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Flashcards in Streptococci Deck (18)
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1
Q

Characteristics of Streptococci?

What is unique about them?

How are they classified?

A
  • Gram positive, coccus shaped, grows in chains
    • Grow in chains because they divide in a plane, unlike staph for example
    • “Streptos” genus = bent/twisted in greek
  • Non-motile, non-endospore forming (despite being positive)
  • Classified by pattern of hemolysis on blood agar (make toxins that destroy RBCs)
2
Q

Classification types?

A
  • α-hemolytic - partial hemolysis (oxidation of hemoglobin)
  • β-hemolytic - total lysis
  • γ-hemolytic - no hemolysis
3
Q

List the α-hemolytic species

Describe the function of each bacteria in the virdians group

A
  1. S. pneumoniae (pneumococcus) (no. 4 killer)
  2. Viridans group:
    • S. viridans - gets into blood, pre-existing damaged heart tissue = endocarditis
    • S. mutans - Kit Kat is fermented by this (on your teeth) = tooth decay
    • S. thermophilus - used industrially to make dairy products; non-pathogenic
4
Q

List the β-hemolytic species (group A-C) and describe their function

A
  1. S. pyogenes (Group A strep) - strep throat (no. 5 killer)
  2. S. agalactiae (Group B strep) - can cause meningitis (neonatal)
  3. S. equi (Group C strep) - horse pathogen
5
Q

List the γ-hemolytic species (group D, N)

What is unique about this group?

A
  1. Enterococcus species (Group D strep) - drug resistant pathogen
  2. Lactococcus lactis (Group N strep) - food grade organism

Not considered streps - too genetically distinct

6
Q

How are strep groups (ex., strep A) decided?

A

Rebecca Lancefield: classified groups using surface carbohydrate antigens which successfuly distinguishes strains

7
Q

Describe the pathogen S. pyogenes

A
  • A common human specific pathogen w/ human reservoir
  • Extracellular; inflammation, neutrophil recruitment, abscesses
  • Pyo = pus
  • 5-15% asymptomatic carriage in school age kids
    • Can carry for >2 years without infection; thus great colonizer
    • Master at hiding from immune system using virulence factors (inhibit innate)
8
Q

What is the main virulence factor for S. pyogenes? What does it do?

Describe the main serotypes

A
  1. M. protein
    • Anti-phagocytic cell surface protein
    • Binds to C4 binding protein (complement proteins) which protects own cells from complement system
      • Strep takes it = protection from complement
    • Antibodies can target M. protein
      • Workaround = strep makes >100 M protein serotypes (1 antibody targets only 1 serotypes)
        • M1, M3 = pharyngitis, invasive disease
        • M18 = rheumatic fever -
        • Unsure why the associations exist
9
Q

What are the other 3 virulence factors?

A
  1. Hyaluronic acid capsule
    1. Polysaccharide on surface
    2. Protects strep from complement (blocks receptor binding to C3b) -
    3. Major component of our OWN tissue as well, thus, cannot make vaccine against capsule
  2. Hemolysins
    1. Makes O and S streptolysins
    2. Made by all group A strains - important
      1. S: produces β-hemolysins
      2. O: oxygen turns it off
  3. Superantigens
    1. Secreted exotoxins (Spe’s)
    2. Function as potent activators of T cells –> cytokine storm –> TSS
    3. Not emetic (vomit-inducing) like staph enterotoxins (SE’s) in Staph Food Poisoning
10
Q

Characteristic of pharyngitis a.k.a. strep throat?

How is it treated?

A
  • Common in school age children, teenagers
  • Severe sore throat; no cough
  • Swollen lymph nodes, pus (tonsillar exudate)
  • Skin rash
  • Treatment:
    1. β-lactams (no documented resistance until recently…)
    2. Erythromycin (resistant strain exists); used in case of penicillin allergy
11
Q

Characteristics of impetigo?

A
  • Also caused by S. aureus (staph)
  • Superficial skin infection; red sores
  • Highly contagious
  • Topical ABx
12
Q

Characteristics of scarlet fever?

A
  • Rash develops during strep throat
  • Strawberry tongue, fever
  • Caused by “scarlet fever toxins”; Streptococcal pyogenic exotoxins (SpeA, SpeC)
    • Thus this rash is NOT a sign of bacteremia
13
Q

What is Rheumatic Fever? What does it cause?

A
  • Occurs 2-3 weeks after infection (of strep throat or scarlet fever)
  • Autoimmunity caused by antibody cross-reactivity with M protein (strep –> response to M –> attack host tissue when no strep left)
  1. Acute rheumatic fever = initial, acute, painful swollen joints
  2. Rheumatic heart disease = damaged heart valves (chronic)
    • Congestive heart failure = increase risk of infective endocarditis by other pathogens

Rare in developed because strep is treated quickly

14
Q

What causes Invasive Streptococcal disease?

A
  1. Bacteremia: blood isolation
  2. Soft tissue: necrotizing fasciitis
  3. Muscle: necrotizing myositis
  4. TSS
    • Combine 2-4 to get flesh eating disease; as dangerous as bubonic plague
15
Q

Describe the risk factors and treatment for invasive strep

A

Risk factor

  1. Tissue injury
  2. Use of nonsteroidal anti-inflammatory agents
  3. Chicken pox (60 fold increase) as the lesions from pox = portal of entry
  4. Postpartum
  5. Lack of immunity to superantigens and M protein
  6. MHC class 2 halotypes; by chance, may bind the superantigens really well = more likely to develop invasive disease

Treatment

  1. ABx
  2. Amputation, debridement
  3. IVIG (intravenous immunoglobulin)
    • To neutralise superantigen activity, opsonize S. pyogenes
16
Q

What is genetic variability in S. pyogenes caused by?

A

Genetic variability in strep is due to mobile elements that have inserted around the chromosome

17
Q

Describe the findings of the mouse model

A
  1. Deletion of SpeA decreases virulence significantly, same with deleting all superantigens
    • Therefore injecting SpeA antibodies = decrease infection in mice (superantigens = potential future vaccine)
  2. Deletion of T cells = inhibition of infection!
    • Making mice immunodeficient = infection goes away
    • Therefore, functional T cells are required for nasopharyngeal infection (unique to S. pyogenes)
18
Q

What is important about the MHC class 2 during a strep infection?

A

Strep is a human-specific pathogen and so is only adapted to the MHC class 2; mouse model with mouse MHC class 2 = minimal colonisation

  • Therefore, MHC class II is an important contributor to host-specific tropism by S. pyogenes