Streptococci
Streptococci are G+ve, non motile, & catalase-negative. Clinically
important genera include Streptococcus & Enterococcus. They are ovoid
to spherical in shape, & occur as pairs or chains. Because of their
complex nutritional requirements, blood-enriched medium is generally
used for their isolation. Streptococcus forms part of the normal flora of
man & animals. Some species (S.pyogenes) are important human
pathogens causing pyogenic infections.
Classification
1-Hemolytic classification
α- hemolytic streptococci cause a chemical change in the hemoglobin of
red cells in blood agar, resulting in the appearance of green pigment that
forms a ring around the colony. β - hemolytic streptococci cause gross
lysis of red blood cells, resulting in a clear ring around the colony. Two
types of β – hemolysins are released. Streptolysin O (inactivated by
atmospheric oxygen) is demonstrable only in deep colonies while
Streptolysin S ( oxygen stable) is responsible for surface colony
haemolysis.
γ- hemolytic is a term applied to streptococci that cause no color change
or lysis of red blood cells.
There are two important antigens of beta-hemolytic streptococci:
a) C- carbohydrate determines the group of β - hemolytic
streptococci. It is located in the cell wall, & its specificity is
determined by an amino sugar.
b) M protein is the most important virulence factor & determines the
type of group A β - hemolytic streptococci. It protrudes from the
outer surface of the cell & interferes with ingestion by phagocytes
(antiphagocytic). There are approximately 80 Grifith serotypes
based on the M protein, which explains why multiple infections
with S.pyogenes that produce certain M protein types are
rheumatogenic ( cause primarily rheumatic fever ), whereas strains
of
S.pyogenes that produce other M protein types are
nephritogenic (cause primarily acute glomerulonephritis).
Although M protein is the main antiphagocytic component of
S.pyogenes, the org also has a polysaccharide capsule that play a
role in retarding phagocytosis.
2-Serological classification (Lancefield)
Many species of streptococci have a polysaccharide in their cell walls
known as C- carbohydrate. The Lancefield scheme classifies primarily β -
hemolytic streptococci into groups A-U on the basis of their Ccarbohydrate. The clinically most important groups of β - hemolytic
streptococci are types A & B.
3-Classification based on Schleifer & Kilpper-Balz
This classification depend on the basis of structure of the cell wall
peptidoglycan together with the G+C content of the DNA & the results of
DNA pairing. They have divided the genus Streptococcus into sex
groups.
a)
b)
c)
d)
e)
f)
Pyogenic streptococci – S.pyogenes
Pneumococci – S.pneumoniae
Oral streptococci – S.mutans
Enterococci – S. faecalis
Lactic streptococci – S.lactice
Other streptococci – S.bovis
Group A β-hemolytic streptococci
S.pyogenes, the most clinically important member of this group of gram
positive cocci, is one of the most frequently encountered bacterial
pathogens of humans worldwide. It can invade apparently intact skin or
mucous membranes, causing some of the most rapidly progressive
infections known. A low inoculum suffices for infection. The growth of
S.pyogenes is inhibited by antibiotic bacitracin, an important diagnostic
criterion.
Structure
1-Capsule (antiphagocytic)
2-Cell wall
a)Fimbriae: the fimbriae contain the major S.pyogenes virulence factor,
M protein.
b)Group A-specific C-carbohydrate
c)Protein F ( fibronectin- binding protein)
3-Extracellular products
Epidemiology
The only reservoir for S.pyogenes in nature is the skin & mucous
membranes of the human host. Respiratory droplets or skin contact
spread Group A streptococcal infection from person to person, especially
in crowded environments such as classrooms or children's play area.
Pathology
S.pyogenes cells, perhaps in an inhaled droplet, attach to the pharyngeal
mucosa via actions of protein F, lipoteichoic acid, & M protein. The
bacteria may simply colonize; the patient is then considered colonized.
Alternatively, bacteria may grow & secrete toxins, causing damage to
surrounding cells, invading the mucosa, and eliciting an inflammatory
response with attendant influx of white cells, fluid leakage, & pus
formation. The patient then has streptococcal pharyngitis. Occasionally,
there is sufficient spread that the blood stream is significantly invaded,
possibly resulting in septicemia &/or seeding of distant sites, where
cellulitis (acute inflammation of subcutaneous tissue), fasciitis
(inflammation of the tissue under the skin that covers a surface of
underlying tissue), or myonecrosis (death of muscle cells) may develop
rapidly or insidiously.
Clinical findings
1-Pyogenic diseases
a-Sore throat ( acute tonsillitis/ & pharyngitis) is the commonest of
streptococcal diseases. The org may spread to surrounding tissue
causing complication like otitis media, mastoiditis,sinusitis,
meningitis,
peritonitis & pneumonia.
b-Skin infection
Local infections in superficial layers of skin due to S.pyogenes
include impetigo & erysipelas.
c-Other pyogenic diseases
* puerperial sepsis ( postpartum infection of uterus).
*Sepsis: Infection of wounds, burns, chronic skin lesion (eczema,
psoriasis).
*Lymphadenitis, septicaemia, acute endocarditis, abscess in internal
organs (brain, liver, lung, & kidney).
2- Toxigenic diseases
a-Scarlet fever
Scarlet fever occurs as a complication of streptococcal infection
(sore throat) when the infecting strain produces erythrogenic toxin &
the patient has got no antitoxic immunity.
b- Streptococcal toxic shock syndrome
This syndrome is mediated by pyrogenic exotoxins that function as
superantigens causing massive, nonspecific T- cell activation &
cytokines release. It is similar to staphylococcal toxic shock
syndrome.
.
3-Immunogenic diseases ( non suppurative infection)
a- Acute glomerulonephritis(AGN): This rare, postinfectious sequela
occur as soon as one week after impetigo or pharyngitis ensues, due to a
few nephritogenic strains of group A streptococci.
Antigen-antibody complexes on the basement membrane of the
glomerulus initiate the disease. The most clinical features are
hypertension, edema of the face and ankles, & smoky urine (due to red
cells in the urine).
b-Acute rheumatic fever: this autoimmune disease occurs two to three
weeks after the initiation of pharyngitis. It is caused by cross reactions
between antigens of the heart & joint tissues, & the streptococcal antigen
(especially the M protein epitopes). It is characterized by fever, rash,
carditis, & arthritis.
Lab. Diagnosis
1-Specimen: Throat swab, pus& lesion samples, sputum, blood , spinal
fluid
2-Smear: G+ve cocci in chains or pairs are found association with pus
cells.
3-culture: Specimen should be inoculated immediately. Specimen is
inoculated in the blood agar medium & incubated at 37C ْ for overnight.
Hemolysis develops better under anaerobic conditions or under 5-10%
CO2. The bacterial colonies are small, dry & surrounded by β-hemolysis.
A simple technique of detection of S.pyogenes ( group A) is done by
agar plate test using paper discs impregnated with bacitracin. S.pyogenes
is more sensitive to bacitracin than other streptococci. S.pyogenes can be
rapidly identified by fluoruesent antibody technique.
4-Antigen detecting tests: ELISA, agglutination tests
5-Serological tests: test for streptococcal antibodies is not helpful in
diagnosing acute infection which may be used to identify & confirm
primary infection. They are more commonly used to diagnose non
suppurative complications.
Treatment
S.pyogenes has not acquired resistance to penicillin G, which remains
the antibiotic of choice for acute streptococcal disease. In a pencillin
allergic patient , Macrolide such as clarithromycin is the preferred drug.
Pencillin G plus clindamycin are used in treating streptococcal toxic
shock syndrome.