Etiology and Epidemiology

Etiology. HSV-2 > HSV-1. See also Section 27.

Prevalence. Highly variable. Depends on many
factors: country, region of residence, population
subgroup, gender, and age. Greater among
higher risk sexual behavior groups. Prevalence
of HSV-2 seropositivity in general population:
United States: 21%; Europe: 815%; Africa:
4050% in 20-year-olds. Strongly associated
with age, increasing from negligible levels in
children <12 to as high as 80% among higher
risk populations. In the United States, approximately
one in five adults infected.
Transmission. Usually skin-to-skin contact.
Seventy percent of transmission occurs during
times of asymptomatic HSV shedding. Transmission
rate in discordant couples (one partner
infected, the other not) approximately 10% per
year; 25% of females become infected, compared
with only 46% of males. Prior HSV-1
infection is protective; in females with anti-
HSV-1 antibodies, 15% become infected with
HSV-2, but in those without anti-HSV-1 antibodies,
30% become infected with HSV-2.
Clinical Manifestation
Only 10% of HSV-2 seropositive individuals
are aware that symptoms are those of GH.
Ninety percent do not recognize symptoms of
GH. Most clinical lesions are minor breaks in
the mucocutaneous epithelium, presenting as
erosion, abrasions, fissures. The classically
described findings are uncommon. Symptoms of
aseptic HSV-2 meningitis can occur with primary
or recurrent GH.
Primary Genital Herpes. Most individuals with
primary infection are asymptomatic. Those
with symptoms report fever, headache, malaise,
myalgia, peaking within the first 34
days after onset of lesions, resolving during
the subsequent 34 days. Erythematous papules
initially evolve to vesicles or pustules, which become
eroded as the overlying epidermis sloughs
(Figs. 30-14, 30-15). Primary infection occurs
anywhere on the anogenital skin, cervix, and
anorectal mucosa. Epithelial defects heal in 24
weeks, often with resulting postinflammatory
hypo- or hyperpigmentation, uncommonly
with scarring.
With host defense defects, lesions tend to be
more extensive and delayed in healing.
Recurrent Genital Herpes. New symptoms may
result from old infections. Most individuals do
not experience classic findings of grouped
Figure 30-14. Genital herpes, primary Multiple,
extremely painful, punched-out, confluent, shallow ulcers
on the edematous vulva and perineum. Micturition is often
very painful. Associated inguinal lymphadenopathy is
common.
vesicles on erythematous base. Common
symptoms are itching, burning, fissure, redness,
and irritation prior to eruption of vesicles.
Dysuria, sciatica, and rectal discomfort.
Lesions may be similar to primary infection
but on a reduced scale. Often a 1- to 2-cm erythematous
plaque with vesicles (Figs. 30-16 to
30-21), which rupture with of erosions.
Distribution. Males. Primary infection: glans,
prepuce, shaft, sulcus, scrotum, thighs, buttocks.
Recurrences: penile shaft, glans, buttocks.
Females. Primary infection: labia majora/
minora, perineum, inner thighs. Recurrences:
labia majora/minora, buttocks.

Anorectal Infection. Occurs following anal

intercourse; characterized by tenesmus, anal
pain, proctitis, discharge, and ulcerations (Figs.
30-18, 30-19) as far as 10 cm into anal canal.
General Findings. Inguinal/femoral lymph nodes
may be enlarged, tender with primary infection.
Signs of aseptic meningitis. Fever, nuchal
rigidity; can occur in the absence of GH. Pain
along sciatic nerve.
Differential Diagnosis
Trauma, candidiasis, syphilitic chancre, fixeddrug
eruption, chancroid, gonococcal erosion.
Laboratory Studies
See Section 27 Herpes Simplex Virus Disease.
Diagnosis
Diagnosis can be made on clinical finding. Confirmation
by viral culture or direct fluorescent antibody
(DFA) or serology may be indicated. Coinfection
with another STD should be ruled out.
Course
GH is a lifetime infection and recurrances are
the rule. Seventy percent are asymptomatic.
Recurrence rates are high in those with an
extended first episode of infection, regardless
of whether antiviral therapy is given. Chronic
suppressive therapy reduces shedding. Treatment
of first-episode infection prevents complications
such as meningitis and radiculitis.
Erythema multiforme may complicate recurrences,
occurring 12 weeks after an outbreak.
Treatment
Prevention. Advise patients to abstain from sexual
activity while lesions are present and encourage
use of condoms during all sexual activity.
First Episode. Oral antivirals. Acyclovir 400 mg
5 times daily for 10 days or until lesions resolve.
Recurrances. Oral antivirals. Acyclovir 400 mg
3 times daily for 5 days or 800 mg twice daily
for 5 days, or 800 mg 3 times daily for 2 days.
Valacyclovir 500 mg twice daily for three days
or 1 mg twice daily for 3 days. Famciclovir 125
mg twice daily for 5 days or 1 g once a day for
5 days.
Maintenance Therapy. Oral antivirals: Daily
suppressive therapy. Acyclovir 400 mg twice
daily. Valcyclovir 5001000 mg once daily.
Famciclovier 250 mg once daily.
Severely Immunocompromised. IV acyclovir
5 mg/kg every 8h for 57 days or oral acyclovir
400 mg 5 times a day for 714 days.
Acyclovir Resistant. IV foscarnet 40 mg/kg every
8h for 1421 days.
Neonates. see Section 27.