JW - Biofilms and Bacteriophage I Flashcards

(18 cards)

1
Q

What is Vibrio cholerae and how does it appear microscopically? (5)

A
  • Gram-negative, curved rod
  • 0.5–0.8 μm wide and 1.4–2.6 μm long
  • Facultative anaerobe
  • Has a single polar flagellum
  • Optimal growth at 20–30°C
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2
Q

How is Vibrio cholerae transmitted? (3)

A
  • Water (infectious dose = 10⁹)
  • Food (infectious dose = 10³)
  • Person-to-person contact
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3
Q

What are the clinical events in cholera? (4)

A
  1. Entry
  2. Colonisation
  3. Disease, hypovolemic shock, acidosis, vomitting, diarrhoea, muscle cramps
  4. Exit (in one to many liters of fluid per day)
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4
Q

What are the clinical manifestations of cholera? (5)

A
  • Severe diarrhea – up to 20–30 L/day
  • Dehydration
  • Shock
  • Acidosis
  • Can be fatal if untreated
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5
Q

Describe the pathology of cholera infection. (4)

A
  • Non-invasive – bacteria do not reach bloodstream
  • V. cholerae colonizes intestinal microvilli
  • Secretes cholera toxin, mucinase, and endotoxin
  • Acts locally in the intestine
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6
Q

How is V. cholerae classified? (2)

A
  • Serogroups – bacteria of the same species with different antigenic determinants on the cell surface
  • Biotypes (biovars) – different strains of the same bacterial species
    distinguished by a group of phenotypic or genetic traits
  • 150 serogroups exist, but only two are epidemic-causing
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7
Q

How is toxigenic Vibrio cholerae classified? (3)

A
  • Divided into two epidemic serotypes:
    • O1
    • O139
  • These two serotypes are responsible for cholera outbreaks
  • Other serotypes exist in the environment but are not epidemic-causing
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8
Q

What is the classification hierarchy for the O1 serotype of V. cholerae?

A
  • O1 is further divided into two biotypes:
    • Classical – caused the first six pandemics
    • El Tor – replaced Classical in 1961
  • Each biotype has three serotypes (ribotypes):
    • Inaba – A & C antigens
    • Ogawa – A & B antigens (mostly A, little C)
    • Hikojima – A, B & C antigens
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9
Q

What is significant about the O139 serotype of V. cholerae? (3)

A
  • Emerged in Southeast Asia in 1992
  • Replaced O1 as the predominant pandemic-causing strain
  • Demonstrates the potential for new epidemic serotypes to emerge
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10
Q

Why are only O1 and O139 of over 150 V. cholerae serotypes toxigenic? (3)

A
  • These two serotypes have acquired key virulence factors (e.g. CTXϕ phage and TCP pili)
  • Environmental strains lack these elements and do not cause severe disease
  • Highlights the role of horizontal gene transfer in pathogenic evolution
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11
Q

What is transduction in bacteria and what are its types? (4)

A
  • Transduction is the transfer of genetic information from one bacterium to another via a bacteriophage
  • The DNA is carried inside the phage particle
  • There are two types of transduction:
    • Generalized transduction – random bacterial DNA is packaged into phage heads
    • Specialized transduction – specific bacterial genes near the prophage insertion site are transferred
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12
Q

What is the structure of the V. cholerae genome? (2)

A

Two circular chromosomes

  • Chromosome I (2.96 Mbp) – essential functions and housekeeping
  • Chromosome II (1.07 Mbp) – includes integron island
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13
Q

What two bacteriophages are associated with V. cholerae virulence in chromosome 1 (2)?

A
  • VPI phage – encodes Toxin-Coregulated Pilus (TCP) for host attachment
  • CTXϕ phage – encodes cholera enterotoxin; integrates into Chromosome I
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14
Q

What is the Toxin-Coregulated Pilus (TCP) (4)?

A
  • Filamentous surface structure on V. cholerae
  • Required for efficient colonization of the small intestine
  • Major subunit = TcpA
  • Genes for TCP production are located on pathogenicity island (VPI) in Chromosome I
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15
Q

How is cholera toxin encoded and regulated? (4)

A
  • Genes: ctxA and ctxB (on phage CTXϕ)
  • Transcription regulated by host and phage proteins
  • Integration site in genome = attRS
  • Toxin expression requires TCP (receptor for CTXϕ)
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16
Q

How does the cholera toxin (CT) function at the cellular level? (5)

A
  • A-B type toxin: 1 A subunit + 5 B subunits
  • Binds to GM1 ganglioside on host cells
  • Internalized via endocytosis → ER
  • A1 subunit modifies GTPase → increases cAMP
  • High cAMP → secretion of Cl⁻, HCO₃⁻, and water → diarrhea
17
Q

Why doesn’t V. cholerae always cause disease? (3)

A
  • Only becomes toxigenic after infection with CTXϕ phage
  • Phage uses TCP to enter the bacterium
  • Integration of CTX genome enables toxin production
18
Q

What broader lesson does V. cholerae teach about phage biology? (3)

A
  • Phage-mediated gene transfer is key in evolution of virulence
  • Many bacterial pathogens acquire virulence factors via phages
  • Phages may also enhance survival and pathogenicity in biofilms