Genital Ulcers and genital lesions

Question 1

syphilis

- epidemiology

Answer 1

Most infectious cases in NZ through MSM, or imported form case

Question 2

syphilis

- pathlogly

Answer 2

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

Question 3

syphilis

- early manifestations

Answer 3

onset 9-90 days post exposure

• anogenital ulceration
• rash
• ocular lesions
• neurological signs

Question 4

Primary syphilis

Answer 4

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

Question 5

syphilus early confirmation of diagnosis

Answer 5

Before serology positive: Dark field microscopy (non-specific depending on site)
Direct fluorescent antibody (DFA) test - specific

Question 6

Secondar Syphilis

Answer 6

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

Question 7

Late manifestations

Answer 7

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

Question 8

Congenital infection: syphilis

Answer 8

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

Question 9

syphilis testing

Answer 9

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)

Question 10

Causes of false positives VDRL/RPR

Answer 10

technical 
Acute biological 
- fever, immunisation, pregnancy 
Chronic biological 
- chronic infection, autoimmune disease, IUD, debilitated states, advancing age

Question 11

Causes of false positive TPHA

Answer 11

SLE, infectious mononucleosis, leprosy

Question 12

Treatment of early syphilis

Answer 12

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

Question 13

Genital herpes - biology

Answer 13

Herpesviridae: alpha sub family, neurotropic, latency
HSV-1 and -2 closely related: morphologically indistinguishable: dense core containing genome, 50% homologous, yet different site preference

Question 14

Genital herpes infection

Answer 14

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

Question 15

Genital herpes tranmission

Answer 15

direct contact with visions from

• blister of ulcer
• sexual contact shedding virus asymptomatically

Question 16

Asymptomatic shedding and virus subtypes

Answer 16

HSV-1
Asymptomatic shedding from oral cavity
HSV-2
all subtypes are infectious, shedding occurs at many sites

Question 17

Factors that reduce transmission

Answer 17

Condoms ~ 50% protection

Antiviral therapy - reduce risk of transmission of symptomatic herpes by 75% Also reduces overall acquisition

Question 18

Genital herpes diagnosis

Answer 18

Best from a vesicle or an ulcer, use DNA amplification techniques

Question 19

Genital herpes techniques

Answer 19

Treatment

• first episode: Aciclovir (antiviral drug)
• Recurrence: Aciclovir larger dose
• Suppression: Aciclovir smaller long term dose

Question 20

Factors that reduce transmission

Answer 20

condoms 50% protection

- antiviral treatment: reduces risk of transmission of symptomatic herpes by 75%

Question 21

Chlamydia trachomatis

Answer 21

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

Question 22

Anogenital warts

Answer 22

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

Question 23

HPV

Answer 23

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

Question 24

HPV and sexual transmission

Answer 24

well established 
Common infection in the recently sexually active 
Most infections are subclinical 
Decreasing prevalence with age 
Incubation period

Question 25

Types/ stages of HPV infection

Answer 25

latent
subclinical
clinical (not very common relatively)

Question 26

Wart treatments

Answer 26

Mainly cosmetic (warts), or to prevent progression, to remove much precancerous tissue, treat cancer
Treatment modalities:
- Physical of chemical ablation

Question 27

Complications of intraepithelial neoplasia

Answer 27

the majority of anogenital HPV infections are benign

In a small minority, the development of high grade dysplasia and anogenital