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H1N1 Flu Update

2009 H1N1 Flu: Situation Update

October 23, 2009, 5:30 PM ET

U.S. Situation Update

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October 23, 2009, 11:30 AM

Each week CDC analyzes information about influenza disease activity in the United States and publishes findings of key flu indicators in a report called FluView. During the week of October 11-17, 2009, a review of the key indictors found that influenza activity continued to increase in the United States from the previous week. Below is a summary of the most recent key indicators:

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  Visits to doctors for influenza-like illness (ILI) increased steeply since last week in the United States, and overall, are much higher than what is expected for this time of the year. ILI activity now is higher than what is seen during the peak of many regular flu seasons.
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  Total influenza hospitalization rates for laboratory-confirmed flu are climbing and are higher than expected for this time of year.
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  The proportion of deaths attributed to pneumonia and influenza (P&I) based on the 122 Cities Report has increased and has been higher than what is expected at this time of year for two weeks. In addition, 11 flu-related pediatric deaths were reported this week; 9 of these deaths were confirmed 2009 H1N1, and two were influenza A viruses, but were not subtyped. Since April 2009, CDC has received reports of 95 laboratory-confirmed pediatric 2009 H1N1 deaths and another 7 pediatric deaths that were laboratory confirmed as influenza, but where the flu virus subtype was not determined.
• 
  Forty-six states are reporting widespread influenza activity at this time. They are: Alabama, Alaska, Arizona, Arkansas, California, Colorado, Delaware, Florida, Georgia, Idaho, Illinois, Indiana, Iowa, Kansas, Kentucky, Louisiana, Maine, Maryland, Massachusetts, Michigan, Minnesota, Mississippi, Missouri, Montana, Nebraska, Nevada, New Hampshire, New Mexico, New York, North Carolina, North Dakota, Ohio, Oklahoma, Oregon, Pennsylvania, Rhode Island, South Dakota, Tennessee, Texas, Utah, Vermont, Virginia, Washington, West Virginia, Wisconsin, and Wyoming. This many reports of widespread activity are unprecedented during seasonal flu.
• 
  Almost all of the influenza viruses identified so far are 2009 H1N1 influenza A viruses. These viruses remain similar to the virus chosen for the 2009 H1N1 vaccine, and remain susceptible to the antiviral drugs oseltamivir and zanamivir with rare exception.

CDC

Natural and Acquired Immunity

Immunity: Natural and Acquired

Long ago, physicians realized that people who had recovered from the plague would never get it again—they had acquired immunity. This is because some of the activated T and B cells had become memory cells. Memory cells ensure that the next time a person meets up with the same antigen, the immune system is already set to demolish it.

Immunity can be strong or weak, short-lived or long-lasting, depending on the type of antigen it encounters, the amount of antigen, and the route by which the antigen enters the body. Immunity can also be influenced by inherited genes. When faced with the same antigen, some individuals will respond forcefully, others feebly, and some not at all.
Antigen, Natural, and Acquired Immunity.

An immune response can be sparked not only by infection but also by immunization with vaccines. Some vaccines contain microorganisms—or parts of microorganisms— that have been treated so they can provoke an immune response but not full-blown disease.

Immunity can also be transferred from one individual to another by injections of serum rich in antibodies against a particular microbe (antiserum). For example, antiserum is sometimes given to protect travelers to countries where hepatitis A is widespread. The antiserum induces passive immunity against the hepatitis A virus. Passive immunity typically lasts only a few weeks or months.

Infants are born with weak immune responses but are protected for the first few months of life by antibodies they receive from their mothers before birth. Babies who are nursed can also receive some antibodies from breast milk that help to protect their digestive tracts.

Immune Tolerance

Immune tolerance is the tendency of T or B lymphocytes to ignore the body’s own tissues. Maintaining tolerance is important because it prevents the immune system from attacking its fellow cells. Scientists are hard at work trying to understand how the immune system knows when to respond and when to ignore an antigen.

Tolerance occurs in at least two ways—central tolerance and peripheral tolerance. Central tolerance occurs during lymphocyte development. Very early in each immune cell’s life, it is exposed to many of the self molecules in the body. If it encounters these molecules before it has fully matured, the encounter activates an internal self-destruct pathway, and the immune cell dies. This process, called clonal deletion, helps ensure that “self-reactive” T cells and B cells, those that could develop the ability to destroy the body’s own cells, do not mature and attack healthy tissues.

Because maturing lymphocytes do not encounter every molecule in the body, they must also learn to ignore mature cells and tissues. In peripheral tolerance, circulating lymphocytes might recognize a self molecule but cannot respond because some of the chemical signals required to activate the T or B cell are absent. So-called clonal anergy, therefore, keeps potentially harmful lymphocytes switched off. Peripheral tolerance may also be imposed by a special class of regulatory T cells that inhibits helper or cytotoxic T-cell activation by self antigens.

Vaccines

For many years, healthcare providers have used vaccination to help the body’s immune system prepare for future attacks. Vaccines consist of killed or modified microbes, parts of microbes, or microbial DNA that trick the body into thinking an infection has occurred.

A vaccinated person’s immune system attacks the harmless vaccine and prepares for invasions against the kind of microbe the vaccine contained. In this way, the person becomes immunized against the microbe. Vaccination remains one of the best ways to prevent infectious diseases, and vaccines have an excellent safety record. Previously devastating diseases such as smallpox, polio, and whooping cough (pertussis) have been greatly controlled or eliminated through worldwide vaccination programs.

NIH

What is the Immune System?

What is the Immune System?

The immune system is a network of cells, tissues, and organs that work together to defend the body against attacks by “foreign” invaders. These are primarily microbes—tiny organisms such as bacteria, parasites, and fungi that can cause infections. Viruses also cause infections, but are too primitive to be classified as living organisms. The human body provides an ideal environment for many microbes. It is the immune system’s job to keep them out or, failing that, to seek out and destroy them.

When the immune system hits the wrong target, however, it can unleash a torrent of disorders, including allergic diseases, arthritis, and a form of diabetes. If the immune system is crippled, other kinds of diseases result.

The immune system is amazingly complex. It can recognize and remember millions of different enemies, and it can produce secretions (release of fluids) and cells to match up with and wipe out nearly all of them.

The secret to its success is an elaborate and dynamic communications network. Millions and millions of cells, organized into sets and subsets, gather like clouds of bees swarming around a hive and pass information back and forth in response to an infection. Once immune cells receive the alarm, they become activated and begin to produce powerful chemicals. These substances allow the cells to regulate their own growth and behavior, enlist other immune cells, and direct the new recruits to trouble spots.

Although scientists have learned much about the immune system, they continue to study how the body launches attacks that destroy invading microbes, infected cells, and tumors while ignoring healthy tissues. New technologies for identifying individual immune cells are now allowing scientists to determine quickly which targets are triggering an immune response. Improvements in microscopy are permitting the first-ever observations of living B cells, T cells, and other cells as they interact within lymph nodes and other body tissues.

In addition, scientists are rapidly unraveling the genetic blueprints that direct the human immune response, as well as those that dictate the biology of bacteria, viruses, and parasites. The combination of new technology and expanded genetic information will no doubt reveal even more about how the body protects itself from disease.

NIH

Postural Tachycardia Syndrome

Synonym(s): Chronic Orthostatic Intolerance, Postural Orthostatic Tachycardia Syndrome

What is postural tachycardia syndrome?

Postural orthostatic tachycardia syndrome (POTS) is one of a group of disorders that have orthostatic intolerance (OI) as their primary symptom. OI describes a condition in which an excessively reduced volume of blood returns to the heart after an individual stands up from a lying down position. The primary symptom of OI is lightheadedness or fainting. In POTS, the lightheadedness or fainting is also accompanied by a rapid increase in heartbeat of more than 30 beats per minute, or a heart rate that exceeds 120 beats per minute, within 10 minutes of rising. The faintness or lightheadeness of POTS are relieved by lying down again. Anyone at any age can develop POTS, but the majority of individuals affected (between 75 and 80 percent) are women between the ages of 15 to 50 years of age. Some women report an increase in episodes of POTS right before their menstrual periods. POTS often begins after a pregnancy, major surgery, trauma, or a viral illness. It may make individuals unable to exercise because the activity brings on fainting spells or dizziness.

Doctors aren’t sure yet what causes the reduced return of blood to the heart that occurs in OI, or why the heart begins to beat so rapidly in POTS, but the current thinking is that they are the result of abnormalities in the sympathetic nervous system (which is responsible for decreasing muscle tone and increasing heartbeat in reaction to situations of stress or emergency) or the parasympathetic nervous system (which does the opposite) or both .

Is there any treatment?

Therapies for POTS are targeted at relieving low blood volume or regulating circulatory problems that could be causing the disorder. No single treatment has been found to be effect for all. Some treatments are more successful than others and are often used together for best results. Simple interventions such as adding extra salt to the diet, and avoiding heavy meals and alcohol are often effective. Some people with POTS avoid faintness by sleeping with the head of the bed tilted up or by using a body stocking. The drugs fludrocortisone (for those on a high salt diet) and midodrine in low doses are often used to increase blood volume and narrow blood vessels. Drinking 16 ounces of water (2 glassfuls) before getting up can also help raise blood pressure. Some individuals are helped by beta receptor blocking agents. There is some evidence that an exercise program can gradually improve orthostatic tolerance.

What is the prognosis?

POTS may follow a relapsing-remitting course, in which symptoms come and go, for years. In most cases (approximately 80 percent), an individual with POTS improves and becomes functional, although some residual symptoms are common.

NINDS

Chronic Inflammatory Demyelinating Polyneuropathy (CIPD)

What is chronic inflammatory demyelinating polyneuropathy (CIPD)?

Chronic inflammatory demyelinating polyneuropathy (CIDP) is a neurological disorder characterized by progressive weakness and impaired sensory function in the legs and arms. The disorder, which is sometimes called chronic relapsing polyneuropathy, is caused by damage to the myelin sheath (the fatty covering that wraps around and protects nerve fibers) of the peripheral nerves. Although it can occur at any age and in both genders, CIDP is more common in young adults, and in men more so than women. It often presents with symptoms that include tingling or numbness (beginning in the toes and fingers), weakness of the arms and legs, loss of deep tendon reflexes (areflexia), fatigue, and abnormal sensations. CIDP is closely related to Guillain-Barre syndrome and it is considered the chronic counterpart of that acute disease.

Is there any treatment?

Treatment for CIDP includes corticosteroids such as prednisone, which may be prescribed alone or in combination with immunosuppressant drugs. Plasmapheresis (plasma exchange) and intravenous immunoglobulin (IVIg) therapy are effective. IVIg may be used even as a first-line therapy. Physiotherapy may improve muscle strength, function and mobility, and minimize the shrinkage of muscles and tendons and distortions of the joints.

What is the prognosis?

The course of CIDP varies widely among individuals. Some may have a bout of CIDP followed by spontaneous recovery, while others may have many bouts with partial recovery in between relapses. The disease is a treatable cause of acquired neuropathy and initiation of early treatment to prevent loss of nerve axons is recommended. However, some individuals are left with some residual numbness or weakness.

NINDS

Neuroacanthocytosis

Synonym(s): Levine-Critchley Syndrome, Choreoacanthocytosis

What is Neuroacanthocytosis?

Neuroacanthocytosis refers to a group of genetic conditions that are characterized by movement disorders and acanthocytosis (abnormal, spiculated red blood cells). Four syndromes are classified as neuroacanthocytosis: Chorea-acanthocytosis, McLeod syndrome, Huntington’s disease-like 2 (HDL2), and panthothenate kinase-associated neurodegeneration (PKAN). Acanthocytosis may not always be observed in HDL2 and PKAN. These disorders are caused by different genetic mutations, and the signs and symptoms vary, but usually include chorea (involuntary, dance-like movements), parkinsonism (slowness of movement), dystonia (abnormal body postures), and problems walking. There may also be muscle weakness, involuntary movements of the face and tongue, tongue/lip biting (which is mostly characteristic of Chorea-acanthocytosis), as well as difficulty with speech and eating, cognitive impairment, psychiatric symptoms, and seizures. Individuals with McLeod syndrome often have cardiac problems. Many features of these disorders are due to degeneration of the basal ganglia, a part of the brain that controls movement. Additional disorders that are also known have neurologic symptoms, acanthocytosis, and either lipoprotein disorders or systemic findings. The diagnosis of neuroacanthocytosis is typically based on the symptoms and clinical observation, a review of family history, and the evaluation of specific laboratory and imaging studies.

Is there any treatment?

There are currently no treatments to prevent or slow the progression of neuroacanthocytosis and treatment is symptomatic and supportive. Medications that block dopamine, such as some of the antipsychotics, may decrease the involuntary movements. Botulinum toxin injections usually improve symptoms of dystonia. A feeding tube may be needed for individuals with feeding difficulties to maintain proper nutrition. Seizures may be treated with a variety of anticonvulsants, and antidepressants may also be appropriate for some individuals. Speech, occupational, and physical therapy may also be beneficial.

What is the prognosis?

Neuroacanthocytosis is a progressive disease, and in some cases may be complicated by poor nutritional status, cardiac abnormalities, and pneumonia.

NINDS

Chorea

What is chorea?

Chorea is an abnormal involuntary movement disorder, one of a group of neurological disorders called dyskinesias,which are caused by overactivity of the neurotransmitter dopamine in the areas of the brain that control movement. Chorea is characterized by brief, irregular contractions that are not repetitive or rhythmic, but appear to flow from one muscle to the next. Chorea often occurs with athetosis, which adds twisting and writhing movements. Chorea is a primary feature of Huntington’s disease, a progressive, hereditary movement disorder that appears in adults, but it may also occur in a variety of other conditions. Syndenham’s chorea occurs in a small percentage (20 percent) of children and adolescents as a complication of rheumatic fever. Chorea can also be induced by drugs (levodopa, anti-convulsants, and anti-psychotics) metabolic and endocrine disorders, and vascular incidents.

Is there any treatment?

There is no standard course of treatment for chorea. Treatment depends on the type of chorea and the associated disease. Treatment for Huntington’s disease is supportive, while treatment for Syndenham’s chorea usually involves antibiotic drugs to treat the infection, followed by drug therapy to prevent recurrence. Adjusting medication dosages can treat drug-induced chorea. Metabolic and endocrine-related choreas are treated according to the cause(s) of symptoms.

What is the prognosis?

The prognosis for individuals with chorea varies depending on the type of chorea and the associated disease. Huntington’s disease is a progressive, and ultimately, fatal disease. Syndenham’s chorea is treatable and curable.

NINDS

Charcot-Marie-Tooth Disease

What is Charcot-Marie-Tooth Disease?

Charcot-Marie-Tooth disease (CMT) is one of the most common inherited neurological disorders, affecting approximately 1 in 2,500 people in the United States.  CMT,  also known as hereditary motor and sensory neuropathy (HMSN) or peroneal muscular atrophy, comprises a group of disorders caused by mutations in genes that affect the normal function of the peripheral nerves.  The peripheral nerves lie outside the brain and spinal cord and supply the muscles and sensory organs in the limbs.  A typical feature includes weakness of the foot and lower leg muscles, which may result in foot drop and a high-stepped gait with frequent tripping or falls. Foot deformities, such as high arches and hammertoes (a condition in which the middle joint of a toe bends upwards), are also characteristic due to weakness of the small muscles in the feet. In addition, the lower legs may take on an “inverted champagne bottle” appearance due to the loss of muscle bulk. Later in the disease, weakness and muscle atrophy may occur in the hands, resulting in difficulty with fine motor skills. Some patients experience pain, which can range from mild to severe.

Is there any treatment?

There is no cure for CMT, but physical therapy, occupational therapy, braces and other orthopedic devices, and orthopedic surgery can help patients cope with the disabling symptoms of the disease. In addition, pain-killing drugs can be prescribed for patients who have severe pain.

What is the prognosis?

Onset of symptoms of CMT is most often in adolescence or early adulthood, however presentation may be delayed until mid-adulthood.  Progression of symptoms is very gradual.  The degeneration of motor nerves results in muscle weakness and atrophy in the extremities (arms, legs, hands, or feet), and the degeneration of sensory nerves results in a reduced ability to feel heat, cold, and pain.  There are many forms of CMT disease.  The severity of symptoms is quite variable in different patients and some people may never realize they have the disorder. CMT is not fatal and people with most forms of CMT have a normal life expectancy.

NINDS

Cerebro-Oculo-Facio-Skeletal Syndrome (COFS)

Synonym(s): COFS, Pena Shokeir II Syndrome, Cockayne Syndrome Type II

What is Cerebro-Oculo-Facio-Skeletal Syndrome (COFS)?

Cerebro-oculo-facio-skeletal syndrome (COFS) is a pediatric, genetic, degenerative disorder that involves the brain and the spinal cord. It is characterized by craniofacial and skeletal abnormalities, severely reduced muscle tone, and impairment of reflexes. Symptoms may include large, low-set ears, small eyes, microcephaly (abnormal smallness of the head), micrognathia (abnormal smallness of the jaws), clenched fists, wide-set nipples, vision impairments, involuntary eye movements, and mental retardation, which can be moderate or severe. Respiratory infections are frequent. COFS is diagnosed at birth. Ultrasound technology can detect fetuses with COFS at an early stage of pregnancy, as the fetus moves very little, and some of the abnormalities result, in part, from lack of movement.

A small number of individuals with COFS have a mutation in the “ERCC6″ gene and are more appropriately diagnosed as having Cockayne Syndrome Type II. Other individuals with COFS may have defects in the xeroderma pigmentosumgenes “XPG” or “XPD.” Still others who are diagnosed with COFS have no identifiable genetic defect and are presumably affected because of mutations in a distinct, as-yet-unknown gene.

NOTE: This disorder is not the same as Cohen’s syndrome (cerebral obesity ocular skeletal syndrome).

Is there any treatment?

Treatment is supportive and symptomatic. Individuals with the disorder often require tube feeding. Because COFS is genetic, genetic counseling is available.

What is the prognosis?

COFS is a fatal disease. Most children do not live beyond five years.

NINDS

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