Intended Learning Outcome (ILO) of this study
At the end of this lecture you will be able to describe:
morphological and cultural properties and classification of Streptococci
pyogenes,
virulence factors, pathogenesis, clinical manifestations of Streptococci pyogenes
diagnosis, prevention and treatment of infections caused by streptococci
Streptococci
The streptococci are gram-positive, nonmotile, and
catalase negative spherical bacteria that characteristically
form pairs or chains during growth. They are widely
distributed in nature. Some are members of the normal
human flora; others are associated with important human
diseases attributable in part to infection by streptococci, in
part to sensitization to them. Streptococci elaborate a
variety of extracellular substances and enzymes.
II. CLASSIFICATION OF STREPTOCOCCI
Streptococci can be classified by several schemes, for
example, by the hemolytic properties of the organisms,
and according to the presence of specific surface antigens
determined by immunologic assays.
A. Hemolytic properties on blood agar
-Hemolytic streptococci cause a chemical change in the hemo-globin of red cells in
blood agar, resulting in the appearance of a green pigment that forms a ring around the
colony (see Figure 9.16).
β-Hemolytic streptococci cause gross lysis of red blood cells, resulting in a clear ring
around the colony (see Figure 9.16).
γ-Hemolytic is a term applied to streptococci that cause no color change or lysis of red
blood cells. The traditional division of streptococci based on the ability of the bacterial
colony to hemolyze erythrocytes in the blood agar medium is still considered the first
step in the classification of streptococci.
B. Serologic (Lancefield) groupings
Many species of streptococci have a polysaccharide in their cell walls known as C-
substance, which is antigenic and easily extractable with dilute acid. The Lancefield
scheme classifies primarily β-hemolytic streptococci into groups A through U on the
basis of their C-sub stance. The clinically most important groups of β-hemolytic
streptococci are Types A and B (Figure 9.2). Commercial kits in which group-specific
antisera are coupled to latex beads are now widely used for identification of β-hemolytic
streptococci.
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Hemolysis on blood agar Lancefield’s Grouping Virulence factors
system
III. GROUP A -HEMOLYTIC STREPTOCOCCI
Streptococcus pyogenes
Streptococcus pyogenes is carried asymptomatically in the pharynx of 5–30% of the
population, more commonly in children. It is transmitted by the aerosol route and by
contact. It can invade apparently intact skin or mucous membranes, causing some of
the most rapidly progressive infections known.
Pathogenesis
S. pyogenes cells, perhaps in an inhaled droplet, attach to the pharyngeal mucosa via
actions of protein F, lipoteichoic acid, and M protein. The bacteria may simply replicate
sufficiently to maintain themselves without causing injury in which case the patient is
then considered colonized. Alternatively, bacteria may grow and secrete toxins, causing
damage to surrounding cells, invading the mucosa, and eliciting an inflammatory
response with attendant influx of white cells, fluid leakage, and pus formation. The
patient then has streptococcal pharyngitis. Occasionally, there is sufficient spread that
the bloodstream is significantly invaded, possibly resulting in septicemia and/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.
Figure 9.4 Cytolytic toxins and other exoenzymes produced by Streptococcus
pyogenes
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D. Clinical significance
S. pyogenes is a major cause of cellulitis. Other more specific syndromes include:
1. Acute pharyngitis or pharyngotonsilitis: Pharyngitis is the most common type of
S. pyogenes infection. S. pyogenes pharyngitis (“strep throat”) is associated with
severe, purulent inflammation of the posterior oropharynx and tonsillar areas (see
Figure 9.16).
2. Impetigo: it can cause severe and extensive lesions on the face and limbs (see
Figure 9.16).
3. Erysipelas: Affecting all age groups, patients with erysipelas experience a fiery red,
advancing erythema, especially on the face or lower limbs (see Figure 9.16).
4. Puerperal sepsis: This infection is initiated during or following soon after, the
delivery of a newborn.
5. Invasive group A streptococcal disease: Patients may have a deep local invasion
either without necrosis (cellulitis) or with it (necrotizing fasciitis/myositis) as shown in
Figure 9.5.
6. Streptococcal toxic shock syndrome: This syndrome is defined as isolation of
group A β-hemolytic streptococci from blood or another normally sterile body site in the
presence of shock and multiorgan failure. The syndrome is mediated by the production
of streptococcal pyrogenic exotoxins that function as superantigens causing massive,
nonspecific T-cell activation and cytokine release.
7. Post-streptococcal sequelae
a. Acute rheumatic fever: This autoimmune disease occurs 2 to 3 weeks after the
initiation of pharyngitis. It is caused by cross reactions between antigens of the heart
and joint tissues, and the streptococcal antigen (especially the M protein epitopes).
b. Acute glomerulonephritis: This rare, postinfectious sequel occurs as soon as 1
week after impetigo or pharyngitis ensues, due to a few nephritogenic strains of group A
streptococci.
E. Laboratory identification
Rapid latex antigen kits for direct detection of group A streptococci in patient samples
are widely used. In a positive test, the latex particles clump together, whereas in a
negative test, they stay separate, giving the suspension a milky appearance (Figure
9.6).
F. Treatment
Antibiotics are used for all group A streptococcal infections. S. pyogenes has not
acquired resistance to penicillin G, which remains the antibiotic of choice for acute
streptococcal disease. In a penicillin allergic patient, a macrolide such as clarithromycin
or azithromycin is the preferred drug (see Figure 9.16).
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Other features are:
toxins are important in their pathogenicity:
erythrogenic toxin associated with scarlet fever;
pyrogenic exotoxins A, B and C associated with toxic shock;
production of S. pyogenes cell envelope proteinase (SpyCEP), which degrades
IL-8 and other cytokines, thereby retarding neutrophil activation;
ability to invade and survive intracellularly making them difficult to eradicate with
penicillin;
production of degrading enzymes (immunoglobulin proteases, hyaluronidase and
collagenases).