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Available therapeutic options against carbapenem-resistant Klebsiella pneumoniae (CR-Kp) are limited because of the high level of resistance to other antimicrobial classes including polymyxins. The double-carbapenem regimen has been recently considered a possible therapeutic strategy. In the present study, we evaluated the in vitro bactericidal and synergistic activity of a double-carbapenem regimen consisting of ertapenem plus high-dose meropenem in a series of patients with healthcare-associated CR-Kp infections in whom the use of colistin was not indicated because of potential nephrotoxicity and/or resistance. In vitro synergy was evaluated using checkerboard and killing studies. A total of 15 patients were included in the study, with sepsis, severe sepsis and septic shock found in two (13.3%), five (33.3%) and one (6.7%) patients, respectively. Overall, the clinical/microbiological response was 12/15 (80%). Synergy was observed in 11/14 (78.6%) isolates using the checkerboard method whereas in killing studies 12/14 (85.7%) and 14/14 (100%) strains were synergistic and bactericidal at 24 h at concentrations of 1 × MIC MEM+1 × MIC ERT and 2 × MEM+1 × MIC ERT, respectively, with a significant decrease of log CFU/mL compared with other combinations (p <0.0001). The double-carbapenem regimen showed clinical and in vitro effectiveness in patients with CR-Kp infections., (Copyright © 2015 European Society of Clinical Microbiology and Infectious Diseases. Published by Elsevier Ltd. All rights reserved.)

Infections due to carbapenemase-producing Klebsiella pneumoniae represent an emerging threat due to the high mortality rate and lack of valid antimicrobial combinations, especially when the strain is colistin-resistant. We report a case of bloodstream infection due to pandrug-resistant K. pneumoniae treated successfully with an innovative regimen comprising a combination of colistin plus double carbapenem, along with an in vitro analysis showing the synergistic and bactericidal effect., (Copyright © 2015 The Authors. Published by Elsevier Ltd.. All rights reserved.)

We present a case of Rhodococcus equi primary retroperitoneal abscesses without pulmonary involvement in an immunocompromised patient with severe nephrotic syndrome. No risk factors for exposure to R. equi were present. The infection was successfully treated with long-term combination antibiotic treatment including linezolid and tigecycline., (Copyright 2009 International Society for Infectious Diseases. Published by Elsevier Ltd. All rights reserved.)

Glycosphingolipids are essential components of plasma membrane and act as antigens, mediators of cell adhesion, and modulators of signal transduction. Following activation of the Fas receptor, gangliosides are recuited in various intracellular compartments. We have evaluated whether the pro-apoptotic anti-CD95 antibody induces a nuclear localization of GD3 in HUT-78 cells. Our data shows that GD3 translocation from cytosol to nuclei is strongly correlated to concomitant rapid phosphorylation of histone H1 shortly after induction of apoptosis. This work advances the hypothesis that GD3 induces a post-translational modification of histone H1 thus influencing the apoptosis process through transcriptional activation/repression of specific genes.

OBJECTIVES: To analyze the expression of the 15- to 17-kDa plasmid-encoded antigens from Rhodococcus equi isolates of 7 AIDS patients and determine the immunologic response to these proteins in the patients' sera. METHODS: The expression of the virulence proteins in R. equi isolates and the specific antibody response were investigated by immunoblotting. Plasmid DNA was analyzed by agarose gel electrophoresis. RESULTS: The only patient infected with a strain carrying the virulence 85-kb plasmid and expressing the 15- to 17-kDa antigens developed a fatal pneumonia and did not produce specific antibodies to the virulence proteins. Of the 6 patients infected with R. equi strains lacking both proteins and plasmid, only 1 subject had a pulmonary disease with poor clinical outcome and exhibited a negligible humoral immune response to R. equi antigenic components, whereas the other patients who produced a remarkable antibody response developed either an asymptomatic infection (1 case) or pneumonia (4 cases) which completely cleared up. CONCLUSIONS: Our findings suggest that R. equi disease can be induced without the expression of the 15- to 17-kDa virulence-associated plasmid-encoded antigens in HIV-infected patients with very low CD4+ cell counts. Nevertheless, both the synthesis of the virulence proteins and a defective humoral immune response to R. equi may contribute to the severity of rhodococcal disease.