Bacterial STIs

Question 1

What cells does chlamydia infect?

Answer 1

Chlamydia can only survive inside cells, and preferentially infects sites with columnar epithelial cells in the mucosa such as the cervix, urethra, pharynx, rectum and eye

Question 2

Chlamydia tranchomatis bacterium traits

Answer 2

• g-, LPS not very endotoxic
• unusual peptidoglycan -> hard to see with light microscopy
• non-motile

Question 3

Replication of chlamydia

Answer 3

Replication
1. elementary bodies enter by receptor mediated endocytosis
3. multiple inclusion bodies in endosomes fuse to form inclusion bodies
4. transition from EB to RB
5. replication and maturation
6. transition from RB to EB
7. exit

Question 4

Two forms of chlamydia

Answer 4

Elementary bodies: extracellular, infectious
Reticulate bodies: intracellular replicative phase

Question 5

Damage from chlamydia infection

Answer 5

• mostly from inflammation
• development of a lymphoid follicle from activation of B, T cells and macrophages, chronic inflammation,
  Cycle of immune activation causes cell damage and scar tissue formation
  activated CD4+ and CD8+ T cells and macrophages produce interferon gamma can cause RB cells to pause their cell cycle until conditions change

Question 6

Pelvic inflammatory disease

Answer 6

Active infection:
- Production of secretory IgA
- Lymphoid follicles form with APC, macrophages, B cells, and T cells
- Cycle of chronic activation and inflammation

Question 7

Chlamydia association with HIV

Answer 7

• People with chlamydia have a higher chance of getting HIV
  Hypothesis:
• Infection of chlamydia can worsen the tightness of the junctions between epithelial cells, giving HIV more access
• Chlamydia recruits the target cells for HIV at site of infection
  Presence of bacterial infection upregulates HIV coreceptors

Question 8

what test is recommended for diagnosis of chlamydia

Answer 8

nucleic acid detection using patient samples

Question 9

Treatment of chlamydia

Answer 9

antimicrobials target RB > need good penetration of tissues and cells, and should be long acting
○ Macrolide antibiotics or tetracyclines: have good tissue penetration, need activity for prolonged time

Question 10

Neisseria gonorrhoeae characteristics

Answer 10

g- diplococcus
fussy
CO2 enriched atmosphere

Question 11

Diseases caused by gonorrhoea

Answer 11

• When symptomatic it presents as urethritis a few days after contact
  May ascend the genital tract and cause pelvic inflammatory disease
  
  • Can cause disseminated disease (unlike chlamydia)
  • Newborns may contract conjunctivitis

Question 12

Target of Neisseria gonorrhoeae

Answer 12

• columnar epithelial cells

Question 13

Entry of Neisseria gonorrhoeae

Answer 13

loose attachment with pili and then closer specific adhesion by outer membrane proteins and lipo-oligosaccharides
replicates at cell surface and spreads in mucosal secretions with twitching motility

Question 14

Inflammation consequences of Neisseria gonorrhoeae infection

Answer 14

Inflammatory response stimulated by lipo-oligosaccharides and peptidoglycan (interaction with PRRs)
Symptoms: pus, pain
TNF production -> product of inflammation -> loss of ciliated epithelial cells in fallopian tubes in gonorrhoeal infections

Question 15

Neisseria gonorrhoeae immune system avoidance

Answer 15

Avoids being killed by polymorphonuclear lymphocytes
Invasive strains are generally less immunogenic, avoid complement cascade and neutrophils by altered LPS or lack of outer membrane proteins
Production of IgA protease (chops up secretory IgA)

Question 16

Diagnosis of Neisseria gonorrhoeae

Answer 16

• swabs from discharge
• cultured on GC biplate if possible to test for antibiotic susceptibility
• gram stain for presumptive diagnosis in men -> look for intra and extra cellular g- diplococci and neutrophils (indicates immune response)

Question 17

Treatment of Neisseria gonorrhoeae

Answer 17

• gonorrhoeae is good at the acquisition of genetic material from other sources (HGT) so it can rapidly develop antibiotic resistance = treatment must be informed by current recommendations on resistance
• treat for chlamydia as well due to high rates of coinfection

Question 18

Spread of Neisseria gonorrhoeae

Answer 18

May be translocated to sub-epithelial tissue before causing inflammation and dissemination
gonorrhoeae is highly antigenically variable in pili and surface proteins -> makes it better at avoiding antibody response

Question 19

Treponema pallidum in pregnancy

Answer 19

can spread to foetus via placenta

Question 20

Treponema pallidum stages

Answer 20

Primary: chancre (painless infectious tissue ulcer) or asymptomatic
goes latent for 2-24 weeks

Secondary: rash, warty genital lesions, both of which are infectious
goes latent for years

Tertiary syphilis: bacteria is found in capillaries of organs and tissues, major damage

Question 21

Treponema pallidum characteristics

Answer 21

• spiral rod that enters the body through contact with body fluids and spreads to the skin and nearby lymph nodes, from where it can then disseminate to the bloodstream.
• g-
• need special techniques to visualise
  motile due to periplasmic contractile flagella
• labile
  > need tissue culture

Question 22

Treponema pallidum diagnosis

Answer 22

swab from primary or mucosal secondary lesion
PCR
More common:
- specific antibodies to treponemal antignes with EIA
- RPR: cardiolipin produced by damage to host cells because of activity, test antibodies associated with this
-> for active treatment

Question 23

Treatment of Treponema pallidum

Answer 23

penicillin
- pregnancies screened for syphilis