Staphylococcus and Streptococcus Part 2 Flashcards

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1
Q

What are the S. aureus enzymes?

A
  1. Coagulase: Converts fibrinogen to fibrin; Makes clots
  2. Catalase
  3. Staphylokinase/Fibrinolysin: Dissolves clots (spreading factor)
  4. Hyaluronidase: Hydrolyzes CT (Spreading factor, carbon source)
  5. Penicillinase (Beta-lactamase)
  6. DNAse, proteases, lipases
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2
Q

What is S. aureus’ resevoir?

A

Human anterior nasopharynx, skin; Normal microbiota. Usually in hair follicles and sweat glands. Transmission by direct contact or aerosol

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3
Q

How does S. aureus attach to surfaces?

A

Fibronectin, collagen, elastin binding proteins; Receptors for sialoprotein and laminin.

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4
Q

Describe a S. aureus infection clinically.

A

Pyogenic, acute, aggressive and locally destructive; Presents with biols, folliculitis. impetigo, TSS, SSS and food poisoning.

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5
Q

Describe TSS

A

No bacteremia, systemic toxin release; Presents with fever, rash and hypotension

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6
Q

Describe SSS

A

Large cutaneous blisters, complete dequamation of epithelium; Recovery following antibody production

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7
Q

Describe Staphylococcal food poisoning.

A

Ingestion of organism is not necessary; Rapid onset with vomiting, diarrhea, nausea but no fever.

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8
Q

What are the systemic infections of S. aureus?

A

Osteomyelitis, septic arthritis, endocarditis, pneumonia, and empyema.

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9
Q

How is virulence regulated in S.aureus?

A

Expression is controlled by cell density; Rna poly 3

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10
Q

How does S. aureus evade the host immune system?

A
  1. Leukocidins and hemolysins kill phagocytic cells.
  2. Protein A blocks antibody function and titrates complement.
  3. Catalase
  4. Staphyloxanthin: carotenoid pigment protects against ROS
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11
Q

How is S. aureus diagnosed?

A

Organism is cultured and identified; yellow on mannitol fermenter, catalase and coagulase positive.

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12
Q

How is S. aureus treated?

A

Vancomycin; Most strains are now penicillin resistant. mecA encodes a PBP2’ to penicillin and other beta-lactams.

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13
Q

Describe S. pyogenes.

A

Gram+, strictly fermentative, catalase negative; Common cause of pharyngitis and tonsillitis

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14
Q

How are Streptococci classified?

A
  1. Antigenic differences
  2. Hemolysis pattern: alpha is partial lysis, beta is complete lysis of rbcs, and gamma is non-hemolytic
  3. Biochemical/Physiological differences
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15
Q

What are the 3 types of disease sS. pyogenes causes?

A
  1. Direct invasion:pharyngitis, skin or wound infections.
  2. Toxin mediated: TSS, scarlet fever, fascitis.
  3. Delayed immunologic reaction: Rheumatic fever, glomerulonephritis.
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16
Q

What are the surface antigens on S. pyogenes?

A

Hyaluronic acid capsule, lipoteichoic acid, and M protein.

17
Q

What role does M protein play?

A

Forms protective coat of fibrin and fibrinogen, degrades C3b, binds IgM

18
Q

What toxins does S. pyogenes have?

A
  1. Streptolysin: oxygen liable, pore forming cytolysin for rbcs, wbcs.
  2. Extracellular enzymes: Streptokinases (fibrinolysin), hyaluronidase, C5a peptidase, DNAses
19
Q

What is S. pyogenes resevoir?

A

Human nasopharynx; Transmission by direct contact or aerosol. Attachment initially by lipotechoic acids via fibronectin.

20
Q

What happens if S. pyogenes releases erythrogenic toxin?

A

Scarlet fever; Usually a couple days after pharyngitis symptoms. Can get sequelae due to delayed immune reaction; Glomerulonephritis, rheumatic fever.

21
Q

What are some S. pyogenes diseases?

A

Impetigo, Erysipelas, necrotizing fascitis, TSS, rheumatic fever

22
Q

Describe Necrotizing fascitis.

A

Deep subcutaneous infection, destruction of fat and muscle; Starts like cellulitis but gets worse.

23
Q

How is S. pyogenes TSS different from S. aureus?

A

S. pyogenes TSS is systemic; Production of pyrogenic exotoxin.

24
Q

How is rheumatic fever caused?

A

Antibody to bacteria cross reacts with heart tissue; Type 2 hypersensitivity. Chronic and progressive damage. Usually following strep throat, not skin infection.