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STREPTOCOCCUS
Dr, Ayman Shahzad
MBBS, M.Phil.
Diseases
S. pyogenes(group A streptococcus) is the leading bacterial
cause of pharyngitis and cellulitis immunologic diseases,
namely, rheumatic fever and acute glomerulonephritis.
Streptococcus agalactiae (group B streptococcus) is the
leading cause of neonatal sepsis and meningitis.
Enterococcus faecalis is an important cause of hospital
acquired urinary tract infections and endocarditis.
Viridans group streptococci are the most common cause of
endocarditis .
Streptococcus bovis also causes endocarditis
Important
Properties
All streptococci are catalase-negative.
One of the most important characteristics for identification of
streptococci is the type of hemolysis.
Hemolytic streptococci form a green zone around their
colonies as a result of incomplete lysis of red blood cells in
the agar. The green color is formed when hydrogen peroxide
produced by the bacteria oxidizes hemoglobin (red color) to
biliverdin (green color).
β-Hemolytic streptococci form a clear zone around their
colonies because complete lysis of the red cells
➢ -streptococcus
➢ -hemolytic streptococcus/
Oppathogensportunistic
➢ -hemolytic/pyogenic
streptococcus
Important
Properties
β-Hemolysis is due to the production of enzymes (hemolysins)
called streptolysin O and streptolysin S .
Some streptococci are nonhemolytic (γ-hemolysis).
There are two important antigens of β-hemolytic streptococci:
C carbohydrate determines the group of β-hemolytic
streptococci. It is located in the cell wall, and its specificity is
determined by an amino sugar.
M protein is the most important virulence factor It protrudes
from the outer surface of the cell and interferes with ingestion
by phagocytes
* M-protein :
◆Anti-phagocytotic
◆Common antigen -- heart muscle cell, glomerular basement membrane
cells, etc.
◆M Ag-Ab complex: type Ⅲ hypersensitivity
There is common antigenicity between M protein and Myocardial cells,
glomerular [ɡ
'lɒ
mrjʊ
lə] basement membrane cells, so the antibody just against M
protein can also combine with these cells, activate complements and result type Ⅱ
hypersensitivity
Such as: poststreptococcal acute glomerulonephritis, rheumatic fever, rheumatic
heart disease.
Pathogenesis
Cause disease by three mechanisms:
(1) Pyogenic inflammation, which is induced locally
at the site of the organisms in tissue;
(2) Exotoxin production, which can cause
widespread systemic symptoms in areas of the body
where there are no organisms;
(3) Immunologic, which occurs when antibody
against a component of the organism cross-reacts
with normal tissue or forms immune complexes that
damage normal tissues
Group A
streptococci
Hyaluronidase degrades hyaluronic
acid
(2) Streptokinase (fibrinolysin)
activates plasminogen to form plasmin,
which dissolves fibrin in clots, thrombi,
(3) DNase (streptodornase) degrades
DNA in exudates or necrotic tissue
Toxins and
Hemolysins:
Erythrogenic toxin causes the rash of scarlet fever. Its
mechanism of action is similar to that of the TSST of S. aureus
(i.e., it acts as a superantigen
Streptolysin O is a hemolysin that is inactivated by oxidation
(oxygen-labile). It is antigenic, and antibody to it (ASO) develops
after group A streptococcal infections. The titer of ASO antibody
can be important in the diagnosis of rheumatic fever
Pyrogenic exotoxin A is the toxin responsible for most cases of
streptococcal toxic shock syndrome (i.e., it is a superantigen)
Exotoxin B is a protease that rapidly destroys tissue and is
produced in large amounts by the strains of S. pyogenes, the so-
called “flesh-eating” streptococci that cause necrotizing fasciitis
Clinical Findings
S. pyogenes causes three types of diseases:
(1) Pyogenic diseases such as pharyngitis and
cellulitis,
(2) Toxigenic diseases such as scarlet fever and
toxic shock syndrome, and
(3) Immunologic diseases such as rheumatic fever
and acute glomerulonephritis (AGN). (See next
section on poststreptococcal diseases.)
Laboratory
Diagnosis
Microbiologic
Cultures remain
the gold
standard
The rapid test
detects bacterial
antigens in a
throat swab
specimen.
ASO titers are
high soon after
group A
streptococcal
infections.
Titers of anti-
DNase B are
high in group A
streptococcal
skin infections
Streptococcus
pneumoniae
(Pneumococcus)
—Gram-positive “lancet-shaped” cocci in
pairs (diplococci) or short chains.
α-Hemolytic colonies. Catalase-negative.
Growth is inhibited by optochin in contrast
to viridians streptococci, which are resistant.
Colonies are bile soluble. Prominent
polysaccharide capsule.
Pathogenesis
Induces inflammatory response.
No known exotoxins.
Polysaccharide capsule retards phagocytosis.
Anti polysaccharide antibody opsonizes the
organism and provides type-specific immunity.
IgA protease degrades secretory IgA on
respiratory mucosa, allowing colonization
Laboratory
diagnosis
Gram-stained smear and culture.
α-Hemolytic colonies on blood agar.
Growth inhibited by bile and optochin.
Quellung reaction occurs (swelling of capsule with type-
specific antiserum). Serologic tests for antibody not useful.
Tests for capsular antigen in spinal fluid and C
polysaccharide in urine can be diagnostic

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Streptococcal Infections: Diseases, Properties, Pathogenesis

  • 2. Diseases S. pyogenes(group A streptococcus) is the leading bacterial cause of pharyngitis and cellulitis immunologic diseases, namely, rheumatic fever and acute glomerulonephritis. Streptococcus agalactiae (group B streptococcus) is the leading cause of neonatal sepsis and meningitis. Enterococcus faecalis is an important cause of hospital acquired urinary tract infections and endocarditis. Viridans group streptococci are the most common cause of endocarditis . Streptococcus bovis also causes endocarditis
  • 3.
  • 4. Important Properties All streptococci are catalase-negative. One of the most important characteristics for identification of streptococci is the type of hemolysis. Hemolytic streptococci form a green zone around their colonies as a result of incomplete lysis of red blood cells in the agar. The green color is formed when hydrogen peroxide produced by the bacteria oxidizes hemoglobin (red color) to biliverdin (green color). β-Hemolytic streptococci form a clear zone around their colonies because complete lysis of the red cells
  • 5. ➢ -streptococcus ➢ -hemolytic streptococcus/ Oppathogensportunistic ➢ -hemolytic/pyogenic streptococcus
  • 6. Important Properties β-Hemolysis is due to the production of enzymes (hemolysins) called streptolysin O and streptolysin S . Some streptococci are nonhemolytic (γ-hemolysis). There are two important antigens of β-hemolytic streptococci: C carbohydrate determines the group of β-hemolytic streptococci. It is located in the cell wall, and its specificity is determined by an amino sugar. M protein is the most important virulence factor It protrudes from the outer surface of the cell and interferes with ingestion by phagocytes
  • 7.
  • 8. * M-protein : ◆Anti-phagocytotic ◆Common antigen -- heart muscle cell, glomerular basement membrane cells, etc. ◆M Ag-Ab complex: type Ⅲ hypersensitivity There is common antigenicity between M protein and Myocardial cells, glomerular [ɡ 'lɒ mrjʊ lə] basement membrane cells, so the antibody just against M protein can also combine with these cells, activate complements and result type Ⅱ hypersensitivity Such as: poststreptococcal acute glomerulonephritis, rheumatic fever, rheumatic heart disease.
  • 9. Pathogenesis Cause disease by three mechanisms: (1) Pyogenic inflammation, which is induced locally at the site of the organisms in tissue; (2) Exotoxin production, which can cause widespread systemic symptoms in areas of the body where there are no organisms; (3) Immunologic, which occurs when antibody against a component of the organism cross-reacts with normal tissue or forms immune complexes that damage normal tissues
  • 10. Group A streptococci Hyaluronidase degrades hyaluronic acid (2) Streptokinase (fibrinolysin) activates plasminogen to form plasmin, which dissolves fibrin in clots, thrombi, (3) DNase (streptodornase) degrades DNA in exudates or necrotic tissue
  • 11. Toxins and Hemolysins: Erythrogenic toxin causes the rash of scarlet fever. Its mechanism of action is similar to that of the TSST of S. aureus (i.e., it acts as a superantigen Streptolysin O is a hemolysin that is inactivated by oxidation (oxygen-labile). It is antigenic, and antibody to it (ASO) develops after group A streptococcal infections. The titer of ASO antibody can be important in the diagnosis of rheumatic fever Pyrogenic exotoxin A is the toxin responsible for most cases of streptococcal toxic shock syndrome (i.e., it is a superantigen) Exotoxin B is a protease that rapidly destroys tissue and is produced in large amounts by the strains of S. pyogenes, the so- called “flesh-eating” streptococci that cause necrotizing fasciitis
  • 12. Clinical Findings S. pyogenes causes three types of diseases: (1) Pyogenic diseases such as pharyngitis and cellulitis, (2) Toxigenic diseases such as scarlet fever and toxic shock syndrome, and (3) Immunologic diseases such as rheumatic fever and acute glomerulonephritis (AGN). (See next section on poststreptococcal diseases.)
  • 13.
  • 14. Laboratory Diagnosis Microbiologic Cultures remain the gold standard The rapid test detects bacterial antigens in a throat swab specimen. ASO titers are high soon after group A streptococcal infections. Titers of anti- DNase B are high in group A streptococcal skin infections
  • 15. Streptococcus pneumoniae (Pneumococcus) —Gram-positive “lancet-shaped” cocci in pairs (diplococci) or short chains. α-Hemolytic colonies. Catalase-negative. Growth is inhibited by optochin in contrast to viridians streptococci, which are resistant. Colonies are bile soluble. Prominent polysaccharide capsule.
  • 16. Pathogenesis Induces inflammatory response. No known exotoxins. Polysaccharide capsule retards phagocytosis. Anti polysaccharide antibody opsonizes the organism and provides type-specific immunity. IgA protease degrades secretory IgA on respiratory mucosa, allowing colonization
  • 17. Laboratory diagnosis Gram-stained smear and culture. α-Hemolytic colonies on blood agar. Growth inhibited by bile and optochin. Quellung reaction occurs (swelling of capsule with type- specific antiserum). Serologic tests for antibody not useful. Tests for capsular antigen in spinal fluid and C polysaccharide in urine can be diagnostic