Lecture 35: Genital Ulcers and lesions

Question 1

Epidemiology of syphilis? pathology?

Answer 1

Infectious cases uncommon in NZ but there is an increasing amount in Auckland. Traditionally was in homosexual men or “imported” however, the number of heterosexual cases is rising esp in oral sex transmission.

T. Pallidum : a spirochaete that evades the immune response in the maintenance of latency (-immunologically priveleged sites, intracellular sites)

Cell-mediated immunity important in the control of proliferation

Much of the clinical disease is due to the immune response to the organism (eg. vasculitis, destruction, fibrosis)

Question 2

Early manifestations?

Answer 2

Onset 9-90 days post-exposure

Common features:

• Hard ulceration differing at the different sites of infection
• Rash
• ocular lesions (Ophthalmic syphilis increasing in frequency)
• Neurological sings (eg. cranial nerve 3,6,7,8)

Question 3

Primary syphilis presentation? diagnosis?

Answer 3

Onset 14-21 days after inoculation

• initially papular and then ulcerations (painless unless secondarily infected or using cabnet creams on them)
• Rubbery inguinal nodes (usually unilateral)
• Diagnosis by dark field microscopy or direct immunofluorescence

Question 4

Secondary syphilis?

Answer 4

Appears 4-10 weeks after primary lesions(s) and may overlap primary lesions(s)

Due to haematogenous spread therfore may have systemic symptoms and/or a rash - macular, papular or papulosquaous (+/- generally unwell feeling)

May have mucous membrane lesions (often in folds), alopecia

Question 5

Late manifestations of syphilis?

Answer 5

Late disease is defined as no longer being infection (but can reactivate beyond this point in immune compromise)

Common features:

• Commonly NONE
• Aortic disease
• Papillary signs
• long tract signs
• cognitive changes
• gummatous changes (localised extreme vasculitis and fibrosis)

Question 6

Congenital syphilis infection?

Answer 6

Infectin occurs as early as 9/40 but no inflammatory response until ≈ 18/40 weeks onwards. 50% undergo mid-trimester abortion or perinatal death if undiagnosed.

Question 7

Tests done to confirm syphilis?

Answer 7

EIA

• uses recombinant proteins in ELISA like test utilising anti-human IgG and anti-human IgM
• overall specificity and sensitivity > 99% with primary syphilis only having sensitivity of 75% and specificity of 61-81%

RPR

• a non-specific or non-treponemal test detecting AB agaisnt lipoidal Ag
• positive 3-5 weeks post-exposure
• Highly specific in healthy people (false positive 1-10%)

TPPA

• Treponema pallidum particle agglutination assay
• specific, indirect agglutination test
• Diagnosis of early and late diesase used as a confirmatory test (false +ve from Ab to other treponemal organisms)

Question 8

False positives in tests for syphilis? Treatment for when it isn’t a false positive and Mr Jones has actually been bumming his business partner?

Answer 8

1. Technical
2. Acut biological (fever, immunisation, pregnancy)
3. Chronic biological (ie >6months)

Primary, secondary or latent = Benzathine penicillin 2x 900mg syringes stat

If allergic then give 100mg doxycycline bid for 14d (unless pregnant!)

(NB: Jarisch-herxheimer reaction - dead and decaying treponines causing an acute febrile illness = give NSAID etc)

Question 9

Herpes virus? Types? Site of infection? Transmission?

Answer 9

They are at a steady state and have been for some time

HSV-1 and HSV-2 are closel related and morphologically indistinguishable. HSV-1 was traditionally orolabial and HSV-2 genital but these have become muddled over time.

Transmission is between mucosal membranes to mucosal membranes replicating in the cells of the epidermis before traveling via unmyelinated sensory nerved to sacral paraspinal ganglia and becoming latent. Reactivation occurs in the same nerve territory as initial infection.

Question 10

Diagnosis of HSV? Treatment?

Answer 10

Best from a vesicle or ulcer - doing PCR test that is quite specific?

Treatment:

• First episode Aciclovir
• Use more Aciclovir for recurrence and also suppression
• Targets an enzyme for virus replication without having really any effect on host enzyme pathways

Question 11

Chlamydia Trachomatis?

Answer 11

Chlamydia infection of lymphatic tissue rather than epithelial tissue, very uncommon in NZ and needs long course of treatment.

Question 12

Anogenital warts? treatment? outcomes?

Answer 12

A common sexually aquired problem due to infection of HPV

Spontaneous regression can occur

HPV needs a differentiating epithelium to grow and cause wart formation - latent, subclinical and clinical states

Ablation using chemial or physical methods - none are really that good that’s why there is so many different types

The majority of anogenital HPV infections are benign but a small amount develop to high grade dysplasia and anogenital cancer occurs that don’t regress and rather persist or progress.