Genetically controlled changes in outer membrane proteins also occur in the course of an infection. This finely controlled expression of the genes for pili and surface proteins changes the adherence pattern to different host cells, increases resistance to cervical proteases, increases resistance to phagocytosis and immune lysis, and is presumably necessary for successful infection. Many pathogenic bacteria exist in nature as multiple antigenic types or serotypes, meaning that they are variant strains of the same pathogenic species. There are 80 different antigenic types of Streptococcus pyogenes based on M-proteins on the cell surface. Based on minor differences in surface structure chemistry there are multiple serotypes of Vibrio cholerae , Staphylococcus aureus , Escherichia coli , Neisseria gonorrhoeae and an assortment of other bacterial pathogens.
Antigenic variation is prevalent among pathogenic viruses as well.
If the immune response is the main defense against a pathogen, then being able to shed old antigens and present new ones to the immune system might allow infection or continued invasion by the pathogen to occur. Furthermore, the infected host would seem to be the ideal selective environment for the emergence of new antigenic variants of bacteria. Perhaps this explains why many bacteria exist in a great variety of antigenic types. Evading Complement Antibodies that are bound to bacterial surfaces will activate complement by the classical pathway and bacterial polysaccharides activate complement by the alternative pathway. Bacteria in serum and other tissues, especially Gram-negative bacteria, need protection from the antimicrobial effects of complement.