1. Herpes simplex &
Herpes Zoster
By .Prof.
EISHA ABDEL MONIEM

2. *Human herpes virus includes:
1.Herpes simplex virus type 1.
2.Herpes simplex virus type 2.
3.Varicella Zoster virus
4.Epestien – Bar virus.
5.Cytomegalovirus.
6.HHV 6,7,8

3.  They are DNA viruses characterized
by tendency to produce :
 Primary infection----Latency ( neurons
or lymphoid tissue). ----Reactivation
(recurrence)
 It replicate intranuclear ,and once
patient become infected ,infection
remain for life.

4. 
HERPES SIMPLEX

5. 
It is the commonest virus
infection of the skin all over
the world.

6. 

7. Type – 1 HSV1: Found mainly in
lesions of the lips ,mouth ,face and non
genital areas(70-90%) ,may also cause
genital lesions.
Type – 2 HSV2: Found mainly in the
genital lesions (70-90%) ,can also induce
oral lesions.

8. Transmission
 HSV spread by direct contact, as
the virus is shed in saliva, tears and
genital secretions.
 Infection results from a kiss given to a
child or adult from a person shedding the
virus.
 The only way to contract HSV 2 is through
direct sexual contact with an infected
individual.[

9. Pathogenesis
[ HSV travels through tiny breaks in
the skin or mucous membranes in the
mouth or genital areas. Even
microscopic abrasions on mucous
membranes are sufficient to allow viral
entry.

10. Pathogenesis
Virus will replicate at the site of infection
inducing primary lesion ,travel by
retrograde axonal flow to the dorsal root
ganglion, and establish latency (virus exists
in a non infectious state) until reactivation
where the virus particles descend via
peripheral nerves to the skin and induces
recurrent lesions.

11. CLINICAL FORMS
1.Primary Infection

2.Recurrent Infection

12. 1.The primary infection
:
-occurs in infants and children who have no
immunity.

-Asymptomatic infection
(subclinical) is the rule( 90%).
-Symptomatic primary infection (clinical)
(10%)occur after 3-7 days of exposure usually show
severe clinical picture with prodrome of fever
,malais, anorexia and painful tender
lympadenopathy, and cutaneous lesions. Resolution
of symptoms occurs within2-6 weeks.

13. Morphology of the primary lesion
Painful vesicles sometimes
umblicated on an erythematous base
,that is followed by progression to
pustules and erosion . Grouped and
scattered vesicles typically develop.
Crusting of lesions and resolution
occur within 2 to 6 weeks.

14. Primary Herpes Simplex
clinical types.
1. Primary gingivostomatitis (Commonest type).
2. Herpetic keratoconjuctivities
3. Herpetic whitlow.
4. Primary genital herpes.
5. Kaposi variclliform eruption.
6. Herpes Encephalitis
7. Neonatal herpes

15. 
• Primary Herpetic gingivostomatitis: .
Most cases occur in children between 1-5 years of
age. After an incubation period of 5 days, the
stomatitis begins with fever, malaise, restlessness
and excessive dribbling. Drinking and eating are
very painful and the breath is foul. The gums are
swollen, inflamed and bleed easily,vesicles on mm
that give white membrane covering erosions on the
tongue and oral mucosa. The regional lymph nodes
are enlarged and tender. The fever subsides after 3-5
days and recovery is usually complete in 2 weeks.

17. • Keratoconjunctivitis: Primary
herpes infection of the eye causes a
severe and often purulent
conjunctivitis with superficial
ulceration of the cornea. The eyelids
are grossly oedematous and there may
be vesicles on the surrounding skin.

18. Herpetic whitlow
A herpetic whitlow is an infection of the herpes virus
around the fingernail. In children, this is often caused
by thumbsucking . It is seen in adult healthcare
workers such as dentists because of increased
exposure to the herpes virus. The use of rubber gloves
prevents herpes whitlow in healthcare workers

21. Kaposi varicelliform eruption
(Eczema herpeticum(
 Infants or children with atopic eczema
can develop a potentially fatal HSV
infection in the area of skin that has the
eczema .Therefore, people with atopic
eczema should avoid being near
anyone with an active herpes infection.

22. Primary Genital Herpes
 The Primary genital HSV infection
(genital herpes) can be severe and
prolonged, with multiple painful
blisters and ulcers in the genital area.
Fever and malaise are common, and
some people have burning during
urination, difficulty or pain during
defecation.
 HSV2 more than HSV1

23. Recurrent Herpes Simplex

24. 

25. RECURRENT HERPES SIMPLEX
-Occurs in individuals who have specific
antibodies and exposed to activating factors.
- Recurrent infections differ from primary
herpes simplex in the smaller size of the
vesicles, their grouping, absence of
constitutional symptoms - usually mild and
heals within 7 days


26. Activating Factors
*Spontaneously.
*Appropriate stimulus:
-Stress and psychic factors
-Ultraviolet light.
-Fever.
-Common cold ,infuenza and other
upper respiratory tract infection.

27.  * Gastrointestinal disturbance as dyspepsia
and diarrhea.
 * Tooth extraction and trauma to lips.
 * immunosuppression
 * Menestruation
*Genital herpes:
 Trauma of coitus
 Stress
 Fatigue.

28. Recurrent Herpes simplex
1.Recurrent herpes libialis
Cold sore
2.Recurrent genital herpes



29. Recurrent herpes libialis
Cold sore.
Develops on the lips. Starts by
tingling sensation , followed by
redness and swelling. Usually, fluid-
filled blisters form on the erythematous
base and break ,open and leaving
sores. The sores quickly form a scab.
After about a week, the scab falls off
and the episode ends..

30. 

32. Recurrent Genital Herpes
Simplex

Burning sensation in the genitalia, buttocks, and thighs
 Small blisters or open sores on genitals or inner thighs; in
women, often occur inside the vagina
 May be painful or not
 In women, vaginal discharge
 Fever, muscle aches
 Headache
 Painful urination
 Swollen lymph glands in the groin


33. If a patient is diagnosed with genital
herpes, testes for other sexually
transmitted diseases such as
Chlamydia and gonorrhea should be
performed.

34. Patology
Epidermis
Intraepidermal supra basal vesicle produced by

Balooning degeneration
Reticular degeneration
of epidermal cells that show intarnuclear eosinophilic
inclusion bodies and multinucleated giant cells (2-15 nuclei)due to
fusion of cells
Dermis
cellular infiltration (neutrophils)
vasculities

36. Prognosis
. Usually the number of outbreaks is
greatest in the first year and higher for
HSV-2 genital lesions than HSV-1 cold
sores. Each year after that, the number
of outbreaks usually goes down and
they become less severe

37. Complications
 Herpetic keratitis –scarring within the cornea and
possible blindness
 Secondary infection
 Persistent herpes infection, with so close attacks.
 Encephalitis and/or meningitis.
 Lung infection.

38. Special Populations
 Newborns – herpes infections contracted during delivery from
the mother can lead to meningitis, herpes infection in the
blood, skin infection, and may even be fatal

When the immune system is suppressed:
HIV
Chemotherapy for cancer
 Long term use of high doses of corticosteroids


39. Differential diagnosis
Herpes Zoster
Thrush stomatitis
Impetigo contagiosum
Acute eczema
Erythema multiformis

40. D.D of genital herpes
Folliculitis
Chancroid
genital sores
Behcet’s disease

41. Diagnosis
 Tzanc smear: to detect giant cells by opening
fresh vesicle and scrape its base.The most rapid
diagnosis is by detection of viral antigen by
immunofluorescence in scrapings from lesions or
the virus seen by electron microscopy in vesicle
fluid. Diagnosis by culture of the virus from vesicle
fluid requires only 1– 5 days. The detection of HSV
DNA in the cerebrospinal fluid( Lumber puncture)

42. Treatment
Antiviral therapy: . In primary
infection or troublesome recurrent
herpes simplex, antiviral therapy is
indicated. Acyclovir interferes with the
action of DNA polymerase. Acyclovir is
of proven clinical value against herpes
simplex and varicella zoster virus.

43. Valacyclovir and famcyclovir are
chemically related to acyclovir and
have the same mechanism of action

44. .The usual oral dose of
Acyclovir: is 200mg five times daily .
for 5 or more days.
Valacyclovir: 500mg three times daily
for 5 days
Famicyclivir: 125 mg three times daily
for 5 days.

45.  Antiviral cream, applied every 2
hours during the attack can shorten
the healing time and duration of
symptoms of a cold sore .

46.  Severe HSV infections, including
herpes encephalitis and infections in
newborns, are treated with
intravenous acyclovir. .

47.  Prophilaxis: Preventing HSV infection is difficult because
people can spread the virus even when they don't have any symptoms
of an active outbreak.
 Avoiding direct contact with an open lesion will lower the risk of
infection.
 People with genital herpes should avoid sexual contact when they
have active lesions, the use of condoms, may lower the risk of
infection.
 People with active HSV lesions should also avoid contact with
newborns, children with eczema, or people with suppressed immune
systems, because these groups are at higher risk for more severe
disease.
 To decrease the risk of infecting newborns, a cesarean delivery (
C-section) is recommended for pregnant women who have an active
HSV infection at the time of delivery.

48. Varicella (chickenpox) and
zoster (shingles)

49. Aetiology
 Varicella and Herpes zoster are caused by
the same virus, herpes virus varicellae
or varicella zoster virus (VZV).Varicella
is the primary infection , after which the
virus persists in nerve ganglion cells,
usually sensory.Herpes Zoster is the result
of reactivation of this residual latent virus

50. Epidemiology
 Primary varicella is an endemic disease. Varicella is
one of the classic diseases of childhood, with the highest
prevalence occurring in the 4 - 10 years old age group.
 Varicella is highly communicable, with an attack rate
of 90% in close contacts.
 Most people become infected before adulthood but
10% of young adults remain susceptible.
 Herpes zoster, in contrast, occurs sporadically and
evenly throughout the year.

51. Transimission
Varicella is transmitted by droplet
infection from the nasopharynx and dry
scales are not infectious. Patients are
infectious to others from 2 days before
to 5 days after the onset of the rash.
Sub clinical infections may occur
2..rash…..5--------------

52. Zoster patients are infectious, from virus
in the lesions and, in some instances, the
nasopharynx. Chickenpox occurs in
susceptible contacts of zoster patients.

53. Chicken pox
Varicella

54. Clinical features
 Incubation period of 14-21 days.
 : After 1-2 days of fever, development of small red papules
takes place which very rapidly become tense clear vesicles
that may turn to pustules, they are surrounded by red areolae.
In 2-4 days a dry crust forms and soon separate, to leave a
shallow pink depression which heals without scarring.these
lesions are associated with pruritis that may be tense.
 The vesicles appear in 3-5 crops over 2-4 days. They are most
numerous on the trunk, then on the face, scalp and limbs. Their
distribution is centripetal. A characteristic feature is the
presence of lesions at different stages in each site. Lesions are
common inside the mouth.

59. Complication
 Most common complication is secondary
bacterial infection of the vesicles.
 Severe complications which may be life
threatening include viral pneumonia,
encephalititis, and haemorrhagic
chickenpox.

60. Herpes Zoster (Shingles(

61. Herpes Zoster (Shingles(
 Herpes Zoster mainly affect a single dermatome of the
skin.
 It may occur at any age but the vast majority of
patients are more than 50 years of age.
 The latent virus reactivates in a sensory ganglion and
tracks down the sensory nerve to the appropriate
segment
 Herpes zoster affecting the eye and face may cause
great problems

64. Triggering factors
1.Old age
2.Trauma to vertb. Column as fracture spine and
disc prolapse.
3.Lymphoma and neoplasm
4.Antimitotic drugs.
5.X-ray therapy.
6.Diabetes.
7.Infection.
8.Disturbed immunity.

65. CLINICAL FEATURES
Symptoms
Pain usually precedes, associates
or follows the eruptions .It ranges from
mild burning to severe agonizing pain
.It may be accompanied by fever,
headache, malaise, and tenderness
localized to areas on one or more
dermatom.

66. Morphology of the lesion
The disease is characterized by sudden
appearance of group of vesicles on
erythematous base on linear
distribution occuring along the
course of the affected nerve or
nerves,lesions are unilateral..The early lesion
contains a clear serum but after few days
become purulent,the wall ruptures and crust
forms.

70.  The pain subsides gradually as the
eruption disappears. Recovery is
complete in 2-4 weeks . Occasionally,
the pain is not followed by the eruption
(zoster sine eruption).

71. Clinical Types

Localization
1.Herpes zoster pectoralis (50%)---Inter costal nerves.
2.Herpes zoster cranialis ----Trigeminal nerve(15%)
a. HZ frontalis ----supraorbital nerve
b. HZ Ophtalmicus---eye affected ,vesicles at the side of the
nose,conjunctiva red and inflammed,superficial or deep keratitis.
c. HZ of the maxillary division—vesicles in the uvula and
tonsilar area
d.Hz of the mandibular division---vesicles on the posterior
part of the tongue ,the floor of the mouth and the buccal mm.

75. e. Ramsy –Hunt syndrome
----geniculate ganglion,pain in the
ear,nausea vomiting nystagmus and loss
of hearing, and vesicles on the pinna of
the ear. Facial palsy is a frequent
complication.

76. 3.HZ cervicalis (10%) -----cervical nerves.
4.HZ abdominalis ---abdominal nerves.
5.Lumbosacral variety (10%):
Sacralis-----urinary bladder symptoms
dysuria,frequency and even retention of
urine may occur.
Femoralis----femoral nerve

77. Morphological classification
1.Abortive type.
2.Hemorrhagic type.
3.Gangrenous ,necrotic type.
4.Generalized or disseminated type.
5.Bilateral type

78. Complications

1.Secondary bacterial infection.
2.Eczematization.

3.Post herpetic neuralgia
4.Ocular complications as keratiti,ophthalmitis and blindness.
5.Gangrene formation.
6.Telengiectasia and skin atrophy.
7.Neuralgic complication :menegities ,encephalitis and facial
polsy.
8.Urinary complication : cystitis and or urinary retension.


79. Differential diagnosis
1.Herpes simplex.
2.Acute eczema.
3.Impetigo contagusum.
4.Erythema multiformis.

80. Prevention
 Preventive measures should be considered
for individuals at risk of contracting severe
varicella infection e.g. leukaemic children,
neonates, and pregnant women
 Where urgent protection is needed, passive
immunization should be given. Zoster
immunoglobulin (ZIG) is the preparation of
choice but it is very expensive.
 A live attenuated vaccine is available .

81. Treatment
General:
Analgesics ,tegretol and
vitamineB12
Local:
Drying agent as gentian violet 1%
acyclovir cream 5%.
local antibiotic as Na fucidate.

82. Varicella Vaccine
usually is given between the ages of 12 to
15 months. The Centers for Disease
Control and Prevention (CDC) also
recommends a booster shot at 4 to 6
years old for further protection. The CDC
also recommends that people 13 years of
age and older who have never had
chickenpox or received the chickenpox
vaccine get two doses of the vaccine.

83. Antiviral therapy
Acyclovir 400 5 times daily for 7 d. Famcyclovir
250mg 3 times daily for 7 d. Valcyclovir 1000 mg 3
times daily fo 7 days. Such treatment prevents
progression of the eruption, reduces the systemic
complications of varicella and zoster, lessens zoster
pain during treatment, reduces the risk of
development of post-herpetic neuralgia and if it
develops, it decreases its duration. Ophthalmic
zoster is treated by antiviral therapy together with
ophthalmologic supervision.

84. 
For post-herpetic neuralgia a tricyclic
anti-depressant is useful.