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STREPTOCOCCI
 Cocci arrange in chain were first seen and describe by Billorth
in purulent exudates from erysipelas and infection who gave
the name streptococci.
 Streptos meaning winded or twisted.
 Rosenbach gave the name Streptococcus pyogenes to cocci
arranged in chain which is isolated from human suppurative
lesions.
CLASSIFICATION
 Based on oxygen requirement:
 Aerobes
 Facultative anaerobes
 Obligate anaerobes
 Based on hemolysis on blood agar:
 Alpha (α) hemolytic
 Beta (β) hemolytic
 Gamma (γ) hemolytic
CLASSIFICATION
 Based on carbohydrate (C) antigen:
 Lancefield groups – A to V (without I and J)
 Based on M proteins:
 Griffith typing – 80 types of S. pyogenes
STREPTOCOCCUS PYOGENES
- Group A streptococci
MORPHOLOGY
 Cocci, spherical or oval, 0.5–1.0 μm in diameter
 Arranged in chains
 Chain formation – cocci divide in one plane, daughter
cells fail to separate completely.
GROWTH CHARACTERISTICS
 Aerobes and facultative anaerobe.
 Fastidious in nutritive requirement, growth occur only in
enriched media containing blood or serum.
 Blood agar – colonies small, semitransparent, circular
with a clear zone of hemolysis around them.
 Liquid media – glucose or serum broth, granular
turbidity with a powdery deposit.
Blood agar: S.pyogenes showing beta hemolysis
BIOCHEMICAL REACTIONS
 Catalase negative (unlike staphylococci)
 Not soluble in 10% bile (unlike pneumococci)
 PYR test positive
 Ferment several sugars producing acid but no gas.
RESISTANCE
 Easily destroyed by heat (54°C for 30 min)
 Rapidly inactivated by antiseptics
 Resistant to crystal violet
 Selective media – crystal violet, nalidixic acid, colistin
sulphate
 Does not develop resistance to drugs
 Sensitivity to bacitracin – S. pyogenes
ANTIGENIC STRUCTURE
 Capsule – Group A streptococci are capsulated, made up
of hyluronic acid.
• Capsule is antiphagocytic but no antigenic.
 Cell wall:
 Outer layer – protein and lipoteichoic acid (helps in
adhesion)
 Middle layer – c carbohydrate antigen.
 Inner layer – peptidoglycan
 Peptidoglycan is responsible for cell wall rigidity.
 Serological grouping depends on the C carbohydrate
antigen. (integral part of cell wall)
 On the basis of carbohydrate C antigen, S.pyogenes –
Lancefield group A
 Outer layer protein layer consist of M, T and R proteins.
 Antigenic relationships have been Demonstrated between:
 Capsular hyaluronic acid and human synovial fluid
 Cell wall proteins and myocardium
 Group A carbohydrates and cardiac valves
 Cytoplasmic membrane antigens and vascular intima
 Peptidoglycans and skin antigens
TOXINS AND VIRULENCE FACTORS
➢ S. pyogenes forms several exotoxins and enzymes
➢ M protein act as virulence factor by inhibiting
phagocytosis
➢ C polysaccharide – toxic effect
➢ Hemolysins
➢ Hemolysins:
 Streptococci produce two hemolysins, streptolysin O and S.
 Streptolysin O : oxygen labile, antigenic
 Anti streptolysin O appears in sera following streptococcal infection.
 ASO test is standard test for diagnosis of streptococcal infection.
 ASO titer in more than 200 units is considered significant and
suggests either recent or recurrent infection.
 ASO titer is more in rheumatic fever .
 Streptolysin S : oxygen stable, not anigenic.
 Protein but not antigenic, responsible for haemolysis around colonies
on the blood agar plates.
STREPTOKINASE (fibrinolysin)
 Promotes lysis of human fibrin clots by activating plasma
precursor – plasminogen.
 Streptokinase is given IV in treatment of early myocardial
infection & thromboembolic disorders.
DEOXYRIBONUCLEASES (streptodornase DNAase)
 Pyogenic exudates contain large amounts of DNA
 Streptodornase causes depolymerisation of DNA and helps
liquefy the thick pus
 May be responsible for the thin serous character of the
streptococcal exudates
 Useful in diagnosis of S.pyogenes infection, particularly in skin
lesions, where ASO titer is low.
HYALURONIDASE
 Breaks down hyaluronic acid of tissues
 This may favour spread of infection along intracellular spaces
 The enzyme is antigenic and specific antibodies appear in
convalescent sera.
PATHOGENICITY
 Disease – suppurative or non- suppurative (including
sequelae to post-streptococcal infections)
 S. pyogenes produces pyogenic lesions with a tendency to
spread locally along lymphatics and through blood stream.
SUPPURATIVE
1) Respiratory infections
2) Skin and soft tissue infections
3) Genital infections
NON-SUPPURATIVE (post-streptococcal sequelae)
1) Acute rheumatic fever
2) Acute glomerulonephritis
SUPPARATIVE COMPLICATION :
RESPIRATORY INFECTIONS
 Primary site of invasion – throat
 Sore throat – most common
 Localised – tonsillitis
 Diffuse – pharyngitis
SKIN AND SOFT TISSUE INFECTION
Two typical streptococcal infections:
▪ Erysipelas
 Diffuse infection involving the superficial lymphatics
 Affected skin red, swollen and indurated,sharply
demarcated from surrounding healthy area
 Seen in older patients
▪ Impetigo
• Impetigo and streptococcal infection of scabies lesions are
the main causes of acute glomerulonephritis in children in
the tropics
 S. pyogenes causes a variety of suppurative infections of
wounds or burns, with a predilection to produce lymphangitis
and cellulitis
 Subcutaneous infections – range from cellulitis to necrotising
fasciitis
 Necrotising fasciitis – more common, caused by mixed
aerobic and anaerobic bacterial infection
 S. pyogenes M types 1 and 3 forming pyrogenic exotoxin A –
may alone be responsible – ‘flesh eating bacteria
Necrotising fasciitis
 Extensive necrosis of subcutaneous and muscular tissue and
adjacent fascia associated with a severe systemic illness – a
toxic shock–like syndrome, with disseminated intravascular
coagulation and multisystem failure.
GENITAL INFECTIONS
 Aerobic and anaerobic streptococci – normal inhabitants of
female genital tract
 S. pyogenes cause puerperal sepsis
Non suppurative complications:
 Non-suppurative post-streptococcal sequelae: two
important sequelae
 Acute rheumatic fever
 Acute glomerulonephritis
 Complications – 1 to 3 weeks after the acute infection
EPIDEMIOLOGY
 Streptococcal infections – respiratory tract -frequent in
children at 5–8 years of age
 More common in winter in the temperate countries
 No seasonal distribution in the tropics
 Crowding – important factor in transmission of infection
 Outbreaks in closed communities – boarding schools or
army camps
LABORATORY DIAGNOSIS
 Acute infections – diagnosis established by culture
 Non-suppurative complications – diagnosis based on
demonstration of antibodies.
Specimen
 Throat swab, pus or exudates
 In rheumatic fever and glomerulonephritis –serum sample
Microscopy
 Gram-stained films from pus – presumptive information
 Smears from throat – no value – streptococci form part of
normal resident flora
Culture
 Sample either plated immediately or transported in Pike’s
medium (blood agar with crystal violet and sodium azide)
 Specimen plated on sheep blood agar – incubated at 37°C
under 5–10% CO2 or anaerobically
Identification
 Hemolytic streptococci – grouped by Lancefield technique –
specific antisera
 Rapid diagnostic tests – streptococcal group A antigen
 Bacitracin sensitivity – S.pyogenes
Serology
 Rheumatic fever and glomerulonephritis – retrospective
diagnosis
 Antistreptolysin O titration (ASO titre) higher than 200
indicative of prior streptococcal infection
 Antideoxyribonuclease B (anti-DNAase B) higher than 300 –
significant
 Streptozyme test – sensitive and specific screening test
TREATMENT
 All beta hemolytic Group A streptococci are sensitive to
penicillin G
 In patients allergic to penicillin, erythromycin or
cephalexin may be used
 Tetracyclines and sulphonamides are not recommended
 Antimicrobial drugs have no effect on established
glomerulonephritis and rheumatic fever
OTHER HEMOLYTIC STREPTOCOCCI
 Besides S. pyogenes, streptococci belonging to groups B, C,
D, F, G and rarely H, K, O and R may also cause human
infection
 Of these B, C and G are more common
GROUP B STREPTOCOCCI :
 Important pathogens of cattle, producing bovine mastitis
 Streptococcus agalactiae – important human pathogen
responsible for:
 Neonatal infections
 Adult infections
Identified by CAMP reaction.
Streptococci.pdf

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Streptococci.pdf

  • 2.  Cocci arrange in chain were first seen and describe by Billorth in purulent exudates from erysipelas and infection who gave the name streptococci.  Streptos meaning winded or twisted.  Rosenbach gave the name Streptococcus pyogenes to cocci arranged in chain which is isolated from human suppurative lesions.
  • 3. CLASSIFICATION  Based on oxygen requirement:  Aerobes  Facultative anaerobes  Obligate anaerobes  Based on hemolysis on blood agar:  Alpha (α) hemolytic  Beta (β) hemolytic  Gamma (γ) hemolytic
  • 4. CLASSIFICATION  Based on carbohydrate (C) antigen:  Lancefield groups – A to V (without I and J)  Based on M proteins:  Griffith typing – 80 types of S. pyogenes
  • 5.
  • 6.
  • 7. STREPTOCOCCUS PYOGENES - Group A streptococci MORPHOLOGY  Cocci, spherical or oval, 0.5–1.0 μm in diameter  Arranged in chains  Chain formation – cocci divide in one plane, daughter cells fail to separate completely.
  • 8. GROWTH CHARACTERISTICS  Aerobes and facultative anaerobe.  Fastidious in nutritive requirement, growth occur only in enriched media containing blood or serum.  Blood agar – colonies small, semitransparent, circular with a clear zone of hemolysis around them.  Liquid media – glucose or serum broth, granular turbidity with a powdery deposit.
  • 9. Blood agar: S.pyogenes showing beta hemolysis
  • 10. BIOCHEMICAL REACTIONS  Catalase negative (unlike staphylococci)  Not soluble in 10% bile (unlike pneumococci)  PYR test positive  Ferment several sugars producing acid but no gas.
  • 11. RESISTANCE  Easily destroyed by heat (54°C for 30 min)  Rapidly inactivated by antiseptics  Resistant to crystal violet  Selective media – crystal violet, nalidixic acid, colistin sulphate  Does not develop resistance to drugs  Sensitivity to bacitracin – S. pyogenes
  • 12. ANTIGENIC STRUCTURE  Capsule – Group A streptococci are capsulated, made up of hyluronic acid. • Capsule is antiphagocytic but no antigenic.  Cell wall:  Outer layer – protein and lipoteichoic acid (helps in adhesion)  Middle layer – c carbohydrate antigen.  Inner layer – peptidoglycan  Peptidoglycan is responsible for cell wall rigidity.  Serological grouping depends on the C carbohydrate antigen. (integral part of cell wall)
  • 13.  On the basis of carbohydrate C antigen, S.pyogenes – Lancefield group A  Outer layer protein layer consist of M, T and R proteins.  Antigenic relationships have been Demonstrated between:  Capsular hyaluronic acid and human synovial fluid  Cell wall proteins and myocardium  Group A carbohydrates and cardiac valves  Cytoplasmic membrane antigens and vascular intima  Peptidoglycans and skin antigens
  • 14.
  • 15. TOXINS AND VIRULENCE FACTORS ➢ S. pyogenes forms several exotoxins and enzymes ➢ M protein act as virulence factor by inhibiting phagocytosis ➢ C polysaccharide – toxic effect ➢ Hemolysins
  • 16. ➢ Hemolysins:  Streptococci produce two hemolysins, streptolysin O and S.  Streptolysin O : oxygen labile, antigenic  Anti streptolysin O appears in sera following streptococcal infection.  ASO test is standard test for diagnosis of streptococcal infection.  ASO titer in more than 200 units is considered significant and suggests either recent or recurrent infection.  ASO titer is more in rheumatic fever .  Streptolysin S : oxygen stable, not anigenic.  Protein but not antigenic, responsible for haemolysis around colonies on the blood agar plates.
  • 17. STREPTOKINASE (fibrinolysin)  Promotes lysis of human fibrin clots by activating plasma precursor – plasminogen.  Streptokinase is given IV in treatment of early myocardial infection & thromboembolic disorders. DEOXYRIBONUCLEASES (streptodornase DNAase)  Pyogenic exudates contain large amounts of DNA  Streptodornase causes depolymerisation of DNA and helps liquefy the thick pus  May be responsible for the thin serous character of the streptococcal exudates  Useful in diagnosis of S.pyogenes infection, particularly in skin lesions, where ASO titer is low.
  • 18. HYALURONIDASE  Breaks down hyaluronic acid of tissues  This may favour spread of infection along intracellular spaces  The enzyme is antigenic and specific antibodies appear in convalescent sera.
  • 19. PATHOGENICITY  Disease – suppurative or non- suppurative (including sequelae to post-streptococcal infections)  S. pyogenes produces pyogenic lesions with a tendency to spread locally along lymphatics and through blood stream. SUPPURATIVE 1) Respiratory infections 2) Skin and soft tissue infections 3) Genital infections NON-SUPPURATIVE (post-streptococcal sequelae) 1) Acute rheumatic fever 2) Acute glomerulonephritis
  • 20. SUPPARATIVE COMPLICATION : RESPIRATORY INFECTIONS  Primary site of invasion – throat  Sore throat – most common  Localised – tonsillitis  Diffuse – pharyngitis SKIN AND SOFT TISSUE INFECTION Two typical streptococcal infections: ▪ Erysipelas  Diffuse infection involving the superficial lymphatics  Affected skin red, swollen and indurated,sharply demarcated from surrounding healthy area  Seen in older patients
  • 21. ▪ Impetigo • Impetigo and streptococcal infection of scabies lesions are the main causes of acute glomerulonephritis in children in the tropics  S. pyogenes causes a variety of suppurative infections of wounds or burns, with a predilection to produce lymphangitis and cellulitis  Subcutaneous infections – range from cellulitis to necrotising fasciitis  Necrotising fasciitis – more common, caused by mixed aerobic and anaerobic bacterial infection  S. pyogenes M types 1 and 3 forming pyrogenic exotoxin A – may alone be responsible – ‘flesh eating bacteria
  • 22.
  • 23. Necrotising fasciitis  Extensive necrosis of subcutaneous and muscular tissue and adjacent fascia associated with a severe systemic illness – a toxic shock–like syndrome, with disseminated intravascular coagulation and multisystem failure. GENITAL INFECTIONS  Aerobic and anaerobic streptococci – normal inhabitants of female genital tract  S. pyogenes cause puerperal sepsis
  • 24. Non suppurative complications:  Non-suppurative post-streptococcal sequelae: two important sequelae  Acute rheumatic fever  Acute glomerulonephritis  Complications – 1 to 3 weeks after the acute infection
  • 25. EPIDEMIOLOGY  Streptococcal infections – respiratory tract -frequent in children at 5–8 years of age  More common in winter in the temperate countries  No seasonal distribution in the tropics  Crowding – important factor in transmission of infection  Outbreaks in closed communities – boarding schools or army camps
  • 26. LABORATORY DIAGNOSIS  Acute infections – diagnosis established by culture  Non-suppurative complications – diagnosis based on demonstration of antibodies.
  • 27. Specimen  Throat swab, pus or exudates  In rheumatic fever and glomerulonephritis –serum sample Microscopy  Gram-stained films from pus – presumptive information  Smears from throat – no value – streptococci form part of normal resident flora
  • 28.
  • 29. Culture  Sample either plated immediately or transported in Pike’s medium (blood agar with crystal violet and sodium azide)  Specimen plated on sheep blood agar – incubated at 37°C under 5–10% CO2 or anaerobically Identification  Hemolytic streptococci – grouped by Lancefield technique – specific antisera  Rapid diagnostic tests – streptococcal group A antigen  Bacitracin sensitivity – S.pyogenes
  • 30. Serology  Rheumatic fever and glomerulonephritis – retrospective diagnosis  Antistreptolysin O titration (ASO titre) higher than 200 indicative of prior streptococcal infection  Antideoxyribonuclease B (anti-DNAase B) higher than 300 – significant  Streptozyme test – sensitive and specific screening test
  • 31. TREATMENT  All beta hemolytic Group A streptococci are sensitive to penicillin G  In patients allergic to penicillin, erythromycin or cephalexin may be used  Tetracyclines and sulphonamides are not recommended  Antimicrobial drugs have no effect on established glomerulonephritis and rheumatic fever
  • 32. OTHER HEMOLYTIC STREPTOCOCCI  Besides S. pyogenes, streptococci belonging to groups B, C, D, F, G and rarely H, K, O and R may also cause human infection  Of these B, C and G are more common GROUP B STREPTOCOCCI :  Important pathogens of cattle, producing bovine mastitis  Streptococcus agalactiae – important human pathogen responsible for:  Neonatal infections  Adult infections Identified by CAMP reaction.