Non Ulcer STDs Flashcards
What are some things to remember about Neisseria gonorrhoeae?
Gram neg diplococci (live in neutrophils/PMN’s)
NO CAPSULE
Need Fe2+ and CO2 to grow
High level of surface antigen variation–>
Rapid antibiotic resistance via transformation and conjugation
What’s the pathogenesis of N. gonorrhoeae?
Mostly adheres to nonciliated epithelial cells
Causes acute inflammatory response (lots of neutrophils, which it can live in for a few hours). Damage is mediated by lipooligosaccharide (LOS) and peptidoglycan fragments
What are the virulence factors of N. gonorrhoeae
Colonization pili that help it attach to epithelial cells and invade
Get Fe3+ with receptors that bind human transferrin, lactoferrin and Hgb (human proteins that usually bind Fe3+ that usually keep Fe3+ away from bacteria)
Cleave IgA1 with it’s IgA protease
Has no capsule so has mechanisms to down regulate complement
What are the 3 surface antigen molecules that N. Gonorrheae can change?
Pili stucture (from gene recombination)
Opacitiy (Opa) protein
LOS (lipooligosaccharide)
There are lots of different versions of surface antigens that gonorrheae can turn on and off
Another way that Gonococcal can avoid complement destruction in the blood stream is by adding a molecule to its lipooligosaccharide that makes it look more like the host. It uses its own enzmye and everything! What is the name of the molecule?
Sialic Acid
What is the lab dx for N. Gonorhheae in urethritis and cervisitis
Urethritis: Gram stain (95% sensitivity and specificity if symptomatic)
Look for gram neg dipplococci esp. in neutrophils
Cervicitis: Gram stain (50-70% sen)
BETTER WAY=PCR/DNA based detection (NAAT: nulceic acid amplification test)
What kind of agar do you use for N. Gonorrheae?
Chocolate agar (for sterile sources)
Thayer Marin/Thayer Lewis (for contaminated sources)
What happens in disseminated gonococcal infection (DGI)
Gonorrhaea can spread through the blood to infect skin and joints leading to:
Dermatitis
Arthritis usually in large joints (can become septic)
In non-menstruating women, N. gonorrhea will manifest NOT as a cervisitis but as ____________
Vaginitis
How do culture rates for N. gonorrhea change with hormonal changes in females
Progesterone causes neg. culture results even when there is an infection, so neg. culture occurs during the secretory phase of the menstrual cycle
Why do young females have high rates of N. Gonorrhoeae and Chalmydia trachomatis
Cervical ectopy causes the exposure of the columnar epithelial cells on the cervix, which are most susceptible to C. tracomatis or N. gonorrhoeae)
Mothers infected with either Neisseria gonorrheae or Chlamydia trachomatis can have babies with neonatal purulent conjuctivitis. How will you tell them apart in the question stem you get on the NBME?
Gonorrheae: early onset (within 1st 5 days)
Chlamydia: usually later onset (~1 week after birth)
What should you remember about Chlamydia trachomatis?
Obligate intracellular, gram neg.
Poor gram staining (may be visualized with Giemsa stain)
No muramic acid in cell wall
There are different types of C. Trachomatis based on different surface antigens. What is the classification of C. Trachomatis and what diseases do they cause (no real easy way to ask this)
D-K: STI’s (urethritis, cervicitis, PID), neonatal pneumonia or conjunctivitis
L1-L3: lymphogramuloma vernereum
A-C: Blindness
Developmental Cycle of Chlamydia
It has 2 main forms:
- Elementary body: Small extracellular infectious form, metabolically inactive, and makes disulfide bonds with membrane proteins
- Reticulate body: Large intracellular replicative form that is metabolically active and osmaotically fragile
Think:
ELEMENTARY ENTERS
RETICULATE REPLICATES
