I was prescribed Zpac antibiotic (zithromax), for bronchitis, in 2003, cured the bronchitis, then gave me Guillain-Barre. It is a form of erythromycin.

azithromycin - An azalide, derived from erythromycin, and a member of a subclass of macrolide antibiotics with bacteriocidal and bacteriostatic activities. Azithromycin reversibly binds to the 50S ribosomal subunit of the 70S ribosome of sensitive microorganisms, thereby inhibiting the translocation step of protein synthesis, wherein a newly synthesized peptidyl tRNA molecule moves from the acceptor site on the ribosome to the peptidyl (donor) site, and consequently inhibiting RNA-dependent protein synthesis leading to cell growth inhibition and cell death.

At this point in time the immune cells, which had been initially activated by the bacteria, had finally reached the peripheral nerves and were attacking them. When this happens the peripheral nerves become inflamed and the myelin sheath that surrounds the nerve fibres gets damaged. One's own immune system should not attack its peripheral nerves, but under certain circumstances it can become confused or conned into doing so because of a process known as 'molecular mimicry'. The proteins that are attached to the bacteria are often very similar, if not the same, to the ones on the surface of the peripheral nerves and the immune system cannot differentiate the two.

When the nerve becomes inflamed and the myelin starts to become damaged, there are certain things that happen to the nerves which cause symptoms. The first is that of conduction block. Instead of the signal being able to propagate all the way down the nerve, it reaches a point where the inflammation is severe and blocked, preventing the conduction from getting through. If this happens in a nerve that is carrying signals from the central nervous system to the muscles, it causes weakness. When it happens to nerves or fibres carrying signals back to the central nervous system, the symptoms include those of numbness and unsteadiness. Sometimes there is damage to the nerve axon (the part that actually conducts the electricity), which is more severe.

The reason for the destruction of myelin in GBS is unknown, although it is thought that the underlying problem is autoimmune in nature. An autoimmune disorder is one in which the body's immune system, trained to fight against such foreign invaders as viruses and bacteria, somehow becomes improperly programmed. The immune system becomes confused, and is not able to distinguish between foreign invaders and the body itself. Elements of the immune system are unleashed against areas of the body, resulting in damage and destruction. For some reason, in the case of GBS, the myelin sheath appears to become a target for the body's own immune system.

The first symptoms of GBS consist of muscle weakness (legs first, then arms, then face), accompanied by prickly, tingling sensations (paresthesias). Symptoms affect both sides of the body simultaneously, a characteristic that helps distinguish GBS from other causes of weakness and paresthesias. Normal reflexes are first diminished, then lost. The weakness eventually affects all the voluntary muscles, resulting in paralysis. When those muscles necessary for breathing become paralyzed, the patient must be placed on a mechanical ventilator which takes over the function of breathing. This occurs about 30% of the time. Very severely ill GBS patients may have complications stemming from other nervous system abnormalities which can result in problems with fluid balance in the body, severely fluctuating blood pressure, and heart rhythm irregularities.

Periodicals:

Fulgham, J. R. "Guillain-Barr� syndrome." Critical Care Clinics (Jan. 1997): 1-15.

Rees, J. H. "Campylobacter jejuni Infection and Guillain-Barr� Syndrome." New England Journal of Medicine (23 Nov. 1995): 1374-79.

Stern, V. "Terror of the Unknown." The Guardian (13 Feb. 1996): T10+.

Walling, A. D. "Comparisons of Treatments for Guillain-Barr� Syndrome." American Family Physician (15 May 1997): 2510+.

Organizations:

American Academy of Neurology. 1080 Montreal Ave., St. Paul, MN 55116. (612) 695-1940. http://www.aan.com

Guillain-Barr� Syndrome Foundation International. PO Box 262, Wynnewood, PA 19096. (610) 667-0131. (610) 667-0131. http://www.webmast.com/gbs

http://www.healthatoz.com/healthatoz/Atoz/ency/guillain-barre_syndrome.html
Source: Gale Encyclopedia of Medicine, Published December, 2002 by the Gale Group
The Essay Author is Rosalyn Carson-DeWitt MD

According to a guideline developed by the American Academy of Neurology (AAN), treating GBS early, within two to four weeks after signs and symptoms first appear, may speed recovery time. Two main treatments, both equally effective, have been shown to speed the recovery from and reduce the severity of GBS in adults:

Plasmapheresis (plaz-muh-fuh-RE-sis). This treatment � also known as plasma exchange � is a type of "blood cleansing" in which damaging antibodies are removed from your blood. Plasmapheresis consists of removing the liquid portion of your blood (plasma) and separating it from the actual blood cells. The blood cells are then put back into your body, which manufactures more plasma to make up for what was removed. It's not clear why this treatment works, but scientists believe that plasmapheresis removes certain antibodies from plasma that contribute to the immune system attack on the peripheral nerves.

Intravenous immunoglobulin (IVIg). Immunoglobulin contains healthy antibodies from blood donors. High doses of immunoglobulin can block the damaging antibodies in your blood that may contribute to GBS.

Sodium
Vitamin D-3
Vitamin B-12 (as methylcobalamin)
Pantothenic Acid (as calcium d-pantothenate)
Calcium (as dibasic calcium phosphate
and calcium ethanolamine phosphate [EAP]
Iodine (as kelp)
Magnesium (as magnesium citrate and malate)
Zinc (as zinc picolinate)
Selenium (as L-selenomethioinine [Selenomax]
Copper (as copper sebecate)
Manganese (as manganese citrate)
Chromium (as chromium picolinate)
Molybdenum (as molybdenum chelate)
Potassium (as potassium citrate)

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What happens?

The lymphocytes set off chemicals called antibodies that circulate in the blood and latch on to, and damage the myelin. They also attract macrophages that are cells that attack and digest myelin. Eventually suppressor lymphocytes stop the action of the harmful lymphocytes, allowing the sheath to regenerate. Occasionally, the attack is directed against the axon (the cable

Are there different types of GBS?

GBS is a syndrome - which means a collection of symptoms - rather than an individual illness. If the nerves become inflamed and lose their myelin, which happens in most cases, it is called acute demyelinating polyradiculoneuropathy (AIDP).

Chronic demyelinating polyradiculoneuropathy

If GBS becomes chronic, it is called chronic demyelinating polyradiculoneuropathy (CIDP). Breathing difficulties are not common in this version of the condition. It is different from GBS, in that it takes more than four weeks to reach its peak. Treatment, which aims to stop the immune reaction of the body against itself, includes the use of drugs, usually steroids or azathioprine, or blood-related treatments such as plasma exchange and intravenous immunoglobulin.

Treatment is tailored to the individual according to the form and severity of their disease. These options will be explained by your doctor. The risk is that while it suppresses the abnormal immune response, treatment can also affect normal immune functions.

Miller Fisher Syndrome

Miller Fisher Syndrome affects 5% of GBS sufferers and causes paralysis of the eye muscles, lack of coordination, loss of tendon reflexes and no weakness.

Jenny Murray, National coordinator, 27 Grenville St, New Plymouth, Phone/fax 06 751 1014, Email [email protected]

Terry Watton, President, 28 Thames Rd, Paeroa, Phone 07 862 6438, Email [email protected]

Robert Gregory, Researcher, Dept of Psychology, Massey University, Private Bag 11222, Palmerston North, Phone 06 350 5799, ext 2053, Email [email protected]