This post, like the first on MS, started with the conversation I had over lunch with Prof Ebringer and has been kicked around in my head for a few months afterwards. Here's the next phase.
The immune system is quite complex. Apart from defending us against microbes it appears to be quite important in healing. The formation of antibodies against damaged tissues seems to be quite routine and is probably part of the normal healing process. When those auto antibodies are made against proteins which are not limited to the damaged tissues you can get auto immune diseases in the aftermath of injury. Best documented is pemphigus, where the initial antibodies to skin proteins can be produced in response to damage by anything from UV radiation or thermal burns to surgery or drug adverse reactions. Sometimes the problem goes away with removal of the trigger or after healing of the injury, other times it's there for ever as a self perpetuating, on going, catastrophic problem with auto immune attack on the skin.
Let's talk optic neuritis and multiple sclerosis. Optic neuritis is an inflammatory injury to the optic nerve. Usually it has no obvious cause (think gluten!) but occasionally it comes directly associated with sinusitis. The sinusitis does not have to be caused by acinetobacter, any infection will do, it can even be subclinical.
Treatment, by aggressive surgical and medical management can produce prompt resolution of both the neuritis and sinusitis if a correct diagnosis is made (difficult if the sinus problem is subclinical and an MRI is not available!). The theory linking the two problems seems to be a localised inflammation, plus venous spread of a frightening soup of inflammatory mediators from the sinus past the optic nerve.
The nerve is clearly injured, as reflected by the chunks of lost vision. The injury is not permanent if the sinusitis is successfully treated. The question to me is whether there is enough damage to the optic nerve for the myelin sheathes to be recognised by the immune system as needing antibody production, aka skin burns and auto antibodies to skin. If the damaged nerve does trigger antibody production you are set up with anti-myelin antibodies, which just might have you set up with an on going anti myelin syndrome, call it MS.
About half to three quarters of the people who get idiopathic optic neuritis go on to develop MS. The question to me is whether these are the half or more who had acinetobacter in their sinuses or those who developed auto antibodies to their myelin as a direct result of inflammatory mediator damage. I don't think there is information available which allows us to come to any conclusion about this. It is even possible that the initial priming of the immune system by direct nerve damage from sinusitis can be maintained and promoted by chronic acinetobacter respiratory infection or vice versa... A number of MS patients may be straight gluten toxicity mediated by the innate immune system in the absence of antibodies to anything.
The idea (somewhat abstract) of antibodies to damaged nerves is interesting as it has similarities to immune mediated damage to nerves seen in the various experimental autoimmune encephalomyelitis models used to study MS. These are interesting in their own right and being injected with nerve tissue, especially from other species, appears to be a particularly potent way of generating "MS like" syndromes. They can be another post.