Background/Purpose: Nosocomial bacterial resistance has been advanced and well studied in Taiwan, but there were few reports describing the antibiotic susceptibility of community-acquired pathogens. Through collecting data from those who received blood cultures in emergency department, we presented an epidemiological study to analyze appropriate empirical therapy for the community-acquired bacteremia in Southern Taiwan. Methods: From July 1998 to June 1999, patients presented at emergency department of Kaohsiung Veterans General Hospital with fever, chills or symptoms of sepsis were routinely performed two sets of blood cultures. Those of positive blood cultures without prior admission history to the hospital within 2 weeks were further analyzed for the etiologic pathogens, antibiotic susceptibility, and risk factors of community-acquired bacteremia. Results: A total of 303 episodes were enrolled for analysis, Escherichia coli, Klebsiella pneumoniae, and Staphylococcus aureus accounted for 76.3% of the isolates. Most of the community-acquired bacteremia was secondary bacteremia. Eighty-four percents of E. coli, 89% of K. pneumoniae, and 76% of S. aureus were susceptible to cefazolin. Susceptible rates of the three major pathogens to gentamicin were 72%, 92%, and 68% respectively. Conclusion: While treating community-acquired bacteremia in Southern Taiwan, the first generation antibiotic, cefazolin plus gentamicin, was effective in vitro for the majority of cases. However, since the community-acquired bacteremia is mostly secondary in origin, it is necessary to explore the underlying primary lesions to attain therapeutic success. Further on-going epidemiological surveillance on bacterial resistance of community-acquired bacteremia is necessary to provide evidence-based appropriateness of empirical therapy. © 2010 Taiwan Society of Microbiology.
T.-G., Y., Y.-S., C., & M.-Y., Y. (2010). Approach of Empirical Antibiotic Treatment: Analyzing Bacterial Resistance of Community-acquired Bacteremia. Journal of Microbiology, Immunology and Infection, 43(1), 43–46. https://doi.org/10.1016/S1684-1182(10)60006-0