chicken pox / bertih / jentungan

 last week, one of my friend asked me regarding chicken pox.Since my hypotalamus not actively storing informations and knowledges, it was a bit tough to explain regarding that topic.I need to revise again before i gave her a call to talk that topic, so that i didn't give wrong informations. Alhamdulillah, i hope it could help her a little bit...

here,i just want to share my notes . so that it can be as a references for me in the future, InsyaAllah

chicken pox :
 • highly contagious illness

• caused by primary infection with varicella zoster virus ZV).

• It usually starts with vesicular skin rash mainly on the body and head rather than at the periphery and become itchy raw pockmarks which mostly heal without scarring.

• Is spread easily through coughs or sneezes of ill individuals, or through direct contact with secretions from the rash. Following primary infection there is usually lifelong protective immunity from further episodes of chickenpox.

• Chickenpox is rarely fatal, although it is generally more severe in adult males than in adult females or children. Pregnant women and those with a suppressed immune system are at highest risk of serious complications. The most common late complication of chicken pox is shingles, caused by reactivation of the varicella zoster virus decades after the initial episode of chickenpox

• A person with chickenpox is infectious from one to five days before the rash appears.

• The contagious period continues until all blisters have formed scabs, which may take 5 to 10 days.

• It takes from 10 to 21 days after contact with an infected person for someone to develop chickenpox.

• is often heralded by a prodrome of anorexia, myalgia, nausea, fever, headache, and malaise in adolescents and adults,

• while in children the first symptom is usually the development of a papular rash, followed by devolopment of malaise, fever [a temperature of 100-102F, but may be as high as 106F in rare cases], and anorexia.

• Rarely cough, rhinitis, abdominal pain, and gastrointestinal distress has been reported in pateints with varicella.Typically, the disease is more severe in adults

Infection in pregnancy and neonates


• For pregnant women, antibodies produced as a result of immunization or previous infection are transferred via the placenta to the fetus.[7]

• Women who are immune to chickenpox cannot become infected and do not need to be concerned about it for themselves or their infant during pregnancy.[8]

• Varicella infection in pregnant women can lead to viral transmission via the placenta and infection of the fetus.

• If infection occurs during the first 28 weeks of gestation, this can lead to fetal varicella syndrome (also known as congenital varicella syndrome).[9]

• Effects on the fetus can range in severity from underdeveloped toes and fingers to severe anal and bladder malformation. Possible problems include:

• Damage to brain: encephalitis,[10] microcephaly, hydrocephaly, aplasia of brain

• Damage to the eye: optic stalk, optic cap, and lens vesicles, microphthalmia, cataracts, chorioretinitis, optic atrophy

• Other neurological disorder: damage to cervical and lumbosacral spinal cord, motor/sensory deficits, absent deep tendon reflexes, anisocoria/Horner's syndrome

• Damage to body: hypoplasia of upper/lower extremities, anal and bladder sphincter dysfunction

• Skin disorders: (cicatricial) skin lesions, hypopigmentation

• Infection late in gestation or immediately following birth is referred to as "neonatal varicella".[11] Maternal infection is associated with premature delivery. The risk of the baby developing the

disease is greatest following exposure to infection in the period 7 days prior to delivery and up to 7 days following the birth.


• The baby may also be exposed to the virus via infectious siblings or other contacts, but this is of less concern if the mother is immune.

• Newborns who develop symptoms are at a high risk of pneumonia and other serious complications of the disease.[12]

Pathophysiology

• Exposure to VZV in a healthy child initiates the production of host immunoglobulin G (IgG), immunoglobulin M (IgM), and immunoglobulin A (IgA) antibodies;

• IgG antibodies persist for life and confer immunity.

• Cell-mediated immune responses are also important in limiting the scope and the duration of primary varicella infection.

• After primary infection, VZV is hypothesized to spread from mucosal and epidermal lesions to local sensory nerves.

• VZV then remains latent in the dorsal ganglion cells of the sensory nerves.

• Reactivation of VZV results in the clinically distinct syndrome of herpes zoster (i.e., shingles), and sometimes Ramsay Hunt syndrome type II

Diagnosis

• Early rash of smallpox vs chickenpox: rash mostly on the torso is characteristic of chickenpox

• The diagnosis of varicella is primarily clinical. In a non-immunized individual with typical early nonspecific, or "prodromal", symptoms associated with the appropriate appearing rash occurring in "crops".

• Confirmation of the diagnosis can be sought through either examination of the fluid within the vesicles, or by testing blood for evidence of an acute immunologic response.

• Vesicular fluid can be examined with a Tsanck smear, or better with examination for direct fluorescent antibody.

• The fluid can also be "cultured", whereby attempts are made to grow the virus from a fluid sample. Blood tests can be used to identify a response to acute infection (IgM) or previous infection and subsequent immunity (IgG).[13]

• Prenatal diagnosis of fetal varicella infection can be performed using ultrasound, though a delay of 5 weeks following primary maternal infection is advised. A PCR (DNA) test of the mother's amniotic fluid can also be performed, though the risk of spontaneous abortion due to the amniocentesis procedure is higher than the risk of the baby developing foetal varicella

Treatment

• Although there have been no formal clinical studies evaluating the effectiveness of topical application of calamine lotion, a topical barrier preparation containing zinc oxide and one of the most commonly used interventions, it has an excellent safety profile.[15]

• It is important to maintain good hygiene and daily cleaning of skin with warm water to avoid secondary bacterial infection.[16]

• Scratching may also increase the risk of secondary infection.[17]

• Addition of a small quantity of vinegar to the water is sometimes advocated.

• To relieve the symptoms of chicken pox, people commonly use anti-itching creams and lotions. These lotions are not to be used on the face or close to the eyes.

• An oatmeal bath also might help ease discomfort.[19]

Children

• If oral acyclovir is started within 24 hours of rash onset it decreases symptoms by one day but has no effect on complication rates.

• Use of acyclovir therefore is not currently recommended for immunocompetent individuals (i.e., otherwise healthy persons without known immunodeficiency or those on immunosuppressive medication).[20]

Adults

• Infection in otherwise healthy adults tends to be more severe and active;

• treatment with antiviral drugs (e.g. acyclovir) is generally advised, as long as it is started within 24–48 hours from rash onset.[21]

• Patients of any age with depressed immune systems or extensive eczema are at risk of more severe disease and should also be treated with antiviral medication.