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Varicella zoster virus (VZV) is a family of human (alpha) herpes viruses.

The virus consists of a


double-stranded DNA genome, covered in a nucleus containing protein and wrapped by
glycoproteins. This virus can cause two types of diseases, namely varicella (chickenpox) and
herpes zoster (shingles).
In 1767, Heberden able to clearly differentiate between chickenpox and smallpox, which is
believed to be the word "chickenpox" is derived from the English language is "gican" which
means itch or is derived from the French language is "Chiche-pois", which describes the size of
the vesicles. In 1888, Von Bokay found an association between varicella and herpes zoster,
varicella suspected he found that the developing of children who terpapapar with someone
suffering from acute herpes zoster. In 1943, Garland learned of herpes zoster due to
reactivation of latent viruses. In 1952, Weller and Stoddard conducted an invitational study,
they found varicella and herpes zoster caused by the same virus.

EPIDEMIOLOGY
Varicella exists throughout the world and there is no difference in race or sex. Varicella mainly
concerns children under the age of 20, especially ages 3 - 6 years and only about 2% occurs in
adults. In America, varicella often occur in children under the age of 10 years and 5% of cases
occur in the over 15 years and in Japan, generally occurs in children under 6 years of age as
much as 81.4%. 1,2,3 The incidence of herpes zoster increases with age and is usually rare in
children. The incidence of herpes zoster based on age ie from birth - 9 years: 0.74 / 1000; age of
10-19 years: 1.38 / 1000; age 20-29 years: 2,58 / 1000. In the US, herpes zoster is rare in
children, of which more than 66% of the more than 50 years of age, less than 10% of the under
20 years of age to the age dan5% less from 15 years. Although herpes zoster is a common
disease in adults, but shingles can also occur in a newborn if the mother is suffering from
shingles during pregnancy. From the research, it was found about 3% of herpes zoster in
children, usually found in children - children who imunokompromis and suffering from
malignant disease.

PATHOGENESIS
The incubation period of varicella is 10-21 days in immunocompetent children (on average 14-
17 days) and in immunocompromised children it is usually shorter, ie less than 14 days. VZV
enters the human body by inhalation from respiratory secretions (droplet infection) or direct
contact with skin lesions. Droplet infection can occur 2 days before up to 5 days after the lesion
appears on the skin. VZV enters the human body through the upper respiratory tract mucosa,
oropharynx or conjunctiva. The first viral replication cycle occurs on days 2-4 located on
regional lymph nodes then followed by the spread of small amounts of virus through blood and
lymph glands, which results in primary viremia (usually occurs on days 4-6 after the first
infection). In most infected patients, replication of the virus can defeat the body's immature
defense mechanisms so that it will continue with the second viral replication cycle that occurs
in the liver and spleen, which results in secondary viremia. In this phase, the virus particles will
spread throughout the body and reach the epidermis on day 14-16, which results in the
appearance of lesions in a typical skin. A child suffering from varicella will be able to transmit it
to others, which is 2 days before up to 5 days after the onset of lesions on the skin. In herpes
zoster, the pathogenesis is not yet fully known. During varicella, VZV moves from skin lesions
and mucosal surfaces to sensory nerve endings and is transported centripetally through sensory
nerve fibers to the sensory ganglion. In the ganglion latent infection (dormant) occurs, where
the virus is no longer contagious and does not multiply, but still has the ability to turn into
infectious in the event of viral reactivation. Reactivation of the virus can be caused by
conditions that reduce cellular immunity as in patients with carcinoma, patients who receive
immunosuppressive treatment include corticosteroids and those receiving transplant organs.
During reactivation, the virus will multiply again so that an inflammatory reaction occurs and
damages the sensory ganglion. Then the virus will spread to the bone marrow and brain stem
and through sensory nerves to skin and then clinical symptoms will arise.

CLINICAL DESCRIPTION
Varicella in older children (puberty) and adults is usually preceded by prodormal symptoms,
namely fever, malaise, headache, nausea and anorexia, which occur 1-2 days before the onset
of lesions on the skin while in children (younger age) who are immunocompetent , prodormal
symptoms are rarely found only fever and mild malaise and occur together with the appearance
of lesions on the skin.
Lesions in varicella, beginning in the face and scalp area, then extending to the chest
(centripetal spread) and then can extend to the extremities. Lesions can also be found in the
oral and genital mucosa. Lesions in varicella are usually very itchy and have a characteristic
picture of the presence of all stages of the lesion at one time. At first a small erythematous
macula arises in the face and chest area, and then changes rapidly within 12-14 hours to
become a papule and then develops into vesicles containing clear fluid with an erythematous
basis. The formed vesicles with an erythematous base have a classic image, which is superficial
and has thin walls that look like a collection of water droplets on the skin (tear drop), 2-3 mm in
diameter, elliptical, with an axis parallel to the folds of skin or vesicles like dewdrops on the
leaves of a rose (dew drop on a rose petal). Vesicle fluid quickly becomes cloudy due to the
entry of inflammatory cells so that on day 2 it will turn into pustules. The lesion will dry out
beginning at the center so that it forms an umbilication (delle) and eventually will become crust
in a time that varies between 2-12 days, then the crust will be released within 1-3 weeks. In the
healing phase varicella rarely forms scar (scar), if not accompanied by bacterial secondary
infection. 1-3, 8.9 Varicella that occurs during pregnancy, can cause intrauterine varicella or
neonatal varicella. Intrauterine varicella, occurs in the first 20 weeks of pregnancy, which can
cause congenital abnormalities such as atrophy, arms and legs, neurological and ocular
abnormalities and mental retardation. Whereas neonatal varicella occurs when a mother gets
varicella (maternal varicella) less than 5 days before or 2 days after giving birth. Babies will be
exposed to secondary viremia from their mothers obtained by transplasental but the baby has
not received antibody protection due to insufficient time for the formation of antibodies to the
mother's body called transplasental antibodies. Prior to the use of varicella zoster
immunoglobulin (VZIG), the neonatal varicella mortality rate was around 30%, this was due to
the occurrence of severe pneumonia and fulminant hepatitis. But if the mother gets varicella
within 5 days or more before giving birth, then the mother has enough time to form and
distribute the antibodies formed (transplasental antibodies) so that the neonate rarely suffers
from severe varicella. Herpes zoster in children is rarely preceded by prodormal symptoms.
Prodormal symptoms that can be found are radicular pain, paresthesia, malese, headache and
fever, usually occurring 1-3 weeks before the rash appears on the skin. Skin lesions that are
typical of herpes zoster are usually unilateral localization and rarely cross the midline of the
body. Locations that are often found are in T3 to L2 dermatomes and nerves to V and VII.
The initial lesions are erythematous macules and papules, then within 12-24 hours they will
develop into vesicles and will continue to become pustules on days 3-4 and finally crusts will
form on days 7-10 and can heal without scarring, unless they occur bacterial secondary
infection. In immunocompromised patients herpes zoster can occur desiminata and can affect
visceral devices such as the lungs, liver, brain and disseminated intravascular coagulophaty
(DIC) so that it can be fatal. Lesions on the skin usually heal longer and can experience necrosis,
hemorrhagic and can form scarring.

COMPLICATION
Varicella
In immunocompetent children, mild varicella is usually found so complications are rare.
Complications that can be found in varicella are:
1. Secondary infection of the skin caused by bacteria
Frequent infections of the skin and occur in children ranging from 5 - 10%. Lesions on the skin
become a place for virulent organisms to enter and if the infection extends it can cause
impetigo, furuncles, cellulitis, and erythema.
The infectious organisms that are often the cause are group A streptococcus and
staphylococcus aureus.
2. Scar
The onset of scar associated with staphylococcus or streptococcus infection originating from
scratching.
3. Pneumonia
Can occur in older children and in adults, which can cause fatal conditions. In adults the
incidence of varicella pneumonia is around 1: 400 cases.
4. Neurology
Acute cerebellar ataxia postinfection
► Ataxia often appears suddenly, always occurs 2-3 weeks after the onset of varicella. This
situation can persist for 2 months.
► The manifestation of being unable to maintain a standing position is unable to stand up and
there is no coordination and dysarthria.
► The incidence ranges from 1: 4000 cases of varicella.
Encephalitis
► These symptoms often arise during the acute occurrence of varicella which is a few days after
the onset of the rash. Lethargy, drowsiness and confusion are symptoms that are often
encountered.
► Some children experience seizures and the rapid development of encephalitis can lead to
deep coma.
► Is a serious complication in which the mortality rate ranges from 5-20%. ► Incidents range
from 1.7 / 100,000 sufferers.
5. Shingles
A slow complication of varicella, namely the onset of herpes zoster, arises several months to
years after the occurrence of primary infection.
Varicella zoster virus remains in the sensory ganglion.
6. Reye syndrome
Characterized by fatty liver with encephalophaty.
This situation is associated with aspirin use, but after widespread use of acetaminophen
(antipyretics), cases of reye start syndrome are rarely found.

Herpes zoster Complications that can be found in herpes zoster are: 1. Secondary infection of
the skin caused by bacteria. 2. Posherpetic neuralgia (PHN) The incidence increases with
increasing age where approximately 50% of PHN sufferers are over 60 years of age and PHN is
usually rare in children.
3. In ophthalmic areas, keratitis, episcleritis, iritis, papillitis and nerve damage can occur.
4. Desiminata herpes zoster which can affect organs such as the brain, lungs and other organs
and can be fatal.
5. Meningoencephalitis.
6. Motor paresis.
7. Form a scar.

LABORATORY EXAMINATION For tests of varicella zoster virus (VZV) several tests can be carried
out, namely:
1. Tzanck smear - Preparations are taken from the new vesicle base, then stained with
hematoxylin-eosin, Giemsa's, Wright's, toluidine blue or Papanicolaou's. By using a light
microscope, multinucleated giant cells will be found.
- This inspection has a sensitivity of around 84%.
- This test cannot distinguish between varicella zoster virus and herpes simplex virus.

2. Direct fluorescent assay (DFA)


- Preparations were taken from vesicle base scraping, but if they were in the form of
examination crust with DFA, they were less sensitive.
- Quick inspection results.
- Requires a fluorescence microscope.
- This test can find varicella zoster virus antigen.
- This examination can distinguish between VZV and herpes simplex virus.
3. Polymerase chain reaction (PCR) - Examination with this method is very fast and very
sensitive. - With this method various types of preparations can be used such as scraping on the
basis of vesicles and if it is crusta-shaped it can also be used as a preparation, and CSF.
- Sensitivity ranges from 97 - 100%.
- This test can find nucleic acid from the varicella zoster virus.
4. Skin biopsy The results of histopathological examination: appear intraepidermal vesicles with
epidermal cell degeneration and acantholysis. In the upper dermis there is lymphocytic
infiltrate.
Varicella DIAGNOSIS
1. Disseminated herpes simplex.
2. Disseminated herpes zoster.
3. Impetigo.
Shingles
1. Herpes simplex virus.
2. Contact dermatitis.
3. Poison ivy.

MANAGEMENT
Varicella and Herpes zoster In immunocompetent children, usually no specific treatment is
needed and the treatment given is symptomatic, namely:
- The lesion is still in the form of vesicles, powder can be given to prevent breakage.
- Vesicles that have ruptured or have formed crusts, can be given antibiotic ointment to prevent
secondary infection.
- Can be given antipyretics and analgesics, but may not be a group of salicylates (aspirin) to
avoid the occurrence of Reye's syndrome.
- The fingernails must be cut to prevent secondary infection from scratching.

Antiviral drugs - Antiviral treatment can reduce the duration of illness, severity and healing time
will be shorter.
- Antiviral administration should be less than 48 - 72 hours after the skin eruption appears.
- Antiviral groups that can be given are acyclovir, valacyclovir and famasiklovir.
- Anti viral dose (oral) for the treatment of varicella and herpes zoster: Neonate: Acyclovir 500
mg / m2 IV every 8 hours for 10 days.
Children (2 - 12 years): Acyclovir 4 x 20 mg / kg BB / day / oral for 5 days. Puberty and adults:
● Acyclovir 5 x 800 mg / day / oral for 7 days.
● Valacyclovir 3 x 1 gr / day / oral for 7 days.
● Famasiklovir 3 x 500 mg / day / oral for 7 days. 1-3, 6,8,11

PREVENTION
In immunocompetent children who have suffered from varicella no precautionary measures are
needed, but preventive measures are aimed at groups at high risk for fatal varicella such as
neonates, puberty or adults, with the aim of preventing or reducing symptoms of varicella.
Preventive measures that can be given are:
1. Passive immunization
● Using VZIG (Varicella zoster immunoglobulin). ● Giving in 3 days (less than 96 hours) after
exposure to VZV, immunocompetent children have been shown to prevent varicellla while
immunocompromised children with VZIG administration can relieve symptoms of varicella. ●
VZIG can be given to: - Children <15 years old who have never had varicella or herpes zoster.
- Puberty age> 15 years who have never had varicella or herpes zoster and do not have
antibodies to VZV. - Newborns, whose mothers suffer from varicella within 5 days before or 48
hours after giving birth.
- Premature infants and infants aged ≤ 14 days whose mothers have never had varicella or
herpes zoster. - Children who suffer from leukemia or lymphoma who have never had varicella.
● Dosage: 125 U / 10 kg BB. - Minimum dose: 125 U and maximum dosage: 625 U. ● IM giving is
not given IV
● The protection obtained is temporary. 1,3,5
2. Active immunization
● The vaccine uses varicella virus vaccine (Oka strain) and acquired immunity can last up to 10
years.
● Used in America since 1995. ● Protection against varicella ranges from 71 - 100%. ● Vaccines
are effective if given at age ≥ 1 year and are recommended given at the age of 12-18 months. ●
Children aged ≤ 13 years who do not suffer from varicella are recommended to be given a
single dose and older children are given in 2 doses at a distance of 4 - 8 weeks. ● Subcutaneous
giving. ● Side effects: Sometimes a fever or a local reaction such as a maculopapular rash or
vesicles can occur, occurring in 3- 5% of children and occurring 10-21 days after administration
at the injection site. ● Varicella vaccine: Varivax.
● It should not be given to pregnant women because it can cause congenital varicella.

PROGNOSIS Varicella and herpes zoster in immunocompetent children without prognosis


complications are usually very good whereas in immunocompromised children, the morbidity
and mortality are significant.

CONCLUSION VZV infection can cause two types of diseases, namely varicella and shingles.
Varicella is often found in children while herpes zoster is more common at older ages. Proper
treatment of the two diseases above can prevent the occurrence of severe complications in
children. Provision of passive and active immunization in children - children, can prevent and
reduce symptoms of the disease that arises.

Referensi:
Sugito T L. Infeksi Virus Varicella - Zoster pada bayi dan anak. Dalam : Boediardja S A editor.
Infeksi Kulit Pada Bayi & Anak, Fakultas Kedokteran Universitas Indonesia, Jakarta, 2003 : 17 -
33.

Hurwitz S. Herpes zoster. In : Clinical Pediatric Dermatology A Texbook of skin Disease of


Childhood and Adolescence, 2 nd edition, Philadelphia ; W.B. Saunders Company, 1993 : 324 -
27.

Frieden I J, Penney N S. Varicella - Zoster Infection. In : Schchner L A, Hansen R C editor.


Pediatric Dermatology, second edition, vol 2, Churchill Livingstone, NewYork, 1995 : 1272 - 75.

Oxman N M, Alani R. Varicella and herpes zoster. In : Fitzpatrick T B, Eisen A Z editor.


Dermatology In General Medicine, 4 th edition, vol 2, McGraw - Hill, Inc, 1993 : 2543 - 67.