Factors of pathogenicity of staphylococci
Staphylococcus is a unique microorganism. It can cause more than 100 different diseases related to eleven classes according to the International Classification of 1968. Staphylococci can affect any tissue, any organ. This property of staphylococci is due to the presence of a large complex of pathogenicity factors.
Adhesion factors - the attachment of staphylococci to tissue cells is due to their hydrophobicity (the higher it is, the more pronounced adhesive properties), as well as the adhesive properties of polysaccharides, possibly also protein A, and the ability to bind fibronectin (the receptor of some cells).
Various enzymes that play the role of "aggression and protection" factors: plasmacoagulase (the main pathogenicity factor), hyaluronidase, fibrinolysin, DNase, lysozyme-like enzyme, lecithinase, phosphatase, proteinase, etc.
Complex of secreted exotoxins:
- membrane-damaging toxins - a, p, 8 and y. Previously, they were described as hemolysins, necroxins, leukocidins, lethal toxins, ie, by the nature of their action: hemolysis of erythrocytes, necrosis with intradermal administration of a rabbit, destruction of leukocytes, death of a rabbit with intravenous administration. However, it turned out that this effect is caused by the same factor - membrane-damaging toxin. It has a cytolytic effect on various types of cells, which manifests itself as follows. The molecules of this toxin first bind to the currently unknown receptors of the target cell membrane or are absorbed non-specifically by the lipids contained in the membrane, and then a 7-molecule fungal heptamer consisting of 3 domains is formed. The domains forming the "hat" and the "edge" are located on the outer surface of the membranes, and the "foot" domain serves as a transmembrane channel-at times. Through it, small molecules and ions enter and exit, leading to the swelling and death of cells that have a nucleus and the osmotic lysis of red blood cells. Several types of membrane-damaging (pore-forming) toxins have been detected: a-, b-, s- and y-hemolysins (a-, b-, S- and y-toxins). They differ in a number of properties. Hemolysin is more often found in staphylococci isolated from a person, it lyses the red blood cells of humans, rabbits and rams. Lethal effect in rabbits is caused by intravenous administration in 3-5 minutes. Hemolysin b is found more often in staphylococci of animal origin, it lyses human and lamb erythrocytes (preferably at a lower temperature). Hemolysin S lysates the erythrocytes of humans and many animal species. Lethal effect on the rabbit with intravenous administration causes in 16-24-48 hours Very often in staphylococci are found a- and 8-toxins at the same time;
- exfoliative toxins A and B are distinguished by their antigenic properties, the ratio to temperature (A is thermostable, B is thermolabile), the localization of genes controlling their synthesis (A is controlled by a chromosomal gene, B is plasmidic). Often, both exfoliatin are synthesized from the same strain of S. Aureus. These toxins are associated with the ability of staphylococci to cause pemphigus in newborns, bullous impetigo, scarlet fever-like rash;
- true leukocidin, a toxin that differs from hemolysins by antigenic properties, selectively acts on leukocytes, destroying them;
- Exotoxin, which causes toxic shock syndrome (STS). It has the properties of superantigen. STS is characterized by an increase in temperature, a decrease in blood pressure, skin rashes followed by desquamation on hands and feet, lymphocytopenia, sometimes diarrhea, kidney damage, etc. More than 50% of strains of S. Aureus are capable of producing and secreting this toxin.
Strong allergenic properties, which possess both components of the cell structure, and exotoxins and other secreted by bacteria products of vital activity. Staphylococcal allergens can cause hypersensitivity reactions of both delayed type (GCHZ) and immediate type (GCHN) - Staphylococcus are the main culprits of skin and respiratory allergies (dermatitis, bronchial asthma, etc.). The peculiarity of the pathogenesis of staphylococcal infection and its tendency to transition to a chronic form are rooted in the effect of GCHZ.
Cross-reacting antigens (with erythrocyte isoantigens A and B, kidney and skin - induction of autoantibodies, development of autoimmune diseases).
Factors that inhibit phagocytosis. Their presence can be manifested in inhibition of chemotaxis, protection of cells from absorption by phagocytes, in ensuring the ability of staphylococci to multiply in phagocytes and blocking the "oxidative explosion". Phagocytosis inhibits the capsule, protein A, peptidoglycan, teichoic acids, toxins. In addition, staphylococci induce the synthesis of suppressors of phagocytic activity by certain cells of the body (for example, splenocytes). The inhibition of phagocytosis not only prevents the purification of the body from staphylococci, but also disrupts the function of processing and representing antigens to T and B lymphocytes, which leads to a decrease in the strength of the immune response.
The presence of a capsule in staphylococci increases their virulence for white mice, makes them resistant to phages, does not allow typing with agglutinating sera and masks protein A.
Teichoic acids not only protect staphylococci from phagocytosis, but, obviously, play an important role in the pathogenesis of staphylococcal infections. It was found that in children with endocarditis, antibodies to teichoic acids are detected in 100% of cases.
Mitogenic action of staphylococci against lymphocytes (protein A, enterotoxins and other products secreted by staphylococci possess this action).
Enterotoxins A, B, CI, C2, C3, D, E. They are characterized by antigenic specificity, thermostability, resistance to formalin (do not turn into toxoids) and digestive enzymes (trypsin and pepsin), are stable in the pH range from 4.5 to 10.0. Enterotoxins are low-molecular proteins with a mass of 26 to 34 kD with the properties of superantigens.
It is also established that there are genetically determined differences in the sensitivity to staphylococcal infection and the nature of its course in humans. In particular, severe staphylococcal purulent-septic diseases are more often found in people with blood groups A and AB, less often in individuals 0 and B groups.
With the synthesis of enterotoxins, the ability of staphylococci to cause food poisoning such as intoxication is associated. Most often they are caused by enterotoxins A and D. The mechanism of action of these enterotoxins has been little studied, but it differs from the action of other bacterial enterotoxins that disrupt the function of the adenylate cyclase system. All types of staphylococcal enterotoxins cause a similar pattern of poisoning: nausea, vomiting, pancreatic pain, diarrhea, sometimes headache, fever, muscle spasm. These features of staphylococcal enterotoxins are due to their superantigenic properties: they induce excessive synthesis of interleukin-2, which causes intoxication. Enterotoxins excite the smooth muscles of the intestine and increase the motility of the gastrointestinal tract. Poisoning is most often associated with the use of dairy products infected with staphylococcus (ice cream, cakes, cakes, cheese, cottage cheese, etc.) and canned oil. Infection of dairy products can be associated with mastitis in cows or with purulent-inflammatory diseases of people related to the production of foods.
Thus, the abundance of various pathogenicity factors in staphylococci and their high allergic properties determine the pathogenesis of staphylococcal diseases, their nature, localization, severity of the course and clinical manifestations. Avitaminosis, diabetes, decreased immunity contribute to the development of staphylococcal diseases.
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Resistance of staphylococci
Among non-spore-forming bacteria, staphylococci, like mycobacteria, have the greatest resistance to external factors. They tolerate drying well and remain viable and virulent for weeks and months in the dryest minute dust, being a source of dust infection. Direct sunlight kills them only for many hours, and scattered acts very weakly. They are resistant to high temperatures: they heat up to 80 ° C for about 30 minutes, dry heat (110 ° C) kills them for 2 hours; low temperatures tolerate well. The sensitivity to chemical disinfectants varies greatly, for example, a 3% solution of phenol kills them for 15-30 minutes, and a 1% aqueous solution of chloramine in 2-5 minutes.