Some bacteria can liberate antigenic surface components in a soluble form into the tissue fluids. Streptococcus pneumoniae and Neisseria meningitidis are known to release capsular polysaccharides during growth in tissues. They are found in the serum of patients with pneumococcal pneumonia and in the cerebrospinal fluid of patients with meningitis. Protein A, produced by S. aureus may remain bound to the staphylococcal cell surface or it may be released in a soluble form. There are probably several ways that pathogens interfere with the antibacterial action of antibody molecules.
Some pathogens produce enzymes that destroy antibodies.
Neisseria gonorrhoeae , N. meningitidis , Haemophilus influenzae , Streptococcus pneumoniae and Streptococcus mutans , which can grow on the surfaces of the body, produce IgA proteases that inactivate secretory IgA by cleaving the molecule at the hinge region, detaching the Fc region of the immunoglobulin. One way bacteria can avoid forces of the immune response is to periodically changing antigens, i.e., to undergo antigenic variation. Some bacteria avoid the host antibody response by changing from one type of fimbriae to another, or by switching fimbrial tips. This makes the original AMI response obsolete by using new fimbriae that do not bind the previous antibodies. Antigenic variation is an important mechanism used by pathogenic microorganisms for escaping the neutralizing activities of antibodies.