonstrated the in vitro bacteriostatic/bactericidal activity of trimebutine against bacteria frequently colonizing the gastrointestinal tract and potentially involved in human gastrointestinal infections that might trigger post-infectious functional gastrointestinal disorders.

Emergence of Klebsiella pneumoniae carrying bla(VIM) and bla(KPC) genes.

A Klebsiella pneumoniae clinical isolate resistant to imipenem was recovered from a wound sample. The patient, a 57-year-old man, underwent a surgical resection of small bowel and sigmoid colon and was treated with multiple courses of antimicrobials. PCR analysis revealed that the clinical isolate was carrying simultaneously bla(VIM-1), bla(KPC-2), bla(SHV) and bla(TEM) genes. The concomitant presence of these genes is alarming and poses therapeutic as well as infection control problems.

Diffuse interstitial lung disease as an early manifestation of ankylosing spondylitis.

A rare case of ankylosing spondylitis with interstitial pulmonary disease of the upper lung field, at an early stage in the disease, is described. The patient, a 35-year-old asymptomatic woman, was admitted to the hospital due to an abnormal chest radiograph that was found during preoperative evaluation for a toxic adenoma of the thyroid gland. Her mother and sister were also found to suffer from ankylosing spondylitis but without lung involvement. History, physical and laboratory examination as well as open lung biopsy excluded other causes of an interstitial pulmonary disease. The diagnosis of ankylosing spondylitis was based on clinical, radiographic, positive human leukocyte antigen (HLA-B27) and histologic findings.