Chapter 128. Pneumococcal Infections (Part 2)

Nonimmunologic Mechanisms Nonimmunologic mechanisms that protect against pneumonia include filtration of air as it passes through the nasopharynx, the glottal reflex, laryngeal closure, the cough reflex, clearance of organisms from the lower airways by ciliated cells, and ingestion by pulmonary macrophages and PMNs of small bacterial inocula that manage to reach alveolar spaces. Respiratory virus infection, chronic pulmonary disease, or heart failure compromises these mechanisms, predisposing to the development of pneumococcal pneumonia.Immunologic MechanismsInnate Immunity Innate immune mechanisms participate in clearance of pneumococci from the nasopharynx as well as in phagocytosis by PMNs and macrophages via the microbial pattern recognition...
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Chapter 128. Pneumococcal Infections (Part 2) Chapter 128. Pneumococcal Infections (Part 2) Nonimmunologic Mechanisms Nonimmunologic mechanisms that protect against pneumonia includefiltration of air as it passes through the nasopharynx, the glottal reflex, laryngealclosure, the cough reflex, clearance of organisms from the lower airways byciliated cells, and ingestion by pulmonary macrophages and PMNs of smallbacterial inocula that manage to reach alveolar spaces. Respiratory virus infection,chronic pulmonary disease, or heart failure compromises these mechanisms,predisposing to the development of pneumococcal pneumonia. Immunologic Mechanisms Innate Immunity Innate immune mechanisms participate in clearance of pneumococci fromthe nasopharynx as well as in phagocytosis by PMNs and macrophages via themicrobial pattern recognition receptor Toll-like receptor 2 (TLR2). Humoral Immunity Immunologically specific humoral mechanisms provide the best protectionagainst pneumococcal infection. Most healthy adults have antibody to constituentsof S. pneumoniae, such as PspA, PsaA, and the cell wall; however, there is noconvincing evidence for an opsonic role of these antibodies, especially at theirusual concentrations. Most healthy adults lack IgG antibody to the majority ofpneumococcal capsular polysaccharides. Antibody appears after colonization,infection, or vaccination. In the first few weeks after colonization, nonspecificmechanisms probably protect the host from infection. Thereafter, newly developedanticapsular antibody provides a high degree of specific protection. Adults whoare at risk of aspirating pharyngeal contents and/or who have diminishedmechanisms of lower airway clearance are at risk of developing pneumonia beforeantibody is produced. Persons with a diminished capacity to form antibodyprobably remain susceptible as long as they are colonized. The risk of serious pneumococcal infection is greatly increased in personswith conditions that compromise IgG synthesis and/or the phagocytic function ofPMNs and macrophages. Most patients hospitalized for pneumococcal pneumoniahave one or more of these conditions (Table 128-1). Once a pneumococcalinfection has been initiated, the absence of a spleen predisposes to fulminantdisease. The liver can remove opsonized (antibody-coated) pneumococci from thecirculation; in the absence of antibody, however, only the slow passage of bloodthrough the splenic sinuses and prolonged contact with reticuloendothelial cells inthe cords of Billroth can result in bacterial clearance. Patients without spleens tendto develop overwhelming pneumococcal disease that rapidly progresses to death. Table 128-1 Conditions that Commonly Predispose to PneumococcalInfection Increased risk of exposure Defective complement function Day-care centers Defective bacterial Military training camps clearancea Prisons Congenital asplenia, Shelters for the homeless hyposplenia Respiratory infection, inflammation Splenectomy Influenza, other viral respiratory Sickle cell diseaseinfections Multifactorial conditions Air pollution Infancy and aging Allergies Cigarette smoking Chronic disease Chronic obstructive pulmonary disease Alcoholism Other causes of chronic pulmonary Prior hospitalizationinflammation or obstruction Malnutrition Anatomical disruption of meninges HIV infection(dural tear) Chronic lung disease Defective antibody formation Glucocorticoid treatment Common variablehypogammaglobulinemia Cirrhosis of the liver Selective IgG subclass deficiency Renal insufficiency Multiple myeloma Diabetes mellitus Chronic lymphocytic leukemia Anemia Lymphoma Coronary artery disease Fatigue, stress, and/or exposure to colda The absence of a spleen predisposes to more fulminant infection (see text).