MAKALAH VARICELLA PDF

Varicella-zoster, also known as Chickenpox, is quite familiar and a worldwide disease. This infectious disease can affect anyone, especially those who have not received immunization. In Indonesia, data records for cases of varicella or chickenpox nationally remains inadequate and limited only in some certain areas. Data from the Banyumas Central Java Province District of Health Office states, during the period from January to November , there were persons affected by varicella. Although Varicella-zoster infection is classified as a mild infection, due to its high probability to become a severe sickness and high possibility of death in immunocompromised patients, this infection should be treated and prevented carefully.

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Varicella-zoster, also known as Chickenpox, is quite familiar and a worldwide disease. This infectious disease can affect anyone, especially those who have not received immunization. In Indonesia, data records for cases of varicella or chickenpox nationally remains inadequate and limited only in some certain areas.

Data from the Banyumas Central Java Province District of Health Office states, during the period from January to November , there were persons affected by varicella. Although Varicella-zoster infection is classified as a mild infection, due to its high probability to become a severe sickness and high possibility of death in immunocompromised patients, this infection should be treated and prevented carefully.

VZV is a family of human herpes viruses. The virus consists of a double stranded DNA genome, covered in a nucleus containing protein and wrapped by glycoprotein.

The VZV can cause primary, latent, and recurrent infections. This disease is very contagious with characteristic reddish vesicle lesions. The latent reactivation of the VZV generally occurs in the sixth decade with the appearance of shingles characterized as vesicular lesions limited to a specific dermatomes and accompanied by severe pain. Chickenpox is a viral infectious disease caused by the Varicella-Zoster virus which can manifest into varicella chickenpox and its latent reactivation causes herpes zoster shingles.

Varicella is usually a limited disease that lasts for four to five days and some symptoms often characterized by fever, malaise, and generalized vesicular rashes usually consisting of lesions. Infants, adolescents, adults, and immunocompromised people are at higher risk for complications. This virus has an envelope, icosahedral shape, and a double chain DNA that encodes more than 70 kinds of proteins.

VZV is a Human Herpes Neurotropic virus that causes less than four million cases of smallpox each year. After smallpox, VZV becomes latent in the cranial nerves, dorsal roots and autonomic nervous system ganglia along the neuraxis. VZV or herpes virus, consists of a double-chain DNA genome surrounded by protein and contained in an envelope of icosahedral and lipids on the outer membrane.

The VZV genome has 69 different genes that encode proteins to form viruses and enter the host cell. Viral DNA replication and new virion synthesis spreads to adjacent uninfected cells. During primary infection, which causes varicella, VZV remains in dorsal sensory root ganglia cells. Classic herpes zoster, with a dermatomal vesicular rash is the most common clinical symptom caused by VZV reactivation, but some HCT recipients have a general vesicular exanthema that resembles varicella, neuropathic pain syndrome, or organ involvement not associated with any rash.

There are no differences according to sex or race. There were 11, cases of varicella hospitalization with people die each year. A lethal perinatal varicella may occur if pregnant women infected by varicella within five days before delivery or 48 hours after giving birth. Death is related to the low immune system among the neonates. Congenital varicella is often characterized by limb hypoplasia, skin lesions, and microcephaly. Overall, the incidence of herpes zoster is per , people per year.

The epidemiology of chickenpox seems to change. There had been a shift in the age distribution of cases over the past 20 years.

This condition is shown in the increased consultation for chickenpox in general practice and more deaths due to varicella in England and Wales. Based on hospital admissions data for chickenpox in young adults, there is similar evidence in the United States. Epidemiological changes have important consequences for the future such as death and risk of infection in health workers and pregnant women. Chickenpox is generally considered a mild disease in countries where most cases occur in children.

In immunocompetent children, complications rarely occur with fewer than 2 deaths per , cases in children aged years. Though, in adults, chickenpox is more often associated with complications and death. Varicella can lead to pneumonia in 1 out of cases and is very severe in smokers.

VZV is a contagious in days before skin lesions appear. It can be transmitted through the respiratory tract and cause lesions in the oropharynx.

These lesions facilitate the spread of the virus through the respiratory tract pathway. In this phase, transmission occurs through droplets to the mucous membranes of healthy people, such as the conjunctiva. The incubation period lasts around 14 days, where the virus will spread to the lymph glands, then expand to the liver and mononuclear cells. VZV in mononuclear cells begins to disappear 24 hours before the onset of the skin rash; in immunocrompomised patients, the virus disappears later that is hours after the onset of the skin rash.

These viruses migrate and replicate from capillaries to skin tissue and cause maculopapular, vesicular and crustal lesions. This infection causes fusion of epithelial cells to form multinucleus cells characterized by intranuclear eosinophilic inclusions.

The spread of lesions on the skin is known to be caused by the presence of ORF47 kinase protein, which is useful in the process of viral replication. VZV can cause disseminated infections that are usually associated with a low immune system. In this phase, the virus particles will spread throughout the body and reach the epidermis between 14 to 16 days, which results in the appearance of lesions on the typical skin. A child who has varicella will transmit it to others ranging from two-days before and up to five-days after the onset of the lesion 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 centripetally transported through sensory nerve fibers to the sensory ganglion.

In the ganglion latent infection occurs, where the virus is no longer contagious and does not multiply, but still has the ability to turn into an infectious virus reactivation. It starts with prodromal symptoms such as fever, malaise, headache, and abdominal pain, which last between 24 to 48 hours before skin lesions appear. Systemic symptoms such as fever, fatigue, and anorexia can occur along with skin lesions.

Symptoms of the respiratory tract and vomiting rarely occur. Initial skin lesions of the scalp, face, body, are usually very itchy, in the form of a reddish macula, then turn into small vesicle lesions and contain fluid in them, similar to the appearance of teardrops. Healing is characterized by the formation of new skin epithelial cells that appear from the base of the lesion.

Hypopigmentation can occur due to healing of the lesion. Scarring due to varicella infection is rare. 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 often shown all stages of the lesion simultaneously.

At first, a small erythematous macule arises in the face and chest area, and then changes rapidly within hours to become a papule and then develops into clear vesicles containing erythematous fluid. The vesicles formed with an erythematous base have a classic form, which is superficial and has thin walls so that it looks like a tear drop, mm in diameter, elliptical in shape, with an axis that is parallel to the skin fold or visible vesicles like dew points 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 lesions will dry out beginning at the center so that they form umbilization delle and eventually become crust within weeks. In the healing phase, varicella rarely forms scar, if not accompanied by bacterial secondary infection. Shingles in children is rarely preceded by prodromal symptoms. Symptoms that can be found are radicular pain, paresthesia, malaise, headache and fever, usually occurring 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. Initial lesions in the form of erythematous macules and papules, then within hours will develop into vesicles and will continue to become pustules on days and finally on the 7th day crusts will form and can heal without scarring, unless there is a secondary bacterial infection.

Laboratory tests are very important for diagnosing patients suspected of having varicella or herpes zoster and for determining appropriate antiviral therapy.

Leukopenia occurs in the first 72 hours, followed by lymphocytosis. Patients with neurological disorders due to varicella usually experience lymphocytic pleocytosis and increased protein in cerebrospinal fluid and glucose, which are generally remains in normal limits.

Virological methods by detecting viral DNA or viral proteins are used as one of the methods of diagnosing VZV infection. One of the serological methods used to diagnose VZV infection is based on the examination of acute serum and convalescence, namely IgM and IgG.

VZV IgM examination has low sensitivity and specificity. VZV reactivation triggers IgM, which is sometimes difficult to distinguish from the presence of IgM in primary infection. IgG examination has clinical importance, in order to know passive antibodies or have received an active vaccine against varicella. The presence of IgG is basically a sign of latent infection unless the patient has received passive antibodies from immunoglobulins.

Another technique is to use membrane antigen assay fluorescents. This examination can detect antibodies that are bound to cells infected by VZV. This test is very sensitive and specific, almost similar to the examination of enzyme immunoassay or immunoblotting.

Another supportive serological examination is latex agglutination, to determine the status of immunity against VZV. Varicella and herpes zoster in immunocompetent children usually do not require specific treatment unless it is symptomatic: 2.

Acetaminophen can reduce discomfort due to fever; antipruritus such as diphenhydramine 1. Topical and systemic antibiotics can be given to treat bacterial superinfection. Antiviral therapy reduces mortality because it can prevent progressive pneumonia, and alters the prognosis of varicella infection in high-risk children.

Acyclovir therapy in immunodeficient children should begin 24 to 72 hours after a skin rash appears. Therapy is continued for 7 days or until no new lesions appear within 48 hours. The most common complication caused by varicella infection is an infection of S. Antibiotics can actually be used to reduce the risk of death, unless there is sepsis.

Secondary infections due to bacteria are usually characterized by the appearance of bullae or cellulitis, regional lymphadenitis and subcutaneous abscesses can appear. Other manifestations are pneumonia, arthritis, and osteomyelitis. Neurological complications such as meningoencephalitis and cerebral ataxia are common. Complications in the central nervous system usually occur in children under 5 years and over the age of 20 years. Varicella vein encephalitis usually resolves on its own within 24 to 72 hours.

Cerebellar ataxia usually disappears in some time. Symptoms such as bleeding, petechiae, purpura, epistaxis, haematuria, gastrointestinal bleeding, and Disseminated Intravascular Coagulation are caused by complications in the form of thrombocytopenia, occurring 1 to 2 weeks after varicella infection.

Viral arthritis can also occur due to the presence of varicella viruses in the joint.

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Varicella commonly known as chickenpox is a highly contagious infection caused by the varicella-zoster virus. It is spread through respiratory droplets in the air formed when an infected person coughs or sneezes. It is also spread through direct contact with skin lesions caused by the virus. People infected with chickenpox generally become immune, but they can be at risk of developing shingles later in life. Primary infection with varicella-zoster virus VZV results in the development of chickenpox.

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