Oh No!!!!!!!!!!!

huhuhuhu... untuk entry kali ni sangat2 la aku rasa huhuhuhuhuhu...<sedih la> sebab i got a German Measles... huhuhuhu... <hah? apa tu "German Measles??"> Rubella la... huhuhuhuh... P macam  xkonfem la gi la... so, tomorrow aku akan p klinik Sg.Buloh untuk dapatkan rawatan.. wawawa.... Mummy!!!! I Need You.... huhuhuhu..... hm, mari kita sama2 baca facts tentang German Measles ni...<hmm, lagi sedap bunyi nya dari Rubella tu...hihihi>

Rubella....

Rubella, commonly known as German measles, is a disease caused by the rubella virus. The name "rubella" is derived from the Latin, meaning little red. Rubella is also known as German measles because the disease was first described by German physicians in the mid-eighteenth century. This disease is often mild and attacks often pass unnoticed. The disease can last one to three days. Children recover more quickly than adults. Infection of the mother by Rubella virus during pregnancy can be serious; if the mother is infected within the first 20 weeks of pregnancy, the child may be born with congenital rubella syndrome (CRS), which entails a range of serious incurable illnesses. Spontaneous abortion occurs in up to 20% of cases.^[1]

Rubella is a common childhood infection usually with minimal systemic upset although transient arthropathy may occur in adults. Serious complications are very rare. Apart from the effects of transplacental infection on the developing fetus, rubella is a relatively trivial infection.

Acquired (i.e. not congenital) rubella is transmitted via airborne droplet emission from the upper respiratory tract of active cases. The virus may also be present in the urine, feces and on the skin. There is no carrier state: the reservoir exists entirely in active human cases. The disease has an incubation period of 2 to 3 weeks.^[2]

In most people the virus is rapidly eliminated. However, it may persist for some months post partum in infants surviving the CRS. These children are a significant source of infection to other infants and, more importantly, to pregnant female contacts.

The name rubella is sometimes confused with rubeola, an alternative name for measles in English-speaking countries; the diseases are unrelated.^[3][4] In some other European languages, rubella and rubeola are synonyms^[which?], and rubeola is not an alternative name formeasles.^[5]

Signs and symptoms

After an incubation period of 14–21 days, German measles causes symptoms that are similar to the flu. The primary symptom of rubella virus infection is the appearance of a rash (exanthem) on the face which spreads to the trunk and limbs and usually fades after three days (that is why it is often referred to as three-day measles). The facial rash usually clears as it spreads to other parts of the body. Other symptoms include low grade fever, swollen glands (sub occipital & posterior cervical lymphadenopathy), joint pains, headache and conjunctivitis.^[6] The swollen glands or lymph nodes can persist for up to a week and the fever rarely rises above 38 ^oC (100.4 ^oF). The rash of German measles is typically pink or light red. The rash causes itching and often lasts for about three days. The rash disappears after a few days with no staining or peeling of the skin. When the rash clears up, the patient may notice that his skin sheds in very small flakes wherever the rash covered it. Forchheimer's sign occurs in 20% of cases, and is characterized by small, red papules on the area of the soft palate.

Rubella can affect anyone of any age and is generally a mild disease, rare in infants or those over the age of 40. The older the person is the more severe the symptoms are likely to be. Up to two-thirds of older girls or women experience joint pain or arthritic type symptoms with rubella. The virus is contracted through the respiratory tract and has an incubation period of 2 to 3 weeks. During this incubation period, the patient is contagious typically for about one week before he develops a rash and for about one week thereafter.

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Congenital rubella syndrome

Main article: Congenital rubella syndrome

Rubella can cause congenital rubella syndrome in the newly born. The syndrome (CRS) follows intrauterine infection by Rubella virus and comprises cardiac, cerebral, ophthalmic and auditory defects.^[7] It may also cause prematurity, low birth weight, and neonatal thrombocytopenia, anaemia and hepatitis. The risk of major defects or organogenesis is highest for infection in the first trimester. CRS is the main reason a vaccine for rubella was developed. Many mothers who contract rubella within the first critical trimester either have a miscarriage or a still born baby. If the baby survives the infection, it can be born with severe heart disorders (PDA being the most common), blindness, deafness, or other life threatening organ disorders. The skin manifestations are called "blueberry muffin lesions." ^[8]

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Cause

Main article: Rubella virus

The disease is caused by Rubella virus, a togavirus that is enveloped and has a single-stranded RNA genome.^[9] The virus is transmitted by the respiratory route and replicates in thenasopharynx and lymph nodes. The virus is found in the blood 5 to 7 days after infection and spreads throughout the body. The virus has teratogenic properties and is capable of crossing the placenta and infecting the fetus where it stops cells from developing or destroys them.^[6]

Increased susceptibility to infection might be inherited as there is some indication that HLA-A1 or factors surrounding A1 on extended haplotypes are involved in virus infection or non-resolution of the disease.^[10] [11]

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Diagnosis

Rubella virus specific IgM antibodies are present in people recently infected by Rubella virus but these antibodies can persist for over a year and a positive test result needs to be interpreted with caution.^[12] The presence of these antibodies along with, or a short time after, the characteristic rash confirms the diagnosis.^[13]

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Prevention

Main article: MMR vaccine

Rubella infections are prevented by active immunisation programs using live, disabled virus vaccines. Two live attenuated virus vaccines, RA 27/3 and Cendehill strains, were effective in the prevention of adult disease. However their use in prepubertile females did not produce a significant fall in the overall incidence rate of CRS in the UK. Reductions were only achieved by immunisation of all children.

The vaccine is now usually given as part of the MMR vaccine. The WHO recommends the first dose is given at 12 to 18 months of age with a second dose at 36 months. Pregnant women are usually tested for immunity to rubella early on. Women found to be susceptible are not vaccinated until after the baby is born because the vaccine contains live virus.^[14]

The immunisation program has been quite successful. Cuba declared the disease eliminated in the 1990s, and in 2004 the Centers for Disease Control and Prevention announced that both the congenital and acquired forms of rubella had been eliminated from the United States.^[15][16]

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Treatment

There is no specific treatment for Rubella; however, management is a matter of responding to symptoms to diminish discomfort. Treatment of newly born babies is focused on management of the complications. Congenital heart defects^{[citation needed]} and cataracts can be corrected by direct surgery.^[17] Management for ocular CRS is similar to that for age-related macular degeneration, including counseling, regular monitoring, and the provision of low vision devices, if required.^[18]

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Prognosis

Rubella infection of children and adults is usually mild, self-limiting and often asymptomatic. The prognosis in children born with CRS is poor.^[19]

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Epidemiology

Rubella is a disease that occurs worldwide. The virus tends to peak during the spring in countries with temperate climates. Before the vaccine to rubella was introduced in 1969, widespread outbreaks usually occurred every 6–9 years in the United States and 3–5 years in Europe, mostly affecting children in the 5-9 year old age group.^[20] Since the introduction of vaccine, occurrences have become rare in those countries with high uptake rates.

Vaccination has interrupted the transmission of rubella in the Americas: no endemic case has been observed since February 2009.^[21] Since the virus can always be reintroduced from other continents, the population still need to remain vaccinated to keep the western hemisphere free of rubella. During the epidemic in the US between 1962–1965, Rubella virus infections during pregnancy were estimated to have caused 30,000 still births and 20,000 children to be born impaired or disabled as a result of CRS.^[22][23] Universal immunisation producing a high level of herd immunity is important in the control of epidemics of rubella.^[24]

In the UK, there remains a large population of men susceptible to rubella who have not been vaccinated. Outbreaks of rubella occurred amongst many young men in the UK in 1993 and in 1996 the infection was transmitted to pregnant women, many of whom were immigrants and were susceptible. Outbreaks still arise, usually in developing countries where the vaccine is not as accessible.^[25]

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History

Rubella was first described in the mid-eighteenth century. Friedrich Hoffmann made the first clinical description of rubella in 1740,^[26] which was confirmed by de Bergen in 1752 and Orlow in 1758.^[27]

In 1814, George de Maton first suggested that it be considered a disease distinct from both measles and scarlet fever. All these physicians were German, and the disease was known as Rötheln (from the German name Röteln), hence the common name of "German measles".^[28] Henry Veale, an English Royal Artillery surgeon, described an outbreak in India. He coined the name "rubella" (from the Latin, meaning "little red") in 1866.^{[26][29][30][31]}

It was formally recognised as an individual entity in 1881, at the International Congress of Medicine in London.^[32] In 1914, Alfred Fabian Hess theorised that rubella was caused by a virus, based on work with monkeys.^[33] In 1938, Hiro and Tosaka confirmed this by passing the disease to children using filtered nasal washings from acute cases.^[30]

In 1940, there was a widespread epidemic of rubella in Australia. Subsequently, ophthalmologist Norman McAllister Gregg found 78 cases of congenital cataracts in infants and 68 of them were born to mothers who had caught rubella in early pregnancy.^[29][30] Gregg published an account, Congenital Cataract Following German Measles in the Mother, in 1941. He described a variety of problems now known as congenital rubella syndrome (CRS) and noticed that the earlier the mother was infected, the worse the damage was. The virus was isolated in tissue culture in 1962 by two separate groups led by physicians Parkman and Weller.^[29][31]

There was a pandemic of rubella between 1962 and 1965, starting in Europe and spreading to the United States.^[31] In the years 1964-65, the United States had an estimated 12.5 million rubella cases. This led to 11,000 miscarriages or therapeutic abortions and 20,000 cases of congenital rubella syndrome. Of these, 2,100 died as neonates, 12,000 were deaf, 3,580 were blind and 1,800 were mentally retarded. In New York alone, CRS affected 1% of all births ^[34]

In 1969 a live attenuated virus vaccine was licensed.^[30] In the early 1970s, a triple vaccine containing attenuated measles, mumps and rubella (MMR) viruses was introduced.^[31]

ni German Measles bagi Baby...