Genital Ulcers and Genial Lesions Flashcards Preview

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Flashcards in Genital Ulcers and Genial Lesions Deck (27):

Epidemiology of Syphilis 

  • Infectious cases uncommon in NZ except MSM
    • smaller heterosexual component, mainly men-men
    • Some "imported" or from contaxt with imported
  • Late latent (non-infectious) syphilis has been previously over-diagnosed in NZ; eg, due to impact of immigration from pacific Islands 


Describe the pathology of Syphilis, the pathogen, and how it evades the immune system....

  • T. pallidum; a spirochaete
  • Evasion of the Immune response is important in maintaining latency:
    • immunologically privledged sites; eye, brain etc
    • intra cellular sites
    • little evidence that antibody is lytic
    • surface of organism is immunologically inert
  • CMI is critical to the control of T.pallidum proliferation
  • Much of the clinical presentation is due to the immune response to the organism; eg; vasculitus → destruction, fibrosis


When do you get early manifestations of Syphilis and what are some of them?

9-90 days post exposure

Common features; anogenital ulceration, rash, ocular lesions, neurological issues


Primary Syphilis occurs when, and looks like

  • Onset is 14-21 days after inoculation
  • Initially papularr, then ulcerates
    • ulcer 1-2cm diameter 
    • usually solitary and painless
    • less typical/unusual in non-genital types
  • Rubbery inguinal node(s) with genital lesions
  • Diagnosis by scraping lesion, doing DFA test (non-specific) or Direct fluorescent (specific) before serology positive
    • see the spirochaete moving around in solution, not actually that easy to do

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Describe Secondary Syphilis

  • Appears 4-10 weeks after a primary lesion(s), may overlap primary lesion(s)
  • Due to haematogenous spread therefore may have systemic symptoms
  • Characteristic Rash  (very variable!!)
    • macular → papular → paulosquamous
    • Trunk, extremeties, palms and soles
  • May also have mucus membrane lesions (look like warts!), alopecia (hair loss)

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Late manifestations of Syphilis

Late Disease: defined as when no longer infectious (but can reactivate beyond this point in immune compromise)

Common features of late disease:
- often NONE
-Aortic disease
- Papillary signs, optic atrophy
-Long tract signs, yramidal signs
-cognitive change
-gummatous change (fibrosis with destruction often in skin or bones)


Congenital infection of Syphilis

  • Infection occurs as early as 9/40, but no inflammatory response until ~18/40 onwards
  • More then 50% undergo mid-trimester abortion or perinatal death
  • Early form
    • most changes appear 1-2months of age
  • Late forms
    • 80% of those liveborn who are infected are undetected early


Syphilis Tests

  • Predictive value of tests poor in low prevalence settings such as NZ
  • Pregnancy is a significant cause of of biological false positive (BFP) results 
  • Screening with EIA
    • if positie then confirmed using RPR and TPPA (or TPHA, "h" is for haem)
    • False posiitive not associated with conventional BFP reactions
    • High sensitivity and speicificity EXCEPT in primary syphilis!
    • If you do too early the result wont be positive



What is the RPR of Syphilis

  • non-specific or non-treponemal test
    • detects ABs against lipoidal Ag
      • ​Liposomes in suspension + unattached charcoal
    • Flocculation type ie; not complement dependent
      • charcoal particules trapped in lattice of Ag-Ab complex
    • Quantitative: used to follow treatment
  • Positive: 3-5wk post-exposure
  • highly specifc in healthy people
    • ​false positive rate 1-10%
  • VDRL highly specific in CSF 


TPPA test?

  • Treponema pallidum particle agglutination assay
  • Indirect agglutination assay
    • gelatin particles are sensitized with T pallidum Ag
    • Patient serum is mixed with these particles
    • In a positive assay the particles aggregate and clump
  • Confirmatory
  • Diagnosis early and late disease for BOTH primary and secondary syphilis
  • False positive reactions can occur due to presence of Ab against other treponemal organisms

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Treatment of early syphilis is?

Benzathine Penicillin

  • If there is a penicillin allergy: Doxycycline 100mg twice daily for 14 days
  • Treat those in sexual contact with patient the same way
  • Still give benzthine penicillin if pregnant, if there is a penicillin allergy then desensitize before B-P, as they cannot usse doxycycline

Also used in rheumatic fever


What is a Jarisch-Herxheimer reaction

What can happen when you treat someone with early Ayphilis with benzthine penicillin.

Due to the systemic release of the breakdown products of infection cause this, eg; T.pallidum, and you get an exaggerated immune reaction. 

Fever, chills


Describe the biology of the herpes virus, and the sub types


  • subfamily 
  • HSV-1 and HSV-2 closely related
    • morphologically indistinguishable; dense core containing genome, witha icosahedral capsid
    • 50% homology of genomes
  • ​HSV-1 and HSV-2 have different site preference
    • commonly found in non-preffered site with altered natural history 



Genital herpes:

Where does it transmit and then replicate. how does it then cause infection

  1. Transmission in mucosa: more vunerable then skin, why females are more at risk from male partner
  2. Replicates in the cells of the epidermis: causing cellular destruction and inflammation
  3. Travels via unmyelinated ensory nerves to sacral paraspinal ganglia​​​
    • ​​enters Latent phase: hidden from host immune system
  4. Reactivation in same nerve territory as initial infection
  • Dual genital infection with both HSV-1 and HSV-2 is possible
  • Duel orolabial and genital infection with HSV-1 is possible

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Why can you never fully eliminate the genital herpes virus?

Because at any one time only some of the latently infected neurons are reactivated and there will always be some still latent and evading the immune system


How do you transmit HSV and what is the transmission risks?

  • Transmitted from direct contact with virions from
    • blister or ulcer
    • sexual contact shedding virus asymptomatically: can occur from genital/anal or oral sites. 
  • Peak Shedding significant just before symptomatic episode but bad also when lesions are actually present
    • presents anxiety for patients as they don't know when they're actually infectious
  • Usually symptomatic new infections are from asymptomatic sexual partners
  • unsure how much virion is needed to cause infection

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Where and how to do a diagnostic test for Genital Herpes?

  • Best to test from a vesicle or ulcer
  • Herpes simplex PCR is performed using Rohe Lightmix kit HSV-1/2 assay
    • The use of HSV type specific serology is not routinel indicated and can be problematic if pitfalls are not well understood


  • First episode: Aciclovir 400 mg for 7 days
  • Recurrence : Aciclovir 800mg for 2 days
  • Suppression: Aciclocir 100mg for 9-12 months



  • Bioavailability 15-20% (low)
  • Once absorbed key step in acitvation involves thymidine kinase
  • Host cell kinases effect change to ACV-TP
  • ACV-TP competitively  inhibits viral DNA polymerase; incorperates itself into viral DNA and causes chain termination
  • HSV resitance uncommon
  • Valaciclovir: aciclovir with L-valine ester added to ACV
    • 55% bioavailabilty


Factors that reduce Transmission of herpes

  • condoms ~50%
  • Antiviral therapy:
    • reduces risk of transmission of symptomatic herpes by 75%
    • reduces overall acquisition of HSV-2 by 48% 
    • Reduces total HSV acquisitions by 61%
    • Rates higher in women


The L serovars of Chlamydia (L1, L2, L3)

  • Presentation depends on gender, site of acquisition and stage of disease
  • Predisposition in infecting lymphocytes and lymphatic tissue
  • Most relevant in developed nations in HIV+ MSM have high risk "serosorted' sex
    • Should be tested for particularly in symptomatic MSM when rectal chlamydia is +
    • lots of sex with lots of different partners
    • doxycycline 100mg for 3 weeks

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Anogenital warts are due to ______. these rates are dropping due to the _________.

Anogenital warts are due to HPV. these rates are dropping due to the Gardasil vaccine.

  • can be difficult to treat
  • spontaneous regression can occur
  • can cause significant patient anxiety
  • some ass. with anogenital neoplasia


what is HPV

  • DNA viruses
  • species and site specific
  • need differentiating epithelium to grow
  • warts are of clonal origin
  • infectiousness may vary with viral type
  • some types can transform or immortalise infected cells
  • get in with 'cracks', microabrasions in the eptithelium

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E6 and E7 of HPV do what?

  • Target Tumor suppresor genes and hence drive DNA replication
  • E7: binds to reticuloblastoma gene→ inhibits transcription factor E2F → transcription of genes involved in cell cycle progression and DNA synthesis


Sexual transmission of HPV

  • Common infection in those whoe are recently sexually active (18-28 yr)
  • Most infections subclinical
  • Decreasing prevalence with age 
  • incubation period: 3-8m for warts, 4-36m for cervical lesions
  • Visible lesions usually at sites of microtrauma byt HPV causes anogenital 'field infection'
  • once one HPV infection resolved onlly have type specific immunity
  • evidence for perinatal transmission

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Types/stages of HPV

  • Latent, subclinical, clinical
  • Latent/subclinical 100x more common then clinical infection
  • long latency with periodic reactivation is the norm

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Treatment of HPV warts

  • mainly cosmetic (warts), or to prevent progression, ofr to remove pre/cancerous tissue
    • Physical or chemical ablation etc (70% efficacy, 30% reccurence)
    • have same levels of recurrence


Intraepithelial neooplasia as a complication of HPV

  • uncommon, usually HPV infection is benign
  • smoking and immune status are important cofacotrs
  • Cervical and vulver IE neoplasia well described
  • Oro-pharyngeal and aanal cance becoming important
  • Prophylactixc vaccination vital
    • packaged in capsule from L1 gene of HPV DNA which is why it works so well