2600. Mannose-Binding Lectin Polymorphisms are Important Modulating Factors in Community- and Hospital-Acquired Pneumonia Caused by Legionella spp.

BACKGROUND: Community-acquired pneumonia (CAP) and hospital-acquired pneumonia (HAP) are the leading causes of death from infection in developed countries. Mannose-binding lectin (MBL) is a C-type serum lectin that plays a central role in the innate pulmonary host defenses against respiratory pathogens. We hypothesized that MBL polymorphisms may increase the risk of developing Legionella pneumonia. Therefore, the aim of this study was to evaluate the role of MBL polymorphisms in susceptibility to CAP and HAP caused by Legionella spp. METHODS: A total of 96 BAL and blood samples collected for routine microbiological analysis from Lithuanian patients presenting with CAP and HAP, were used for this study. MBL polymorphisms in the 54 codon (54 G/G, 54 G/A, and 54 A/A) were detected by BanIRFLP. Legionella spp. were detected by nested PCR. RESULTS: Polymorphisms in the 54 codon of MBL were determined in 96 patients. Among 96 patients with CAP and HAP, the most commonly observed 54 codon MBL variant was 54 G/G (69.8%, n = 67), followed by 54 G/A (21.9%, n = 21), and 54 A/A (8.3%, n = 8). By using nested PCR, Legionella pneumonia was detected among 15.6% (n = 15) of patients diagnosed with CAP and HAP. Legionella spp. were detected among 7 patients with MBL 54 codon G/G variant (10.4%), while 3 patients with MBL 54 G/A (14.3%), and 5 patients with MBL 54 codon A/A variant (62.5%). During this study Legionella spp. were detected more frequently (P < 0.05) among patients with the A/A variant of the 54 codon vs. those with other variants of MBL 54 codon. There were no significant differences found among those with Legionella infection and G/A (14.3%) or G/G (10.4%) variants of MBL gene 54 codon. CONCLUSION: MBL gene 54 codon variant A/A polymorphisms may play an important role in increased susceptibility to lower respiratory infectionscaused by Legionella spp. DISCLOSURES: All authors: No reported disclosures.