Streptococcus pneumonia

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1 Streptococcus pneumonia The pneumococci (S. pneumoniae) are gram-positive diplococci. Often lancet shaped or arranged in chains, possessing a capsule of polysaccharide that permits typing with specific antisera. Pneumococci are normal inhabitants of the URT of 5 40% of humans and can cause pneumonia, sinusitis, otitis, bronchitis, bacteremia, meningitis, and other infections. Morphology and Identification With age, Pneumococcus rapidly become gram negative and tend to lyse spontaneously. Viridans streptococci do not lyse and are thus easily differentiated from pneumococci. On solid media, the growth of pneumococci is inhibited around a disk of optochin; viridans streptococci are not inhibited by optochin Capsule swelling test, or quellung reaction is used for capsule The exact makeup of the capsule is unique and distinctly antigenic for each of more than 90 serotypes. Pneumococcal cell wall structure is similar to other streptococci. Teichoic acid, LPA, and phosphocholine are rooted in the peptidoglycan extending outward into the capsule where they provide binding domains for a variety of surface proteins.

2 Growth characteristic On blood agar, pneumococci produce round, glistening colonies surrounded by a zone of ἀ-hemolysis. Both colonies and broth cultures have a tendency to undergo autolysis due the action of autolysins, a family of pneumococcal enzymes that degrade peptidoglycan. Extracellular products All pneumococci produce pneumolysin, which is a member of the family of transmembrane pore-forming toxins. The pneumococcus does not secrete pneumolysin but it is released on lysis of the organisms (autolysin's primary role was to release pneumolysin to an extracellular location). Pneumolysin has a number of other effects on the host cells, including its ability to stimulate cytokines and disrupt the cilia of human respiratory epithelial cells. Pneumococci also produce a neuraminidase, which cleaves sialic acid present in host mucin and involved in host colonization and involved in biofilm formation, Pneumococcal Diseases The most common form of infection with S. pneumoniae is pneumonia, which begins with fever and a shaking chill followed by signs that localize the disease to the lung. These include difficulty breathing and cough with production of purulent sputum, sometimes containing blood. The pneumonia typically fills part or all of a lobe of the lung with inflammatory cells, and the bacteria may spread to the bloodstream and thus other organs. The most important of the latter is the CNS and leads to acute purulent meningitis. EPIDEMIOLOGY Infections are derived from colonization of the nasopharynx, where pneumococci can be found in 5 to 40% of healthy persons depending on age, season, and other factors. Respiratory secretions containing pneumococci may be transmitted from person to person by direct contact or from the microaerosols created by coughing and sneezing in close quarters. Such conditions are favored by crowded living conditions, particularly when colonized persons are mixed with susceptible ones, as in child care centers, recruitment barracks, and prisons.

3 As with other bacterial pneumonias, viral respiratory infection and underlying chronic disease are important predisposing factors. Pathogenesis Aspiration of respiratory secretions containing these pneumococci is the initial event leading to pneumonia. Normally, aspirated organisms are cleared rapidly by the defense mechanisms of the lower respiratory tract, including the cough and other reflexes; the mucociliary blanket; and phagocytosis by alveolar macrophages. Host factors that impair the combined efficiency of these defenses can allow pneumococci to reach the alveoli and multiply there. These include - chronic pulmonary diseases - damage to bronchial epithelium from smoking or air pollution - respiratory dysfunction from alcoholic intoxication, narcotics, anesthesia, and trauma. The polysaccharide capsule of S. pneumoniae is the major determinant of virulence. Unencapsulated mutants do not produce disease in humans or laboratory animals. Pneumolysin s toxicity for pulmonary endothelial cells and direct effect on cilia contributes to the disruption of the endothelial barrier and facilitates the access of pneumococci to the alveoli and eventually their spread beyond into the bloodstream. Pneumococcal surface protein A (PspA) is found in virtually all pneumococci and has been shown to interfere with complement deposition. Initial alveolar multiplication produces a profuse outpouring of serous edema fluid, which is then followed by an influx of PMNs and erythrocytes. By the second or third day of illness, the lung segment has increased threeto fourfold in weight through accumulation of this cellular, hemorrhagic fluid typically in a single lobe of the lung. A remarkable feature of pneumococcal pneumonia is the lack of structural damage to the lung, which usually leads to complete resolution on recovery.\

4 IMMUNITY Immunity to S. pneumoniae infection is provided by antibody directed against the specific pneumococcal capsular type. When antibody binds to the capsular surface, C3b is deposited by classical pathway mechanisms, and phagocytosis can proceed. DIAGNOSIS Gram smears of material from sputum and other sites of pneumococcal infection typically show Gram-positive, lancet-shaped diplococci

5 S. pneumoniae grows well overnight on blood agar medium and is usually distinguished from viridans streptococci by susceptibility to (Optochin) or by a bile solubility Quellung Reaction: When pneumococci of a certain type are mixed with specific antipolysaccharide serum of the same type or with polyvalent antiserum (OMNISERUM) on a microscope slide Bacteremia is common in pneumococcal pneumonia and meningitis, and blood cultures are valuable supplements to cultures

6 Detection of pneumococcal capsular antigen in body fluids is possible but valuable primarily when cultures are negative. PREVENTION A vaccine prepared from capsular polysaccharide extracted from the 23 most common serotypes of S. pneumoniae is available. However, this vaccine cannot be administered to infants below 2 years of age and to immunodeficient patients perhaps due to an immature or a sensitive immune system It is recommended for patients who are particularly susceptible to pneumococcal infection because of advanced age, underlying disease. A seven-valent conjugate vaccine (PCV-7) is now available and recommended for use beginning at 2 months of age.

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