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While bacterial virulence has experienced a long host/pathogen-dependent evolutionary process, antimicrobial resistance has had a very different, shorting and changing evolution due to the biological pressure caused by the introduction of the antimicrobials in human medicine. This strong pressure has forced the microorganisms to adapt to these changing conditions, continuously acquiring or developing new resistance mechanisms, causing major changes in cellular functions and finally influencing the virulence and bacterial fitness. Multiple factors may mediate in the relationship between virulence and resistance. The genes often involved in both phenomena have the same transport and dispersion mediums. Islands, integrons, transposons and other genetic elements could also facilitate the combined selection of virulence and resistance genes. The increase in resistance can affect virulence in different ways, mainly depending on the bacterial species, the environment, and the mechanism of resistance. This review presents the different phenomena in which the genetic mechanism that provides an advantage over the antimicrobials directly affects the virulence and fitness, such as changes in the structure of the cellular wall, efflux pumps, porins or two-component regulatory systems. The co-selection of virulence and antimicrobial resistance factors and the relative ease of bacteria to develop compensatory mutations can favour, particularly in environments with high antibiotic pressure, the emergence of prevalent clones. These can be virulent and with few treatment options, and could be a major health problem in the near future., (Copyright © 2011 Elsevier España, S.L. All rights reserved.)