Mucosal ulcerative disorders in adolescent females can be caused by sexually transmitted as well as nonsexually transmitted diseases. In this chapter, common mucosal ulcerative disorders are discussed sequentially and include:

1. 
   

   Vulvar herpes simplex virus (HSV) infection

   
   
2. 
   

   Syphilis in teenage females

   
   
3. 
   

   Chancroid

   
   
4. 
   

   Behcet Disease

See Chapter 114, Herpes Simplex, for information on all types of herpes simplex infections.

Patient Story

A 16-year-old girl presents with vulvar swelling, pain, and difficulty urinating. She admits to being sexually active. On examination, ulcerative lesions are noted on the inner aspects of the labia minora (Figure 75-1). She is treated with analgesics and oral acyclovir for presumed Herpes simplex virus type 2 (HSV-2). She is also tested for other STDs including blood tests for syphilis, HIV, and urine tests for gonorrhea and chlamydia. Her culture of the lesions is positive for HSV-2 as expected. Her other tests are all negative. Her lesions resolve after 2 weeks.

Introduction

HSV-2 is a sexually transmitted infection that usually causes vesicles and ulcers in the genito-anal region. HSV-1 usually involves infections found extra-genitally. HSV-2 infections present with painful genital ulcerative lesions. HSV-1 can occur in the genito-anal region and HSV-2 can occur on the oral mucosa. There are many people with positive serologies for both types of herpes simplex that are not aware of having a “herpes infection” with symptoms.

Epidemiology

• 
  

  The prevalence of HSV increases with age.^1–4

  
  
• 
  

  By age 15 years of age, 40 percent will be infected with HSV-1.²

  
  
• 
  

  The prevalence of HSV-1 is greater than HSV-2 in most areas of the world and since HSV-2 is primarily sexually transmitted, it is not as common in children.

  
  
• 
  

  Data from the Centers for Disease Control and Prevention (CDC) monitored through the National Health and Nutrition Examination Survey (NAHNES) found the overall prevalence of HSV-2 from 2005 to 2008 to be 16.2 percent; of those testing positive for HSV-2 infection, 81.1 percent said they had never been told by a doctor or health care professional that they had genital herpes.²

  
  
• 
  

  In this study, seroprevalence increased with age, ranging from 1.4 percent among those aged 14 to 19 years to 26.1 percent among those aged 40 to 49 years.²

  
  
• 
  

  HSV-2 seroprevalence is greater among women (20.9%) than men (11.5%).²

Etiology and Pathophysiology

• 
  

  Genital herpes is usually caused by HSV-2 but may also be caused by HSV-1.

  
  
• 
  

  Transmission occurs more commonly from an infected male to a female partner.

  
  
• 
  

  Infection occurs as a result of exposure to mucosal tissue that has active lesions or as a result of exposure to the secretion of an individual who has active HSV infection.

  
  
• 
  

  Incubation period is about 4 days but can range from 2 to 12 days.

  
  
• 
  

  It may be divided into two categories: first episode versus recurrences. Patients experiencing their first outbreak may not have any antibodies to type 1 or 2 HSV or they may have an antibody to usually type 1.

  
  
• 
  

  The virus usually remains in the sensory ganglia of the autonomic nervous system. Once triggered the virus can travel down the sensory nerve and reactivate the same region as the initial infection.

Risk Factors

• 
  

  Found more commonly in females and African Americans.²

  
  
• 
  

  Found more commonly in individuals with lower socioeconomic status.¹

Diagnosis

Clinical Features

• 
  

  Vesicles are noted on the labia minora and vestibule (Figure 75-1). Lesions may also be noted in the vagina and on the cervix.

  
  
• 
  

  The vesicles are small, on an erythematous base, and rupture into painful shallow ulcerations.

  
  
• 
  

  Skin lesions are usually preceded by prodromal symptoms that include: fever, malaise, burning, and paresthesia at the site, loss of appetite, and headaches. Lymphadenopathy may also be noted.

  
  
• 
  

  Recurrences occur as a result of triggers such as stress, fatigue, and menstruation.

Laboratory Testing

• 
  

  Viral culture may be obtained from an active lesion. In these cases, the base of the unroofed lesion must be swabbed vigorously. The cells are then evaluated for HSV infection.

  
  
• 
  

  Direct fluorescent antibody (DFA)—This technique identifies the presence of viral antigens. It is rapid, sensitive, and relatively inexpensive. Tzanck smear-cells obtained from the base of a vesicle are stained and then assessed for multinucleated giant cells. This is not as specific as culture and DFA and only valuable if done by persons well trained in this testing.

  
  
• 
  

  Polymerase chain reaction (PCR)—May be used to detect the presence of herpes virus DNA in the CSF when herpes encephalitis is suspected. It is used less often for genital herpes infections.

  
  
• 
  

  Serologic assays—Used primarily for diagnosing recurrent infection. This is generally not helpful in acute diagnosis and management.

Differential Diagnosis

• 
  

  Other sexually transmitted infections must be considered and include syphilis and chancroid.

  
  
• 
  

  Other diagnoses to consider are candida infection, Behcet disease (as discussed in this chapter), lichen planus, lichen sclerosis, herpes zoster, and trauma. These entities can usually be distinguished based on their characteristic appearance and usual involvement in areas other than the genital tract.

  
  
• 
  

  Prepubertal children who develop genital herpes must be evaluated for sexual abuse (see Chapter 9, Child Sexual Abuse).

Management

Prevention

• 
  

  Patients must be educated about the mode of transmission and understand the concept of asymptomatic shedding.

Medications

• 
  

  Systemic antiviral drugs can modestly improve the signs and symptoms of herpes episodes when used to treat first clinical and recurrent episodes, or when used as daily suppressive therapy.⁵

  
  
• 
  

  Antiviral drugs do not eradicate latent virus.

  
  
• 
  

  Acyclovir, valacyclovir and famciclovir have been shown to provide clinical benefit for genital herpes.⁵ SOR B

  
  
• 
  

  Oral acyclovir has been approved for use in children with primary genital HSV infection. The medication should be started within 6 days of onset of disease. Oral acyclovir may also be used in recurrent HSV within 2 days of onset.

  
  
• 
  

  Recommended maximum dose is 80 mg/kg/day (1200 mg/day) for 7 to 10 days for a primary infection and 5 days for a recurrent infection.

  
  
• 
  

  Supportive therapy may be necessary for control of pain associated with the lesions.

  
  
• 
  

  At times chronic suppressive therapy may be necessary and may be more effective than episodic therapy for recurrent infection. The maximum dose is 1000 mg/day of acyclovir.

Prognosis

• 
  

  The treatment of genital herpes does not lead to cure.

Patient Education

• 
  

  Patients have to be educated about the modes of transmission of herpes virus.

  
  
• 
  

  Patients with active lesions need to avoid direct contact of their lesions with other individuals.

  
  
• 
  

  Condoms should be used at all other times.

  
  
• 
  

  They should be educated about the factors that may precipitate a recurrence.

See Chapter 181, Syphilis, for information on all types of syphilis infections.

Patient Story

A 16-year-old female noted several nonpainful bumps while shaving her vulvar area (Figure 75-2). She noted in the ensuing couple days that the surface of the some of the bumps eroded into ulcers. While this was not painful she was scared and presented to her physician for evaluation. She admitted to having had intercourse (unprotected) for the first time 6 weeks ago. The physician noted flat-topped raised plaques that could be condyloma lata or HPV. Her serum RPR test and confirmatory treponemal test were positive. She was treated with one dose of 2.4 million units of benzathine penicillin given intramuscularly. An HIV screen and an HIV DNA PCR were performed and fortunately, were negative.

Introduction

Syphilis is an infection caused by the spirochete Treponema pallidum. It causes ulcerative lesions on the external genitalia.

Epidemiology

• 
  

  The rate of syphilis in the US in 2011 was 1.0 case per 100,000 adult population.⁶

  
  
• 
  

  The rate of primary and secondary syphilis in 15 to 19 year olds in the US in 2011 was 2.4 per 100,000 population.⁶

Etiology and Pathophysiology

• 
  

  Acquired syphilis is transmitted by direct contact with syphilis lesions. The spirochete enters through areas of micro trauma in the mucous membranes.

  
  
• 
  

  Syphilis is categorized as early (primary, secondary and early latent <2 years of infection) versus late (>2 years of infection).