Overwhelming post-splenectomy infection pathophysiology: Difference between revisions
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Latest revision as of 18:36, 18 September 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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Pathophysiology
The spleen contains many macrophages (part of the reticuloendothelial system), immune cells which phagocytose (eat) and destroy bacteria. In particular, these macrophages are activated when bacteria are bound by IgG antibodies (IgG1 or IgG3) or complement component C3b. These types of antibodies and complement are immune substances called opsonizers, molecules which bind to the surface of bacteria to make them easier for macrophages to phagocytose and destroy the bacteria.
When the spleen is gone, IgG and complement component C3b are still bound to bacteria, but they cannot be removed from the blood circulation because the spleen, which contained the macrophages, is gone. The bacteria therefore are free to cause infection.
Patients without spleen often need immunizations against pathogens that normally require opsonization and phagocytosis by macrophages in the spleen. These include common human pathogens with capsules (Streptococcus pneumoniae, Salmonella typhi, Neisseria meningitidis, E. Coli, Hemophilus influenzae, Streptococcus Agalactiae, Klebsiella pneumoniae). Capsules (made of polysaccharides) are an evolutionary development by bacteria to evade phagocytosis by macrophages alone, since only proteins are directly recognized by macrophages in phagocytosis. Humoral immunity in the form of IgG and complement proteins is the answer of the human immune system to allow these pathogens marked for destruction.