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d Natural killer T (NKT) cells are known to play a protective role in the immune responses of mice against a variety of infectious pathogens. However, little is known about the detailed information of NKT cells in patients with Mycobacterium tuberculosis infection. The aims of this study were to examine NKT cell levels and functions in patients with active M. tuberculosis infection, to investigate relationships between NKT cell levels and clinical parameters, and to determine the mechanism responsible for the poor response to ␣-galactosylceramide (␣-GalCer). NKT cell levels were significantly lower in the peripheral blood of pulmonary tuberculosis and extrapulmonary tuberculosis patients, and the proliferative responses of NKT cells to ␣-GalCer were also lower in patients, whereas NKT cell levels and responses were comparable in latent tuberculosis infection subjects and healthy controls. Furthermore, this NKT cell deficiency was found to be correlated with serum C-reactive protein levels. In addition, the poor response to ␣-GalCer in M. tuberculosis-infected patients was found to be due to increased NKT cell apoptosis, reduced CD1d expression, and a defect in NKT cells. Notably, M. tuberculosis infection was associated with an elevated expression of the inhibitory programmed death-1 (PD-1) receptor on NKT cells, and blockade of PD-1 signaling enhanced the response to ␣-GalCer. This study shows that NKT cell levels and functions are reduced in M. tuberculosis-infected patients and these deficiencies were found to reflect the presence of active tuberculosis.

Previously, Pseudomonas putida was considered a low-virulence pathogen and was recognized as a rare cause of bacteremia. Recently, however, multidrug-resistant and carbapenem-resistant P. putida isolates have emerged, causing difficult-to-treat nosocomial infections in seriously ill patients. Currently, the outcome of multidrug-resistant or carbapenem-resistant P. putida bacteremia remains uncertain. Here, we report 18 cases of P. putida bacteremia with high rates of carbapenem resistance and mortality. From January 2005 through December 2011, all cases of nosocomial P. putida bacteremia were identified and analyzed at Chonnam National University Hospital and Chonnam National University Hwasun Hospital. Electronic medical records were reviewed retrospectively. Four (22%) and five (23%) of 18 P. putida isolates were resistant to imipenem and meropenem, respectively. Common primary infection sites were central venous catheter (7, 39%), pneumonia (5, 28%), and cholangitis (2, 11%). Fourteen (78%) patients had indwelling devices related to the primary site of infection. The 30-day mortality rate was 39% (7/18): 40% (2/5) in patients with carbapenem-resistant P. putida bacteremia vs. 38% (5/13) in patients with carbapenem-susceptible P. putida bacteremia. Nosocomial P. putida bacteremia showed high resistance rates to most potent β-lactams and carbapenems and was associated with high mortality rates.

BackgroundFew clinical data are available on the relationship between genospecies and outcome of Acinetobacter bacteremia, and the results are inconsistent. We performed this study to evaluate the relationship between genospecies and the outcome of Acinetobacter bacteremia.MethodsClinical data from 180 patients who had Acinetobacter bacteremia from 2003 to 2010 were reviewed retrospectively. The genospecies were identified by rpoB gene sequence analysis. The clinical features and outcomes of 90 patients with A. baumannii bacteremia were compared to those of 90 patients with non-baumannii Acinetobacter bacteremia (60 with A. nosocomialis, 17 with Acinetobacter species “close to 13 TU”, 11 with A. pittii, and two with A. calcoaceticus).Results A. baumannii bacteremia was associated with intensive care unit-onset, mechanical ventilation, pneumonia, carbapenem resistance, and higher APACHE II scores, compared to non-baumannii Acinetobacter bacteremia (P<0.05). In univariate analyses, age, pneumonia, multidrug resistance, carbapenem resistance, inappropriate empirical antibiotics, higher APACHE II scores, and A. baumannii genospecies were risk factors for mortality (P<0.05). Multivariate analysis revealed A. baumannii genospecies (OR, 3.60; 95% CI, 1.56–8.33), age, pneumonia, and higher APACHE II scores to be independent risk factors for mortality (P<0.05).Conclusion A. baumannii genospecies was an independent risk factor for mortality in patients with Acinetobacter bacteremia. Our results emphasize the importance of correct species identification of Acinetobacter blood isolates.

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