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Streptococcus pneumoniae

 

Streptococcus pneumoniae

Streptococcus pneumoniae
S. pneumoniae in spinal fluid. FA stain (digitally colored).
Scientific classification
Domain: Bacteria
Phylum: Firmicutes
Class: Cocci
Order: Lactobacillales
Family: Streptococcaceae
Genus: Streptococcus
Species: S. pneumoniae
Binomial name
Streptococcus pneumoniae
(Klein 1884)
Chester 1901

Streptococcus pneumoniae, or pneumococcus, is a Gram-positive, alpha-hemolytic, facultative anaerobic 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.

S. pneumoniae resides asymptomatically in the nasopharynx of healthy carriers. The respiratory tract, sinuses, and nasal cavity are the parts of host body that are usually infected. However, in susceptible individuals, such as elderly and immunocompromised people and children, the bacterium may become pathogenic, spread to other locations and cause disease. S. pneumoniae is the main cause of community acquired pneumonia and meningitis in children and the elderly, and of septicemia in HIV-infected persons. The methods of transmission include sneezing, coughing, and direct contact with an infected person.

Despite the name, the organism causes many types of pneumococcal infections other than pneumonia. These invasive pneumococcal diseases include bronchitis, rhinitis, acute sinusitis, otitis media, conjunctivitis, meningitis, bacteremia, sepsis, osteomyelitis, septic arthritis, endocarditis, peritonitis, pericarditis, cellulitis, and brain abscess.[2]

S. pneumoniae is one of the most common causes of bacterial meningitis in adults and young adults, along with Neisseria meningitidis, and is the leading cause of bacterial meningitis in adults in the USA. It is also one of the top two isolates found in ear infection, otitis media.[3] Pneumococcal pneumonia is more common in the very young and the very old. It also is a major bacterium for invasive diseases like pneumonia and meningitis in South Asian children 12 years of age, though the evidence is of low quality and scarce.[4]

S. pneumoniae can be differentiated from serotypes are known, and these types differ in virulence, prevalence, and extent of drug resistance.

Contents

  • History 1
  • Genetics 2
  • Transformation in S. pneumoniae 3
  • Infection 4
  • Vaccine 5
  • Interaction with Haemophilus influenzae 6
  • Diagnosis 7
  • See also 8
  • References 9
  • External links 10

History

In 1881, the organism, known later in 1886 as the pneumococcus[5] for its role as an [etiologic agent] of pneumonia, was first isolated simultaneously and independently by the U.S. Army

  • GAVI Alliance
  • PneumoADIP
  • PATH's Vaccine Resource Library pneumococcal resources
  • Centers for Disease Control and Prevention (2012). "Ch. 16: Pneumococcal Disease". In Atkinson W, Wolfe S, Hamborsky J. Epidemiology and Prevention of Vaccine-Preventable Diseases (12th ed.). Washington DC: Public Health Foundation. pp. 233–248. 

External links

  1. ^ Ryan KJ; Ray CG (editors) (2004). Sherris Medical Microbiology. McGraw Hill.  
  2. ^ a b Siemieniuk, Reed A.C.; Gregson, Dan B.; Gill, M. John (Nov 2011). "The persisting burden of invasive pneumococcal disease in HIV patients: an observational cohort study". BMC Infectious Diseases 11: 314.  
  3. ^ Dagan R (2000). "Treatment of acute otitis media—challenges in the era of antibiotic resistance". Vaccine 19 (Suppl 1): S9–S16.  
  4. ^ Jaiswal, Nishant; Singh, Meenu; Thumburu, Kiran Kumar; Bharti, Bhavneet; Agarwal, Amit; Kumar, Ajay; Kaur, Harpreet; Chadha, Neelima; et al. (5 May 2014). "Burden of Invasive Pneumococcal Disease in Children Aged 1 Month to 12 Years Living in South Asia: A Systematic Review". PLoS ONE 9 (5): e96282.  
  5. ^ a b  
  6. ^  .
  7. ^  .
  8. ^ Winslow, C., and J. Broadhurst (1920). "The Families and Genera of the Bacteria: Final Report of the Committee of the Society of American Bacteriologists on Characterization and Classification of Bacterial Types". J Bacteriol 5 (3): 191–229.  
  9. ^  
  10. ^  
  11. ^ Avery OT, MacLeod CM, and McCarty M (1944). "Studies on the chemical nature of the substance inducing transformation of pneumococcal types: induction of transformation by a desoxyribonucleic acid fraction isolated from pneumococcus type III". J Exp Med 79 (2): 137–158.  
  12. ^ Lederberg J (1994). "The Transformation of Genetics by DNA: An Anniversary Celebration of Avery, Macleod and Mccarty (1944)". Genetics 136 (2): 423–6.  
  13. ^ van der Poll T, Opal SM (2009). "Pathogenesis, treatment, and prevention of pneumococcal pneumonia". Lancet 374 (9700): 1543–56.  
  14. ^ Claverys JP, Prudhomme M, Martin B (2006). "Induction of competence regulons as a general response to stress in gram-positive bacteria". Annu. Rev. Microbiol. 60: 451–75.  
  15. ^ Engelmoer DJ, Rozen DE (December 2011). "Competence increases survival during stress in Streptococcus pneumoniae". Evolution 65 (12): 3475–85.  
  16. ^ Michod RE, Bernstein H, Nedelcu AM (May 2008). "Adaptive value of sex in microbial pathogens". Infect. Genet. Evol. 8 (3): 267–85.  http://www.hummingbirds.arizona.edu/Faculty/Michod/Downloads/IGE%20review%20sex.pdf
  17. ^ 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.  
  18. ^ 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.   Full text
  19. ^ Pikis, A; Campos, JM; Rodriguez, WJ; Keith, JM (2001). : mechanism, significance, and clinical implications"Streptococcus pneumoniae"Optochin resistance in . Journal of Infectious Diseases 184 (5): 582–590.  
  20. ^ Zheng CJ, Sohn MJ, Kim WG. (2006). "Atromentin and  

References

See also

Atromentin and leucomelone possess antibacterial activity, inhibiting the enzyme enoyl-acyl carrier protein reductase, (essential for the biosynthesis of fatty acids) in S. pneumoniae.[20]

Diagnosis is generally made based on clinical suspicion along with a positive culture from a sample from virtually any place in the body. An ASO Titre of >200 units is significant.[2] S. pneumoniae is, in general, optochin sensitive, although optochin resistance has been observed.[19]

Diagnosis

It is unclear why H. influenzae is not affected by the immune system response.[18]

  1. When H. influenzae is attacked by S. pneumoniae, it signals the immune system to attack the S. pneumoniae
  2. The combination of the two species sets off an immune system alarm that is not set off by either species individually.

Two scenarios may be responsible for this response:

Lab tests show 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.

When both bacteria are placed together into the nasal cavity of a mouse, 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.

Both Haemophilus influenzae (H. influenzae) and S. pneumoniae can be found in the human upper respiratory system. A study of competition in vitro revealed S. pneumoniae overpowered H. influenzae by attacking it with hydrogen peroxide.[17]

Interaction with Haemophilus influenzae

Vaccine

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, like 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.

Infection

Competence, in S. pneumoniae, is induced by DNA-damaging agents such as mitomycin C, a DNA inter-strand cross-linking agent, and the fluoroquinolone antibiotics norfloxacin, levofloxacin and moxifloxacin, topoisomerase inhibitors that cause double-strand breaks.[14] Transformation protects S. pneumoniae against the bactericidal effect of mitomycin C.[15] Michod et al.[16] summarized evidence that induction of competence in S. pneumoniae is associated with increased resistance to oxidative stress and increased expression of the RecA protein, a key component of the recombinational repair machinery for removing DNA damages. On the basis of these findings, they suggested that transformation is an adaptation for repairing oxidative DNA damages. S. pneumoniae infection stimulates polymorphonuclear leukocytes (granulocyte) to produce an oxidative burst that is potentially lethal to the bacteria. The ability of S. pneumoniae to repair the oxidative DNA damages in its genome, caused by this host defense, likely contributes to this pathogen’s virulence.

Natural bacterial transformation involves the transfer of DNA from one bacterium to another through the surrounding medium. Transformation is a complex, developmental process requiring energy, dependent on expression of numerous genes. In S. pneumoniae at least 23 genes are required. In order for a bacterium to bind, take up and recombine exogenous DNA into its chromosome it must enter a special physiological state, called competence.

Transformation in S. pneumoniae

The genome of S. pneumoniae is a closed, circular DNA structure that contains between 2.0 and 2.1 million base pairs, depending on the strain. It has a core set of 1553 genes, plus 154 genes in its virulome, which contribute to virulence, and 176 genes that maintain a noninvasive phenotype. Genetic information can vary up to 10% between strains.[13]

Genetics

S. pneumoniae played a central role in demonstrating 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.[10] In 1944, Oswald Avery, Colin MacLeod, and Maclyn McCarty demonstrated the transforming factor in Griffith's experiment was DNA, not protein, as was widely believed at the time.[11] Avery's work marked the birth of the molecular era of genetics.[12]

The organism was termed Diplococcus pneumoniae from 1920[8] because of its characteristic appearance in Gram-stained sputum. It was renamed Streptococcus pneumoniae in 1974 because it was very similar to streptococci.[5][9]

[7].Louis Pasteur and the French chemist [6]

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