ABSTRACT
OBJECTIVES: The main function of HLA is to present antigens to lymphocytes and to initiate specific immune responses. Autoimmune, viral, allergic, and neurologic diseases have been found to be related to HLA molecules. In renal transplant, the main target of the recipient's immune system is the HLA molecules on the surface of donor cells. HLA also plays a role in the development of an immune response to viral infections. After renal transplant, BK virus infections may occur due to immunosuppression. Here, we investigated the relationship between HLA and BK virus in renal transplant recipients. MATERIALS AND METHODS: This retrospective study investigated HLA-A, HLA-B, and HLA-DR tissue typing before renal transplant. DNA was isolated from whole blood, and tissue typing tests were performed based on polymerase chain reaction. Patients were tested for BK virus posttransplant using DNA isolated from urine and/or plasma samples. RESULTS: We found HLA-B*13 allele to be a protective factor (P < .049; odds ratio: 0.131; 95% confidence interval, 0.017-1.029) and HLA-DRB1*03 allele to be a possible risk factor (P < .029; odds ratio: 2.521; 95% confidence interval, 1.157-5.490) against BK virus. No significant relationships were found between BK virus and age, sex, donor type, and HLA mismatch. CONCLUSIONS: HLA class I molecules are known to be effective against viruses with the help of cytotoxic T cells. HLA-B*13 alleles within the HLA class I molecules were identified as protective factors against BK virus. HLA class II is associated with CD4-positive T cells that help secrete immune system cytokines, playing a role in stimulating and suppressing the immune system. We demonstrated that HLA-DRB1*03 allele could be a risk factor against BK virus. This allele may be associated with immunomodulatory cytokine secretion of the immune system.
Subject(s)
BK Virus/genetics , DNA, Viral/blood , HLA Antigens/genetics , Kidney Transplantation/adverse effects , Opportunistic Infections/virology , Polyomavirus Infections/virology , Tumor Virus Infections/virology , BK Virus/immunology , Female , Gene Frequency , HLA Antigens/blood , Host-Pathogen Interactions , Humans , Immunocompromised Host , Immunosuppressive Agents/adverse effects , Male , Opportunistic Infections/blood , Opportunistic Infections/diagnosis , Opportunistic Infections/immunology , Polyomavirus Infections/blood , Polyomavirus Infections/diagnosis , Polyomavirus Infections/immunology , Retrospective Studies , Treatment Outcome , Tumor Virus Infections/blood , Tumor Virus Infections/diagnosis , Tumor Virus Infections/immunology , Viral LoadABSTRACT
This article describes the emergence of resistance and predictors of fatality for 1556 cases of healthcare-associated Gram-negative bloodstream infection in 2014 and 2015. The colistin resistance rate in Klebsiella pneumoniae was 16.1%, compared with 6% in 2013. In total, 660 (42.4%) cases were fatal. The highest fatality rate was among patients with Acinetobacter baumannii bacteraemia (58%), followed by Pseudomonas aeruginosa (45%), Klebsiella pneumoniae (41%), Enterobacter cloacae (32%) and Escherichia coli (28%). On multi-variate analysis, the minimum inhibitory concentrations for carbapenems [odds ratio (OR) 1.02, 95% confidence interval (CI) 1.01-1.04; P = 0.002] and colistin (OR 1.1, 95% CI 1.03-1.17; P = 0.001) were found to be significantly associated with fatality.
Subject(s)
Anti-Bacterial Agents/pharmacology , Bacteremia/mortality , Colistin/pharmacology , Cross Infection/mortality , Gram-Negative Bacteria/drug effects , Gram-Negative Bacterial Infections/mortality , Adult , Aged , Aged, 80 and over , Bacteremia/microbiology , Carbapenems/pharmacology , Cross Infection/microbiology , Female , Gram-Negative Bacteria/isolation & purification , Gram-Negative Bacterial Infections/microbiology , Humans , Male , Microbial Sensitivity Tests , Middle Aged , Retrospective StudiesABSTRACT
This article describes the prevalence of antibiotic resistance and predictors of mortality for healthcare-associated (HA) Gram-negative bloodstream infections (GN-BSI). In total, 831 cases of HA GN-BSI from 17 intensive care units in different centres in Turkey were included; the all-cause mortality rate was 44%. Carbapenem resistance in Klebsiella pneumoniae was 38%, and the colistin resistance rate was 6%. Multi-variate analysis showed that age >70 years [odds ratio (OR) 2, 95% confidence interval (CI) 1.22-3.51], central venous catheter use (OR 2.1, 95% CI 1.09-4.07), ventilator-associated pneumonia (OR 1.9, 95% CI 1.1-3.16), carbapenem resistance (OR 1.8, 95% CI 1.11-2.95) and APACHE II score (OR 1.1, 95% CI 1.07-1.13) were significantly associated with mortality.
Subject(s)
Bacteremia/mortality , Cross Infection/mortality , Drug Resistance, Bacterial , Gram-Negative Bacteria/drug effects , Gram-Negative Bacteria/isolation & purification , Gram-Negative Bacterial Infections/mortality , Adult , Aged , Bacteremia/epidemiology , Bacteremia/microbiology , Cross Infection/epidemiology , Cross Infection/microbiology , Female , Gram-Negative Bacteria/classification , Gram-Negative Bacterial Infections/epidemiology , Gram-Negative Bacterial Infections/microbiology , Humans , Intensive Care Units , Male , Middle Aged , Prevalence , Prognosis , Retrospective Studies , Risk Factors , Survival Analysis , Turkey/epidemiologyABSTRACT
Antimicrobial therapy of Brucella spp. infection is difficult because there are relatively few effective treatment regimens, and single-agent therapy has generally been considered inadequate due to unacceptably high relapse rates. tigecycline, the first in a new class of antimicrobials, the glycylcyclines, is a 9-t-butylglycylamido derivate of minocycline. in this study, the in vitro activity of tigecycline in combination with gentamicin, streptomycin, rifampin, co-trimoxazole, levofloxacin, and minocycline was investigated using the checkerboard method to evaluate 16 Brucella melitensis isolates. The time-kill method was used to determine the bactericidal activities of combinations of tigecycline with rifampin, gentamicin, and levofloxacin, which were found (via the checkerboard method) to have a synergistic effect in combinations with tigecycline. Using the checkerboard method, combinations of rifampin, gentamicin, and levofloxacin with tigecycline showed synergistic effects against 5 (31.2%), 3 (18.9%), and 8 (50%) of the isolates. No synergy was observed with tigecycline in combination with minocycline, streptomycin, or co-trimoxazole. tigecycline with gentamicin achieved the earliest complete killing at 4x miC (in 6 h), while complete killing with the other combinations was delayed up to 24 h. the time-kill method showed that the combination of tigecycline and levofloxacin had an antagonistic effect, while the checkerboard method detected synergy and no interaction effects. these data suggest that a combination regimen of tigecycline with gentamicin and rifampin may be a good choice for treating brucellosis.