infectious diseases
Factors Facilitating Microbial Invasion
Virulence Factors
Virulence factors assist pathogens in invasion and resistance of host defenses; these factors include Capsule Enzymes Toxins Some organisms (eg, certain strains of pneumococci, meningococci, Haemophilus Infections ) have a capsule that blocks phagocytosis, making these organisms more virulent than nonencapsulated strains. However, capsule-specific opsonic antibodies can bind to the bacterial capsule and facilitate phagocytosis. ) facilitate local tissue spread. Invasive organisms (eg, Shigellosis , Some bacteria (eg, Pneumococcal Infections , Organisms may release toxins (called exotoxins), which are protein molecules that may cause disease (eg, Diphtheria , Endotoxinis a lipopolysaccharide produced by gram-negative bacteria and is part of the outer membrane of these organisms. Endotoxin triggers humoral enzymatic mechanisms involving the complement, clotting, fibrinolytic, and kinin pathways and causes much of the morbidity in gram-negative bacterial sepsis. Some microorganisms are more virulent because they do the following: Impair antibody production Destroy protective antibodies Resist the lytic effects of serum complement Resist the oxidative steps in phagocytosis Produce superantigens Many microorganisms have mechanisms that impair antibody production by inducing suppressor cells, blocking antigen processing, and inhibiting lymphocyte mitogenesis. Many mucosal pathogens, includingNeisseria gonorrhoeae,N. meningitidis,S. pneumoniae, andH. pneumoniae, produce proteases that cleave immunoglobulin A (IgA). IgA is the predominant immunoglobulin class produced at mucosal surfaces. Resistance to the lytic effects of serum complement confers virulence. Some organisms resist the oxidative steps in phagocytosis. For example, Legionella Infections and Some viruses and bacteria produce superantigens that bypass the immune system, cause nonspecific activation of inordinate numbers of naive T cells, and thus cause excessive and potentially destructive inflammation mediated by massive release of proinflammatory cytokines (eg, staphylococcal and streptococcal Toxic Shock Syndrome (TSS) ). 