Genital Warts And Genital Ulcer Disease Flashcards

1
Q

Papillomaviruses (HPV)

A
  • Papovavirus family
    • naked, icosahedral DNA virus (so will survive in the environment)
    • > 200 diff. Types of HPV have been recognized
    • > 40 are assoc. w/ genital infections
  • Latent and transforming infections
    • treatment will not clear latent infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Papillomaviruses (HPV) Transmission

A
  • Breaks in skin
  • Sexually transmitted
  • Birth canal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

HPV Wart Pathogenesis

A
  • Viral replication depends on epithelial cell differentiation
  • HPV infects basal cells
  • Induces cell proliferation and thickening in the basal layer, stratum spinosum and stratum granulosum
  • As cells differentiate, nuclear factors expressed in diff layers promote transcription of diff viral genes
  • The late genes encoding structural proteins are expressed only in terminally differentiated cells
  • New viral particles are shed w/ dead cells of the upper layer of skin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Risk factors for genital warts

A

Women

  • Young age (<25)
  • Multiple sex partners
  • Male partner sexual behavior

Men

  • Multiple sex partners
  • Being uncircumcised

Immunosuppressed

  • Larger and more treatment-resistant genital warts
  • Higher rates of recurrence
  • Higher rates of malignant transformation of anogenital warts

Persistent HPV infection (oncogenic subtype) is a risk factor for developing cervical cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Genital HPV infection Symptoms

A
  • Infection is often subclinical; only noticed during exam
  • Subclinical infection often resolves on its own
    • ~70% resolve 1 year
    • ~90% within 2 years
    • 20-30% of pts have a recurrence within a few months
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

HPV Genital Infection incubation period

A
  • 3wks to 8 months
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

HPV Transforming Infections

A
  • Viral DNA is usually integrated
  • Basal cells replace more differentiated epithelial cells
  • Clinical outcome = dysplasia and carcinomas
  • Integration inactivates an HPV early gene —> no viral DNA replication but express of some genes
  • Continued expression of HPV E6 and E7 genes
    • E6 protein binds p53 and targets it for degradation
    • E7 protein binds and inactivates retinoblastoma protein
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

HPV subtypes causing warts

A
  • 1, 2, 3, 4, 10
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

HPV subtypes causing genital warts

A
  • 6, 11
  • Also cause laryngeal papillomas
  • Low cancer risk subtypes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

HPV Genital Warts Diagnosis

A
  • Usually made by clinical appearance
  • No FDA-approved serological or blood tests to detect HPV infection
    • not all ppl mount an antibody response to HPV and antibody titers may decline over time
    • HPV may become latent (undetectable) with the potential for reactivation, so neg. test does not rule out infection
  • Biopsy can be used to confirm the diagnosis and rule out malignancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

HPV Genital Warts Treatment

A
  • Main indication: alleviation of bothersome symptoms
    • pruritus, bleeding, burning, tenderness, vaginal discharge, pain, obstruction of the vagina, dyspareunia
  • No medical indication for treatment of asymptomatic warts
    • do not pose serious risks, may want to wait for spontaneous resolve
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

HPV cyto-destructive treatment

A
  • Podophyllotoxin
  • Trichloroacetic acid and bichloroacetic acid
  • 5-Fluorouracil
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

HPV immune-mediated treatment

A
  • Imiquimod
  • Interferons
  • HPV vaccines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

HPV genital warts surgical treatment

A
  • Ablative procedures

- Excision

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Herpes Simplex Viruses

A
  • Enveloped DNA virus
    • HSV-1 and 2 are closely related alpha herpesviruses
  • Potential for latency and reactivation
  • Reactivation may be asymptomatic, but virus is still shed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

HSV Transmission

A
  • Sexually or perinatally
  • Sexual transmission from men to women is more efficient than women to men
  • Fomite transmission unlikely-sensitive to drying and detergents
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Genital Herpes Clinical Course

A
  • Primary infection
    • both localized and systemic symptoms
    • mean duration ~3wks
  • Reactivation
    • prodrome
    • localized symptoms
    • duration ~5-10 days
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

HSV Primary Infection

A
  • Vesicular-ulcerative lesions on the penis, cervix, vagina or vulva
    • vesicles—>ulcers—>crusts
  • Fever, malaise, dysuria
  • Lymphadenopathy (inguinal lymph nodes)
  • HSV cervicitis
  • HSV proctitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

HSV Recurrent Disease

A
  • Frequency of recurrence depends on
    • severity and duration of the initial episode
    • infecting serotype- HSV-2 reactivates more often than HSV-1
    • host factors (immune status)
  • Reactivation becomes less common over time
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Potential complication of genital herpes

A
  • Aseptic meningitis (assoc. w/ HSV-2)
    • more likely to occur w/ primary infection than reactivation
    • self resolves and neurological sequelae are unlikely
    • recurrent episodes of meningitis can occur (Mollaret’s meningitis); may not have evidence of genital lesions at time of meningitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Genital herpes and HIV

A
  • HSV-2 genital ulcer disease assoc. w/ an increased risk for HIV-1 infection
    • HSV-2 genital lesions cause local inflammation and disruption of the genital mucosa
    • immune response to HSV-2 infection recruits CD4 T-cells to genital tract
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Genital ulcer disease differential

A
  • Infectious causes = genital herpes, syphilis and chancroid
  • Genital herpes
    • multiple, shallow, tender ulcers that may be vesicular
    • recurrent disease
  • Primary syphilis
    • painless, indurated, clean-based ulcer, called a chancre
  • Chancroid
    • deep, purulent ulcer
    • may be assoc. w/ painful inguinal lymphadenitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Herpes Treatment

A
  • Antiviral therapy
  • First clinical episode
    • Acyclovir
  • Treatment after primary infection
    • episodic treatment
    • continuous (suppression) treatment
  • Does NOT eliminate latent/asymptomatic shedding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Herpes Screening

A
  • Routine screening not recommended for asymptomatic pts
  • Screening asymptomatics assoc. w/ a low specificity and high false-pos rate
  • Serologic tests for HSV-1 cannot differentiate oral from genital infection
  • Asymptomatic individuals not treated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

HSV Diagnosis

A
  • Based on appearance not accurate
  • Should be lab confirmed
    *Virologic tests
    +PCR or viral culture
    *type-specific serologic tests
    +western blots or ELISA
    +IgM assays do not differentiate b/w HSV-1 and 2
26
Q

Type-specific Serologic Tests

A
  • Type-specific and nonspecific antibodies to HSV develop within several weeks following infection and persist indefinitely
    • tests can differentiate b/w HSV-1 and 2
  • Presence of HSV-2 antibody indicates genital infection
  • Presence of HSV-1 antibody does not distinguish genital from oral infection
27
Q

Treponema pallidum

A
  • Organism that causes syphilis
  • Humans only natural host
  • Think, coiled spirochete (no visualized under light microscopy)
  • Labile and cannot be spread by fomites
  • Lacks species-specific antigens on cell surface
28
Q

Treponema pallidum transmission

A
  • Organism that causes syphilis

- Transmitted through sexual, congenital, blood transfusion

29
Q

Treponema pallidum pathogenicity

A
  • Consequence of pts immune response
  • Can remain latent: lipid outer surface relative paucity of extruding proteins allow the organism to escape immune control and establish a chronic infection
30
Q

Primary Syphilis Clinical Manifestations

A

Chancre

  • Early: macule/papule —> erodes
  • Late: clean based, painless, indurated ulcer w/ smooth firm borders
  • Unnoticed in 15-30% of pts
  • Resolves in 1-5wks
  • HIGHLY INFECTIOUS
31
Q

Syphilis Progression

A
  • Primary: painless chancre
  • Secondary: Rash, fever, neuro symptoms (can even resemble chickenpox)
  • Latency: may got into latency
  • Tertiary Syphilis: 5-50yrs of infection, bone, cardiac, nerve disease
32
Q

Syphilis Treatment

A
  • Penicillin
33
Q

Syphilis Diagnosis

A
  • RPR lab test

- Followed by TPPA and FTA

34
Q

Jarsich-Herxheimer reaction

A
  • Immune reaction from massive release of treponemal antigens due to antibodies working and the organism being lysed
  • Manifested by fever, headache, myalgia
  • Occurs within 24hrs
  • Treatment = steroids
35
Q

Malignant Syphilis Presentation

A
  • Painful skin ulcers all over body, fever
36
Q

Prozone Effect

A
  • In syphilis refers to a false-neg response from overwhelming antibody titers that interfere w/ formation of the Ag-Ab network necessary to a pos reaction
37
Q

Syphilitic Proctitis Presentation

A
  • Painful bowel movements and rectal bleeding (dyschezia and hematochezia)
  • Rash on palms/soles
38
Q

RPR Titer

A
  • RPR measures the viral load

- 1:xx where x = the viral load (higher the number the more viral particles)

39
Q

Tabes dorsalis

A
  • Ataxia and loss of proprioception
  • Pupils do not react to light
  • Product of Ocular syphilis
40
Q

Haemophilus ducreyi

A
  • Causes chancroid

- Painful necrotizing genital ulcers that may be accompanied by lymphadenopathy

41
Q

Chancroid Symptoms

A
  • Caused by Haemophilus ducreyi
  • Starts as a tender papule-pustule-then ulcer w/ a ragged undermined edge; is friable and a grey-yellowish discharge
  • Painful, indurated, ‘ragged’ genital ulcers and tender suppurative inguinal adenopathy
  • ## Painful inguinal lymphadenopathy in 50%, fluctuant buboes may rupture spontaneously
42
Q

Chancroid Diagnosis

A
  • Culture of material from the ulcer base or edges or aspirate (80% sensitive)
  • PCR
43
Q

Chancroid Treatment

A
  • Caused by Haemophilus ducreyi

- Treatment: Azithromycin 1g PO x1 OR Ceftriaxone 250mg IM x1 (erythromycin and ciprofloxacin may also be used)

44
Q

Genital Ulcers Differentiation (Herpes vs. Chancroid vs. Primary syphilis)

A
  • Genital Herpes: painful lesions w/ b/l painful inguinal adenopathy (pain, b/l)
  • Chancroid: painful lesions w/ unilateral painful adenopathy (pain, u/l)
  • Primary Syphilis: No painful lesions w/ b/l painless adenopathy (no pain, b/l)
45
Q

Chancroid Transmission

A
  • Microabrasion in skin during intercourse
46
Q

Klebsiella granulomatis

A
  • Granuloma inguinale or Donovanosis
  • Causes painless, progressive (destructive), “serpiginous” ulcerative lesions, w/o regional lymphadenopathy; beefy red w/ white border and highly vascular
47
Q

Granuloma Inguinale OR Donovanosis Diagnosis

A
  • Cause by Klebsiella granulomatis

- Dx: tissue biopsy

48
Q

Granuloma Inguinale OR Donovanosis Treatment

A
  • Caused by Klebsiella granulomatis

- Rx: Doxycycline 100mg PO BID x3wks

49
Q

Granuloma Inguinale (Donovanosis)

A
  • Chronic, progressively destructive infection, as beefy (velvety) red, friable and non-tender ulcers. Lesions are elevated w/ a smooth rolled edge. May have a serpiginous outline.
  • Kissing lesions- extension along skin folds and contact on opposed surfaces
50
Q

Granuloma Inguinale (Donovanosis) Complications

A
  • Elephantiasis, stricture and pelvic abscess, proctitis, lymphangitis, lymphadenitis, discharging sinuses
51
Q

Lymohogranuloma venereum

A
  • Chlamydia trachomatis

- “Groove sign”; painful elongated sausage-shaped swellings in inguinal area above and below the Poupart ligament

52
Q

Chlamydia trachomatis Symptoms

A
  • Lymphogranuloma Venereum
  • Short-lived painless genital ulcer accompanied by painful inguinal lymphadenopathy
  • Outbreaks in US assoc. w/ proctitis particularly among MSM (gays)
  • Rectal pain, tenesmeus, rectal bleeding/discharge
  • May be mistaken for IBD on biopsy
53
Q

Lymphogranuloma Venereum Treatment

A
  • Caused by Chlamydia trachomatis

- Rx: Doxycycline OR Erythromycin

54
Q

Lymphogranulma Venereum Stages

A
  • 1st stage: small painless papule/pustule at site of inoculation. May erode into small ulcer
  • 2nd stage: painful inflammation/infection of inguinal lymph nodes, may become fluctuant and rupture or may develop into hard, nonsuppurative masses’ along w/ fever, arthralgia, malaise
  • 3rd stage: proctocolitis, perirectal abscesss, fistulas, strictures, stenosis and scarring, may lead to elephantiasis
55
Q

Lymphogranuloma Venereum Diagnosis

A
  • Caused by Chlamydia trachomatis

- Dx: culture and cell typing, serology, immunoflourescence, PCR

56
Q

Chlamydia Risk Factors

A
  • Women >25 who have a new sex partner, >1 sex partner, a sex partner w/ concurrent partner, or a sex partner who has a STI
  • Women <25 and older women w/ risk factors need testing every year (CDC)
57
Q

Neurosyphilis

A
  • Can occur at any stage of Infection
58
Q

Mycoplasma genitalium

A
  • Organism that can cause PID
59
Q

Mycoplasma Genitalium Treatment

A
  • Azithromycin

- Moxifloxacin

60
Q

HPV Latent Infection

A
  • Viral DNA is not integrated

- Treatment will not clear