Metallo-beta-lactamase producing gram-negative bacterial isolates.

BACKGROUND: The global emergence of metallo-ß-lactamase (MBL) producing bacterial isolates causing lower respiratory tract infection (LRTI) has resulted in fewer therapeutic options in treatment modalities. However, to our knowledge no studies regarding MBLs had been done so far in Nepal. Therefore, this study was carried out to assess the current level of MBL producing bacterial isolates in our setup. METHODS: This was a cross-sectional study conducted over a period of six months (June to November 2008) at Bacteriology laboratory of a teaching hospital. A total of 1120 specimens representing lower respiratory tract (sputum, endotracheal secretion and bronchial washing) were processed from outpatients and inpatients, with suspected LRTI, at TUTH. The specimens were collected and processed according to the standard methodology. Combination disk method and Double disk synergy test methods were used for the detection of MBL producing isolates. RESULTS: Respiratory pathogens were recovered from 497 (44.4%) of suspected cases. Among these, gram-negative bacteria were observed in 448 (84.0%). Multidrug resistance (MDR) was found in 286 (53.7%) of the total bacterial isolates. MBL was present in 6 (1.3%) of the total 448 gram-negative isolates. MBL was detected by both DDST and CD methods in 3 isolates each of Pseudomonas aeruginosa and Acinetobacter spp. from inpatients. All MBL producers were MDR. CONCLUSIONS: MBL-producing gram negative bacteria were detected from LRTI isolates in this study and this data can be used as base-line information of this novel type of ß-lactamase in our setup.

Granulocyte colony-stimulating factor dosing in pegylated interferon alpha-induced neutropenia and its impact on outcome of anti-HCV therapy.

Many patients with chronic hepatitis C (HCV) infection undergoing treatment with pegylated interferon-alpha (PEG-IFN-alpha) and ribavirin develop neutropenia requiring dose reduction or granulocyte colony-stimulating factor (G-CSF) supplement. We analysed the database of patients who completed treatment for chronic HCV infection between 2003 and 2006. Patients with absolute neutrophil counts below 1000 cells/microL were initiated on G-CSF (G-CSF group) while a matching group of patients who received anti-HCV treatment without developing neutropenia were used as a control group (non-G-CSF group). Patients on the G-CSF arm were divided into two subgroups based on the timing of G-CSF administration relative to PEG-IFN-alpha administration. Of the 163 patients with HCV infection, 30 patients received G-CSF, most of who were maintained on 300 microg of G-CSF once a week. Administration of G-CSF 2 days before or after each dose of PEG-IFN-alpha did not make a significant difference in the neutrophil counts. In the G-CSF arm, 23 of 30 patients (77%) had undetectable end-of-treatment viral response which was comparable with 27 of 30 in the control group (90%; P = 0.17). There was no statistically significant difference in the sustained viral response between the two groups (61%vs 76%, P = 0.18). In most patients PEG-IFN-alpha induced neutropenia improved with a once-a-week dose of G-CSF with a comparable virological outcome. Timing of G-CSF administration did not make any significant impact on the patient's neutrophil counts but was better tolerated when given 2 days apart from PEG-IFN-alpha.

Lymphoproliferative responses to mitogens and prepared antigens of M. avium complex in patients with HIV infection.

Published reports have demonstrated that antigens of Mycobacterium avium complex (MAC) can suppress the normal response to mitogens in lymphoproliferation assays. We therefore studied the lymphoproliferative (LP) function of PBMC from 55 HIV-infected patients and 16 controls in response to mitogens with and without MAC antigen. As expected, LP responses decline with progressive decline in CD4 count; MAC antigen in combination with PHA further suppresses that response in a dose-dependent manner. More relevant were the LP responses in those with CD4 counts less than 100. All patients with MAC disease had poor responses (stimulation index, SI < 10) to PHA or anti-CD3 with or without MAC antigen. Those who did not have nor subsequently developed MAC were both good (SI > 10) or poor responders (SI < 10). The suppressive effect of MAC on lymphocyte function may serve as a weak virulence factor which is only relevant in severely immunocompromised HIV patients.