Among the 91 patients with MSSA bacteremia identified over the 3-year study period, two patients who did not receive antibiotic treatment, two patients who received initial vancomycin treatment, and three patients who were aged <18 years were excluded. Among the 84 adult patients included in the study, 28 (33.3%) received initial teicoplanin treatment and 56 (66.7%) initial β-lactam treatment. Subsequently, we stratified these two groups based on propensity score matching according to the outcome analysis using the logistic regression model (Figure 1).
Comparisons of the demographics, comorbidities, severity of blood stream infection at onset, source of bacteremia, rate of adequate infection source control, infection by strains with teicoplanin MICs ≥1.5 mg/L, and clinical outcomes between the two groups before and after propensity score matching are presented in Table 1. Before propensity score matching, no statistically significant differences were observed in terms of sex, age, length of hospital stay, and the proportion of S, aureus strains with teicoplanin MICs ≥1.5 mg/L between the groups. A significantly higher prevalence of coronary artery disease (42.9% versus 8.9%, p<0.01) and congestive heart failure (39.3% versus 7.1%, p<0.01) was observed in the initial teicoplanin treatment group. There was no statistically significant difference in disease severity (Pittsburgh bacteremia score ≥4) between the groups or infection sources of bacteremia. The adequate infection source control rate was higher in the initial teicoplanin treatment group than in the β-lactam treatment group (78.9% versus 41.7%, p=0.01). We did not find statistically significant differences in short-term favorable outcome, favorable outcome at the time of completion of teicoplanin or β-lactam therapy, persistent bacteremia and the 30-day overall mortality rate between the two groups (Table 1).
The risk factors for unfavorable clinical response at the completion of teicoplanin or β-lactam therapy in the unadjusted univariate analysis included higher disease severity (Pittsburgh bacteremia score ≥4 (94.1% versus 20.9%, p<0.01) and infective endocarditis as the source of bacteremia (23.5% versus 3.0%, p=0.01) (Table 2). After adjustments were made in the multivariate analysis, we observed that the Pittsburgh bacteremia score ≥4 (odds ratio, 60.6; 95% CI, 7.4–496.8) was independently associated with unfavorable outcome at the time of completion of teicoplanin or β-lactam therapy (Table 2). There was no significant evidence of lack of fit in any of the final models, as the p-values were >0.05 in the Hosmer-Lemeshow goodness-of-fit tests.
All patients included in the study were divided into the initial teicoplanin treatment (n=28) and β-lactam treatment (n=28) groups after 1:1 propensity score matching with Pittsburgh bacteremia score ≥4 (the independent risk factor for unfavorable outcome) and age. After matching, there were no statistically significant differences in terms of sex, length of hospital stay, and the proportion of S. aureus strains with teicoplanin MICs ≥1.5 mg/L between the groups. The incidence of coronary artery disease and congestive heart failure was higher (42.9% versus 10.7%, p=0.03 and 39.3% versus 10.7%, p=0.04, respectively) among patients receiving initial teicoplanin treatment than in those receiving β-lactam treatment even after propensity score matching. No statistically significant differences were observed in the source of bacteremia and the rate of adequate infection source control between the two groups after matching. We did not find statistically significant differences in short-term favorable outcome, favorable outcome at the time of completion of teicoplanin or β-lactam therapy, persistent bacteremia and 30-day overall mortality rate between the groups after propensity score matching.
Among the patients in the initial teicoplanin treatment group, 21 (75.0%) switched to β-lactam treatment and three (14.3%) died within 30 days of hospitalization after the onset of MSSA bacteremia. Altogether, 71.5% (15/21) of the patients switched to β-lactam treatment within 4 days after the onset of bacteremia, which was consistent with the time of availability of final susceptibility test results (Supplementary Figure). On the other hand, the 30-day mortality rate was 14.3% in patients with initial teicoplanin treatment without a switch to β-lactam treatment for MSSA bacteremia (Table 1). The clinical data of seven patients with MSSA bacteremia who received continuous teicoplanin treatment are shown in Supplementary Table. The MIC distributions of teicoplanin in the MSSA strains isolated from patients in the initial teicoplanin treatment group (n=28) and the β-lactam treatment group (n=56) are shown in Figure 2(A). The MIC distributions in post propensity-matching group (both n=28) were showed in Figure 2(B). We observed that 78.6% (22/28) of the MSSA strains in the initial teicoplanin treatment group exhibited teicoplanin MICs <1.5 mg/L, while 60.7% (34/56) of the MSSA strains in the initial β-lactam treatment group exhibited teicoplanin MICs <1.5 mg/L (Figure 2(A)). In the propensity-matching group, 78.6% (22/28) of patients in the initial teicoplanin treatment group with MSSA bacteremia had teicoplanin MICs <1.5 mg/L and 67.9% (19/28) of patients in the initial ß-lactam treatment group with MSSA bacteremia had teicoplanin MICs <1.5 mg/L (Figure 2(B)).
The Kaplan-Meier curves for 30-day survival in patients with MSSA bacteremia are presented in Figure 3. The cases were grouped according to the initial treatment (teicoplanin or β-lactam) before propensity score matching (Figure 3(i)) and were further stratified as the initial teicoplanin treatment group or the β-lactam treatment group after propensity score matching (Figure 3(ii)). The 30-day survival was not significantly different between the two groups before propensity score matching (hazard ratio, 1.84; 95% CI, 0.60–5.64, p=0.29) as well as after propensity score matching (hazard ratio, 3.12; 95% CI, 0.98–9.99, p=0.06).