CT Scan : A diagnostic Breakthrough in Medicine

Computed tomography (CT), originally known as computed axial tomography (CAT or CT scan) and body section roentgenography, is a medical imaging method employing tomography where digital geometry processing is used to generate a three-dimensional image of the internals of an object from a large series of two-dimensional X-ray images taken around a single axis of rotation. The word "tomography" is derived from the Greek tomos (slice) and graphein (to write). CT produces a volume of data which can be manipulated, through a process known as windowing, in order to demonstrate various structures based on their ability to block the X-ray beam. Although historically (see below) the images generated were in the axial or transverse plane (orthogonal to the long axis of the body), modern scanners allow this volume of data to be reformatted in various planes or even as volumetric (3D) representations of structures.


History
The first commercially viable CT scanner was invented by Godfrey Newbold Hounsfield in Hayes, England at Thorn EMI Central Research Laboratories using X-rays. Hounsfield conceived his idea in 1967, and it was publicly announced in 1972. It is claimed that the CT scanner was "the greatest legacy" of the Beatles; the massive profits from their record sales enabled EMI to fund scientific research.[1] Allan McLeod Cormack of Tufts University, Massachusetts, USA independently invented a similar process and they shared a Nobel Prize in medicine in 1979.

The prototype CT scanner
The original 1971 prototype took 160 parallel readings through 180 angles, each 1° apart, with each scan taking a little over five minutes. The images from these scans took 2.5 hours to be processed by algebraic reconstruction techniques on a large computer.
The first production X-ray CT machine (called the EMI-Scanner) was limited to making tomographic sections of the brain, but acquired the image data in about 4 minutes (scanning two adjacent slices) and the computation time (using a Data General Nova minicomputer) was about 7 minutes per picture. This scanner required the use of a water-filled Perspex tank with a pre-shaped rubber "head-cap" at the front, which enclosed the patient's head. The water-tank was used to reduce the dynamic range of the radiation reaching the detectors (between scanning outside the head compared with scanning through the bone of the skull). The images were relatively low resolution, being composed of a matrix of only 80 x 80 pixels. The first EMI-Scanner was installed in Atkinson Morley's Hospital in Wimbledon, England, and the first patient brain-scan was made with it in 1972.

a historic EMI-Scanner
In the U.S., the first installation was at the Mayo Clinic. As a tribute to the impact of this system on medical imaging the Mayo Clinic has an EMI scanner on display in the Radiology Department.
The first CT system that could make images of any part of the body, and did not require the "water tank" was the ACTA scanner designed by Robert S. Ledley, DDS at Georgetown University.

Schizophrenia: A short summary

Historical Background: in 1896, Emil Kraepelin differentiated psychiatric illness into 2 major groups.

• Dementia Precox
• Mani depressive illness( psychosis)

Eugen Bleuer's Fundamental Symptoms of Schizophremi: Ambivalence Autism Affective Flattening Association disorder

First Rank symptoms
I. Hallucinations
1. Audible thoughts/thought echo 2. Voices heard arguing 3. Voices giving running commentary II. Thought Alienation Phenomenon a) Thought withdrawal b) Thought insertion c) Thought broadcasting
III. Passivity Phenomenon A. Made feelings B. Made volition C. Made impulses IV. Delusional Perception

Epidemiology; Point prevalence of Schizophrenia is 0.5 to 1 %. The Incidence is about 0.5 in 1000 persons

Clinical features Thought and speech Disorders Autistic thinking, loosening of association, thought blocking, neologism, paraphasias, mutism, perseveration, verbigeration Delusions: primary and secondary Disorders Of Perception Hallucinations Disorders of Affect Disorders of Motor Behaviour Negative Symptoms Suicidal Tendency

Clinical types: Simple Schizophrenia Hebephrenic Schizophrenia Catatonic Schizophrenia Residual Schicophrenia Undifferentiated Schizophrenia Post-schizophrenic depression Others

Bad Prognostic Factors Male Negative Symptoms Early Onset Insidious progression Chronic Course

Diagnostic Criteria: According to DSM IV TR 2 or more of the following is required with 6 months of duration of disease with at least 1 month of Active symptoms 1. Delusion Hallucinations Bizzare Behaviour Bizzare thoughts

MANAGEMENT: 1. Pharmacological Treatment: Generally the treatment is continued for 6 months to 1 year for the first episode, for 1-2 year for subsequent episodes. Fluphenazine 25-30 mg IM every 2-3 weeks Penfluridol Flupenthixol Haloperidol ECT ( Electroconvulsive Therapy) Miscellaneous Treatments Limbic Leucotomy Psychosocial Treatment.

Organic Metal Disorders and Delirium

Organic Mental Disorders are behavioral or psychological disorders associated with permanent or transient brain dysfunction and include only those mental and behavioral disorders that are due to demonstrable cerebral disease or disorders, either primary or secondary. Sub Categories of Organic Mental Disorders: OMD are

• Delirium
• Dementia
• Organic Amnestic Syndrome
• Other organic mental disorders

Delirium:
commonest type
synonyms: Acute Confusional state, acute brain syndrome, acute organic reaction, toxic psychosis, metabolic encephalopathy.

Clinical Features:
1. A relative Acute Onset
2. Clouding of Consciousness
3.Disorientation to time place and person.
other: Disturbed sleep-wake sleep cycle
sun downing( aggravated in the evening and night)
Motor disturbances- asterixis,Carphologia. etc
Psychomotor disturbances

Diagnosis:
According to ICD10
Symptoms should be present in each one area:
1. Impairment of attention and consciousness
2.Global disturbance of cognition
3. Psychomotor disturances
4.Disturbed slepp wake sleep cycle
5. Emotional disturbances.

Important causes of Delirium are:

1. Metabolic causes: hypoxia, narcosis,hypoglycemia, CCF, Metabolic acidosis or alkalosis, fever , anemia, shock.
2. Endocrine : Hypo/hyper thyroid,adrenal,pituitary and parathyroid.
3. Drug: Digitalis, quinidine, alcohol, anti hypertensives, sedatives,barbiturates,TCA, Antipsychotics.
4. Nutritional deficiency: Thiamin, Niacin, Pyridoxine, folic acid, B12
5. Systemic Infections.
6. Intracranial causes: Epilepsy, tumors, migraine, head injury, infections
7. post operative

Management of Delirium:
Ix: CBC, BGA, Sugar level, po2 and co2, TFT, serum b1 and foalte, toxic screen, csf, etc
Identificaton of the cause and its immediate correction.
Symptomatic measures
Supportive medical and nursing ccare.

Guinea Worm : Dracunculiais CDC article

Source: CDC

What is dracunculiasis?

Dracunculiasis, more commonly known as Guinea worm disease (GWD), is a preventable infection caused by the parasite Dracunculus medinensis. Infection affects poor communities in remote parts of Africa that do not have safe water to drink.

Currently, many organizations, including The Global 2000 program of The Carter Center of Emory University, UNICEF, Centers for Disease Control and Prevention (CDC), and the World Health Organization (WHO) are helping the last 5 countries in the world (Sudan, Ghana, Mali, Niger, and Nigeria) to eradicate the disease. Since 1986, when an estimated 3.5 million people were infected annually, the campaign has eliminated much of the disease.

In 2007, only 9,585 cases of GWD were reported. Most of those cases were from Sudan (61%) and Ghana (35%). All affected countries are aiming to eliminate Guinea worm disease as soon as possible.

How does Guinea worm disease spread?

Approximately 1 year after a person drinks contaminated water, the adult female Guinea worm emerges from the skin of the infected person. Persons with worms protruding through the skin may enter sources of drinking water and unwittingly allow the worm to release larvae into the water. These larvae are ingested by microscopic copepods (tiny "water fleas") that live in these water sources. Persons become infected by drinking water containing the water fleas harboring the Guinea worm larvae.

Once ingested, the stomach acid digests the water fleas, but not the Guinea worm larvae. These larvae find their way to the small intestine, where they penetrate the wall of the intestine and pass into the body cavity. During the next 10-14 months, the female Guinea worm larvae grow into full size adults, 60-100 centimeters (2-3 feet) long and as wide as a cooked spaghetti noodle. These adult femal worms then migrate and emerge from the skin anywhere on the body, but usually on the lower limbs.

A blister develops on the skin at the site where the worm will emerge. This blister causes a very painful burning sensation and it ruptures within 24-72 hours. Immersion of the affected limb into water helps relieve the pain but it also triggers the Guinea worm to release a milky white liquid containing millions of immature larvae into the water, thus contaminating the water supply and starting the cycle over again. For several days after it has emerged from the ulcer, the female Guinea worm is capable of releasing more larvae whenever it comes in contact with water.

What are the signs and symptoms of Guinea worm disease?

Infected persons do not usually have symptoms until about one year after they become infected. A few days to hours before the worm emerges, the person may develop a fever, swelling, and pain in the area. More than 90% of the worms appear on the legs and feet, but may occur anywhere on the body.

People, in remote, rural communities who are most commonly affected by Guinea worm disease (GWD) frequently do not have access to medical care. Emergence of the adult female worm can be very painful, slow, and disabling. Frequently, the skin lesions caused by the worm develop secondary bacterial infections, which exacerbate the pain, and extend the period of incapacitation to weeks or months. Sometimes permanent disability results if joints are infected and become locked.

What is the treatment for Guinea worm disease?

There is no drug to treat Guinea worm disease (GWD) and no vaccine to prevent infection. Once the worm emerges from the wound, it can only be pulled out a few centimeters each day and wrapped around a piece of gauze or small stick. Sometimes the worm can be pulled out completely within a few days, but this process usually takes weeks or months. Analgesics, such as aspirin or ibuprofen, can help reduce swelling; antibiotic ointment can help prevent bacterial infections. The worm can also be surgically removed by a trained doctor in a medical facility before an ulcer forms.

Where is Guinea worm disease found?

Dracunculiasis now occurs only in 5 countries in sub-Saharan Africa. Transmission of the disease is most common in very remote rural villages and in areas visited by nomadic groups. In 2007, the two most endemic countries, Sudan and Ghana, reported 9,173; 5,815 and 3,358 cases of Guinea worm disease (GWD), respectively. Other endemic countries reporting cases of GWD in 2007 were: Mali (313 cases), Nigeria (73 cases), and Niger (14 cases).

Asia is now free of the disease. Transmission of GWD no longer occurs in several African countries, including Benin, Burkina Faso, Cameroon, Central African Republic, Chad, Cote d'Ivoire, Ethiopia, Kenya, Mauritania, Senegal, Togo, and Uganda. No locally acquired cases of disease have been reported in these countries in the last year or more. The treat of case importations from the remaining endemic countries requires that surveillance be maintained in formerly endemic areas until offical certification. The World Health Organization has certified 180 countries free of transmission of dracunculiasis, including six formerly endemic countries: Pakistan (in 1996), India (in 2000), Senegal and Yemen (in 2004), Central African Republic and Cameroon (in 2007).

Who is at risk for infection?

Anyone who drinks standing pond water contaminated by persons with GWD is at risk for infection. People who live in villages where the infection is common are at greatest risk.

Is Guinea worm disease a serious illness?

Yes. The disease causes preventable suffering for infected persons and is a heavy economic and social burden for affected communities. Emgerence of the adult female worms can be very painful, slow, and disabling. Parents who have active Guinea worm disease may not be able to care for their children. They are also prevented from working in their fields and tending their animals. Because worm emergence usually occurs during planting and harvesting season, heavy crop losses may result leading to financial problems for the entire family. Children may be required to work the fields or tend animals in place of their disabled parents, preventing them from attending school. Therefore, GWD is both a disease of poverty and also a cause of poverty because of the disability it causes.

Is a person immune to Guinea worm disease once he or she has it?

No. Infection does not produce immunity, and many people in affected villages suffer disease year after year.

How can Guinea worm disease be prevented?

Because GWD can only be transmitted via drinking contaminated water, educating people to follow these simple control measures can completely prevent illness and eliminate transmission of the disease:

Drink only water from underground sources (such as from borehole or hand-dug wells) free from contamination.

Prevent persons with an open Guinea worm ulcer from entering ponds and wells used for drinking water.

Always filter drinking water, using a cloth filter, to remove the water fleas.

Additionally, unsafe sources of drinking water can be treated with an approved larvicide, such as ABATE®*, that kills copepods, and communities can be provided with new safe sources of drinking water, or have existing dysfunctional ones repaired.

*Use of trade names is for identification only and does not imply endorsement by the Public Health Service or by the U.S. Department of Health and Human Services.

Giant baby 8.7 kg born in Indonesia

Read ......

Seasonal hyperacute panuveitis (SHAPU) In Nepal

Seasonal hyperacute panuveitis (SHAPU), characterized by an unusual form of unilateral severe hyper acute diffused intraocular inflammation, is one of the mysterious eye diseases of which the definite cause and treatment remains yet to be tound out. In this study, a total of six cases were included. Aqueous and vitreous samples were subjected to direct microscopy and culture (bacterial or fungal). Of the six cases included, two yielded Streptococcus pneumoniae and one Acinetobactor sp. on culture. All three culture positive samples showed pus cells in direct microscopic examination (gram stain). All cases were subjected to vitrectomy and intravitreal antibiotic and steroid injection, along with oral antibiotics and steroid. Five cases were also treated with antiviral agent. After treatment four cases showed reversal of hypotony and three cases recovered some vision.

Moths have been reported to increase the prevalence of this disease. Complications can be as devastating as blindness.

Read NMJ journal Article...Read

Magic Johnson: Fight Against HIV/AIDS

Magic Johnson: Personal life and His Commitment against AIDS

Personal life

Johnson first fathered a son in 1981, when Andre Johnson was born to Melissa Mitchell. Although Andre was raised by his mother, he visited Johnson each summer, and as of October 2005 was working for Magic Johnson Enterprises as a marketing director. In 1991, Johnson married Earlitha "Cookie" Kelly, with whom he had one son, Earvin III; the couple adopted a daughter, Elisa, in 1995.

In 1998, Johnson hosted a late night talk show on the Fox network called The Magic Hour, but the show was canceled after two months due to low ratings. He runs Magic Johnson Enterprises, a company that has a net worth of $700 million; its subsidiaries include Magic Johnson Productions, a promotional company; Magic Johnson Theaters, a nationwide chain of movie theaters; and Magic Johnson Entertainment, a movie studio. Johnson has also worked as a motivational speaker. He is a supporter of the Democratic Party—in 2005, he publicly endorsed Phil Angelides for governor of California, and Hillary Clinton for president of the United States. Johnson was an NBA commentator for Turner Network Television for seven years, before becoming a studio analyst for ESPN's NBA Countdown in 2008.

After announcing his infection in November 1991, Johnson created the Magic Johnson Foundation to help combat HIV, although he later diversified the foundation to include other charitable goals. In 1992, he joined the National Commission on AIDS, but left after eight months, saying that the commission was not doing enough to combat the disease. He was also the main speaker for the United Nations (UN) World AIDS Day Conference in 1999, and has served as a United Nations Messenger of Peace.

HIV had been associated with drug addicts and homosexuals, but Johnson's campaigns sought to show that the risk of infection was not limited to those groups. Johnson stated that his aim was to "help educate all people about what [HIV] is about" and teach others not to "discriminate against people who have HIV and AIDS". Johnson was later criticized by the AIDS community for his decreased involvement in publicizing the spread of the disease.

To prevent his HIV infection from becoming AIDS, Johnson takes a daily combination of drugs from GlaxoSmithKline and Abbott Laboratories. He has advertised GlaxoSmithKline's drugs,^[91] and partnered with Abbott Laboratories to publicize the fight against AIDS in African American communities.

Top 10 Epidemics of All time

Plague

Smallpox

Measles

is

Number 10

Approx 454,000 people, died worldwide in 2004, aka rubeola.

Polio

is

Number 9

Caused more than 27,000 cases and 7,000 deaths in 1916.

Yellow Fever

is

Number 8

1878 New Orleans killed 13,000 people 200,000 estimated cases of yellow fever, with 30,000 deaths, per year.

AIDS

is

Number 7

(Acquired Immune Deficiency Syndrome) The leading cause of death of 15-to-49-year-olds totaling 45 million in 2005.

Malaria

is

Number 6

Over 1 million people a year die, (parasites of the genuis Plasmodium). Annually 300 million–500 million cases of malaria occur worldwide!

Tuberculosis (TB)

is

Number 5

2 million die annually with one-third of world’s population are thought to be infected

Cholera

is

Number 4

This water-borne disease in the summer of 1832, killed 3,000+ in New York, World Health Organization said that 56 countries officially reported 101,383 cholera cases, including 2,345 deaths.

Plague (bubonic and Pneumonic)

is

Number 3

Killed one-third of Europe’s population in 1348-50, (Yersinia pestis). World Health Organization reports 1,000-3,000 cases annually

Smallpox

is

Number 2

Ancient disease (variola virus)

Influenza or “flu”

is

Number 1

Kills 36,000 people annually, (RNA virus).

Myasthenia Gravis and Lambert Eaton

Myasthenia gravis

Myasthenia gravis (literally "serious muscle-weakness") is a neuromuscular disease leading to fluctuating muscle weakness and fatiguability. It is an autoimmune disorder, in which weakness is caused by circulating antibodies that block acetylcholine receptors at the post-synaptic neuromuscular junction, inhibiting the stimulative effect of the neurotransmitter acetylcholine. Myasthenia is treated medically with cholinesterase inhibitors or immunosuppressants, and, in selected cases, thymectomy. At 200–400 cases per million it is one of the less common autoimmune disorders.

Signs and symptoms

Ptosis of the left eye.

The hallmark of myasthenia gravis is fatiguability. Muscles become progressively weaker during periods of activity and improve after periods of rest. Muscles that control eye and eyelid movement, facial expression, chewing, talking, and swallowing are especially susceptible. The muscles that control breathing and neck and limb movements can also be affected. Often the physical examination is within normal limits.^[3]

The onset of the disorder can be sudden. Often symptoms are intermittent. The diagnosis of myasthenia gravis may be delayed if the symptoms are subtle or variable.

In most cases, the first noticeable symptom is weakness of the eye muscles. In others, difficulty in swallowing and slurred speech may be the first signs. The degree of muscle weakness involved in MG varies greatly among patients, ranging from a localized form, limited to eye muscles (ocular myasthenia), to a severe or generalized form in which many muscles - sometimes including those that control breathing - are affected. Symptoms, which vary in type and severity, may include asymmetrical ptosis (a drooping of one or both eyelids), diplopia (double vision) due to weakness of the muscles that control eye movements, unstable or waddling gait, weakness in arms, hands, fingers, legs, and neck, a change in facial expression, dysphagia (difficulty in swallowing), shortness of breath and dysarthria (impaired speech, often nasal due to weakness of the velar muscles).

In myasthenic crisis a paralysis of the respiratory muscles occurs, necessitating assisted ventilation to sustain life. In patients whose respiratory muscles are already weak, crises may be triggered by infection, fever, an adverse reaction to medication, or emotional stress.^[4] Since the heart muscle is stimulated differently, it is never affected by MG.

Diagnosis

Myasthenia can be a difficult diagnosis, as the symptoms can be subtle and hard to distinguish from both normal variants and other neurological disorders. A thorough physical examination can reveal easy fatiguability, with the weakness improving after rest and worsening again on repeat of the exertion testing. Applying ice to weak muscle groups characteristically leads to improvement in strength of those muscles. Additional tests are often performed, as mentioned below. Furthermore, a good response to medication can also be considered a sign of autoimmune pathology.

Physical examination

Muscle fatigability can be tested for many muscles.A thorough investigation includes:

• looking upward and sidewards for 30 seconds: ptosis and diplopia.
• looking at the feet while lying on the back for 60 seconds
• keeping the arms stretched forward for 60 seconds
• 10 deep knee bends
• walking 30 steps on both the toes and the heels
• 5 situps, lying down and sitting up completely
• "Peek sign": after complete initial apposition of the lid margins, they quickly (within 30 seconds) start to separate and the sclera starts to show

Blood tests

If the diagnosis is suspected, serology can be performed in a blood test to identify certain antibodies:

• One test is for antibodies against the acetylcholine receptor. The test has a reasonable sensitivity of 80–96%, but in MG limited to the eye muscles (ocular myasthenia) the test may be negative in up to 50% of the cases.

• A proportion of the patients without antibodies against the acetylcholine receptor have antibodies against the MuSK protein.

• In specific situations (decreased reflexes which increase on facilitation, co-existing autonomic features, suspected presence of neoplasm, especially of the lung, presence of increment or facilitation on repetitive EMG testing) testing is performed for Lambert-Eaton syndrome, in which other antibodies (against a voltage-gated calcium channel) can be found.

electromyography, which is considered to be the most sensitive (although not the most specific) test for MG

Edrophonium test

Tensilon test

Imaging

A chest CT-scan showing a thymoma (red circle).

A chest X-ray is frequently performed; it may point towards alternative diagnoses (e.g. Lambert-Eaton due to a lung tumor) and comorbidity. It may also identify widening of the mediastinum suggestive of thymoma, but computed tomography (CT) or magnetic resonance imaging (MRI) are more sensitive ways to identify thymomas, and are generally done for this reason.

Pulmonary function test

Restrictive pattern on spirometry

Associations

Myasthenia Gravis is associated with various autoimmune diseases, including:

• Thyroid diseases, including Hashimoto's thyroiditis and Graves' disease
• Diabetes mellitus type 1
• Rheumatoid arthritis
• Lupus, and
• Demyelinating CNS diseases

When Did AIDS Begin? How?

When Did AIDS

Begin?

Reprinted from Times Magazine, By Christine Gorman

Spring 1988

A new study of the oldest known HIV suggests the virus jumped from animals to humans in the 1940s.

The year was 1959, location: The central African city of Leopoldville, now called Kinshasa, shortly before the waves of violent rebellion that followed the liberation of the Belgian Congo. A seemingly healthy man walked into a hospital clinic to give blood for a Western backed study of blood diseases. He walked away and was never heard from again. Doctors analyzed his sample, froze it in a test tube and forgot about it. A quarter-century later, in the mid-1980s, researchers studying the growing AIDS epidemic took a second look at the blood and discovered that it contained HIV, the virus that causes AIDS.

And not just any HIV. The Leopoldville sample is the oldest specimen of the AIDS virus ever isolated and may now help solve the mystery of how and when the virus made the leap from animals (monkeys or chimpanzees) to humans, according to a report published last week in Nature. Dr. David Ho, director of the Aaron Diamond AIDS Research Center in New York City and one of the study's authors, says a careful genetic analysis of the sample's DNA pushes the origin of the AIDS epidemic back at least a decade, to the early '50s or even the '40s.

Over the past 15 years, scientists have identified at least 10 subtypes of the virus. But they couldn't tell whether they were seeing variations on one changeable virus or the handiwork of several different viruses that had made the jump from primates to man. A look at the genetic mutations in the Leopoldville sample strongly suggests that all it took to launch the epidemic was one unlucky turn of events.

By comparing the DNA of the 1959 virus with that of samples taken from the '80s and '90s. Ho and his colleagues constructed a viral family tree in which the Leopoldville isolate sits right at the juncture where three subtypes branch out. The 39-year-old specimen is also strikingly similar to the other seven subtypes. The clear implication: all the viral strains can be traced back to a single event or a closely related group of events. One theory is that AIDS started through contact with infected monkeys in a remote area and spread to the rest of the population through urbanization and mass inoculations.

The findings underscore how rapidly HIV can adapt to its surroundings, making it difficult to develop effective vaccines. No one knows how many more subtypes of HIV will sprout in the next 40 years, but chances are they will be every bit as lethal as the ones we see today, if not more so.

Porphyria: A Fact about Vampires?

Porphyria - the true story about Vampire

Legend tells us that vampires come out at night. They are night creatures because the sun can hurt and even kill them. They come out at night to seek fresh blood because without it they will suffer agonizing pain and will die. Their bodies dry up due to lack of blood, and new blood refreshes their bodies and gives them energy and certain powers.

It has been long believed that the condition associated with vampire legends is porphyria. Vampire characteristics are similar to those of porphyrics and this may have led to the misconception in the early 1400-1600's that porphyria sufferers were vampires. Vampire legends are in every country and porphyria is also found throughout the world. Porphyria comes from the Greek word meaning purple.

Of course, we now know that porphyria patients are NOT vampires, but porphyria might have contributed to the origin of the vampire legends.

EXPLAINING PORPHYRIA

Porphyria is a group of disorders caused by the abnormal production of heme which is the base material responsible for making hemoglobin and chlorophyll. Most types of porphyria are inherited. A child needs to inherit the defective gene from only one parent to develop the disease.

Heme is a substance found in all body tissues. The largest amounts of heme are found in the blood and bone marrow, and heme is also found in the liver and red blood cells. Multiple enzymes are required for the body to convert chemical compounds called porphyrins into heme. If any of the enzymes are abnormal, the process is disturbed and cannot continue. This allows the porphyrins to build up in the body.

Excessive porphyrin in the body causes photosensitivity which is oversensitivity to sunlight. When porphyrins are exposed to light and oxygen, they generate a charged, unstable form of oxygen that can damage the skin. Nerve damage, pain and paralysis can occur in some porphyrias. Sometimes an attack is so severe it can also lead to respiratory paralysis and the patient is unable to speak, breath or swallow. At times, this if fatal.


ABOUT:
Congenital Erythropoietic Porphyria - Hypersensitivity to Light

Fewer than 200 cases of congenital erythropoietic porphyria have ever been documented, and not just because physicians can’t pronounce the name. Due to a gene mutation, the skin becomes extremely sensitive to sunlight. Areas of exposed skin can become blistered and infected. Sunlight exposure can also lead to scarring, changes in skin pigmentation and increased hair growth. Such symptoms have unfairly linked people suffering from the condition with the lore of vampires and werewolves. On overcast or very cold winter days, the symptoms of congenital erythropoietic porphyria (also called erythropoietic protoporphyria) are sometimes attenuated, allowing some safe exposure to indirect sunlight.

Synesthesia is not considered to be a disease (though it has not been well studied, either) and tends to affect people who are bright and colorful—er, that is, people who are intelligent and creative

Swine Flu : CDC Recommendation

Novel H1N1 Vaccination Recommendations

With the new H1N1 virus continuing to cause illness, hospitalizations and deaths in the US during the normally flu-free summer months and some uncertainty about what the upcoming flu season might bring, CDC's Advisory Committee on Immunization Practices has taken an important step in preparations for a voluntary novel H1N1 vaccination effort to counter a possibly severe upcoming flu season. On July 29, ACIP met to consider who should receive novel H1N1 vaccine when it becomes available.

Novel H1N1 Vaccine

Every flu season has the potential to cause a lot of illness, doctor’s visits, hospitalizations and deaths. CDC is concerned that the new H1N1 flu virus could result in a particularly severe flu season this year. Vaccines are the best tool we have to prevent influenza. CDC hopes that people will start to go out and get vaccinated against seasonal influenza as soon as vaccines become available at their doctor’s offices and in their communities (this may be as early as August for some). The seasonal flu vaccine is unlikely to provide protection against novel H1N1 influenza. However a novel H1N1 vaccine is currently in production and may be ready for the public in the fall. The novel H1N1 vaccine is not intended to replace the seasonal flu vaccine – it is intended to be used along-side seasonal flu vaccine.

CDC’s Advisory Committee on Immunization Practices (ACIP), a

panel made up of medical and public health experts, met July 29, 2009, to make recommendations on who should receive the new H1N1 vaccine when it becomes available. While some issues are still unknown, such as how severe the virus will be during the fall and winter months, the ACIP considered several factors, including current disease patterns, populations most at-risk for severe illness based on current trends in illness, hospitalizations and deaths, how much vaccine is expected to be available, and the timing of vaccine availability.

The groups recommended to receive the novel H1N1 influenza vaccine include:

• Pregnant women because they are at higher risk of complications and can potentially provide protection to infants who cannot be vaccinated;
• Household contacts and caregivers for children younger than 6 months of age because younger infants are at higher risk of influenza-related complications and cannot be vaccinated. Vaccination of those in close contact with infants less than 6 months old might help protect infants by “cocooning” them from the virus;
• Healthcare and emergency medical services personnel because infections among healthcare workers have been reported and this can be a potential source of infection for vulnerable patients. Also, increased absenteeism in this population could reduce healthcare system capacity;
• All people from 6 months through 24 years of age
  • Children from 6 months through 18 years of age because we have seen many cases of novel H1N1 influenza in children and they are in close contact with each other in school and day care settings, which increases the likelihood of disease spread, and
  • Young adults 19 through 24 years of age because we have seen many cases of novel H1N1 influenza in these healthy young adults and they often live, work, and study in close proximity, and they are a frequently mobile population; and,
• Persons aged 25 through 64 years who have health conditions associated with higher risk of medical complications from influenza.

We do not expect that there will be a shortage of novel H1N1 vaccine, but flu vaccine availability and demand can be unpredictable and there is some possibility that initially, the vaccine will be available in limited quantities. So, the ACIP also made recommendations regarding which people within the groups listed above should be prioritized if the vaccine is initially available in extremely limited quantities. For more information see the CDC press release CDC Advisors Make Recommendations for Use of Vaccine Against Novel H1N1.

Once the demand for vaccine for the prioritized groups has been met at the local level, programs and providers should also begin vaccinating everyone from the ages of 25 through 64 years. Current studies indicate that the risk for infection among persons age 65 or older is less than the risk for younger age groups. However, once vaccine demand among younger age groups has been met, programs and providers should offer vaccination to people 65 or older.