Streptococcus pneumoniae, or pneumococcus, is a Gram-positive,
alpha-hemolytic (under aerobic conditions) or beta-hemolytic (under
anaerobic conditions), facultative anaerobic member of the genus
Streptococcus. They are usually found in pairs (diplococci) and do
not form spores and are non-motile. 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
S. pneumoniae resides asymptomatically in healthy carriers typically
colonizing the respiratory tract, sinuses, and nasal cavity. However,
in susceptible individuals with 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
autoinoculation in persons carrying the bacteria in their upper
respiratory tract. It can be a cause of neonatal infections.
S. pneumoniae is the main cause of community acquired pneumonia and
meningitis in children and the elderly, and of septicemia in those
infected with HIV. The organism also causes many types of pneumococcal
infections 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
S. 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,
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 90 different serotypes
are known, and these types differ in virulence, prevalence, and extent
of drug resistance.
4 Diseases and Symptoms
6 Interaction with Haemophilus influenzae
8 See also
10 External links
In 1881, the organism, known later in 1886 as the pneumococcus for
its role as a cause of pneumonia, was first isolated simultaneously
and independently by the U.S. Army physician George Sternberg and
the French chemist Louis Pasteur.
The organism was termed Diplococcus pneumoniae from 1920 because
of its characteristic appearance in Gram-stained sputum. It was
Streptococcus pneumoniae in 1974 because it was very similar
S. pneumoniae played a central role in demonstrating that 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. In 1944 Oswald Avery, Colin
Maclyn McCarty demonstrated the transforming factor in
Griffith's experiment was not protein, as was widely believed at the
time, but DNA. Avery's work marked the birth of the molecular era
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
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. 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.
Competence in S. pneumoniae is induced by DNA-damaging agents such as
mitomycin C, fluoroquinolone antibiotics (norfloxacin, levofloxacin
and moxifloxacin), and topoisomerase inhibitors. Transformation
protects S. pneumoniae against the bactericidal effect of mitomycin
C. Michod et al. 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
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 the
DNA damages in its genome, caused by this host defense,
likely contributes to this pathogen’s virulence. Consistent with
this premise Li et al. reported that, among different highly
transformable S. pneumoniae isolates, nasal colonization fitness and
virulence (lung infectivity) depend on an intact competence system.
Main article: Pneumococcal infection
S. pneumoniae is part of the normal upper respiratory tract flora. As
with many natural flora it can become pathogenic under the right
conditions, typically when 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. After S. pneumoniae colonizes the 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 pneumonia. It is susceptible to
Diseases and Symptoms
Pneumonia is the most common and most serious of the S. pneumoniae
diseases which include symptoms like fever and chills, cough, rapid
breathing, difficulty breathing, chest pain. For the elderly they may
include confusion, low alertness, and less of the former listed
Pneumococcal meningitis is an infection of the tissue covering the
brain and spinal cord. Symptoms include: stiff neck, fever, headache,
confusion and photophobia.
Sepsis is caused by overwhleming 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.
Main article: Pneumococcal vaccine
Due to the importance of disease caused by S. pneumoniae several
vaccines have been developed to protect against invasive infection.
World Health Organization
World Health Organization recommend routine childhood pneumococcal
vaccination; it is incorporated into the childhood immunization
schedule in a number of countries including the United Kingdom,
United States, and South Africa.
Interaction with Haemophilus influenzae
Haemophilus influenzae (H. 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. However, in a
study adding both bacteria to the nasal cavity of a mouse within 2
weeks only H. influenzae survives; further analysis showed that
neutrophils exposed to dead H. influenzae were more aggressive in
attacking S. pneumoniae.
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. S. pneumoniae is, in
general, optochin sensitive, although optochin resistance has been
The recent advances in next-generation sequencing (NGS) 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.
Atromentin and leucomelone possess antibacterial activity, inhibiting
the enzyme enoyl-acyl carrier protein reductase, (essential for the
biosynthesis of fatty acids) in S. pneumoniae. Optochin
sensitivity in a culture of
Pneumococcal Awareness Council of Experts
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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.
Type strain of
Streptococcus pneumoniae at
BacDive - the Bacterial
Firmicutes (low-G+C) Infectious diseases
Bacterial diseases: G+
primarily A00–A79, 001–041, 080–109
Viridans streptococci: S. mitis
bacitracin susceptible: S. pyogenes
Group A streptococcal infection
bacitracin resistant, CAMP test+: S. agalactiae
Group B streptococcal infection
Streptococcus iniae infection
Urinary tract infection
Staphylococcal scalded skin syndrome
Toxic shock syndrome
Clostridial necrotizing enteritis
Peptostreptococcus (non-spore forming)