## 1 Introduction  
The increase in antimicrobial resistance due to the emergence of multi-drug resistant (MDR) pathogens is one of the world's greatest public health challenges, as it can lead to an era without effective antibiotics [1]. Recently, the World Health Organization (WHO) published a list of \"priority pathogens\", which includes those microorganisms considered a serious threat to human health. Some members of this list are carbapenem-resistant pathogens and are known under the acronym of ESKAPE, including among other species, _Klebsiella pneumoniae_[1; 2; 3]. _K. pneumoniae_ is a Gram-negative, opportunistic bacteria pathogen associated with a wide range of diseases such as urinary tract infections, pneumoniae, septicemia, wounds, and soft tissue infections [4]. Carbapenem resistance is increasing rapidly worldwide, particularly among _K. pneumoniae_. The main carbapenem-resistance mechanism is acquisition of plasmid-encoded carbapenemases, which may belong to the molecular class A (i.e., KPC-type), B (i.e., impenem (IMP)-type, VIM-type, NDM-type) and D (i.e., OXA-48-type). The high-risk clones of _K. pneumoniae_, in contrast to low-risk clones, have an extraordinary ability to persist and spread in the nosocomial environment, disseminating these carbapenemases and therefore being involved in nosocomial outbreaks [4]. Nevertheless, much less attention has been paid to the presence or occurrence of resistance to antiseptics and biocides, such as chlorhexidine (CHLX) [5], widely used in hospital settings. CHLX is a symmetric bis-biguanide molecule comprising two chloroguanide chains that are connected by a central hexamethylene chain, and carry two positive charges at physiological pH. CHLX is sparingly soluble in water, and thereby normally formulated with either acetate or gluconate to form water-soluble salts [6]. The antimicrobial effect of this compound is based on damaging the bacterial membrane, leading to the subsequent leakage of cytoplasmatic material. Therefore, mechanisms conferring resistance toward CHLX include multidrug efflux pumps and cell membrane changes [5]. Moreover, CHLX adaptation has been associated with the emergence of stable resistance to the last-resort antibiotic colistin (polymyxin E) [7; 8; 9]. In general, the failure of antibiotic treatments has been associated with resistance mechanisms. However, it has recently been noted that other mechanisms such as tolerance and persistence were also involved [10]. The recovery of persistent cells is one of the main causes of prolonged and recurrent infections, that can lead to the complete failure of antibiotic treatments [11]. In this context, it is important to distinguish between resistant, tolerant, and persistent bacteria [12]. The term resistance is generally used to describe the inherited ability of a bacterial population to grow in the presence of high concentrations of antibiotics, regardless of the duration of treatment [12], due to active defense mechanisms associated with mutations [10]. Whereas, the term tolerance is used to describe the ability, inherited or not, of a bacterial population to survive the transient exposure of high concentrations of antibiotics without causing changes in minimum inhibitory concentrations (MICs), due to the deceleration of essential biological processes [10; 11; 12]. It is important to emphasize that despite the slow-growth rate, tolerant bacteria keep a metabolically active state. In contrast to resistance and tolerance, persistence is characterized by the ability, not inherited, of a bacterial subpopulation (around 0.001-1%) [10] to resist antibiotics by growth arrest due to the inactivation of their metabolism and their non-replicative state, thus it is due to their dormant state. Persistent bacteria exhibit transient levels of tolerance to antibiotics that do not affect their MICs, so once the drug pressure is removed and their metabolism is reactivated, they can rapidly re-grow.