Streptococcus pneumoniae
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| Streptococcus pneumoniae | ||||||||||||||
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| Streptococcus pneumoniae (Klein 1884) Chester 1901 |
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. pneumoniae 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.
S. pneumoniae is a gram-positive cocci (shphere-shaped bacterium) that demonstrates alpha-hemolysis when cultures on a blood agar plate. Alpha-hemolysis refers to a characteristic pattern of incomplete destruction of red blood cells around a colony growing in sheep's blood agar. It has a carbohydrate capsule that is an important virulence factor for the organism. Because of the chemical make-up of the capsule (it is a polysaccharide) it will not cause an immune response in neonates and very young children (because they have not yet developed humoral immunity).
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Pathogensis
S. pneumoniae is normally found in the nasopharynx of 5-10% of healthy adults, and 20-40% of healthy children. It can be found in higher amounts in certain environments, especially those where people are spending a great deal of time in close proximity to each other (day cares, army barracks). 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 it can cause sinusitis and otis media, respectively. 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 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 (where it can cause bacteremia) and is carried to the meninges, joint spaces, bones, and peritoneal cavity, and may result in meningitis, brain abscess, septic arthritis, or osteomyelitis.
S. pneumoniae has several virulence factors, including the polysaccharide capsule mentioned earlier, that help it evade a host's immune system. It has pneumococcal surface proteins that inhibit activation of complement, and it secretes IgA1 protease that will destroy secretory IgA produced by the body.
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 (Overwhelming post-splenectomy infection) and prevention measures are indicated (see asplenia).
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
Treatment is usually with β-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.
More advanced beta-lactam antibiotics (cephalosproins) are commonly used in combination with other drugs such as vancomycin to treat meningitis and community-acquired pneumonia. An amoxicillin and clavulonic acid combination is often used to treat otis media.
Prevention
Pneumococcal vaccine (Pneumovax™ is one brand) gives at least 85% protection in those under 55 years of age for five years or longer. Immunization is suggested for those at highest risk of infection, including those 65 years or older, and generally should be a single lifetime dose (high risk side effects if repeated). The standard 23-valent vaccines are ineffective for children under two years old; a conjugated 13-valent vaccine is effective for them and should be reinforced with the standard 23-valent vaccine upon reaching the age of 2 years. It should also be administered before a splenectomy.
The current guidelines of the American College of Physicians call for administration of the immunization between ages 2 and 65 when indicated, or at age 65. If someone received the immunization before age 60, the guidelines call for a one-time revaccination.
Revaccination at periodic intervals is also indicated for those with other conditions such as asplenia or nephrotic syndrome. Product license suggests every 5-10 years and with immunity testing generally being unhelpful clinically, revaccination every six years has gained ground; aiming for 5 yearly risks greater side-effects if revaccination is performed prematurely due to a miscalculated interval.
Interaction with Haemophilus influenzae
Both of H. influenzae and S. pneumoniae can be found in the upper respitoray system of humans. A study of competition in a laboratory revealed that, in a petrì dish, S. pnumoniae always overpowered H. influenzae by attacking it with a hydrogen peroxide and stripping off surface molecules that H. influenzae needs for survival.
When both bacteria are placed together into a nasal cavity, within 2 weeks, only H. influenzae survives. When both are placed separately into a nasal cavity, each one survives. Upon examining the upper respiratory tissue from mice exposed to both bacteria, an extraordinaririly large number of neutrophils immune cells were found. In mice exposed to only one bacteria, the cells were not present.
Lab tests show that neutrophils that were exposed to already dead H. influenzae were more aggressive in attacking S. pneumoniae than unexposed neutrophils. Exposure to killed H. influenzae had no effect on live H. influenzae.
Two scenarios may be responsible for this response:
- When H. influenzae is attacked by S. pneumoniae, it signals the immune system to attack the S. pneumoniae
- The combination of the two species together sets off an immune system alarm that is not set off by either species individually.
It is unclear why H. influenzae is not affected by the immune system response. (Lysenko, et al., 2005)
References
- Lysenko, E.S., A.J. Ratner, A.L. Nelson, and J.N. Weiser. In press. The role of innate immune responses in the outcome of interspecies competition for colonization of mucosal surfaces. PLoS Pathogens.
- McDaniel, Larry. Professor, Department of Microbiology, University of Mississippi Medical Center. "Gram Positive Cocci." Lecture to 2nd-year medical students. 09/20/2005.
