Streptococcus Pyogenes Flashcards by Rachel cyr

Q

Streptococcus Pyogeneous

Overview

A

G +
Cocci, pairs or chains
Facultative Anaerobe
Catalase -
Ferment glucose —> lactic acid
complex growth requirements
Lance Field Group A

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Q

S.pyogenes

Encounter

A

Normal flora of skin
Normal flora also the nasopharynx (5-15% humans)
disease is caused by recently acquired strains.

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Q

S.pyogenes

Entry

A

Wound infection of skin
Inhalation for nasopharynx infection

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Q

S.pyogenes

Spread

A

Person to person thorugh respiratory droplets
Skin to skin contact
Contact with fomite

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Q

S.pyogenes

Multiplication

A

Xtrcl growth on mucous membranes
Skin
Deep tissue

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Q

S.pyogenes

Damage

A

Pharyngitis
Pyoderma
Scarlet Fever
Prysipelas
Cellulits
Necrotizing fasciitis
Glumulonephritis
Rheumatic fever

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Q

S.pyogenes

Diagnosis

A

Throat or skin culture on blood agar
β hemolysis
Immunodetection assays

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Q

S.pyogenes

Treatment

A

Remain sensitive penicillins/cephalosporins
Treatment prevent local infection from becoming invasive rheumatic fever and Person to Person spread

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Q

S.pyogenous Virulence Factor (Structural)

Cell Wall

A

Cell wall contains specific Ags.
Group specific carbohydrate (Lancefield Group A Ag)

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Q

S.pyogenous Virulence Factor (Structural)

M Protein

A

Extends through cell wall and capsule.
Contributes to adhesion, by binding fibrinogen
Prevents C3b binding, preventing complement activation and opsonization

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Q

S.pyogenous Virulence Factor (Structural)

Pili

A

allow attachment to host tissues
in S. pyogenes they are encoded by the FCT
pathogenicity island

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Q

S.pyogenous Virulence Factor (Structural)

F Protein

A

binds fibronectin allowing adherence to respiratory cells

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Q

S.pyogenous Virulence Factor (Structural)

Capsule

A

Composed of hyaluronic acid
Hyaluronic acid is commonly found in connective tissue and recognized as “self” by the immune system.
Thus capsule allows S. pyogenes to mask itself as a normal component and avoid destruction by the immune system

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Q

S.pyogenous Virulence Factor (Structural)

C5a Peptidase

A

Protease that inactivates C5a preventing C5a from attracting phagocytic cells to the site of infection

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Q

S.pyogenous Virulence Factor (Cytotoxin)

Streptolysin S (SLS)

A

disrupts membranes by an unknown mechanism
Peptide encoded by sagA that is extensively modified prior to secretion
Active against WBCs, RBCs, and platelets
Oxygen stable
non immunogenic
Responsible for Beta hemolysis observed on blood agar plates

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Q

S.pyogenous Virulence Factor (Cytotoxin)

Streptolysin O

A

Pore forming cytotoxin, binds to cholestrol
Oxygen labile
Very immunogenic —> Antistreptolysin O antibodies (ASO)
Free cholesterol in skin inhibits toxin binding to membranes —>Cutaneous infections do not develop ASO.

Q

S.pyogenous Virulence Factor

Pyrogenic Exotoxins (SPE)

A

Four toxins (SpeA-D)
All act as superantigens
SpeA and SpeC are encoded by a lysogenic bacteriophage.
Play a role in specific diseases
Not all strains posses pyrogenic toxins

Q

S.pyogenous Virulence Factor (enzymes)

Streptokinase A & B

A

Enzyme that cleaves human plasminogen releasing activated plasmin
Plasmin goes on to cleave fibrin and fibrinogen.
Action is to break blood clots facilitate rapid spread of the S. pyogenes from the site of the infection.

Q

S.pyogenous Virulence Factor (enzymes)

Streptodornases A-D

A

Deoxyribonuclease enzymes that can break down free DNA in the environment (Dnases)
B and D can also break down RNA.
Thought to facilitate spread by breaking down nucleic acids present in pusand decreasing the viscosity of the pus.
Immunogenic
AB to Dnase B are one test for cutaneous infection.

Q

S.pyogenous Virulence Factor (enzymes)

Hyaluronidase

A

cleaves hyaluronic acid in host connective tissue.
Thought to play a role in the spread of the organism from the original site of infection.
Also cleaves the S. pyogenes capsule!

Q

S.pyogenes Diseases

A

S. pyogenes disease breaks down into two categories:

Suppurative disease or pus producing diseases
Non supparative disease, non pus producing

usually a complication of an infection causing supparative disease
Example: Rheumatic fever

Q

S.pyogenes **Suppurative **Diseases:

Pharyngitis

A

Most common
Spread by saliva or nasal secretions from infected person.
Organism is inhaled and adheres to and colonizes the nasopharynx
Incubation 2-4 days
S/Sx: Sore throat, fever, malaise, and headache.
Characteristic erythematous rash on back of throat (red rash caused by dilated and congested capillaries)
Left untreated it can lead to abscess in pharynx and tonsils and disseminated disease.

Q

S.pyogenes Suppurative Diseases:

Scarlet Fever

A

Scarlet Fever is a complication of Strep. pharyngitis
Occurs when the infecting S. pyogenes contains a gene w/ a Spe toxin.
The resulting inflammation produces a characteristic erythematous rash on the upper chest and extremities 1-2 days after symptoms of pharyngitis
Also produces a rash on the tongue called “strawberry tongue
Rash clears in 5-7 days.

Q

S.pyogenes Suppurative Diseases:

Necrotizing Fascciitis

A

Rare, and seen primarily in immuno-compromised individuals.
Most often associated with S. pyogenes
Characterized by massive deep tissue destruction (deep tissue, below dermis) which spreads along the fascia (the connective tissue that surrounds muscle, blood vessels, and nerves).
S. pyogenes is introduced through a wound in the skin and disseminates to the deep tissues.
SpeB protease activity is not very specific, it degrades complement components, antibody, extracellular matrix proteins, destroying tissues.
Spe(A-D) superantigen action causes a massive inflammation response contributing to edema (swelling) and tissue destruction.
Disease will progress quickly leading to septic shock and multiple organ failure.
Aggressive treatment required including both antibacterial treatment and surgical removal of infected tissues.

**S.pyogenes Non-Suppurative Diseases:** **Rheumatic Fever**

* Complication of Strept. Pharyngitis * Chronic inflammation of the heart, joints, skin and possibly brain. * Believed to be caused cross reactivity of anti-streptococcal AB to host proteins. * Antibody to M protein may cross react with myosin of heart muscle fibers. * This leads to immune system attack of heart valves and reduced heart function.