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Medsci 202 > Lecture 6: Streptococci and Disease > Flashcards

Lecture 6: Streptococci and Disease Flashcards

1
Q

is strep gram + or -

A

gram +

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2
Q

how do strep often grow

A

in chains, some produce capsules

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3
Q

can strep be treated with penicillin

A

yes - no beta lacatmase gene found

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4
Q

how are streptococci classified

A

by serologic specificity of cell wall group specific carbohydrates

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5
Q

where can strep be found

A

asymptomatic colonisation of upper respiratory tract (~20% carriers)

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6
Q

how is strep transmitted

A

human to human, respiratory droplets, wound infections

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7
Q

incidence in populations

A

highest in maori and pacific island populations

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8
Q

the species can be further divided into different ____ based on variations in the ____

A

M serotypes, M protein

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9
Q

List the strep virulence factors

A

Adhesins, Pili, Cytolysins, Spreading factors, Superantigens, Immune evasion factors

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10
Q

MSCRAMMS

A

Microbial surface components recognizing adhesive matrix molecules

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11
Q

explain how adhesins/MSCRAMMS work

A
  • cell wall-attached proteins found in Gram-positive bacteria
  • bind to host extracellular matrix proteins eg. fibronectin, elastin, laminin, vitronectin and collagen.
  • important for tissue colonization.
  • Examples are M protein (binds to fibronectin,
    fibrinogen, CD46), F protein (binds to fibronectin) and Cpa (collagen-binding protein).
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12
Q

Explain how Pili work

A
  • long hair-like structures protruding from cell surface. - - cell wall-anchored
  • built from covalently assembled protein monomers that form the pilus fiber.
  • A tip protein is believed to function as an adhesin
  • Pili have also been implicated in cell
    aggregation (biofilm formation).
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13
Q

What are the two cytolsins in strep

A

streptolysin O
streptolysin S

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14
Q

Streptolysin O

A

(SLO): oxygen-labile cytolysin that forms pores in host cell membrane

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15
Q

Streptolysin S

A
  • (SLS): oxygen-stable cytolysin
  • lyses leucocytes, erys and platelets.
  • Completely lyses red blood cells = β-hemolysis.
  • highly antigenic
  • anti-SLO antibodies are tested for diagnostic of previous S. pyogenes infection in suspected cases of acute rheumatic fever.
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16
Q

what are spreading factors

A

proteins that facilitate spreading from a localized infection (e.g., abscess) to surrounding tissue or blood (causing bacteremia).

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17
Q

give examples of spreading factors

A

lipases, nucelases, hyaluronidase, proteases, streptokinase (fibrinolysin)

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18
Q

lipases

A

hydrolyse lipids, for invasion of cutaneous tissues

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19
Q

nucleases

A

hydrolyses DNA, decrease viscosity of pus

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20
Q

hyaluronidase

A

hydrolyses hyaluronic acid in connective tissue

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21
Q

proteases

A

streptococcal cysteine protease (SCP) with wide substrate spectrum

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22
Q

Streptokinase (fibrinolysin)

A

causes fibrinolysis (dissolves clots)

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23
Q

The streptococcal SAgs are ____ and ____ related to the staphylococcal superantigens, however, they do not cause ____ (in contrast to some staphylococcal
SAgs). SAgs trigger massive release of ____ (TNF-α, IFN-γ) and over-stimulation of the host ____, resulting in systemic ____.

A

structurally, functionally, food poisoning, pro-inflammatory cytokines, immune response, inflammation

24
Q

What are the immune evasion factors of strep

A

capsule, m protein, C5a peptidase

25
Q

capsule

A

a dense hyaluronic acid coat that prevents opsonisation with ab and complement
(inhibits phagocytosis). Only in some strains

26
Q

M-protein

A

in addition to its function as an adhesin, M protein prevents complement factor
C3b from opsonising (antiphagocytic).

27
Q

C5a peptidase

A

a protease that cleaves complement factor C5a (a chemoattractant) preventing neutrophil migration to the site of infection.

28
Q

S. pyogenes and diseases

A

impetigo, pharyngitis, scarlet fever, cellulitis, necrotising fasciitis (flesh eating disease), Sreptococcal toxic shock syndrome (STSS), rheumatic fever and rheumatic heart disease

29
Q

pyoderma/Impetigo

A
  • localised purulent cutaneous infection
  • S. pyogenes colonisaition after contact with inferted person or fomites
  • subcutaneous tissue infection through breaks in skin
  • Highly communicable
  • crowded places with hot/humid climate.
  • kids most affected
30
Q

Pharyngitis

A
  • develops 2-4 days after exposure to S. pyogenes.
  • sore throat, fever, reddened pharynx, tonsillitis, pus filled vesicles on tonsils.
31
Q

Scarlet fever

A
  • complication of pharyngitis
  • can develop into serious systemic disease.
  • Caused by strains that produce the superantigen pyrogenic exotoxin A (SPE-A) = “scarlet fever toxin”. = superantigen
  • fever, sore trhoat, “strawberry tongue”, rash on chest
32
Q

Cellulitis

A
  • infection of skin that involves subcutaneous tissue.
  • acute and rapidly spreading infection (hyaluronidase, DNAse)
33
Q

Necrotising fasciitis (flesh eating disease)

A
  • deep infection of the skin, 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, and hyaluronidase)
  • often develops into severe systemic disease with high mortality (toxic shock syndrome).
34
Q

STSS: often follows ____ and ____.
STSS has a mortality rate of ____ (more severe than staphylococcal TS). Massive release
of ____ occurs in response to ____ secretion. Overstimulation of the immune response leads to ____. Symptoms include ____, ____, ____ and ____.

A

necrotising fasciitis, sepsis, 30-70%, pro-inflammatory cytokines, superantigen, systemic inflammation, fever, headace, multiorgan failure, shock

35
Q

Rheumatic Fever and Rheumatic Heart Disease:
Develops after ____ due to S. pyogenes. Inflammation of
endocardium, myocardium, pericardium results in thickened and deformed ____ and
____ in myocardium. The disease often starts with ____in joints
(arthritis).

ARF is an ____, NOT an infection! It is triggered by ____, an antibody cross-reaction where antibodies generated against the M protein also bind (cross-
react) to ____ (cardiac myosin, collagen in joints, …). This triggers a ____ immune response.

A

untreated/chronic sore throats, heart valves, granulomas, inflammatory changes, autoimmune disease, molecular mimicry, host proteins, type II hypersensitivity

36
Q

S. agalactiae (group B streptococcus)

A

A gram-positive coccus that grows in long chains. It is either β-hemolytic or non-hemolytic and carries the Lancefield group B specific carbohydrate.

37
Q

S. agalactiae (group B streptococcus)

A

A gram-positive coccus that grows in long chains. It is either β-hemolytic or non-hemolytic and carries the Lancefield group B specific carbohydrate.

38
Q

group B streptococcus causes ____ of ____ and ____. Most infections in newborns are acquired from mother during ____ or at ____.

A

asymptomatic colonisation, upper respiratory, genitourinary, pregnancy, time of birth

39
Q

neonatal disease of s. agalactiae (GBS)

A

pneumonia, becteremia, sepsis, menigitis

40
Q

infections in pregnant women (GBS)

A

UTI, bacteremia

41
Q

viridans streptococci

A

Asymptomatic colonisation of oropharynx, gastrointestinal tract and genitourinary tract.
Commensales of mouth flora (S. mitis, S. mutants, …)

42
Q

virulence factors of viridans strep

A

Less virulent than S. pyogenes (less immune evasion toxins). Some carry adhesins/pili for
binding to teeth, biofilm (dental plaque).

43
Q

Viridans strep diseases

A
  • dental caries: S. mutants, S. sobrinus
  • bacterial endocarditis: S. gordonii, S. mitis
  • septic shock in immuno-compromised patients
44
Q

Streptococcus pneumoniae shape

A

Lancet-shaped’ diplococci or short chains. Most strains have outer capsule

45
Q

strep penumoniae epidemiology

A

Endogenous spread from colonised pharynx to lungs, sinuses, ears, …
Conditions that interfere with bacterial clearance are risk factors (e.g.,
immunocompromised patients)

46
Q

Streptococcus pneumoniae - virulence

A

S.pneumoniae carries antiphagocytic capsule and produces pneumolysin, a cytolysin that
destroys ciliated epithelial cells.

47
Q

Streptococcus pneumoniae - diseases

A
  • Pneumonia (60% of bacterial pneumonias), agzer aspiration, bacteria multiply in alveolar space, infiltration of neutrophils and alveolar machrohages, inflammaion (most damage caused by immune response), symptoms: fever, yellowish sputum, chest pain
  • Meningitis: headache, fever, sepsis, high mortality
  • Bacteremia: more common in patients with meningitis
  • sinusitus and otitis media: usually after virus infection
48
Q

rheumatic fever and rheumatic heart disease mechanism

A

conserved region in GAS protein structurally resembles certain host antigen (molecular mimicry)

GAS - group a strep. RF is Autoimmune disease

49
Q

molecular mimicry

A

different proteins share antibody epitopde

50
Q

epitope

A

small region with a protein or sugar that us recognized by an antibody or T cell receptor

51
Q

RF autoimmune anitbody reaction

A

s. pyogenes, m protein, antibody binding
antibody cross reaction to protein from eg. cardiac myofibre (note, - this is not M protein but a different ptotein that is structurally similar)
antibody rects with own tissue
causes RF

52
Q

explain how Acute rheumatic fever (ARF) comes about

A
  • cross reactive antibodies trigger a type II hypersensitivity reaction
53
Q

explain type II hypersensitivity reaction

A
  1. neutrophil adherence to host tissue
  2. frustrated phagocytosis - cant phagocytose large tissue
  3. extracellular enzyme release
54
Q

explain the normal antimicrobial action

A
  1. microbe opsonised by c3b and labeled for destruction
  2. phacoytes like neutrophils have Fc receptro for andtibody adn C3b receptor to bind to C3b
  3. phagocytsis
  4. lysosome fusion
55
Q

streptococcus pneumonia - shape

A

gram - postive diplococcus

56
Q

pneumonia risk factors and incidence

A

30-60% children and <10% carriers
- young age, close contact, viral inections

Medsci 202 (28 decks)

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