A microbial invasion can be facilitated by: virulence factors Microbial adherence antibiotic resistance defects in the mechanisms of host defense virulence virulence factors supporting pathogenic microorganisms in the invasion and neutralize host defenses. These factors include capsules enzymes toxins capsules Some organisms (eg. As certain strains of pneumococci, meningococci, Haemophilus influenzae type b) have a capsule blocked phagocytosis, and these organisms thus virulent than non-encapsulated strains makes However, capsule-specific opsonic antibodies of bind the bacterial capsule and phagocytosis erleichtern.Enzyme bacterial proteins with enzymatic activity (eg., protease, hyaluronidase, neuraminidase, elastase, collagenase) facilitate the local spread in the tissue. Invasive microorganisms (eg. As Shigella flexneri, Yersinia enterocolitica) can penetrate intact eukaryotic cells and they traverse, which makes them the penetration through mucosal surfaces. Some bacteria (e.g., Neisseria gonorrhoeae, H. influenzae, Proteus mirabilis, Clostridium species, Streptococcus pneumoniae.) Form IgA-specific proteases that cleave secretory IgA on mucosal surfaces and inaktivieren.Toxine organisms can release toxins (known as exotoxins) – protein molecules which may be the cause of a disease (z. B. diphtheria, cholera, tetanus, botulism) increase or decrease the severity of the disease. Most toxins bind to specific receptors on target cells. With the exception of preformed toxins which are responsible for some food poisoning (z. B. botulism, food poisoning by staphylococci or Bacillus cereus), toxins from microorganisms during the course of a local or systemic infection are formed. Endotoxin is a formed of gram negative bacteria and lipopolysaccharide component of the cell wall. Endotoxin triggers humoral enzymatic mechanisms that affect the complement, coagulation, fibrinolysis and activation of kinin have and responsible for a significant proportion of the morbidity of gram-negative sepsis sind.Andere factors Some microorganisms are more virulent because they do the following: Impaired antibody production Resist the lytic effects of serum complement escaping the oxidative processes in phagocytosis. Produce superantigens Many microorganisms have mechanisms that can affect antibody production, eg. For example by stimulation of suppressor cells, blocking the antigen and inhibition of Lymphozytenmitogenese. The resistance to the lytic effects of serum complement is also a virulence factor. Serum resistant N. gonorrhoeae strains often lead via the local infection addition to disseminated infection. Some organisms can escape oxidative processes in phagocytosis. For example, the oxidative step in Legionella and Listeria is either not triggered or actively suppressed, while other microorganisms produce enzymes (eg. B. catalase, glutathione, superoxide dismutase), which suppress the action of the oxidative substances. Some viruses and bacteria produce superantigens that evade the immune system, cause a non-specific activation of inordinate numbers of naïve T cells and thus excessive and potentially destructive inflammation, mediated by massive release of proinflammatory cytokines. Microbial Adherence The adherence of microorganisms on surfaces makes it easier for them to build a base from which they can penetrate the fabric. Crucial for adherence factors such as adhesins (microbial molecules which allow the attachment to a cell) to which the antibodies adhesins, as well as host-side receptors. To the receptors of the host include sugar residues of the cell surface, and cell surface proteins (eg. B. fibronectin), which increase the binding of certain Gram-positive bacteria (eg. B. staphylococci). Other adherence factors are delicate structures on certain bacterial cells (eg. As streptococci), the fibrils are called and which bind some types of bacteria to human epithelial cells. Other bacteria such. B. enterobacteria such as Escherichia coli have specific adhesive organelles that fimbriae or pili are called. Fimbriae enable microorganisms to attach to almost all human cells, including neutrophils and epithelial cells of the urinary tract, oral cavity and small intestine. Biofilm A biofilm is a slime layer, which may form around certain bacteria around and represents a protective factor against phagocytosis and antibiotics. A biofilm develops around Pseudomonas aeruginosa in the lungs of patients with cystic fibrosis and to coagulase-negative staphylococci on synthetic medical products such. As intravenous catheters, vascular prostheses and surgical sutures. The probability that a biofilm developed on such medical products is influenced by the roughness of the material, the chemical composition and water-repellent material properties. Antimicrobial resistance microorganisms have an extraordinary genetic variability. The use of antimicrobial drugs performs selection ultimately to the survival of strains which are able to resist them. Emergence of antimicrobial resistance may be due to a spontaneous mutation of chromosomal genes. In many cases, resistant strains of bacteria have acquired mobile genetic elements from other microorganisms. These elements are encoded on plasmids or transposons and allow to synthesize enzymes that alter the antimicrobial agent on or off which alter the ability of the bacterial cell, the antimicrobial agent to accumulate the inhibition by the antimicrobial agent withstand the microorganisms, it is an important the public health sector task to minimize the inappropriate use of antibiotics. For further discussion, overview of antibacterial substances: antibiotic resistance. Defects in host defense mechanisms Two types of immune deficiency conditions affect the ability of the host to fight infection: Primary Immunodeficiency Secondary (acquired) immunodeficiency Primary immunodeficiencies are genetic in origin; > 100 primary immune deficiency states have been reported. Most primary immunodeficiencies are detected in infancy, but up to 40% only in adolescence or adulthood. Acquired immune deficiencies are due to other diseases (eg. B cancer, HIV infection, chronic disease) caused by the action or a chemical or a drug which is toxic to the immune system. Mechanisms lack of immune responses may involve Cellular Immunity Humoral immunity Cellular phagocytic complement defects are usually T-cell or combined immunodeficiencies. T cells contribute to the destruction of intracellular organisms; thus can opportunistic infections such as Pneumocystis jirovecii or cryptococcal occur with T-cell defects in patients. A chronic infections that can lead to failure to thrive, chronic diarrhea and persistent oral candidiasis. Humoral defects are typically caused by B-cell patients will not be with this type of defect usually have infections with encapsulated organisms (eg. As H. influenzae, streptococci) into functional immunoglobulins. In these patients, poor growth, diarrhea and recurrent sinopulmonary infections can occur. A defect of phagocytic affects the immediate immune response to a bacterial infection and can lead to the formation of recurrent abscesses or severe pneumonia. Primary complement system deficiencies are particularly rare. Patients with this type of defect can with recurrent infections with pyogenic bacteria present (z. B. encapsulated bacteria, Neisseria sp) and an increased risk of autoimmune diseases (eg. As SLE).