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Varicella is an acute infectious disease caused by varicella zoster virus (VZV).

If the infection is
recurrent it is known as herper zoster.

VZV  a DNA virus and is a member of the herpesvirus group. Like other herpesvirus, VZV has the
capacity to persist in the body after the primary infection as a latent infection. VZV persists in
sensory nerve ganglia.

Pathogenesis

VZV enters through the respiratory tract and conjunctiva. The virus is believed to replicate at the site
of entry in the nasopharynx and in regional lymph nodes. Primary viremia occurs 4 to 6 days after
infection and disseminates the virus to other organs, such as the liver, spleen and sensory ganglia.
Further replication occurs in the viscera, followed by a secondary viremia, with viral infection of the
skin.

Virus can be cultured from mononuclear cells of an infected person.

Clinical Features

The incubation period  14 to 16 days after exposure (may range 10-21 days)

1. Gejala prodromal: demam, nyeri kepala dan lesu sebelum timbul ruam kulit
2. Ruam kulit muncul mulai dari wajah, scalp dan menyebar ke tubuh. Lesi menyebar
sentrifugal (dari sentral ke perifer) sehingga dapat ditemukan lesi baru di ekstremitas,
sedangkan di badan lesi sudah berkrusta.
3. Lesi berupa makula eritematosa yang cepat berubah menjadi vesikel “dewdrop on rose petal
appearence”. Dalam beberapa jam sampai 1-2 hari vesikel dengan cepat menjadi keruh,
menjadi pustul dan krusta kemudian mulai menyembuh. Ciri khas varisela adalah
ditemukannya lesi kulit berbagai stadium di berbagai area tubuh.

4. Pada anak, erupsi kulit terutama berbentuk vesikular beberapa kelompok vesikel timbul 1-2
hari sebelum erupsi meluas. Jumlah lesi bervariasi, mulai dari beberapa sampai ratusan.
Umumnya pada anak-anak lesi lebih sedikit, biasanya lebih banyak pada bayi usia <1 tahun,
pubertas dan dewasa.
5. Kadang lesi dapat berbentuk bula atau hemoragik.
6. Selaput lendir sering terkena, terutama mulut, konjungtiva palpebra dan vulva
7. Keadaan umum dan tanda-tanda vital terganggu dan memberikan petunjuk tentang berat
ringannya penyakit
8. Status imun pasien perlu diketahui untuk menuntukan apakah obat antivirus perlu diberikan.
Untuk itu perlu diperhatikan beberapa hal yang dapat membantu menentukan status imun
pasien, antara lain: keadaan imunokompromais (keganasan, HIV/AIDS, pengobatan dengan
imunosupresan, misalnya kortikosteroid jangka panjang atau sitostatik, kehamilan, bayi
berat badan rendah).

Pathomechanism:

The pathogenesis of varicella differs from herpes zoster cutaneous lesions. VZV infects numerous
endothelial cells from smasll cutaneous capillaries through capture of the virus from the blood
circulation via specific adhesion molecules expressed on endothelial cells. After internalization of the
virus, the endothelial cells permit some viral replication during which these cells exhibit a more
swollen appearance.

Once arrived in the basal keratinocytes, active viral replication is taken place with secondary
dissemination to surrounding, overlying keratinocytes. These keratinocytes in the suprabasal layer
then become swollen, their nuclei present intranuclear inclusion bodies and their cytoplasm
becomes more eosinophilic and sometimes present giant syncytial cell formation, the will lead to the
formation of intraepidermal blisters. This is called the cytopathic effect (CPE).

The innate and adaptive cutaneous immune systems finally limit the extension of the infection.
There will be a neutrophilic infiltration of the blisters, clinically recognizable as pustules, followed by
the formation of a crusted lesion that will dissapeaer after about 5-7 days.

In HZ, the virus is transported via the axonal microtubular system to a predetermined dermatome
where the intra-epidermal free nerve endings and those surrounding the pilosebaceous structures
nurture the keratinocytes with infecting virus. After hte release of the virus in the basal layer
epidermal and or follicular keranitocytes the pathogenic process is identical for that described for
the varicella skin lesion.

Diagnosis

The majority of cases  clinical recognition


Sometimes, a Tzanck smear is required to prove or to exclude other vesiculobullous disorders.
Advantage is it can be easily performed and analyzed. Tzanck test/smear is scraping of an ulcer base
to look for Tzank cells.

1. Unroof vesicle and scrape base with sterile no. 15 scalpel blade
2. Smear onto clean glass slide
3. Fix with gentle heat or air dry
4. Fix with methanol.
5. Stain with giemsa, methylene blue
6. Microscopic examination using oil immersion lens (look for multinucleate giant cells/datia
berinti banyak).

Immunohistochemistry has a high sensitivity and specificity and can distinguish VZV from HSV.

Gold standard  viral culture

Differential diagnosis:

1. Herpes zoster
2. Hand foot and mouth disease
3. Dermatitis kontak iritan toxic

Varicella in Pregnancy:

When chickenpox is contracted during pregnancy, the fetus may present a congenital varicella
infection through transplacental passage during primary or secondary viremia.

Neonatal chickenpox  newborn that develops chickenpox within the first 2 weeks of life.

The overall absolute risk of embryopathy is about 2% during pregnancy varicella.

The fetal risks are variable according to the developmental age, the most dangerous period being
the one associated with development of neural structures during the second trimester. Before the
20th week of pregnancy, fetal infection is responsible for rare cases of ocular, skeletal or
neurological malformations.

The skin of the newborn may present typical varicella scars after in utero chickenpox. Some
neurological deficiencies may someimes not be noticed at birth and velop only later in infancy.

At term, the highest risk is when varicella occurs between 4-8 days before delivery and 2 days after
delivery, as the mother has not yet developed protective IgM and IgG antibodies that are
transmitted to the baby. In the absence of treatemnt there is a mortality rate of 30% for neonatal
chickenpox.

Childhood Varicella:

A progressive cephalo-caudal spreading vesicular rash emerging in 3-6 day period is usual for
chickenpox. Furthermore, exanthema has a centripetal distribution with more trunkal and proximal
lesions than vesicles on the distal extremities.

The average duration from onset to complete clinical healting of the lesions lasts around 8-10 days.

Small macular lesion after 1-2 days  papular  vesicle up to 2-3 mm


The first 2 days the vesicle fluid is celar, then it may become pustular. A small dark crust forms after
4 to 5 days. The scab may remain for 1 to 3 weeks. Young children have between 200-250 leasions.
In older children is may exceed 500.

Penatalaksanaan

1. Topical
a. Lesi vesikular: diberi bedak agar vesikel tidak pecah, dapat ditambahkan mentol 2%
atau antipruritus yang lain
b. Vesikel yang sudah pecah/krusta: salap antibiotik
2. Sistemik
a. Antivirus: dapat diberikan pada anak, dewasa, pasien yang tertular orang serumah,
neonatus dari ibu yang menderita varisela 2 hari sebelum sampai 4 hari sesudah
melahirkan. Berdasarkan CDC neonatus dari ibu yang menderita varisela 2-4 hari
sebelum melahirkan sebaiknya diberikan imunoglobulin.
i. Asiklovir: dosis bayi/anak 4x10-20 mg/kg (max 800 mg/hari) selama 7 hari.
Dewasa 5x800 mg/hari selama 7 hari atau
ii. Valasiklovir: Dewasa 3x1 gr/hari selama 7 hari
b. Pada ibu hamil pemberian asiklovir perlu dipertimbangkan risiko dan manfaat
pemberiannya. Asiklovir oral dapat diberikan pada ibu hamil usia >20 meinggu dengan
awitan varisela <24 jam. Pemberian asiklovir sebelum usia gestasi 20 minggu perlu
dipertimbangkan risiko dan manfaat.
c. Anti piretik bila demam, hindari salisilat (Reye’s syndrome)
d. Antipruritus
3. Edukasi
a. Bila mandi, harus hati-hati agar vesikel tidak pecah
b. Jangan menggaruk dan dijaga agar vesikel tidak pecah, biarkan mengering dan lepas
sendiri
c. Istirahat pada masa aktif sampai semua lesi sudah mencapai stadium krustasi
d. Rawat bila berat, bayi, usia lanjut dan dengan komplikasi
e. Makan lunak bila terdpat banyak lesi di mulut.