Streptococcus pneumoniae
| Streptococcus pneumoniae | |
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| SEM micrograph of S. pneumoniae. | |
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| Species: | S. pneumoniae
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| Binomial name | |
| Streptococcus pneumoniae (Klein 1884)
Chester 1901 | |
Streptococcus pneumoniae, or pneumococcus, is gram-positive, alpha-hemolytic, bile soluble aerotolerant anaerobe and a member of the genus Streptococcus.[1] A significant human pathogenic bacterium, S. pneumoniae was recognized as a major cause of pneumonia in the late 19th century and is the subject of many humoral immunity studies.
Despite the name, the organism causes many types of pneumococcal infection other than pneumonia, including acute sinusitis, otitis media, meningitis, bacteremia, sepsis, osteomyelitis, septic arthritis, endocarditis, peritonitis, pericarditis, cellulitis, and brain abscess.
S. pneumoniae is the most common cause of bacterial meningitis in adults and children and dogs and is one of the top two isolates found in ear infection, otitis media.[2] Pneumococcal pneumonia is more common in the very young and the very old.
S. pneumoniae can be differentiated from Streptococcus Viridans, some of which are also alpha hemolytic, using an optochin test, as S. pneumoniae is optochin sensitive. S. pneumoniae can also be distinguished based on its sensitivity to lysis by bile. The encapsulated, gram-positive coccoid bacteria have a distinctive morphology on gram stain, the so-called, "lancet shaped" diplococci. It has a polysaccharide capsule that acts as a virulence factor for the organism; more than 90 different serotypes are known, and these types differ in virulence, prevalence, and extent of drug resistance.
History
In 1881, the organism, then known as the pneumococcus for its role as an etiologic agent of pneumonia, was first isolated simultaneously and independently by the U.S Army physician George Sternberg and the French chemist Louis Pasteur.
The organism was termed Diplococcus pneumoniae from 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.
S. pneumoniae played a central role in demonstrating that genetic material consists of DNA. In 1928, Frederick Griffith demonstrated transformation of life, turning harmless pneumococcus into a lethal form by co-inoculating the live pneumococci into a mouse along with heat-killed, virulent pneumococci. In 1944, Oswald Avery, Colin MacLeod, and Maclyn McCarty demonstrated that the transforming factor in Griffith's experiment was DNA, not protein as was widely believed at the time.[3] Avery's work marked the birth of the molecular era of genetics.[4]
Genetics
The genome of S. pneumoniae is a closed, circular DNA structure that contains between 2 million and 2.1 million basepairs, depending on the strain. It has a core set of 1553 essential genes, plus 154 genes in its virulome, which contribute to virulence, and 176 genes that maintain a non-invasive phenotype. There is up to 10% genetic variation between strains.[5]
S. pneumoniae is part of the normal upper respiratory tract flora but as with many natural flora, it can become pathogenic under the right conditions (e.g., if the immune system of the host is suppressed). Invasins such as Pneumolysin, an anti-phagocytic capsule, various adhesins and immunogenic cell wall components are all major virulence factors.
Vaccine
Interaction with Haemophilus influenzae
Both H. influenzae and S. pneumoniae can be found in the human upper respiratory system. A study of competition in a laboratory revealed that, in a petrì dish, S. pneumoniae always overpowered H. influenzae by attacking it with hydrogen peroxide.[6]
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 extraordinarily large number of neutrophil immune cells were found. In mice exposed to only one bacterium, 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.[7]
Diagnosis
S. pneumoniae is generally Optochin sensitive, although Optochin resistance has been observed. [8]
See also
- Pneumonia
- Pneumococcal infection
- Pneumococcal vaccine
- Pneumococcal polysaccharide vaccine
- Pneumococcal conjugate vaccine
- Child mortality
- PneumoADIP
- Otitis media
- Sepsis
- Meningitis
- H. influenzae
References
- ^ Ryan KJ; Ray CG (editors) (2004). Sherris Medical Microbiology. McGraw Hill. ISBN 0-8385-8529-9.
{{cite book}}:|author=has generic name (help)CS1 maint: multiple names: authors list (link) - ^ Dagan R (2000). "Treatment of acute otitis media - challenges in the era of antibiotic resistance". Vaccine. 19 Suppl 1: S9–S16. PMID 11163457.
- ^ Avery OT, MacLeod CM, and McCarty M (1944). "Studies on the chemical nature of the substance inducing transformation of pneumococcal types." J Exp Med 79:137-158.
- ^ Lederberg J (1994). "The transformation of genetics by DNA: an anniversary celebration of Avery, MacLeod and McCarty (1944)". Genetics. 136 (2): 423–6. PMC 1205797. PMID 8150273.
- ^ van der Poll T, Opal SM (2009). "Pathogenesis, treatment, and prevention of pneumococcal pneumonia". Lancet. 374 (9700): 1543–56. doi:10.1016/S0140-6736(09)61114-4. PMID 19880020.
- ^ Pericone, Christopher D., Overweg, Karin, Hermans, Peter W. M., Weiser, Jeffrey N. (2000). "Inhibitory and Bactericidal Effects of Hydrogen Peroxide Production by Streptococcus pneumoniae on Other Inhabitants of the Upper Respiratory Tract". Infect Immun. 68 (7): 3990–3997. doi:10.1128/IAI.68.7.3990-3997.2000. PMC 101678. PMID 10858213.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ^ Lysenko ES, Ratner AJ, Nelson AL, Weiser JN (2005). "The role of innate immune responses in the outcome of interspecies competition for colonization of mucosal surfaces". PLoS Pathog. 1 (1): e1. doi:10.1371/journal.ppat.0010001. PMC 1238736. PMID 16201010.
{{cite journal}}: CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link) Full text - ^ "Optochin resistance in Streptococcus pneumoniae: mechanism, significance, and clinical implications", Journal of Infectious Diseases, 184 (5): 582–590, 2001, doi:10.1086/322803, PMID 11474432
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External links
- GAVI Alliance
- PneumoADIP
- Pneumococcal Awareness Council of Experts
- PATH's Vaccine Resource Library pneumococcal resources
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