VARICELLA ZOSTER

VIRUS
INFECTIONS
• Varicella (Chicken Pox)
• Herpes Zoster (Shingles)

By JOHN PAUL CAMELLO, MD

Etiology
• Herpesviridae
• Eosinophilic intracellular inclusions and multinucleated giant cells
-alterations seen in tissue culture

Varicellovirus
Virus classification
Group: Group I (dsDNA
)
Order: Herpesvirales
Family: Herpesviridae
Subfamily: Alphaherpesviri
nae
Genus: Varicellovirus
Pathogenesis and Pathology
• Primary Infection
• Respiratory route -> localized replication -> seeding of lymphatic and RES
->viremia (diffuse and scattered nature of lesions)
• Vesicles ( involve the corium, and dermis with degenerative changes)
• Vesicular fluid may become cloudy (PMNS and deg cells and fibrin)
Pathogenesis and Pathology
• Recurrent Infection
• Mechanism of reactivation of VZV that results in HZ is unknown
• Dorsal Root Ganglia
• Pulmonary
• Interstitial Pneumonitis, multinucleated giant cell formation, intranuclear inclusions and
pulmonary hemorrhage
• CNS
• Perivascular cuffing (similar to measles and viral encephalitides)
• perivascular cuffing. the accumulation of lymphocytes or plasma cells in a dense mass around
the vessel. An indication of inflammation or of an immune reaction.
• Focal Hemorrhagic necrosis of the brain is infrequent
Epidemiology and Clinical Manifestations
• CHICKEN POX
• Humans (only known reservoir)
• Highly contagious
• Endemic and epidemic during seasonal peaks late winter and early spring
• Children 5-9 yrs old most commonly affected (50% of all cases)
• 10% of population in US >15yrs is susceptible
• Incubation Period
• 10 to 21 days but usually 14-17 days
• Secondary attack rates of 70%-90% within a household
Epidemiology and Clinical Manifestations
• CHICKEN POX
• Infectious ~48h before onset of vesicular rash, during period of vesicular
formation( 4-5 days) and until all vesicles are crusted
• Rash, low grade fever and malaise
• Skin lesions —the hallmark of the infection—include maculopapules, vesicles,
and scabs in various stages of evolution
• evolve from maculopapules to vesicles over hours to days, appear on the trunk and face and
rapidly spread to involve other areas of the body. Most are small and have an erythematous
base with a diameter of 5–10 mm. Successive crops appear over a 2- to 4-day period.
• most common infectious complication of varicella is secondary bacterial
superinfection of the skin, which is usually caused by Streptococcus pyogenes or
Staphylococcus aureus, including strains that are methicillin-resistant
 Close-up of lesions of disseminated zoster. Note
Varicella lesions at various stages of evolution: lesions at different stages of evolution, including
vesicles on an erythematous base, umbilical vesicles, and crusts. pustules and crusting.
(Photo courtesy of Lindsey Baden; with permission.)
Epidemiology and Clinical Manifestations
• CHICKEN POX
• The most common extracutaneous site of involvement in children is the CNS
• Acute cerebellar ataxia and meningeal inflammation
• appears ~21 days after onset of the rash and rarely develops in the pre-eruptive phase
• Benign complication of VZV in children
• Aseptic meningitis, encephalitis, transverse myelitis, and Guillain-Barre syndrome can
also occur
• Reyes Syndrome – aspirin
• Other than supportive care, no specific therapy (e.g., acyclovir administration)has proved
efficacious for patients with CNS involvement.
Epidemiology and Clinical Manifestations
• CHICKEN POX
• Varicella Pneumonia
• most serious complication
• 20% of adult cases and usually severe in pregnant women
• Pneumonia due to VZV usually has its onset 3–5 days into the illness
• tachypnea, cough, dyspnea, and fever
• Cyanosis, pleuritic chest pain, and hemoptysis are frequently noted
• nodular infiltrates and interstitial pneumonitis on xray
• Resolution of pneumonitis parallels improvement of the skin rash
• patients may have persistent fever and compromised pulmonary function for weeks.
Epidemiology and Clinical Manifestations
• CHICKENPOX
• Other complications of Chicken Pox
• include myocarditis, corneal lesions, nephritis, arthritis, bleeding diatheses, acute
glomerulonephritis, and hepatitis.
• Hepatic involvement, distinct from Reye’s syndrome and usually asymptomatic, is common in
chickenpox and is generally characterized by elevated levels of liver enzymes, particularly
aspartate and alanine aminotransferases.
• Perinatal Varicella
• High mortality rates 30% when maternal disease develops within 5 days before delivery or
within 48 h thereafter ~~~newborn does not receive protective transplacental antibodies and
has an immature immune system
• Congenital varicella
• with clinical manifestations of limb hypoplasia, cicatricial skin lesions, and microcephaly at birth,
is extremely uncommon
Epidemiology and Clinical Manifestations
• HERPES ZOSTER (Shingles)
• sporadic
• reactivation of latent VZV from dorsal root ganglia
• occurs at all ages, but its incidence is highest (5–10 cases per 1000 persons)
among individuals in the sixth decade of life and beyond
• unilateral vesicular dermatomal eruption, often associated with severe pain.
• T3-L3
• zoster ophthalmicus (ophthalmic branch of the trigeminal nerve is involved)
• Can cause blindness if without antiviral therapy
• In children,reactivation is usually benign; in adults, it can be debilitating
because of pain.
Epidemiology and Clinical Manifestations
• HERPES ZOSTER (Shingles)
• onset of disease is heralded by pain within the dermatome, which may precede lesions
by 48–72 h; an erythematous maculopapular rash evolves rapidly into vesicular lesions
• In the normal host, these lesions may remain few in number and continue to form for
only 3–5 days. The total duration of disease is generally 7–10 days; however, it may take
as long as 2–4 weeks for the skin to return to normal
• zoster sine herpetica (characteristic localization of pain to a dermatome with serologic
evidence of herpes zoster in the absence of skin lesions)
• Ramsay Hunt syndrome is defined as an acute peripheral facial neuropathy associated
with erythematous vesicular rash of the skin of the ear canal, auricle (also termed
herpes zoster oticus), and/or mucous membrane of the oropharynx. patients lose their
sense of taste in the anterior two-thirds of the tongue while developing ipsilateral facial
palsy.
Epidemiology and Clinical Manifestations
• HERPES ZOSTER (Shingles)
• the most debilitating complication of herpes zoster is pain associated with
acute neuritis and postherpetic neuralgia.
• CNS involvement may follow localized herpes zoster
• Like chickenpox, herpes zoster is more severe in immunocompromised than
immunocompetent individuals
• Lesions continue to form for >1 week, and scabbing is not complete in most cases until 3
weeks into the illness.
• Herpes zoster in a thoracic dermatome
• Grouped vesicles on erythematous plaques.
• Herpes zoster in distribution of the ophthalmic branch of the trigeminal
nerve. Crusts at sites of resolving vesicles on an erythematous plaque.
Differential Diagnosis
• Disseminated HSV infection in patients with atopic dermatitis
• Disseminated vesiculopapular lesions
• coxsackievirus infection, echovirus infection and or atypical measles
• these rashes are more commonly morbilliform with a hemorrhagic component
rather than vesicular or vesiculopustular
• Rickettsialpox (herald spot)

• Smallpox (Unilateral vesicular lesions in a dermatomal pattern should

lead rapidly to the diagnosis of herpes zoster, although the occurrence of
shingles without a rash has been reported
Differential Diagnosis
• HSV and coxsackievirus infections can cause dermatomal vesicular
lesions.
Laboratory Findings
• PCR (detects VZV DNA)
• Tzanck smear
• Serologic
• immunofluorescent detection of antibodies to VZV membrane antigens
• fluorescent antibody to membrane antigen (FAMA) test
• immune adherence hemagglutination
• enzyme-linked immunosorbent assay (ELISA)
• FAMA and ELISA are most sensitive
TREATMENT
• Medical management of chickenpox in the immunologically normal
host is directed toward the prevention of avoidable complications
• good hygiene includes daily bathing and soaks
• Secondary bacterial infection of the skin can be avoided by
meticulous skin care, particularly with close cropping of fingernails
• Pruritus can be decreased with topical dressings or the administration
of antipruritic drugs
• Tepid water baths and wet compresses are better than drying lotions
for the relief of itching
TREATMENT
• Acyclovir (800 mg by mouth five times daily), valacyclovir (1 g three
times daily), or famciclovir (250 mg three times daily) for 5–7 days is
recommended for adolescents and adults with chickenpox of ≤24 h
duration.
• Valacyclovir is licensed for use in children and adolescents.Famciclovir
is recommended but not licensed for varicella.
• Acyclovir therapy may be of benefit to children <12 years of age if
initiated early in the disease (<24 h) at a dose of 20 mg/kg every 6 h.
• Aluminum acetate soaks for the management of herpes zoster can be
both soothing and cleansing
• Acyclovir is administered at a dosage of 800 mg five times daily for 7–
10 days
• Valacyclovir, the prodrug of acyclovir, accelerates healing and
resolution of zoster associated pain more promptly than acyclovir. The
dose is 1 g by mouth three times daily for 5–7 days.
• Patients with herpes zoster benefit from oral antiviral therapy, as
evidenced by accelerated healing of lesions and resolution of zoster-
associated pain
• In severely immunocompromised hosts (e.g., transplant recipients,
patients with lymphoproliferative malignancies), both chickenpox and
herpes zoster (including disseminated disease) should be treated, at
least at the outset, with IV acyclovir, which reduces the occurrence of
visceral complications but has no effect on healing of skin lesions or
pain. The dose is 10 mg/kg every 8 h for 7 days
• For low-risk immunocompromised hosts, oral therapy with
valacyclovir or famciclovir appears beneficial. If medically feasible, it is
desirable to decrease immunosuppressive treatment concomitant
with the administration of IV acyclovir
• management of acute neuritis and/or postherpetic neuralgia
• nonnarcotics to narcotic derivatives
• gabapentin, pregabalin, amitriptyline hydrochloride, lidocaine(patches), and
fluphenazine hydrochloride
• glucocorticoid therapy administered early in the course of localized herpes
zoster significantly accelerated such quality-of-life improvements as a return
to usual activity and termination of analgesic medications
• The dose of prednisone administered orally is 60 mg/d on days 1–7, 30 mg/d on days 8–
14, and 15 mg/d on days 15–21.
• appropriate only for relatively healthy elderly persons with moderate or severe pain at
presentation.
• Glucocorticoids should not be used without concomitant antiviral therapy.
PREVENTION
• First method
• live attenuated varicella vaccine (Oka)
• all children >1 year of age (up to 12 years of age) who have not had
chickenpox and for adults known to be seronegative for VZV
• Two doses are recommended for all children: the first at 12–15 months of age
and the second at ~4–6 years of age.
• VZV-seronegative persons >13 years of age should receive two doses of
vaccine at least 1 month apart
• In individuals >50 years of age, a VZV vaccine with 18 times the viral content
of the Oka vaccine decreased the incidence of shingles by 51%, the burden of
illness by 61%, and the incidence of postherpetic neuralgia by 66%.
• Second Method
• VZIG
• administer varicella-zoster immune globulin (VZIG) to individuals who are
susceptible, are at high risk for developing complications of varicella, and
have had a significant exposure
• should be given within 96 h (preferably within 72 h) of the exposure
Recommendations for VZIG Administration

• 1. Exposure to a person with chickenpox or zoster

• A. Household: residence in the same household
• B. Playmate: face-to-face indoor play
• C. Hospital
• Varicella: same 2- to 4-bed room or adjacent beds in large ward, faceto- face contact with
infectious staff member or patient, visit by a person deemed contagious
• Zoster: intimate contact (e.g., touching or hugging) with a person deemed contagious
• D. Newborn infant
• onset of varicella in the mother ≤5 days before delivery or ≤48 h after delivery; VZIG not
indicated if the mother has zoster
• 2. Patient should receive VZIG as soon as possible but not >96 h after
exposure
• Candidates (Provided They Have Significant Exposure) Include:
1. Immunocompromised susceptible children without a history of varicella
or varicella immunization
2. Susceptible pregnant women
3. Newborn infants whose mother had onset of chickenpox within 5 days
before or within 48 h after delivery
4. Hospitalized premature infant (≥28 weeks of gestation) whose mother
lacks a reliable history of chickenpox or serologic evidence of protection
against varicella
5. Hospitalized premature infant (<28 weeks of gestation or ≤1000-g birth
weight), regardless of maternal history of varicella or VZV serologic status
• THIRD METHOD
• antiviral therapy can be given as prophylaxis to individuals at high risk who
are ineligible for vaccine or who are beyond the 96-h window after direct
contact
• Therapy is instituted 7 days after intense exposure. At this time, the host is
midway into the incubation period. This approach significantly decreases
disease severity, if not totally preventing disease.
• THANK YOU!!!!