Mechanism 3 Capsule Some bacteria produces excess of molecular weight polysaccharides also called

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Mechanism 3: Capsule Some bacteria produces excess of molecular weight polysaccharides, also called exopolysaccharides, when separated from clinical view of samples. This extracellular sucrose coating is normally referred as capsule. Different varieties of bacteria uses the diversified sugars to produce this capsule. The process of capsule production is one of the major virulence factors used by bacteria to escape clearance from another viral and infectious site. The capsule is specially designed to provide bacteria with protection from both the host immune response and the antibiotics (Munford, 2008). Research reveals that some capsules immunomodulatory effects. The capsule hinders bacteria from phagocytosis by hindering opsonizing antibodies to be recognized by phagocytic host defence cells (including, macrophages and neutrophils). When the phagocytes gets “frustrated” it results to severe inflammatory response as the macrophages and neutrophils releases more inflammatory cytokines in a trial to clear the bacteria. The enhanced inflammatory response can results into increased tissue damage or rapture as more neutrophils and macrophages are subjected to defence protocol in the site of infection. The most invasive species of bacteria producing capsules are the Neisseria meningitides (meningococcal), Streptococcus pneumonia (pneumococcus) and Pseudomonas aeruginosa (Walker, 2014). The pneumococcus capsular polysaccharide is regarded as the most primary virulence factors. The pneumococci utilize the genetic constituents of 24 biosynthetic genes to produce their capsule. There exist at least 90 different types of capsules, of which 23 types of these capsules are regarded the most vital and research shows that they causes more than 90% of invasive disease worldwide. Professional Application For a nurse, understanding these mechanisms enables important considerations when prescribing antimicrobial therapy. This included obtaining an accurate diagnosis of infection; understanding the difference between empiric and definitive therapy; identifying opportunities to switch to narrow-spectrum, cost-effective oral agents for the shortest duration necessary; understanding drug characteristics that are peculiar to antimicrobial agents (such as pharmacodynamics and efficacy at the site of infection); accounting for host characteristics that influence antimicrobial activity; and in turn, recognizing the adverse effects of antimicrobial agents on the host.