A few more thoughts on this...

I'm also surprised that Actinomyces showed up in this study in such seemingly small proportions. Having nothing else to firmly associate with sinus tracts, I had it figured for a major presence and a major player in tissue reconstruction... I think that too may have overshadowed the significance of Prevotella.

Prevotella isn't exactly a new discovery either, it's been found in HS before, and so has its relative and sometimes synonym, Bacteriodes, which literature also makes to sound like a big player other areas of the "follicular occlusion triad".

I tried to round up data on the spectrum of activity of the antibiotics that the Pasteur Institute used to achieve such dramatic improvements in HS - what all microbes do they work on in other words - and for some reason while that data says that metronidazole works on Actinomyces, I have other new references that say the opposite.

If these new references are right, that might explain a great deal, because nowhere else in my data is there any indication of anything else that might be effective against Actinomyces being used in the Pasteur Institute's remarkable studies.

Since the Pasteur Institute otherwise beat even severe HS cases into temporary remission with antibiotics, I'm really wondering if Actinomyces being missed by antibiotics - and possibly setting up a small protected reservoir of other microbes - could have been the only reason their results were only temporary?

Also, this isn't the first time one of their microbiological studies has shown a seemingly exclusive relationship between Staphylococcus lugdunensis and Stage I HS, so possibly it's particularly important if you have Stage I HS, to be a little more careful about avoiding the additional infections seen in later stages?

I've gone to look up an organism detected in HS only to suddenly find myself studying dentistry, because that organism is a normal dweller of the human mouth, enough times now that I try to be more vigilant about saliva, mine and that of other creatures. Seems like some possibility that if I were raised to wash my hands BEFORE using the restroom as well as after, or not to sing in the shower (shower spray can displace saliva), or simple things like that, just maybe I might have been spared Hurley 2/3? Also it seems like there may be a lot of hand-to-mouth activity while smoking or snacking that might get saliva or oral bacteria onto the hands where it can be transmitted elsewhere while using the lavatory or while scratching some godforsaken itch.

Hopefully we're forming a good picture of HS and having all kinds of observances and avoidances may be behind us soon, but there's some stuff I wish I'd thought of sooner.

Of all the microbes ever found in HS, I'm not sure what it's made out of but Staph, and in advanced cases, Strep, Prevotella / Bacteroides, and maybe a little Actinomyces making it particularly persistent? I'm hoping for some kind of confirmation soon.

I have to keep trying sometimes to remember that all of this is very hopeful, since it's started to seem like a HS diagnosis makes many doctors get out a rubber stamp and stamp "hopeless" across your forehead...

I think the authors of this latest study are probably being too modest in their discussion of the significance of the research, and a little too tender to the prevailing dermatological paradigm - after seeing their work, I have a hard time seeing what's dermatological about HS anymore...

All I seem to see anymore is that there is some kind of immune impairment which prevents the immune system from doing its job and cleaning up the mess, and that this presumably comes from some kind of microbial toxins. When the Pasteur Institute uses enough antibiotics to beat all kinds of creatures into submission, we see the immune system get back to work and, amazingly, mop up even hypertrophic scarring in HS, as if they'd beaten up the very cause of the dysfunction...

And in spite of all the discussion in HS literature of early follicular events, it almost seems like these affected follicles wouldn't be such an issue if the immune system didn't seem to be failing to clean up even those little messes, that early in the progression?

I hope I'm not being too hopeful here, but I'm not quite sure what makes more sense to me than this.

Medscape Medical News
Study Suggests New Treatment for Hidradenitis Suppurativa
Kate Johnson
March 19, 2012
http://www.medscape.com/viewarticle/760502

Complete remission of severe hidradenitis suppurativa obtained in 4 patients using wide-spectrum antimicrobial treatment
Aude Nassif, MD, Institut Pasteur, Paris, France; Helene Coignard, MD, Hpital Necker-Enfants Malades, Paris, France; Olivier Join-Lambert, MD, PhD
Journal of the American Academy of Dermatology
April 2012 Volume 66, Issue 4, Supplement 1, Page AB46
http://www.jaad.org/article/S0190-9622(11)01430-7/abstract
"We report 4 cases of complete remission (CR), defined as
absence of any inflammatory lesion, obtained with compassionate usage of antimicrobial treatment based on intravenous (IV) ertapenem or an association of IV ceftriaxone and oral metronidazole as induction treatment."

Poster Ertapenem in the Treatment of Severe Hidradenitis Suppurativa
http://www.globale-dermatologie.com/en/poster-ertapeneme-dans-le-traitement-de-lhidosadenite-suppuree-severe.html
"One case of complete remission (disappearance of all inflammatory lesions) occured in a patient with a severity of stage 2 (of Hurley). A reduction of one stage of Hurley was observed in 7 patients with stage 2 ans also 7 patients with stage 3 of the disease."

Efficacy of rifampin-moxifloxacin-metronidazole combination therapy in hidradenitis suppurativa.
Join-Lambert O1, Coignard H, Jais JP, Guet-Revillet H, Poire S, Fraitag S, Jullien V, Ribadeau-Dumas F, Thze J, Le Guern AS, Behillil S, Leflche A, Berche P, Consigny PH, Lortholary O, Nassif X, Nassif A.
Dermatology. 2011 Feb;222(1):49-58. doi: 10.1159/000321716. Epub 2010 Nov 25.
"Complete remission was obtained in 16 patients, including 6/6, 8/10 and 2/12 patients with Hurley stage 1, 2 and 3, respectively (p=0.0004). The median duration of treatment to obtain complete remission was 2.4 (range 0.9-6.5) and 3.8 months (range 1.6-7.4) in stage 1 and 2 patients, respectively, and 6.2 and 12 months in the 2 stage 3 patients"

Microbiologic profiles of hidradenitis suppurativa lesions
Olivier Join-Lambert, MD, PhD; Aude Nassif, MD; Hlne Guet-Revillet, MD; Xavier Nassif, MD, PhD.
Journal of the American Academy of Dermatology
Volume 66, Issue 4, Supplement 1, Page AB110, April 2012

Antimicrobial susceptibility testing of Actinomyces species with 12 antimicrobial agents
A. J. Smith1,*, V. Hall2, B. Thakker3 and C. G. Gemmell4
J. Antimicrob. Chemother. (August 2005) 56 (2): 407-409.
http://jac.oxfordjournals.org/content/56/2/407.long
"It should be noted that metronidazole should not be used to treat actinomycotic infections without added antimicrobial agents, since metronidazole is not active against the pathogenic actinomycetes."

Actinomyces species (Actinomycoses)
Michael M. McNeil, M.D., MP.H. , Dr. med. habil., Klaus P. Schaal
http://www.antimicrobe.org/b73.asp
"However, metronidazole alone is not suitable for treating actinomycotic infections because fermentative actinomycetes are generally resistant to this drug""
"It should be noted that all of the fermentative actinomycetes are resistant to metronidazole"

Oops, left out a link. Here's this one

Efficacy of rifampin-moxifloxacin-metronidazole combination therapy in hidradenitis suppurativa.
http://www.ncbi.nlm.nih.gov/pubmed/21109728

Very cool. Thanks for sharing.

good info

Interesting, I've been suspecting as much for a while now. I've been washing regularly with Hibiclens for the last several months, and my HS is the most inactive it's been in years.

Stay hopeful... I don't know why the next paper from this team couldn't boast actual cures of HS. They've done enough bacteriology and antibiotic work to get there provided all else goes well.

They can boast COMPLETE REMISSIONS (if only temporary) of even Stage 3 HS, and that is literally (and not figuratively like in older HS literature where "remission" often only means "some improvement").

I know the notion prevails among doctors and patients alike that HS does not begin as a bacterial phenomena, but let me ask this - what aspect of Stage 1 HS can NOT be accounted for by the virulence properties of Staphyloccoci?

Shame on me maybe if I accept an explanation of HS from authorities who:

a. do not understand HS, by their own admission
b. do not understand the first thing about how to make HS better, also often by their own admission

I did try to believe for nine years of HS that bacteria had nothing to do with the cause of it, which got me exactly nowhere.

Honestly, someone besides me is due to go back and try to find where everyone got the idea of non-bacterial HS -- from clean swabs? There is NO WAY that swab is actually clean considering where they stuck it!

Often "clean swab" means something like "there was nothing on it that I, the Lab Technician, was ever taught was of importance to the matter" - that's what my last bacteriological work looks like, even when they find something they don't bother naming it, not even the bacteria that almost hospitalized me or worse last year. I had three unnamed "commensal" flora - i.e., "Oh, never mind those, those are just ordinary bacteria of the skin, that I, The Lab Technician, was not taught could do anything like this".

I'd rather take my explanations from people who may have the best understandings as exhibited by the best RESULTS, even if these researchers aren't quite willing to haul off and utterly declare yet that HS is that much a bacterial phenomenon. They are of course very modest and allow the possibility of fastidious ("unculturable") organisms since the paper in question was a genomic study of bacterial cultures from HS lesions, but the instances of complete remissions suggest to me that any fastidious bacteria yet to be identified in HS still had the tar beaten out of them by the antibiotics.

I don't think you could get those kind of results by missing a significant organism, does that make sense?

Perhaps most importantly, the more horrible a symptom of HS, the more likely it can be directly traced to bacteria - boils, abscesses and even sinus tracts (as a variation of abscess) are well-known bacterial phenomena, and within the known capabilities of the most commonly isolated bacteria from HS (Staphylococcus, Streptococcus, etc). Even if HS "isn't curable," INFECTIONS ARE.

At least that's why I'm still very enthused about this work, even if I'm not sure I'm a candidate. I do sympathize for others who are certain they aren't candidates for antibiotics - I doubt I'd want metronidazole or even ertapenem myself - but I remain optimistic that the more we can clear up the origins of HS, the more viable options will be open to us.

I'm even sorely tempted to just haul off and try to describe here off the top of my head what I think a successful antibiotic therapy looks like categorically... it might look SOMETHING like

Antibiotic or combination of antibiotics:

1. Is preferrably bacteriocidal (not bacteriostatic) at concentrations used.

2. Targets detected organisms (or most frequently detected organisms in HS) that are capable of interfering with phagocytosis
and ideally takes into consideration any unusual resistance mechanisms amongst members of this category detected in a specific patient.

3. Targets detected Actinomycetales to prevent colonies thereof from shielding other organisms against antibiotics, thus forming a reservoir of requisite HS bacteria that may cause recurrence of symptoms following suspension of antibiotics.

If there's an error or omission there, lemme hear about it.

(And that MAY even read that if the research in question had just throw in some penicillin - most often called for in literature against Actinomyces - they might already be boasting cures. You might also be able to spot in that why something like ertapenem can prove so useful - it's broad antibiotic range likely covers most of criterion 2 singlehandedly).

Keep an eye on number 3, though - it may be the one overlooked the most. If for the sake of experiment we take Tara Grant to McD's and feed her a French Fry with ketchup (OMG! TWO nightshades) and her HS comes rip-roaring back, then I'm tempted to at least suspect that she's still packing a reservoir of HS-related bacteria in the wrong places. Replace "antibiotic" in item 3 with "dietary measures," or any other remedy for HS, in other words.

Let me repeat this - even if HS "isn't curable," INFECTIONS ARE - and that may also go for any attendant "incurable" co-morbidities of HS. Before you or your doctor decide that co-moribidities of HS (OR of smoking) can't have a bacterial origin or at least a strong participation of bacteria, consider browsing the literature a little, and better yet, maybe look a little into what frequently associated microbes may be capable of.

I just gave this same advice to my wife this very day because she has an appointment where she's going to inquire about surgery to have her ovaries removed to reduce the risk of ovarian cancer from PCOS. She's still skeptical of a possible microbial origin, but I pointed out to her that JUST MAYBE she is a candidate for 5-alpha-reductase inhibitors because some microbes produce 5-alpha-reductase, and while PCOS "isn't curable," an infection might be.

One of the microbes that can do that, is one the ones that has been closely associated with another of MY co-morbidities. In that one, there are a lot of implicated periodontal bacteria that may not have even required a HS lesion to find their way into the bloodstream to raise hell. (Of course, in the literature it's another incurable disease - in this case "incurable" means that doctors were chopping off people's limbs BEFORE it occurred to them to use antibiotics on obvious cases of gangrene!!!!! Just hack us up and don't even bother with bacteriology! FINALLY someone wrote a real medical paper a few years ago bringing up the folly of THAT, thank God!!!)

If something vaguely similar has happened in HS, where currently my situation is the option of surgery and no options of antibiotics even doxy, I'll probably be able to say I have seen the likes of it before.

Is that enough emphasis yet on the importance of the possible role that bacteria may play in a number of diseases, whether the literature says so or not?

From what I read, there are A LOT of us with HS, and I'm thrilled at the idea that even a fraction of that number might be helped or even eventually cured by the research of Nassif & Nassif et al, because even 1% of them would be a lot of people!

I'm saddened a bit though that the work of Nassif and Nassif hasn't proven to be more exemplary on the part of other researchers yet. I'm even wondering why COMPLETE REMISSIONS wasn't front page news on any HS-dot-orgs to the best of my knowledge. Helloooo? Don't let this work fall through the cracks! Keep talking it up like it's about the best thing that ever happened to us, because it could be. :-)

Also - again - for anyone who may still be only reading such advice for the first time - if you only have Stage 1 HS, please consider getting your bacteriology checked into if you haven't already done so, so that you can might get something done about it while it may be a simple infection, before it becomes a microbial zoo. Resistance aside, if our information is good then at that stage of HS, a single antibiotic or antimicrobial might still do a lot of good.

If anyone gets any good out of this advice, please let me know, BTW. I'm not a doctor but I am trying very hard to be able to give decent advice or insights to you, me, or anybody with HS, and any successes from ID of bacteria to alleviation of symptoms may be helpful and encouraging to all of us.

One last thing, to all you lovely people on this board, forgive me for being too stupid to figure out the hug button - I'm also too dumb to figure out blogs, mp3 players, and hundreds of other simple everyday items. Consider yourselves hugged, daily. :-)

Keep the faith!!!!!

As time allows, I'll try and look more into alternatives to antibiotics. I haven't done much of that because the focus so far has been very much on exactly what we'd want to aim at with those, which is quite a subject.

It struck me as a cheerful thought in a way though this morning that some of the stuff I might come up with might already be out there and isn't waiting on the likes of me. Sometimes I follow a lead and it leads right to something we already know about, like turmeric / curcumin or zinc or whatever, so I may not be other only one who's trying to give some serious thought to the subject.

Lately I've been looking at human beings' natural antimicrobial lipids (as opposed to antimicrobial peptides), yet another subject that's very new to me but may well lead me to known approaches like coconut oil if not any unknown ones. I'm thinking about giving coconut oil a try myself shortly, just trying to figure out now if the best thing to do might be dietary use, as opposed to topical application?

Thankfully my wife's doctor doesn't think PCOS puts her at increased risk for ovarian cancer.

The following would probably be better suited reading for caregivers - it gets pretty intense - but for anyone curious, parts of this article that are understandable to us normal people might be informative?

Role of sex steroid hormones in bacterial-host interactions
Free full text: http://www.hindawi.com/journals/bmri/2013/928290

There might also be something in it that helps explain why HS flares might be linked to hormones, bacteriologically speaking? - perhaps including,

"Sex steroid hormones play important roles in diverse functions of mammals, such as the modulation of the immune response. Testosterone, estradiol, and progesterone can differentially regulate responses against bacterial infections and alter metabolic pathways of pathogenic and microbiota bacteria. In general, testosterone acts as an immunosupressor, while estradiol acts as an activator, and progesterone acts as a modulator of the immune system. These effects are related to the sexual dimorphism found in bacterial infections, where men and male animals are in many cases more susceptible to bacterial infections than females. The stage of the menstrual or estrous cycles and pregnancy also determines the outcome of bacterial infections due to the changes in the levels of sex hormones."

Or even, since I have expressed concerns here about a possible major role of Prevotella or related Bacteroidales in HS, this passage:

"Prevotella intermedius (previously Bacteroides melaninogenicus subsp. intermedius [60]) is found among these anaerobic bacteria, and interestingly, it uptakes estradiol and progesterone, which in turn enhance bacterial growth"

?????

Okay, one last thing (it's the last one for now, honest) since I broached the subject of natural human antimicrobial lipids. One of them is purported to be sphingosine, and some of us might recall a product called Emu Aid that used to boast a content of .1% of an active ingredient phytosphingosine?

Don't let them fool you, "Phyto-" means it comes from plants, not Emus, and potential dietary sources even if generally scarce in foods will hopefully turn out to mean I might not have to worry about rubbing it on sore parts in order to enjoy benefits, but we might be able to see one non-antibiotic antimicrobial strategy of some sort at work there (it might even say so in the Emu Aid patent?), maybe one that's just waiting to be made better use of, or to be used more effectively in combination?

I at least like the idea of maybe being able to use antimicrobials systemically that otherwise might be limited mainly to certain tissues, and I also like the idea that some of them might be available through nutrition if I used food smarter in that respect.

I did a random sampling of 3 significant Staph in HS and all may have degradation pathways for sphingosine. I don't know yet if they are using these capabilities but they may at least have the genes for it, and Staph may have to be resisting or degrading some of the antimicrobial lipids as well as antimicrobial peptides in order to occupy the niche that it may hold in HS. Still, strategies along these lines might be help with some of the complications invited by Staph, because hopefully some antimicrobial lipids will still be able to help arrest some of its little party guests?

Anyway, more reading that's probably a headache for us non-professionals, and maybe more antimicrobial lipids have been discovered since this paper was written in 2007, but here's a link

Thematic Review Series: Skin Lipids. Antimicrobial lipids at the skin surface
Free full text: http://www.jlr.org/content/49/1/4.full

"The chemical structures of the antimicrobial lipids known to present at the human skin surface are given in Fig. 1:
lauric acid
sapienic acid
sphingosine
dihydrosphingosine
6-hydroxysphingosine"

I was going over some papers on Staphylococcus lugdunensis again. I'm still trying to figure out why other Staphylococci don't really seem to have been caught on the scene when HS starts, in any quality microbiological work that I can think of. I hang on to hopes that if it can be figured out if there's anything going on that truly acts as an invitation to this particular bacteria in HS that it can be remedied once identified.

For caregivers this paper from 2008 is one of the articles goes into more detail about how Staphylococcus lugdunensis can be distinguished from Staphylococcus aureus (of which MRSA is a strain). I wonder if doctors mistaking the two species might make them more hesitant to try antibiotics or more skeptical that antibiotics would be worthwhile to try in HS, but if I'm not mistaken this paper actually paints a fairly optimistic picture where the general trend seems to be that Staphylococcus lugdunensis has broad susceptibility to common antibiotics rather than broad resistance.

Perhaps that's additional incentive for those who have the opportunity to try to get HS dealt with at Stage 1, if there may be not only just a single responsible organism to have do in at that stage, but an easy one to do in as well? - provided that caregivers are aware or made aware of what they need to know, of course.

From Clinical Microbiology to Infection Pathogenesis: How Daring To Be Different Works for Staphylococcus lugdunensis
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2223846

I think that it is because over a period of time we come into contact with the various organisms from wounds being open. Think about it... How many of you disinfect public toilet sets before you go? How many wash there hands before using the bathroom? Do you carry your personal tissue supply? The tissues are exposed to organisms. Infection is easy post wounds open. How many have pets and their pets are on there beds? You sit in the bed, lay on the bed... think about it. The bacteria infections can be treated with antibiotics but the HS does not go away. I have stage three n have had all kinds of organisms but staph has never been. I think they need to focus on why some glands cells will not release oil and other junk. Why does the body try to contain it by forming scar tissue and allow the fluid/puss to tunnel. Our whole body is covered with skin, we don't hs all over, correct the dysfunction.