Streptococcus pneumoniae
Streptococcus pneumoniae | |
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S. pneumoniae in spinal fluid. FA stain (digitally colored). | |
Scientific classification | |
Domain: | Bacteria |
Phylum: | Bacillota |
Class: | Bacilli |
Order: | Lactobacillales |
Family: | Streptococcaceae |
Genus: | Streptococcus |
Species: | S. pneumoniae
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Binomial name | |
Streptococcus pneumoniae (Klein 1884) Chester 1901
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Streptococcus pneumoniae, or pneumococcus, is a
Streptococcus pneumoniae resides asymptomatically in healthy carriers typically colonizing the respiratory tract, sinuses, and
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.
The capsular polysaccharide (CPS) serves as a critical defense mechanism against the host immune system. It composes the outermost layer of encapsulated strains of S. pneumoniae and is commonly attached to the peptidoglycan of the cell wall. [7] It consists of a viscous substance derived from a high-molecular-weight polymer composed of repeating oligosaccharide units linked by covalent bonds to the cell wall. The virulence and invasiveness of various strains of S. pneumoniae vary according to their serotypes, determined by their chemical composition and the quantity of CPS they produce. Variations among different S. pneumoniae strains significantly influence pathogenesis, determining bacterial survival and likelihood of causing invasive disease. [8] Additionally, the CPS inhibits phagocytosis by preventing granulocytes’ access to the cell wall. [9]
History
In 1881, the organism, known later in 1886 as the pneumococcus[10] for its role as a cause of pneumonia, was first isolated simultaneously and independently by the U.S. Army physician George Sternberg[11] and the French chemist Louis Pasteur.[12]
The organism was termed Diplococcus pneumoniae from 1920[13] because of its characteristic appearance in Gram-stained sputum. It was renamed Streptococcus pneumoniae in 1974 because it was very similar to streptococci.[10][14]
Streptococcus pneumoniae played a central role in demonstrating that genetic material consists of
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.[18] The pneumococcal genome is known to contain a large and diverse repertoire of antimicrobial peptides, including 11 different lantibiotics.[19]
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.[20] Competence in S. pneumoniae is induced by DNA-damaging agents such as
Infection
Streptococcus pneumoniae is part of the normal
S. pneumoniae undergoes spontaneous phase variation, changing between transparent and opaque colony phenotypes. The transparent phenotype has a thinner capsule and expresses large amounts of phosphorylcholine (ChoP) and choline-binding protein A (CbpA), contributing to the bacteria’s ability to adhere and colonize in the nasopharynx. [26] The opaque phenotype is characterized by a thicker capsule, resulting in increased resistance to host clearance. [27] It expresses large amounts of capsule and pneumococcal surface protein A (PspA) which help the bacteria survive in the blood. [28] Phase-variation between these two phenotypes allows S. pneumoniae to survive in different human body systems.
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,
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;[30] it is incorporated into the childhood immunization schedule in a number of countries including the United Kingdom,[31] the United States,[32] and South Africa.[33]
Currently, there are two vaccines available for S. pneumoniae: the pneumococcal polysaccharide vaccine (PPV23) and the pneumococcal conjugate vaccine (PCV13). PPV23 functions by utilizing CPS to stimulate the production of type-specific antibodies, initiating processes such as complement activation, opsonization, and phagocytosis to combat bacterial infections. It elicits a humoral immune response targeting the CPS present on the bacterial surface. [34] PPSV23 offers T-cell-independent immunity and requires revaccination 5 years after the first vaccination because of its temporary nature. [35] PCV13 was developed when determining its low efficacy in children and infants. PCV13 elicits a T-cell-dependent response and provides enduring immunity by promoting interaction between B and T cells, leading to an enhanced and prolonged immune response. [36]
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
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.[40] There is also evidence that S. pneumoniae uses hydrogen peroxide as a virulence factor.[41] 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.[42]
Diagnosis
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.[43]
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.[44]
Atromentin and leucomelone possess antibacterial activity, inhibiting the enzyme enoyl-acyl carrier protein reductase, (essential for the biosynthesis of fatty acids) in S. pneumoniae.[45]
Resistance
Resistant pneumococcal strains are called penicillin-resistant pneumococci (PRP),[46] penicillin-resistant Streptococcus pneumoniae (PRSP),[47] Streptococcus pneumoniae penicillin resistant (SPPR)[48] 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.[49]
See also
References
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- ^ Sternberg GM (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..
- ^ Pasteur L (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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- ^ "Pneumococcal Vaccination: Information for Health Care Providers". cdc.org. Archived from the original on 23 July 2016. Retrieved 26 July 2016.
- ^ "Critical decline in pneumococcal disease and antibiotic resistance in South Africa". NICD. Retrieved 20 July 2015.
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External links
- GAVI Alliance Archived 2014-08-20 at the Wayback Machine
- 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 (eds.). Epidemiology and Prevention of Vaccine-Preventable Diseases (12th ed.). Washington DC: Public Health Foundation. pp. 233–248. Archived from the original on 2017-03-10.
- Type strain of Streptococcus pneumoniae at BacDive - the Bacterial Diversity Metadatabase Archived 2020-04-20 at the Wayback Machine