Categories
Ailmemts & Remedies

SARS (Severe acute respiratory syndrome)

Description:
SARS, or Severe acute respiratory syndrome, is the disease caused by SARS coronavirus. It causes an often severe illness marked initially by systemic symptoms of muscle pain, headache, and fever, followed in 2–10 days by the onset of respiratory symptoms,[3] mainly cough, dyspnea, and pneumonia. Another common finding in SARS patients is a decrease in the number of lymphocytes circulating in the blood.

You may click to see the picture: ....(01 )   (1)…….(2)

Virus classification:-

Group: Group IV ((+)ssRNA)

Order: Nidovirales

Family: Coronaviridae

Genus: Coronavirus

Species: SARS coronavirus

SARS coronavirus is a positive and single stranded RNA virus belonging to a family of enveloped coronaviruses. Its genome is about 29.7kb, which is one of the largest among RNA viruses. The SARS virus has 13 known genes and 14 known proteins. There are 265bp in the 5’UTR and 342bp in the 3’UTR. SARS is similar to other coronaviruses in that its genome expression starts with translation of two large ORFs 1a and 1b, which are two polyproteins.

The functions of several of these proteins are known:  ORFs 1a and 1b encode the replicase and there are four major structural proteins: nucleocapsid, spike, membrane and envelope. It also encodes for eight unique proteins, known as the accessory proteins, with no known homologues. The function of these accessory proteins remains unknown.
In the SARS outbreak of 2003, about 9% of patients with confirmed SARS infection died. The mortality rate was much higher for those over 50 years old, with mortality rates approaching 50% for this subset of patients.

Coronaviruses usually express pp1a (the ORF1a polyprotein) and the PP1ab polyprotein with joins ORF1a and ORF1b. The polyproteins are then processed by enzymes that are encoded by ORF1a. Product proteins from the processing includes various replicative enzymes such as RNA dependent polymerase, RNA helicase, and proteinase. The replication complex in coronavirus is also responsible for the synthesis of various mRNAs downstream of ORF 1b, which are structural and accessory proteins. Two different proteins, 3CLpro and PL2pro, cleave the large polyproteins into 16 smaller subunits.

SARS-Coronavirus follows the replication strategy typical of the Coronavirus genus.

In the SARS outbreak of 2003, about 9% of patients with confirmed SARS infection died. The mortality rate was much higher for those over 50 years old, with mortality rates approaching 50% for this subset of patients.

Causes:
SARS is caused by a strain of coronavirus, the same family of viruses that causes the common cold. Until now, these viruses have never been particularly dangerous in humans, although they can cause severe disease in animals. For that reason, scientists originally thought that the SARS virus might have crossed from animals to humans. It now seems likely that it evolved from one or more animal viruses into a completely new strain.
 
How do SARS spread:
Most respiratory illnesses, including SARS, spread through droplets that enter the air when someone with the disease coughs, sneezes or talks. Most experts think SARS spreads mainly through face-to-face contact, but the virus also may be spread on contaminated objects — such as doorknobs, telephones and elevator buttons.

Symptoms:
Once a person has contracted SARS, the first symptom that they present with is a fever of at least 38°C (100.4°F) or higher. The early symptoms last about 2–7 days and include non-specific flu-like symptoms, including chills/rigor, muscle aches, headaches, diarrhea, sore throat, runny nose, malaise, and myalgia (muscle pain). Next, they develop a dry cough, shortness of breath, and an upper respiratory tract infection.

SARS typically begins with flu-like signs and symptoms — signs and symptoms include:

*Fever of 100.4 F (38 C) or higher
* Dry cough
*Shortness of breath

Complications:
The main complication of SERS  is that most people develop pneumonia. Breathing problems can become so severe that a mechanical respirator is required. SARS is fatal in some cases, often due to respiratory failure. Other possible complications include heart and liver failure.

People older than the age of 60 — especially those with underlying conditions such as diabetes or hepatitis — are at highest risk of serious complications.

Risk Factors:
In general, people at greatest risk of SARS have had direct, close contact with someone who’s infected, such as family members and health care workers.

Diagnosis:
At that time, a chest x-ray is ordered to confirm pneumonia. If the chest appears clear and SARS is still suspected, a HRCT scan will be ordered, because it is visible earlier on this scan. In severe cases, it develops into respiratory failure and acute respiratory distress syndrome (ARDS), and in 70-90% of the cases, they develop lymphopenia (low count of lymphocyte white blood cells).

The incubation period for SARS-CoV is from 2–10 days, sometimes lasting up to 13 days, with a mean of 5 days.  So symptoms usually develop between 2–10 days following infection by the virus. As part of the immune response, IgM antibody to the SARS-CoV is produced. This peaks during the acute or early convalescent phase (week 3) and declines by week 12. IgG antibody is produced later and peaks at week 12.

Tests:
When SARS first surfaced, no specific tests were available to help doctors diagnose the disease. Now several laboratory tests can help detect the virus. But no known transmission of SARS has occurred anywhere in the world since 2004.

Treatment:
Although global efforts are still on, scientists have not yet found out any effective treatment for SARS. Antibiotic drugs don’t work against viruses and antiviral drugs haven’t shown much benefit.

Prevention:
Researchers are working on several types of vaccines for SARS, but none has been tested in humans.Engineering of SARS virus has been done. In a paper published in 2006, a new transcription circuit was engineered to make recombinant SARS viruses. The recombination allowed for efficient expression of viral transcripts and proteins. The engineering of this transcription circuit reduces the RNA recombinant progeny viruses. The TRS (transcription regulatory sequences) circuit regulates efficient expression of SARS-CoV subgenomic mRNAs. The wild type TRS is ACGAAC.

A double mutation results in TRS-1 (ACGGAT) and a triple mutation results in TRS-2 (CCGGAT). When the remodeled TRS circuit containing viruses are genetically recombined with wild type TRS circuits, the result is a circuit reduced in production of subgenomic mRNA. The goal of modifying the SARS virus with this approach is to produce chimeric progeny that have reduced viability due to the incompatibility of the WT and engineered TRS circuits.

Novel subunit vaccine constructs for an S protein SARS vaccine based on the receptor binding domain (RBD) are being developed by the New York Blood Center. The re-emergence of SARS is possible, and the need remains for commercial vaccine and therapeutic development. However, the cost and length of time for product development, and the uncertain future demand, result in unfavorable economic conditions to accomplish this task. In the development of therapeutics and next-generation vaccines, more work is required to determine the structure/ function relationships of critical enzymes and structural proteins.

If SARS infections resume, follow these safety guidelines if you’re caring for an infected person:

 *Wash your hands. Clean your hands frequently with soap and hot water or use an alcohol-based hand rub containing at least 60 percent alcohol.

* Wear disposable gloves. If you have contact with the person’s body fluids or feces, wear disposable gloves. Throw the gloves away immediately after use and wash your hands thoroughly.

* Wear a surgical mask. When you’re in the same room as a person with SARS, cover your mouth and nose with a surgical mask. Wearing eye glasses also may offer some protection.

* Wash personal items. Use soap and hot water to wash the utensils, towels, bedding and clothing of someone with SARS.

* Disinfect surfaces. Use a household disinfectant to clean any surfaces that may have been contaminated with sweat, saliva, mucus, vomit, stool or urine. Wear disposable gloves while you clean and throw the gloves away when you’re done.

Follow all precautions for at least 10 days after the person’s signs and symptoms have disappeared. Keep children home from school if they develop a fever or respiratory symptoms within 10 days of being exposed to someone with SARS. Children can return to school if signs and symptoms go away after three days.

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/SARS_coronavirus
http://www.mayoclinic.com/health/sars/DS00501/DSECTION=prevention

Categories
Health Alert

HEALTH ALERT

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SOME CAUSES OF BRAIN DAMAGE…………………

_CLICK & SEE THE PICTURES

1.           No Breakfast  People who do not take breakfast are going to have a lower blood sugar level. This leads to an insufficient supply of nutrients to the brain causing brain degeneration.

      
2.           Overeating:   It causes hardening of the brain arteries, leading to a decrease in mental power.

3.           Smoking :   It causes multiple brain shrinkage and may lead to Alzheimer disease.

4.           High Sugar consumption:   Too much sugar will interrupt the absorption of proteins and nutrients causing malnutrition and may interfere with brain development.

5.           Air Pollution  The brain is the largest oxygen consumer in our 20 body. Inhaling polluted air decreases the supply of oxygen to the brain, bringing about a decrease in brain efficiency.

6.           Sleep Deprivation :   Sleep allows our brain to rest… Long term deprivation from sleep will accelerate the death of brain cells…

7.           Head covered while sleeping :   Sleeping with the head covered increases the concentration of carbon dioxide and decrease concentration of oxygen that may lead to brain damaging effects.

8.           Working your brain during illness :   Working hard or studying with sickness may lead to a decrease in effectiveness of the brain as well as damage the brain.

9.           Lacking in stimulating thoughts:   Thinking is the best way to train our brain, lacking in brain stimulation thoughts may cause brain shrinkage.

10.       Talking Rarely :   Intellectual conversations will promote the efficiency of the brain.

 

SOME CAUSES OF LIVER DAMAGE

1.           Sleeping too late and waking up too late are main cause.
   
2.           Not urinating in the morning.
   
3.           Too much eating.
   
4.           Skipping breakfast.
   
5.           Consuming too much medication.
   
6.           Consuming too much preservatives, additives, food colouring, and artificial sweetener.
 
7.           Consuming unhealthycooking oil. As much as possible reduce cooking oil when frying, which includes even the best cooking oils like olive oil. Do not consume fried foods when you are tired, except if the body is very fit.

8.           Consuming raw (overly done) foods also add to the burden of liver. Veggies should be eaten raw or cooked 3-5 parts. Fried veggies should be finished in one sitting, do not store.

We should prevent this without necessarily spending more. We just have to adopt a good daily lifestyle and eating habits. Maintaining good eating habits and time condition are very important for our bodies to absorb and get rid of unnecessary chemicals according to ‘schedule.’

TOP FIVE CANCER CAUSING FOODS:

1.     Hot Dogs……...CLICK & SEE

Because they are high in nitrates, the Cancer Prevention Coalition advises that children eat no more than 12 hot dogs a month. If you can’t live without hot dogs, buy those made withoutsodium nitrate.

2.     Processed meats and Bacon…...CLICK & SEE

Also high in the same sodium nitrates found inhot dogs, bacon, and other processed meats raise the risk of heart disease. The saturated fat in bacon also contributes to cancer.

3.     Doughnuts…….CLICK & SEE
.

Doughnuts are cancer-causing double trouble. First, they are made with white flour, sugar, andhydrogenated oils, then fried at high temperatures. Doughnuts may be the worst food you can possibly eat to raise your risk of cancer.

4.     French fries…...CLICK & SEE

Like doughnuts, French fries are made withhydrogenated oils and then fried at high temperatures. They also contain cancer- causing acryl amides which occur during the frying process. They should be called cancer fries, not French fries.

5.     Chips, crackers, and cookies……..CLICK & SEE


All are usually made with white flour and sugar. Even the ones whose labels claim to be free of trans-fats generally contain small amounts of trans-fats.

Categories
Herbs & Plants

Cynanchum glaucescens

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Botanical Name :Cynanchum glaucescens
Family: Asclepiadaceae

Common Name ;

Habitat : Cynanchum glaucescens is native to  E. Asia – China. It grows in  Mountains, riversides; 100-800. Fujian, Guangdong, Guangxi, Hunan, Jiangsu, Jiangxi, Sichuan, Zhejiang

Description:
Cynanchum glaucescens is a perennial Climber growing to 0.6m.
It is hardy to zone 0. It is in flower from June to October, and the seeds ripen from July to October. The flowers are hermaphrodite (have both male and female organs)
YOU MAY CLICK TO SEE THE PICTURES

The Herbs is rhizomatous, roots fibrous, fascicled at nodes. Stems erect, to 60 cm, pubescent along 2 lines. Leaves opposite, subsessile; leaf blade glabrous, elliptic, oblong-lanceolate, or oblong, 1-7 cm × 7-12 mm, base cuneate or rounded, apex rounded to ± acute; lateral veins 3-5 pairs, obscure. Inflorescences umbel-like, sometimes with 2 cymules separated by a short rachis, shorter than leaves, glabrous or puberulent. Sepals oblong-lanceolate, ca. 2.3 × 1 mm, glabrous, basal glands 5. Corolla yellow, rotate, ca. 8 mm in diam.; lobes ovate-oblong, ca. 3.5 × 2.3 mm, obtuse. Corona shallowly cupular, 5-lobed; lobes ovate, fleshy, incurved, slightly shorter than anthers and adnate to them. Pollinia ovoid. Stigma head convex. Follicles fusiform, 4.5-6 cm × 6-10 mm. Seeds oblong, ca. 5 mm; coma ca. 2 cm. Fl. May-Nov, fr. Jul-Dec.
The plant prefers light (sandy), medium (loamy) and heavy (clay) soils. The plant prefers acid, neutral and basic (alkaline) soils. It can grow in semi-shade (light woodland) or no shade. It requires moist soil.

Cultivation:
We have very little information on this species and do not know if it will be hardy in Britain, though judging by its native range it could succeed outdoors in many parts of this country. It probably does not have any special cultivation requirements and will probably succeed in most soils in a sunny position.

Propagation:
Seed – sow spring in the greenhouse. When they are large enough to handle, prick the seedlings out into individual pots and grow them on in the greenhouse for at least their first winter. Plant them out into their permanent positions in late spring or early summer, after the last expected frosts. Division in spring.

Medicinal Uses:

Antitussive; Expectorant.

The fragrant root is used in Chinese medicine.  The roots and stems are used to treat coughs, pneumonia, uneasy breathing, and lung diseases.  They are also used in the treatment of asthma with profuse sputum, coughs etc.

The dried root and stem are antitussive and expectorant. They are used in the treatment of asthma with profuse sputum, coughs etc.

Known Hazards:There are some reports of toxins in this genus

Disclaimer : The information presented herein is intended for educational purposes only. Individual results may vary, and before using any supplements, it is always advisable to consult with your own health care provider

Resources:
http://digedibles.com/database/plants.php?Cynanchum+glaucescens
http://www.herbnet.com/Herb%20Uses_C.htm
http://www.showyourplant.com/Cynanchum_glaucescens/

http://www.efloras.org/florataxon.aspx?flora_id=2&taxon_id=200018553

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Categories
Ailmemts & Remedies

Severe Acute Respiratory Syndrome (SARS)

Definition::
Severe acute respiratory syndrome  is a respiratory disease in humans which is caused by the SARS coronavirus (SARS-CoV). There was one near pandemic, between the months of November 2002 and July 2003, with 8,422 known infected cases and 916 confirmed human deaths (a case-fatality rate of 10.9%) worldwide being listed in the World Health Organization’s (WHO) 21 April 2004 concluding report. Within a matter of weeks in early 2003, SARS spread from Hong Kong to rapidly infect individuals in some 37 countries around the world.

CLICK & SEE THE PICTURES

As of today, the spread of SARS has been fully contained, with the last infected human case seen in June 2003 (disregarding a laboratory induced infection case in 2004). However, SARS is not claimed to have been eradicated (unlike smallpox), as it may still be present in its natural host reservoirs (animal populations) and may potentially return into the human population in the future.

Mortality by age group as of 8 May 2003 is below 1% for people aged 24 or younger, 6% for those 25 to 44, 15% in those 45 to 64 and more than 50% for those over 65. For comparison, the case fatality rate for influenza is usually around 0.6% (primarily among the elderly) but can rise as high as 33% in locally severe epidemics of new strains. The mortality rate of the primary viral pneumonia form is about 70%.

Symptoms:
The main symptoms of SARS are:

•High fever (above 38°C)
•Dry cough
•Breathing difficulties
*Other breathing symptoms
•Headache
•Muscular aches and stiffness
•Loss of appetite
•Malaise or tiredness
•Confusion
•Rash

The most common symptoms are:
*Chills and shaking
*Cough — usually starts 2-3 days after other symptoms
*Fever
*Headache
*Muscle aches

Less common symptoms include:
*Cough that produces phlegm (sputum)
*Diarrhea
*Dizziness
*Nausea and vomiting
*Runny nose
*Sore throat

These symptoms are typical of many severe respiratory infections. There have only ever been a few cases of SARS reported in the UK, so if you’ve similar symptoms, it’s far more likely to be a more typical form of pneumonia. Even if you’ve recently returned from south-east Asia, there’s little risk that you have SARS as the virus has been contained.

Causes:
Coronaviruses are positive-strand, enveloped RNA viruses that are important pathogens of mammals and birds. This group of viruses cause enteric or respiratory tract infections in a variety of animals including humans, livestock and pets.

CLICK & SEE

Initial electron microscopic examination in Hong Kong and Germany found viral particles with structures suggesting paramyxovirus in respiratory secretions of SARS patients. Subsequently, in Canada, electron microscopic examination found viral particles with structures suggestive of metapneumovirus (a subtype of paramyxovirus) in respiratory secretions. Chinese researchers also reported that a Chlamydophila-like disease may be behind SARS. The Pasteur Institute in Paris identified coronavirus in samples taken from six patients, so did the laboratory of Malik Peiris at the University of Hong Kong, which in fact was the first to announce (on 21 March 2003) the discovery of a new coronavirus as the possible cause of SARS after successfully cultivating it from tissue samples and was also amongst the first to develop a test for the presence of the virus. The CDC noted viral particles in affected tissue (finding a virus in tissue rather than secretions suggests that it is actually pathogenic rather than an incidental finding). Upon electron microscopy, these tissue viral inclusions resembled coronaviruses, and comparison of viral genetic material obtained by PCR with existing genetic libraries suggested that the virus was a previously unrecognized coronavirus. Sequencing of the virus genome — which computers at the British Columbia Cancer Agency in Vancouver completed at 4 a.m. Saturday, 12 April 2003 — was the first step toward developing a diagnostic test for the virus, and possibly a vaccine. A test was developed for antibodies to the virus, and it was found that patients did indeed develop such antibodies over the course of the disease, which is highly suggestive of a causative role.

On 16 April 2003, the WHO issued a press release stating that a coronavirus identified by a number of laboratories was the official cause of SARS. Scientists at Erasmus University in Rotterdam, the Netherlands demonstrated that the SARS coronavirus fulfilled Koch’s postulates thereby confirming it as the causative agent. In the experiments, macaques infected with the virus developed the same symptoms as human SARS victims.

An article published in The Lancet identifies a coronavirus as the probable causative agent.

In late May 2003, studies from samples of wild animals sold as food in the local market in Guangdong, China found that the SARS coronavirus could be isolated from palm civets (Paguma sp.), but the animals did not always show clinical signs. The preliminary conclusion was that the SARS virus crossed the xenographic barrier from palm civet to humans, and more than 10,000 masked palm civets were destroyed in Guangdong Province. Virus was also later found in raccoon dogs (Nyctereuteus sp.), ferret badgers (Melogale spp.) and domestic cats. In 2005, two studies identified a number of SARS-like coronaviruses in Chinese bats. Phylogenetic analysis of these viruses indicated a high probability that SARS coronavirus originated in bats and spread to humans either directly, or through animals held in Chinese markets. The bats did not show any visible signs of disease, but are the likely natural reservoirs of SARS-like coronaviruses. In late 2006, scientists from the Chinese Centre for Disease Control and Prevention of Hong Kong University and the Guangzhou Centre for Disease Control and Prevention established a genetic link between the SARS coronavirus appearing in civet cats and humans, bearing out claims that the disease had jumped across species

Viral replication:
Coronavirus (CoV) genome replication takes place in the cytoplasm in a membrane-protected microenvironment and starts with the translation of the genome to produce the viral replicase. CoV transcription involves a discontinuous RNA synthesis (template switch) during the extension of a negative copy of the subgenomic mRNAs. The requirement for base pairing during transcription has been formally demonstrated in arteriviruses and CoVs. The CoV N protein is required for coronavirus RNA synthesis and has RNA chaperon activity that may be involved in template switch. Both viral and cellular proteins are required for replication and transcription. CoVs initiate translation by cap-dependent and cap-independent mechanisms. Cell macromolecular synthesis may be controlled after CoV infection by locating some virus proteins in the host cell nucleus. Infection by different coronaviruses cause in the host alteration in the transcription and translation patterns, in the cell cycle, the cytoskeleton, apoptosis and coagulation pathways, inflammation and immune and stress responses. The balance between genes up- and down-regulated could explain the pathogenesis caused by these viruses. Coronavirus expression systems based on single genome constructed by targeted recombination, or by using infectious cDNAs, have been developed. The possibility of expressing different genes under the control of transcription regulating sequences (TRSs) with programmable strength and engineering tissue and species tropism indicates that CoV vectors are flexible. CoV based vectors have emerged with high potential vaccine development and possibly for gene therapy

Possible Complications:
*Respiratory failure
*Liver failure
*Heart failure
.
Diagnosis:
SARS may be suspected in a patient who has:

1.Any of the symptoms, including a fever of 38 °C (100.4 °F) or higher, and
2.Either a history of:
…..1.Contact (sexual or casual) with someone with a diagnosis of SARS within the last 10 days OR
…..2.Travel to any of the regions identified by the WHO as areas with recent local transmission of SARS (affected regions as of 10 May 2003[13] were parts of China, Hong Kong, Singapore and the province of Ontario, Canada).

A probable case of SARS has the above findings plus positive chest X-ray findings of atypical pneumonia or respiratory distress syndrome.

With the advent of diagnostic tests for the coronavirus probably responsible for SARS, the WHO has added the category of “laboratory confirmed SARS” for patients who would otherwise fit the above “probable” category who do not (yet) have the chest x-ray changes but do have positive laboratory diagnosis of SARS based on one of the approved tests (ELISA, immunofluorescence or PCR).

The chest X-ray (CXR) appearance of SARS is variable. There is no pathognomonic appearance of SARS but is commonly felt to be abnormal with patchy infiltrates in any part of the lungs. The initial CXR may be clear.

White blood cell and platelet counts are often low. Early reports indicated a tendency to relative neutrophilia and a relative lymphopenia — relative because the total number of white blood cells tends to be low. Other laboratory tests suggest raised lactate dehydrogenase and slightly raised creatine kinase and C-Reactive protein levels.

With the identification and sequencing of the RNA of the coronavirus responsible for SARS on 12 April 2003, several diagnostic test kits have been produced and are now being tested for their suitability for use.

Three possible diagnostic tests have emerged, each with drawbacks. The first, an ELISA (enzyme-linked immunosorbent assay) test detects antibodies to SARS reliably but only 21 days after the onset of symptoms. The second, an immunofluorescence assay, can detect antibodies 10 days after the onset of the disease but is a labour and time intensive test, requiring an immunofluorescence microscope and an experienced operator. The last test is a polymerase chain reaction (PCR) test that can detect genetic material of the SARS virus in specimens ranging from blood, sputum, tissue samples and stools. The PCR tests so far have proven to be very specific but not very sensitive. This means that while a positive PCR test result is strongly indicative that the patient is infected with SARS, a negative test result does not mean that the patient does not have SARS.

The WHO has issued guidelines for using these diagnostic tests.  There is currently no rapid screening test for SARS and research is ongoing.

Treatment:
Antibiotics are ineffective as SARS is a viral disease. Treatment of SARS so far has been largely supportive with antipyretics, supplemental oxygen and ventilatory support as needed.

Suspected cases of SARS must be isolated, preferably in negative pressure rooms, with complete barrier nursing precautions taken for any necessary contact with these patients.

There was initially anecdotal support for steroids and the antiviral drug ribavirin, but no published evidence has supported this therapy.

Researchers are currently testing all known antiviral treatments for other diseases including AIDS, hepatitis, influenza and others on the SARS-causing coronavirus.

There is some evidence that some of the more serious damage in SARS is due to the body’s own immune system overreacting to the virus – a cytokine storm. Research is continuing in this area.

In December 2004 it was reported that Chinese researchers had produced a SARS vaccine, it has been tested on a group of 36 volunteers, 24 of whom developed antibodies against the virus.

A 2006 systematic review of all the studies done on the 2003 SARS epidemic found no evidence that antivirals, steroids or other therapies helped patients. A few suggested they caused harm.

The clinical treatment of SARS has been relatively ineffective with most high risk patients requiring artificial ventilation. Currently, corticosteroids and Ribavirin are the most common drugs used for treatment of SARS (Wu et al., 2004). In vitro studies of Ribavirin have yielded little results at clinical, nontoxic concentrations. Better combinations of drugs that have yielded a more positive clinical outcome (when administered early) have included the use of Kaletra, Ribavirin and corticosteroids. The administration of corticosteroids, marketed as Prednisone, during viral infections has been controversial. Lymphopenia can also be a side effect of corticosteroids even further decreasing the immune response and allowing a spike in the viral load; yet physicians must balance the need for the anti-inflammatory treatment of corticosteroids (Murphy 2008). Clinicians have also noticed positive results during the use of human interferon and Glycyrrhizin. No compounds have yielded inhibitory results of any significance. The HIV protease inhibitors Ritonavir and Saquinavir did not show any inhibitory effect at nontoxic levels. Iminocyclitol 7 has been found to have an inhibitory effect on SARS-CoV in that it disrupts the envelope glycoprotein processing. Iminocyclitol 7 specifically inhibits the production of human fucosidase and in vitro trials yielded promising results in the treatment of SARS, yet one problem exists. A deficiency of fucosidase can lead to a condition known as fucosidosis in which there is a decrease in neurological function.

Prognosis:
The death rate from SARS was 9 to 12% of those diagnosed. In people over age 65, the death rate was higher than 50%. The illness was milder in younger patients.

Many more people became sick enough to need breathing assistance. And even more people had to go to hospital intensive care units.

Public health policies have been effective at controlling outbreaks. Many nations have stopped the epidemic in their own countries. All countries must continue to be careful to keep this disease under control. Viruses in the coronavirus family are known for their ability to change (mutate) in order to spread among humans.
.
Prevention:
The WHO set up a network for doctors and researchers dealing with SARS, consisting of a secure web site to study chest x-rays and a teleconference.

A SARS-treating hospital in Taiwan.Attempts were made to control further SARS infection through the use of quarantine. Over 1200 were under quarantine in Hong Kong, while in Singapore and Taiwan, 977 and 1147 were quarantined respectively. Canada also put thousands of people under quarantine.[14] In Singapore, schools were closed for 10 days and in Hong Kong they were closed until 21 April to contain the spread of SARS.

On 27 March 2003, the WHO recommended the screening of airline passengers for the symptoms of SARS.

In Singapore, a single hospital, Tan Tock Seng Hospital, was designated as the sole treatment and isolation centre for all confirmed and probable cases of the disease on 22 March. Subsequently, all hospitals implemented measures whereby all staff members were required to submit to temperature checks twice a day, visitorship was restricted only to pediatric, obstetric and selected other patients, and even then, only one person was allowed to visit at a time. To overcome this inconvenience, videoconferencing was utilised. A dedicated phoneline was designated to report SARS cases, whereupon a private ambulance service was dispatched to transport them to Tan Tock Seng Hospital.

On 24 March, Singapore’s Ministry of Health invoked the Infectious Diseases Act, allowing for a 10-day mandatory home quarantine to be imposed on all who may have come in contact with SARS patients. SARS patients who have been discharged from hospitals were under 21 days of home quarantine, with telephone surveillance requiring them to answer the phone when randomly called up. Discharged probable SARS patients and some recovered cases of suspected SARS patients are similarly required to be home quarantined for 14 days. Security officers from CISCO, a Singaporean auxiliary police force, were utilised to serve quarantine orders to their homes, and installed an electronic picture (ePIC) camera outside the doors of each contact. Sparked in particular by the news surrounding an elderly man who disregarded the quarantine order, flashing it to the public as he strolled to eating outlets and causing a minor exodus of patrons which persisted until the fears over the disease abated, the Singapore government called for an urgent meeting in Parliament on 24 April to amend the Infectious Disease Act and include penalties for violations, revealing at least 11 other violators of quarantine orders. These amendments included:

…*the requirement of suspected persons of infectious diseases to be brought to designated treatment centres, and their prohibition from going to public places;

…*the designation of contaminated areas and the restriction of access to them, and the destruction of suspected sources of infection;

…*the introduction of the power to tag offenders who break home quarantine (persons who failed to be contacted three times by phone consecutively) with electronic wrist tags, and the imposition of fines without court trial;

…*the ability to charge repeated offenders in court which may lead to imprisonment; and

…*the prosecution of anyone caught lying to health officials about their travel to SARS-affected areas or contacts with SARS patients.

Thermal imaging at Taoyuan Airport’s International checkpoint.On 23 April the WHO advised against all but essential travel to Toronto, noting that a small number of persons from Toronto appear to have “exported” SARS to other parts of the world. Toronto public health officials noted that only one of the supposedly exported cases had been diagnosed as SARS and that new SARS cases in Toronto were originating only in hospitals. Nevertheless, the WHO advisory was immediately followed by similar advisories by several governments to their citizens. On 29 April WHO announced that the advisory would be withdrawn on 30 April. Toronto tourism suffered as a result of the WHO advisory, prompting The Rolling Stones and others to organize the massive Molson Canadian Rocks for Toronto concert, commonly known as SARSstock, to revitalize the city’s tourism trade.

Also on 23 April, Singapore instituted thermal imaging scans to screen all passengers departing Singapore from Singapore Changi Airport. It also stepped up screening of travelers at its Woodlands and Tuas checkpoints with Malaysia. Singapore had previously implemented this screening method for incoming passengers from other SARS affected areas but was to include all travelers into and out of Singapore by mid- to late May.

In addition, students and teachers in Singapore were issued with free personal oral digital thermometers. Students took their temperatures daily, usually two or three times a day, but the temperature-taking exercises were suspended with the waning of the outbreak.

Taiwan Taoyuan International Airport also added SARS checkpoints with an infrared screening system similar to Singapore’s Changi Airport.

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/Severe_acute_respiratory_syndrome
http://health.nytimes.com/health/guides/disease/severe-acute-respiratory-syndrome-sars/overview.html
http://www.bbc.co.uk/health/physical_health/conditions/sars1.shtml

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Myelodysplastic Syndrome

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Definition:
The myelodysplastic syndromes (MDS, formerly known as “preleukemia”)  are a group of disorders caused by poorly formed or dysfunctional blood cells.Myelodysplastic syndromes occur when something goes wrong in your bone marrow — the spongy material inside our bones where blood cells are made.

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Patients with MDS often develop severe anemia and require frequent blood transfusions. In most cases, the disease worsens and the patient develops cytopenias (low blood counts) due to progressive bone marrow failure. In about one third of patients with MDS, the disease transforms into acute myelogenous leukemia (AML), usually within months to a few years.

The myelodysplastic syndromes are all disorders of the stem cell in the bone marrow. In MDS, hematopoiesis (blood production) is disorderly and ineffective. The number and quality of blood-forming cells decline irreversibly, further impairing blood production.

There is no cure for myelodysplastic syndromes. Treatment for myelodysplastic syndromes usually focuses on reducing or preventing complications of the disease and of treatments. In certain cases, myelodysplastic syndromes are treated with a bone marrow transplant, which may help prolong life.

The median age at diagnosis of a MDS is between 60 and 75 years; a few patients are younger than 50; MDS diagnoses are rare in children. Males are slightly more commonly affected than females.

The exact number of people with MDS is not known because it can go undiagnosed and there is no mandated tracking of the syndrome. Some estimates are on the order of 10,000 to 20,000 new cases each year in the United States alone. The incidence is probably increasing as the age of the population increases, and some authors propose that the incidence in patients over 70 may be as high as 15 cases per 100,000 per year

Symptoms:
Myelodysplastic syndromes rarely cause signs or symptoms in the early stages of the disease.The symptoms are nonspecific and generally related to the blood cytopenias:

In time, myelodysplastic syndromes may cause:

*Anemia—chronic tiredness,fatigue, shortness of breath, chilled sensation, sometimes chest pain

*Neutropenia (low neutrophil count) —increased susceptibility to  frequent infections

*Pinpoint-sized red spots just beneath the skin caused by bleeding (petechiae)

*Thrombocytopenia (low platelet count) —increased susceptibility to bleeding and ecchymosis (bruising), as well as subcutaneous hemorrhaging resulting in purpura or petechia.

Many individuals are asymptomatic, and blood cytopenia or other problems are identified as a part of a routine blood count:

*neutropenia, anemia and thrombocytopenia (low cell counts of white and red blood cells, and platelets, respectively);

*splenomegaly or rarely hepatomegaly;

*abnormal granules in cells, abnormal nuclear shape and size; and/or

*chromosomal abnormalities, including chromosomal translocations and abnormal chromosome number.

Although there is some risk for developing acute myelogenous leukemia, about 50% of deaths occur as a result of bleeding or infection. Leukemia that occurs as a result of myelodysplasia is notoriously resistant to treatment.

Causes:
Myelodysplastic syndromes occur when something happens to disrupt the orderly and controlled production of blood cells. People with myelodysplastic syndromes have blood cells that are immature and defective, and instead of developing normally, they die in the bone marrow or just after entering your bloodstream. Over time, the number of immature, defective cells begins to surpass that of healthy blood cells, leading to problems such as anemia, infections and excess bleeding.

Doctors divide myelodysplastic syndromes into two categories based on their cause:

*Myelodysplastic syndromes with no known cause. Called de novo myelodysplastic syndromes, doctors don’t know what causes these. De novo myelodysplastic syndromes are often more easily treated than are myelodysplastic syndromes with a known cause.

*Myelodysplastic syndromes caused by chemicals and radiation. Myelodysplastic syndromes that occur in response to cancer treatments, such as chemotherapy and radiation, or in response to chemical exposure are called secondary myelodysplastic syndromes. Secondary myelodysplastic syndromes are often more difficult to treat.

Types of myelodysplastic syndromes:
The World Health Organization divides myelodysplastic syndromes into subtypes based on the type of cells involved. Myelodysplastic syndrome subtypes include:

*Refractory cytopenia with unilineage dysplasia. In this type, one or two blood cell types are low in number — most commonly, the red blood cells are affected. Also, one type of blood cell appears abnormal under the microscope.

*Refractory anemia with ringed sideroblasts. This differs from refractory anemia in that existing red blood cells contain excess amounts of iron (ringed sideroblasts).

*Refractory cytopenia with multilineage dysplasia. In this myelodysplastic syndrome, two of the three types of blood cells are abnormal, and less than 1 percent of the cells in the bloodstream are immature cells (blasts).

*Refractory anemia with excess blasts — types 1 and 2. In both these syndromes, any of the three types of cells — red blood cells, white blood cells or platelets — may be low in number and appear abnormal under a microscope.

*Myelodysplastic syndrome, unclassified. In this uncommon syndrome, there are reduced numbers of one of the three types of mature blood cells, and either the white blood cells or platelets look abnormal under a microscope.

*Myelodysplastic syndrome associated with isolated del(5q) chromosome abnormality. People with this syndrome have low numbers of red blood cells, and the cells have a specific defect in their DNA.
Risk Factors:
Factors that may increase your risk of myelodysplastic syndromes include:

*Older age. Most people with myelodysplastic syndromes are adults older than 60. Anyone can develop myelodysplastic syndromes, but they’re rare in younger people.

*Being male. Myelodysplastic syndromes occur more frequently in men than in women.

*Treatment with chemotherapy or radiation. Your risk of myelodysplastic syndromes is increased if you received chemotherapy or radiation, both of which are commonly used to treat cancer.

*Exposure to certain chemicals. Chemicals linked to myelodysplastic syndromes include tobacco smoke, pesticides and industrial chemicals, such as benzene.

*Exposure to heavy metals. Heavy metals linked to myelodysplastic syndrome include lead and mercury.

Complications:
Complications of myelodysplastic syndromes include:

*Anemia. Reduced numbers of red blood cells can cause anemia, which can make you feel tired.

*Recurrent infections. Having too few white blood cells increases your risk of serious infections.

*Bleeding that won’t stop. Lacking platelets in your blood to stop bleeding can lead to excessive bleeding that won’t stop.

*Increased risk of cancer. Some people with myelodysplastic syndromes may eventually develop leukemia, a cancer of the blood cells.

Diagnosis:
MDS must be differentiated from anemia, thrombocytopenia, and/or leukopenia. Usually, the elimination of other causes of these cytopenias, along with a dysplastic bone marrow, is required to diagnose a myelodysplastic syndrome.

A typical investigation includes:
*Full blood count and examination of blood film. The blood film morphology can provide clues about hemolytic anemia, clumping of the platelets leading to spurious thrombocytopenia, or leukemia.

*Blood tests to eliminate other common causes of cytopenias, such as lupus, hepatitis, B12, folate, or other vitamin deficiencies, renal failure or heart failure, HIV, hemolytic anemia, monoclonal gammopathy. Age-appropriate cancer screening should be considered for all anemic patients.

*Bone marrow examination by a hematopathologist. This is required to establish the diagnosis, since all hematopathologists consider dysplastic marrow the key feature of myelodysplasia.

*Cytogenetics or chromosomal studies. This is ideally performed on the bone marrow aspirate. Conventional cytogenetics requires a fresh specimen, since live cells are induced to enter metaphase to enhance chromosomal staining. Alternatively, virtual karyotyping can be done for MDS,[10] which uses computational tools to construct the karyogram from disrupted DNA. Virtual karyotyping does not require cell culture and has dramatically higher resolution than conventional cytogenetics, but cannot detect balanced translocations.

*Flow cytometry is helpful to establish the presence of any lymphoproliferative disorder in the marrow.

Anemia dominates the early course. Most symptomatic patients complain of the gradual onset of fatigue and weakness, dyspnea, and pallor, but at least half the patients are asymptomatic and their MDS is discovered only incidentally on routine blood counts. Previous chemotherapy or radiation exposure is an important historic fact. Fever and weight loss should point to a myeloproliferative rather than myelodysplastic process. Children with Down syndrome are susceptible to MDS, and a family history may indicate a hereditary form of sideroblastic anemia or Fanconi anemia.

The average age at diagnosis for MDS is about 65 years, but pediatric cases have been reported. Some patients have a history of exposure to chemotherapy (especially alkylating agents such as melphalan, cyclophosphamide, busulfan, and chlorambucil) or radiation (therapeutic or accidental), or both (e.g., at the time of stem cell transplantation for another disease). Workers in some industries with heavy exposure to hydrocarbons such as the petroleum industry have a slightly higher risk of contracting the disease than the general population. Males are slightly more frequently affected than females. Xylene and benzene exposure has been associated with myelodysplasia. Vietnam veterans that were exposed to Agent Orange are at risk of developing MDS.

The features generally used to define a MDS are: blood cytopenias; ineffective hematopoiesis; dyserythropoiesis; dysgranulopoiesis; dysmegakaropoiesis and increased myeloblast.

Dysplasia can affect all three lineages seen in the bone marrow. The best way to diagnose dysplasia is by morphology and special stains (PAS) used on the bone marrow aspirate and peripheral blood smear. Dysplasia in the myeloid series is defined by:

Granulocytic series
1.Hypersegmented neutrophils (also seen in Vit B12/Folate deficiency)
2.Hyposegmented neutrophils (Pseudo-Pelger Huet)
3.Hypogranular neutrophils or pseudo Chediak Higashi large granules
4.Auer rods – automatically RAEB II (if blast count <5% in the peripheral blood and <10% in the bone marrow aspirate) also note Auer rods may be seen in mature neutrophils in AML with translocation t(8;21)
5.Dimorphic granules (basophilic and eosinophilic granules) within eosinophils
Erythroid series
1.Binucleated erythroid percursors and karyorrhexis
2.Erythroid nuclear budding
3.Erythroid nuclear strings or internuclear bridging (also seen in congenital dyserythropoietic anemias)
4.Loss of E-cadherin in normoblasts is a sign of aberrancy
5.PAS (globular in vacuoles or diffuse cytoplasmic staining) within erythroid precursors in the bone marrow aspirate (has no bearing on paraffin fixed bone marrow biopsy). Note: One can see PAS vacuolar positivity in L1 and L2 blasts (AFB classification; the L1 and L2 nomenclature is not used in the WHO classification)
6.Ringed sideroblasts seen on Prussian blue iron stain (10 or more iron granules encircling 1/3 or more of the nucleus and >15% ringed sideroblasts when counted amongst red cell precursors)
Megakaryocytic series (can be the most subjective)
1.Hyposegmented nuclear features in platelet producing megakaryocytes (lack of lobation)
2.Hypersegmented (osteoclastic appearing) megakaryocytes
3.Ballooning of the platelets (seen with interference contrast microscopy)
Other stains can help in special cases (PAS and napthol ASD chloroacetate esterase positivity) in eosinophils is a marker of abnormality seen in chronic eosinophilic leukemia and is a sign of aberrancy.

On the bone marrow biopsy high grade dysplasia (RAEB-I and RAEB-II) may show atypical localization of immature precursors (ALIPs) which are islands of immature precursors cells (myeloblasts and promyelcytes) localized to the center of intertrabecular space rather than adjacent to the trabeculae or surrounding arterioles. This morphology can be difficult to recognize from treated leukemia and recovering immature normal marrow elements. Also topographic alteration of the nucleated erythroid cells can be seen in early myelodysplasia (RA and RARS), where normoblasts are seen next to bony trabeculae instead of forming normal interstitially placed erythroid islands.

Myelodysplasia is a diagnosis of exclusion and must be made after proper determination of iron stores, vitamin deficiencies, and nutrient deficiencies are ruled out. Also congenital diseases such as congenital dyserythropoietic anemia (CDA I through IV) has been recognized, Pearson’s syndrome (sideroblastic anemia), Jordans anomaly – vacuolization in all cell lines may be seen in Chanarin-Dorfman syndrome, ALA (aminolevulinic acid) enzyme deficiency, and other more esoteric enzyme deficiencies are known to give a pseudomyelodysplastic picture in one of the cell lines, however, all three cell lines are never morphologically dysplastic in these entities with the exception of chloramphenicol, arsenic toxicity and other poisons.

All of these conditions are characterized by abnormalities in the production of one or more of the cellular components of blood (red cells, white cells other than lymphocytes and platelets or their progenitor cells, megakaryocytes).

 

Treatment :
No definitive cure or treatment for myelodysplastic syndromes exists. Instead, most people receive supportive care to help manage symptoms such as fatigue and to prevent bleeding and infections.

Blood transfusions
Blood transfusions can be used to replace red blood cells, white blood cells or platelets in people with myelodysplastic syndromes.

Medications :
Medications used to increase the number of healthy blood cells your body produces include:

*Medications that increase the number of blood cells your body makes. Called growth factors, these medications are artificial versions of substances found naturally in your bone marrow. Some growth factors, such as erythropoietin or darbepoietin, can reduce the need for blood transfusions by increasing red blood cells. Others may help prevent infections by increasing white blood cells in people with certain myelodysplastic syndromes.Medications that stimulate blood cells to mature, rather than remain immature.
*Medications such as azacitidine (Vidaza) and decitabine (Dacogen) may improve the quality of life of people with certain myelodysplastic syndromes and help delay progression to acute myelogenous leukemia. But these drugs aren’t effective in all people, and some can cause further blood cell problems. Medications that suppress your immune system.

*Medications used to suppress the immune system may be used in certain myelodysplastic syndromes.Medication for people with a certain genetic abnormality. If your myelodysplastic syndrome is associated with a genetic abnormality called isolated del(5q), your doctor may recommend lenalidomide (Revlimid). Lenalidomide may reduce the need for blood transfusions in people with this abnormality.

*Bone marrow stem cell transplant
During a bone marrow stem cell transplant, your defective blood cells are destroyed using powerful chemotherapy drugs. Then the abnormal bone marrow stem cells are replaced with healthy, donated cells (allogeneic transplant). Unfortunately, few people are candidates for this procedure because of the high risks involved in transplanting in older adults — those most likely to have myelodysplastic syndromes. Even among young, relatively healthy people, the number of transplant-related complications is high.

Prognosis:
Indicators of a good prognosis Younger age; normal or moderately reduced neutrophil or platelet counts; low blast counts in the bone marrow(<20%) and no blasts in the blood; no Auer rods; ringed sideroblasts; normal karyotypes of mixed karyotypes without complex chromosome abnormalities and in vitro marrow culture- non leukemic growth pattern.

Indicators of a poor prognosis Advanced age; Severe neutropenia or thrombocytopenia ; high blast count in the bone marrow (20-29%) or blasts in the blood; Auer rods; absence of ringed sideroblasts; abnormal localization or immature granulocyte precursors in bone marrow section all or mostly abnormal karyotypes or complex marrow chromosome abnormalities and in vitro bone emarrow culture-leukemic growth pattern.

Prognosis and karyotype Good: Normal, -Y, del(5q), del(20q)
Intermediate or variable: +8, other single or double anomalies
Poor; Complex (>3 chromosomal aberrations); chromosome 7 anomalies

The International Prognostic Scoring System (IPSS) is the most commonly used tool in MDS to predict long-term outcome.

Cytogenetic abnormalities can be detected by conventional cytogenetics, a FISH panel for MDS, or Virtual Karyotype.

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://www.mayoclinic.com/health/myelodysplastic-syndromes/DS00596
http://en.wikipedia.org/wiki/Myelodysplastic_syndrome

http://www.bmj.com/content/314/7084/883.full

http://www.medicalook.com/Blood_disorders/Myelodysplastic_syndrome.html

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