Many microorganisms have mechanisms that impair antibody production at different sites by inducing suppressor cells, blocking antigen processing, and inhibiting lymphocyte mitogenesis. Bacterial resistance to the lytic effects of serum components is associated with virulence. Microbes have also developed methods to elude, inactivate, or ignore steps in phagocytosis. For example, some microbes adhere via fibrillae, which are fine structures on bacterial cells that bind streptococci to human epithelial cells. Fimbriae enable the organism to attach to almost all human cells, including neutrophils and epithelial cells in the GU tract, mouth, and intestine.
Colonization is enhanced by the materials' roughness, chemical composition, and hydrophobicity.
The exact pathogenesis of this adherence is unknown, but the microbe's ability to produce a slime layer may play a role in the pathogenesis of coagulase-negative staphylococcal foreign body infections. Genetic variability, essential for this microbial evolution, may occur via various mechanisms. Microevolutionary change involves point mutations in a nucleotide base pair, altering the target site of an antimicrobial agent and interfering with its activity. Genetic variability in bacteria may also be created by acquisition of foreign DNA carried by plasmids, bacteriophages, or transposable genetic elements. An example of this phenomenon is the spread of a tetracycline-resistant transposon among Neisseria gonorrhoeae, Mycoplasma hominis, and Ureaplasma urealyticum.