(B) Lecture 16: Bacterial STDs Flashcards
Sexually transmitted disease
A RECOGNIZABLE DISEASE state that has developed from an infection
Sexually transmitted infection
A pathogen that causes INFECTION through sexual contact
Most common STIs
- HIV
- HPV
- Hepatitis virus
- Neisseira gonorrhoeae
- Chlamydia trachomatis
- Treponema pallidum
History of Syphillis
Treponema pallidum
- old disease (3000 BC)
- “stranger” disease
- mercury is first treatment for syph
- COMPOUND 606 was the first potent treatment
History of Gonorrhea
Neisseria gonorrhoeae
- not clear when it officially appeared
- some say it’s a disease from Ancient Greece
- SULFONAMIDES decreased incidence
History of Chlamydia
Chlamydia trachomatis
- HIDDEN disease under gonorrhoea and syph
- Eric Dunlop was first to identify C. trachomatis as the cause of this genital infection
- MOST COMMON bacterial STI since late 1990s
Obligate human pathogens
- must be in contact w/ their host to survive and replicate
- bacterial STDs have no other niche than human body (human-human contact is needed)
Treponema pallidum
agent of SYPHILLIS
- spirochetes
- unculturable (does not tolerate high temp, atmospheric O2 level)
- sexual or mother/child transmission
T. pallidum disease
- stage 1: no signs; maybe a sore
- stage 2: body rash
- stage 3: nothing visible outside; affects INTERNAL organs
T. pallidum virulence factors
- slow to grow but need FEW cells to transmit
- NO LPS and internal flagella
- evade immune response
- outer membrane proteins: attachment to epithelial cells (adheres to cell wall) and extracellular matrix
T. pallidum treatment
Diagnosis
- PCR
- serologic tests
NO vaccine available
Antibiotics treatment
- penicillin or doxycycline
Neisseria gonnorrhoeae
- gram-NEGATIVE bacteria
- diplococci
- non-motile (adheres to cell wall)
- obligate human pathogen
- sexual transmission and mother/child
N. gonnorhoeae disease
MORE POTENT than syphillis
Female
- abdominal pain
- increased vaginal discharge
- painful urination
- painful intercourse
- vaginal bleeding btwn periods
Male
- DISCHARGE/EXUDATE from penis -
- swollen testicles
- painful urination
- UTI
- inflammation of penile
N. gonnorhoeae gender differences
Females are usually asymptomatic
Men are usually SYMPTOMATIC
Gonococcal conjunctivitis
white discharge from eyes
especially seen in mother/child transmission
N. gonorrhoeae cycle
- adherence to urogenital epithelium
- competition w/ resident microbiota
- colonization + invasion of epithelium
- release of peptidoglycans
- cytokine, chemokine and inflammatory response
- influx of neutrophils; phagocytosis of N. gonorrhoeae
- neutrophil-rich EXUDATE helps w/ transmission
N. gonnorrhoeae virulence factors
Colonization/invasion:
- Type IV Pili
- Opa (Opacity protein)
- cell wall antigen (LOS)
- PorB (OM porin)
Immune modulation
- prevents complement activation, opsonization and bacterial killing
- modulates activities of macrophages, DCs and neutrophils
- modulates T cell function to avoid adaptive immunity
N. gonorrhoea treatment
Diagnosis
- PCR
- culture
NO vaccine available
Antibiotics RESISTANCE (Mtr efflux pump) - antibiotics pumped out before it effects target
Urgent need for new therapeutics
N. gonnorhoea antibiotic resistance
Antibiotics keep becoming resistant
Some antibiotics are no longer first-line antibiotics = keeps resistance low
Last resort: cephalosporin
Visible complication to gonorrhoea
White discharge/exudate from neutrophils
Chlamydia trachomatis
- gram-NEGATIVE bacteria
- thin or no PG layer
- obligatory INTRACELLULAR pathogen (must be inside human)
- sexual or mother/child transmission
C. trachomatis disease
MOST ppl are asymptomatic
Female = 80-90% asymptomatic
- cervicitis
- prolonged menses, spotting + discharge
- tubing infertility or ectopic pregnancy
Male = Up to 90% asymptomatic
- urethritis (inflammation of urethra)
- dysuria + penile discharge
C. trachomatis life cycle
Has 2 states: EB and RB
Elementary body = INFECTIOUS
Reticulate body = NOT infectious; made to REPLICATE; within cell
- infectious EB enters
- EB is circled by inclusion and differentiates to RB
- RB fuses and replicates
- persistent form reactivates; RB form differentiates to EB
- EB accumulates and is released then exocytoses
C. trachomatis virulence factors
LPS = presumably bind CFTR
MOMP (Major outer membrane protein) = mannose receptor on surface
Secretion system (T3SS, T2SS, T5SS)
- T3SS is the most important
- inject molecules that manipulate cytoskeleton to form inclusion around
