S. Pneumonia Report
I remember getting a bad lung infection, pneumonia, caused by Streptococcus pneumoniae, a few years back. I was very sick with a high fever, shortness of breath, fatigue, chest pain, and greenish-yellow – sometimes even bloody – mucus, which I consistently coughed up. I suffered for roughly a month or so before my pneumonia finally disappeared and I healed up. Being an otherwise healthy individual, yet still experiencing the symptoms for such a lengthy amount of time, made me wonder about how S. pneumoniae affects individuals who are immunocompromised. If this infection can cause a healthy person to be debilitated for over a month, what happens to individuals who unfortunately do not have the system in place to fight this infection? I chose
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Certain complement proteins, such as C3b, bind to bacteria, like S. pneumoniae, and mediate effective phagocytosis of the bacteria by using either antibody-dependent or antibody-independent mechanisms, or by use of both (2). Congenital deficiencies of the complement pathway, such as missing factor C2 or C3 in either the classical or the alternative pathway can put people at higher risk for invasive infection by S. pneumoniae, as the factors in effective opsonisation of the bacterium are missing and therefore the microorganism in question – S. pneumoniae in this case – cannot be phagocytosed (2). The lack of certain antibodies, as discussed above, also plays a role in decreasing the effectiveness of the complement system, as the polysaccharide capsule around S. pneumoniae cannot be breached for proper phagocytosis to occur.
Individuals with either deficiencies listed above are at a much higher risk of mortality from pneumococcal disease (2). This is because they lack the proper components, such as antibodies and/or complement proteins, which are crucial in effective immune response, from their system. What may start as a lung infection, can eventually spread and become a more invasive disease such as pneumococcal meningitis and cause severe systemic effects, including brain damage and death. Having a combination of these deficiencies makes matters worse and increases the risk even
Certain complement proteins, such as C3b, bind to bacteria, like S. pneumoniae, and mediate effective phagocytosis of the bacteria by using either antibody-dependent or antibody-independent mechanisms, or by use of both (2). Congenital deficiencies of the complement pathway, such as missing factor C2 or C3 in either the classical or the alternative pathway can put people at higher risk for invasive infection by S. pneumoniae, as the factors in effective opsonisation of the bacterium are missing and therefore the microorganism in question – S. pneumoniae in this case – cannot be phagocytosed (2). The lack of certain antibodies, as discussed above, also plays a role in decreasing the effectiveness of the complement system, as the polysaccharide capsule around S. pneumoniae cannot be breached for proper phagocytosis to occur.
Individuals with either deficiencies listed above are at a much higher risk of mortality from pneumococcal disease (2). This is because they lack the proper components, such as antibodies and/or complement proteins, which are crucial in effective immune response, from their system. What may start as a lung infection, can eventually spread and become a more invasive disease such as pneumococcal meningitis and cause severe systemic effects, including brain damage and death. Having a combination of these deficiencies makes matters worse and increases the risk even