(MAC/MAI) Mycobacterium Avium Complex Pulmonary Disease: Join us

Just be careful and look after yourself

@oldkarl I'm with @windwalker Terri. I have never heard of chronic being used with bronchiectasis. I thought bronchiectasis IS chronic. Once you are diagnosed with it's for life. There is no cure. When you put chronic and bronchiectasis together, it is as if bronchiectasis can be transient and curable. That makes no sense to me.

@flib I wasn't taking into account that some mouthpieces have that little outlet valve or flap to allow exhaled breath to escape through. The main thing is to get the mist into the lungs.

@ling123 That was exactly my thought process when I read Karl's post.

@heathert I think I need a Pari nebulizer!

@windwalker I had one when in the Amakacin trial so when I finished I bought my own, fantastic nebuliser and no tubes so easy to clean!

I know. I saw that video too some time ago and also another one. In both the mouth is not removed from the nebulizer...i.e. the person is exhaling back into the nebulizer which seems all wrong. However, if you take you mouth piece out to exhale you are losing some of the mist. Flib

Exactly what I was thinking.Thanks, Flib

Thanks, Terri. My conclusion also. My nebulizer doesn't have any holes but I manage to exhale to the side and get the mist in. All this fun, I can hardly stand it.

@windwalker, I'm not gonna argue with anyone. All I have to go on is Mayo and the doctors who have diagnosed me. But there is a big difference between simple or acute bronchiectasis, and Chronic Bronchiectasis. Simple bronchi... is the result of bacterial infection. it is hard to control, and can be deadly. But if you can control, even kill, the bacteria, no more damage will be done. Chronic, on the other hand, owes its existence to misfolding and dying prions of protein. These prions, or proteins with autoimmune problems, often clone themselves a few times before they die. Then each clone repeats, and so on, putting their clone out into the blood stream. When they die, their carcasses work their way into body tissue, stack themselves into tiny water tubes called fibrils, and START doing their damage to the tissue. For instance, if the fibrils get into the lung tissues, it is these dead carcases that leatherize the tissues or make them enlarge, or mess up skin, or corneas, or stack themselves in the brain, or whatever. They are tiny, about a thousandth the width of a human hair. But because they are already dead, their existence is chronic and cannot now be stopped as bacteria can. At this point in time, science has no way to get them out of the body if the kidneys fail, and no way to stop them from forming. The fibrils only live for 2-3 hours, not long enough to take a hammer and beat the little buggers into submission. So they just keep doing their damage until after the person is dead. That is the difference. Nothing stops them, especially not their death. With the bacteria, they may be difficult to kill, but they can be stopped, at least theoretically. Acute bronchi.... is dangerous only as long as the bacteria is alive. Amyloid fibrils are dangerous only after they are dead. Then localized fibrils attach whatever tissue they can attach to. Some can go only to heart walls, or blood vessel linings. Some go after these, and kidneys, and toenails and corneas, for instance. It depends on their exact shape, elasticity, size, atomic weight, whatever, after they are dead and reformed into fibrils. If bacteria, it lives to damage. If protein prions, they die to damage.