Genital Ulcers and genital lesions Flashcards
syphilis
- epidemiology
Most infectious cases in NZ through MSM, or imported form case
syphilis
- pathlogly
T. palladium
Maintains latency through evasion of immune responses
- immunologically privileged sites e.g. brain and eyes
- intracellular sites
- little evidence that antibody is lytic
- surface of organism is immunologically inert
Cell mediated immunity critical to control of its proliferation
Much clinical disease due to immune response to organism e.g. vasculitis, destruction, fibrosis
syphilis
- early manifestations
onset 9-90 days post exposure
- anogenital ulceration
- rash
- ocular lesions
- neurological signs
Primary syphilis
Onset 14-21 days post inoculation
Typically papular then ulcerates
- usually solidarity, painless
- less typical in non-genital sites (mouth anus)
Rubbery inguinal nodes with genital lesions
syphilus early confirmation of diagnosis
Before serology positive: Dark field microscopy (non-specific depending on site)
Direct fluorescent antibody (DFA) test - specific
Secondar Syphilis
Appears 4-10 weeks after primary lesions may overlap with primary lesions
Due to haematogenous spread therefore may have systemic symptoms
highly variable rash, on trunk, palms and soles
may also have mucous membrane lesions, alopecia
Late manifestations
late disease: When no longer infectious (but can reactivate beyond this point in immune compromise) Common features of late disease - commonly none - Aortic disease - papillary signs, optic atrophy - long tract sings, pyramidal sings
Congenital infection: syphilis
Infection occurs as early as 9/40 weeks but no inflammatory response until about 18/40
More than 50% undergo mid trimester abortion or perianal death
Early form - most changes appear 1-2 months of age
late forms - 80% of those liveborns who are infected are undetected early
syphilis testing
predictive values poor in low prevalence settings such as NZ
Pregnancy a significant cause of biological false positive results
Screen with EIA then if positive confirm using RPR (highly specific in heathy people) and TPPA (diagnosis early and late disease)
Causes of false positives VDRL/RPR
technical Acute biological - fever, immunisation, pregnancy Chronic biological - chronic infection, autoimmune disease, IUD, debilitated states, advancing age
Causes of false positive TPHA
SLE, infectious mononucleosis, leprosy
Treatment of early syphilis
Primary, secondary or early latent (<2 years)
Benzathine penicillin
Penicillin allergy: doxycycline
Pregnancy: benzathine penicillin, if allergic to penicillin –> desensitise
Possible Jarish-herxheimer reaction due to systemic release of breakdown products of infection
Genital herpes - biology
Herpesviridae: alpha sub family, neurotropic, latency
HSV-1 and -2 closely related: morphologically indistinguishable: dense core containing genome, 50% homologous, yet different site preference
Genital herpes infection
Transmission: mucosa more vulnerable than skin, females more at risk from male partner
Replicates in the cells of the epidermis
- cellular destruction and inflammation
travels via unmyelinated neurons to sacral paraspinal ganglia: enters latent phase
Reactivation in same nerve territory as initial infection
Genital herpes tranmission
direct contact with visions from
- blister of ulcer
- sexual contact shedding virus asymptomatically
Asymptomatic shedding and virus subtypes
HSV-1
Asymptomatic shedding from oral cavity
HSV-2
all subtypes are infectious, shedding occurs at many sites
Factors that reduce transmission
Condoms ~ 50% protection
Antiviral therapy - reduce risk of transmission of symptomatic herpes by 75% Also reduces overall acquisition
Genital herpes diagnosis
Best from a vesicle or an ulcer, use DNA amplification techniques
Genital herpes techniques
Treatment
- first episode: Aciclovir (antiviral drug)
- Recurrence: Aciclovir larger dose
- Suppression: Aciclovir smaller long term dose
Factors that reduce transmission
condoms 50% protection
- antiviral treatment: reduces risk of transmission of symptomatic herpes by 75%
Chlamydia trachomatis
L2 most common subtype in NZ
- presentation depends on gender, site of acquisition and stage of disease
Most relevant in developed nations in HIV + MSM have high serosorted sex
Anogenital warts
a common sexually acquired problem due to infection with mucosotropic types of HPV
- can be difficult to treat
- spontaneous regression can occur
- can cause significant patient anxiety
- some association with anogenital neoplasia
HPV
DNA virus Species and site specific Need differentiating epithelium to grow Warts are of colonel origin Infectiousness may vary with viral type Some types can transform or immortalise infected cells
HPV and sexual transmission
well established Common infection in the recently sexually active Most infections are subclinical Decreasing prevalence with age Incubation period
Types/ stages of HPV infection
latent
subclinical
clinical (not very common relatively)
Wart treatments
Mainly cosmetic (warts), or to prevent progression, to remove much precancerous tissue, treat cancer
Treatment modalities:
- Physical of chemical ablation
Complications of intraepithelial neoplasia
the majority of anogenital HPV infections are benign
In a small minority, the development of high grade dysplasia and anogenital
