Lecture 24 - Burkholderia Flashcards
(11 cards)
describe the bukholderia genera and list the 4 pathogenic species
- G-ve rods, 70+ species, diverse niches, most non-pathogenic
1. cepecia complex (BCC)
2. mallei
3. pseudomallei
4. Thailandensis
what is the location, disease and resistance of Bulkholderia cepecia complex (BCC)?
- 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
list the 5 pathogenic components ofBulkholderia cepecia complex (BCC)
- Cable pilus = epithelial invasion
- Biofilms
3.Exopolysac (EPS) cepacian = colonisation and persistence - Antimicrobial resistance
- B cepacia epidemic strain marker (BCESM) on genomic island for metabolism and virulence
describe b mallei and the animal/human disease forms it causes
- 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
describe the history of b mallei
- 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
how does the mallein test for b mallei work? who made it and when?
- glycerin fluid with glanders put in horses eyes = swelling after 1-2 days positive
- russians 1891
describe the transmission, location, disease and risk factors of b pseudomallei
- 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
describe the history of b pseudomallei
- 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
compare and contrast pseudomallei and mallei
- 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
describe the 3 main virulence factors of burkholderia
- capusle = CPS of -3)-2-O-acetyl 6-deoxy-β-D-manno-heptopyranose essential for survival and rep in macrophages
- LPS = heteropolymer of d-glucose and l-talose units ( -3)-β-d-
glucopyranose-6-deoxy-α-l-talopyranose-) - T3SS-3 to escape vesciles + required for full virulence; T3SS-1 and -2 only mallei/thailandensis
describe the 5 step intracellular invasion process of burkholderia using the virulence factors involved
- Invasion = FliC and PilA, BoaA and BoaB, Sap1
- Phagosome survival = sigma factors, catalase, DpsA
- Phagosome escape = T3SS
- Host actin polymerisation = BimA, surface associated protein,
- Host cell apoptosis and bacterial spread = T6SS