Phagocytic insufficiency.
Intact skin and mucous membranes are an effective barrier against the penetration of microorganisms into the human body, but when they are damaged, they become the entrance door for infections caused mainly by representatives of the normal resident microflora. The barrier functions of the skin do not work due to extensive injuries, penetrating injuries, burns, surgical operations, pressure sores, etc.
Violation of humoral immunity
Phagocytic cells are macrophages and leukocytes, polymorphonuclears (PMN, macrophages), representing the next line of defense of innate (nonspecific immunity) after the skin and mucous membranes. The main representatives of PMN are neutrophil granulocytes, and their decrease in peripheral blood levels to less than 1,500 cells/ml is called neutropenia. This condition leads to frequent bacterial and fungal infections, and if they fall below 500 cells/ml (severe neutropenia), microorganisms can enter the bloodstream and cause bacteremia and sepsis. Microbial agents that cause infection with severe neutropenia are extracellular pathogens: staphylococci (S. aueus) and purulent streptococci, Nocardia, Pseudomonas aeruginosa, H.influenzae, Legionella, Serratia, Candida, Burkholderia, Aspergillus, Chromobacterium and others.
Defects in acquired immunity
Phagocyte dysfunction occurs mainly due to congenital defects in chemotaxis, adhesion and absorption of opsonized pathogens, formation of phagolysosomes and intracellular digestion of microbes. In these cases, infections caused by cocobacteria such as S. aureus and S. pyogenes develop. Victims often have recurrent upper respiratory tract infections, pneumonia, skin abscesses, cellulite, etc., which can be complicated by sepsis.
Infections due to defects in the complement system.
The lack of components of the complement system is due to genetic defects that do not allow for their adequate synthesis. With a deficiency of the C3 component or the C3-converting enzyme, frequent infections with extracellular bacteria develop due to defective immune adhesion and bacterolysis. In the absence of C5-C9 components, recurrent bacteremia with Neisseria meningitidis and N. gonorrhoeae is possible due to the inability of effective lysis of bacterial walls. Patients with defective components C3 and C5-C9 have recurrent synopulmonary and invasive infections due to encapsulated bacteria such as S. pneumoniae, P. aeroginosa, Proteus, H. influenzae, and N. meningitidis. En choisissant le
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