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Abstract: Currently, one of the most serious threats to public health is the rapid spread of multidrug–resistant (MDR) and highly virulent Klebsiella pneumoniae (hvKp). In these strains, various antibiotic resistance genes (ARGs) are frequently detected, including several novel ones first identified in this bacterial species, such as carbapenemases of the KPC, NDM–1, and OXA–48 types. The widespread prevalence of environmental ARGs, which can be transferred between microbiota, particularly among clinical pathogens and human commensals, has significantly contributed to the emergence of antimicrobial resistance (AMR) in K. pneumoniae. Resistance is caused by mechanisms such as drug inactivation, increased efflux, or altered binding to target sites. Moreover, this resistance is further enhanced by the production of various beta-lactamases, mainly extended–spectrum beta-lactamases (ESBLs), or by biofilm formation. Particularly concerning in K. pneumoniae, the main species representing the carbapenemase–producing Enterobacterales (CPE) group, is the emergence of plasmid–mediated resistance to carbapenems and polymyxins, which are considered “last–resort drugs” for treating infections caused by these pathogenic microorganisms. The growing resistance of K. pneumoniae to antibiotics and other antimicrobial agents remains one of the most important problems in epidemiological surveillance, microbiological diagnostics, and the global treatment of infections. The high mortality rate among infected patients and the difficulty in treating infections caused by MDR K. pneumoniae have led to this bacterium being classified as one of the most common and dangerous human pathogens in both Polish and global healthcare. This article characterizes the factors determining antibiotic resistance in K. pneumoniae, both in terms of biochemical mechanisms and molecular features. In addition, the current epidemiological situation regarding the spread of invasive, resistant K. pneumoniae isolates in Europe and Poland is described, and treatment regimens for infections caused by these high–alert pathogens are presented.