Lecture 35 - Genital ulcers and genital lesions Flashcards

1
Q

Syphilis - how do you get it?

A

-Not very common, except for men having sex with men
T. pallidum - a spirochaete
-can easily evade the immune response

-a lot of the clinical disease is due to immune response to organism e.g vasculitis, destruction, fibrosis

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2
Q

Common features of syphilis

A
  • rash, lesions, neurological signs
  • occurs 14-21 days after inoculation
  • can have ulcers on mouth or genital or anal regions
  • can get a rubbery lymph node
  • with serology can see the spiral shaped organisms, they can move and twist a lot
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3
Q

Secondary syphilis

A
  • can occur later on after primary lesion (4-10 weeks later)
  • due to haematgenous spread, and may have systemic symptoms
  • rash - macular, papular, papulosquamous
  • trunk, extremities, palms, osles
  • may have mucous membrane lesions - wart like lesions
  • patches on tongue
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4
Q

late disease

A
  • when no longer infectious

- can get aortic disease, cognitive change

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5
Q

Congenital disease

A
  • occurs as early as 9 weeks of pregnancy, and inflammatory response goes on for a while
  • more than 50% undergo abortion or perinatal death
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6
Q

Tests

A
  • Quite hard to interpret
  • can get false positives
  • murex ICE is an EIA test which uses 3 recombinant proteins - representing immunodominant epitopes from T. pallidum
  • uses anti igG and anti-human igM

RPR test - non specific test, looking for antigen
-uses charcol particles

TPPA

  • high specificity
  • but can still get false positives

can see that tests work best in secondary stages of the disease

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7
Q

false positives

A

e.g technical, biological, acute biological - pregnancy

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8
Q

Treatment

A
Benzathine penicillin
(same type used for rhuematic fever)
-If have penicillin allergy, use doxycycline
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9
Q

Genital herpes

A

Type 1 - oral
Type 2 - genital

risk of getting it is higher for women , due to anatomy and amount of mucosa

replicates in cells of epidermis, cellular destruction and inflammation

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10
Q

Transmission

A
  • normally from a blister, or an ulcer
  • people can shed virus asymptomatically
  • most peopel get it from an asymptomatic partner
  • at the beginning, shed a low amount of virus, but then this amount increases
  • short incubation period
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11
Q

Diagnosis

Treatment

A

Best from a vesicle or ulcer
-herpes simplex PCR is performed

Treatment - aciclovir
-this becomes actiavated, and can the inhibit viral DNA poly,erase and causes viral chain termination

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12
Q

reducing transmission

A
  • Condoms

- antiviral therapy - reduces risk by 75%

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13
Q

Chlamydia trachomatis

A

L2 - most common in NZ

  • infect lympocytes and lymphatic tissue
  • presentation depends on gender, site of acquisition and stage of disease
  • most of the complications are due to chornic disease that has not been controlled e.g in developign countries
  • most relevant in developed nations where they are HIV positive, adn have no condom use ect.
  • lots of partners, also havign sex with HIV+ partners
  • requires doxycycline for 3 weeks (longer course of treatment)
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14
Q

Anogenital warts

A
  • a common sexually acquired problem due to infection with HPV
  • normally treated because patients want them gone
  • unusual to have warts associated
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15
Q

HPV

A

DNA virus

  • warts are common
  • can also get neoplasia with hpv
  • there are species specific and site specific
  • wart is of clonal origin, all virus in wart will be similar
  • need differentiating epithelium to grow
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16
Q

Molecular biology

A
  • they can cause changes in cells they infecitn - this can cause cancer
  • go in cracks in epithelium
  • infects basal cells, where uncoating, early transcription and chronic maintenance of viral genome ocurs
  • HPV induce hyperplasia is induce in the stratum spinosum
  • HPV induced hyperplasia is induced in stratum spiniosim
  • highest levels of viral replicaiton cocur in more differentiatied stratum

E6 and E7 - important, and target tumour supressor genes and drive DNA replication

17
Q

Sexual transmission

A
  • Well established
  • incubation period - about 3 months
  • most people get it when they have had a previous infection and can test antibodies
  • stages - latent, subclinical, clinical - infectiousness
  • Latent/subclinical infectios ins 100 times more common than clinical infection
  • long latency with period reactivation is the norm
18
Q

Wart treatments

A

mainly cosmetic warts, to prevent progression, remove pre cancerous tissue treat cancer
-many treatment modalities - physical or chemical ablation

19
Q

Complications of intraepithelial neoplasia

A
  • Majority of anogenital HPV infections are benign
  • the development of high grade dysplasia and anogenital cancer occurs
  • in a small minority, the development of high grade dysplasia and anogential cancer occurs - smoking, immune status important co-factors
20
Q

Vaccine

A

Gardisal 9

  • packaged in a capsule with dna form l1 gene expression
  • synthetic virus like particals
  • get better immunity from virus then from exposure