varicella inggris

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(CHICKEN POX)

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Page 1: Varicella Inggris

(CHICKEN POX)

Page 2: Varicella Inggris

• An acute, highly

contagious exanthem.

• Most often occurs in

childhood.

• Result of primary infection

of a susceptible individual.

Page 3: Varicella Inggris

EPIDEMIOLOGY

1.Worldwide in distribution,

whereas the proportion of

susceptible adults is even

higher in Asia, Africa, and

the Middle East.

2.No difference in racial or

sexual susceptibility.

Page 4: Varicella Inggris

3.Humans are the only

known reservoir.

4.Vectors play no role in

transmission.

5.The mean incubation

period is 14 or 15 days,

with a rarge of 10 to 23

days.

Page 5: Varicella Inggris

6.The major route by which

varicella is acquired and

transmitted is thought to

be the respiratory tract

7.Airborne droplets

constitute an important

mechanism of transmission,

but can also be spread by

direct contact

Page 6: Varicella Inggris

ETIOLOGY

1.VZV is a member of the

herpes virus family.

2.There is only one VZV

serotype.

Page 7: Varicella Inggris

3.A number of antigens are

present in the virion and

produced infected cells.

4.Studies of molecular

biology and its

pathogenesis have been

hampered.

Page 8: Varicella Inggris

PATHOGENESIS

1.Entry of the virus is

through the mucosa of

the upper respiratory

tract and oropharynx.

Page 9: Varicella Inggris

2.Initial multiplication at this portal dissemination small amounts of virus blood and lymphatics (primary viremia) by cells of RES.

3.Incubating infection is partially contaired by innate host defenses and by developing immune responses.

Page 10: Varicella Inggris

4.Virus replication eventually overwhelms these still undeveloped defenses secondary viremia occurs (zweeks often infection) fever and malaise and disseminates throughout the body especially skin and mucous membranes.

Page 11: Varicella Inggris

5.Cyclic viremia is terminate after about 3 days.

6.Host immune responses terminate viremia and limit the progression of varicella lesions.

7.IgG, IgM, and IgA of VZV are detectable 2 to 5 days after onset of clinical varicella.

Page 12: Varicella Inggris

8.Reach maximum titers during second or third week decline slowly persist in low levels for life

9.Cell mediated immunity is more important than humoral immunity in recovery from varicella.

Page 13: Varicella Inggris

CLINICAL MANIFESTATIONS

Prodrome of Varicella1.Uncommon in young

children.2.In older children and

adults, rash preceded by 2 to 3 day of fever , chills, malaise, headache, anorexia, severe backache.

Page 14: Varicella Inggris

Rash of Varicella1.Benigns on the face and

scalp.2.Spreads rapidy to the

trunk, with relative sparing of the extremities.

3.Central in distribution.4.More profuse in lows and

protected parts of the body.

Page 15: Varicella Inggris

5.Rose colored macules papule vesicles pustules crusts.

6.Vesicle is superficial and thin walled like a drop of water

7.Vesicle can also develop in the mucous membranes

8.Fever that persist is proportional to the severity of rash.

Page 16: Varicella Inggris

COMPLICATIONS OF VARICELLA

1.Secondary bacterial

infection of skin lesion

(children).

2.Primary varicella

pneumonia (adult).

Page 17: Varicella Inggris

3.Congenital VZV infection :

asymptomatic infection

severe congenital

malformation.

4.Morbidity and mortality

are markedly increased in

immuno compromised

patients.

Page 18: Varicella Inggris

5.CNS complication :• Reye’s syndrome.• Acute cerebellar atoxia.• Encephalitis or

meningoencephalitis.• Acute ascending or

transverse myelitis.• Guillain-barre

syndrome.6.Mild hepatitis.

Page 19: Varicella Inggris

PATHOLOGY

1.Histologically, can’t be

distinguished from herpes

zoster.

2.Ballooning degeneration

(characteristic changes).

Page 20: Varicella Inggris

CLINICAL DIAGNOSIS

1.The development papulo

vesikular eruption after a

brief and mild (or absent)

prodrome symptoms.

Characteristic diagnostic include:

Page 21: Varicella Inggris

2.Appearance of lesions in

crops with central

distribution.

3.Rapid evolution of lesions.

4.Presence of lesions in all

stages of development in

any area throughout the

acute disease.

Page 22: Varicella Inggris

5.Presence of lesions in

the mucous membranes

of the mouth.

Page 23: Varicella Inggris

LABORATORY DIAGNOSIS

1.Routine blood test are

not helpful.

2.Asymptomatic elevation

in ALT and AST.

Page 24: Varicella Inggris

3.Punch biopsies more

rediable for histologig

examinations.

4.Defenitive diagnosis from

isolation of virus in cell

cultures.

5.Serologic tests.

Page 25: Varicella Inggris

TREATMENT

Antiviral agents :

• Acyclovir.

• Famciclovir.

• Laciclovir.

• Vidarabine.

• Foscarnet.

Page 26: Varicella Inggris

TREATMENT OF VARICELLA

1.Generally benign and self-limited.

2.Locally :• Cool compresses.• Calamine lotion.

Orally :• Antihistamines.• Antipyretics.• Antiviral agents.

Page 27: Varicella Inggris

PREVENTION & CONTROL

1.Passive

immunization.

2.Chemoprophylactic.

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