I'm reading about pneumonia online and have found there's a lot about it that is surprising, including the many types of pneumonia. Here's a section that gets into diagnosis that includes a reference to 'tie-dying':

"The bacterial kingdom is divided into those that dye purple called Gram positive, and those that dye pink, called Gram negative. (Pneumococcal is Gram positive and nursing home pneumonia is Gram negative.)

The stain we use was invented in 1878 by a young Dane named Hans Christian Gram. It is similar to tie-dying. The first dye is crystal violet and is fixed or mordanted in Gram positive bacteria by iodine. (In tie-dying the mordant is alum.)

The dye washed out of the Gram negative bacteria with alcohol and a pick counter stain, safranin, is added to color them so they can be easily seen.

Gram positive bacteria are usually sensitive to penicillin; gram negative bacteria are not. The latter require complex and new antibiotics that are often difficult to choose."

Well, I find all that interesting, particularly the use of the words tie-dye and mordant.

But toward the end of the article there is this curious statement regarding sleeping pills, of all things, as increasing the likelihood of contraction of pneumonia, which puzzles the heck out of me. Any comment wwh or wof'?

"Once you get into a nursing home, your chances of having these bacteria in your throat rise to 12 percent, and in a skilled nursing home to 37 percent. In the acute care hospital, 60 percent of the elderly carry these potentially dangerous bacteria in their throat. When this happens, a heavy dose of sleeping pills or a stroke allows you to breathe these potentially deadly organisms into your lungs."


http://www.vh.org/adult/patient/internalmedicine/aba30/1992/pneumoniadiagnosis.html

*Let me know whether the link is too long. If it is, I'll just get rid of it.

Maybe you breathe differently when under the influence of sleeping pills. Maybe then you can suck the bacteria into your lungs from your throat. Any docs wanna explain?

I see not point in mentioning tie dying. It just happens that one large group of bacteria will take the blue dye, and the remainder won't. The big problem in all enclosed places is that aerosols of bacteria are produced, and susceptible people inhale them. Especially susceptible patients have to be put into tent of clear plastic, with oxygen from tanks.

as far as I remember both types take the blue dye in. but gram-positive bacteria have many more layers of peptido-glycan which forms the cell wall of the majority of bacteria. so crystal violet will be washed from gram-negative but not gram-positive cells.

the "sleeping pill and stroke" thing puzzles me
but I am not a MD

the "sleeping pill and stroke" thing puzzles me
but I am not a MD

Dear vika: I am an ancient and obsolete former MD, but
I see little sense in that sentence.

how about an idea that both stroke and a heavy sleep after taking sleeping pills causes breathing through the mouth rather than though the nose. therefore air comes via throat and can carry bacteria to the lungs

Vika, my guess is that you're probably right about the sleeping pills; plus, I imagine that under sedation, we move less, and so instead of turning onto our side and resuming nose-breathing, we might lie on our backs and mouth-breathe the whole time.

WW, thanks for this thread--I had completely forgotten this use of mordant, and had to LIU in Atomica:
mor·dant (môr'dnt)
adj.

Bitingly sarcastic: mordant satire.
Incisive and trenchant: an inquisitor's mordant questioning.
Bitingly painful.
Serving to fix colors in dyeing.
n.
A reagent, such as tannic acid, that fixes dyes to cells, tissues, or textiles or other materials.
A corrosive substance, such as an acid, used in etching.
tr.v., -dant·ed, -dant·ing, -dants.
To treat with a mordant.

[French, from Old French, present participle of mordre, to bite, from Vulgar Latin *mordere, from Latin mordēre.]

mor'dan·cy n.
mor'dant·ly adv.
--------------------------------------------------------------------------------
The American Heritage® Dictionary of the English Language, Fourth Edition Copyright © 2000 by Houghton Mifflin Company. Published by Houghton Mifflin Company. All rights reserved.

About the sleeping pills, there are a few factors. Under sedation or after a stroke you move around less and secretions can pool in the lowest part of the lungs allowing bacteria to thrive. Sedation will also sedate the cilia, the little hairs of the cells lining the lungs, which act as an escalator to move bacteria and gunk (technical term) up and out. Also after a stroke or if someone is over-sedated the muscles which protect the airway can become unco-ordinated and allow food and saliva into the lungs carrying bacteria.

In reply to:

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Sedation will also sedate the cilia, the little hairs of the cells lining the lungs, which act as an escalator to move bacteria and gunk (technical term) up and out.

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Now that's the kind of inside information I knew we'd eventually get around to hearing about! Thanks, Zed. The sleeping pill statement was extremely puzzling--and the open-mouth theory just didn't strike me as being quite plausible since I doubted that all who took sleeping pills automatically slept with their mouths open. But your points make more sense, and this point about the sedated cilia is fascinating.

...the sedated cilia is fascinating.

eah, poor wee cilia

eah, poor wee cilia
vika, you've become Scottish, now?

Agree with the cilia, Zed. Depressed cough and swallow reflexes are a big contributory factor

For anyone who's interested, look up "aspiration pneumonia" on whichever medical site or search engine floats your boat. With sedation secondary to sleeping tablets, the body's natural reflexes are diminished. One of these is the gag reflex which prevents you from inhaling liquids and solids. In the presence of vomiting or regurgitation (cf reflux) - both of which are common in institutionalised patients - when the gag reflex is diminished or absent, oral and GIT micro-organisms gain access to the lungs. In institutionalised patients, these organisms are often less treatable than in a community setting, having been exposed to antibiotics and having developed resistance. Strokes affecting certain parts of the brain can also interfere with the gag reflex or with swallowing producing the same result, namely an aspiration pneumonia.

Any questions?

(Better late than never.)

The lungs have an intrinsic mechanism for clearing the gunk (official term "sputum," once called "phlegm") automatically: the surface layer of cells in the bronchi (epithelium) has little hairlike extensions (cilia, pl of cilium) that sweep any adherent mucus, plus whatever germs or cellular debris may be in it, up and out. That's what we're doing when we clear our throat—get the gunk out into the mouth, so we can expectorate it or swallow it, but either way it's out of our lungs. This process is helped along by coughing, which hurls the sputum further up and out faster. Toxins (see * below) or infections or other noxious influences can paralyze this ciliary mechanism, temporarily or permanently.

Sedatives, or strokes or other neurological damage, or drinking, can impair or paralyze the cough mechanism.

Age, or sedatives, or alcohol, or strokes big or mini-, can interfere with swallowing mechanisms so that mouth organisms fail to be diverted away from the lungs, and pathogens can be introduced that would ordinarily be shunted elsewhere.

Mouth breathing has nothing to do with anything except that the nasal passages moisten the air on the way into the lungs. They also filter out the largest of particles; some are caught in the hairs, and some stick to the moist surfaces in the upper airway. Air that is too dry can parch the lungs and render them more susceptible to infection, but that's not a major factor.

Nursing homes may have more than the usual percentage of pathogens in the ambient environment because of a lot of antibiotics (necessary ones, we trust) having eliminated the competing susceptible commensal organisms, leaving more pathogens (and often selecting for the drug-resistant ones).

* (Btw, cigarette smoke is one such inhibitor of normal ciliary activity. Anybody ever notice that your "smokers' cough" often begins a day or two after stopping? ["I never coughed like this while I was smoking!"] The reason is that it takes that long for the cilia to regain their activity, so that now, for the first time in years, they can resume their normal function of clearing out the crud that's been accumulating all this time...)