1. Herpes infection
Ghodiwala Tossif
Ml-610

2. Herpesviridae
Virus classification
Group:
Group I (dsDNA)
Order:
Herpesvirales
Family:
Herpesviridae

3. INTRODUCTION
A. Herpesviridae - large, enveloped dougle
stranded DNA viruses; morphologically alike;
share a common mode of replication.
B. Herpesviruses - ubiquitous and cause
infections ranging from painful skin ulcers to
chickenpox to encephalitis.

4. C. An outstanding property - the ability to
establish latent infections, to persist
indefinitely in infected hosts, and to periodically
become reactivated.
D. With all these viruses, immunocompromised
patients, especially those with altered cellular
immunity, have more frequent and severe
infections, including severe disease from
reactivation of the virus
E. Effective antiviral drugs available to treat
these infections.

5. CLASSIFICATION
A. Alphaherpesviruses are fast growing,
cytolytic viruses that establish latent infections
in neurons. Herpes simples virus type 1 and
2 (HSV-1 and HSV- 2) and Varicella- zoster virus
(VSV) are members of this subfamily. These
three viruses produce vesicular rashes both in
their primary infections and in reactivation.

6. B. Betaherpesviruses include the slow growing
Cytomegalovirus (CMV) - so named because it
causes the cells it infects to become cytomegalic –
become massively enlarged. These viruses become
latent in secretory glands and kidneys. This
subfamily also includes the newly identified human
Herpesviruses 6 and 7.
• Human herpesvirus 6 causes a common
childhood illness – sixth disease – roseola
infantum.
• Human herpesvirus 7 – is closely related to
human herpesvirus 6, but is not firmly associated
with human disease.

7. C. Gammaherpesviruses, exemplified by Epstein
Barr virus (EBV) infect and become latent in
lymphoid cells. A new herpesvirus – also called
Kaposi's sarcoma associated herpesvirus has
been detected in over 90% of Kaposi's sarcomas
and a rare type of B cell lymphoma from AIDS
patients.

9. Structure

12. Replication Cycle
• 1. Virus attaches to the cell receptors
(heparan sulfate moiety of cellular
proteoglycans) via glycoprotein spikes.
• 2. Enters the cell after pH independent fusion
with the cell membrane.
• 3. Tegument proteins are released, one of
which shuts down cellular protein synthesis.

13. • 4. The nucleocapsid is transported along the
cytoskeleton to a nuclear pore where viral
DNA is released, enters the nucleus, and
circularizes.
• 5. Viral gene expression is tightly regulated,
with three classes of mRNA's, alpha, beta, and
gamma, being transcribed in an ordered
sequence by cellular RNA polymerase II.

14. • 6. The virus buds through the nuclear
membrane.
• 7. Enveloped virions accumulate in
endoplasmic reticulum and the mature virions
are released by exocytosis. The length of the
replication cycle varies from 18h (HSV) to over
70h (CMV).

16. Pathogenesis
Entry by skin or mucous membranes
viral multiplication
sensory nerve
lysis of cells
root ganglia
vesicles
latency
ulcers
REACTIVATION
COLD
FEVER
SURGERY
UNKNOWN

17. HOW IS LATENCY MAINTAINED?
Not fully understood.
If interested read about HHV Latency Associated Transcript

18. HERPES SIMPLEX VIRUS DISEASE:

19. Course of the Disease
• The incubation period for herpes - 2 to 7 days.
• Persons with primary herpetic lesions are
infectious for about 7 to 12 days.
• Genital, rectal, or oral herpes recurs in 60 to
80% of persons whose primary infection was
symptomatic.
• These recurrent episodes of herpes are milder
and of shorter duration than the initial
outbreak.

20. Epidemiology
• HSV-1 and 2 infections are life-long.
• The virus is found in the lesions on the skin
but can be present in body fluids including
saliva and vaginal secretions.
• As a result of poor hygiene in underdeveloped
countries, HSV-1 antibodies are found in more
than 90% of children.

21. Epidemiology 2
• HSV-2 is normally spread sexually and is found in the
anus, rectum and upper alimentary tract as well as
the genital area.
• An infant can be infected at birth by a genitallyinfected mother.
• The infant can also be infected in utero if the
mother’s infection spreads.
• Because of the infant’s underdeveloped immune
system, the resulting infection can be very severe
and sometimes be deadly.

22. Definitions of Infection Types
First Clinical Episode
• Primary infection
– First infection ever with either HSV-1 or HSV-2
– No antibody present when symptoms appear
– Disease is more severe than recurrent disease
• Non-primary infection
– Newly acquired HSV-1 or HSV-2 infection in an
individual previously seropositive to the other
virus
– Symptoms usually milder than primary infection
– Antibody to new infection may take several
weeks to a few months to appear
22

23. Definitions of Infection Types
Recurrent symptomatic infection
• Antibody present when symptoms appear
• Disease usually mild and short in duration
Asymptomatic infection
• Serum antibody is present
• No known history of clinical outbreaks
23

24. Types of Infection
Infection Type
Lesions/
Symptoms
Type-specific
antibody at time of
presentation
HSV-1
HSV-2
First episode, Primary
(Type 1 or 2)
+/Severe,
bilateral
-
-
First episode, Non-primary
Type 2
+/Moderate
+
-
First episode, Recurrence
Type 2
+/Mild
+/-
+
Symptomatic, Recurrence
Type 2
+/Mild,
unilateral
+/-
+
Asymptomatic, Infection
Type 2
-
+/-
+
24

25. Transmission
a. HSV-1- usually transmitted in saliva (kissing,
sharing of glasses, etc.)
b. HSV-2 transmitted by
• 1. sexual contact (HSV-2 can infect genitalia,
anorectal tissues, or the orpharynx)
• 2. autoinoculation
• 3. during pregnacy and labour
c. Both types can cause oral and genital lesions.

26. Special “at risk” groups:
• Neonates
• Immunocompromised
• Physicians, nurses, dentists, etc. in
contact with oral and genital secretions.

27. Immunity
a. During primary infection, interferon and natural killer cells limit the
progression of the infection.
b. Antibody directed against envelope glycoproteins can neutralize
extracellular viruses and help limit their spread. Antibody can also
participate in ADCC. Viruses can escape antibody neutralization and
clearance by:
• (1) Direct cell-to cell spread- limiting their time spent outside the
cell.
• (2) Latent infections of the neurons
• (3) Binding the antibody “upside down” with Fc receptors and/or
inhibiting C3b
c. Cell mediated immunity is essential for controlling and resolving HSV
infections. Without functional cell mediated immunity, the virus may
disseminate to vital organs and the brain
ADCC-Antibody-dependent cellular cytotoxicity

28. Clinical Presentations
• The classical presentation of HSV-1 and 2 is
the lesion – a clear vesicle on an
erythematous base – “the dewdrop on a rose
petal”- which then progresses to pustular
lesions, ulcers, and crusted lesions.

30. • Primary herpes infection may be
asymptomatic or symptomatic.
• In women, the primary infection is usually
more severe than in men.
• lymphadenopathy, as well as flu-like
symptoms including fever, headache, malaise,
and muscle aches during the first few weeks
of infection.

31. Recurrent oral infection is more common with HSV-1
infections than with HSV-2.
Symptoms typically progress in a series of eight stages
• Latent (weeks to months incident-free): The
remission period; After initial infection, the
viruses move to sensory nerve ganglia
(Trigeminal ganglion), where they reside as
lifelong, latent viruses. Asymptomatic
shedding of contagious virus particles can
occur during this stage.

32. • Prodromal (day 0–1): Symptoms often
precede a recurrence. Symptoms typically
begin with tingling (itching) and reddening of
the skin around the infected site. This stage
can last from a few days to a few hours
preceding the physical manifestation of an
infection and is the best time to start
treatment.

33. • Inflammation (day 1): Virus begins
reproducing and infecting cells at the end of
the nerve. The healthy cells react to the
invasion with swelling and redness displayed
as symptoms of infection.

34. • Pre-sore (day 2–3): This stage is defined by the
appearance of tiny, hard, inflamed papules
and vesicles that may itch and are painfully
sensitive to touch. In time, these fluid-filled
blisters form a cluster on the lip (labial) tissue,
the area between the lip and skin (vermilion
border), and can occur on the nose, chin, and
cheeks.

35. • Open lesion (day 4): This is the most painful
and contagious of the stages. All the tiny
vesicles break open and merge to create one
big, open, weeping ulcer. Fluids are slowly
discharged from blood vessels and inflamed
tissue. This watery discharge is teeming with
active viral particles and is highly contagious.
Depending on the severity, one may develop a
fever and swollen lymph glands under the jaw.

36. • Crusting (day 5–8): A honey/golden crust starts to
form from the syrupy exudate. This yellowish or
brown crust or scab is not made of active virus
but from blood serum containing useful proteins
such as immunoglobulins. This appears as the
healing process begins. The sore is still painful at
this stage, but, more painful, however, is the
constant cracking of the scab as one moves or
stretches their lips, as in smiling or eating. Virusfilled fluid will still ooze out of the sore through
any cracks.

37. • Healing (day 9–14): New skin begins to form
underneath the scab as the virus retreats into
latency. A series of scabs will form over the sore
(called Meier Complex), each one smaller than
the last. During this phase irritation, itching, and
some pain are common.
• Post-scab (12–14 days): A reddish area may linger
at the site of viral infection as the destroyed cells
are regenerated. Virus shedding can still occur
during this stage.

38. HSV-1
•
•
•
•
•
•
•
Oral Herpes – Herpetic Gingivostomatitis
Herpes labialis (fever blisters or cold sores)
Herpetic whitlow
Eczema herpeticum
Keratoconjunctivitis
Encephalitis
Disseminated infections

39. HSV-2
• Genital herpes
• Neonatal herpes
• Aseptic meningitis

41. Herpes labialis
(fever blisters or cold sores)
• a milder, recurrent form of infection
characterized by crops of vesicles, usually at
the mucocutanous junction of the lips or nose.
Reoccurs frequently at the same site usually
with less severe symptoms.

44. Oral Herpes :
Herpetic Gingivostomatitis
• an infection of the oral mucosa characterized
by redness of oral tissues, formation of
multiple vesicles, painful ulcers and fever.
Occurs primarily in children characterized by
fever, irritability and vesicular mouth lesions.
Primary disease is more severe and lasts
longer than recurrences. Lesions heal
spontaneously in 2-3 weeks. Many children
have asymptomatic primary disease and
produce neutralizing antibody.

45. Symptoms
The symptoms can be mild or severe and may
include:
• Not able to chew or swallow
• Sores on the inside of the cheeks or gums
• Fever
• General discomfort, uneasiness, or ill feeling
• Very sore mouth with no desire to eat
• Halitosis (bad breath)

48. Herpetic whitlow
• A herpetic whitlow is a lesion (whitlow) on a
finger or thumb caused by the herpes simplex
virus.
• Herpes whitlow can be caused by infection by
HSV-1 or HSV-2.
• HSV-1 whitlow is often contracted by health care
workers that come in contact with the virus; it is
most commonly contracted by dental workers
and medical workers exposed to oral secretions.

51. Herpes gladiatorum
• Individuals that participate in contact sports such
as wrestling, rugby, and soccer sometimes
acquire a condition caused by HSV-1 known as
herpes gladiatorum, scrumpox, wrestler’s herpes,
or mat herpes, which presents as skin ulceration
on the face, ears, and neck.
• Symptoms include fever, headache, sore throat
and swollen glands. It occasionally affects the
eyes or eyelids.

53. Eczema herpeticum
• Eczema herpeticum is a rare but severe
disseminated infection that generally occurs at
sites of skin damage produced by, for example,
atopic dermatitis, burns, long term usage of
topical steroids or eczema.
• It is also known as Kaposi varicelliform eruption,
Pustulosis varioliformis acute and KaposiJuliusberg dermatitis.
• This infection affects multiple organs, including
the eyes, brain, lung, and liver, and can be fatal.

54. Keratoconjunctivitis

55. • Keratoconjunctivitis is inflammation of the
cornea and conjunctiva.
• Primary infection typically presents as swelling
of the conjunctiva and eyelids
(blepharoconjunctivitis), accompanied by
small white itchy lesions on the surface of the
cornea. The effect of the lesions varies, from
minor damage to the epithelium (superficial
punctate keratitis), to formation of dendritic
ulcers.

56. Herpes esophagitis
• Herpes esophagitis is a viral infection of the
esophagus caused by Herpes simplex virus.
• While the disease most often occurs in
immunocompromised patients, including
post-chemotherapy, immunosuppression with
organ transplants and in AIDS.

57. • Patients with herpes esophagitis experience
odynophagia, or painful swallowing and
dysphagia.
• Other symptoms can include food impaction,
hiccups, weight loss, fever and on rare
occasions upper gastrointestinal bleeding and
tracheoesophageal fistula.

60. Herpesviral encephalitis
• Herpes simplex encephalitis (HSE) is a rare,
but severe viral infection of the human central
nervous system. It is estimated to affect at
least 1 in 500,000 individuals per year.
• The majority of cases of herpes encephalitis
are caused by herpes simplex virus-1 (HSV-1)
• About 10% of cases of herpes encephalitis are
due to HSV-2, which is typically spread
through sexual contact.

61. • About 1 in 3 cases of HSE result from primary
HSV-1 infection, predominantly occurring in
individuals under the age of 18;
• 2 in 3 cases occur in seropositive persons, few
of whom have history of recurrent orofacial
herpes.
• Approximately 50% of individuals that
develop HSE are over 50 years of age.

62. Pathophysiology
• HSE is thought to be
caused by the
retrograde
transmission of virus
from a peripheral site
on the face following
HSV-1 reactivation,
along a nerve axon, to
the brain.

64. • HSE results in rapid death in approximately
70% of cases.
• survivors suffer severe neurological damage.
• Only a small population of survivors (2.5%)
regain completely normal brain function.
• Earlier treatment (within 48 hours of symptom
onset) improves the chances of a good
recovery.

65. Genital Herpes
• painful vesicular lesions of the male and
female genitals and anal area.
• Lesions more severe and protracted in primary
disease than in recurrence.
• Asymptomatic infections occur in both men
and women.
• Many infections are asymptomatic – many
people have antibody to HSV-2 but have no
history of disease.

66. How common is genital herpes?
• CDC estimates that, annually, 776,000 people
in the United States get new herpes infections.
• Nationwide, 16%, or about one out of six,
people aged 14 to 49 years have genital HSV-2
infection.
• Over the past decade, the percentage of
persons with genital herpes infection in the
United States has remained stable.

67. • Transmission from an infected male to his
female partner is more likely than from an
infected female to her male partner.
• Because of this, genital HSV-2 infection is
more common in women (approximately one
out of five women aged 14 to 49 years) than in
men (about one out of nine men aged 14 to
49 years).

68. symptoms of genital herpes
• Most individuals infected with HSV-1 or HSV-2
experience either no symptoms or have very
mild symptoms that go unnoticed or are
mistaken for another skin condition. Because
of this, most people infected with HSV-2 are
not aware of their infection. When symptoms
do occur, they typically appear as one or more
blisters on or around the genitals, rectum or
mouth. The blisters break and leave painful
sores that may take two to four weeks to heal.

69. • Itching or burning feeling in the genital or anal
area
• Flu-like symptoms, including fever
• Swollen glands
• Pain in the legs, buttocks, or genital area
• Vaginal discharge

72. Clinical Manifestations
Genital Herpes: Primary Lesions
Source: Cincinnati STD/HIV Prevention Training Center
72

73. Clinical Manifestations
Genital Herpes: Multiple Ulcers
Source: Cincinnati STD/HIV Prevention Training Center
73

74. Clinical Manifestations
Genital Herpes: Recurrent Ulcer
Source: Cincinnati STD/HIV Prevention Training Center
74

75. Clinical Manifestations
Genital Herpes: Periurethal Lesions
Source: Cincinnati STD/HIV Prevention Training Center
75

76. Clinical Manifestations
Genital Herpes: Cervicitis
Source: Cincinnati STD/HIV Prevention Training Center
76

77. Clinical Manifestations
Herpes on the Buttock
Source: Cincinnati STD/HIV Prevention Training Center
77

78. Neonatal herpes simplex
• Neonatal herpes simplex is a rare but serious
condition, usually caused by vertical
transmission of herpes simplex virus from
mother to newborn.

79. Transmission
• The majority of cases (85%) occur during birth
when the baby comes in contact with infected
genital secretions in the birth canal, most
common with mothers that have newly been
exposed to the virus,
• an estimated 5% are infected in utero, and
approximately 10% of cases are acquired
postnatally. Detection and prevention is difficult
because transmission is asymptomatic in 60% 98% of cases.

82. FACTORS INFLUENCING TRANSMISSION
•
•
•
•
•
Type of maternal infection (primary/recurrent)
Maternal antibody status
Duration of rupture of membranes
Integrity of mucocutaneous barriers
Mode of delivery (C-section/vaginal)

83. INCIDENCE OF NEONATAL DISEASE
• 2/1000 mothers are HSV culture + at delivery
asymptomatic
• 50-70% affected infants born to women
asymptomatic at the time of delivery
• Antepartum cultures are not useful in
assessing risk of neonatal infection
• Increased risk w/ primary vs recurrent
infection
• Incidence from 1/2000 to 1/5000 live births
and increasing

84. RISK OF NEONATAL HSV INFECTION
• 50% risk: Infants born to women w/ primary
infection near the time of delivery
• 30% risk: Infants born to mothers with first
episode, non-primary infection (antibody to
type 1, new acquisition type 2 and vice versa)
• 1 to 3% of infants born to mothers w/
recurrent infection
• Passive immunity protects against infection ,
but has little effect on the severity of disease

85. TIMES OF TRANSMISSION
•
HSV of the newborn is acquired during one
of three distinct time intervals:
1. Intrauterine (in utero 5%)
2. Peripartum (perinatal 85%)
3. Psotpartum (postnatal 10%)

86. DISEASE CLASSIFICATION
• Disease localized to the skin, eyes and mouth
SEM disease accounting for 45% of cases
• Encephalitis w/ or w/out CNS involvement
accounting for 30%
• Disseminated infection including CNC, lungs,
etc. accounting for 25%
• This classification is predictive of morbidity
and mortality

87. DIAGNOSTIC TESTS
• Cultures from skin lesions, mouth,
nasopharynx, conjunctiva, urine, stool/anorectum and CSF.
• Positive cultures at more than 48 hrs are
consistent w/ viral replication as opposed to
colonization
• Serologic tests should not be relied on
• PCR testing for CSF HSV DNA is the diagnostic
method of choice for HSV encephalitis

88. TREATMENT AND FOLLOW UP
•
•
•
•
Acyclovir is the treatment of choice
SEM 14 days of treatments
CNS and disseminated disease 21 days
Oral acyclovir contraindicated in neonates for
HSV treatment
• Ocular involvement requires trifluridine

90. Diagnosis
HSV Diagnosis
• Clinical diagnosis is insensitive and nonspecific
• Clinical diagnosis should be confirmed by
laboratory testing:
– Virologic tests
– Type-specific serologic tests
90

91. Diagnosis
Virologic Tests
•
Viral culture (gold standard)
–
–
–
–
–
•
Preferred test if genital ulcers or other mucocutaneous lesions are present
Highly specific (>99%)
Sensitivity depends on stage of lesion; declines rapidly as lesions begin to
heal
Positive more often in primary infection (80%–90%) than with recurrences
(30%)
Cultures should be typed
Polymerase Chain Reaction (PCR)
–
–
More sensitive than viral culture; has been used instead of culture in
some settings; however PCR tests are not FDA-cleared or widely available
Preferred test for detecting HSV in spinal fluid
91

92. Diagnosis
Virologic Tests
(continued)
• Antigen detection (DFA or EIA)
– Fairly sensitive (>85%) in symptomatic shedders
– Rapid (2-12 hours)
– May be better than culture for detecting HSV in
healing lesions
• Cytology (Tzanck or Pap)
– Insensitive and nonspecific and should not be relied
on for HSV diagnosis
92

93. Diagnosis
Type-specific Serologic Tests
• Type-specific and nonspecific antibodies to HSV
develop during the first several weeks to few months
following infection and persist indefinitely
• Presence of HSV-2 antibody indicates anogenital
infection
• Presence of HSV-1 does not distinguish anogenital
from orolabial infection
93

94. Diagnosis
Uses of Type-specific Serologic Tests
• Type-specific serologic assays might be
useful in the following scenarios:
– Recurrent or atypical genital symptoms with
negative HSV cultures
– A clinical diagnosis of genital herpes without
laboratory confirmation
– A sex partner with herpes
– As part of a comprehensive evaluation for STDs
among persons with multiple sex partners, HIV
infection, and among MSM at increased risk for
HIV acquisition
94

95. Diagnosis
Evaluation of Genital Ulcer
• All patients with genital ulcers should be
evaluated with a serologic test for syphilis and
a diagnostic evaluation for genital herpes
• In settings where chancroid is prevalent, a test
for Haemophilus ducreyi should also be
performed
95

96. Management
• There is no method to eradicate herpes virus
from the body, but antiviral medications can
reduce the frequency, duration, and severity
of outbreaks.
• Analgesics such as ibuprofen and
acetaminophen can reduce pain and fever.
• Topical anesthetic treatments such as
prilocaine, lidocaine, benzocaine or tetracaine
can also relieve itching and pain

97. Antiviral
There are several antivirals that are effective for
treating herpes including:
• aciclovir (acyclovir),
• valaciclovir (valacyclovir),
• famciclovir,
• and penciclovir.

98. Management
CDC-Recommended Regimens for First
Clinical Episode
• Acyclovir 400 mg orally 3 times a day for 7-10 days,
or
• Acyclovir 200 mg orally 5 times a day for 7-10 days,
or
• Famciclovir 250 mg orally 3 times a day for 7-10 days,
or
• Valacyclovir 1 g orally twice a day for 7-10 days
98

99. Management
CDC-Recommended Regimens for
Suppressive Therapy
•
•
•
•
Acyclovir 400 mg orally twice a day, or
Famciclovir 250 mg orally twice a day, or
Valacyclovir 500 mg orally once a day, or
Valacyclovir 1 g orally once a day
99

100. Management
CDC-Recommended Regimens for
Episodic Therapy
• Acyclovir 400 mg orally 3 times a day for 5 days, or
• Acyclovir 800 mg orally twice a day for 5 days, or
• Acyclovir 800 mg orally 3 times a day for 2 days, or
• Famciclovir 125 mg orally twice a day for 5 days, or
• Famciclovir 1000 mg orally twice a day for 1 day, or
• Valacyclovir 500 mg orally twice a day for 3 days, or
• Valacyclovir 1 g orally once a day for 5 days
100

101. Management
Severe Disease
• IV acyclovir should be provided for patients with
severe disease or complications requiring
hospitalization
• CDC-Recommended Regimen:
– Acyclovir 5-10 mg/kg IV every 8 hours for 2-7 days or until
clinical improvement
– Follow with oral antiviral therapy to complete at least 10
days total therapy
101

102. Management
Allergy, Intolerance, and Adverse
Reactions
• Allergic and other adverse reactions to acyclovir,
valacyclovir, and famciclovir are rare
• Desensitization to acyclovir is described by Henry
RE, et al., Successful oral acyclovir desensitization.
Ann Allergy 1993; 70:386-8
102

103. Management
Herpes in HIV-Infected Persons
• HIV-infected persons may have prolonged,
severe, or atypical episodes of genital,
perianal, or oral herpes
• HSV shedding is increased in HIV-infected
persons
103

104. Management
CDC-Recommended Regimens for
Daily Suppressive Therapy in
HIV-Infected Persons
• Acyclovir 400-800 mg orally twice a day or
three times a day, or
• Famciclovir 500 mg orally twice a day, or
• Valacyclovir 500 mg orally twice a day
104

105. Management
CDC-Recommended Regimens for Episodic
Infection in
HIV-Infected Persons
• Acyclovir 400 mg orally 3 times a day for 5-10
days, or
• Famciclovir 500 mg orally twice a day for 5-10
days, or
• Valacyclovir 1 g orally twice a day for 5-10
days
105

106. Management
Genital Herpes in Pregnancy
• Majority of mothers of infants who acquire neonatal
herpes lack histories of clinically evident genital
herpes
• Risk for transmission to neonate is high (30%-50%)
among women who acquire genital herpes near the
time of delivery
• Risk is low (<1%) in women with histories of recurrent
herpes at term or who acquire genital HSV during the
first half of pregnancy
106

107. Management
Genital Herpes in Pregnancy (continued)
• Prevention of neonatal herpes depends on:
✓ avoiding acquisition of HSV during late pregnancy
✓ avoiding exposure of the infant to herpetic lesions during
delivery
• All pregnant women should be asked whether they
have a history of genital herpes
107

108. Management
Genital Herpes in Pregnancy (continued)
• At the onset of labor:
– All women should be questioned carefully about
symptoms of genital herpes, including prodromal
– All women should be examined carefully for herpetic
lesions
• Women without symptoms or signs of genital herpes
or its prodrome can deliver vaginally
108

109. Management
Genital Herpes in Pregnancy (continued)
• Safety of acyclovir, valacyclovir, famciclovir in
pregnancy not definitively established, but no
clear evidence for increased birth defects
• Oral acyclovir may be given for first-episode or
severe recurrent herpes; IV acyclovir should be
used for severe infection
• Suppressive acyclovir late in pregnancy reduces
frequency of cesarean sections in women with
recurrent genital herpes; many specialists
recommend it
109

110. Prevention
110

111. Prevention
Patient Counseling and Education
• Goals
– Help patients cope with the infection
– Prevent sexual and perinatal transmission
• Counsel initially at first visit
• Education on chronic aspects may be beneficial after
acute illness subsides
• HSV-infected persons may express anxiety about
genital herpes that does not reflect the actual clinical
severity of their disease
111

112. Prevention
Patient Counseling and Education
• Counseling should include:
–
–
–
–
Natural history of the infection
Treatment options
Transmission and prevention issues
Neonatal HSV prevention issues
• Emphasize potential for recurrent episodes,
asymptomatic viral shedding, and sexual
transmission
112

113. Prevention
Counseling: Natural History
•
Recurrent episodes likely following a first
episode; with HSV-2 more than HSV-1
–
–
–
•
Frequency of outbreaks may decrease over time
Stressful events may trigger recurrences
Prodromal symptoms may precede outbreaks
Asymptomatic viral shedding is common and
HSV transmission can occur during
asymptomatic periods
113

114. Prevention
Counseling: Treatment
• Suppressive therapy available and effective in
preventing symptomatic recurrences
• Episodic therapy sometimes useful in shortening
duration of recurrent episodes
• When and how to take antiviral medications
• Recognition of prodromal symptoms to know
when to begin episodic therapy
114

115. Prevention
Counseling: Transmission and Prevention
• Inform current and future sex partners about genital
herpes diagnosis
• Abstain from sexual activity with uninfected partners
when lesions or prodrome present
• Correct and consistent use of latex condoms might
reduce the risk of HSV transmission
• Valacyclovir suppressive therapy decreases HSV-2
transmission in heterosexual couples in which source
partner has recurrent herpes
115

116. Prevention
Counseling: Neonatal Herpes
Prevention
• Risk of neonatal HSV infection should be explained
to all patients, including men
• Pregnant women should inform their
prenatal/perinatal providers that they have genital
herpes
• Pregnant women without HSV-2 infection should
avoid intercourse during third trimester with men
who have genital herpes
• Pregnant women without HSV-1 infection should
avoid oral sex from a partner with oral herpes
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117. Prevention
Counseling for Asymptomatic Persons
• Give asymptomatic persons diagnosed with
HSV-2 infection the same counseling messages
as symptomatic persons
• Teach the common manifestations of genital
herpes, as many patients will become aware
of them with time
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118. Prevention
Partner Management
• Symptomatic sex partners
– Evaluate and treat in the same manner as patients
who have genital lesions
• Asymptomatic sex partners
– Ask about history of genital lesions
– Educate to recognize symptoms of herpes
– Offer type-specific serologic testing
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