My mother is 84 years old and has been in good health most of her life. But the past few years, she has had pulmonary problems: difficulty catching her breath (not necessarily exersize-induced), excessive phlegm build-up. Her pulmonologist originally considered idiopathic pulmonary fibrosis but had rejected this later. She is on inhalants, including using a machine twice a day to deliver medication.
Her significant background includes:
non-smoker.
has lived in the L.A. basin for 47 years.
survived a severe case of the Spanish Flu as an infant. (Her two brothers did not survive, and she was ill enough to have a premature memento mori photo taken of her when they thought she would die as well.)
Now I consider living in smog-ridden L.A. a very significant factor (and we’ve repeatedly asked her to move to New Jersey but she’d sooner walk down Whittier Boulevard naked than leave her house, stubborn Finn). I’m wondering if a pre-existing condition may make her more susceptible to smog. Does anyone know if influenza (especially the Spanish flu) can scar lung tissue or otherwise have long-term effects?
“Idiopathic” is a word that just means “we don’t know what causes this”. So all kinds of stuff can get into your lungs and mess things up permanently.
Don’t mean to sound snide, but you’re looking for a “known cause”, there it is right there: Environmental exposure. She’s lived in L.A. for 47 years. As your body ages, it gets less able to deal with contaminants and to heal itself, so when she was 37, in 1955, she moved her already-aging (I say this from the exalted height of 47 and trust me, 37 is “already aging” ), possibly already scarred lungs to one of the most smog-ridden cities in the U.S. It can’t have been good for her.
Anyway, the air’s much cleaner there now, or so they say , and the damage is done. [shrug] I’d say let her stay there as long as she’s able to look after herself.
While the flu, or influenza, is generally a serious illness with a limited duration, it can cause permanent lung damage. However, since mom has survived to the age of 84, it’s doubtful that her lungs were permanently seriously affected by the flu. She may just be suffering from the normal decline of lung function with the passage of time. Lungs deteriorate with time. That’s normal. Especially with living in LA for nearly half a century. I suspect her case of influenza had little or nothing to do with her current status. And even if it did, there’s not much to do differently because of it now.
Essentially, everyone will die when their lungs give out. If something else doesn’t give out first.
Of course this question would be better addressed to her doc, who’s examined her, and has first-hand knowledge of her specific situation.
And the name “spanish flu” was just a name hung on that year’s influenza virus strain. Which knocked off a lot of soldiers, if I recall correctly. They’re still trying to figure out which strain it was and why it was so virulent.
QtM, MD
Thanks DDG and QtM. I guess I’m just a little frustrated with no diagnosis (don’t know why the pulmonologist rejects IPF), the various treatments that they’ve tried and have not worked, and living 3000 miles away. I guess I want to know why she’s going through this, and grabbing at any possibility, however farfetched. An increased suscepibility to smog (as compared to her cohorts) is probably as far as we’ll get. Hell, I spent my first 20-some very odd years in Southern California, and thought that painful lungs were par for the course. I learned better when I moved (which is why we want to get her out of there).
(And no, DDG, I don’t think you sound snide. Thanks for the lnk. )
“I guess I’m just a little frustrated with no diagnosis”
It always nice to have a neat explanation for things but reaching a definite dagnosis often has a cost that outweighs any practical benefit. I’m not just talking about money, but about discomfort and danger. For example, has your mother’s pulmonologist bronchoscoped her? Has she had a lung biopsy performed? Both procedures are likely to yield important information that would enable the pulmonologist to make a definitive diagnosis but they are expensive, uncomfortable, and risky in an 84 year old. More important, although they might yield a diagnosis that would ease your frustration, they probably wouldn’t yield information that would cause her physician to change your mother’s treatment in a way that significantly improve her comfort or prolong her life. This has a lot to do with age, if she had the same problem at age 24, her physician would pursue a definite diagnosis much more aggressively but at 84 there’s not much point. Have you spoken with you mohter’s physician about her prognosis?
I know that this has nothing to do with the OP per se, but it’s related so I thought I might add it.
The Spanish flu killed somewhere between 20 and 30 million people mainly in 1918, a large portion of the victims were soldiers in the trenches in France and Belgium, but it struck all over the world and most of the victims were not soldiers.
In 1997 an American researcher, Dr Jeffrey Taubenberger managed to isolate the virus from the frozen body of a female victim buried in Alaska. This was the second virus retrieved from bodies buried in permafrost, the previous one from a site in Svalbard.
Taubenberger and his team confirmed that the viruses where identical. They were also able to perform a complete DNA sequencing of the virus. The sequencing showed that it was a mutated version of a Type A form of swinevirus, that had gotten extremely virulent in its mutative form. The matching swinevirus was found to be of North American origin. It was already known that some of the earliest cases of Spanish Flu where reported in the US, the extreme speed that the disease killed with, and a relatively short incubation time at first gave reason to believe that the flu was not one, but several pandemics.
Taubenberger research rpoovided a more plausible explanation. It is now believed the disease arose in the US sometime around 1915, and in 1918 it hit the army where tight living conditions for huge amounts of new conscripts provided an ideal ground for spreading. The infected soldiers where shipped en masse to the war in Europe where the trenches provided an even better base for the virus to spread. Within a year the virus had gone around the globe and killed mre people by one disease than any pandemic since the Black Death in the 1350s. Around 1919 those that had been exposed, but not killed had developed immunity and the pandemic slowly subsided.
IIRC the hog farm where the virus mutated was identified as somewhere in Ohio last year, but I can’t seem to locate the article where I read that and I don’t have a subscription to Science Magazine where the Taubenberger research with subsequent finds has been published.
In fact the Spanish Flu levels are correct (if you call a 20 million discrepancy correct… fact is that we will never know). However the Plague still holds the record. In Europe in the 1350s the Black Death pandemic killed off over 30% of the population, which already there is above the lower estimate for Spanish Flew worldwide. The Plague then kept returning every other year for an other couple of hundred years decimating the population with at times up to 15%. It took till the mid 1500s for Europe to reach pre-Plague level population. The fact that the Spanish Flu was so virulent, but that it was a virus to which we develop immunity is probably what stopped it from reaching Plague levels.
As far as I understand the Spanish Flu kills faster, spreads faster and we develop better immunity to flu viruses than to bacteria like Y. Pestis. But I ain’t the best to answer that. Tamerlane amongst others would probably be able to either debunk or confirm this.
Immunity is much more easily conferred by viruses than by bacteria. Since viruses have relative simple protein coats, that don’t easily mutate. When one gets the flu, even a mild case, immunity quickly follows.
For gram negative bacilli, like Y. pestis, your immune system has a much more difficult time breaking the barrier of the outer membrane. It’s simply harder for your system to fight off. Moreover, if you do manage to fight off a bacterial infection, you may get it again because it hasn’t conferred immunity.
Yeah, mom has gone through a number of tests, including being scoped, MRIs (but I don’t think she’s had a biopsy done yet, but if it’s not necessary, then you’re right, it shouldn’t be done). She’s also had her pulmonologist changed on her 3 times by her HMO (but that’s a Pit-type of story that I don’t have the venom for - yet). Fortunately, she likes the take-action nature of this last one (“he vill do sometink!”) and my brother happens to be in the states and will be with her on her next visit this coming week. We want her to be comfortable and not in pain. (Plus, the biologist in me is just curious.) bio-brat, thanks for the link - a lot of the points seem very cogent and applicable to Mom. I talked with her about it, and she wrote down a few things to bring up with her doctor (exercise to increase her lung capacity, non-opioid painkillers). QtM, that’s frightening about PF.
Sparc, I remember when those findings came out and being amazed yet again at what the dead can reveal. Thanks for the info.
Well, we’ve been trying to get the protocol for a blocking ELIZA to analyze West Nile samples here in the Mosquito Research and Control Unit and so I’ve been learning (or at least trying to learn) about viral immune responses. With the flu virus (an orthomyxovirus), you can develop an immune response that might protect you with subsequent exposures. Flu viruses have two surface proteins (pretty simple, as bio-brat says) that bind them or incorporate them into host cells (hemoglutinin and neurominidase, or something close) and these are also the proteins that hosts target for antibody production. The viral RNA that codes for these two proteins can change enough that antibodies produced one year will not provide protection against the following year’s viral population (antigenic shift/antigenic drift). So we get flu shots each year, based on prediction (I believe) on what the viral population will be (and I think they base these predictions on what is happening in pig farms in China, right?).
Are the membranes of bacteria so devoid of proteins that can initiate an immune response or do they change more rapidly than viral proteins (a sort of Red Queen scenario)?
Actually brachyrhynchos bacterial outer membranes are rife with proteins. Here is a sample of P. aeruginosa’s outer membrane proteins. These proteins are often highly mutatable, making them much more elusive targets.
I found this website which has all sorts of cool information on how bacteria (and some viruses) avoid the immune system.
), possibly already scarred lungs to one of the most smog-ridden cities in the U.S. It can’t have been good for her.
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