Streptococcous Flashcards

1
Q

Describe Streptococci

A
  • Gram-positive, coccus shaped,
  • aerotolerant anaerobes, grow in chains
  • ”Streptos” – Greek for bent or twisted
  • non-motile, non-endospore forming
  • Initially classified by their pattern of hemolysis on blood agar
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2
Q

what is the difference between alpha-hemolytic

beta-hemolytic and gamma-hemolytic streptococci how are they classified?

A

“Lancefield Classification
• classified on the basis of surface carbohydrate antigens

Alpha

  • S. pneumoniae (pneumococcus)
  • viridans group including:
  • S. viridans - endocarditis (important for causing infection but non pathogenic)
  • S. mutans – tooth decay
  • S. thermophilus – dairy food (not infectious)

Beta (disease causing)

  • S. pyogenes (Group A Streptococcus)
  • S. agalactiae (Group B Streptococcus)
  • S. equi (Group C Streptococcus)

Gamma

  • Enterococcus species (Group D Streptococcus)
  • Lactococcus lactis (Group N Streptococcus)
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3
Q

describe S. pyogenes

A

Common human specific pathogen

extracellular pthogen

“pyo” = pus

5-15% asymptomatic arriage

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4
Q

What does S. pyogenes cause?

A

historically a major cause of mortality due to

  • scarlet fever
  • pueperal sepsis
  • wound infections in soldiers

Today a common cause of

  • Pharyngitis
  • impetigo
  • sever invasive stretococcal disease
  • streptococcal toxic shock syndrome (flesh eating disease)
  • important cause of post infection sequelae including acute rheumatic fever (Get infection, infection goes away and disease appears)
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5
Q

How dangerous are S. pyogenes virulence factors?

A

Arsenal of key virulence factors

a mastero at hiding from immune system

armed to cause severe damage

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6
Q

What does the M protein do in S. pyogenes?

A

an anti-phagocytic cell surface expressed protein
– binds “Factor H” of the complement system
– Factor H is a complement regulatory protein that
protects self cells from C3b deposition
– >100 M protein serotypes
– hypervariable(changing) N-terminus – basis for M protein serotypes
• e.g. M1, M3 typically cause pharyngitis and
invasive disease
• e.g. M18 typically cause acute rheumatic fever

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7
Q

How can humans combat M proteins?

A

antibodies to a particular M protein serotype will opsonize and kill these bacteria

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8
Q

What are the 2 hemolysins(targets red cells and other cells) S. pyogenes makes?

A

Streptolysins (O and S)
– streptolysin S produces β-hemolysis
– streptolysin O is “O2-sensitive” – can be seen under anaerobic conditions

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9
Q

What is a hyaluronic acid capsule in S. pygoenes

A
  • a polysaccharide
  • hyaluronic acid is a major component of host tissues – bacteria “look like self”
  • can also block opsonization through
  • C3b (typical of other capsules)
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10
Q

What are streptococcal pyrogenic exotoxins and what do they do? (Spe’s)

A
  • Secreted exotoxins
  • superantigens
  • all S. pyogenes strains make between 4 and 8 different superantigens
  • function as potent activators of T cells resulting in a cytokine storm disease known as the toxic shock syndrome
  • Not emetic like the staphylococcal enterotoxins
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11
Q

What does the DNAse (Streptodornase) do?

A
  • Lets bacteria escape from NET
  • enzyme that degrades DNA
  • secreted exotoxin
  • targets NETs (Neutrophil extracellular traps)
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12
Q

How do NETs form?

A
  1. Activation leads to formation of reactive O2 species
  2. Loss of nuclear structure – spilling into cytoplasm
  3. DNA mixes with granules
  4. Loss of cell membrane integrity and release of NETs
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13
Q

what deomgraphic is pharyngitis most common in?

A

school aged children and teenagers

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14
Q

What are symtoms of pharyngitis

A
  • fever and severe sore throat
  • typically absence of cough
  • swollen cervical lymph nodes
  • tonsillar exudate (pus)
  • skin rash
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15
Q

How do you determine if strep throat (pharyngitis) is viral or bacterial?

A

diagnosed by a rapid strep test

  • positive test = strep throat = antibiotics
  • negative test = throat culture

treated with antibiotics

  • penicillins (no documented resistance!!!!)
  • erythromycin (resistant strain exist)
  • erythromycin only if allergic to penicillin

untreated pharyngitis can lead to a number of complications including acute rheumatic fever

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16
Q

Describe Impetigo

A
  • most common among children
  • also caused by S. aureus
  • a superficial skin infection
  • red sores that forms crusts, normally on the face
  • highly contagious through direct contact (especially children)
17
Q

Describe the Scarlet fever

A

“scarlatina”

rash that develops typically during strep throat

5-15 years of age

high fever, “strawberry tongue”

rash – small red bumps

  • normally on the chest and stomach
  • can look like a sunburn
  • rough sandpaper
  • lasts 2-7 days

toxin mediated - caused by the “scarlet fever toxins” (superantigens)

  • same toxins as streptococcal pyrogenic exotoxins
18
Q

Describe Acute Rheumatic fever

A

a “post infection” sequelae

occurs 2-3 weeks after infection (e.g. strep throat or scarlet fever)

typically occurs in children 5-15 years of age

caused by antibody cross reactivity with the M protein

a form of autoimmunity

rare in developed counties since 1960s but endemic in many developing countries

19
Q

What can Acute rheumatic fever cause

A

can cause painful swollen joints

heart tissue targeted = damages heart valves

acute rheumatic fever = the initial flare up

rheumatic heart disease = when the valves are damaged

can be permanent

can lead to congestive heart failure – heart can’t pump enough blood

patients are at increased risk for infective endocarditis by other pathogens

20
Q

Is group A strep a top 10 killer for individual pathogens?

A

Yes it is # 9 on the list of global mortality from individual pathogens

21
Q

Describe invasive streptococcal disease

A
  • rare in developed countries but very serious
  • • “invasive streptococcal disease” is defined as isolation of S. pyogenes from a normally sterile site
  • • blood isolation = bacteremia
  • • if soft tissue involved = necrotizing fasciitis
  • • if muscle involved = necrotizing myositis
  • The disease: Invasive streptococcal disease
  • • streptococcal toxic shock syndrome = flesh-eating disease
22
Q

Describe events of Day 0 - 4 of invasive streptococcal disease

A

Trauma (day zero)

  • Discomfort in the general region of the
  • Pain that is out of proportion with the

severity of the injury (day one)

  • Influenza-like symptoms
  • Swelling or sunburn-type redness in the general region of the injured area (day two)
  • Worsening of the condition and less frequent urination
  • Large, boil-like blisters (bullae) containing pus (day 2-3)
  • Haemorrhage from the bullae
  • Gangrene (day four)
23
Q

What is treatment for Invasive Streptococcal disease

A
  • Antibiotics
  • Supportive therapy
  • Debridement/amputation - take tissue out
  • Intravenous immunoglobulin (IVIG) - pooled antibodies
  • neutralize superantigen activity
  • opsonization of S. pyogenes
24
Q

What are risk factors for invasive streptococcal disease?

A

Tissue injury (penetrating and nonpenetrating)

Prior use of nonsteroidal antiinflammatory agents

Chicken pox in children (58-fold increased risk)

  • should get vaccine

Postpartum

Lack of immunity to superantigens and M protein

MHC class II haplotypes (ie. superantigen receptors)

  • Some bind better to superantigen making the disease mroe infections
25
Q

What does the superantigen do to the T cell

A

Binds to less variable regions (B region)

only 50 possibilities in humans

26
Q

How many superantigens of S. pyogenes are there?

A

Many including

SmeZ

SpeG

SpeA

SpeC

SpeLM

many mobile genetic elements

maybe why strep is associated with different diseases depending on the strain

27
Q

What is the mouse model of S. pyogenes?

A
  • S. pyogenes poorly colonizes the mouse nasopharynx
  • mouse MHC class II are poorly bound by bacterial superantigens
28
Q

what happens in transgenic mice that express human MHC class II?

A

There is a 100 000 fold difference in infections due to human MHC II markers

29
Q

Can strep colonize w/o certain superantigens?

A

In the mouse model strep has been observed to colonize much less efficiently without the superantigen SpeA