I've probably posted things like this before but I'm not very sure any of those posts are still around.

This is always the first article I'd point anyone at

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4257786
https://www.researchgate.net/publication/268788920_Bacterial_Pathogens_Associated_with_Hidradenitis_Suppurativa_France
https://wwwnc.cdc.gov/eid/article/20/12/14-0064_article

I so rarely find a paper I'm Googling for hosted at a CDC URL that this paper seems worth paying close attention to for that fact alone.

There are others, but this looks at bacteriology at different stages of HS, and seems to shows Staphylococcus lugdunensis dominating Stage 1 HS cultures, and Prevotella bivia dominating later stage HS cultures. I'm very tempted to take those findings very seriously since they seem to match my own experiences, my HS started with what sounds like a textbook case of Staphylococcus lugdunensis infection as the Mayo Clinic describes it, and the only time I know of them actually identifying a species from one of my abscesses, it was Prevotella bivia. I marvelled at them finding the very same thing in France, literally half a world away.

I may have actually caught this unusual Staph at a local clinic where I started going with unusual frequency because of increasing problems with pilonidal cyst, and likely already had problems with anaerobes like Prevotella or Bacteroides in (and probably leaking from) the pilonidal cyst so these anerobes may have present and ready, and quickly able to join in with the Staph and turn it into Stage 2 HS barely one week after it started. That's how long I was at Stage 1, a week. I've been Stage 2 or 3 ever since, for 13 years now.

With the exception that older HS research may claim to have found Staphylococcus aureus, because prior to the 1990s, nobody knew the difference between S. aureus and S. lugdunensi, and the two can still be hard to sort out, the latest work linked above may simply do a better job than ever giving evidence of the sort of things that have been found all along in HS.

We often read about "CNS" (occasionally "CoNS") or Coagulase-Negative Staphylococci being found in HS. That can include Staphylococcus lugdunensis, which is otherwise similar to S. aureus/MRSA in many ways, with the similarities easily contributing to the confusion between the two. "CNS" may also include Staphylococcus epidermidis, which may often be found in HS but from experience it seems like a relatively minor player more than being likely to be a major contributor, which seems consistent with its reputation.

Staphylococcus lugdunensis may not have a lot of acquired resistance going for it, and may still be susceptible to a number of antibiotics, provided it isn't mistaken for MRSA, a mistake that could cause antibiotic treatment to begin and end with vancomycin, which may be one of few things that Staphyloccoccus lugdunensis may have acquired resistance to, and possibly because of quite often being mistaken for MRSA and being treated as if it were.

I believe that one of my doctors got rid of the S. lugdunensis with erythromycin, which put an end to the large sinus tract formation, and because S. lugdunensis apparently isn't part of my ordinary environment for me to catch it back, it's never returned to make more sinus tracts, which has generally improved the management of my HS greatly.

The research I point to sometimes finds Staphylococcus aureus, but it may tend to be separate from sites with S. lugdunensis, or may take up residence if S. lugdunensis has been eliminated. Staphylococcus lugdunensis is supposed to make an antibiotic (called lugdunin) that kills S. aureus/MRSA, which has been of interest before to researchers trying to find things that work on MRSA.

Staph aureus may not be as keen to form the partnerships with anaerobic bacteria like Prevotella or Bacteroides that S. lugdunensis may like to form. S. lugdunensis may not mind so much the putrefactive activities of anaerobes that may produce malodor associated with HS, since S. lugdunensis may dabble in these activities somewhat itself (S. lugdunensis is ODC positive, which may be the best test short of genetic analysis to tell it from S. aureus), or at least these are the things I've read in various literature. I've seen it stated flat out in scientific journals that there is only a single known strain of S. aureus (USA 300) that wants to get involved in that.

Prevotella on its own may not normally raise a lot of concern and just to prove it there may be relatively few papers written about it, but it may be able to partner with Staphylococcus lugdunensis to cause unexpected trouble. This combination may produce the large sinus tract networks associated with later stage HS. Getting rid of the S, lugdunensis may be able to break up a partnership (called "synergy") that may bring out the worst in Prevotella.

My impression of Bacteroides based on experience is that it may not be a terribly obnoxious player either, but may be good at getting into damaged areas and taking up residence and preventing healing from happening. That's how my pilonidal cyst surgery went, for months it healed normally if slowly, but when the tiny, hard, round, waxy, leathery, burning, itching boils appeared right where the surgery was the healing stopped and things have stayed that way ever since. I still have some small remains of the original sinus tracts where it seems to have taken up residence, while the rest of them disappeared.

I also get small sores on other parts of my body and if they take on those same characteristics as many sores or small lesions do, then the healing seems to go no further. Pimples may take on these characteristics and never heal, I have examples on my thighs. They are ten years old and continue to produce pus, but they are surrounded by a waxy, leathery area and never go away whereas those that don't make this transformation into something HS-like can disappear in a day. Even a sliver can take on these characteristics of HS, and may refuse to come out if it does. I've got examples of that on my person too.

It's odd that I don't hear so much about it now, but maybe that's because of the number of doctors I've been to who seem to have let their trusted sources' HS literature mistakenly talk them into thinking that infection is uncommon and atypical, but back when the doctors still thought it was infection (and were most likely very right), they used to urge me to get it dealt as soon as I could with to keep it from "seeding" infection throughout my system. I finally had my pilonidal cyst operated on it case the HS was coming from there, I had the last of my teeth out in case the HS was coming from infected teeth.

I guess the part they may not realize so easily is that an infection that's been "seeded" that way may be able to maintain a low profile under the right conditions, although they're still good about recognizing an infection gotten out of hand and that's causing a lot of trouble.

Particularly if one looks at one of the reviews of HS bacteriological research if a free copy can be found, there's one that displays a number of important studies in a color-coded chart where we can see how often S. lugdunensis, Prevotella, and Bacteroides may be found in HS (after adjusting for the likely earlier misidentification of S. lugdunensis). The copy I saw and saved is no longer free but the abstract is here:

Bacteriology of hidradenitis suppurativa/acne inversa: A review.
J Am Acad Dermatol. 2015 Nov;73(5 Suppl 1):S12-8. doi: 10.1016/j.jaad.2015.07.041.
https://www.ncbi.nlm.nih.gov/pubmed/26470608

Naturally other infections are frequently found (typically 20% of cases may have this one or that one) but S, lugdunensis, Prevotella and Bacteroides may well represent the most consistent findings, with some studies finding Corynebacterium where we'd ordinarily find Bacteroides, as if the two shared some property that may make them interchangeable in HS. (An apparent case of HS with Corynebacterium in place of Bacteroides or other typical HS bacteria was probably the first one studied by affiliates of the Pasteur Institute in Paris, who have given us such fantastic HS research in recent years).

The other thing we may get a lot of in later stage HS (Stage 2-3) is Streptococcus, although there doesn't seem to be a particular species that's all that typical to find in everyone. Numerous reports of periodontal Strep (Streptoccocus millerii group) and throat Strep (Streptococcus pyogenes) in HS exist. The first textbook on HS (by van der Zee) projected that 1/3 of us could have throat Strep in our later Stage HS although that might be a bit of a high figure.

I suspect I have throat Strep keeping my HS going, often appearing as pea-sized lumps that can pop up overnight, and with enough inflammation can grow to the size of a grape or fig overnight, making me want to avoid inflammation at almost any cost. One of the pea-sized lumps ruptured beneath the skin once, and the large abscess that formed within hours and the high concern level of the hospital staff upon arrival may support the idea of this nasty species of Strep having been present (and still being there because the same characteristic lumps eventually returned in the same place at a notable depth, independent of any new lesions, suggesting that the particular choice of antibiotics may not have been fully up to the task of clearing out quite enough of the infection to prevent eventual recurrence).

I hope I'm not oversimplifying or being otherwise misleading here. I've poured over HS articles for years like I've poured over nothing else trying to gain an understanding of what this very promising research is trying to tell us.

Some might think I'm overcomplicating things with "S. lugdunensis, Prevotella, Bacteroides and Strep" but I really am trying to break it down - probably more than 100 different microbes have been isolated from HS lesions or abscesses, and personally I find 4 a lot easier to deal with than 100, a lot of which may be merely opportunists, and some of which may even be innocent bystanders.

If any doctor is ever inclined to follow recommendations about trying to get susceptibility testing of microbes in order to try to see what antibiotics may be needed (not that this always works because of the differences that there can be between what happens in a culture dish and what happens in the human body), culturing and testing up to 4 microbes may also be a lot easier than trying to culture and test several dozen different ones.

Aside from the confusion between S. lugdunensis and S. aureus (many medical practitioners may not yet be aware that S. lugdunensis exists for never having thought to look, although the Mayo Clinic has some good materials on it), I think it may have been a good enough rule of thumb that the less excited that bacteriological research in general seems to be about an organism found in HS, the less it may be worth worrying about, although not all of us may get the opportunity to look up 100 organisms one at a time. Sometimes just the number of Google hits for a search can be revealing. I don't suppose there that many worrisome organisms likely to have gotten past modern science, even if modern science may still be underestimating what some of them may be capable of.

I might note that various species of Actinomyces have also been reported with notable frequency in HS and it's even been suggested by one notable paper that it may play a key role in sinus tract formation, but findings may still be inconsistent and although it's credited with being able to cause abscesses of the jaw, somehow it seems to have trouble assuming a lead role in the architecture of HS symptoms, with the more frequently reported species themselves probably being perfectly capable of accounting for most if not all of the symptoms.

Like the various Streptococcus species isolated from HS cases, the various species of Actinomyces found in HS may prove to be no more than an opportunistic infection, secondary to the most common and more consistent findings of S. lugdunensis, Prevotella bivia, and Bacteroides.

Prevotella bivia and Bacteroides fragilis are two of the most common resident microbes of the human gut or gastointestinal tract. The tiniest amount of them may not have to travel far on someone's undergarments in order to be introduced into a S, lugdunensis lesion, which may turn Stage 1 HS into Stage 2 and pave the way for Stage 3.

"Studies and statistical analyses have identified the different bacterial genera in gut microbiota and their associations with nutrient intake. Gut microflora is mainly composed of three enterotypes: Prevotella, Bacteroides, and Ruminococcus"
https://en.wikipedia.org/wiki/Gut_flora

Judging from my experiences, Bacteroides may be able to create low-profile systemic infections, in order to make the appearances in new sores or lesions distant from the HS site that it does, and turn them into characteristic HS lesions. Its close relatives - formerly classified as species of Bacteroides themselves - have been found in the circulatory system of patients with one of the HS "co-morbidities" I've been diagnosed with, and Bacteroides fragilis has also been implicated in pilonidal cysts that are unresponsive to keflex as mine was.

It's certainly possible for other microbes worth targeting with antibiotics to find their way into open HS lesions (perhaps things like E. coli, Pseudomonas, or even relatives of Clostridium), and they have been reported but that may be worth addressing on more of a case-by-case basis since they may not appear consistently in HS. The first things to look for, if necessary, and the easiest things to justify looking for, may be the things we can most expect to find in any and all patients based on the research that we have.

I could be wrong about any and all of this, but I really don't know where there is a single work that aspires to cover all of the details I've attempted to cover here. Hopefully this will help turn some of the wonderful HS research and some of the complicated technical writings about HS into something a little easier for most of us (including myself) to comprehend and work with.

Sometimes we may have to be as prepared as possible to help keep our doctors on the right course, based on the guidance we have from research.

Many of our medications may have the reputation of being "double-edged swords" that might promote the advancement of infections while suppressing the symptoms of infection, such as things that block or lower TNF-a (although it can be hard to generalize here whether we can expect them to make things better or worse and it might depend on which specific infections are present, and other factors).

These concerns tends to make it sound like careful choices of antibiotics to eradicate the typical infections, rather than treating the inflammation that is likely to come from infection or the inflammation that may encourage infections (or both), may still be the best approach.

Lastly, I might point to the methods used in the first and most important reference and link in this post. "Perilesional" swabs were taken - that is, swabs were taken both from lesions and from normal skin near to lesions to help sort out whether lesions contained microbes typically found on patients' skin, which in general they apparently they did not.

That will hopefully someday help lay to rest the long-standing rumors that HS lesions contain normal "commensal" flora of the skin, something that seems to have produced a great deal of confusion in HS research literature, possibly by tricking the people commenting into thinking that microbes harmless on the skin are also harmless when introduced into the body, even though problematic Staphylococcus of one species or another was frequently present.

Also, any time that anaerobic bacteria have been successfully cultured from a swab, bear in mind that this is doing something that my doctors have insisted can't be done because of the sensitivity of anaerobes to aerobic conditions, ending in refusal to even attempt cultures.

One more thing, it's been said before that a great majority of HS patients may have a characteristic gene (a gamma secretase gene variant) that causes a healing deficit, but alert readers may spot how many times I've described things that imply that any healing deficit is localized as is infection, and to the same places, and may more likely be the work of the infections themselves and their various weapons that can keep the immune system from cleaning these infections or any other refuse.

What these "HS genes" might actually do - and this is probably the most controversial thing I'm going to say here - is often give us a bactericidal defect that may make it harder for us to clear infections without the aid of something else that kills them. These genes variants may prevent us from making a protein that's been proven in vitro to kill a wide range of microbes, that may be a normal immune response to many different infections.

Lastly, it may not be worth arguing with anyone whether any of these bacteria cause HS or not - the worst of these bacteria are generally the kind of thing that call for treatment because of the kind of things they can cause that aren't the subject of controversy. Whatever they're doing there, it probably isn't good and they shouldn't be left to do it. Very similar and probably very wise sentiments come to us from the people who gave us what is likely the finest HS research we've ever seen - from the abstract for the article in the first link in this post:

"Whether these pathogens are the cause of the lesions or are secondary infectious agents, these findings support targeted antimicrobial treatment of HS."

I hope this helps anyone and my apologies for being long overdue at having another try at it.

I think this disease may have already been beaten, it just doesn't know it yet so it hasn't thought to inform the doctors.

Which antibiotics?

Which antibiotics can depend on a lot of things - which microbes the doctor is trying to get rid of, and what kind of resistance those microbes may have acquired. Not all antibiotics kill every bacteria, for starters, and bacteria with acquired resistance can require even more careful choices of antibiotics.

However, the Staph species that's closely associated with HS may still be susceptible to a lot of things as long as they don't use vancomycin, is my understanding of the work that the Mayo Clinic participated in, and I think that is probably how my doctor got rid of the Staph just using erythromycin. If there's Strep infection present, it may respond to the typical antibiotics they might use for it if we're lucky. If not it may take a different choice.

I don't think I've heard very much about Prevotella having a lot of acquired resistance, either. It may also start to behave itself more if they get rid of the Staph that it may form aggressive partnerships with, although it may also be able to form partnerships with Strep.

I'm sure it's important for the doctor to realize that more than one important infection may be present or it may look antibiotics have failed if they get only one or two when more are present. That's happened to me before my doctor or I ever knew what HS was, and we thought it was a single infection of some kind.

One other thing that may be important is that in the Pasteur Institute research, they seem to have gotten poorer results for combining antibiotics than they might have gotten by not doing so. They looked into it and published a paper about how two of the antibiotics they combined, rifampin and clindamycin, may not be compatible, and other research has given warnings about other combinations of antibiotics interfering with each other also.

There may also be interference between metronidazole, and clindamycin or other antibiotics, since the Pasteur Institute seemed without exception to include metronidazole to address the presence of anaerobic bacteria. I'm not sure it that's been confirmed that metronidazole can interfere with other antibiotics, but that is what the results seem to suggest - the combination of metronidazole and clindamycin may have failed to do what clindamycin alone may have proven itself capable of. Sadly, so far the Pasteur Institute studies may have shown us more about what not to do with antibiotics, than what to do with them.

It may be best for doctors to try to go after the most typical infections one at a time rather than all at once, and narrow spectrum antibiotics might carry less risk of creating resistant strains than broad spectrum antibiotics, so that is hopefully more of an attractive option for them? I think my own case of HS and my partial success story likely shows that we can do go about things that way.

Clindamycin by itself seems to have given good results in clinical studies as we might expect, although a study last year warned that with topical clindamycin there was a risk of creating superbugs, but they didn't seem to see that problem with oral clindamycin. I'm not sure why that is, but that's the research we have.