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7 - Streptococcus Pyogenes

The document provides an overview of Streptococcus pyogenes, detailing its morphological, cultural, and biochemical characteristics, as well as its classification and virulence factors. It discusses various clinical conditions caused by this pathogen, including both suppurative and non-suppurative diseases, and outlines laboratory investigations for diagnosis. Additionally, the document covers treatment options and antibiotic resistance related to Streptococcus pyogenes infections.

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sahil sahil
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0% found this document useful (0 votes)
10 views22 pages

7 - Streptococcus Pyogenes

The document provides an overview of Streptococcus pyogenes, detailing its morphological, cultural, and biochemical characteristics, as well as its classification and virulence factors. It discusses various clinical conditions caused by this pathogen, including both suppurative and non-suppurative diseases, and outlines laboratory investigations for diagnosis. Additionally, the document covers treatment options and antibiotic resistance related to Streptococcus pyogenes infections.

Uploaded by

sahil sahil
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd

Streptococcus pyogenes

(Group A Streptococci)
Session Learning Outcomes
• Describe the main morphological, culture, and
biochemical characteristics of Streptococci.
• Classify streptococci with relation to antigenic structures
and give examples
• Relate virulence factors to the pathogenesis and clinical
spectrum of illness caused by Group A Streptococci
(Streptococcus pyogenes)
• Discuss different clinical conditions including suppurative
and non-suppurative sequelae of Streptococcus pyogenes
infection.
• Discuss laboratory investigations for diagnosing
Streptococcus pyogenes infections.
no for
need • List the antibiotics used for treatment of Streptococcus
exam pyogenes and any resistance.
Genus streptococci
from
benefits
gets hosts harm
without

• Includes many species, commensals/ pathogens


• Gram-stain characteristics: Generally appear as gram-
positive cocci arranged in chains or pairs
• Catalase negative (unlike Staphylococci which are catalase positive)
• Facultative Anaerobes or aerobes
having
• claritiondrequirements
Fastidious Growth Requirements
• Can form capsules and slime layer
thisslide
Recstartsfrom
Streptococci
Aerobes and Facultative anaerobes
. ( O2 requirement )
Obligate anaerobes
( HEMOLYSIS) 02
growwithout
(peptostreptococci)

1.ALPHA 3.GAMMA
( The viridans group) ( The Enterococcus group)
2.BETA
( the hemolytic streptococci)
serological Group specific C carbohydrate antigen

20 Lancefield groups(ABCDEFGH KL
MNOPQRSTUV)
Group A – streptococcus pyogenes (GAS)

Serological typing ( M protein )


Griffith typing ( 1,2,3, etc.)
clearareaaroundcolony

eg pneumococci
strep

eg pyrogenic
strep

nohemolysis
Classification of Genus Streptococcus
Rebecca Lancefield - serogrouping system

 beta-hemolytic streptococci classifies by group-specific cell


wall carbohydrate (CHO) antigen
(As of 1992, Serogroups A to H and K to V ( except I & J )
emostpyrogenicvariety
 Groups A, B, C, D, and G are most
commonly associated with human disease

Streptococcus pyogenes (Group A) – further classified :


encoded
by it gene
1. Griffith typing based on M Protein
2. Emm classification: based on emm locus. Characterize and measure the genetic
diversity among isolates of S pyogenes
Cell surface structure of S pyogenes and extracellular
substances. (virulence factors)
Extracellular Virulence Factors
1. Exotoxins:
Onlabile when itisexposedto Oz itmakes itinactivated
a. Streptolysin O (SLO): Hemolytic and Cytolytic: make cell leaky
Tmorphonuclearleukocytesneutrophils
(RBC's, WBC’s, PMN's, platelets, etc.) and Causes sub-surface hemolysis
on Blood agar.
Eigas
ASLO (ASO)titer indicates recent infection (300-500 in pediatric populations)
02Stable associated
withsurface
b. Streptolysin S (SLS): Hemolytic and Cytolytic - lytic for red and
white blood cells and Causes surface hemolysis on Blood Agar
inducefever
can
c. Pyrogenic (Erythrogenic) Exotoxins (Types A, B &C)
Produced by more than 90% of Grp A strep

 Mediate pyrogenicity (fever)


 Causes scarlet fever (scarlatiniform) rash
 Increase susceptibility to endotoxic shock
 Immunomodulators (superantigens)
Extracellular Virulence Factors (cont.)

2. Enzymes:
a. Nucleases: Four antigenic types (A,B,C,D)
Facilitate liquefication of pus generating growth substrates
 Nucleases A, C have DNase activity
 Nucleases B, D also have RNase activity
b. Streptokinases: Two different forms
Lyse blood clots: catalyze conversion of plasminogen to
plasmin, leading to digestion of fibrin(spread of lesion)
pimpforrecruitmentof
neutrophils

c. C5a Peptidase destroys C’ chemotactic signals (C5a)


1bheifai.tn fnd
d. Hyaluronidase hydrolyzes hyaluronic acid(Dissolves pus)
e. Others: Proteinase, NADase, ATPase, phosphatase, etc.
Clinical infections caused by Group A streptococci (GAS)
• One of Most Important Human
Pathogens

1. Suppurative Diseases:
Pharyngitis; Scarlet Fever;
Cutaneous & Soft Tissue
Infections; Systemic Disease

2. Non-Suppurative Sequalae chroni complications


there
• ARF (Acute rheumatic fever) p Tater
• RHD (Rheumatic Heart Disease)
• AG (Acute Glomerulonephritis)
Group A Streptococcus (S. pyogenes):
Diverse group of acute suppurative (pus-forming) & nonsuppurative diseases

1. Suppurative Streptococcal Diseases


*Pharyngitis (& tonsilitis):
in childrens
Scarlet fever: Complication of streptococcal pharyngitis
when infecting strain is lysogenized; Frequently develop
scarletina rash (sandpaper like) on upper chest spreading to
extremities and Strawberry tongue.
*Cutaneous & Soft Tissue Infections.
1.Pyoderma (Impetigo): contagious pyoderma with
superficial yellow weeping lesions or crusted honey colored)

2.Erysipelas: Acute superficial cellulitis of skin with


lymphatic involvement; face and lower extremities; skin and
subcutaneous involvement
Classical features of Scarlet fever
Erysipelas

NOTE:
 erythema
 bullae
Erysipelas is raised bright red patch of skin with a sharply demarcated
but rapidly advancing margin. Bullae are fluid-filled sacs or lesions that appear
when fluid is trapped under a thin layer of skin

or pyoderma
Impetigo
Cutaneous & Soft Tissue Infections(cont.)
3.Cellulitis: Involvement of deeper subcutaneous tissues;
Deeper invasion with systemic symptoms
cancausedistractionof
muscles
4.Necrotizing fasciitis: (“flesh-eating bacteria”): Infection
deep in subcutaneous tissues that spreads along fascial planes,
destroying muscle and fat;
Initially cellulitis followed by bullae
(fluid filled blisters), gangrene,
systemic toxicity, multiorgan failure and
mortality in more than 50% of patients
5.Wound Infections
Necrotising fasciitis

Other Suppurative Diseases


*Puerperal & neonatal sepsis
*Lymphangitis: Inflammation of lymphatic vessel(s)
*Pneumonia
Systemic Disease
toxin mediated
1.Streptococcal Toxic Shock Syndrome (TSS):
Multisystem toxicity following soft tissue infection progressing
to shock and organ failure (not to be confused with Staphylococcal Toxic
Shock Syndrome where hyper absorbent tampons have been identified as an
important risk factor)

causedwhenthe streptococcienterstobloodstream
2. Bacteremia

Beta-hemolytic colonies on blood agar


Group A Streptococcal Diseases (cont.)
Nonsuppurative Sequelae

itisnotcurofinfectionbutcuzof immunologicalreactions
Post-infection complications of Group A streptococcal disease;
Serious complications in pre-antibiotic era; still important in
developing countries
1. Acute rheumatic fever (ARF): Inflammation of
heart, joints, blood vessels, sub-cutaneous tissues
2. Rheumatic heart disease (RHD): Chronic,
progressive heart valve damage
3. Acute glomerulonephritis (AG): Acute
inflammation of renal (kidney) glomeruli
4. PANDAS: Pediatric Autoimmune Neuropsychiatric
Disorders Associated with Streptococcus
Nonsuppurative Sequelae
Acute Glomerulonephritis :
 Follows either respiratory (pharyngitis) or cutaneous
(pyoderma) streptococcal infection
 Associated with well-defined group of M-types
 Most often seen in children manifesting as dark, smoky urine
with RBC's, RBC casts, white blood cells, depressed serum
complement, decreased glomerular filtration rate
 Latent period: 1-2 weeks after skin infection and 2-3 weeks
after pharyngitis
 Granular accumulations of immunoglobulin due to deposition of
so immune complexes within the kidney
G(Type ??III Hypersensitivity)

Nonsuppurative Sequelae
Acute Rheumatic Fever (ARF)
 Inflammatory reaction characterized by arthritis, carditis, chorea
(disorder of CNS with involuntary spastic movements), erythema
marginatum (skin redness with defined margin), or subcutaneous
nodules
 Within 2-3 weeks following pharyngitis
• Epidemic pharyngitis: ARF in as many as 3%
• Sporadic pharyngitis: ARF in 1 per 1000

 Morbidity & mortality linked to subsequent disease of heart valve


(Rheumatic Heart Disease)
 Poorly understood pathogenesis with several proposed theories including
cross-reactivity of heart tissues & strep antigens
• (Type ??
II hypersensitivity, exotoxins, direct invasion)
Laboratory diagnosis - by staining and culture
• Specimen – Blood, Pus, Throat swab, Blood for ASO
• Transported in Pike`s media
1. Smear and Grams staining -- cocci in
chains with pus cells
2. Blood agar incubated with 10% co2: pinpoint, beta
hemolytic
– Selective media- crystal violet blood agar
3. Streptococcus. pyogenes are
i. Bacitracin Sensitive ,
ii. PYR test positive and
iii. rapid fluorescent Ab test positive
Catalase Negative: -
Differentiates from
Staphylococcus

Bacitracin test:
Mstnsetive presumptively distinguishing between
Group A beta-hemolytic streptococci
(bacitracin Positive) and other beta-
hemolytic streptococci that are isolated
from pharyngeal swabs (95% sensitivity
for Grp A strep)
Laboratory diagnosis - by serology test
• Lancefield grouping and typing done by precipitation and co
agglutination
• ASO test and anti-DNase B done by latex agglutination or
turbidometry (retrospective diagnosis of a past GAS infection, especially
in cases of rheumatic fever or post-streptococcal glomerulonephritis)
• Antistreptolysin O (ASO test) >200 IUs is positive
• Antideoxyribonuclease B (ADNaseB) >300-350 units is
positive

• Rapid antigen detecting test: below


noneedfor
exam Treatment
• Penicillin drug of choice, no drug resistance
 For most adult patients or children - oral Penicillin V or
oral Amoxicillin
 For patients with a history of acute rheumatic fever -
options include oral penicillin, oral amoxicillin, or single-
dose intramuscular (IM) benzathine penicillin

• For patients allergic to penicillin - Macrolides like


Erythromycin; or Oral Cephalosporins
(Erythromycin resistance has been increasing)

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