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
2
Q
Papillomaviruses (HPV) Transmission
A
- Breaks in skin
- Sexually transmitted
- Birth canal
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
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
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
6
Q
HPV Genital Infection incubation period
A
- 3wks to 8 months
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
8
Q
HPV subtypes causing warts
A
- 1, 2, 3, 4, 10
9
Q
HPV subtypes causing genital warts
A
- 6, 11
- Also cause laryngeal papillomas
- Low cancer risk subtypes
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
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
12
Q
HPV cyto-destructive treatment
A
- Podophyllotoxin
- Trichloroacetic acid and bichloroacetic acid
- 5-Fluorouracil
13
Q
HPV immune-mediated treatment
A
- Imiquimod
- Interferons
- HPV vaccines
14
Q
HPV genital warts surgical treatment
A
- Ablative procedures
- Excision
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
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
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
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
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
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
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
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
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
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
