During my studies on neuropathies from Bordetella Pertussis in Men, a patient with Multiple Sclerosis, who was undergoing an infection by B. Pertussis in S-phase (virulent and contagious), told me that her daughter was affected by Myasthenia Gravis and that she was getting worse and worse though she had been thymectomized and though she was submitting herself to frequent plasmapheresis.

To be scrupulous, I asked for a research of anti-Bordetella antibodies also in this daughter’s serum: the result was definitely positive. Also other four patients affected by myasthenia, of whom two were thymectomized as well, came out to be positive.

To verify if there could be an etiopathogenic relationship between BP and MG, I analysed again in literature the anatomic, immunologic and biomolecular characteristics of MG.

It results that in MG there is a decrease of acetylcholine receptors (AchR) at the level of neuromuscular junction and that in its pathogenesis anti-AchR antibodies are surely involved. From general Phisiology we know that membrane receptors (of surface) can be divided into three groups:

• receptors connected to ionic channels;
• receptors connected to G-proteins; receptors connected to enzymes.

After a synthetic description of acetylcholine receptors at the level of neuromuscular junction, I describe, in a more general way, receptors linked to ionic channels (with indications about the electrical qualities of membrane) and receptors linked to G-proteins.

Keeping in mind these notions, I reasses experimental myasthenia gravis and the spontaneous MG in the animals and, considering the natural and experimental pathogenic power of bordetella toxins, I examine the cellular mechanisms of reception, transportation and metabolization of neurotransmitters; I pay particular attention to receptors which are linked to G-proteins, to the effects of the ADP-rybosilaction of these proteins due to Pertussis Toxin, and to the effects of the ATPasi (main regulator of “channels loosing K+”) due to the Dermonecrotic Toxin (probably responsible for “myasthenic crisis”).

Reconsidering the role of Thymus in MG, we see that the lymphoid organ at first suffers the attack of anti-AchR antibodies and of T-lymphocytes made autocytotoxic by Pertussis Toxin, then, producing abnormal quantities of thymopoietin, it interferes directly with muscular contraction.

We have to issue that:

• if MG can be due to a reinfection by Bordetella Pertussis, in all patients is compulsory to search for anti-pertussis antibodies with proper methods;
• if the research comes out to be positive, the disease is perfectly curable: with the specific antibiotic treatment (eritrocina) we avoid the patient become disabled.