4. Varicella (Chickenpox)
Highly contagious
Mainly Children
Generalized Vesicular eruptions on Skin and
Mucous membranes
Severe manifestations in Adults and Immune
compromised.
PRODROME: Brief of low-grade fever, URT
symptoms, and mild malaise may occur
Rapid appearance of pruritic asynchronous
exanthem
6. Varicella (Chickenpox)
Pathogenesis
MODE OF TRANSMISSION:
- Airborne droplets and direct contact from varicella
patients.
- Vesicular fluid of Zoster patients can be the source
of Varicella in susceptible individuals.
PRIMARY VIREMIA and spread to liver and
spleen.
SECONDARY VIREMIA follows with viral spread
to the skin.
9. Varicella (Chickenpox)
Occurs year-round, peaks in
late autumn and late winter
through early spring
INCUBATION PERIOD14-21d.
Lesions appear in crops -
typically have 3 crops begin in
trunk and scalp, then spread
peripherally
Lesions begin as tiny
erythematous papules, that
develop central vesicles
surrounded by red halos
(‘dew drops on a rose petal’)
Hallmark - lesions in all stages of evolution
Macule
Varicella (Chickenpox)
C/P
13. Varicella (Chickenpox)
C/P
Lesions began to dry, umbilicated
appearance, then surrounding
erythema fades and a scab forms.
All scabs slough off 10-14 days
Scarring not typical unless
superinfected
Cluster in areas of previous skin
irritation
Painful lesions along the oral, rectal,
and vaginal mucosa, external
auditory canal, tympanic membrane
14. Varicella (Chickenpox)
C/P
Severe in the
immunocompromised host -
can be fatal
Need to get varicella-zoster
immunogloblin 96 hours
post-exposure to possible
varicella
16. CONGENITAL VARICELLA SYNDROME
(CVS) & NEONATAL VARICELLA
• Primary maternal infection during the 1st
trimester may lead to spontaneous
abortions or CVS (serious) skin lesions,
hypoplasia of limbs, chorio-retinitis &
CNS defects
• Primary maternal infection near the time
of birth can lead to widely disseminated
infection in the new born with mortality
rate of 35%
• If rash began a week or more before
delivery, maternal Abs transferred via
placenta – baby gets the infection but
escapes clinical disease
21. IMMUNOCOMPETENT
1. Neonate: Acyclovir, 500 mg/m2 q8h × 10 days
2. Child: Symptomatic treatment alone, or acyclovir, 20 mg/kg PO
qid × 5 days
3. Adolescent, adult; Acyclovir, 800 mg PO 5×/day × 7 days
IMMUNOCOMPROMISED
1. Mild varicella or mild compromise; Acyclovir, 800 mg PO
5×/day × 7-10 days
2. Severe varicella or severe compromise; Acyclovir, 10 mg/kg
IV q8h × 7 days or longer;
3. Acyclovir resistant (advanced acquired immunodeficiency
syndrome) Foscarnet, 40 mg/kg IV q8h until healed.
Varicella (Chickenpox)
Treatment
22. Varicella (Chickenpox)
Prevention
VARICELLA ZOSTER IMMUNEGLOBULIN(VZIG)
• Postexposure prophylaxis in cases of inadvertent
exposure to the virus,
• 125 IU/10kg IM; not to exceed 625 IU/dose given
within 96 hours of initial contact can severity of the
disease though not prevent it protection up to 3 wk
• VZIG given to neonates whose mothers became
infected shortly before birth.
VACCINATION
• live attenuated varicella vaccine is effective, a two-
dose SC in children.
• One-time live-attenuated VZV vaccine for eligible
persons older than 50 years.
25. Herpes Zoster (Shingles)
Caused by varicella-zoster virus
After primary infection, virus lies dormant in genome of sensory
nerve root cell
Age of Onset; More than 66% are >50 years of age.
Reactivation results in a sensory neuritis
Incidence, severity and risk of complications increase significantly
with age and immunosuppression due to a decline in specific cell-
mediated immune response to VZV
Occasionally localized dysesthesia but no cutaneous eruption
(‘zoster sine herpete’)
27. PRODROME:
Pain/pruritis, tingling, hyperesthesia,
Pre eruptive pain (pre-herpetic
neuralgia), unilateral, dermatomal,
precedes the eruption by 4 to 5 ds.
Prodromal symptoms may be
absent, particularly in children.
If cranial nerve involvement -
prodrome of severe HA, facial pain,
or auricular pain prior to the eruption.
Herpes Zoster (Shingles)
C/P
28. ERUPTIVE PHASE:
Single dermatome; Does not cross midline
red, swollen plaque of varying sizes and
spreads to involve part or all of a dermatome
The vesicles arise in clusters (grouped) from
the erythematous base and become cloudy with purulent fluid by day
3 or 4.
Vesicles either umbilicate or rupture before forming a crust, which
falls off in 2 to 3 weeks.
The elderly or debilitated patients may have a prolonged and
difficult course.
The major morbidity is post-herpetic neuralgia (PHN).
+/- fever or constitutional symptoms. Regional LAD common
Herpes Zoster (Shingles)
C/P
29. Herpes Zoster (Shingles)
COMPLICATIONS “8”
1. Post-herpetic neuralgia (PHN). The most
frequent problem, which is more in elderly
2. Post-herpetic itch (PHI).
3. Local Scarring.
4. Secondary bacterial infection
5. Ramsay-Hunt syndrome
(Herpes Zoster Oticus)
6. Disseminated zoster: >20 vesicles Requires intravenous acyclovir
7. Corneal scarring and loss of vision dt. ophthalmic zoster
8. Visceral involvement: pneumonitis; meningoencephalitis; hepatitis
30. Herpes zoster (ophthalmic zoster). Involvement of
the first branch of the fifth nerve. Hutchinson’s sign is the presence of vesicles at
the tip, side, or bridge of the nose indicating Involvement of the nasociliary branch
of the trigeminal nerve, Which also innervates the cornea.
31.
32. Shingles
When it occurs in a child as young as this 8 month
old it is often as a result of primary infection in utero.
36. Systemic antivirals are recommended in all patients over 50
with pain in whom blisters are still present, even if they are
not given within the first 72 h of the eruption but
within 7 days may also be helpful
Herpes Zoster (Shingles)
Rx
I. ANTIVIRAL THERAPY
37. Herpes Zoster (Shingles)
Rx
II. ORAL ANALGESIA
1. Acetaminophen 2. NSAIDs 3. Opiate analgesia
Antiviral therapy and analgesics aid acute pain control
III. TOPICAL THERAPY
1. Wet dressings with 5% aluminum acetate (Burow solution), applied for
30-60 minutes 4-6 times daily;
2. Lotions (such as calamine).
3. Local anesthetics, such as 10% lidocaine in gel form, or lidocaine
patches may acutely pain
IV. CORTICOSTEROIDS
Controversial (40-60 mg every morning) typically is administered as early
as possible in the course of the disease and is continued for 1 week,
followed by a rapid taper over 1-2 weeks.
38. Herpes Zoster (Shingles) Rx of
POST-HERPETIC NEURALGIA
1. Antiviral therapy: The only consistently successful
method of treating PHN is to prevent it via prompt
treatment of acute zoster and its associated pain.
Initiation as early as possible in the course of acute
zoster within 72 hours of onset
2. Local anesthetic: (e.g. Lidocaine patch 5 %),
3. Capsaicin: 5 times daily
4. Oral analgesics: Narcotic & nonnarcotic e.g. ibuprofen
5. Anticonvulsants: (Carbamazepine600-800 mg/d.
/Gabapentin 900-1800mg/d /Pregabalin).
6. Tricyclic anti-depressants (TCA):
(e.g. amitriptyline 10-25 mg PO up to 75 mg/d)
7. Local anesthetic blocking of sympathetic nerves may
produce transient relief, their effectiveness in reducing
the protracted pain of PHN remains to be determined.
8. Neurosurgery- if necessary helpful in exceptional cases.
42. Infectious Mononucleosis
Acute self-limiting illness of children and young
adults caused by EBV.
Transmission by oral contact, sharing eating
utensils, transfusion, or transplantation
Incubation period 30-50 days (shorter, 14-20 days,
in transfusion-acquired infection)
Asymptomatic in children, but symptomatic in
adolescents and young adults
43.
44.
45. Infectious Mononucleosis
C/P
Latency is established in B lymphocytes
~95% of adults worldwide are seropositive.
PRODROME:
Fatigue, malaise, anorexia, HA, sweats, chills
lasting 3-5 days.
46. Infectious Mononucleosis
C/P
1. Classically, ~80% present with triad of fever, pharyngitis, and
lymphadenopathy
i. Fever - can have wide daily fluctuations.
ii. Pharyngitis, tonsillar and adenoidal enlargement, or s.
exudate, halitosis, palatal petechiae.
iii. LAD: - anterior cervical and posterior cervical - in classic
cases, - generalized LAD toward end of wk 1
2. Splenomegaly: develops in 50% of patients in 2nd-3rd wk
3. Hepatomegaly: in 10% of patients
4. Exanthem: nonspecific erythematous, maculopapular, rash in 5-
10% of patients on trunk and proximal extremities, with spread to
face and forearms
5. Ampicillin-induced eruption
55. I. Immunocompetent hosts: rarely colitis,
encephalitis, myocarditis, and anterior uveitis.
II. Congenital and neonates: congenital deafness;
mental retardation TORCH infections
(toxoplasmosis, rubella, cytomegalovirus and
herpes virus).
III. AIDS patients: blindness.
CYTOMEGALOVIRUS (CMV)
Complications
56. CYTOMEGALOVIRUS (CMV)
Dx
(1) Serologies (e.g. IgM and IgG antibodies).
(2) Molecular amplification techniques (e.g. PCR);
(3) Cultures (helpful to determine if drug resistance is
present).
(4) CMV antigenemia assays (helpful in
immunosuppressed hosts).
(5) Biopsy of cutaneous lesions (e.g. ulcerations) may
show characteristic findings of enlarged endothelial cells
with prominent intranuclear inclusions (‘owl’s eyes’).
57. CYTOMEGALOVIRUS (CMV)
Rx
• Uncomplicated CMV infection in
immunocompetent hosts: primarily supportive.
• Immunocompromised hosts or in those with
complicated infections: systemic therapy
1. Ganciclovir Intravenous,
2. Valganciclovir Oral,
3. Cidofovir,
4. Foscarnet.
• Prevention: is possible by matching CMV serologies
between donor and transplant recipients.
61. Exanthem subitum (Roseola
infantum, Sixth disease)
• 3–5 days of high fever followed by cutaneous
eruption as fever fades
• Discrete circular ‘rose red,’ 2- to 5-mm macules or
maculopapules, often surrounded by a white halo
• Enanthem of red papules on soft palate (Nagayama’s
spots)
62. Human Herpesvirus 7
PRIMARY INFECTION:
Usually asymptomatic
Exanthem subitum (roseola, sixth disease) but is
less common than HHV-6
REACTIVATION INFECTION:
Possibly pityriasis rosea
DRESS
