bacterial virulence Flashcards

1
Q

what is impedin

A

enables the organism to avoid host defence mechanisms

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2
Q

what is aggressin

A

causes damage to the host directly

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3
Q

what is modulin

A

induces damage to the host indirectly

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4
Q

what are the main staphylococcal infectons of the skin

A

S.aureus

  • 20%-(60%) colonisation (carriage)
  • coagulase positive
  • nasal strain can protect

S.epidermis

  • 100% colonisation
  • skin and mucosa membranes
  • coagulase negative
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5
Q

explain the pathology of S.aureus

A

Superficial lesions - boil to abscesses

Systemic - life threatening

Toxinoses - toxic shock, scaled skin syndrome

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6
Q

what are superantigens

A

Common theme disrupting immune system and coordination by over stimulation. Activate 1 in 5 T cells. TSST-1 in particular is associated with toxic shock. Massive release of cytokines and inappropriate immune response.

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7
Q

what is diagnostic criteria for toxic shock syndrome

A

Fever 39*
Diffuse macular rash and desquamation
Hypotension < 90 mmHg (adults)
>3 organ systems involved eg liver, blood, renal, mucous membranes

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8
Q

what are adhesions

A

extra cellular matrix molecules present on epithelial, endothelial surfaces as well as components of blood clots

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9
Q

what is panton-valentine leukocidin

A
  • A toxin produced by certain types of staph aureus
  • Specific toxicity for leukocytes
  • PVL associated with severe skin infections
  • PVL and alpha-toxin associated with CA-MRSA responsible for necrotising pneumonia and contagious severe skin infections
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10
Q

what is streptococcus pyogenes

A

common presentation as pharyngitis or streptococcal sore throat, scarlet fever

  • Group A streptococci
  • Skin infections can be impetigo, cellulitis, necrotising fasciitis
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11
Q

what is the lance field system

A

Lancefield grouping is a system of classification that classifies catalase-negative Gram-positive cocci based on the carbohydrate composition of bacterial antigens found on their cell walls.

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12
Q

what are GAS skin diseases

A
  • Impetigo (usually face)
  • Cellulitis - deeper skin infection in the dermis that is not associated with necrosis
  • Erysipelas (localised) - fever, rigours and nausea
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13
Q

how can new strains of a disease emerge

A

horizontal gene transfer

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14
Q

what do opportunistic infections and toxinoses depend on

A

genotype and expression of virulence proteins

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15
Q

what are some pyogenic infections caused by staph aureus

A
  • boils, carbuncles
  • surgical site infection
  • abscesses
  • impetigo
  • mastitis
  • pneumonia eg ventilator assisted
  • endocarditis
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16
Q

what are some toxin-mediated infections

A
  • scaled skin syndrome
  • pemphigus neonatorum
  • toxic shock syndrome
  • food poisoning
17
Q

what is the effects of s aureus manipulating B cells

A

inability to develop adaptive immunity

18
Q

what is the effect of s aureus manipulating plasma blasts

A

inability to develop adaptive immunity

19
Q

what is the effect of s aureus manipulating T cells

A

inability to develop adaptive immunity

20
Q

how can understanding virulence factors impact on clinical care

A
  • next generation sequencing (more rapid diagnosis)
  • molecular techniques (PCR/antibodies etc)
  • diagnoses and understanding pathology/risk
  • isolation and quarantine
  • vaccines/anti-infectives
21
Q

what is a virulence factor

A

component of micro-organism that can be assigned to its ability to cause that disease

22
Q

what do opportunistic infections and toxinoses depend on

A

genotype and expression of virulence proteins

23
Q

where are s.pyrogenes normally found

A

pharynx and also adheres to skin

24
Q

what os the variation in disease and virulence an effect of

A

variation in genes and the proteins expressed by pathogen