Streptococcus pneumoniae

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Invasive pneumococcal disease
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Streptococcus pneumoniae
S. pneumoniae in spinal fluid. FA stain (digitally colored).
Scientific classification Edit this classification
Domain: Bacteria
Phylum: Bacillota
Class: Bacilli
Order: Lactobacillales
Family: Streptococcaceae
Genus: Streptococcus
Species:
S. pneumoniae
Binomial name
Streptococcus pneumoniae
(Klein 1884) Chester 1901

Streptococcus pneumoniae, or pneumococcus, is a

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.[citation needed
]

Streptococcus pneumoniae resides asymptomatically in healthy carriers typically colonizing the respiratory tract, sinuses, and

weaker immune systems, such as the elderly and young children, the bacterium may become pathogenic and spread to other locations to cause disease. It spreads by direct person-to-person contact via respiratory droplets and by auto inoculation in persons carrying the bacteria in their upper respiratory tracts.[3] It can be a cause of neonatal infections.[4]

Streptococcus pneumoniae is the main cause of

Streptococcus pneumoniae can be differentiated from the viridans streptococci, 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 so-called "bile solubility test". The encapsulated, Gram-positive, coccoid bacteria have a distinctive morphology on Gram stain, lancet-shaped diplococci. They have a polysaccharide capsule that acts as a virulence factor for the organism; more than 100 different serotypes are known, and these types differ in virulence, prevalence, and extent of drug resistance.

History

In 1881, the organism, known later in 1886 as the pneumococcus[7] for its role as a cause of pneumonia, was first isolated simultaneously and independently by the U.S. Army physician George Sternberg[8] and the French chemist Louis Pasteur.[9]

The organism was termed Diplococcus pneumoniae from 1920[10] because of its characteristic appearance in Gram-stained sputum. It was renamed Streptococcus pneumoniae in 1974 because it was very similar to streptococci.[7][11]

Streptococcus pneumoniae played a central role in demonstrating that genetic material consists of

virulent pneumococci.[12] In 1944, Oswald Avery, Colin MacLeod, and Maclyn McCarty demonstrated that the transforming factor in Griffith's experiment was not protein, as was widely believed at the time, but DNA.[13] Avery's work marked the birth of the molecular era of genetics.[14]

Genetics

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.[15] The pneumococcal genome is known to contain a large and diverse repertoire of antimicrobial peptides, including 11 different lantibiotics.[16]

Transformation

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 and is dependent on expression of numerous genes. In S. pneumoniae, at least 23 genes are required for transformation. For a bacterium to bind, take up, and recombine exogenous DNA into its chromosome, it must enter a special physiological state called competence.[17] Competence in S. pneumoniae is induced by DNA-damaging agents such as

DNA damage. On the basis of these findings, they suggested that transformation is an adaptation for repairing oxidative DNA damage. S. pneumoniae infection stimulates polymorphonuclear leukocytes (granulocytes) to produce an oxidative burst that is potentially lethal to the bacteria. The ability of S. pneumoniae to repair oxidative DNA damage in its genome caused by this host defense likely contributes to the pathogen's virulence. Consistent with this premise, Li et al.[21]
reported that, among different highly transformable S. pneumoniae isolates, nasal colonization fitness and virulence (lung infectivity) depend on an intact competence system.

Infection

Streptococcus pneumoniae is part of the normal

lungs, the body responds by stimulating the inflammatory response, causing plasma, blood, and white blood cells to fill the alveoli. This condition is called bacterial pneumonia.[22]

Diseases and symptoms

Pneumonia is the most common of the S. pneumoniae diseases which include symptoms such as fever and chills, cough, rapid breathing, difficulty breathing, and chest pain. For the elderly, they may include confusion, low alertness, and the former listed symptoms to a lesser degree.[citation needed]

Pneumococcal meningitis is an infection of the tissue covering the brain and spinal cord. Symptoms include stiff neck, fever, headache, confusion, and photophobia.[citation needed]

Sepsis is caused by overwhelming response to an infection and leads to tissue damage,

organ failure, and even death. The symptoms include confusion, shortness of breath, elevated heart rate, pain or discomfort, over-perspiration, fever, shivering, or feeling cold.[23]

Vaccine

Due to the importance of disease caused by S. pneumoniae, several vaccines have been developed to protect against invasive infection. The World Health Organization recommends routine childhood pneumococcal vaccination;[24] it is incorporated into the childhood immunization schedule in a number of countries including the United Kingdom,[25] the United States,[26] and South Africa.[27]

Biotechnology

Components from S. pneumoniae have been harnessed for a range of applications in biotechnology. Through engineering of surface molecules from this bacterium, proteins can be irreversibly linked using the

glycoside hydrolases have also been cloned from S. pneumoniae to help analysis of cell glycosylation.[30]

Interaction with Haemophilus influenzae

Historically, Haemophilus influenzae has been a significant cause of infection, and both 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.[31] There is also evidence that S. pneumoniae uses hydrogen peroxide as a virulence factor.[32] However, in a study adding both bacteria to the nasal cavity of a mouse within two weeks, only H. influenzae survives; further analysis showed that neutrophils exposed to dead H. influenzae were more aggressive in attacking S. pneumoniae.[33]

Diagnosis

Optochin sensitivity in a culture of Streptococcus pneumoniae (white disk)
Example of a workup algorithm of possible bacterial infection in cases with no specifically requested targets (non-bacteria, mycobacteria etc.), with most common situations and agents seen in a New England community hospital setting. Streptococcus pneumoniae is mentioned at gram stain near top right, and again in the alpha-hemolytic workflow in lower left quadrant.

Diagnosis is generally made based on clinical suspicion along with a positive culture from a sample from virtually any place in the body. S. pneumoniae is, in general, optochin sensitive, although optochin resistance has been observed.[34]

The recent advances in next-generation sequencing and comparative genomics have enabled the development of robust and reliable molecular methods for the detection and identification of S. pneumoniae. For instance, the Xisco gene was recently described as a biomarker for PCR-based detection of S. pneumoniae and differentiation from closely related species.[35]

Atromentin and leucomelone possess antibacterial activity, inhibiting the enzyme enoyl-acyl carrier protein reductase, (essential for the biosynthesis of fatty acids) in S. pneumoniae.[36]

Resistance

Resistant pneumococcal strains are called penicillin-resistant pneumococci (PRP),[37] penicillin-resistant Streptococcus pneumoniae (PRSP),[38] Streptococcus pneumoniae penicillin resistant (SPPR)[39] or drug-resistant Strepotococcus pneumoniae (DRSP). In 2015, in the US, there were an estimated 30,000 cases, and in 30% of them the strains were resistant to one or more antibiotics.[40]

See also

References

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  2. ^ "Streptococcus pneumoniae". microbewiki.kenyon.edu. Retrieved 2017-10-24.
  3. ^ "Transmission". cdc.org. Retrieved 24 Oct 2017.
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  8. ^ Sternberg, George Miller (30 April 1881). "A fatal form of septicaemia in the rabbit produced by the subcutaneous injection of human saliva. An experimental research". Bulletin of the National Board of Health..
  9. ^ Pasteur, Louis (1881). "Sur une maladie nouvelle provoquée par la salive d'un enfant mort de rage". Comptes Rendus de l'Académie des Sciences de Paris. 92: 159..
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  17. ^ Bernstein H, Bernstein C, Michod RE. Sex in microbial pathogens. Infect Genet Evol. 2018 Jan;57:8-25. doi: 10.1016/j.meegid.2017.10.024. Epub 2017 Oct 27. PMID 29111273
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  22. ^ Anderson, Cindy. "Pathogenic Properties (Virulence Factors) of Some Common Pathogens" (PDF).
  23. ^ "Symptoms and Complications". Centers for Disease Control and Prevention. 24 July 2023.
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  25. ^ "Children to be given new vaccine". BBC News. 8 February 2006.
  26. ^ "Pneumococcal Vaccination: Information for Health Care Providers". cdc.org. Archived from the original on 23 July 2016. Retrieved 26 July 2016.
  27. ^ "Critical decline in pneumococcal disease and antibiotic resistance in South Africa". NICD. Retrieved 20 July 2015.
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External links