Lecture 24 - Burkholderia Flashcards

(11 cards)

1
Q

describe the bukholderia genera and list the 4 pathogenic species

A
  • G-ve rods, 70+ species, diverse niches, most non-pathogenic
    1. cepecia complex (BCC)
    2. mallei
    3. pseudomallei
    4. Thailandensis
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2
Q

what is the location, disease and resistance of Bulkholderia cepecia complex (BCC)?

A
  • soil, plants (onion rot), mammals = recycling organics
  • Cystic fibrosis = nosocomial opportunistic, immunocomp
  • contaminated hospital equipment and liquids
  • Fatal cepacia syndrome = necrotising pneumonia, resp failure, bacteremia
  • Resistant to aminoglycosides, quinolones, polymyxins, beta lactams
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3
Q

list the 5 pathogenic components ofBulkholderia cepecia complex (BCC)

A
  1. Cable pilus = epithelial invasion
  2. Biofilms
    3.Exopolysac (EPS) cepacian = colonisation and persistence
  3. Antimicrobial resistance
  4. B cepacia epidemic strain marker (BCESM) on genomic island for metabolism and virulence
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4
Q

describe b mallei and the animal/human disease forms it causes

A
  • g-ve aerobic non-motile facultative intracellular
  • never isolated from environ
  • glanders in horses = swelling below jaw and mucous discharge from nostrils
  • humans = nodular lung lesions, fever, septicaemia, death
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5
Q

describe the history of b mallei

A
  • hippocrates, aristotle, apsyrtus
  • Isolated 1882 by loffler and schutz and french scientists
  • 1900 control programs
  • WW1 and 2 bioterrorism = germany vs russia, japan, russia vs afghan
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6
Q

how does the mallein test for b mallei work? who made it and when?

A
  • glycerin fluid with glanders put in horses eyes = swelling after 1-2 days positive
  • russians 1891
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7
Q

describe the transmission, location, disease and risk factors of b pseudomallei

A
  • melioidosis = rapid growth, motile, no lesions meant not glanders
  • tropical, contaminated soil/air/water esp after rain
  • Endemic in SE asia and N aussie
  • Cutaneous infection = asymptomatic, acute septicaemia/chronic/latent
  • fever, pneumonia, abscesses, life-threatening
  • risks = diabetes and renal disease
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8
Q

describe the history of b pseudomallei

A
  • whitmore and krishnaswami in morphia addicts in burma 1911
  • stanton and fletcher 1932 = melioidosis
  • 40% dead in thailand
  • australian Currie’s study in QLD/WA over 23yrs
  • australia = contaminated wound saline
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9
Q

compare and contrast pseudomallei and mallei

A
  • both g-ve safety pin rods, intracellular, 2 chromosomes Chr1 and Chr2
  • Pseudo motile vs mallei not
  • Pseudo wrinkled on ashdown agar
  • Mallei host restricted
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10
Q

describe the 3 main virulence factors of burkholderia

A
  1. capusle = CPS of -3)-2-O-acetyl 6-deoxy-β-D-manno-heptopyranose essential for survival and rep in macrophages
  2. LPS = heteropolymer of d-glucose and l-talose units ( -3)-β-d-
    glucopyranose-6-deoxy-α-l-talopyranose-)
  3. T3SS-3 to escape vesciles + required for full virulence; T3SS-1 and -2 only mallei/thailandensis
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11
Q

describe the 5 step intracellular invasion process of burkholderia using the virulence factors involved

A
  1. Invasion = FliC and PilA, BoaA and BoaB, Sap1
  2. Phagosome survival = sigma factors, catalase, DpsA
  3. Phagosome escape = T3SS
  4. Host actin polymerisation = BimA, surface associated protein,
  5. Host cell apoptosis and bacterial spread = T6SS
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