Hidradenitis Suppurativa Support Group
Hidradenitis suppurativa (hi-drad-uh-NIE-tis sup-yoo-ruh-TIE-vuh) is rare, long-term skin condition that features small, painful lumps under the skin. The disease manifests as clusters of chronic abscesses or boils, sometimes as large as baseballs, that are extremely painful to the touch and may persist for years with occasional to frequent periods of inflammation,...
I keep double-checking my concepts about HS just to be sure I haven't missed something or gotten something wrong...
One of the most important topics to me is unusual means of persistence of either HS itself or of associated infection, because basically I am looking for what would have caused relapses after the stunning successes by the Pasteur Institute-affiliated researchers in treating HS using only broad-spectrum antibiotics.
As far as I'm concerned they were probably only a hair away from curing HS, and ever since then I've wondered what little thing might have gone wrong.
ACTINOMYCOSIS?
One such mechanism for infection that I've mentioned before (with links in previous posts about it) would be an actinomycosis, where infection with a species of Actinomyces may create a colony that can shield small numbers of other bacteria from antibiotics as well as the immune system, so that infection would be able to return out of hiding one antibiotic use stops.
The Pasteur Institute-affiliated bacteriological studies so far seemed to show a fairly consistent presence of Actinomyces, which may lend plausibility to the idea that this kind of complication may not be uncommon in HS patients past Stage 1 of the disease.
Unless the presence of Actinomyces is detected or suspected, it may be unlikely that the patient will receive an appropriate antibiotic that will address Actinomyces. None may have been used in the Pasteur Institute affiliated studies, thus actinomycosis has been near the top of my list of what might have gone wrong.
DIFFERENTIAL PENETRANCE?
Had to just make that up I think, phew... Don't know what real medical professionals call that. This would be when how good an antibiotic is at penetrating an infected cell to kill the infection within may depend on the type of cell. If there is a single type of cell that is infected that a particular antibiotic cannot get into to kill the infection, then there may be a reservoir of infectious organisms waiting to spring forth and cause relapse after when antibiotic treatment is completed.
However possible or plausible this sort of situation may or may not be, it doesn't seem to have posed an obstacle to successes brought about by the P.I. related antibiotic work?
UNUSUAL HOST BARRIERS?
I have often read descriptions of cysts like mine as being created when the immune system is forced to wall off an infectious organism that it is not equipped to fight, so it does the only thing it can next and tries to imprison it, creating a stalemate that may never be resolved.
Based on personal experiences, I have to make the inference that what keeps the microbes IN the cyst, may also keep antibiotics OUT - and this might correspond with the frequency with which surgery is resorted to with such cysts? - yet statistically a number of patients in the antibiotic studies might have had similar cysts which we presume might have responded to treatment, so I'm having a hard time thinking of even these as an impossible obstacle to any number of known antibiotics.
BIOFILM INFECTION?
https://en.wikipedia.org/wiki/Biofilm
Probably the most common suggestion for unusual persistence of infection that I have seen offered in HS literature (especially more recent bacteriological papers) is a biofilm infection, in which species or types of infectious organisms can cooperate in producing different substances known as biofilm. They can often be creative in this process, so that not all biofilms are created equal.
Biofilms can protect infection-causing organisms from various threats, including antibiotics, which may make them an attractive prospect for explaining the stubborn nature of some HS infections hence their relatively frequent mention in literature.
However, I have seen very little literature describing how one can actually tell whether a biofilm infection is present without laboratory proceedures. One article describes the presence of biofilm infection in HS sinus tracts as blatantly evidenced by a mucous-like discharge from lesions.
I have had this happen on several occasions including very recently, however this has been very rare and has always cleared up seemingly all by itself in about a week. I have also taken tea extract supplements *just in case* since some components of tea are reported to help break up SOME of the many possible biofilms, but tea drinkers may already be covered here.
My feeling has been that this type of complication did not present a significant obstacle to temporary successes of antibiotics against HS that were achieved in the French studies under discussion here.
L-FORM BACTERIA, CWD (Cell Wall Deficient) BACTERIA?
https://en.wikipedia.org/wiki/L-form_bacteria
If I understand correctly, an important means by which these versions of different organisms may cause complication is that, because they lack the normal cell wall of these organisms, that antibiotics which target bacterial cell walls therefore have no such target in the case of these organisms, which may require antibiotics with a different mechanism.
Also note that this kind of bacteria can be CREATED by antibiotics, which is often how they are created in the laboratory for research, so we can infer that they can originate with imprecise application of antibiotics by caregivers.
This part is also a bit of a challenge for me, but if I've inferred correctly,
under more ordinary circumstances, this is not of great concern because many pathogenic microbes carry certain defenses against the immune system in their cell walls, so that stripping them of the cell wall with antibiotics when in the body would actually render them more vulnerable to being killed by the immune system normally.
However, that does imply that a healthy immune system is required to move the process along to that desirable outcome - but a healthy immune system may be the most important thing that a person does NOT have when they have HS, especially in the HS-afflicted areas themselves. This may be another reason to emphasize the possible importance of careful bacteriological work-ups.
My feeling with this type of infection is that in the long run, it posed no insurmountable obstacle to successes with the broad-spectrum antibiotic treatment, even if it may be a frequent complication of poorly-founded antibiotic prescription for HS.
SMALL-COLONY VARIANTS (SCVs)?
I may have made a mistake in overlooking this type of infection previously. As described, they are often slower-growing and less aggressive or toxic than their ordinary forms, so they don't necessarily sound as if they are cause for much concern even though in SCV form, microbes may no longer respond to antibiotics.
What I did not quite realize until recently is that SCVs CAN REVERT TO THEIR ORDINARY FORMS - I though of them as mutants that could only continue to produce more SCVs! - and I think that might have been a terrible mistake, because these may actually turn out to be the best match for a description of the way that HS may relapse even after seemingly being cured?
So I still have a LOT to study concerning this type of situation, but I would not be surprised if these turn out to be a primary cause for relapses of HS following apparent cure.
In cases where an apparent cure was NOT achieved, perhaps any number of these might be contributors to the lack of results, as may be resistant strains and etc.
Anyway, we hear more and more about just how much of a role that infection may play in HS (mostly from me lately) and naturally the first question that everyone including me wants to ask is why we can't make it go away and STAY AWAY with antibiotics...
I will keep looking for answers because there always seem to be surprises left...
But just maybe the answer to that most important of HS questions is somewhere in this very post?
Also, as I am beginning to look more and more at the antibacterial and antimicrobial properties of herbs (the list slowly grows more and more impressive even though I haven't officially started on it yet), it may be accurate enough to substitute those for "antibiotics" in this paper. What made trouble for the Pasteur Institute's efforts may also present obstacles to the complete effectiveness of turmeric, for example?
Lastly: THE USUAL DISCLAIMER - this post is the work of a completely uneducated, opinionated and sleep-deprived individual. It is not science and cannot aspire to be science. Contrary to proper protocols, this work has been published without being reviewed by a Science Editor - or any editor!
However, if you can find a better work like this at the moment, let me at it. As far as I know, I may be the first person to bring up as many as three of four of these concerns in writing about HS. So just in case there's a microscopic speck of PROGRESS in it somewhere, just thought I'd throw it out there.
Have a great weekend and may we all be feeling better on Monday!
One of the most important topics to me is unusual means of persistence of either HS itself or of associated infection, because basically I am looking for what would have caused relapses after the stunning successes by the Pasteur Institute-affiliated researchers in treating HS using only broad-spectrum antibiotics.
As far as I'm concerned they were probably only a hair away from curing HS, and ever since then I've wondered what little thing might have gone wrong.
ACTINOMYCOSIS?
One such mechanism for infection that I've mentioned before (with links in previous posts about it) would be an actinomycosis, where infection with a species of Actinomyces may create a colony that can shield small numbers of other bacteria from antibiotics as well as the immune system, so that infection would be able to return out of hiding one antibiotic use stops.
The Pasteur Institute-affiliated bacteriological studies so far seemed to show a fairly consistent presence of Actinomyces, which may lend plausibility to the idea that this kind of complication may not be uncommon in HS patients past Stage 1 of the disease.
Unless the presence of Actinomyces is detected or suspected, it may be unlikely that the patient will receive an appropriate antibiotic that will address Actinomyces. None may have been used in the Pasteur Institute affiliated studies, thus actinomycosis has been near the top of my list of what might have gone wrong.
DIFFERENTIAL PENETRANCE?
Had to just make that up I think, phew... Don't know what real medical professionals call that. This would be when how good an antibiotic is at penetrating an infected cell to kill the infection within may depend on the type of cell. If there is a single type of cell that is infected that a particular antibiotic cannot get into to kill the infection, then there may be a reservoir of infectious organisms waiting to spring forth and cause relapse after when antibiotic treatment is completed.
However possible or plausible this sort of situation may or may not be, it doesn't seem to have posed an obstacle to successes brought about by the P.I. related antibiotic work?
UNUSUAL HOST BARRIERS?
I have often read descriptions of cysts like mine as being created when the immune system is forced to wall off an infectious organism that it is not equipped to fight, so it does the only thing it can next and tries to imprison it, creating a stalemate that may never be resolved.
Based on personal experiences, I have to make the inference that what keeps the microbes IN the cyst, may also keep antibiotics OUT - and this might correspond with the frequency with which surgery is resorted to with such cysts? - yet statistically a number of patients in the antibiotic studies might have had similar cysts which we presume might have responded to treatment, so I'm having a hard time thinking of even these as an impossible obstacle to any number of known antibiotics.
BIOFILM INFECTION?
https://en.wikipedia.org/wiki/Biofilm
Probably the most common suggestion for unusual persistence of infection that I have seen offered in HS literature (especially more recent bacteriological papers) is a biofilm infection, in which species or types of infectious organisms can cooperate in producing different substances known as biofilm. They can often be creative in this process, so that not all biofilms are created equal.
Biofilms can protect infection-causing organisms from various threats, including antibiotics, which may make them an attractive prospect for explaining the stubborn nature of some HS infections hence their relatively frequent mention in literature.
However, I have seen very little literature describing how one can actually tell whether a biofilm infection is present without laboratory proceedures. One article describes the presence of biofilm infection in HS sinus tracts as blatantly evidenced by a mucous-like discharge from lesions.
I have had this happen on several occasions including very recently, however this has been very rare and has always cleared up seemingly all by itself in about a week. I have also taken tea extract supplements *just in case* since some components of tea are reported to help break up SOME of the many possible biofilms, but tea drinkers may already be covered here.
My feeling has been that this type of complication did not present a significant obstacle to temporary successes of antibiotics against HS that were achieved in the French studies under discussion here.
L-FORM BACTERIA, CWD (Cell Wall Deficient) BACTERIA?
https://en.wikipedia.org/wiki/L-form_bacteria
If I understand correctly, an important means by which these versions of different organisms may cause complication is that, because they lack the normal cell wall of these organisms, that antibiotics which target bacterial cell walls therefore have no such target in the case of these organisms, which may require antibiotics with a different mechanism.
Also note that this kind of bacteria can be CREATED by antibiotics, which is often how they are created in the laboratory for research, so we can infer that they can originate with imprecise application of antibiotics by caregivers.
This part is also a bit of a challenge for me, but if I've inferred correctly,
under more ordinary circumstances, this is not of great concern because many pathogenic microbes carry certain defenses against the immune system in their cell walls, so that stripping them of the cell wall with antibiotics when in the body would actually render them more vulnerable to being killed by the immune system normally.
However, that does imply that a healthy immune system is required to move the process along to that desirable outcome - but a healthy immune system may be the most important thing that a person does NOT have when they have HS, especially in the HS-afflicted areas themselves. This may be another reason to emphasize the possible importance of careful bacteriological work-ups.
My feeling with this type of infection is that in the long run, it posed no insurmountable obstacle to successes with the broad-spectrum antibiotic treatment, even if it may be a frequent complication of poorly-founded antibiotic prescription for HS.
SMALL-COLONY VARIANTS (SCVs)?
I may have made a mistake in overlooking this type of infection previously. As described, they are often slower-growing and less aggressive or toxic than their ordinary forms, so they don't necessarily sound as if they are cause for much concern even though in SCV form, microbes may no longer respond to antibiotics.
What I did not quite realize until recently is that SCVs CAN REVERT TO THEIR ORDINARY FORMS - I though of them as mutants that could only continue to produce more SCVs! - and I think that might have been a terrible mistake, because these may actually turn out to be the best match for a description of the way that HS may relapse even after seemingly being cured?
So I still have a LOT to study concerning this type of situation, but I would not be surprised if these turn out to be a primary cause for relapses of HS following apparent cure.
In cases where an apparent cure was NOT achieved, perhaps any number of these might be contributors to the lack of results, as may be resistant strains and etc.
Anyway, we hear more and more about just how much of a role that infection may play in HS (mostly from me lately) and naturally the first question that everyone including me wants to ask is why we can't make it go away and STAY AWAY with antibiotics...
I will keep looking for answers because there always seem to be surprises left...
But just maybe the answer to that most important of HS questions is somewhere in this very post?
Also, as I am beginning to look more and more at the antibacterial and antimicrobial properties of herbs (the list slowly grows more and more impressive even though I haven't officially started on it yet), it may be accurate enough to substitute those for "antibiotics" in this paper. What made trouble for the Pasteur Institute's efforts may also present obstacles to the complete effectiveness of turmeric, for example?
Lastly: THE USUAL DISCLAIMER - this post is the work of a completely uneducated, opinionated and sleep-deprived individual. It is not science and cannot aspire to be science. Contrary to proper protocols, this work has been published without being reviewed by a Science Editor - or any editor!
However, if you can find a better work like this at the moment, let me at it. As far as I know, I may be the first person to bring up as many as three of four of these concerns in writing about HS. So just in case there's a microscopic speck of PROGRESS in it somewhere, just thought I'd throw it out there.
Have a great weekend and may we all be feeling better on Monday!
Also, it seems like a good time to bring up the concept of *pulsed doses of antibiotics,* where they are used intermittently instead of continuously during the course of treatment. This may give some unusual forms of bacteria the opportunity to revert to their normal, antibiotic-susceptible forms so that they can be zapped by the next dose instead of hiding out until after a continuous course of antibiotics has been completed.
Thus there could be cases where relapses come not from the wrong choice of antibiotics, but perhaps from suitable antibiotics not being applied in the most effective manner for a particular situation?
I guess if there were a moral to the story, it might be that we probably shouldn't be too hasty in playing down the role of infection in HS just because antibiotics don't seem to be able play a decisive role.
Also I want to say that I think it's fantastic that we have this group - I am so very grateful - and I think it's important that we have whatever exchanges we can. A half-dozen times here now I've gone to try to see if I could help answer someone's question on HS and just for trying I've stumbled over something that may be very important.
It's all very new to me but offhand it looks like the very same qualities of bacteria that could cause clotting in a boil may be able to help bring on this phenomena of "small colony variants" (???) and that sounds likes getting close to being able to know more things to do about them if they really turn out to be big trouble makers in HS.
I have a couple of things still on my mind though about what might be going on when antibiotics DON'T make HS go away...
DISTRIBUTED RESISTANCE?
Most of us I'm sure are familiar with the idea that microbes can develop resistance to antibiotics. Quite often, the discussion concerns how one organism will develop resistance to an antibiotic as a genetic trait on the part of the bacteria, and then under certain circumstances, may be able to give away this resistance to certain other infectious organisms that might be present. This definitely sounds like something that might be at work in some stubborn cases of HS...
I most often seem to see literature discussing antibiotic resistance involving the production of bacterial enzymes which can literally degrade and digest antibiotics. On account of this, doctors sometimes might try enzyme inhibitors with antibiotics to try and make sure that the antibiotics are being degraded before they can work. That's something my own doctor did early on in trying different things is to give me an antibiotic plus a beta-lactamase inhibitor in case this kind of enzyme might have been present.
I thought that might deserve a little emphasis because at least on paper it sounds as if one microbe that makes these enzymes may be able to protect other infections that might be present from antibiotics this way, at least on paper.
Imagine what this might look like in real life, you could have six different infections that all seem to behave as if they have extraordinary antibiotic resistance, when it might turn out to be that just one of them is chewing up the antibiotics on behalf of the rest of them, and may be nowhere as hopeless a situation as it might appear?
Anyway, this might help further underscore the importance of trying to unravel one's HS bacteriology as soon as possible before more confusing complications such as this can set in, even though this would be advice that I still have to work at following myself.
I tend to only want to go bother the doctor when things have really gotten out of hand, but this presents the doctor with a situation where there just isn't time to wait for lab results and so they just have to proceed by making the best guesses that they can in an emergency.
EFFLUX PUMPS?
I strongly suspect that the biggest bane of my existance could be microbes that have acquired this trait or are expressing it to an usual extreme. This is why I haven't rushed off to see an infectious diseases specialist yet even though my doctor was kind enough to offer me a referral, because when the time comes I would like to know what to do about this in case the specialist doesn't.
What it sounds like might have happened is that at first, I might had just your usual type of Bacteriodes infection without such special equipment, and back then when I would have pilonidal cyst flare up, they would prescribe the old workhouse Keflex and hot baths and it worked like magic. The cysts went away and would stay away for years at a time.
What might have happened next is that I came in contact with a species or strain of Bacteroides that has this type of special resistance and all of the sudden Kelfex and hot baths stopped helping whatsoever, and the pilonidal cysts began to walk all over me.
I don't have much business doing this because I really don't know what I'm talking about, but the way I'm interpreting what I've read so far, it sounds like it might be possible that this type of infection is capable of spitting antibiotics right back in doctor's faces, and this might just explain why no antibiotic including I've had ever since then (including the one I'm currently one and the impressive cocktail of antibiotics I got when nearly hospitalized by a ruptured cyst last fall) seems to have put the slightest dent in either what's left of my pilonidal cyst, or my HS.
I have no idea how likely it might be that anyone else with HS might have something so stubborn, but more and more I think that might be what's going on in my case. It might even mean that the amazing results in the Pasteur Institute-affiliated efforts with antibiotics that I find so very inspiring, aren't actually something I could aspire to myself if I have such a nasty problem bacteria on board. I will definitely be taking this up with a specialist.
Also, I could take the opportunity to emphasize the possible role of Bacteroides species or related organisms from the same order of bacteria as more of them are implicated in some of my co-morbidities. Again and again, these bacterial DO appear prominently in HS literature and the possibility of them playing a substantial role in HS should not be overlooked.
So anyway, I am still NOT sure that infection is entirely to blame for HS - mainly I'm trying to look at it that way simply because I don't think enough people are doing that, and I think there is plenty of reason to experiment with trying to think about HS that way.
I don't know if I've gotten wise yet to every dirty trick that infections can play on someone (probably not) so I will keep trying to learn, but I can see plenty here already that might easily trick doctors or patients into adopting a sense of hopelessness about HS that it just may not really deserve.