Streptococcus Flashcards
• anti-phagocytic → protects the organism from being phagocytosed
Component of MUCOID COLONIES
Hyaluronic acid capsule
• 80 types
• inhibits activation of complement
* Precipitates fibrinogen → clumps platelets and WBC
* Inhibits the migration of WBC
• anti-phagocytic
→ M protein
Group-specific cell wall antigen
• Group A sugar:
RHAMNOSE-N-ACETYLGLUCOSAMINE
• binds to Fc region of IgG or IgA
* the Fc region is usually reserved for the immune cells
* Leads to no antigen-antibody
complex which usually initiates the complement activity
→ IgG & IgA-binding proteins
cleaves C5a component of complement → inhibits neutrophil chemotaxis in vitro
• leads to problems in initiating inflammatory reaction
C5a protease
• allows binding to FIBRONECTIN
in pharyngeal epithelium
→ F protein
Attached to M protein
• May allow binding to FIBRONECTIN
* Fibronectin is the binding site for our organisms on membranes of host cells or structures
Lipoteichoic acid
Fibronolysin that lyses blood clots
STREPTOKINASE
Degrades hosts DNA &RNA
STREPTODORNASE
Hydrolyze or break down hyaluronic acid which is part of the connective tissue
HYALURONIDASE
Associated with the organism’s ability to destroy WBCS
DIPHOSPHOPYRIDINE
NUCLEOTIDASE
→ Exotoxin A→ most potent
Acquired through LYSOGENY
Associated with fever and rashes in scarlet fever
Associated with Streptococcal
Toxic Shock Syndrome (TSS)
• more fatal
PYROGENIC EXOTOXINS/ ERYTHROGENIC
TOXINS (A,B,C)
Oxygen stable
Surface HEMOLYSIN
• toxic to human cells
→ Antiphagocytic
NOT antigenic
STREPTOLYSIN-S
→ Antigenic
• Induce antibody response
Detect serologically
Also produced by group
C and G
Oxygen liable
STREPTOLYSIN-O
I.C.E. → skin infections
Impetigo
Cellulitis
Erysipelas
→ Begins as fluid-filled blisters that erupt
→ Creating weeping lesions
→ Lesions would release fluid and eventually cross over (mouth, nose, etc.)
→ Common in young children
IMPETIGO
→ Inflammation/infection
of deep tissues including the skin
→ Common in middle-aged individuals
CELLULITIS
→ Itchy and feels hot than the
rest of the body
→ NO PUS PRODUCTION
→ There is EXOTOXIN production
→ increased temperature and rashes
ERYSIPELAS (SAINT ANTHONY’S FIRE)
→ Red swollen tonsils
→ PUS FORMATION
→ Lasts 3-5 days
STREPTOCOCCAL PHARYNGITIS
Occurs after Streptococcal pharyngitis or other infections
PYROGENIC EXOTOXIN is present
→ fever, rashes, strawberry tongue
Rashes start from the neck, chest, and arms
SCARLET FEVER
TOXIN MEDIATED
There is hypotension, multiorgan
failure, fever, erythema, swelling, tachycardia, acute respiratory distress, renal impairment, and shock is observed
Milder compared to
staphylococcal TSS
STREPTOCOCCAL TOXIC SHOCK SYNDROME
cells turn black removed to stop the infection
Acquired through puncture of a structure that contains the
organism (plant thorn, abrasion by bushes)
Does not go deep but it spreads
NECROTIZING FASCIITIS
→ Cardiac inflammation and scarring
→ Triggered by autoimmune reaction to infection with the GAS group
RHEUMATIC HEART DISEASE
→ In the acute stage, the condition may consists of PANCARDITIS
→ Entire layers of the heart may be INFECTED or INFLAMMED (Myocardium, endocardium, epicardium)
RHEUMATIC HEART DISEASE
→ Systemic disease that affects the CONNECTIVE TISSUE
around the ARTERIOLES
→ Occur after an untreated strep throat due to GAS
ACUTE RHEUMATIC FEVER
Comprises a specific set of
RENAL DISEASES
• Immunologic mechanism →
triggers inflammation and
proliferation of glomerular tissue that can result in damage to the basement membrane
→ Antigen-antibody complex is
involved
ACUTE GLOMERULONEPHRITIS
Comprises a specific set of
RENAL DISEASES
• Immunologic mechanism →
triggers inflammation and
proliferation of glomerular tissue that can result in damage to the basement membrane
→ Antigen-antibody complex is
involved
ACUTE GLOMERULONEPHRITIS
