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Rift Valley Fever

Rift Valley fever
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Defibition:
Rift Valley Fever (RVF) is a viral zoonosis (affects primarily domestic livestock, but can be passed to humans) causing fever. It is spread by the bite of infected mosquitoes, typically the Aedes or Culex genera.

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The disease is caused by the RVF virus, a member of the genus Phlebovirus (family Bunyaviridae). The disease was first reported among livestock in Kenya around 1915, but the virus was not isolated until 1931. RVF outbreaks occur across sub-Saharan Africa, with outbreaks occurring elsewhere infrequently (but sometimes severely – in Egypt in 1977-78, several million people were infected and thousands died during a violent epidemic. In Kenya in 1998, the virus claimed the lives of over 400 Kenyans. In September 2000 an outbreak was confirmed in Saudi Arabia and Yemen).

In humans the virus can cause several different syndromes. Usually sufferers have either no symptoms or only a mild illness with fever, headache, myalgia and liver abnormalities. In a small percentage of cases (< 2%) the illness can progress to hemorrhagic fever syndrome, meningoencephalitis (inflammation of the brain), or affecting the eye. Patients who become ill usually experience fever, generalized weakness, back pain, dizziness, and weight loss at the onset of the illness. Typically, patients recover within 2-7 days after onset.

RVF virus is a member of the Phlebovirus genus, one of the five genera in the family Bunyaviridae. The virus was first identified in 1931 during an investigation into an epidemic among sheep on a farm in the Rift Valley of Kenya. Since then, outbreaks have been reported in sub-Saharan and North Africa. In 1997-98, a major outbreak occurred in Kenya, Somalia and Tanzania and in September 2000, RVF cases were confirmed in Saudi Arabia and Yemen, marking the first reported occurrence of the disease outside the African continent and raising concerns that it could extend to other parts of Asia and Europe.

Approximately 1% of human sufferers die of the disease. Amongst livestock the fatality level is significantly higher. In pregnant livestock infected with RVF there is the abortion of virtually 100% of fetuses. An epizootic (animal disease epidemic) of RVF is usually first indicated by a wave of unexplained abortions.

TRANSMISSION TO HUMANS:
*The vast majority of human infections result from direct or indirect contact with the blood or organs of infected animals. The virus can be transmitted to humans through the handling of animal tissue during slaughtering or butchering, assisting with animal births, conducting veterinary procedures, or from the disposal of carcasses or fetuses. Certain occupational groups such as herders, farmers, slaughterhouse workers and veterinarians are therefore at higher risk of infection. The virus infects humans through inoculation, for example via a wound from an infected knife or through contact with broken skin, or through inhalation of aerosols produced during the slaughter of infected animals. The aerosol mode of transmission has also led to infection in laboratory workers.

*There is some evidence that humans may also become infected with RVF by ingesting the unpasteurized or uncooked milk of infected animals.

*Human infections have also resulted from the bites of infected mosquitoes, most commonly the Aedes mosquito.

*Transmission of RVF virus by hematophagous (blood-feeding) flies is also possible.

*To date, no human-to-human transmission of RVF has been documented, and no transmission of RVF to health care workers has been reported when standard infection control precautions have been put in place.

*There has been no evidence of outbreaks of RVF in urban areas.

CLINICAL FEATURES IN HUMANS
Mild form of RVF in humans

*The incubation period (interval from infection to onset of symptoms) for RVF varies from two to six days.

*Those infected either experience no detectable symptoms or develop a mild form of the disease characterized by a feverish syndrome with sudden onset of flu-like fever, muscle pain, joint pain and headache.

*Some patients develop neck stiffness, sensitivity to light, loss of appetite and vomiting; in these patients the disease, in its early stages, may be mistaken for meningitis.

*The symptoms of RVF usually last from four to seven days, after which time the immune response becomes detectable with the appearance of antibodies and the virus gradually disappears from the blood.

Severe form of RVF in humans:

*While most human cases are relatively mild, a small percentage of patients develop a much more severe form of the disease. This usually appears as one or more of three distinct syndromes: ocular (eye) disease (0.5-2% of patients), meningoencephalitis (less than 1%) or haemorrhagic fever (less than 1%).

*Ocular form: In this form of the disease, the usual symptoms associated with the mild form of the disease are accompanied by retinal lesions. The onset of the lesions in the eyes is usually one to three weeks after appearance of the first symptoms. Patients usually report blurred or decreased vision. The disease may resolve itself with no lasting effects within 10 to 12 weeks. However, when the lesions occur in the macula, 50% of patients will experience a permanent loss of vision. Death in patients with only the ocular form of the disease is uncommon.

*Meningoencephalitis form: The onset of the meningoencephalitis form of the disease usually occurs one to four weeks after the first symptoms of RVF appear. Clinical features include intense headache, loss of memory, hallucinations, confusion, disorientation, vertigo, convulsions, lethargy and coma. Neurological complications can appear later (> 60 days). The death rate in patients who experience only this form of the disease is low, although residual neurological deficit, which may be severe, is common.

*Haemorrhagic fever form: The symptoms of this form of the disease appear two to four days after the onset of illness, and begin with evidence of severe liver impairment, such as jaundice. Subsequently signs of haemorrhage then appear such as vomiting blood, passing blood in the faeces, a purpuric rash or ecchymoses (caused by bleeding in the skin), bleeding from the nose or gums, menorrhagia and bleeding from venepuncture sites. The case-fatality ratio for patients developing the haemorrhagic form of the disease is high at approximately 50%. Death usually occurs three to six days after the onset of symptoms. The virus may be detectable in the blood for up to 10 days, in patients with the hemorrhagic icterus form of RVF.

The total case fatality rate has varied widely between different epidemics but, overall, has been less than 1% in those documented. Most fatalities occur in patients who develop the haemorrhagic icterus form.

DIAGNOSIS
Acute RVF can be diagnosed using several different methods. Serological tests such as enzyme-linked immunoassay (the “ELISA” or “EIA” methods) may confirm the presence of specific IgM antibodies to the virus. The virus itself may be detected in blood during the early phase of illness or in post-mortem tissue using a variety of techniques including virus propagation (in cell cultures or inoculated animals), antigen detection tests and RT-PCR.

TREATMENT AND VACCINE

*As most human cases of RVF are relatively mild and of short duration, no specific treatment is required for these patients. For the more severe cases, the predominant treatment is general supportive therapy.

*An inactivated vaccine has been developed for human use. However, this vaccine is not licensed and is not commercially available. It has been used experimentally to protect veterinary and laboratory personnel at high risk of exposure to RVF. Other candidate vaccines are under investigation.

RVF VIRUS IN ANIMAL HOSTS
*RVF is able to infect many species of animals causing severe disease in domesticated animals including cattle, sheep, camels and goats. Sheep appear to be more susceptible than cattle or camels.

*Age has also been shown to be a significant factor in the animal’s susceptibility to the severe form of the disease: over 90% of lambs infected with RVF die, whereas mortality among adult sheep can be as low as 10%.

*The rate of abortion among pregnant infected ewes is almost 100%. An outbreak of RVF in animals frequently manifests itself as a wave of unexplained abortions among livestock and may signal the start of an epidemic.

RVF VECTORS
*Several different species of mosquito are able to act as vectors for transmission of the RVF virus. The dominant vector species varies between different regions and different species can play different roles in sustaining the transmission of the virus.

*Among animals, the RVF virus is spread primarily by the bite of infected mosquitoes, mainly the Aedes species, which can acquire the virus from feeding on infected animals. The female mosquito is also capable of transmitting the virus directly to her offspring via eggs leading to new generations of infected mosquitoes hatching from eggs. This accounts for the continued presence of the RVF virus in enzootic foci and provides the virus with a sustainable mechanism of existence as the eggs of these mosquitoes can survive for several years in dry conditions. During periods of heavy rainfall, larval habitats frequently become flooded enabling the eggs to hatch and the mosquito population to rapidly increase, spreading the virus to the animals on which they feed.

*There is also a potential for epizootics and associated human epidemics to spread to areas that were previously unaffected. This has occurred when infected animals have introduced the virus into areas where vectors were present and is a particular concern. When uninfected Aedes and other species of mosquitoes feed on infected animals, a small outbreak can quickly be amplified through the transmission of the virus to other animals on which they subsequently feed.

PREVENTION AND CONTROL
Controlling RVF in animals

*Outbreaks of RVF in animals can be prevented by a sustained programme of animal vaccination. Both modified live attenuated virus and inactivated virus vaccines have been developed for veterinary use. Only one dose of the live vaccine is required to provide long-term immunity but the vaccine that is currently in use may result in spontaneous abortion if given to pregnant animals. The inactivated virus vaccine does not have this side effect, but multiple doses are required in order to provide protection which may prove problematic in endemic areas.

*Animal immunization must be implemented prior to an outbreak if an epizootic is to be prevented. Once an outbreak has occurred animal vaccination should NOT be implemented because there is a high risk of intensifying the outbreak. During mass animal vaccination campaigns, animal health workers may, inadvertently, transmit the virus through the use of multi-dose vials and the re-use of needles and syringes. If some of the animals in the herd are already infected and viraemic (although not yet displaying obvious signs of illness), the virus will be transmitted among the herd, and the outbreak will be amplified.

*Restricting or banning the movement of livestock may be effective in slowing the expansion of the virus from infected to uninfected areas.

*As outbreaks of RVF in animals precede human cases, the establishment of an active animal health surveillance system to detect new cases is essential in providing early warning for veterinary and human public health authorities.

Public health education and risk reduction:

*During an outbreak of RVF, close contact with animals, particularly with their body fluids, either directly or via aerosols, has been identified as the most significant risk factor for RVF virus infection. In the absence of specific treatment and an effective human vaccine, raising awareness of the risk factors of RVF infection as well as the protective measures individuals can take to prevent mosquito bites, is the only way to reduce human infection and deaths.

Public health messages for risk reduction should focus on:

*reducing the risk of animal-to-human transmission as a result of unsafe animal husbandry and slaughtering practices. Gloves and other appropriate protective clothing should be worn and care taken when handling sick animals or their tissues or when slaughtering animals.
*reducing the risk of animal-to-human transmission arising from the unsafe consumption of fresh blood, raw milk or animal tissue. In the epizootic regions, all animal products (blood, meat and milk) should be thoroughly cooked before eating.

*the importance of personal and community protection against mosquito bites through the use of impregnated mosquito nets, personal insect repellent if available, by wearing light coloured clothing (long-sleeved shirts and trousers) and by avoiding outdoor activity at peak biting times of the vector species.
Infection control in health care settings
*Although no human-to-human transmission of RVF has been demonstrated, there is still a theoretical risk of transmission of the virus from infected patients to healthcare workers through contact with infected blood or tissues. Healthcare workers caring for patients with suspected or confirmed RVF should implement Standard Precautions when handling specimens from patients.

*Standard Precautions define the work practices that are required to ensure a basic level of infection control. Standard Precautions are recommended in the care and treatment of all patients regardless of their perceived or confirmed infectious status. They cover the handling of blood (including dried blood), all other body fluids, secretions and excretions (excluding sweat), regardless of whether they contain visible blood, and contact with non-intact skin and mucous membranes. A WHO Aide–memoire on Standard Precautions in health care is available at: http://www.who.int/csr/resources/publications/standardprecautions/en/index.html

*As noted above, laboratory workers are also at risk. Samples taken from suspected human and animal cases of RVF for diagnosis should be handled by trained staff and processed in suitably equipped laboratories.

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Vector control
*Other ways in which to control the spread of RVF involve control of the vector and protection against their bites.
*Larviciding measures at mosquito breeding sites are the most effective form of vector control if breeding sites can be clearly identified and are limited in size and extent. During periods of flooding, however, the number and extent of breeding sites is usually too high for larviciding measures to be feasible.

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RVF FORESCASTING AND CLIMATIC MODELS
Forecasting can predict climatic conditions that are frequently associated with an increased risk of outbreaks, and may improve disease control. In Africa, Saudi Arabia and Yemen RVF outbreaks are closely associated with periods of above-average rainfall. The response of vegetation to increased levels of rainfall can be easily measured and monitored by Remote Sensing Satellite Imagery. In addition RVF outbreaks in East Africa are closely associated with the heavy rainfall that occurs during the warm phase of the El Niño/Southern Oscillation (ENSO) phenomenon.

These findings have enabled the successful development of forecasting models and early warning systems for RVF using satellite images and weather/climate forecasting data. Early warning systems, such as these, could be used to detect animal cases at an early stage of an outbreak enabling authorities to implement measures to avert impending epidemics.

Within the framework of the new International Health Regulations (2005), the forecasting and early detection of RVF outbreaks, together with a comprehensive assessment of the risk of diffusion to new areas, are essential to enable effective and timely control measures to be implemented.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
http://en.wikipedia.org/wiki/Rift_Valley_fever
http://www.who.int/mediacentre/factsheets/fs207/en/

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Avoid Flu Shots With the One Vitamin that Will Stop Flu in Its Tracks

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Another influenza season is beginning, and the U.S. Center for Disease Control and Prevention (CDC) will strongly urge Americans to get a flu shot. In fact, the CDC mounts a well-orchestrated campaign each season to generate interest and demand for flu shots.

But a recent study published in the October issue of the Archives of Pediatric & Adolescent Medicine found that vaccinating young children against the flu appeared to have no impact on flu-related hospitalizations or doctor visits during two recent flu seasons.

At first glance, the data did suggest that children between the ages of 6 months and 5 years derived some protection from vaccination in these years. But after adjusting for potentially relevant variables, the researchers concluded that “significant influenza vaccine effectiveness could not be demonstrated for any season, age, or setting” examined.

Additionally, a Group Health study found that flu shots do not protect elderly people against developing pneumonia — the primary cause of death resulting as a complication of the flu. Others have questioned whether there is any mortality benefit with influenza vaccination. Vaccination coverage among the elderly increased from 15 percent in 1980 to 65 percent now, but there has been no decrease in deaths from influenza or pneumonia.

There is some evidence that flu shots cause Alzheimer’s disease, most likely as a result of combining mercury with aluminum and formaldehyde. Mercury in vaccines has also been implicated as a cause of autism.

Three other serious adverse reactions to the flu vaccine are joint inflammation and arthritis, anaphylactic shock (and other life-threatening allergic reactions), and Guillain-Barré syndrome, a paralytic autoimmune disease.

One credible hypothesis that explains the seasonal nature of flu is that influenza is a vitamin D deficiency disease.

Vitamin D levels in your blood fall to their lowest point during flu seasons. Unable to be protected by the body’s own antibiotics (antimicrobial peptides) that are released by vitamin D, a person with a low vitamin D blood level is more vulnerable to contracting colds, influenza, and other respiratory infections.

Studies show that children with rickets, a vitamin D-deficient skeletal disorder, suffer from frequent respiratory infections, and children exposed to sunlight are less likely to get a cold. The increased number of deaths that occur in winter, largely from pneumonia and cardiovascular diseases, are most likely due to vitamin D deficiency.

Unfortunately, now, for the first time, flu vaccination is also being pushed for virtually all children — not just those under 5.

This is a huge change. Previously, flu vaccine was recommended only for youngsters under 5, who can become dangerously ill from influenza. This year, the government is recommending that children from age 6 months to 18 years be vaccinated, expanding inoculations to 30 million more school-age children.

The government argues that while older children seldom get as sick as the younger ones, it’s a bigger population that catches flu at higher rates, so the change should cut missed school, and parents’ missed work when they catch the illness from their children.

Of course, this policy ignores the fact that a systematic review of 51 studies involving 260,000 children age 6 to 23 months found no evidence that the flu vaccine is any more effective than a placebo.

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Rubella (German Measles)

Transmission electron micrograph of rubella virus.

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Definition:
Rubella — commonly known as German measles or 3-day measles — is an infection that primarily affects the skin and lymph nodes. It is caused by the rubella virus (not the same virus that causes measles), which is usually transmitted by droplets from the nose or throat that others breathe in. It can also pass through a pregnant woman‘s bloodstream to infect her unborn child. As this is a generally mild disease in children, the primary medical danger of rubella is the infection of pregnant women, which may cause congenital rubella syndrome in developing babies.

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It is a disease caused by Rubella virus. The name 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 five 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.

Rubella is a common childhood infection usually with minimal systemic upset although transient arthropathy may occur in adults. Serious complications are very rare. If it were not for the effects of transplacental infection on the developing foetus, 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, faeces 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.

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

Before a vaccine against rubella became available in 1969, rubella epidemics occurred every 6 to 9 years. Kids ages 5 to 9 were primarily affected, and many cases of congenital rubella occurred as well. Now, due to immunization of children, there are much fewer cases of rubella and congenital rubella.

Most rubella infections today appear in young, non-immunized adults rather than children. In fact, experts estimate that 10% of young adults are currently susceptible to rubella, which could pose a danger to any children they might have someday.

Signs and Symptoms:

After an incubation period of 14-21 days, 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. Other symptoms include low grade fever, swollen glands (post cervical lymphadenopathy), joint pains, headache, conjunctivitis. 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 disappears after a few days with no staining or peeling of the skin. 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 one-third 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 carrier is contagious but may show no symptoms.

The rubella rash can look like many other viral rashes. It appears as either pink or light red spots, which may merge to form evenly colored patches. The rash can itch and lasts up to 3 days. As the rash clears, the affected skin occasionally sheds in very fine flakes.

Other symptoms of rubella, which are more common in teens and adults, may include: headache; loss of appetite; mild conjunctivitis (inflammation of the lining of the eyelids and eyeballs); a stuffy or runny nose; swollen lymph nodes in other parts of the body; and pain and swelling in the joints (especially in young women). Many people with rubella have few or no symptoms at all.

When rubella occurs in a pregnant woman, it may cause congenital rubella syndrome, with potentially devastating consequences for the developing fetus. Children who are infected with rubella before birth are at risk for growth retardation; mental retardation; malformations of the heart and eyes; deafness; and liver, spleen, and bone marrow problems.

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. 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.

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

The cause of rubella is a virus that’s passed from person to person. It can spread when an infected person coughs or sneezes, or it can spread by direct contact with an infected person’s respiratory secretions, such as mucus. It can also be transmitted from a pregnant woman to her unborn child. A person with rubella is contagious from one week before the onset of the rash until about one to two weeks after the rash disappears.

Rubella is rare in the United States because most children receive a vaccination against the infection at an early age. However, cases of rubella do occur, mostly in unvaccinated foreign-born adults.

The disease is still common in many parts of the world, although more than half of all countries now use a rubella vaccine. The prevalence of rubella in some other countries is something to consider before going abroad, especially if you’re pregnant.

Contagiousness:
The rubella virus passes from person to person through tiny drops of fluid from the nose and throat. People who have rubella are most contagious from 1 week before to 1 week after the rash appears. Someone who is infected but has no symptoms can still spread the virus.

Infants who have congenital rubella syndrome can shed the virus in urine and fluid from the nose and throat for a year or more and may pass the virus to people who have not been immunized.

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. The presence of these antibodies along with, or a short time after, the characteristic rash confirms the diagnosis.

Complications:
Rubella is a mild infection. Once you’ve had the disease, you’re usually permanently immune. About 70 percent of adult women with rubella experience arthritis in the fingers, wrists and knees, which generally lasts for about one month. In rare cases, rubella can cause an ear infection (otitis media) or inflammation of the brain (encephalitis).

However, if you’re pregnant when you contract rubella, the consequences for your unborn child may be severe. Up to 85 percent of infants born to mothers who had rubella during the first 11 weeks of pregnancy develop congenital rubella syndrome. This can cause one or more problems, including growth retardation, cataracts, deafness, congenital heart defects and defects in other organs. The highest risk to the fetus is during the first trimester, but exposure later in pregnancy also is dangerous.

Fortunately, an average of fewer than 10 babies are born with congenital rubella syndrome in the United States each year. Rubella occurs most frequently in adults who never received vaccinations because they came from other countries where the MMR vaccine isn’t widely used.

Modern Treatment:
Rubella cannot be treated with antibiotics because antibiotics do not work against viral infections. Unless there are complications, rubella will resolve on its own.

Any pregnant woman who has been exposed to rubella should contact her obstetrician immediately.
Symptoms are usually treated with paracetamol until the disease has run its course. Treatment of newly born babies is focused on management of the complications. Congenital heart defects and cataracts can be corrected by surgery. 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.

Home Treatment:
Rubella is typically a mild illness, especially in kids. Infected children usually can be cared for at home. Monitor your child’s temperature, and call the doctor if the fever climbs too high.

To relieve minor discomfort, you can give your child acetaminophen or ibuprofen. Avoid giving aspirin to a child who has a viral illness because its use in such cases has been associated with the development of Reye syndrome, which can lead to liver failure and death.

Prognosis:
Rubella infection of children and adults is usually mild, self-limiting and often asymptomatic. The prognosis in children born with CRS is poor.

Self-care:
In rare instances when a child or adult is infected with rubella, simple self-care measures are required:

* Rest in bed as necessary.
* Take acetaminophen (Tylenol, others) to relieve discomfort from fever and aches.
* Tell friends, family and co-workers — especially pregnant women — about your diagnosis if they may have been exposed to the disease.

Don’t give aspirin to children who have a viral illness. Aspirin in children has been associated with Reye’s syndrome — a rare, but serious illness that can affect the blood, liver and brain of children and teenagers after a viral infection

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. Since the introduction of vaccine, occurrences have become rare in those countries with high uptake rates. However, 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.

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. Universal immunisation producing a high level of herd immunity is important in the control of epidemics of rubella.

Prevention:
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 given as part of the MMR(measles-mumps-rubella ) 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.

The immunization program has been quite successful with Cuba declaring the disease eliminated in the 1990s. 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.


History:

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

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”. 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.

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

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. Gregg published an account, Congenital Cataract Following German Measles in the Mother, in 1941. He described a variety of problems now know 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.

There was a pandemic of rubella between 1962 and 1965, starting in Europe and spreading to the United States. 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

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

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose

Resources:
http://en.wikipedia.org/wiki/Rubella
http://kidshealth.org/parent/infections/skin/german_measles.html
http://www.mayoclinic.com/health/rubella/DS00332/DSECTION=1

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Hope Over High Blood Pressure Jab

A four-monthly jab may one day replace the need to regularly take pills to control blood pressure, scientists say.

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High blood pressure is a risk factor for heart disease

A team from the Swiss biotechnology firm Cytos found the vaccine against a hormone in the blood significantly cut blood pressure, the Lancet reported.

The jab was tested on 72 patients with high blood pressure and it was found to work without serious side-effects.

The researchers and independent experts said the findings were promising but large-scale trials were now needed.

High blood pressure, which affects a quarter of all adults, doubles the risk of dying from heart disease or stroke and is blamed for 60,000 deaths a year in UK.

Those who are being treated for it often have to take a daily course of pills to keep it under control.

But many people do not keep to their treatment regimes as people with high blood pressure do not display symptoms.

The researchers believe the vaccine, which works against the hormone angiotensin, which causes blood vessels to constrict and increase blood pressure, may offer a simple alternative.

They tested two different doses of the vaccine – 300 microgrammes and 100 microgrammes – as well as a dummy vaccine during the 14-week trial.

Resistance

The jabs were given at the start, and after four weeks and 12 weeks – enough to give a patient four-month resistance.

Neither dose significantly lowered blood pressure at night.

But during the day the larger dose significantly lowered blood pressure, especially during the late morning peak when blood pressure is known to increase.

And, importantly, the vaccine did not have any serious side-effects with the worst being mild flu-like symptoms.

Lead researcher Dr Martin Bachmann said the vaccine could offer a much more simple way of controlling blood pressure and could be administered during regular visits to the doctor.

“Such a regimen is likely to promote adherence to treatment, but will need to be supported by clinical data.”

Professor Jeremy Pearson, of the British Heart Foundation, agreed more research was needed, but described the results as promising.

“Immunisation may be of particular benefit to people who find it difficult to stick to high blood pressure medication, but there is still a long way to go before this approach replaces the highly-effective current treatments.

“Looking after your heart through regular exercise, cutting down on salt, and only drinking in moderation remain the best ways in which we can prevent high blood pressure.”

Other firms are also known to be testing blood pressure vaccines.

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Anger Slows Down Healing Process

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The adage that laughter is the best medicine has been backed by an unusual investigation which says that people who seethe with anger take longer to recover from injury.

Previous studies have linked ill tempered behaviour, whether brow-beating or road rage, with higher incidence of coronary heart disease, hypertension and stroke, especially among men.

But the new study, published on Wednesday in the British journal Brain, Behaviour, Immunity, is the first controlled experiment that directly measures the impact of ire on the healing process.

Researchers at the University of Ohio inflicted minor burns on the forearms of 98 volunteers who were then monitored over eight days to see how quickly the skin repaired itself.

The subjects had each taken a battery of psychological tests beforehand to assess how easily and often they felt and expressed wrath, and were then ranked on an “anger scale”.

Persons who took certain pharmaceutical drugs, smoked cigarettes or drank excessive quantities of caffeine-laden coffee were excluded, along with individuals who were extremely over- or under-weight.

The results were startlingly clear: individuals who had trouble controlling expressions of anger were four times likelier to need more than four days for their wounds to heal, compared with counterparts who could master their anger.

But the researchers were also surprised to find that anger has its nuances, too.

Subjects described as showing “anger out” (regular outbursts of aggression or hostility) or “anger in” (repressed rage) healed almost as quickly as individuals who ranked low on all anger scales.

Only those who tried but failed to hold in their feelings of upset and distemper took longer to heal.

This same group also showed a higher secretion of the stress hormone cortisol, which could at least partly explain the difference in healing time, the study noted.

Earlier research has shown a clear link between cortisol and anger. Hostile men who yelled at spouses during marital spats secreted more of the endocrine modulator within minutes, as did teachers experiencing high levels of stress in the classroom.

High levels of cortisol appears to decrease the production at the point of injury of two cytokines crucial to the repair process, suggests the study.

Cytokines are proteins released by immune-system cells. They act as signallers to generate a wider immune response. “The ability to regulate the expression of one’s anger has a clinically relevant impact on wound healing,” concludes lead author Jean-Philippe Gouin, a psychologist at the University of Ohio. “Those who has low anger control secreted more cortisol following exposition to this stressor. This individual difference in the response to the blistering was related to longer healing,” Gouin added.

Anger-control therapy could help patients recovering from surgery or injury heal more quickly, the paper says.

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Laughter, the best medicine

Laugh loudly and get rid of many illness

Sources: The Times Of India

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