Do you have a fever? Track your temperature closely. If you do have a fever, it probably is infected.

I wish I had an intelligent comment for you. I've had this happen on several occasions (also sometimes dark red fluid that might have similiar origins?) You might inquire if this is what bacterial coagulase enzymes do? I have not studied that yet because I already think of coagulase enzymes as being probably far from the most important bacterial enzymes in HS, but even being as ignorant as I am, clots naturally make me think of coagulation, so I looked it up.

Sounds as if it might be the work of some Staphylococcus? Of those listed below at least, Staphyloccus aureus might be the best match to HS literature so far? The other names are more unfamiliar from HS studies, I think.

Also perhaps look out concerning fevers - I'm not sure if absence of fever necessarily equals absence of infection, as I have never managed a fever even with high likelihood of infection or sometimes confirmed infection.

Lastly you've probably heard this before, but being the maverick I still don't see any proven difference between HS and infection. I think that HS may simply be a specialized infection that often quickly gets so complicated that most don't quite know how to make heads of tails of it. All of the microbes most frequently found complicating HS from Stage 2 onward may be equipped (they seem to be) to paralyze the immune system mainly in the vicinity of lesions.

This may be why we see such dramatic results with broad-spectrum antibiotics in the Pasteur Institute-affiliated studies, the most significant of which so far may be the remarkably broad-spectrum IV antibiotic ertapenem.

(I don't really have anything for you to read about that except what I can piece together from bits of MANY articles and sources, and I'm still not finished with the research to have gotten so far as having something prepared for people's consideration. When you get to the end of the quoted text below and it mentions *phagocytosis,* my HS microbe suspect list is centered on the impact that toxins from strains of any of all the suspect bacteria can have on that particular immune process).

Lastly, I've been doing some philosophizing lately about the nature of HS and HS "cures" - mainly that I think the bacteriology of HS can be very individualized and therefore a HS "cure" or successful treatment may be equally individualized. In some cases - probably still simple infections without target bacteria that have already acquired resistance the antibiotics use - Clindamycin alone or in combination with one other antibiotic has been talked about before as if has ended some cases of HS. Does that mean that for SOME people with a PARTICULAR collection of bacteria, it really was an HS cure?

Probably at any stage of HS/infection, the earlier the intervention the easier it may be to achieve success with it and the fewer antibiotics may be required - and the more that complication by additional infection might be avoided. I'm still trying to avoid antibiotics but usually at least once a year I get to take some whether I want to or not because things have gotten so bad - most recently, this very day.

I should probably just start my own thread about this instead of cr*pping on everyone else's threads with my bacteriological theories, but it's easy to get me started on the subject as important to HS as I personally believe that it is. You can keep in mind that I have mountains of stuff left that I can learn but already I'm almost 100% convinced that *the sooner you can get HS looked at the easier it may be to treat successfully*.

While I'm at it, there may be some more ways that infected lesions that end up registering as sterile, and one of them may be that prior to the first ID and naming in 1988 of that bacteria associated with Stage 1 HS in the French studies (Staphyloccus lugdunensis) that it might have come out looking like such an impossible strain of Staphyloccus aureus that some doctors might have decided that the test results had to be faulty and just threw them right out?

The "why" of any genuine exclusive association of Staphyloccus lugdunensis with Stage 1 HS might be because S. lugdunensis may come equipped with several particularly nasty sets of several different toxin types for which it might be hard to find equals. These might it particularly qualified to be what starts HS rather than it being the work of "just any old infection" - so possibly what's been written about it HS, may actually match its capabilities?

My favorite paper from the French studies, which has been posted before, is one of the ones that describes this role for that species of Staph: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4257786

And now at last, back to your actual questions... Thanks for your patience. Hope these are of any help:

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Staphylococcus
From Wikipedia, the free encyclopedia
https://en.wikipedia.org/wiki/Staphylococcus

"Coagulase production
One of the most important phenotypical features used in the classification of staphylococci is their ability to produce coagulase, an enzyme that causes blood clot formation.

Six species are currently recognised as being coagulase-positive: S. aureus, S. delphini, S. hyicus, S. intermedius, S. lutrae, S. pseudintermedius, and S. schleiferi subsp. coagulans. These species belong to two separate groups the S. aureus (S. aureus alone) group and the S. hyicus-intermedius group (the remaining five). S. aureus can also be found as being coagulase-negative.
A seventh species has also been described Staphylococcus leei from patients with gastritis.[11]

S. aureus is coagulase-positive, meaning it produces coagulase. However, while the majority of S. aureus strains are coagulase-positive, some may be atypical in that they do not produce coagulase"

Coagulase
From Wikipedia, the free encyclopedia
https://en.wikipedia.org/wiki/Coagulase

"Coagulase is a protein enzyme produced by several microorganisms that enables the conversion of fibrinogen to fibrin. In the laboratory, it is used to distinguish between different types of Staphylococcus isolates. Importantly, S. aureus is generally coagulase-positive, meaning that coagulase negativity usually excludes S. aureus. However it is now known that not all S. aureus are coagulase-positive.[1][2]"
...

"Coagulase reacts with prothrombin in the blood. The resulting complex is called staphylothrombin, which enables the enzyme protease to convert fibrinogen, a plasma protein produced by the liver, to fibrin. This results in clotting of the blood. Coagulase is tightly bound to the surface of the bacterium S. aureus and can coat its surface with fibrin upon contact with blood. The fibrin clot may protect the bacterium from phagocytosis and isolate it from other defenses of the host.[4] It has been proposed that fibrin-coated staphylococci resist phagocytosis, making the bacteria more virulent. Bound coagulase is part of the larger family of MSCRAMM."

That's really interesting. Let me see if I am following you:

Certain strands of staph, especially s. aureus, are known to produce a compound (or hormone, or protein, or something) that coagulates blood?

So I could have a small lesion infected with these staph bacteria, and as they took over and grew into the tissue basically, it ruptured small blood vessels, caused bleeding inside the sore, and the blood came into contact with this coagulase and clotted, causing the messy stuff inside my sore?

That's gross, but also fascinating. And also the best answer I've ever had as to the etiology of how this works.

Thank you so much!

That very much sounds like to me like what the literature is saying basically... and coagulases would be proteins (enzymes more specifically being what type of proteins they are).

There another part I'm still confused about though, which is where there are free coagulases and bound coagulases (bound to the bacteria responsible). Staphylococcus aureus is credited with being able to have both kinds, and it's still not clear to me what can be expected from each type as to the extent of the clotting that might be seen.

As I read a little more, Staphyloccus lugdunensis even though listed as coagulase-negative, may possess a membrane-bound form of coagulase. I still can't clarify for anyone including myself whether what you're referring to in the original post could be the work of S. lugdunensis, although the answer must be somewhere on there in literature.

Offhand, I'm tempted to think that S. lugdunensis can do exactly that (cause clotting) as looking backwards, my first recognized HS symptom spung up overnight and by day 2 or 3 had earned the nickname "The blood boil from Hell" because I had never seen the likes before (I still have hypertropic scarring from the original boil that rapidly gave way to sinus tracts) but me just totally guessing probably isn't very good evidence.

Thank you so much for finding all that information!

Does this clotting symptom happen to other people with HS? Is it a known thing, or do I have a different kind of infection?

I only ask because my dermatologist is adamant that my sores are not true HS, but a bacterial infection gone awry. I disagree looking at the symptoms, which are so typical of HS according to others that I talk to. I'm just curious!

Yes it is very common

And no you do not have to have an infection to see this. Area of HS common to be hot...Dr. Hazen from HS institute says it looks like all blood but it is a mixture of blood n puse. He says it is not blood alone.

That's what I was told also and mine in my armpits especially always feel like they are on fire. Hope you feel better soon if even for a day :)