Many apologies, I may be misadvising people on the subject of SCV (small colony variant) microbes as the likeliest cause of recurrence of HS following improvements caused by antibiotics. I'm still not entirely sure, it's a pretty complicated subject, but I thought I might owe people a warning.
One place where I may have gone wrong is that I've seen SCVs associated with long courses of antibiotics (without further clarification how long "long" actually is) so that in that sense they try to sound plausible as one of the things that might go wrong in the Pasteur Institute studies (which might have otherwise cured even some of the worst HS patients had the HS not come right back when the antibiotics stopped), because their initial studies involved relatively long courses of antibiotics which sometimes ran as long as six months.
Another reason this may have tried to sound (mistakenly?) attractive as a reason for HS recurrence is that if one goes to wonder how in the very first stages of recurrence, when there is presumably a minimum number of surviving bacteria, how a sprinkling of troublemakers left behind after successful antibiotic treatment are getting the better of the immune system, so microbes that persist as small colonies (small colony variants) might sound somewhat plausible, since these colonies may be more fit to fight off immune cells by sticking together. SCVs also try to sound plausible because they can be created by antibiotic use.
The past week, I've tried to sort out the difference between SCVs and similar bacterial phenomena more carefully than ever, and ended up less sure than ever that SCVs deserve the top nomination. (It's a little hard for me to do the subject much justice, mainly in earlier or simpler cases of HS we'd probably be talking about Staphylococcus, whereas in the last year or so I've been called up on to study other microbes in HS, other pathologies, and now I seem to be having to even study antibiotics themselves in trying to understand why they've failed).
However, if something like this is to blame for HS so famously staging a comeback when antibiotics stop, maybe the L-form phenomena makes a better suspect than SCVs?
It's not even my idea, I'm sure I have at least one research paper on HS specifically where L-forms are is proposed as a reason for HS being difficult to successfully treat (which for some reason isn't coming out of Google today when I look for "L-form" and "HS". I though that at least one of these research papers also mentions biofilms (which may have more to do with some cases that may not be so easy to put into remission with antibiotics in the first place?) but adding "biofilm" for a keyword didn't help either today, I'll try to find it in my notes later. There are plenty of papers that have been written on L-form Staphylococcus aureus, although I'm not sure yet exactly how much of it applies to other common Staphylococcus species in HS.
I haven't taken biofilm as a possible part of HS very seriously yet because even if it were part of my HS, it doesn't seem to have stopped them from saving my life with antibiotics on more than one occasion, and it doesn't seem to have stopped antibiotics from putting HS into remission in numerous cases.
This author seems to be willing to haul off and nearly give biofilms credit for a great deal http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4278191
"Because the skin lesions in HS are chronic and recurring and require long courses of antibiotics for treatment, it seems likely that HS is a biofilm disease."
Although I'm not as sure myself that sometimes long course of antibiotics aren't "required" because the doctors don't know quite know when to quit, and that may even include the outstanding studies by the Pasteur Institute workers, just as they still may not be hunting Staphylococcus with the best antibiotics yet even though Staphylococcus dominated their Stage 1 HS cultures. The first thing likely to jump out at someone about L-forms is how they are created in laboratories by feeding them antibiotics that target the cell wall of microbes.
"L-forms can be generated in the laboratory from many bacterial species that usually have cell walls... This is done by inhibiting peptidoglycan synthesis with antibiotics or treating the cells with lysozyme, an enzyme that digests cell walls."
The Pasteur Institute has done great things with ertapenem for HS, probably because ertapenem kills enough different troublemaking microbes to clean up most of what could be the problem and most bugs haven't shown resistance to it yet, but carbapenems such as ertapenem target the microbial cell wall.
That isn't to say that SCVs don't appear in HS, or play some kind of role - there may be a role for a type of organism that doesn't make a rapid comeback, but might reappear futher down the line, or might remain unnoticed by anyone indefinitely, and one or more of those might be where they fit into the picture. There's a report of several cases of HS that were apparently successfully treated (cured?) where careful inspection years later still revealed some immune system abnormalities that might owe to a persistent infection. I still haven't gotten the literature to be perfectly clear on this, but L-forms and SCVs might also be able to appear simultaneously, since antibiotics can be involved in their creation or selection.
Anyway, I'm sure HS is confusing enough without me misleading anyone, so I truly hope that isn't what I've been doing, and I do apologize. A person probably can't help going out on a limb with this stuff since much of it can be obscure or poorly understood, but I continue in my faith that maybe even the data we've already been given on HS by the Pasteur Institute and others, may be enough to understand HS if we can find the opportunity to think it over carefully enough.
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