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Medsci 202 > Lecture 11- Streptococci and disease > Flashcards

Lecture 11- Streptococci and disease Flashcards

1
Q

Describe the general characteristics of streptococci?

A
  • Gram positive cocci
  • Grow in chains
  • Some strains produce capsules
  • Susceptible to penicillin(no B lactamase found)
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2
Q

Classify streptococci

A 
Group A= S.PYOGENES
Group B= S.Agalactiae
Group C= S.Disgalactiae. S.equi
Group D= S. bovis, Enterococcus spp
Group F= S. intermedius
No lancefield antigen: S.pneumoniae, viridans group
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3
Q

Describe diagnostic lab test to identify Streptococci?

A

Catalase test should give no bubbles for streptococci. Distinguish from S. aureus which gives bibbles

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4
Q

Describe diagnostic lab tests to classify streptococci?

A

If hemolysis on blood agar= B hemolytic Streptococci
If no hemolysis: 3 tests can be performed
Test 1- Bacitracin. If bacitracin susceptible then GAS species. If bacitracin resistant then GBS species of streptococci
Test 2- Bile esculin agar. If hydrolyse esculin then it is GDS Enterococcus. If no hydrolysis of esculin then do further tests
Test 3- antibiotic test with OPTOCHIN. If optochin susceptible then S.pneumoniae. If optochin resistant then viridans strep

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5
Q

Describe S. pyogenes epidemiology

A
  • Asymptomatic colonisation
  • can survive on dry surfaces
  • spread from wound infections or respiratory droplets from person to person(crowding)
  • Higher infection rates in maori and pacific island populations
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6
Q

List the streptococcal virulence factors of Group A S. Pyogenes- adhesins?

A

1) MSCRAMMS
- cell wall attached proteins
- bind to host extracellular matrix proteins
- Examples= M protein(antiphagocytic), F protein(binds fibronectin) and Cpa(collagen binding protein)
2) Pili
- Long hair like structures
- cell wall anchored
- tip protein functions as adhesin
- Cell aggregation(biofilm formation)

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7
Q

List the streptococcal virulence factors of Group A S. Pyogenes- cytolysins?

A
  • Streptolysin O (SLO)= oxygen liable-forms pores in host cell membrane
  • Streptolysin S(SLS)= oxygen-stable- lyses red blood cells(B-hemolysis), antigenic, anti SLO antibodies test for acute rheumatic fever
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8
Q

List the streptococcal virulence factors of Group A S. Pyogenes- spreading factors?

A

Same as S. aureus except Staphylokinase is called Streptokinase

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9
Q

What are the superantigens associated with S.pyogenes?

A

Streptococcal pyogenic exotoxins(SPE-A)
Streptococcal mitogenic exotoxin Z(SMEZ)
Structurally and functionally related to S. aureus superatigens ie result over-response and inflammation. However they do not cause food poisoning like S. aureus

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10
Q

List the immune invasion factors for S.pyogenes?

A

Capsule
- Hyaluronic acid coat= inhibits phagocytosis
-M protein= adhesin and functions to prevent complement factor C3b from opsonising(antiphagocytic).
C5a peptidase= cleaves complement factor C5a preventing neutrophil migration to the site of infection.

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11
Q

What are the three types of streptococcal diseases?

A 
Non-invasive disease
- pharyngitis, tonsillitis
- pyoderma (impetigo) 
- cellulitis
Invasive disease
- necrotising fasciitis (flesh-eating disease)
- streptococcal toxic shock syndrome
Post-streptococcal disease
- acute rheumatic fever!
- acute glomerulonephritis
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12
Q

Describe characteristics of pharyngitis and tonsillitus?

A

Develops 2-4 days after exposure to S. pyogenes (sore throat, fever, reddened pharynx, pus-filled vesicles on tonsils)

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13
Q

Describe characteristics of scarlet fever?

A
  •   complication of pharyngitis!
  •   production of pyrogenic exotoxin A (SPE-A) = “scarlet fever toxin” = superantigen!
  •   can develop into serious systemic disease!
  •   fever, sore throat, “strawberry tongue”, characteristic rash on chest
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14
Q

Describe characteristics of impetigo?

A
  •   purulent infection of the skin (“derma”)!
  •   S. pyogenes colonisation after contact with infected person or fomites!
  •   spread to subcutaneous tissue through break in skin (e.g. scratch)!
  •   highly communicable, often in hot/humid climate!
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15
Q

Describe characteristics of cellulitis?

A
  •   infection of skin that involves subcutaneous tissue!

*   acute, rapidly spreading infection (hyaluronidase, DNAse)!

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16
Q

Describe characteristics of Necrotising fasciitis(flesh eating disease)?

A

•  deep infection of the skin that involves destruction of muscles
•  S. pyogenes is introduced through e.g. minor cuts, trauma, burn
surgery or vesicular viral infection
•  deep tissue infection is supported by spreading factors!
(DNAses, proteases, hyaluronidase)
•  often development into severe systemic disease with high mortality

17
Q

Describe characteristics of streptococcal toxic shock syndrome(STSS)?

A

•  deep infection of the skin that involves destruction of muscles
•  S. pyogenes is introduced through e.g. minor cuts, trauma, burn,!
surgery or vesicular viral infection.!
•  deep tissue infection is supported by spreading factors!
(DNAses, proteases, hyaluronidase)!
•  often development into severe systemic disease with high mortality

18
Q

Describe rheumatic fever and rheumatic heart disease?

A
  •   Develops after untreated/chronic sore throats due to GAS
  •   inflammation of endocardium, myocardium, pericardium resulting in thickened and deformed valves and granulomas in myocardium
  •   inflammatory changes in joints (arthritis), blood vessels!
  •   Autoimmune disease, NOT infection !!

Mechanism: a conserved region in GAS protein structurally resembles certain host antigens (‘molecular mimicry’). Molecular mimicry is when different proteins share antibody epitope. So M. protein from S.pyogenes amd a host protein share a small section which is similar and this results in a antibody cross reaction. Hypersensitivity reaction- inflammation

19
Q

Describe S. agalactiae- group B streptococcus physiology, epidemiology and disease?

A

Physiology
•  Gram-positive cocci in long chains
•  -hemolytic or non-hemolytic
•  carry Lancefield group B specific carbohydrate
Epidemiology
•  asymptomatic colonisation of upper respiratory & genitourinary tract
•  most infections in newborns acquired from mother during pregnancy, at time of birth or the first week after birth
Disease
•  neonatal disease: pneumonia, bacteremia, sepsis, meningitis
• Urinary tract infections in pregnant women

20
Q

Describe physiology, epidemiology and disease caused by Viridans Streptococci?

A

Physiology
•  hemolytic or non-hemolytic
•  carry no specific Lancefield group antigen
Epidemiology
•  asymptomatic colonisation of oropharynx, gastrointestinal tract and genitourinary tract
•  commensales of mouth flora (S. mitis, S. mutants, …)
Virulence Factors
•  less virulent than S. pyogenes (less immune evasion toxins)
•  adhesins/pili for binding to teeth, biofilm (dental plaque), S. mutants
Disease!
•  dental caries
•  subacute endocarditis
•  septic shock in immuno-compromised patients

21
Q

Describe physiology, epidemiology and virulence by Streptococcus pneumoniae?

A

Physiology
•  ‘lancet-shaped’ diplococci or short chains
•  most strains with outer capsule
Epidemiology
•  endogenous spread from colonised pharynx to lungs, sinuses, ears,..
•  conditions that interfere with bacterial clearance are risk factors
e.g. recent viral lung infection, chronic pulmonary disease, diabetes
Virulence
•  antiphagocytic polysaccharide capsule
•  pneumolysin: destroys ciliated eptithelial cells

22
Q

Describe diseases caused by Streptococcus pneumoniae?

A

•  Pneumonia (60% of bacterial pneumonia)
- after aspiration, bacteria multiply in alveolar spaces
- infiltration of neutrophils and alveolar macrophages
-  inflammation, most damage caused by immune response
-  Symptoms: Fever, yellowish sputum, chest pain
•  Meningitis: headache, fever, sepsis, high mortality
children and elderly have increased risk
•  Bacteremia: more common in patients with meningitis
•  Sinusitis and Otitis Media: usually after virus infection

23
Q

Describe Enterococcus spp?

A
  •   formerly known as group D streptococcus
  •   colonise the gastrointestinal tract (very common)
  •   can spread to other mucosal surfaces when normal gut flora is suppressed by broad-spectrum antibiotics
  •   increased risk in patients with prolonged hospitalisation
  •   UTIs, wound infection, bacteremia and subacute endocarditis

Medsci 202 (15 decks)

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