ENCEPHALO-MEDULLOPATHIES BY BORDETELLA PERTUSSIS
According to the experimental pathology we know that (See notes 1, 2, 3, 4, 5):
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.
- 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;
- 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;
- antibodies anti HLA-antigens of II class inhibit the onset of EAE;
- we can find soluble adehesion molecules (s-ICAM) in MS, not in the non-inflammatory
neuropathies (including ALS).
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:
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 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.
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 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
- 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
- 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.
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Allergic Encephalomyelitis with Antibody to T-cell subset Marker.Science.
Vol 222. Pages: 415-417.
- 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.
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Scienze. Anno XXII. Vol XLII, No 25), (Giugno 1989). Pag. 54-62.
- Troiano M.: Immunopatogenesi della Sclerosi Multipla:
ruolo della barriera emato-encefalica. Volume Abstract del Congresso
SNO. Otranto-2000. Pag. 15-16.
- Troiano M. et Altri: Soluble intercellular adhesion
] in multiple sclerosis. Neurology 47 (1996): Pag.
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Diagnosi, terapia, profilassi. - Attualità e Prospettive. Volume
degli Abstrac del Congresso S N O. Otranto 2000. 96-70
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delle encefalo-medullopatie da Bordetella Pertussis" - EOS, n°
3, vol XX, (2000). Pag. 63-70.