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MICR3330 > 21 - Neisseria gonorrhoeae > Flashcards

21 - Neisseria gonorrhoeae Flashcards

1
Q

Neisseria gonorrhoeae in men

A
  • Colonises the urethra
  • Incubation period: 1 to 7 days
  • Transmitted only by intimate sexual contact
  • 95% show symptoms of acute infection
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2
Q

Symptoms in men

A

Dysuria, urethral discharge

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3
Q

Complications in men

A
  • Epididymitis
  • Urethral stricture (narrowing of the urethra)
  • Prostatitis
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4
Q

Treatment in men

A

Antibiotics

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5
Q

Neisseria gonorrhoeae in woman

A
  • Colonises the endocervix
  • 20% to 80% are asymptomatic
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6
Q

Symptoms (if symptomatic) in woman

A
  • Abdominal pain
  • Vaginal bleeding
  • Fever
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7
Q

Complications in woman

A
  • Pelvic inflammatory disease (PID)
  • Ascending infection into the fallopian tubes (Sterility, Ectopic pregnancy)
  • Perihepatitis
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8
Q

Treatment in woman

A

Antibiotics do not prevent PID but do prevent transmission

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9
Q

Other clinical manifestations

A
  • Disseminated gonococcal disease
  • Gonococcal arthritis
  • Ophthalmia neonatorum (infection in the eye) during delivery
  • Pharyngitis
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10
Q

Multi drug resistance

A

Decreased susceptibility to one currently recommended therapy (cephalosporin OR azithromycin) PLUS
resistance to at least two other antimicrobials (penicillin, tetracycline, erythromycin, ciprofloxacin)

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11
Q

Lab diagnosis

A
  • Plate within 6 hours onto Thayer Martin (MTM) agar
  • Microscopy (gram -ve diplococci)
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12
Q

Extreme drug resistance

A

Decreased susceptibility to two currently recommended therapies (cephalosporin AND azithromycin) PLUS resistance to at least two other antimicrobials (penicillin, tetracycline, erythromycin, ciprofloxacin)

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13
Q

Antimicrobial resistance

A

Driven by point mutation and acquisition of resistance
markers by natural transformation

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14
Q

Mechanisms of resistance to Sulphonamides

A
  • Over-synthesis of para-aminobenzoic acid
  • Chromosomal mutations in the dihydropteroate synthetase gene to prevent binding by sulphonamides
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15
Q

Mechanism of resistance to Quinolones

A

Chromosomal mutations in the gyrA and parC genes (DNA replication machinery)

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16
Q

Mechanisms of resistance to Macrolides

A
  • Chromosomal mutations in the 23S rRNA rrl to prevent antibiotic binding to ribosome
  • Mutations in the mtrR and mtrR gene to increase efflux from the MtrCDE pump
17
Q

MtrR

A
  • Repressor of the transcription of the multidrug efflux pump, MtrCDE
  • Mutation results in high constitutive expression of the pump thus increased drug resistance
18
Q

MtrCDE

A

ABC transporter for the removal of drugs

19
Q

Mechanisms of resistance to tetracyclines

A
  • Chromosomal mutations in the rpsJ (30S ribosomal protein S19) to exclude binding to ribosome
  • penB to exclude antibiotic
  • mtrR promoter and gene to efflux antibiotic
  • Plasmid-mediated production of the TetM protein
20
Q

Mechanisms of resistance to spectinomycin

A
  • Chromosomal mutations in the spc locus
  • Plasmid-mediated resistance (very rare)
  • Not recommended as a first-line agent due to the ease with which resistance may occur
21
Q

Mechanisms of resistance to aminoglycosides

A

Chromosomal mutations in the kan gene

22
Q

Do gonococcal infections increase
transmission of other STIs

A

Yes, in particular HIV.

23
Q

Why are vaccines difficult to design

A
  • Neisseria gonorrhoeae is naturally transformable
  • High antigenic variation and genetic drift
24
Q

EptA

A

Enzyme that adds phosphoethanolamine to lipid A headgroups in the periplasm of gram negative bacteria

25
Q

What is EptA required for

A
  • Resistance to cationic antimicrobial peptides (CAMPs) by removing negative charges on bacterial membrane
  • Resistance to complement mediated lysis
  • Attachment to host cells
26
Q

Cathelcidins and human beta defensins

A

Positively charged peptides (CAMPs) that bind negatively charged surfaces of bacteria

MICR3330 (29 decks)

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