multiple sclerosis amyotrophic lateral sclerosis pseudobulbar syndrome motoneuron disease neurogenous muscolar dystrophy hemiparkinson spastic tetraparesis balo's concentric sclerosis
Dr. Domenico Fiore: sclerosi multipla Dr. Domenico FIORE
V.le Madonna delle Grazie, 17
35028 Piove di Sacco (Padova)


According to the experimental pathology we know that (See notes 1, 2, 3, 4, 5):

  1. to induce the experimental allergic ancephalitis (EAE) in the laboratory animals with the classic method it is necessary not only to immunize them by subcutaneous injections of spinal marrow homogenate, but also to inject endovenously or intra-peritoneum two doses of anti-pertussis vaccine: the first one during the immunization and the second one within 48 hours after the last injection of spinal marrow homogenate; without these two administrations of killed Bordetella (about some billions of killed bacteria) it is not possible to induce EAE;
  2. in a certain animal species we can induce EAE in the form which is considered experimental model of human MS only in the races with astrocytes producers of II class HLA-Antigens; the disease does not arise in the races that have astrocytes not-producers of II class HLA-Antigens;
  3. antibodies anti HLA-antigens of II class inhibit the onset of EAE;
  4. we can find soluble adehesion molecules (s-ICAM) in MS, not in the non-inflammatory neuropathies (including ALS).
Having found (See note 6) a toxi-infection by B. Pertussis in the 95,47% out of 92 patients affected by Multiple Sclerosis (MS) and expecting to find "negative" the patients with neuropathies different from Multiple Sclerosis, as a comparison/check I searched for anti-pertussis antibodies in 20 neurologic patients for whom MS had been excluded (the clinic diagnosis were: Amyotrophic Lateral Sclerosis, Pseudobulbar Syndrome, Motoneuron Disease, Neurogenous Muscolar Dystrophy; Hemiparkinson, Spastic Tetraparesis, Balo's Concentric Sclerosis). In all these patients the nuclear magnetic resonance (NMR) had excluded the presence of patches.
The research of Anti-Bordetella antibodies I asked for came out to be positive in all cases (see the Report example + E-M Scan).
These results demonstrate that (See note 7) , in subjects with a muco-ciliar barrier defect, a re-infection by Bordetella can cause:
  • the multiple sclerosis, in individuals with astrocytes producers of HLA-Antigens of II class;
  • various clinical forms of neuropathies, in individuals with astrocytes not-producers of HLA-antigens of II class.
In these cases the clinical form will depend on the ratio toxins/antibodies (zone phenomenon, Arthus reaction) and on the phenotype (that is, on the metabolic and receptor features) of the neurones, astrocytes and oligodendrocytes preferentially damaged by pertussis toxins.

The substantial pathogenetic differences that exhist between the two types of neuropathies by B. Pertussis (with or without patches) implies a strong difference in the expected "functional recover":

  • in MS (prevailing damages caused by immune complexes precipitation, but also direct toxin damages, caused by the toxins "escaped" from the incorporation into the immune complexes), the functional recover can be very good, but it will be inversally proportional to the disease duration (damages already consolidated and, most of all, direct toxin damages).
  • in the neuropathies without patches (toxins attacking directly neuroepithelia) the damages already suffered at the moment of the etiological diagnosis will not be repaired, all the neurepithelia with toxin "parasitization", being at first only suffering, will end by dying.
In all the cases the benefits will come from the timeliness of the etiological diagnosis and of the subsequent specific antibiotic treatment; for this reason: in all neuropathies which cannot be etiologically qualified ex ante, as the prognosis can be positively modified (at the moment the most part of SM patients is bound to a severe disability; the ALS patients have infaust prognosis, after terrible sufferings), it becomes compulsory to search also for anti-Bordetella antibodies with appropriate methods


  1. Waldor M.F. et Altri (1985): Reversal of Experimental Allergic Encephalomyelitis with Antibody to T-cell subset Marker.Science. Vol 222. Pages: 415-417.
  2. Waisman A. et Altri (1996): Suppressive vaccinati on with DNA encoding a variable region gene of the T-cell receptor prevents autoimmune encephalomyelitis and activate Th2 immunity. Nature Medicine. Vol. 2, (August 1996). Pages: 891-895.
  3. Kimelberg H.K.- Norenberg M.D.: Gli Astrociti. Le Scienze. Anno XXII. Vol XLII, No 25), (Giugno 1989). Pag. 54-62.
  4. Troiano M.: Immunopatogenesi della Sclerosi Multipla: ruolo della barriera emato-encefalica. Volume Abstract del Congresso SNO. Otranto-2000. Pag. 15-16.
  5. Troiano M. et Altri: Soluble intercellular adhesion molecule.1 […] in multiple sclerosis. Neurology 47 (1996): Pag. 1535-1541.
  6. Fiore D.: Sclerosi Multipla - Diagnosi, terapia, profilassi. - Attualità e Prospettive. Volume degli Abstrac del Congresso S N O. Otranto 2000. 96-70
  7. Fiore D.: " I fattori immunologici nella patogenesi delle encefalo-medullopatie da Bordetella Pertussis" - EOS, n° 3, vol XX, (2000). Pag. 63-70.
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