MULTIPLE SCLEROSIS: MICROBIOLOGY, SEROLOGY, TREATMENT
Neurology World Congress- Buenos Aires 1997
Bordetella (BB) in S-phase produce lots of endotoxins (LPF, LPS, etc.);
in R-phase they produce prevalently LPS. LPF irreversibly activates all
the immunocompetent cells: it initially induces normal secondary immune
response (IgG, activated T- lymphocytes, armed macrophages); by protracted
action, it makes T-lymphocytes autocytotoxic.
LPS induces protracted IgM production alternated with immune complexes
building-up. Endotoxins (that are not neutralized by antiserums) + IgM
form immune circulating complexes (ICC) that inhibit antibodies production
and end up precipitating (provoking an attack); IgM production starts again;
the cycle repeats itself. Normally, BB-toxins does not pass into blood.
In individuals with a primitive or secondary muco-ciliar barrier defect,
after reinfection by Bordetella we can have:
- rapid reclamation of respiratory mucosa: transient passage of toxins
into blood; LPF actions prevail; anti-BB IgG and average-low ICC levels
are found in serum; it is Multiple Sclerosis (MS) with IgG, remittent.
- colonization of mucosas (BB on R-phase): protracted passage of toxins
into blood. Autocytotoxic T-lymphocytes, high levels of ICC and/or anti-BB
IgM are found in the blood; it is MS with IgM, chronic-evolutive with free
intervals.
If an attack produces serious vascular damages:
- new toxins + residue/neophormed specific antibodies form ICC that immediatly
precipitate into previous lesions;
- lacking antibodies, new toxins fixed themselves to neuroepithelia; with
new antibodies (also locally neoproduced) they form immune complexes where
the lesion is.
Neither ICC, nor anti-BB antibodies are found in serum: it is seronegative-MS,
chronic-evolutive without free intervals (always active patches; in subjects
with astrocytes producers of II class Ag-HLA autoimmunity can occur).
MS is a toxi-infective disease: environmental factor is Bordetella;
individual factor is a primitive or secondary muco-ciliar barrier defect
which permits toxins passage into blood; clinical forms depend on the relationship
established between Host and bacterium; precocious etiological diagnosis
is possible searching for ICC and for anti-BB IgM and IgG in serum.
Specific treatment: protracted administration of erytromycin
|
