Streptococcus pneumoniae is a
Gram-positive, non-spore-forming, non-motile,
lancet-shaped coccus anaerobe and a member of
the Streptococcaceae family of bacteria (Figure
1). This organism has a capsule comprised of
peptidoglycan and teichoic acid that protecting
it from complement C3b opsonization, and is
Choline residues that make-up teichoic acid
lipoteichoic acid found on the cell wall allow
the bacterium to adhere to choline-binding
receptors on human cells. Choline-binding
receptors are located on cells found throughout
the whole body, thus permitting S.
pneumoniae bacteria to effortlessly enter
targeted areas. Individual bacteria are between
0.5 and 1.25 µm (micrometres) in diameter, and
are found normally in the upper respiratory
tract, including the throat and nasal passages.
They are mesophillic, living optimally at
temperatures between 30°C
Figure 1. An
electron micrograph of nonencapsulated
Streptococcus pneumoniae bacteria [Bar: 1
The difference between S.
pneumoniae and other species of the
Streptococcus genus is that they lack
This pathogen also ferments glucose to lactic
acid, and chemically hydrolyzes insulin. S.
pneumoniae genome is a closed circular DNA
containing 2 to 2.1 million base pairs.
Colonization occurs when the pathogen engages
with the host, proliferates, and attempts to
invade the lower airways. When this occurs, the
host deploys innate, cell-mediated, and humoral
defense mechanisms to prevent the pathogen from
entering past tissue barriers. If colonization
is successful, it will be carried throughout the
nasopharynx for up to four to six weeks.
The pathogenicity of S. pneumoniae has
been attributed to various structures, most of
which are situated on its surface. S.
pneumoniae contains more than 500 different
surface proteins. A notable group is the family
of choline-binding proteins, and among these
proteins are found important determinants of
virulance, including pneumococcal surface
protein (PspA), autolysins (LytA, LytB, and
LytC), and adhesin (CbpA). Other factors,
including cell wall components and the
intracellular toxin pneumolysin, are involved
mainly in the inflammation caused by infection.
The inflammation process probably fully develops
only after lysis of bacteria by autolysin. Since
inflammation is thought to induce most of the
symptoms of pneumococcal disease, this group of
virulence factors may thus be more directly
responsible for the morbidity and mortality
caused by this pathogen once bacteria have
infected the host.
et al., 1995).
Since the amount of hydrogen peroxide produced
by S. pneumoniae is similar to that
produced by activated neutrophils, this oxidant
might be involved in the pathogenesis of this
organism by causing lung injury.
Virulence: The capsule works by
preventing the activation of the alternative
complement pathway and by resisting
phagocytosis. The cell wall, not to be confused
with capsule, plays a role in inflammation; it
activates the alternative complement pathway,
resulting in anaphylatoxin production. It also
enhances vascular permeability, mast cell
degranulation, and polymorphonuclear leukocyte
activation. It induces the
generation of interluekin-1 (IL-1), which is
cytopathic for endothelium, and is a mediator of
attachment to endothelial cells. Pneumolysins
are cytolytic at high concentrations; they
inhibit ciliary movement and disruption of
epithelium, inhibit of bactericidal activity of
lymphocyte proliferation, and antibody
synthesis. Furthermore, autolysins produced by
S. pneumoniae release pneumolysin and
cell wall products, while peptide permeases
enhance adhesion of the bacterium to the target
cell. Finally, complement factor H-binding
component inhibits complement activation and
et al., 1995).
infection can lead to the inflammation of the
sinus, brain, heart, or the whole body (sepsis).
It can also cause repeated ear infections
(otitis media), meningitis, infection of the
bone marrow, or even death, especially since
there are multiple antibiotic-resistant S.
pneumoniae stains. The transmission of this
organism is person to person. Those most
susceptible to infection are either very young,
very old or are immunocompromised (people with
AIDS or cancer). Persons most at increased risk
are those who are present in child-care centers,
old age homes and those who use antimicrobial
agents. The main disease caused by S.
pneumonia. Pneumonia can be
broken down into two forms, namely, bronchial
and lobar. Bronchial pneumoniae is prevalent in
infants, children, and aged adults. Lobar
pneumoniae, involving a single lobe, or section,
of a lung, occurs mainly in younger adults. The
majority of lobar pneumonia cases are caused by
Streptococcus species. One of the
ongoing issues of this disease is that it occurs
mainly in children less than the age of two
because of their lack of immunity. The main
study today is to accomplish making a vaccine
for under the age of two to prevent
life-threatening infections cause by S.
pneumoniae, since it is one of the leading
Alonso DeVelasco, E., Verheul, A.F.M., et al.
(1995). Streptococcus pneumoniae:
Virulence Factors, Pathogenesis, and Vaccines.
Microbiological Reviews, 59(4):