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Hospital-acquired bacterial infection is a common problem in post-operative patients and contributes to increased morbidity, mortality, hospitalization time and health care expenditure [ 1 ]. Once surgical site infections (SSI) are detected in patients in medical intensive care, antibacterial/antifungal therapy is implemented. However, the efficacy of antimicrobial treatment largely depends on accurate diagnoses of the microbes causing SSI. To date, bacterial culture is considered the gold standard procedure to identify pathogens that causing SSI. Staphylococcus aureus, Escherichia coli, Enterococcus spp. , Pseudomonas aeruginosa, Enterobacter spp. , Candida albicans, Klebsiella pneumonia, Gram-positive anaerobes and Proteus mirabilis are the most common causative pathogens of SSI [ 2 ]. However, the classical blood culture procedure has two intrinsic problems: (i) it detects only culturable microbes, thus reducing the chance to identify infectious microorganisms from patients treated with antibiotics; (ii) it takes 24 to 48 hours to achieve first test results of cultures, which hampers accurate treatment and risks the patient’s life [ 3 ]. Although a broad spectrum of antibiotics is administered post-operatively to control SSI, the increasing occurrence of pathogens resistant to a wide spectrum of antibiotics is alarming, such as meticillin-resistant S.aureus (MRSA) or resistance of betalactamases (ESBL)/carbapenemases enterobacteriacea [ 4 , 5 ]. So far, more than one thousand betalactamase genes encoding either ESBL or the carbapenemase phenotype have been recognized [ 6 ] ( http://www.lahey.org/studies/webt.asp ). The distribution of these clinical phenotypes differs greatly between geographical settings and displays distinct local patterns. If conventional bacterial cultures fail to generate colonies, antibiotic resistance profiles cannot be generated.
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Trung et al. (2015) studied this question.
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