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methicillin-resistance in S. aureus, van genes associated with vancomycin resistance in enterococci, and some β-lactamase genes encoding enzymes associated with resis­tance to third- and fourth-generation cephalosporins (extended- spectrum β-lactamases) and carbapenems (carbapenemases) [31]. Genotypic detection of resistance determinants can be very useful to rapidly inform about drugs that should or should not be used. For instance, genotypic detection of a S. aureus and of the cognate mecA gene in a clinical specimen obtained from a surgical infection suggests an MRSA infection and, consequently, the need for using antimicrobial chemother­apy with anti-MRSA coverage. On the other hand, genotypic detection of a Klebsiella pneumoniae and of a carbapenemases gene KPC in a clinical specimen suggests an infection by KPC-producing K. pneumoniae and, consequently, the need for using an antimicrobial regimen with anti-KPC coverage [32]; while genotypic detection of a Pseudomonas aeruginosa and of a VIM carbapenemases gene suggest an infection by P. aeruginosa producing the VIM metallo-enzyme and, consequently, the need for using an antimicrobial regimen with coverage for this type of resistant pathogen [33]. Genotypic detection of resistance determinants, also called genotypic antibiogram, returns actionable information as described in previous examples which, however, is notably different from that of conventional phenotypic antibiogram. In fact, the pres­ence or absence of a resistance determinant does not inform about MIC values but only allows prediction of a likely resistance or susceptibility prole to some antimi­crobial agents. For instance, detection of a K. pneumoniae and of a KPC carbapene­mase gene allows us to predict a likely resistance to older β-lactams including amoxicillin-clavulanate, piperacillin- tazobactam, ceftolozane-tazobactam, third- and fourth-generation cephalosporins, and carbapenems, and a likely susceptibility to new BLICs with anti-KPC activity (e.g., ceftazidime-avibactam, meropenem-vabor­bactam, and imipenem-relebactam) and cederocol, while no information is pro­vided about susceptibility/resistance to non-β-lactam agents such as aminoglycosides, colistin, trimethoprim- sulfamethoxazole, and tigecycline. Despite these limitations, this is very valuable information to rapidly review empiric antimicrobial chemo­therapy if anti-KPC coverage was initially not included. In fact, the rapid detection of carbapenemase genes has become a very valuable tool for guiding antimicrobial stewardship and the appropriate use of the novel antibiotics active against DTR Gram-negatives, since the prole of activity of these novel antibiotics differs, depend­ing on the resistance determinant (Fig.9.2). Clearly, this advantage is greater in set­tings where the prevalence of DTR Gram-negatives is expected to be higher, as in South-Eastern Europe, North Africa, Middle East, Latin America, and Southeast Asia [34, 35].

advantages but should also be aware of their limitations to avoid overinterpreting and to properly contextualize the results. Genotypic antibiogram, in particular, is becoming increasingly popular in settings characterized by a high prevalence of antimicrobial resistant pathogens to rapidly predict the presence of clinically rele­vant resistances and support antimicrobial stewardship. However, it has also some limitations, mostly related with possible discrepancies between genotype and phe­notype, which can result in misleading predictions causing overtreatment or under­treatment. In this scenario of increasing complexity, the importance of a consulting role by experienced clinical microbiologists who are fully familiar with the novel diagnostic technologies should be emphasized.