Genital Human Papillomavirus (HPV) Infection [Slide 2]
Upon completion of this content, the learner will be able to;
Describe the epidemiology of genital HPV infection in the U.S.;
Describe the pathogenesis of genital HPV;
Discuss the clinical manifestations of genital HPV infection;
Identify methods used to diagnose genital warts and cervical cellular abnormalities;
Discuss the CDC-recommended treatment regimens for genital warts;
Summarize appropriate prevention counseling messages for genital HPV infection;
Describe public health measures for the prevention of genital HPV infection.
Epidemiology of genital HPV infection in the U.S.
Clinical manifestations and sequelae
Diagnosis of genital warts and cervical cellular abnormalities
Patient counseling and education
Partner management and public health measures
Lesson I: Epidemiology of Genital HPV Infection in the U.S. [Slide 5]
Genital HPV infection is one of the most common STDs.
More than 40 types of HPV are sexually transmitted and can infect the genital tract.
Genital HPV types are divided into two groups, based on their association with cancer.
Infections with low-risk types (nononcogenic types) can cause genital warts and benign or low-grade cellular changes (e.g. mild Pap test abnormalities), but are not associated with increased risk of cancer.
Infections with high-risk types (oncogenic types) can cause cervical dysplasia (both low-grade and high-grade cervical cellular changes), moderate to severe Pap test abnormalities, and, in rare cases, cancers of the cervix. In addition, these types of HPV infection have been associated with cancers of the vulva, vagina, anus, penis, and oropharynx (back of the throat including base of tongue and tonsils).
Most genital HPV infections, whether caused by low-risk or high-risk types, are transient (go away on their own), asymptomatic, and have no clinical consequences.
Incidence in the U.S.
incidence and prevalence estimates on genital HPV infection are limited by the fact that
Genital HPV infection is not nationally reportable, as most infections are brief, asymptomatic, or subclinical (have no visible clinical manifestations), and have no clinical consequences.
Incidence in the U.S.
The estimated annual incidence of sexually-transmitted HPV infection is 14.1 million cases.
An estimated $1.7 billion spent annually in direct medical costs to treat conditions associated with genital HPV infection (e.g. warts, cervical dysplasia, cancer).
Prevalence in the U.S.
It is estimated that 100% of sexually active men and women acquire genital HPV infection at some point in their lives.
An estimated 79 million women aged 14–59 years are infected with HPV, with the highest prevalence in those aged 20–24 years.
Incidence and Prevalence of HPV-associated Diseases
Prevalence estimates for genital warts are relatively imprecise.
Limited data suggest that annual incidence may be as high as 100 per 100,000 population.
An estimated 1.4 million (1% of the sexually active U.S. population) may be affected at any one time.
Rates of cervical cancer have fallen by approximately 75% since the introduction of Pap screening programs.
From 2004 to 2008, the age-standardized incidence of cervical cancer for all races in the U.S. was 8.1 per 100,000 women.
Approximately 12,200 new cases in 2010
Approximately 4,210 deaths in 2010
Age-Adjusted Delay-Adjusted Incidence of Cervical Cancer by Race: 1975–2009
Graph: Age-Adjusted Delay-Adjusted Incidence of Cervical Cancer by Race: 1975–2009. Although cervical cancer rates continue to decline for both white and black women in the U.S., black women continue to suffer a disproportionate burden of disease.
Transmission of Genital HPV
Predominantly associated with sexual activity, including vaginal and anal intercourse, oral sex, a nonpenetrative sexual activity (genital-genital contact). Likely requires contact with viable HPV and microtrauma to skin or mucous membranes to establish infection.
Can occur from asymptomatic and subclinically infected patients.
Treatment of warts or cervical cellular abnormalities may reduce, but likely does not eliminate infectiousness.
Transmission by fomites (inanimate objects such as environmental surfaces and clothing) has never been documented.
Rarely, genital HPV infection with low-risk types is transmitted from mother to newborn during delivery and can cause respiratory tract warts in the child, known as juvenile-onset recurrent respiratory papillomatosis (JORRP).
Estimates of the incidence rate of JORRP are imprecise; they range from 0.4–1.2 cases per 100,000 children.
The preventive value of cesarean delivery is unknown and, thus, should not be performed solely to prevent transmission of genital HPV to the newborn.
Condoms might reduce the risk for HPV-associated diseases (e.g. genital warts and cervical cancer). Consistent and correct condom use also may reduce the risk for genital HPV acquisition. HPV infection can occur in areas that are not covered or protected by a condom (e.g., scrotum, vulva, or perianus)
Risk Factors for Women
Risk factors consistently associated with genital HPV infection in women
Risk increases with increasing number of recent and lifetime sex partners
Early age of first sexual intercourse
Sexual behavior of sex partners
Risk increases for women whose sex partners have had multiple sex partners.
HPV is more likely to be detected in immunosuppressed women (e.g., HIV-infected persons, women on dialysis, and after kidney transplant).
Risk factors less consistently associated with genital HPV infection in women
Oral contraceptive use
Nutritional factors (poor nutrition)
Lack of circumcision of male partners
Risk Factors for Men
Greater number of recent and lifetime sex partners
Being uncircumcised increases risk
Lesson II: Pathogenesis [Slide 15]
Key features of HPV
Double-stranded DNA virus that belongs to the Papillomaviridae family
Small , nonenveloped virions
Over 100 characterized types
Number of recognized HPV types is gradually increasing as more types are identified and genetically characterized.
Genital types have specific affinity for genital skin and mucosa.
Very limited animal models and no widely available system for in vitro cultivation
Infection is identified by the detection of HPV DNA.
HPV Genotyping System
Types are distinguished by different DNA sequences (>10% difference), primarily those which express L1 capsid (surface) protein.
Genital HPV types are generally characterized in terms of their oncogenic potential (ability to cause cancer).
Low-risk types (nononcogenic types), e.g. HPV types 6 and 11
Associated with genital warts and benign or low-grade cervical cellular changes (associated with mild Pap test abnormalities)
Most genital warts are caused by HPV types 6 and 11.
Recurrent respiratory papillomatosis, a rare condition, is usually associated with HPV types 6 and 11.
High-risk types (oncogenic types), e.g. HPV types 16 and 18
Associated with low-grade cervical cellular changes, high-grade cervical cellular changes (mild, moderate, and severe Pap test abnormalities), and cervical dysplasia, and, in rare cases, cancers of the cervix. In addition, HPV infection has also been associated with cancers of the vulva, vagina, anus, penis, and oropharynx (back of throat including base of tongue and tonsils).
HPV types 16 and 18 account for 70% of cervical cancers.
Most women infected with high-risk HPV types have normal Pap test results and never develop cervical cellular changes or cervical cancer.
Genital HPV infects the basal cell layer of stratified squamous epithelium and stimulates cellular proliferation.
Affected cells display a broad spectrum of changes, ranging from benign hyperplasia, to dysplasia, to invasive carcinoma.
Natural History of HPV
Most infections are transient, asymptomatic or subclinical, and have no clinical consequences in immunocompetent individuals.
Time to development of clinical manifestations is unclear, but most likely
3 weeks to months for genital warts,
Several months to years for cervical cellular abnormalities, and
Decades for cervical cancers.
The median duration of new cervical infections (measured by detection of HPV DNA) is 8 months, but varies.
70% of new infections clear within 1 year.
90% of new infections clear within 2 years.
The gradual development of an effective immune response is thought to be the likely mechanism for HPV DNA clearance.
Natural History of HPV (continued)
Persistent HPV infection is infection that is not cleared by the immune system and is characterized by persistently detectable type-specific HPV DNA.
Persistent oncogenic HPV infection is the most important risk factor for precancerous (high-grade) cervical cellular changes and cervical cancer.
Factors associated with persistent infection include
Certain HPV types, and
It is unclear whether HPV infection that becomes nondetectable at mucosal surfaces has completely cleared or remains latent in basal cells with potential for later reactivation.
Lesson III: Clinical Manifestations and Sequelae [Slide 21]
HPV-associated cancers United States, 2004-2008
Clinical Manifestations and Sequelae
In most cases genital HPV infection is transient and has no clinical manifestations or sequelae.
Clinical manifestations of genital HPV infection include
Cervical cellular abnormalities detected by Pap tests,
Some anogenital squamous cell cancers,
Some oropharyngeal cancers, and
Recurrent respiratory papillomatosis
The two most common clinically significant manifestations of genital HPV infection are
Genital warts that are visualized without magnification, and
Cervical cellular abnormalities that are detected by Pap test screening.
Genital warts have four morphologic types.
Skin-colored, pink, or hyperpigmented
May be keratotic on skin; generally nonkeratinized on mucosal surfaces.
More commonly found on internal structures (i.e., cervix), but also occur on external genitalia
Thick horny layer resembling common warts or seborrheic keratosis
Genital warts appear most commonly in areas of coital friction.
Men—penis, scrotum, urethral meatus, and perianal area
Women—introitus, vulva, perineum, and perianal area
Less common genital warts sites—
Cervix and vaginal walls in women
Pubic area, upper thighs, or crural folds in men and women
Perianal warts do not necessarily imply anal intercourse, but may be secondary to autoinoculation, sexual activity other than intercourse, or spread from a nearby genital wart site.
Intra-anal warts are seen predominantly in patients who have had receptive anal intercourse.
HPV types causing genital warts can occasionally cause lesions on oral, upper respiratory, upper GI, and ocular locations.
Patients with visible warts are frequently infected simultaneously with multiple HPV types.
Genital warts usually cause no symptoms.
Vulvar warts can cause dyspareunia, pruritis, and burning discomfort.
Penile warts occasionally cause pruritis.
Urethral meatal warts occasionally cause hematuria or impairment of urinary stream.
Vaginal warts occasionally cause discharge, bleeding, or obstruction of birth canal (due to increased wart growth in pregnancy).
Perianal and intra-anal warts occasionally cause pain, bleeding on defecation, or pruritis.
Most patients have fewer than ten genital warts, with total wart area of 0.5–1.0 cm2.
Genital Warts—Duration and Transmission
Genital warts may regress spontaneously or persist with or without proliferation.
Frequency of spontaneous regression is unclear. A few studies indicate a regression rate of 10%–30% within three months.
Persistence of infection occurs, but frequency and duration is unknown.
Recurrences after treatment are common (20%–50% recurrence rate at 3–6 months).
Few studies on transmission, but available information suggests that genital warts are highly transmissible. Partners should be told about diagnosis and appropriate prevention strategies should be used.
Abstinence until warts are gone
Consistent and correct condom use
Genital Warts and High-Risk HPV
High-risk HPV types occasionally are found in visible genital warts and have been associated with external genital (i.e., vulvar, penile, and anal) squamous intraepithelial lesions (i.e., squamous cell carcinoma in situ, Bowenoid papulosis, Erythroplasia of Queyrat, or Bowen’s disease of the genitalia).
The most commonly recognized clinical manifestation of external genital squamous intraepithelial lesions (SIL) is Bowenoid papulosis, dome-shaped or flat papules that are often hyperpigmented.
These lesions can sometimes be clinically indistinguishable from genital warts, but on biopsy demonstrate high-grade SIL.
They occur in what is usually macroscopically normal epithelium and mucosal tissue.
Genital Warts in Preadolescent Children
May be due to sexual abuse although this condition is not diagnostic for sexual abuse. Their appearance should prompt an evaluation by a clinician.
May also result from vertical transmission, transmission of nongenital HPV types to genital surface, and possibly fomite transmission, although fomite transmission has never been documented.
Cervical Cellular Abnormalities
Cervical cellular abnormalities are usually subclinical.
Lesions associated with these abnormalities can be detected by Pap test or colposcopy, with or without biopsy.
Magnification by colposcopy can enhance detection of cervical cellular abnormalities; biopsy and histology are used to confirm and stage cervical intraepithelial neoplasia.
Cervical cellular abnormalities are usually caused by HPV
Low gradecervical cellular abnormalities attributed to HPV often regress spontaneously without treatment.
Classification of Cervical Cellular Abnormalities
The 2001 Bethesda System classifies cervical cellular abnormalities into one of several categories.
Atypical squamous cells (ASC) are cells that do not appear to be completely normal.
ASC–US—atypical squamous cells of undetermined significance. These changes are often caused by HPV infection. ASC–US changes are usually mild abnormalities.
ASC–H—atypical squamous cells cannot exclude a high-grade squamous intraepithelial lesion. ASC–H changes are more likely to be associated with precancerous abnormalities than ASC-US.
Low-grade squamous intraepithelial lesion (LSIL) generally are transient, and caused by infection with HPV.
High-grade squamous intraepithelial lesion (HSIL) generally are changes due to persistent infection with a high-risk HPV type. Lesions associated with HSIL may have a higher risk for progression to cervical cancer.
See the American Society for Colposcopy and Cervical Pathology Consensus Guidelines on Management of Women with Cytological Abnormalities for more information on the Bethesda Classification System. http://www.asccp.org/consensus/cytological.shtml
Anogenital Squamous Cell Cancers
HPV infection is causally associated with cervical cancer and other anogenital squamous cell cancers (e.g., anal, penile, vulvar, vaginal).
Over 99% of cervical cancers have HPV DNA detected within the tumor.
Persistent infection with a high-risk HPV type (e.g., infection which is not cleared by the immune system and which is characterized by persistently detectable HPV DNA) is necessary, but not sufficient, for the development of cervical cancer.
There have been other risk factors that increase risk of developing cervical cancer precursors and cervical cancer, including immune suppression, specific HPV types, and possibly others.
Recurrent Respiratory Papillomatosis
HPV infections in infants and children may present as laryngeal papillomatosis, also known as juvenile onset recurrent respiratory papillomatosis (JORRP).
Respiratory papillomatosis is a rare condition, usually associated with HPV types 6 and 11.
Lesson IV: Diagnosis of Genital Warts and Cervical Cellular Abnormalities [Slides 39-40]
Diagnosis of Genital Warts
Diagnosis is usually made by visual inspection with bright light. Usually the diagnosis is made clinically.
Diagnosis can be confirmed by biopsy.
Consider biopsy when
Diagnosis is uncertain;
Patient is immunocompromised;
Warts are pigmented, indurated, or fixed;
Lesions do not respond or worsen with standard treatment; or
There is persistent ulceration or bleeding.
Use of type-specific HPV DNA tests for routine diagnosis and management of genital warts is not recommended.
Application of acetic acid to evaluate external genitalia is not routinely recommended, but may be useful in some settings.
Low specificity (many false positives)
Acetowhitening will occur at sites of prior trauma or inflammation.
External genital warts are not an indication for cervical colposcopy or increased frequency of Pap test screening (assuming patient is receiving screening at intervals recommended by her healthcare provider).
Differential Diagnosis of Genital Warts
Condylomata lata–tend to be smoother, moist, more rounded, and darkfield-positive for Treponema pallidum. This is a manifestation of secondary syphilis and serologic tests for syphilis are typically positive.
Molluscum contagiosum–papules with central dimple, caused by a pox virus; rarely involves mucosal surfaces.
A useful screening test to detect cervical dysplasia (not HPV per se)
Provides indirect evidence of HPV because it detects squamous epithelial cell changes that are almost always due to HPV
No need for more frequent Pap test screening if external genital warts are present (assuming patient is receiving screening at intervals recommended by her healthcare provider).
Limitations of Pap tests
Specimen adequacy—Pap test occasionally must be repeated when the laboratory judges the specimen unsatisfactory for evaluation.
Variable sensitivity (estimates suggest the sensitivity of a single Pap test is 60%–80% for high-grade lesions, and lower for low-grade lesions).
Technologies using liquid collection media (ThinPrep® Pap Test™, Autocyte Prep™) and computer-assisted reading may enhance sensitivity, but reduce specificity.
Nucleic acid tests
A definitive diagnosis of HPV is based on detection of viral nucleic acid (DNA or RNA).
Clinical tests that detect high-risk types of HPV DNA in cells scraped from the cervix are commercially available.
The FDA has approved these tests for:
To triage women with atypical cells of undetermined significance (ASC-US) Pap test results
As an adjunct to the Pap test screening for cervical cancer in women 30 years or older
Use of HPV DNA tests for women with Pap abnormalities worse than AS-CUS (e.g. LSIL or HSIL) is unnecessary because the vast majority of these women are infected with high-risk HPV.
External genital warts are not an indication for HPV DNA testing.
Use of HPV testing in women 20 years and younger is not recommended, primarily because these women will frequently have HPV that is transient in nature.
HPV tests are not FDA-approved for use in men, or as a general test for STDs.
Indication for colposcopy is guided by physical exam and Pap test findings, with or without HPV DNA test findings.
External genital warts are not an indication for cervical colposcopy.
Indications for cervical biopsy include
Visible exophytic lesions on the cervix;
Pap test with HSIL; and
Pap test with ASCUS and HPV-positive, ASC-H or LSIL with colposcopic abnormalities.
For more information on guidelines for managing women with cervical cytologic abnormalities, refer to the 2006 Consensus Guidelines for the Management of Women with Cervical Cytologic Abnormalities. http://www.asccp.org/consensus/cytological.shtml
Lesson V: Patient Management [Slides 47–48]
General Treatment of Genital Warts
Primary goal is removal of warts.
If left untreated, visible genital warts may regress spontaneously or persist with or without proliferation.
In most patients, treatment can induce wart-free periods.
Currently available therapies may reduce, but probably do not eradicate, infectivity.
Effect of current treatment on future transmission is unclear.
No evidence that presence of genital warts or their treatment is associated with development of cervical cancer.
Because of uncertainty regarding the effect of treatment on future transmission and the possibility for spontaneous resolution, some patients may choose to forgo treatment and await spontaneous resolution.
Consider screening persons with newly diagnosed genital warts for other STDs (e.g., chlamydia, gonorrhea, HIV, syphilis).
The presence of genital warts is not an indication for HPV testing, a change in the frequency of Pap tests, or cervical colposcopy.
Patient-applied and provider-administered treatment regimens are available.
The safety of sinecatechins has not been established in pregnancy or HIV- or HSV-coinfected individuals
Using patient-applied treatments
Provider should identify warts for treatment and teach patients how to apply substance.
Patient must be able to identify and reach warts to be treated.
Podofilox 0.5% solution or gel, an antimitotic drug that destroys warts, is relatively inexpensive, easy to use, and safe.
Most patients experience mild or moderate pain or local irritation after treatment with podofilox.
Imiquimod is a topically active immune enhancer that stimulates production of interferon and other cytokines.
Local inflammatory reactions are common with use of imiquimod and sinecatechins; these reactions include redness and irritation and are usually mild to moderate.
Follow-up is not required, but may be useful several weeks into therapy to determine appropriateness of medication use and response to treatment.
CDC-Recommended Regimens for External Genital Warts (Provider Administered)
Cryotherapy with liquid nitrogen or cryoprobe
Repeat applications every one to two weeks.
May be used on internal or external warts and during pregnancy.
Podophyllin resin 10%–25% in compound tincture of benzoin
Apply a small amount to each external wart and allow to air dry.
The treatment can be repeated weekly if needed.
To avoid the possibility of complications associated with systemic absorption and toxicity, two important guidelines should be followed.
Application should be limited to < 0.5 mL of podophyllin or < 10 cm2 of warts per session.
No open lesions or wounds should exist in the area to which treatment is administered.
Some specialists suggest that the preparation area be thoroughly washed off one to four hours after application to reduce local irritation. Local irritation is common.
Podophyllin resin preparations differ in the concentration of active components and contaminants. The shelf life and stability of podophyllin preparations is uncertain.
The safety of podophyllin during pregnancy has not been established.
Trichloroacetic acid (TCA) or bichloroacetic acid (BCA) 80%–90%
Apply a small amount only to warts and allow to air dry (white “frosting” develops).
If excess amount of acid is applied, powder the treated area with talc or sodium bicarbonate (i.e., baking soda), or with liquid soap preparations to remove unreacted acid.
Repeat weekly if necessary.
Can be used on vaginal and anal warts as well as on external warts and during pregnancy.
Surgical removal—tangential scissor excision, tangential shave excision, curettage, or electrosurgery
Surgical therapy is most beneficial for patients who have large numbers or areas of genital warts.
Can be used on accessible internal warts and during pregnancy
Can usually eliminate warts at a single visit
Requires substantial clinical training, additional equipment, and a longer office visit
Alternative Treatment Regimens
Systemic interferon is not effective.
Intralesional interferon is probably effective because of antiviral and/or immunostimulating effects. Administration of intralesional interferon is associated with stinging, burning, and pain at the injection site, and sometimes systemic effects.
Not recommended as a modality because of inconvenient routes of administration, frequent office visits, and the association between its use and a high frequency of systemic adverse effects.
Carbon dioxide laser and surgery, topical cidofovir might be useful in management of extensive warts or intraurethral warts, particularly for those that have not responded to other treatments. Topical cidofovir has challenges as the preparation is not readily available and must be formulated by a pharmacist.
CDC-Recommended Regimens for Cervical Warts
For women who have exophytic cervical warts, high-grade SIL must be excluded before treatment is initiated.
Management should include biopsy and consultation with a specialist.
CDC-Recommended Regimens for Vaginal Warts
Treat only if symptomatic, since most treatments also affect normal tissue and could cause scarring and pain.
The use of a cryoprobe in the vagina is not recommended because of risk for vaginal perforation and fistula formation.
TCA or BCA 80%–90% applied to warts
Apply small amount only to warts and allow to air dry (white “frosting” develops).
If an excess amount of acid is applied, powder the treated area with talc, sodium bicarbonate (i.e., baking soda), or with liquid soap preparations to remove unreacted acid.
Repeat weekly, if needed.
CDC-Recommended Regimens for Urethral Meatal Warts
Cryotherapy with liquid nitrogen
Podophyllin 10%–25% in compound tincture of benzoin
Treatment area must be dry before contact with normal mucosa.
Repeat weekly if needed.
Note:The safety of podophyllin during pregnancy has not been established.
Although data evaluating the use of podofilox and imiquimod for the treatment of distal meatal warts are limited, some specialists recommend their use in certain patients.
CDC-Recommended Regimens for Anal Warts
Cryotherapy with liquid nitrogen
TCA or BCA 80%–90% applied to warts
Apply small amount only to warts and allow to dry (white “frosting” develops).
If an excess amount of acid is applied, powder the treated area with talc, sodium bicarbonate (i.e., baking soda), or with liquid soap preparations to remove unreacted acid.
Repeat weekly if needed.
Warts on the rectal mucosa should be managed in consultation with a specialist.
Many persons with warts on the anal mucosa also have warts on the rectal mucosa, so persons with anal warts can benefit from an inspection of the rectal mucosa by digital examination or anoscopy.
Management in Pregnancy
Genital warts can proliferate and become more friable during pregnancy.
Cytotoxic agents (podophyllin, podofilox, imiquimod) should not be used.
Cryotherapy, TCA, BCA, and surgical removal may be used.
HPV types 6 and 11 can cause recurrent respiratory papillomatosis in children. The route of transmission (i.e., transplacental, perinatal, or postnatal) is not completely understood.
The prevention value of cesarean delivery is unknown; thus, C-section should not be performed solely to prevent transmission to neonate.
Cesarean delivery may be indicated for women with genital warts, if the pelvic outlet is obstructed, or if vaginal delivery would result in excessive bleeding.
Genital Warts in HIV-Infected Patients
No data suggest that treatment modalities for external genital warts should be different.
Might have larger or more numerous warts
Might not respond as well to therapy
Might have more frequent recurrences after treatment
Squamous cell carcinomas arising in or resembling genital warts might occur more frequently, therefore, requiring biopsy for confirmation of diagnosis.
Pap Test Screening in Immunodeficient Patients
Provide cervical Pap test screening every six months for one year, then annually for all HIV-infected women with or without genital warts.
There is an increased incidence of anal cancer in HIV-infected MSM. Some experts screen for anal intraepithelial neoplasia by cytology—however, this is not routinely recommended, because evidence is limited on natural history of anal intraepithelial neoplasias, reliability of screening methods, safety and response to treatments, and programmatic considerations.
Ablative modalities usually are effective, but careful follow-up is essential.
Genital Wart Follow-up
Counsel patients to
Watch for recurrences (most frequent in first three months after treatment), and
Continue regular Pap screening at the same intervals as recommended for women without genital warts. The presence of genital warts is not an indication for increase in frequency of Pap test screening (assuming patient is receiving screening at intervals recommended by her healthcare provider), or for cervical colposcopy.
Communicate to current sex partners about genital warts and the risk of transmission. Patients should have no sexual activity until warts are gone.
External genital warts can be difficult to identify, so it might be useful for patients to have a follow-up evaluation three months after treatment.
Earlier follow-up visits also might be useful for some patients to
Monitor or treat complications of therapy,
Document the absence of warts, and
Reinforce patient education and counseling messages.
Patients concerned about recurrences should be offered a follow-up evaluation three months after treatment.
Treatment of Cervical Dysplasia
Detailed discussion of treatment of cervical dysplasia is beyond the scope of this educational offering.
For more information on managing women with cervical dysplasia refer to the following sources:
2006 Consensus Guidelines for the Management of Women with Cervical Cytologic Abnormalities http://www.asccp.org/consensus/cytological.shtml
CDC National Breast and Cervical Cancer Early Detection Program http://www.cdc.gov/cancer/nbccedp/index.htm
Lesson VI: Patient Counseling and Education [Slide 69]
The Nature of HPV Infection
Genital HPV infection is common in sexually active adults.
The majority of sexually active adults will have HPV infection at some point in their lives, although the majority of them will never know because the infection usually has no symptoms and clears on its own.
Natural history of HPV infection is usually benign.
Low-risk genital HPV types are associated with mild Pap test abnormalities and genital warts.
High-risk types are associated with mild to severe Pap test abnormalities, and rarely, cancers of the cervix, vulva, vagina, anus, penis, and oropharynx.
Most women infected with HPV infection do not develop cervical cancer.
Recurrence of genital warts within the first several months after treatment is common.
Genital HPV infection is usually sexually transmitted (through vaginal intercourse, anal intercourse, oral sex, and also possible through nonpenetrative sexual activity such as genital-genital contact).
Infection is often shared between partners
The incubation period (i.e., the interval between initial exposure and established infection or disease) is variable, and determining the timing and source of infection is frequently difficult.
Within ongoing sexual relationships, sex partners are usually infected by the time of the patient’s diagnosis, although they may have no symptoms or signs of infection.
Recurrences usually are not reinfection.
Treatment for genital warts can reduce HPV infection, but whether treatment results in a reduction in risk for transmission of HPV to sex partners is unclear. The duration of infectivity after wart treatment is unknown.
The value of disclosing a past diagnosis of genital HPV infection to future partners is unclear, although candid discussions about past STD should be encouraged and attempted whenever possible.
HPV testing is not indicated for partners of persons with genital warts or cervical cellular abnormalities due to HPV.
Assess patient’s behavior-change potential.
Develop individualized risk-reduction plans with the patient for lasting results.
Discuss prevention strategies such as abstinence, mutual monogamy, condoms, limiting number of sex partners, etc.
Consistent and correct male condom use reduces the risk for genital HPV acquisition and HPV-associated diseases (e.g., genital warts and cervical cancer).
HPV infections can occur in male and female genital areas that are not covered by a latex condom (e.g., scrotum, vulva, or perianus).
Patient Counseling and Education Resources
Division of STD Prevention. Available at: http://www.cdc.gov/std/hpv/default.htm
American Sexual Health Association, National HPV and Cervical Cancer Prevention Resource Center. Available at: http://www.ashastd.org/std-sti/hpv.html
CDC Cervical Cancer Screening Fact Sheet http://www.cdc.gov/cancer/cervical/pdf/cc_basic.pdf
National Cancer Institute Cervical Cancer Screening Information For Patients http://www.cancer.gov/cancertopics/pdq/screening/cervical/Patient
American Society of Colposcopy and Cervical Cancer Pathology http://www.asccp.org/EducationeLearning/EducatetheEducatorsbrHPVResourceCenter/tabid/5980/Default.aspx
Lesson VII: Partner Management and Public Health Measures [Slide 74]