# Streptococcus pneumoniae

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Species of bacterium

Streptococcus pneumoniae S. pneumoniae in spinal fluid. FA stain (digitally colored). Scientific classification Domain: Bacteria Kingdom: Bacillati 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 [Gram-positive](/source/Gram-positive), spherical bacteria, [alpha-hemolytic](/source/Hemolysis_(microbiology)) member of the [genus](/source/Genus) *[Streptococcus](/source/Streptococcus)*.[1] *S. pneumoniae* cells are usually found in pairs ([diplococci](/source/Diplococci)) and do not form [spores](/source/Bacterial_morphological_plasticity) and are non motile.[2] As a significant human [pathogenic bacterium](/source/Pathogenic_bacterium) *S. pneumoniae* was recognized as a major cause of [pneumonia](/source/Pneumonia) in the late 19th century, and is the subject of many [humoral immunity](/source/Humoral_immunity) studies.[*[citation needed](https://en.wikipedia.org/wiki/Wikipedia:Citation_needed)*]

*Streptococcus pneumoniae* resides asymptomatically in healthy carriers, typically colonizing the respiratory tract, sinuses, and [nasal cavity](/source/Nasopharynx). However, in susceptible individuals with [weaker immune systems](/source/Immunocompromised), such as the elderly and young children, the bacterium may become [pathogenic](/source/Pathogen) and spread to other locations to cause disease. It spreads by direct person-to-person contact via [respiratory droplets](/source/Respiratory_droplet) and by auto-inoculation in persons carrying the bacteria in their upper respiratory tracts.[3] It can be a cause of [neonatal infections](/source/Neonatal_infection).[4]

*Streptococcus pneumoniae* is the main cause of [community acquired pneumonia](/source/Community_acquired_pneumonia) and [meningitis](/source/Meningitis) in children and the elderly,[5] and of [sepsis](/source/Sepsis) in those infected with [HIV](/source/HIV). The organism also causes many types of [pneumococcal infections](/source/Pneumococcal_infection) other than [pneumonia](/source/Pneumonia). These invasive pneumococcal diseases include [bronchitis](/source/Bronchitis), [rhinitis](/source/Rhinitis), [acute sinusitis](/source/Acute_sinusitis), [otitis media](/source/Otitis_media), [conjunctivitis](/source/Conjunctivitis), [meningitis](/source/Meningitis), sepsis, [osteomyelitis](/source/Osteomyelitis), [septic arthritis](/source/Septic_arthritis), [endocarditis](/source/Endocarditis), [peritonitis](/source/Peritonitis), [pericarditis](/source/Pericarditis), [cellulitis](/source/Cellulitis), and [brain abscess](/source/Brain_abscess).[6]

*Streptococcus pneumoniae* growth on blood agar.

*Streptococcus pneumoniae* can be differentiated from the [viridans streptococci](/source/Viridans_streptococci), some of which are also [alpha-hemolytic](/source/Hemolysis_(microbiology)), using an [optochin](/source/Optochin) test, as *S. pneumoniae* is optochin-sensitive. *S. pneumoniae* can also be distinguished based on its sensitivity to [lysis](/source/Lysis) by [bile](/source/Bile), the so-called "bile solubility test". The [encapsulated](/source/Bacterial_capsule), Gram-positive, [coccoid](/source/Coccus) bacteria have a distinctive morphology on Gram stain, [lancet](/source/Scalpel)-shaped diplococci. They have a [polysaccharide](/source/Polysaccharide) capsule that acts as a [virulence factor](/source/Virulence_factor) for the organism; more than 100 different [serotypes](/source/Serotype) are known[7] , and these types differ in [virulence](/source/Virulence), [prevalence](/source/Prevalence), and extent of [drug resistance](/source/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.[8] 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](/source/Pathogenesis#:~:text=In_pathology,_pathogenesis_is_the_to_its_progression_and_maintenance.), determining bacterial survival and likelihood of causing invasive disease.[9] Additionally, the CPS inhibits [phagocytosis](/source/Phagocytosis) by preventing [granulocytes](/source/Granulocyte)' access to the cell wall.[10]

## History

In 1881, the organism, known later in 1886 as the pneumococcus[11] for its role as a cause of pneumonia, was first isolated simultaneously and independently by the U.S. Army [physician](/source/Physician) [George Sternberg](/source/George_Miller_Sternberg)[12] and the French chemist [Louis Pasteur](/source/Louis_Pasteur).[13]

The organism was termed *Diplococcus pneumoniae* from 1920[14] because of its characteristic appearance in [Gram-stained](/source/Gram_stain) [sputum](/source/Sputum). It was renamed *Streptococcus pneumoniae* in 1974 because it was very similar to [streptococci](/source/Streptococcus).[11][15]

*Streptococcus pneumoniae* played a central role in demonstrating that genetic material consists of [DNA](/source/DNA). In 1928, [Frederick Griffith](/source/Frederick_Griffith) demonstrated [transformation](/source/Transformation_(genetics)) of life, turning harmless pneumococcus into a lethal form by co-inoculating the live pneumococci into a mouse along with heat-killed [virulent](/source/Virulent) pneumococci.[16] In 1944, [Oswald Avery](/source/Oswald_Avery), [Colin MacLeod](/source/Colin_Munro_MacLeod), and [Maclyn McCarty](/source/Maclyn_McCarty) demonstrated that the transforming factor in [Griffith's experiment](/source/Griffith's_experiment) was not [protein](/source/Protein), as was widely believed at the time, but DNA.[17] Avery's work marked the birth of the [molecular era of genetics](/source/Molecular_genetics).[18]

## Genetics

The [genome](/source/Genome) of *S. pneumoniae* is a closed, circular DNA structure that contains between 2.0 and 2.1 million [base pairs](/source/Base_pair) depending on the [strain](/source/Strain_(biology)). It has a core set of 1553 [genes](/source/Gene), plus 154 genes in its [virulome](https://en.wiktionary.org/wiki/virulome), which contribute to virulence, and 176 genes that maintain a noninvasive [phenotype](/source/Phenotype). Genetic information can vary up to 10% between strains.[19] The pneumococcal genome is known to contain a large and diverse repertoire of antimicrobial peptides, including 11 different [lantibiotics](/source/Lantibiotics).[20]

### 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](/source/Energy) and depends on the 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](/source/Exogenous_DNA) into its [chromosome](/source/Chromosome), it must enter a special physiological state called [competence](/source/Natural_competence).[21] Competence in *S. pneumoniae* is induced by DNA-damaging agents such as [mitomycin C](/source/Mitomycin_C), [fluoroquinolone](/source/Fluoroquinolone) [antibiotics](/source/Antibiotic) ([norfloxacin](/source/Norfloxacin), [levofloxacin](/source/Levofloxacin) and [moxifloxacin](/source/Moxifloxacin)), and [topoisomerase inhibitors](/source/Topoisomerase_inhibitor).[22] Transformation protects *S. pneumoniae* against the bactericidal effect of mitomycin C.[23] Michod et al.[24] summarized evidence that induction of competence in *S. pneumoniae* is associated with increased resistance to [oxidative stress](/source/Oxidative_stress) and increased expression of the RecA protein, a key component of the [recombinational repair](/source/Recombinational_repair) machinery for removing [DNA damage](/source/DNA_damage). Based on these findings, they suggested that transformation is an adaptation for repairing oxidative DNA damage. *S. pneumoniae* infection stimulates [polymorphonuclear leukocytes](/source/Granulocyte) (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.[25] reported that, among different highly transformable *S. pneumoniae* isolates, nasal colonization fitness and virulence (lung infectivity) depend on an intact competence system.

## Infection

Main article: [Pneumococcal infection](/source/Pneumococcal_infection)

*Streptococcus pneumoniae* is part of the normal [upper respiratory tract](/source/Upper_respiratory_tract) [flora](/source/Human_microbiome). As with many natural flora, it can become pathogenic under the right conditions, typically when the host's immune system is [suppressed](/source/Immunosuppression). [Invasins](/source/Invasins), such as [pneumolysin](/source/Pneumolysin), an anti[phagocytic](/source/Phagocytic) [capsule](/source/Bacterial_capsule), various [adhesins](/source/Bacterial_adhesin), and [immunogenic](/source/Immunogenic) [cell wall components](/source/Bacterial_cell_structure) are all major [virulence factors](/source/Virulence_factors). After *S. pneumoniae* colonizes the [air sacs](/source/Pulmonary_alveolus) of the [lungs](/source/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.[26]

*S. pneumoniae* undergoes spontaneous [phase variation](/source/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.[27] 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 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.[29] 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, shallow breathing and can affect a person's ability to sleep, cause chest pain, and decrease appetite.[30]

While different bacterial infections can cause meningitis, S. pneumoniae is a leading cause. Pneumococcal meningitis occurs when the bacteria spread from the bloodstream 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, limb removal, or death.[31] 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.[32]

An overwhelming response to an infection that causes tissue damage causes sepsis, which can lead to [organ failure](/source/Organ_failure), and even death. The symptoms include confusion, shortness of breath, elevated heart rate, pain or discomfort, overperspiration, fever, shivering, or feeling cold.[33][34]

Less severe illnesses that can be caused by pneumococcal infection include conjunctivitis (pink eye ), otitis media (middle ear infection), Bronchitis (airway inflammation), and sinusitis (sinus infection).[35]

## Vaccine

Main article: [Pneumococcal vaccine](/source/Pneumococcal_vaccine)

Due to the importance of disease caused by *S. pneumoniae*, several [vaccines](/source/Vaccine) have been developed to protect against invasive infection. The [World Health Organization](/source/World_Health_Organization) recommends routine childhood pneumococcal vaccination;[36] it is incorporated into the childhood immunization schedule in a number of countries including the United Kingdom,[37] the United States,[38] Greece,[39] and South Africa.[40]

Currently, two vaccines are available for S. pneumoniae: the pneumococcal polysaccharide vaccine (PPV23 or PPSV23) 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.[41] PPSV23 offers [T-cell](/source/T_cell)-independent immunity and requires revaccination 5 years after the first vaccination because of its temporary nature.[42] PCV13 was developed after determining PPSV23's low efficacy in children and infants. PCV13 elicits a T-cell-dependent response and provides enduring immunity by promoting interaction between [B](/source/B_cell) and T cells, leading to an enhanced, prolonged immune response; it is most effective in young children.[42]

## Biotechnology

Components from *S. pneumoniae* have been harnessed for a range of biotechnology applications. Through engineering of surface molecules from this bacterium, proteins can be irreversibly linked using the [sortase](/source/Sortase) enzyme[43] or using the SnoopTag/SnoopCatcher reaction.[44] Various [glycoside hydrolases](/source/Glycoside_hydrolases) have also been cloned from *S. pneumoniae* to help analysis of cell [glycosylation](/source/Glycosylation).[45]

## Interaction with *Haemophilus influenzae*

Historically, *[Haemophilus influenzae](/source/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](/source/In_vitro)* revealed *S. pneumoniae* overpowered *H. influenzae* by attacking it with [hydrogen peroxide](/source/Hydrogen_peroxide).[46] There is also evidence that *S. pneumoniae* uses hydrogen peroxide as a virulence factor.[47] However, in a study adding both bacteria to the [nasal cavity](/source/Nasal_cavity) of a [mouse](/source/Mouse) within two weeks, only *H. influenzae* survives; further analysis showed that [neutrophils](/source/Neutrophil) (a type of phagocyte) exposed to dead *H. influenzae* were more aggressive in attacking *S. pneumoniae*.[48]

## Diagnosis

Optochin sensitivity in a culture of *Streptococcus pneumoniae* (white disk)

Example of a [workup algorithm](/source/Medical_test) 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](/source/Medical_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](/source/Optochin) sensitive, although optochin resistance has been observed.[49]

The recent advances in next-generation sequencing and [comparative genomics](/source/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.[50]

[Atromentin](/source/Atromentin) and leucomelone possess antibacterial activity, inhibiting the [enzyme](/source/Enzyme) [enoyl-acyl carrier protein reductase](/source/Enoyl-acyl_carrier_protein_reductase), (essential for the [biosynthesis](/source/Fatty_acid_metabolism#Synthesis) of [fatty acids](/source/Fatty_acid)) in *S. pneumoniae*.[51]

## Resistance

Main article: [Pneumococcal infection § Treatment](/source/Pneumococcal_infection#Treatment)

Resistant pneumococcal strains are called penicillin-resistant pneumococci (**PRP**),[52] penicillin-resistant *Streptococcus pneumoniae* (**PRSP**),[53] *Streptococcus pneumoniae* penicillin resistant (**SPPR**)[54] 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.[55]

Beyond penicillin*, S. pneumoniae* also demonstrates high resistance to other antibiotic classes, including [macrolides](/source/Macrolide) (such as [erythromycin](/source/Erythromycin)), [lincosamides](/source/Lincosamides) (such as [clindamycin](/source/Clindamycin)), and [tetracyclines](/source/Tetracycline_antibiotics), as reported in a study of Chinese isolates.[56] However, novel antibiotics such as [eravacycline](/source/Eravacycline), [omadacycline](/source/Omadacycline), [contezolid](/source/Contezolid), and [nemonoxacin](/source/Nemonoxacin) have exhibited considerable in vitro antimicrobial activity against *S. pneumoniae*.

*S. pneumoniae*'s higher sensitivity to eravacycline and omadacycline compared to previous generations of tetracyclines is due to structural modifications in these antibiotics that enhance target binding and reduce recognition. Tetracycline resistance in *S. pneumoniae* is associated with mutations in *tet* genes as well as *rpsJ* and *rpsC* genes.[56]

[Fluoroquinolones](/source/Quinolone_antibiotic) such as nemonoxacin are an effective treatment for [community-acquired pneumonia](/source/Community-acquired_pneumonia) (CAP) and resistance in *S. pneumoniae* is relatively low; resistance may be acquired through point mutations in resistance genes *gyrA*, *gyrB*, *parC*, *parE*, *patA*, and *patB*.[56]

[Oxazolidinones](/source/Oxazolidinone), such as Contezolid, show in vitro efficacy against many Gram-positive cocci. Oxazolidinone resistance in *S. pneumoniae* is associated with mutations in the [peptidyl transferase](/source/Peptidyl_transferase_center) central loop of the ribosomal [23S rRNA](/source/23S_ribosomal_RNA) domain V.[56]

## See also

- [Transformation (genetics)](/source/Transformation_(genetics))

- [Pneumococcal Awareness Council of Experts](/source/Pneumococcal_Awareness_Council_of_Experts)

- [Facultative anaerobic organism](/source/Facultative_anaerobic_organism)

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## External links

Wikimedia Commons has media related to [Streptococcus pneumoniae](https://commons.wikimedia.org/wiki/Category:Streptococcus_pneumoniae).

- [GAVI Alliance](http://www.gavialliance.org) [Archived](https://web.archive.org/web/20140820234029/http://www.gavialliance.org/) 2014-08-20 at the [Wayback Machine](/source/Wayback_Machine)

- [PneumoADIP](http://www.preventpneumo.org)

- [PATH's Vaccine Resource Library pneumococcal resources](http://www.path.org/vaccineresources/pneumococcus.php)

- Centers for Disease Control and Prevention (2012). ["Ch. 16: Pneumococcal Disease"](https://web.archive.org/web/20170310044843/https://www.cdc.gov/vaccines/pubs/pinkbook/table-of-contents.html). In Atkinson W, Wolfe S, Hamborsky J (eds.). [*Epidemiology and Prevention of Vaccine-Preventable Diseases*](https://www.cdc.gov/vaccines/pubs/pinkbook/table-of-contents.html) (12th ed.). Washington DC: Public Health Foundation. pp. 233–248. Archived from [the original](https://www.cdc.gov/vaccines/pubs/pinkbook/pneumo.html) on 2017-03-10.

- [Type strain of *Streptococcus pneumoniae* at Bac*Dive* - the Bacterial Diversity Metadatabase](http://bacdive.dsmz.de/index.php?search=14749&submit=Search) [Archived](https://web.archive.org/web/20200420161937/https://bacdive.dsmz.de/index.php?search=14749&submit=Search) 2020-04-20 at the [Wayback Machine](/source/Wayback_Machine)

v t e Bacillota (low-G+C) Infectious diseases Bacterial diseases: G+ Bacilli Lactobacillales (Cat-) Streptococcus α optochin susceptible S. pneumoniae Pneumococcal infection optochin resistant Viridans streptococci: S. mitis S. mutans S. oralis S. sanguinis S. sobrinus S. anginosus group β A bacitracin susceptible: S. pyogenes Group A streptococcal infection Streptococcal pharyngitis Scarlet fever Erysipelas Rheumatic fever B bacitracin resistant, CAMP test+: S. agalactiae Group B streptococcal infection ungrouped Streptococcus iniae Cutaneous Streptococcus iniae infection γ D BEA+: Streptococcus bovis Enterococcus BEA+: Enterococcus faecalis Urinary tract infection Enterococcus faecium Bacillales (Cat+) Staphylococcus Cg+ S. aureus Staphylococcal scalded skin syndrome Toxic shock syndrome MRSA Cg- novobiocin susceptible S. epidermidis novobiocin resistant S. saprophyticus Bacillus Bacillus anthracis Anthrax Bacillus cereus Food poisoning Listeria Listeria monocytogenes Listeriosis Clostridia Clostridium (spore-forming) motile: Clostridium botulinum Botulism Clostridium tetani Tetanus nonmotile: Clostridium perfringens Gas gangrene Clostridial necrotizing enteritis Clostridioides (spore-forming) Clostridioides difficile [Clostridium difficile] Pseudomembranous colitis Finegoldia (non-spore forming) Finegoldia magna Mollicutes Mycoplasmataceae Ureaplasma urealyticum Ureaplasma infection Mycoplasma genitalium Mycoplasma pneumoniae Mycoplasma pneumonia Anaeroplasmatales Erysipelothrix rhusiopathiae Erysipeloid

Taxon identifiers Streptococcus pneumoniae Wikidata: Q221179 Wikispecies: Streptococcus pneumoniae BacDive: 14749 CoL: 52Y4L EoL: 974503 EPPO: STRCPN GBIF: 3227089 iNaturalist: 1066670 IRMNG: 10033301 ITIS: 966484 LPSN: streptococcus-pneumoniae NCBI: 1313 NZOR: 5ad242c7-8276-415a-b117-5318292d35a9 Open Tree of Life: 699152 SeqCode Registry: 20045

Authority control databases International GND National United States France BnF data Czech Republic Spain Latvia Israel Other Yale LUX

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Adapted from the Wikipedia article [Streptococcus pneumoniae](https://en.wikipedia.org/wiki/Streptococcus_pneumoniae) by Wikipedia contributors ([contributor history](https://en.wikipedia.org/wiki/Streptococcus_pneumoniae?action=history)). Available under [Creative Commons Attribution-ShareAlike 4.0 International](https://creativecommons.org/licenses/by-sa/4.0/). Changes may have been made.