Toll-like receptor 2 (TLR2) is an immune sensor for gram-positive bacterial cell wall components. Single-nucleotide polymorphisms (SNPs) in the TLR2 gene that impair its function may, therefore, influence the risk and outcomes of gram-positive bacterial infections. In a cohort of 694 liver transplant recipients, we assessed the TLR2 SNP that is translated into an amino acid substitution of arginine for glutamine at position 753 (R753Q), and we found that its presence was associated with the clinical characteristics and outcomes of gram-positive bacterial infections. The proportions of patients with the TLR2 R753Q SNP did not significantly differ between those with gram-positive bacterial infections and those without grampositive bacterial infections (9.6% versus 9.6%, P ¼ 0.999). However, in patients with the TLR2 R753Q SNP, higher rates of infection recurrence (27.8% versus 11.8%, P ¼ 0.07) and initial septic shock (11.1% versus 1.2%, P ¼ 0.047) were observed. Chronic hepatitis C [relative risk (RR) ¼ 3.37, 95% confidence interval (CI) ¼ 1.24-9.13, P ¼ 0.02], initial septic shock (RR ¼ 15.13, 95% CI ¼ 2.84-80.54, P ¼ 0.001), and central venous catheter-related bacteremia (RR ¼ 7.22, 95% CI ¼ 2.54-20.51, P < 0.001) were significantly associated with 90-day all-cause mortality after gram-positive bacterial infections. In contrast, the presence of the TLR2 R753Q SNP was not significantly associated with mortality.