Editing Streptococcus pneumoniae

{{Short description|Species of bacterium}}
{{cs1 config|name-list-style=vanc}}
{{Speciesbox
| image = Pneumococcus_CDC_PHIL_ID1003.jpg
| image_caption = ''S. pneumoniae'' in spinal fluid. FA stain (digitally colored).
| genus = Streptococcus
| species = pneumoniae
| authority = (Klein 1884) Chester 1901
}}

'''''Streptococcus pneumoniae''''', or '''pneumococcus''', is a [[Gram-positive]], spherical bacteria, [[hemolysis (microbiology)|alpha-hemolytic]] member of the [[genus]] ''[[Streptococcus]]''.<ref name=Sherris>{{cite book |veditors = Ryan KJ, Ray CG |title = Sherris Medical Microbiology |publisher = McGraw Hill |year = 2004 |isbn = 978-0-8385-8529-0 }}</ref> ''S. pneumoniae'' cells are usually found in pairs ([[diplococci]]) and  do not form [[Bacterial morphological plasticity|spores]] and are non motile.<ref>{{Cite web|url=https://microbewiki.kenyon.edu/index.php/Streptococcus_pneumoniae|title=Streptococcus pneumoniae|website=microbewiki.kenyon.edu|access-date=2017-10-24}}</ref> As 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.{{citation needed|date=June 2022}}

''Streptococcus pneumoniae'' resides asymptomatically in healthy carriers typically colonizing the respiratory tract, sinuses, and [[nasopharynx|nasal cavity]]. However, in susceptible individuals with [[immunocompromised|weaker immune systems]], such as the elderly and young children, the bacterium may become [[pathogen]]ic and spread to other locations to cause disease. It spreads by  direct person-to-person contact via [[respiratory droplet]]s and by auto inoculation in persons carrying the bacteria in their upper respiratory tracts.<ref>{{cite web |url= https://www.cdc.gov/pneumococcal/clinicians/transmission.html|title= Transmission|website= cdc.org |access-date= 24 Oct 2017 }}</ref> It can be a cause of [[neonatal infection]]s.<ref name="BaucellsMercadal Hally2015">{{cite journal |last1=Baucells |first1=B.J. |last2=Mercadal Hally |first2=M. |last3=Álvarez Sánchez |first3=A.T. |last4=Figueras Aloy |first4=J. |title=Asociaciones de probióticos para la prevención de la enterocolitis necrosante y la reducción de la sepsis tardía y la mortalidad neonatal en recién nacidos pretérmino de menos de 1.500g: una revisión sistemática |journal=Anales de Pediatría |volume=85 |issue=5 |pages=247–255 |year=2015 |issn=1695-4033 |doi=10.1016/j.anpedi.2015.07.038|pmid=26611880 |doi-access=free }}</ref>

''Streptococcus pneumoniae'' is the main cause of [[community acquired pneumonia]] and [[meningitis]] in children and the elderly,<ref name="NEJM">{{cite journal|last1=van de Beek|first1=Diederik|last2=de Gans|first2=Jan|last3=Tunkel|first3=Allan R.|last4=Wijdicks|first4=Eelco F.M.|title=Community-Acquired Bacterial Meningitis in Adults|journal=New England Journal of Medicine|date=5 January 2006|volume=354|issue=1|pages=44–53|doi=10.1056/NEJMra052116|issn=0028-4793|pmid=16394301}}</ref> and of [[sepsis]] in those infected with [[HIV]]. The organism also causes many types of [[pneumococcal infection]]s other than [[pneumonia]].  These invasive pneumococcal diseases include [[bronchitis]], [[rhinitis]], [[acute sinusitis]], [[otitis media]], [[conjunctivitis]], [[meningitis]], sepsis, [[osteomyelitis]], [[septic arthritis]], [[endocarditis]], [[peritonitis]], [[pericarditis]], [[cellulitis]], and [[brain abscess]].<ref name="Siemieniuk 2011">{{cite journal|last=Siemieniuk|first=Reed A.C.|author2= Gregson, Dan B. |author3=Gill, M. John |title=The persisting burden of invasive pneumococcal disease in HIV patients: an observational cohort study|journal=BMC Infectious Diseases|date=Nov 2011|volume=11|doi=10.1186/1471-2334-11-314|pmid=22078162|pmc=3226630|pages=314 |doi-access=free }}</ref>
[[File:Streptococcus pneumoniae on agar plates.jpg|thumb|238x238px|S.pneumoniae growth on blood agar.]]
''Streptococcus pneumoniae'' can be differentiated from the [[viridans streptococci]], some of which are also [[hemolysis (microbiology)|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 [[bacterial capsule|encapsulated]], Gram-positive, [[coccus|coccoid]] bacteria have a distinctive morphology on Gram stain, [[scalpel|lancet]]-shaped diplococci. They have a [[polysaccharide]] capsule that acts as a [[virulence factor]] for the organism; more than 100 different [[serotype]]s are known<ref>{{cite journal |last1=Ganaie |first1=F.A. |last2=Beall |first2=B.W. |last3=Yu |first3=J. |last4=van der Linden |first4=M. |last5=McGee |first5=L. |last6=Satzke |first6=C. |last7=Manna |first7=S. |last8=Lo |first8=S.W. |last9=Bentley |first9=S.D. |last10=Ravenscroft |first10=N. |last11=Nahm |first11=M.H. |title=Update on the evolving landscape of pneumococcal capsule types: new discoveries and way forward |journal=Clinical Microbiology Reviews |date=January 29, 2025 |volume=8 |issue=1 |pages=e0017524 |doi=10.1128/cmr.00175-24 |pmid=39878373|pmc=11905375 |pmc-embargo-date=January 29, 2026 }}</ref>
, 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.<ref>{{Cite journal |last1=Paton |first1=James C. |last2=Trappetti |first2=Claudia |date=2019-04-12 |editor-last=Fischetti |editor-first=Vincent A. |editor2-last=Novick |editor2-first=Richard P. |editor3-last=Ferretti |editor3-first=Joseph J. |editor4-last=Portnoy |editor4-first=Daniel A. |editor5-last=Braunstein |editor5-first=Miriam |editor6-last=Rood |editor6-first=Julian I. |title=Streptococcus pneumoniae Capsular Polysaccharide |journal=Microbiology Spectrum |language=en |volume=7 |issue=2 |doi=10.1128/microbiolspec.GPP3-0019-2018 |pmid=30977464 |issn=2165-0497|pmc=11590643 }}</ref> 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#:~:text=In pathology, pathogenesis is the,to its progression and maintenance.|pathogenesis]], determining bacterial survival and likelihood of causing invasive disease.<ref>{{Cite journal |last1=Morais |first1=Victor |last2=Dee |first2=Valerie |last3=Suárez |first3=Norma |date=2018-10-12 |title=Purification of Capsular Polysaccharides of Streptococcus pneumoniae: Traditional and New Methods |journal=Frontiers in Bioengineering and Biotechnology |volume=6 |page=145 |doi=10.3389/fbioe.2018.00145 |doi-access=free |issn=2296-4185 |pmc=6194195 |pmid=30370268}}</ref> Additionally, the CPS inhibits [[phagocytosis]] by preventing [[granulocyte]]s' access to the cell wall.<ref>{{Citation |last1=Dion |first1=Christopher F. |title=Streptococcus pneumoniae |date=2024 |work=StatPearls |url=http://www.ncbi.nlm.nih.gov/books/NBK470537/ |access-date=2024-04-15 |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=29261971 |last2=Ashurst |first2=John V.}}</ref>

==History==
In 1881, the organism, known later in 1886 as the pneumococcus<ref name=Plotkin2012/> for its role as a cause of pneumonia, was first isolated simultaneously and independently by the U.S. Army [[physician]] [[George Miller Sternberg|George Sternberg]]<ref name = Sternberg>{{Cite journal | last = Sternberg | first = George Miller | author-link = George Miller Sternberg | date = 30 April 1881 | title = A fatal form of septicaemia in the rabbit produced by the subcutaneous injection of human saliva. An experimental research | journal = Bulletin of the National Board of Health }}.</ref> and the French chemist [[Louis Pasteur]].<ref name = Pasteur>{{Cite journal | last = Pasteur | first = Louis | author-link = Louis Pasteur | date = 1881 | title = Sur une maladie nouvelle provoquée par la salive d'un enfant mort de rage | journal =  Comptes Rendus de l'Académie des Sciences de Paris | volume = 92 | page = 159 }}.</ref>

The organism was termed ''Diplococcus pneumoniae'' from 1920<ref>{{cite journal |author=Winslow, C. |author2=J. Broadhurst |year=1920 |title=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 |journal=J Bacteriol |volume=5 |issue=3 |pages=191–229 |doi=10.1128/JB.5.3.191-229.1920 |pmid=16558872 |pmc=378870}}</ref> because of its characteristic appearance in [[Gram stain|Gram-stained]] [[sputum]]. It was renamed ''Streptococcus pneumoniae'' in 1974 because it was very similar to [[Streptococcus|streptococci]].<ref name=Plotkin2012>{{cite book |last1=Plotkin |first1=Stanley |author-link1=Stanley Plotkin|last2=Orenstein |first2=W |author-link2=Walter Orenstein |last3=Offit |first3=PA |author-link3=Paul Offit |date=September 22, 2012 |title=Vaccines |url=https://books.google.com/books?id=TRyXTLXNA2YC |publisher=Elsevier – Saunders |page=[https://books.google.com/books?id=TRyXTLXNA2YC&pg=PA542&lpg=PA542&dq=%22Streptococcus%20Pneumoniae%20in%201974%22 542] |isbn=978-1-4557-0090-5 |access-date=July 2, 2015 }}</ref><ref name=Wainer2014>{{cite book |last=Wainer |first=Howard |author-link=Howard Wainer |year=2014 |title=Medical Illuminations: Using Evidence, Visualization and Statistical Thinking to Improve Healthcare |url=https://books.google.com/books?id=23tpAgAAQBAJ |publisher=Oxford University Press |page=[https://books.google.com/books?id=23tpAgAAQBAJ&pg=PA53&lpg=PA53&dq=%22Looking%20at%20this%20display%22 53] |isbn=978-0-19-966879-3 |access-date=July 4, 2015 }}</ref>

''Streptococcus pneumoniae'' played a central role in demonstrating that genetic material consists of [[DNA]].  In 1928, [[Frederick Griffith]] demonstrated [[transformation (genetics)|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.<ref name=Griffith1928>{{cite journal |last=Griffith |first=Fred |author-link=Frederick Griffith |date=January 1928 |title=The Significance of Pneumococcal Types |journal=Journal of Hygiene |volume=27 |issue=2 |pages=113–159 |doi=10.1017/S0022172400031879 |pmc=2167760 |pmid=20474956}}</ref>  In 1944, [[Oswald Avery]], [[Colin Munro MacLeod|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.<ref>{{cite journal |vauthors =Avery OT, MacLeod CM, McCarty M |year=1944 |title=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 |journal=J Exp Med |volume=79 |issue=2 |pages=137–158 |pmc=2135445 |pmid=19871359 |doi=10.1084/jem.79.2.137}}</ref> Avery's work marked the birth of the [[molecular genetics|molecular era of genetics]].<ref>{{cite journal |author=Lederberg J |title=The Transformation of Genetics by DNA: An Anniversary Celebration of Avery, Macleod and Mccarty (1944) |journal=Genetics |volume=136 |issue=2 |pages=423–6 |year=1994 |doi=10.1093/genetics/136.2.423 |pmid=8150273 |pmc=1205797}}</ref>

==Genetics==
The [[genome]] of ''S. pneumoniae'' is a closed, circular DNA structure that contains between 2.0 and 2.1 million [[base pair]]s depending on the [[strain (biology)|strain]]. It has a core set of 1553 [[gene]]s, plus 154 genes in its [[wikt:virulome|virulome]], which contribute to virulence and 176 genes that maintain a noninvasive [[phenotype]]. Genetic information can vary up to 10% between strains.<ref>{{cite journal |title=Pathogenesis, treatment, and prevention of pneumococcal pneumonia |vauthors =van der Poll T, Opal SM |journal=Lancet |year=2009 |volume=374 |issue=9700 |pages=1543–56 |pmid=19880020 |doi=10.1016/S0140-6736(09)61114-4|s2cid =28676845 }}</ref> The pneumococcal genome is known to contain a large and diverse repertoire of antimicrobial peptides, including 11 different [[lantibiotics]].<ref>{{cite journal|last1=Rezaei Javan|first1=Reza|last2=Van Tonder|first2=Andries|last3=King|first3=James|last4=Harrold|first4=Caroline|last5=Brueggemann|first5=Angela|title=Genome Sequencing Reveals a Large and Diverse Repertoire of Antimicrobial Peptides|journal=Frontiers in Microbiology|date= August 2018|volume=2012|issue=9|pages=2012|doi=10.3389/fmicb.2018.02012|pmid=30210481|pmc=6120550|doi-access=free}}</ref>

===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 [[natural competence|competence]].<ref>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</ref>
Competence in ''S. pneumoniae'' is induced by DNA-damaging agents such as [[mitomycin C]], [[fluoroquinolone]] [[antibiotic]]s ([[norfloxacin]], [[levofloxacin]] and [[moxifloxacin]]), and [[topoisomerase inhibitor]]s.<ref>{{cite journal |vauthors=Claverys JP, Prudhomme M, Martin B |title=Induction of competence regulons as a general response to stress in gram-positive bacteria |journal=Annu. Rev. Microbiol. |volume=60 |pages=451–75 |year=2006 |pmid=16771651 |doi=10.1146/annurev.micro.60.080805.142139 }}</ref> Transformation protects ''S. pneumoniae'' against the bactericidal effect of mitomycin C.<ref>{{cite journal |vauthors=Engelmoer DJ, Rozen DE |title=Competence increases survival during stress in Streptococcus pneumoniae |journal=Evolution |volume=65 |issue=12 |pages=3475–85 |date=December 2011 |pmid=22133219 |doi=10.1111/j.1558-5646.2011.01402.x |s2cid=24634666 |doi-access=free }}</ref>  Michod et al.<ref>{{cite journal |vauthors=Michod RE, Bernstein H, Nedelcu AM |title=Adaptive value of sex in microbial pathogens |journal=Infect. Genet. Evol. |volume=8 |issue=3 |pages=267–85 |date=May 2008 |pmid=18295550 |doi=10.1016/j.meegid.2008.01.002 |bibcode=2008InfGE...8..267M |url=http://www.hummingbirds.arizona.edu/Faculty/Michod/Downloads/IGE%20review%20sex.pdf}}</ref> 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 damage]]. On the basis of these findings, they suggested that transformation is an adaptation for repairing oxidative DNA damage. ''S. pneumoniae'' infection stimulates [[granulocyte|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.<ref name="pmid27068094">{{cite journal |vauthors=Li G, Liang Z, Wang X, Yang Y, Shao Z, Li M, Ma Y, Qu F, Morrison DA, Zhang JR |title=Addiction of Hypertransformable Pneumococcal Isolates to Natural Transformation for In Vivo Fitness and Virulence |journal=Infect. Immun. |volume=84 |issue=6 |pages=1887–901 |year=2016 |pmid=27068094 |doi=10.1128/IAI.00097-16 |pmc=4907133}}</ref> reported that, among different highly transformable ''S. pneumoniae'' isolates, nasal colonization fitness and virulence (lung infectivity) depend on an intact competence system.

==Infection==
{{Main|Pneumococcal infection}}

''Streptococcus pneumoniae'' is part of the normal [[upper respiratory tract]] [[human microbiome|flora]]. As with many natural flora, it can become pathogenic under the right conditions, typically when the immune system of the host is [[immunosuppression|suppressed]]. [[Invasins]], such as [[pneumolysin]], an anti[[phagocytic]] [[bacterial capsule|capsule]], various [[bacterial adhesin|adhesins]], and [[immunogenic]] [[bacterial cell structure|cell wall components]] are all major [[virulence factors]]. After ''S. pneumoniae'' colonizes the [[Pulmonary alveolus|air sacs]] of the [[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.<ref>{{cite web|last1=Anderson|first1=Cindy|title=Pathogenic Properties (Virulence Factors) of Some Common Pathogens|url=http://faculty.mtsac.edu/cbriggs/Pathogenic%20Properties%20from%20CAnderson.pdf}}</ref>

''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.<ref name="ReferenceA">{{Cite journal |last1=Wang |first1=Juanjuan |last2=Li |first2=Jing-Wen |last3=Li |first3=Jing |last4=Huang |first4=Yijia |last5=Wang |first5=Shaomeng |last6=Zhang |first6=Jing-Ren |date=2020-03-18 |editor-last=Wessels |editor-first=Michael R. |title=Regulation of pneumococcal epigenetic and colony phases by multiple two-component regulatory systems |journal=PLOS Pathogens |language=en |volume=16 |issue=3 |pages=e1008417 |doi=10.1371/journal.ppat.1008417 |doi-access=free |issn=1553-7374 |pmc=7105139 |pmid=32187228}}</ref> The opaque phenotype is characterized by a thicker capsule, resulting in increased resistance to host clearance.<ref name="ReferenceA"/> It expresses large amounts of capsule and pneumococcal surface protein A (PspA) which help the bacteria survive in the blood.<ref>{{Cite journal |last1=Loughran |first1=Allister J. |last2=Orihuela |first2=Carlos J. |last3=Tuomanen |first3=Elaine I. |date=2019-04-12 |editor-last=Fischetti |editor-first=Vincent A. |editor2-last=Novick |editor2-first=Richard P. |editor3-last=Ferretti |editor3-first=Joseph J. |editor4-last=Portnoy |editor4-first=Daniel A. |editor5-last=Braunstein |editor5-first=Miriam |editor6-last=Rood |editor6-first=Julian I. |title=Streptococcus pneumoniae : Invasion and Inflammation |journal=Microbiology Spectrum |language=en |volume=7 |issue=2 |doi=10.1128/microbiolspec.GPP3-0004-2018 |pmid=30873934 |pmc=6422050 |issn=2165-0497}}</ref> Phase-variation between these two phenotypes allows ''S. pneumoniae'' to survive in different human body systems.

==Diseases and symptoms==
Pneumonia is the most prevalent disease caused by ''Streptococcus pneumoniae.'' Pneumonia is a lung infection characterized by symptoms such as fever, chills, coughing, rapid or labored breathing, and chest pain.<ref>{{Citation |last=Lim |first=Wei Shen |title=Pneumonia—Overview |date=2022 |encyclopedia=Encyclopedia of Respiratory Medicine |pages=185–197 |url=https://doi.org/10.1016/b978-0-12-801238-3.11636-8 |access-date=2024-12-05 |publisher=Elsevier |doi=10.1016/b978-0-12-801238-3.11636-8 |isbn=978-0-08-102724-0|pmc=7241411 }}</ref> For the elderly, those who contract pneumonia have also shown these lesser nonspecific symptoms, but also tend to show that they have tachypnea a few days before clinical certainty that they have contracted the bacterial illness. Tachypnea is characterized by rapid and shallow breathing and can affect a person’s ability to sleep, chest pain, and a decreased appetite.<ref>{{Cite journal |last1=Zalacain |first1=Rafael |last2=Torres |first2=Antoni |date=July 2004 |title=Pneumonia in the Elderly |url=https://journals.lww.com/00045413-200407000-00002 |journal=Clinical Pulmonary Medicine |language=en |volume=11 |issue=4 |pages=210–218 |doi=10.1097/01.cpm.0000132888.49928.86 |issn=1068-0640|url-access=subscription }}</ref>

While a few different bacterial infections can lead to meningitis, S. pneumoniae is one of the leading causes of this infection. Pneumococcal meningitis occurs when the bacteria goes from the blood to the central nervous system, which is made up of the brain and the spinal cord. Here, the infection will spread and cause inflammation, leading to severe disabilities like brain damage or hearing loss or limb removal or death.<ref>{{Cite journal |last1=Gil |first1=Eliza |last2=Wall |first2=Emma |last3=Noursadeghi |first3=Mahdad |last4=Brown |first4=Jeremy S. |date=2023-01-04 |title=Streptococcus pneumoniae meningitis and the CNS barriers |journal=Frontiers in Cellular and Infection Microbiology |language=English |volume=12 |doi=10.3389/fcimb.2022.1106596 |doi-access=free |pmid=36683708 |pmc=9845635 |issn=2235-2988}}</ref> Symptoms include common problems such as head aches, fevers, and nausea, but the more telling signs that a bacterial infection may have reached the brain are sensitivity to light, seizures, having limited range in neck movement, and easy bruising all over the body.

Osteomyelitis, or bone infection, is a rare occurrence but has been seen in patients who were diagnosed to have a S. pneumoniae infection that went untreated for too long.<ref>{{Cite journal |last1=Sheybani |first1=Fereshte |last2=Figueiredo |first2=Ana Helena A. |last3=Brouwer |first3=Matthijs C. |last4=van de Beek |first4=Diederik |date=October 2021 |title=Vertebral osteomyelitis in bacterial meningitis patients |journal=International Journal of Infectious Diseases |volume=111 |pages=354–359 |doi=10.1016/j.ijid.2021.08.069 |pmid=34487853 |issn=1201-9712|doi-access=free }}</ref>

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.<ref>{{cite web|title=Symptoms and Complications|url=https://www.cdc.gov/pneumococcal/about/symptoms-complications.html|website=Centers for Disease Control and Prevention|date=24 July 2023 }}</ref><ref>{{cite web|title=Pneumonia after coronavirus|url=https://kdl.ru/patient/blog/pnevmoniya-kak-oslozhnenie-koronavirusa|website=KDL|date=21 October 2024 }}</ref>

Less severe illnesses that can be caused by pneumococcal infection are conjunctivitis (pink eye ), otitis media (middle ear infection), Bronchitis (airway inflammation), and sinusitis (sinus infection).<ref>{{Cite web |title= |url=https://my.clevelandclinic.org/health/diseases/24231-pneumococcal-disease |access-date=December 3, 2024}}</ref>

== Vaccine ==
{{Main|Pneumococcal vaccine}}
Due to the importance of disease caused by ''S. pneumoniae'', several [[vaccine]]s have been developed to protect against invasive infection. The [[World Health Organization]] recommends routine childhood pneumococcal vaccination;<ref name=WHO2012>{{cite journal|title=Pneumococcal vaccines WHO position paper--2012|journal=Wkly Epidemiol Rec|date=Apr 6, 2012|volume=87|issue=14|pages=129–44|pmid=24340399|url=https://www.who.int/wer/2012/wer8714.pdf?ua=1}}</ref> it is incorporated into the childhood immunization schedule in a number of countries including the United Kingdom,<ref name="BBCVac">{{cite web |title=Children to be given new vaccine |date=8 February 2006 |work=BBC News |url=http://news.bbc.co.uk/1/hi/health/4692908.stm}}</ref> the United States,<ref>{{cite web |url= https://www.cdc.gov/vaccines/vpd-vac/pneumo/hcp/index.html |title= Pneumococcal Vaccination: Information for Health Care Providers |author= <!--Staff writer(s); no by-line.--> |website= cdc.org |access-date= 26 July 2016 |archive-url= https://web.archive.org/web/20160723094817/http://www.cdc.gov/vaccines/vpd-vac/pneumo/hcp/index.html |archive-date= 23 July 2016 |url-status= dead |df= dmy-all }}</ref> Greece,<ref>{{cite web |title=Greek Ministry of Health 2023 Immunisation schedule for children and adolescents |url=https://www.moh.gov.gr/articles/health/dieythynsh-dhmosias-ygieinhs/emboliasmoi/ethniko-programma-emboliasmwn-epe-paidiwn-kai-efhbwn/11252-programma-emboliasmwn-paidiwn-efhbwn-2023?fdl=24973 |access-date=16 July 2024}}</ref>and South Africa.<ref>{{cite web|url=http://www.nicd.ac.za/?page=alerts&id=5&rid=448|title=Critical decline in pneumococcal disease and antibiotic resistance in South Africa|work=NICD|access-date=20 July 2015}}</ref>

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.<ref>{{Cite journal |last1=Aliberti |first1=S. |last2=Mantero |first2=M. |last3=Mirsaeidi |first3=M. |last4=Blasi |first4=F. |date=May 2014 |title=The role of vaccination in preventing pneumococcal disease in adults |journal=Clinical Microbiology and Infection |language=en |volume=20 |issue=5 |pages=52–58 |doi=10.1111/1469-0691.12518 |pmc=4473770 |pmid=24410778}}</ref> PPSV23 offers [[T cell|T-cell]]-independent immunity and requires revaccination 5 years after the first vaccination because of its temporary nature.<ref name="Lavida R. K 2018">{{Cite journal |last1=Brooks |first1=Lavida R. K. |last2=Mias |first2=George I. |date=2018-06-22 |title=Streptococcus pneumoniae's Virulence and Host Immunity: Aging, Diagnostics, and Prevention |journal=Frontiers in Immunology |volume=9 |page=1366 |doi=10.3389/fimmu.2018.01366 |doi-access=free |issn=1664-3224 |pmc=6023974 |pmid=29988379}}</ref> 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 cell|B]] and T cells, leading to an enhanced and prolonged immune response.<ref name="Lavida R. K 2018"/>

==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 [[sortase]] enzyme<ref>{{cite journal |author=Nikghalb, Kevyan D. |title=Expanding the Scope of Sortase-Mediated Ligations by Using Sortase Homologues |journal=ChemBioChem |volume=19 |issue=7 |pages=185–195 |year=2018 |pmid=29124839 |doi=10.1002/cbic.201700517 |s2cid=23874288 }}</ref> or using the SnoopTag/SnoopCatcher reaction.<ref>{{cite journal |author=Veggiani, Gianluca |title=Programmable polyproteams built using twin peptide superglues  |journal=PNAS |volume=113 |issue=5 |pages=1202–1207 |year=2014 |pmid=26787909 |doi=10.1073/pnas.1519214113 |pmc=4747704 |bibcode=2016PNAS..113.1202V |doi-access=free }}</ref> Various [[glycoside hydrolases]] have also been cloned from ''S. pneumoniae'' to help analysis of cell [[glycosylation]].<ref>{{cite journal |author=Gregg, Katie J |title=Structural Analysis of a Family 101 Glycoside Hydrolase in Complex with Carbohydrates Reveals Insights into Its Mechanism |journal=Journal of Biological Chemistry |volume=290 |issue=42 |pages=25657–69 |date=16 October 2015 |doi=10.1074/jbc.M115.680470 |doi-access=free |pmid=26304114 |pmc=4646209}}</ref>

==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]].<ref>{{cite journal |author=Pericone, Christopher D. |author2=Overweg, Karin |author3=Hermans, Peter W. M. |author4=Weiser, Jeffrey N. |title=Inhibitory and Bactericidal Effects of Hydrogen Peroxide Production by Streptococcus pneumoniae on Other Inhabitants of the Upper Respiratory Tract |journal=[[Infection and Immunity|Infect Immun]] |volume=68 |issue=7 |pages=3990–3997 |year=2000 |pmid=10858213 |doi=10.1128/IAI.68.7.3990-3997.2000 |pmc=101678}}</ref> There is also evidence that ''S. pneumoniae'' uses hydrogen peroxide as a virulence factor.<ref>{{cite journal |author=Mraheil, MA. |title=Dual Role of Hydrogen Peroxide as an Oxidant in Pneumococcal Pneumonia |journal=Antioxid Redox Signal |volume=20 |issue=34 |pages=962–978 |year=2021 |pmid=32283950|doi=10.1089/ars.2019.7964 |pmc=8035917}}</ref> 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 [[neutrophil]]s (a type of phagocyte) exposed to dead ''H. influenzae'' were more aggressive in attacking ''S. pneumoniae''.<ref name="PLosPathog2006-Lysenko">{{cite journal | vauthors=Lysenko ES, Ratner AJ, Nelson AL, Weiser JN | title=The Role of Innate Immune Responses in the Outcome of Interspecies Competition for Colonization of Mucosal Surfaces | journal=[[PLOS Pathogens|PLOS Pathog]] | year=2005 | pages=e1 | volume=1 | issue=1 | pmid=16201010 | doi=10.1371/journal.ppat.0010001 | pmc=1238736 | doi-access=free }} [https://archive.today/20130113064742/http://pathogens.plosjournals.org/perlserv/?request=get-document&doi=%2310.1371/journal.ppat.0010001#10.1371/journal.ppat.0010001 Full text]</ref>

== Diagnosis ==
[[File:S. pneumoniae.jpg|thumb|Optochin sensitivity in a culture of ''Streptococcus pneumoniae'' (white disk)]]
[[File:Diagnostic algorithm of possible bacterial infection.png|thumb|Example of a [[Medical test|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.]]
[[Medical 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.<ref>{{cite journal
  |title = Optochin Resistance in Streptococcus pneumoniae: Mechanism, Significance, and Clinical Implications
  |last1 = Pikis
  |first1 = Andreas
  |last2 = Campos
  |first2 = Joseph M.
  |last3 = Rodriguez
  |first3 = William J.
  |last4 = Keith
  |first4 = Jerry M.
  |journal = [[The Journal of Infectious Diseases]]
  |issn = 0022-1899
  |volume = 184
  |issue = 5
  |year = 2001
  |pages = 582–90
  |pmid = 11474432
  |doi = 10.1086/322803
  |jstor = 30137322
  |doi-access = free
  }}</ref>

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.<ref>{{Cite journal|last1=Salvà-Serra|first1=Francisco|last2=Connolly|first2=Gwendolyn|last3=Moore|first3=Edward R. B.|last4=Gonzales-Siles|first4=Lucia|date=2017-12-15|title=Detection of "Xisco" gene for identification of Streptococcus pneumoniae isolates|journal=Diagnostic Microbiology and Infectious Disease|volume=90|issue=4|pages=248–250|doi=10.1016/j.diagmicrobio.2017.12.003|issn=1879-0070|pmid=29329755|url=https://arrow.tudublin.ie/scschbioart/310 |url-access=subscription}}</ref>

[[Atromentin]] and leucomelone possess antibacterial activity, inhibiting the [[enzyme]] [[enoyl-acyl carrier protein reductase]], (essential for the [[fatty acid metabolism#Synthesis|biosynthesis]] of [[fatty acid]]s) in ''S. pneumoniae''.<ref name=Zheng2006>{{cite journal |vauthors=Zheng CJ, Sohn MJ, Kim WG |year=2006 |title=Atromentin and leucomelone, the first inhibitors specific to enoyl-ACP reductase (FabK) of ''Streptococcus pneumoniae'' |journal=Journal of Antibiotics |volume=59 |issue=12 |pages=808–12 |doi=10.1038/ja.2006.108 |pmid=17323650|doi-access=free }}</ref>

== Resistance ==
{{Main|Pneumococcal infection#Treatment}}
Resistant pneumococcal strains are called penicillin-resistant pneumococci ('''PRP'''),<ref>{{cite journal |last1=Nilsson |first1=P |last2=Laurell |first2=MH |title=Carriage of penicillin-resistant ''Streptococcus pneumoniae'' by children in day-care centers during an intervention program in Malmo, Sweden. |journal=The Pediatric Infectious Disease Journal |volume=20 |issue=12 |pages=1144–9 |pmid=11740321 |year=2001 |doi=10.1097/00006454-200112000-00010 }}</ref> penicillin-resistant ''Streptococcus pneumoniae'' ('''PRSP'''),<ref>{{cite journal |last1=Block |first1=SL |last2=Harrison |first2=CJ |last3=Hedrick |first3=JA |last4=Tyler |first4=RD |last5=Smith |first5=RA |last6=Keegan |first6=E |last7=Chartrand |first7=SA |title=Penicillin-resistant ''Streptococcus pneumoniae'' in acute otitis media: risk factors, susceptibility patterns and antimicrobial management. |journal=The Pediatric Infectious Disease Journal |volume=14 |issue=9 |pages=751–9 |pmid=8559623 |year=1995 |doi=10.1097/00006454-199509000-00005 }}</ref> ''Streptococcus pneumoniae'' penicillin resistant ('''SPPR''')<ref>{{cite journal |last1=Koiuszko |first1=S |last2=Bialucha |first2=A |last3=Gospodarek |first3=E |title=The drug susceptibility of penicillin-resistant ''Streptococcus pneumoniae''. |journal=Medycyna Doswiadczalna I Mikrobiologia |volume=59 |issue=4 |pages=293–300 |pmid=18416121 |year=2007 }}</ref> 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.<ref>{{cite web |title=Drug Resistance |url=https://www.cdc.gov/pneumococcal/drug-resistance.html |website=cdc.gov |access-date=17 February 2019}}</ref>

==See also==
* [[Transformation (genetics)]]
* [[Pneumococcal Awareness Council of Experts]]
* [[Facultative anaerobic organism]]

==References==
{{Reflist|2}}

==External links==
{{Commons category|Streptococcus pneumoniae}}
* [http://www.gavialliance.org GAVI Alliance] {{Webarchive|url=https://web.archive.org/web/20140820234029/http://www.gavialliance.org/ |date=2014-08-20 }}
* [http://www.preventpneumo.org PneumoADIP]
* [http://www.path.org/vaccineresources/pneumococcus.php PATH's Vaccine Resource Library pneumococcal resources]
* {{cite book |author=Centers for Disease Control and Prevention |chapter=Ch. 16: Pneumococcal Disease |chapter-url=https://www.cdc.gov/vaccines/pubs/pinkbook/pneumo.html |editor=Atkinson W |editor2=Wolfe S |editor3=Hamborsky J |title=Epidemiology and Prevention of Vaccine-Preventable Diseases |publisher=Public Health Foundation |location=Washington DC |year=2012 |edition=12th |url=https://www.cdc.gov/vaccines/pubs/pinkbook/table-of-contents.html |pages=233–248 |url-status=dead |archive-url=https://web.archive.org/web/20170310044843/https://www.cdc.gov/vaccines/pubs/pinkbook/table-of-contents.html |archive-date=2017-03-10 }}
* [http://bacdive.dsmz.de/index.php?search=14749&submit=Search Type strain of ''Streptococcus pneumoniae'' at Bac''Dive'' -  the Bacterial Diversity Metadatabase] {{Webarchive|url=https://web.archive.org/web/20200420161937/https://bacdive.dsmz.de/index.php?search=14749&submit=Search |date=2020-04-20 }}

{{Gram-positive bacterial diseases}}
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[[Category:Bacteria described in 1884]]
[[Category:Gram-positive bacteria]]
[[Category:Pathogenic bacteria]]
[[Category:Pneumonia]]
[[Category:Polysaccharide encapsulated bacteria]]
[[Category:Streptococcaceae]]