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Streptococcus Pneumonia

Streptococcus pneumoniae is a species of Streptococcus that is a major human pathogen. It was recognized as a major cause of pneumonia in the 1880s, and is the subject of many humoral immunity studies.

The organism was originally named Diplococcus pneumonia in 1926 because of its characteristic appearance in Gram-stained sputum. It was renamed Streptococcus pneumoniae in 1974 because of its growth in chains in liquid media. Because of its role as the etiologic agent of pneumonia, it has long been known informally as the pneumococcus.

Despite the name, the organism causes many types of infection other than pneumonitis, including acute sinusitis, otitis media, meningitis, osteomyelitis, septic arthritis, endocarditis, peritonitis, pericarditis, cellulitis, and brain abscess.

S. pneumonia is the most common cause of bacterial meningitis in adults, and is one of the top two isolates found in otitis media. Pneumococcal pneumonia is more common in the very young and the very old. Contents

Pathogensis of streptococcus pneumoniae

S. pneumoniae is normally found in the nasopharynx of 5-10% of healthy adults, and 20-40% of healthy children. It attaches to nasopharyngeal cells through interaction of bacterial surface adhesins and epithelial cells. This normal colonization can become infection if the organisms are carried into areas, such as the Eustachian tube or nasal sinuses, where their clearance is hindered (as it might be if allergies or viral infection is present). Pneumonia occurs if the organisms are inhaled into the lungs and not cleared (again, viral infection, or smoking-induced ciliary paralysis might be contributing factors). Once the organism makes its way to a site where it is not normally found, it activates the complement protein group, stimulates cytokine production, and attracts white blood cells (specifically polymorphonuclear neutrophils). The organism's polysaccharide capsule makes it resistant to phagocytosis, and if there is no pre-existing anticapsular antibody, alveolar macrophages cannot adequately kill the pneumococci. The organism spreads to the blood stream and is carried to the meninges, joint spaces, bones, and peritoneal cavity, and may result in meningitis, brain abscess, septic arthritis, or osteomyelitis.

The risk of pneumococcal infection is much increased in persons with impaired IgG synthesis, impaired phagocytosis, or defective clearance of pneumococci. In particular, the absence of a functional spleen, through congenital asplenia, splenectomy, or sickle cell disease predisposes one to a more severe course of infection.

Humoral immunity
In the 19th century, it was demonstrated that immunization of rabbits with killed pneumococci protected them against subsequent challenge with viable pneumococci. Serum from immunized rabbits or from humans who had recovered from pneumococcal pneumonia also conferred protection. In the 20th century, the efficacy of immunization was demonstrated in South African miners. It was discovered that the pneumococcus's capsule made it resistant to phagocytosis, and in the 1920s it was shown that an antibody specific for capsular polysaccharide aided the killing of S. pneumoniae. In 1936, a penumococcal capsular polysaccharide vaccine was used to abort an epidemic of pneumococcal pneumonia. In the 1940s, experiments on capsular transformation by pneuococci first identified DNA as the material that carries genetic information.

In 1900, it was recognized that different serotypes of pneumococci exist, and that immunization with a given serotype did not protect against infection with other serotypes. Since then over ninety serotypes have been discovered, each with a unique polysaccharide capsule. Because some of these serotypes are more commonly the cause of disease, it is possible to provide reasonable protection by immunizing with less than 90 serotypes; the current vaccine contains 23 serotypes (i.e., it is "23-valent").

The serotypes are numbered according to two systems: the American system, which numbers them in the order in which they were discovered, and the Danish system which groups them according to antigenic similarities.

Treatment of streptococcus pneumoniae

Treatment is usually with ?-lactam antibiotics. In the 1960s, nearly all strains of S. pneumoniae were susceptible to penicillin, but since that time, there has been an increasing prevalence of resistance, especially in areas of high antibiotic use. A varying proportion of penicillin-resistant strains may also be resistant to erythromycin, macrolides, and clindamycin and the quinolones. Most remain susceptible to vancomycin, which is a less desirable antibiotic because of dosing and tissue penetration issues. Susceptibility testing is routine, with empiric antibiotic treatment, guided by resistance patterns in the community in which the organism was acquired, pending the results.

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