Bacterial STIs Flashcards
What cells does chlamydia infect?
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
Chlamydia tranchomatis bacterium traits
- g-, LPS not very endotoxic
- unusual peptidoglycan -> hard to see with light microscopy
- non-motile
Replication of chlamydia
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
Two forms of chlamydia
Elementary bodies: extracellular, infectious
Reticulate bodies: intracellular replicative phase
Damage from chlamydia infection
- 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
Pelvic inflammatory disease
Active infection:
- Production of secretory IgA
- Lymphoid follicles form with APC, macrophages, B cells, and T cells
- Cycle of chronic activation and inflammation
Chlamydia association with HIV
- 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
what test is recommended for diagnosis of chlamydia
nucleic acid detection using patient samples
Treatment of chlamydia
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
Neisseria gonorrhoeae characteristics
g- diplococcus
fussy
CO2 enriched atmosphere
Diseases caused by gonorrhoea
- 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
Target of Neisseria gonorrhoeae
- columnar epithelial cells
Entry of Neisseria gonorrhoeae
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
Inflammation consequences of Neisseria gonorrhoeae infection
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
Neisseria gonorrhoeae immune system avoidance
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)
Diagnosis of Neisseria gonorrhoeae
- 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)
Treatment of Neisseria gonorrhoeae
- 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
Spread of Neisseria gonorrhoeae
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
Treponema pallidum in pregnancy
can spread to foetus via placenta
Treponema pallidum stages
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
Treponema pallidum characteristics
- 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
Treponema pallidum diagnosis
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
Treatment of Treponema pallidum
penicillin
- pregnancies screened for syphilis
