Porth's Essentials of Pathophysiology, 4e

1051

Sexually Transmitted Infections

C h a p t e r 4 1

Diagnosis andTreatment Diagnosis of genital warts is usually made by visualiza- tion or palpation of nontender papillomatous genital lesions. A diagnosis of genital warts may be confirmed by biopsy. There are no approved serologic tests for HPV or routine methods for culturing the virus. 7 As HPV infec- tion is confined to the epithelium and cells are shed, the infection results in a minimal immune response and not all those infected produce antibodies to the virus that are detected using serology tests. HPV tests are available for women older than 30 years of age who are under- going cervical cancer screening. These tests detect HPV nuclear DNA, ribonucleic acid (RNA), or capsid pro- teins. Four tests have been approved by the Food and Drug Administration (FDA), two of which indicate the presence of one or more high-risk HPV types, and two which provide individual detection of HPV 16 and 18. 7 None of these tests have been approved for use in men, for women older than 20 years of age, or as a general test for STIs. The choice of treatment for genital warts is based on the number, size, site, and morphology of the lesions, as well the person’s preference. If left untreated, the warts may resolve spontaneously, so expectant manage- ment is acceptable if the person is comfortable with this approach. Evaluation and treatment of sexual partners may be suggested, although this may be difficult consid- ering that warts often do not become clinically apparent for several years after exposure. Treatment regimens canbe classified as patient-applied or provider-applied. Patient-applied products include cytoxic agents (podofilox [5%]), an immune enhancer (imiquimod), or a green tea extract (sinecatechin). 4–6 Podofilox is a topical antimitotic agent that results in visible necrosis of wart tissue. The safety of podofilox during pregnancy has not been established. Imiquimod stimulates the body’s immune system (i.e., production of interferon- α and other cytokines). Imiquimod is a category B drug and therefore potentially safe for use in pregnancy. Sinecatechins are thought to destroy wart tissue by inducing cell cycle arrest and apoptosisis. 5 The safety of sinecatechins during pregnancy has not been established. 6 Provider-administered treatments include podophyl- lin resin [10% or 25%], trichloroacetic acid (TCA), or bichloracetic acid (BCA). Podophyllin resin is a topical cytotoxic agent that has long been used for treatment of visible external growths. Multiple applications may be required for resolution of lesions. The amount of drug used and the surface area treated should be limited with each treatment session to avoid systemic absorption and toxicity. This treatment is contraindicated in pregnancy for the same reason. An alternative therapy involves the topical application of a solution of TCA or BCA. These weak destructive agents produce an initial burning in the affected area, followed in several days by a sloughing of the superficial tissue. Several applications at 1- to 2-week intervals may be necessary to eradicate the lesion. Sexual abstinence is suggested during any type of treatment to enhance healing.

Genital warts also may be removed using cryotherapy (i.e., freezing therapy) with liquid nitrogen or a cyro- probe, laser vaporization, electrocautery, or surgical excision. 4 Cryotherapy and BCA or TCA are the recom- mended treatments for cervical HPV lesions. Laser sur- gery can be used to remove large or widespread lesions of the cervix, vagina, or vulva, or lesions that have failed to respond to other first-line methods of treatment. Electrocautery treatment has become more widespread for these types of lesions because it does not require suturing and is beneficial for persons who have a large number of warts. 4 Vaccination is currently regarded as one of the most effective strategies for controlling HPV-related diseases. Two vaccines are available to protect females against the type of HPV that causes cervical cancer—a quadrivalent vaccine (Gardasil) that protects against HPV types 6, 11, 16, and 18. 8 and a bivalent vaccine (Cevarix) that pro- tects against HPV types 16 and 18. 7 The quadrivalent (Gardasil) vaccine can be given to males for protection from genital warts. 8 There is no treatment, however, to eradicate the virus once a person has become infected. Genital Herpes Genital herpes is a common cause of genital ulcers, affecting more than 50 million people in the United States. 1,2 Because herpesvirus infection is not reportable in all states, reliable data on its true incidence and prev- alence are lacking. Etiology and Pathogenesis Genital herpes is caused by the herpes simplex virus (HSV), a large double-stranded DNA virus. 9–13 Herpes simplex infections are highly contagious. There are eight types of HSV; however, only two are considered sexu- ally transmitted. These are HSV-1 (usually associated with fever blisters and cold sores) and HSV-2 (usually associated with genital herpes). 13 HSV-1 and HSV-2 are genetically similar; both cause a similar set of primary and recurrent infections; and both can cause oropharyn- geal and genital lesions, but HSV-2 is most commonly found only in the genitals. 12 HSV-1 and HSV-2 are neurotropic viruses, meaning that they grow in neurons and share the biologic prop- erty of latency. 9 Latency refers to the ability to maintain disease potential in the absence of clinical signs and symptoms. In genital herpes, the virus ascends through the peripheral nerves to the sacral dorsal root ganglia (Fig. 41-2). The virus can remain dormant in the dor- sal root ganglia, or it can reactivate, in which case the viral particles are transported back down the nerve root to the skin, where they multiply and cause a lesion to develop. During the dormant or latent period, the virus replicates in a different manner so that the immune sys- tem or available treatments have no effect on it. It is not known what reactivates the virus. It may be that the body’s defense mechanisms are altered. Numerous studies have shown that host responses to infection influence initial development of the disease, severity of