LGT - Pyogenic Cocci - Strept - DR.S Zeiny

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University of Baghdad

College of Medicine
2022-2023

Title: Pyogenic Cocci: Genus Streptococci

Grade: 3rd
Module: Infectious Diseases Module
Speaker: Sarmad Zeiny
Date: 11 – Oct - 2022
Pyogenic Cocci
Gram positive cocci
Genus Streptococci

Department of Microbiology, College of Medicine, University of Baghdad


Dr. Sarmad M.H Zeiny (M.B.Ch.B, M.Sc., F.I.C.M./Path)
OBJECTIVES:
Upon completion of this lecture, the student will:

 Outline the medically important Streptococci species.


 Describing the morphology & physiology for Streptococci.
 Determine the virulence factors for Streptococci.
 Analyze the diseases & pathogenicity for Streptococci.
 Demonstrate the epidemiology/transmission for Streptococci.
 Outline the laboratory diagnosis for Streptococci.
Clinically important Gram +ve cocci

S.Pyogenes S.aureus
S.agalactia
Streptococci Staphylococci S.epidermidis
Viridans S.
S.saprophyticus

S.Pneumoniae
Staphylococcus
lugdunensis
S.enterococci
Streptococci
(Gram+ve cocci
catalase –ve)
General characteristic for genus streptococci :

 G+ve cocci, arrange in chains or pairs.


 Some strains are capsulated
 Majority are facultative anaerobic, few are obligatory
anaerobic.
 Catalase –ve
 Non motile.
 Non spore forming
 Fastidious microorganism
Gram slide for genus streptococci
Genus Streptococcus

Hemolysis Lancefield (serology)

Serogroups (cell wall polysaccharide


β hemolysis α hemolysis γ hemolysis Ag)

S. Pyogenes S.Pneumoniae
S.Bovis Group A Group B Group D
Enterococcus
Viridans
S. agalactiae
Streptococci
S. Pyogenes S. agalactiae S.bovis

80 Serotypes,
(M-protein)
S.pyogenes
(Group A β- hemolytic,GABH):

M-protein

>80 serotypes

Reservoir Transmission
Human throat and skin Spread by respiratory droplets or
direct contact
Virulence factors:
Virulence factors & Pathogenesis for S.pyogenes

1) M protein and capsule.


2) Streptolysin O*: destroys RBC & WBC, antigenic. anti-streptolysin O (ASO)
antibodies develop.
3) Streptolysin S: destroys RBC, not antigenic.
4) Pyrogenic exotoxin (erythrogenic toxin): few strains,
scarlet fever, few strains superantigens. streptococcal toxic shock syndrome
5) Streptokinase* plasmin  breaks fibrin  spreading factor

6) Hyaluronidase  spreading factor

7) Streptodornases (DNAases)  spreading factor


8) (Anti-C5a) peptidase anti-inflammatory
9) Diphosphopyridine Nucleotidase  kill leukocyte
* Used clinically for diagnosis and for treatment.
DISEASES of S.pyogenes
LOCAL INFECTIONS (invasion)

• Sore throat (acute pharyngitis, pharyngotonsillitis).


• Skin infections: (Wound infection, cellulitis, fasciitis and
myonecrosis (flesh-eating), Impetigo, Erysipelas.

SYSTEMIC INFECTION (invasion &/or toxin)


• Sepsis.
• Meningitis.
• Puerperal Sepsis.
• Streptococcus toxic shock syndrome
• Scarlet fever

POST STREPTOCOCCAL sequel (delayed antibody mediated diseases)

• Rheumatic fever
• Acute Glomerulonephritis
Erysipelas
POST STREPTOCOCCAL complication
(delayed antibody mediated diseases)

 Rheumatic fever:
- After pharyngitis only.
- Type 2 hypersensitivity reaction.
- Involves heart and joints.

 Acute Glomerulonephritis:
- After pharyngitis or skin infections.
- Type 3 hypersensitivity reaction.
- Involves kidney.
Rheumatic fever (Rheumatic heart disease):
 It usually strikes children 5-15 years of age. When it
occurs, it has been shown to follow untreated beta-
hemolytic group A streptococcal pharyngitis (but NOT
after a skin infection).

 Rheumatic fever is antibody-mediated.There are antigens in


the heart that are similar to the antigens of the beta-
hemolytic group A streptococci.Therefore, the antibodies
that forms to eradicate this particular streptococcus also
cross-react with antigens in the heart.
Acute post-streptococcal glomerulonephritis (PSGN)
 It occurs after infection of either the pharynx OR skin by nephritogenic
(having the ability to cause glomerulonephritis) strains of beta-hemolytic group
A streptococci.

 Certain antigens from these nephritogenic streptococci induce an antibody


response. The resulting antigen-antibody complexes travel to and are
deposited in the glomerular basement membrane, where they activate the
complement cascade. This leads to local glomerular destruction in the kidney.

 Clinically, a child will show up in your office, and his mother will complain that
his face is puffy. This is caused by the retention of fluid from his damaged
kidney. His urine is darker than normal (tea or Coca-Cola colored) due to
hematuria (blood in the urine).
ASO test:
 Measure Anti-Streptolysin O Ab.
 ASO test uses in poststreptococcal infection. This test used to
determine significance of current (recent) streptococcal
infection by measuring the ASOT:
 ASOT (Ab Titer):
Normal < 200 > significance result (recent infection)
Laboratory study

Laboratory diagnostic steps


Direct
Specimens
Gram’s Slide

Biochemical Culture

Antibiotics
Serology
sensitivity
S.agalactia
(Group B β- hemolytic):
Normal flora of female genital tract (15-20% of woman), male
urethra & GIT.

Leading Cause for neonatal sepsis, pneumonia & meningitis. (acquire


these bacteria during delivery).
Diagnostic Lab. features

Bacitracin resistant, PYR -VE

Hydrolyzes hippurate. (purple color)

cAMP test-positive produces definitive arrow when close to


Staphylococcus aureus.
Summary
• Streptococci classified according to the type of hemolysis & antigenic components.
• S.pyogenes is the most pathogenic species because of their virulent factors.
• S.pyogenes can cause post-infection severe complications.
• ASO test used in suspected case of rheumatic fever.
• Streptococci easily diagnosed in the lab. By using Gram’s staining, culture and
biochemical tests.
• S.agalactia is the leading Cause for neonatal sepsis, pneumonia & meningitis.
• streptococci infections can be prevented by regular hygiene precautions and by
antibiotics, no vaccine.
Reference:

Jawetz Melnick & Adelbergs Medical Microbiology -


27E (2016)

THANKS

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