Flashcards in Lecture 35: genital ulcers and genital lesions Deck (13):
Epidemiology of syphilis
-Uncommon in NZ except MSM
Pathology of syphilis?
-Immune evasion responses important in maintenance of latency
-CMI is critical and to the control of proliferation of T. pallidum
-Immune response causes much of clinical disease
Early manifestations of syphilis/Primary syphilis?
Early confirmation of syphilis diagnosis?
-Dark field microscopy
-Direct fluorescent antibody test
-appears 4-10 weeks after primary lesions
-due to haematogenous spread therefore may have systemic symptoms
-rash on trunk, extremeties, pamls and soles
-no longer infectious
EIA test: overall pretty good, although might have to wit some timeas for primary syphilis not perfect
RPR: detects and AB against lipoidal Ag. Positive 3-5 weeks post exposure
TPPA: confirmatory, in early and late disease.
Treatment for syphilis?
-Infected <2 years, benzathine penicillin IM
- Contacts are treated
-Pregnant: benzatine penicillin
Transmission: mucosa more vulnerable
Replicates in epidermis
Travels via unmyelinated sensory neurons, where it can enter a latent phase
HSV1 and HSV2
Herpes treatment (Aciclovir facts)
Aciclovir- 15-20% bioavailability
-Activation involves viral thymidine kinase
- host cell metabolises to ACV triphosphate
-This competitively inhibits DNA polymerase, incorporates into DNA chain and terminates chain
-HSV resistance uncommon
-L-valine ester makes valaciclovir, more bioavailable
Chlamydia trachomatis and serovars L1,L2 and L3 (most common here is L2)
Presentation depends on site, and gender: transient anogenital ulcer, cervicitis , proctitis
Causes lymphogranuloma vereneum
-needs differentiating epithelial tissue to grow
-Anogenital warts it can cause, with some association with anogenital neoplasia
-E6 and E7 gene target TS genes and drive replication