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,...
chronic99
If you've been reading here very long, you know me - I get my undergarments in a major twist every time I hear of someone's doctor telling them there is such a thing as HS without bacteria, or of someone's doctor using a medication besides antibiotics on HS. I'm sure that's still hard for some of us to understand because we've probably been let down by a number of antibiotics if we still have HS, and that's certainly true even in my case.
But always curious where this idea of HS without bacteria ever got started in the first place, so I started retracing the steps again a little.
To my knowledge there are only two medical books devoted to HS... (See how easy it is to be a grumpy HS expert? You only have to read two books and you get to say, "Shut up, I've read every book there is on this subject!!!") :-)
And even if we were lucky enough to get our doctors to read one of these two books, they might end up a little confused...
The book on HS by van der Zee
repub.eur.nl/pub/32091/111207_Zee-Hindrik-Hessel-van-der.pdf
informs us that
"At first sight the clinical aspects of HS do suggest infection. But
results of bacterial cultures, despite the volume of discharge, are often negative or do only yield skin commensal microbiota67,68. In a retrospective study, axillary bacterial cultures from HS patients demonstrated that the most prevalent aerobic bacteria species were Staphylococcus aureus, Streptococcus pyogenes, and Pseudomonas aeruginosa, the most frequent anaerobic bacteria were Streptostreptococcus species, Prevotella species, microaerophilic
streptococci, Fusobacterium species, and Bacteroides species67. However, these bacteria were collected by epidermal swabs which
were potentially contaminated with skin commensals. Later, this contamination factor was circumvented in a study aspirating pus from the deeper parts of HS lesions68. Using this method bacteria were cultured in only half of the samples68. The most frequently cultured bacteria were S. aureus and coagulase-negative staphylococci (S.
epidermidis and S. hominis), so again skin commensals68."
And the book organized by Gregor Jemec (here is the chapter on HS bacteriology) http://eknygos.lsmuni.lt/springer/197/86-94.pdf
informs us that
"Despite the volume of the discharge the HS lesions are often found to be sterile [29, 33], but sometimes a large variety of microorganisms
can be isolated from the sinuses, particularly staphylococci, streptococci, Gram-negative rods, and anaerobic bacteria (Table 1.2)."
So naturally the reader wants to interpret this to mean that often, up to half the time, HS lesions have no bacteria in them.
Unless your doctor does a second thing that they might not actually be able to take the time to do, which is follow up the references here, they might not notice that BOTH OF THESE SOURCES may be mincing up a study by Jemec et al with the study by Lapins et al in order to be able to make it sound like this.
van der Zee ref 67 = Jemec ref 29 =
The bacteriology of hidradenitis suppurativa.
Jemec GB, Faber M, Gutschik E, et al (1996)
Dermatology 193:203206
van der Zee ref 68 = Jemec ref 33 =
Coagulase-negative staphylococci are the most common bacteria found in cultures from the deep portions of hidradenitis suppurativa lesions, as obtained by carbon dioxide laser surgery.
Lapins J, Jarstrand C, Emtestam L (1999)
Br J Dermatol 140:9095
What the study by Lapins et al of aspirated pus finds is NOT that half of these deep samples show no bacterial presence, what it actually found is that BACTERIA WERE FOUND FROM DEEP LEVELS IN ALL BUT 3 OF 22 SAMPLES....
Coagulase-negative staphylococci are the most common bacteria found in cultures from the deep portions of hidradenitis suppurativa lesions, as obtained by carbon dioxide laser surgery.
Lapins J, Jarstrand C, Emtestam L.
Br J Dermatol. 1999 Jan;140(1):90-5.
Abstract
...Aerobic and anaerobic cultures from superficial and deep levels were taken during surgery. The regions treated were axillary in eight and perineal in 17 cases. Bacterial cultures were positive for one or more specimens from at least one level in all cases and from deep levels in all but three cases. Sixteen different species or sub-species were found. Staphylococcus aureus and coagulase-negative staphylococci (CNS) were the species most frequently found. Peptostreptococcus species and Propionibacterium acnes were not uncommon. S. aureus was detected in a total of 14 cases, six of which were from the deep levels. S. aureus was the sole bacterium isolated in two deep cultures. CNS were found in 21 patients and 16 of these isolates were from the deep levels. In nine of the 16 deep samples CNS were the only bacteria detected. These findings motivate a re-evaluation of the significance of bacteria in the progress of HS and in particular they suggest that CNS are true pathogens...
PMID: 10215774 [PubMed - indexed for MEDLINE]
THAT'S 13.5% NOT 50%... is that not correct?
And by the way, van der Zee doesn't seem to have noticed this article asserting that CNS Staph infections are troublemakers, being seemingly amazed at the thought of them causing the abscesses they are found in.
At least, the idea that our troubles come from commensal species of bacteria that are already everywhere provides that we probably don't need to worry about others catching HS from us, although given the laundry lists of bacteria that have been isolated from HS, I DO worry about contracting additional infections, which I seem to be good at.
And if one of these studies only used surface specimens from lesions as van der Zee states and it WASN'T Lapins et al?
It would be Jemec's study that only shows COMMENSAL, SKIN-SURFACE flora in only 50% of surface samples when they should probably be finding ordinary skin flora in up to 100% of samples, which could cast considerable doubt on the veracity of Jemec's study.
Unfortunately, I'm having trouble finding a free full text of Jemec's study
but if I can at least take that much of what van der Zee has to say seriously...?
It's just like those "sterile" swab results I've gotten - there's no way the swab has no bacteria on it - after being taken from the skin surface in my crack, it should offer at least a few commensal skin flora to culture, casting plenty of doubts on whether these results were worth wasting a swab. I have no idea what went wrong in Jemec's study but it certainly sounds like something did to judge by all this.
One other thing I could mention is that there are still bacteria which are "unculturable" and can't be grown in a dish from specimens (at least not until someone figures out what to feed them, all bacteria are "unculturable" until that happens obviously) and causal browsing of literature suggests there's good likelihood that these kind of organisms can come from the order of Bacteriodales that frequent isolates from HS like Bacteroides and Prevotella belong to, and they could be very similar in behavior and antibiotic response to the usually encountered types for all anyone knows.
Naturally if they can't get it to grow in a dish so they can try out different antibiotics to see what kills it instead of wasting antibiotics that aren't going to work, this poses a challenge, but nothing I've seen so far suggests that these elusive microbes could be at work in any more than about 10-15% of HS cases.
HS without bacteria? Is there such at thing? According to whom exactly?
As always my best advice to others with HS would be
1. Help your doctor to not underestimate the possible role of bacteria in causing your HS symptoms, and don't let them confuse an incurable disease with a treatable infection if you can possibly help it.
2. Encourage your doctor to be aware how common that problem-causing bacteria like Staphylococcus, Streptococcus and Bacteroides can be in HS, to do bacterial cultures, and if at all possible, to do susceptibility testing on cultures. The more stubborn someone's HS is, the more stubborn a bug they may have, the longer they've had it and the more antibiotics have failed them, the more likely it may become that they have something that could require these measures to find an antibiotic to successfully involve an infection.
I have an upcoming appointment where I intend to practice what I'm preaching here and see how it goes. It will be a new thing to get my doctor interested in my bacteriology outside of emergencies for once.
I could be wrong about all this stuff of course... but I do try not to be, because I hate this disease, I've had doctors threaten to saw me clean in half over this or obvious complications of it, the way it puts out a constant welcome mat for some of the scarier bacteria.
I know everyone else hates it too, I really wish I could come up with a "Treating HS for Dummies" for us all, but I wouldn't begin to know what advice to give someone without knowing their bacteriology, and if your doctor had that, they might not need some goofy patient like me to go and try to make it into a no-brainer for them.
But always curious where this idea of HS without bacteria ever got started in the first place, so I started retracing the steps again a little.
To my knowledge there are only two medical books devoted to HS... (See how easy it is to be a grumpy HS expert? You only have to read two books and you get to say, "Shut up, I've read every book there is on this subject!!!") :-)
And even if we were lucky enough to get our doctors to read one of these two books, they might end up a little confused...
The book on HS by van der Zee
repub.eur.nl/pub/32091/111207_Zee-Hindrik-Hessel-van-der.pdf
informs us that
"At first sight the clinical aspects of HS do suggest infection. But
results of bacterial cultures, despite the volume of discharge, are often negative or do only yield skin commensal microbiota67,68. In a retrospective study, axillary bacterial cultures from HS patients demonstrated that the most prevalent aerobic bacteria species were Staphylococcus aureus, Streptococcus pyogenes, and Pseudomonas aeruginosa, the most frequent anaerobic bacteria were Streptostreptococcus species, Prevotella species, microaerophilic
streptococci, Fusobacterium species, and Bacteroides species67. However, these bacteria were collected by epidermal swabs which
were potentially contaminated with skin commensals. Later, this contamination factor was circumvented in a study aspirating pus from the deeper parts of HS lesions68. Using this method bacteria were cultured in only half of the samples68. The most frequently cultured bacteria were S. aureus and coagulase-negative staphylococci (S.
epidermidis and S. hominis), so again skin commensals68."
And the book organized by Gregor Jemec (here is the chapter on HS bacteriology) http://eknygos.lsmuni.lt/springer/197/86-94.pdf
informs us that
"Despite the volume of the discharge the HS lesions are often found to be sterile [29, 33], but sometimes a large variety of microorganisms
can be isolated from the sinuses, particularly staphylococci, streptococci, Gram-negative rods, and anaerobic bacteria (Table 1.2)."
So naturally the reader wants to interpret this to mean that often, up to half the time, HS lesions have no bacteria in them.
Unless your doctor does a second thing that they might not actually be able to take the time to do, which is follow up the references here, they might not notice that BOTH OF THESE SOURCES may be mincing up a study by Jemec et al with the study by Lapins et al in order to be able to make it sound like this.
van der Zee ref 67 = Jemec ref 29 =
The bacteriology of hidradenitis suppurativa.
Jemec GB, Faber M, Gutschik E, et al (1996)
Dermatology 193:203206
van der Zee ref 68 = Jemec ref 33 =
Coagulase-negative staphylococci are the most common bacteria found in cultures from the deep portions of hidradenitis suppurativa lesions, as obtained by carbon dioxide laser surgery.
Lapins J, Jarstrand C, Emtestam L (1999)
Br J Dermatol 140:9095
What the study by Lapins et al of aspirated pus finds is NOT that half of these deep samples show no bacterial presence, what it actually found is that BACTERIA WERE FOUND FROM DEEP LEVELS IN ALL BUT 3 OF 22 SAMPLES....
Coagulase-negative staphylococci are the most common bacteria found in cultures from the deep portions of hidradenitis suppurativa lesions, as obtained by carbon dioxide laser surgery.
Lapins J, Jarstrand C, Emtestam L.
Br J Dermatol. 1999 Jan;140(1):90-5.
Abstract
...Aerobic and anaerobic cultures from superficial and deep levels were taken during surgery. The regions treated were axillary in eight and perineal in 17 cases. Bacterial cultures were positive for one or more specimens from at least one level in all cases and from deep levels in all but three cases. Sixteen different species or sub-species were found. Staphylococcus aureus and coagulase-negative staphylococci (CNS) were the species most frequently found. Peptostreptococcus species and Propionibacterium acnes were not uncommon. S. aureus was detected in a total of 14 cases, six of which were from the deep levels. S. aureus was the sole bacterium isolated in two deep cultures. CNS were found in 21 patients and 16 of these isolates were from the deep levels. In nine of the 16 deep samples CNS were the only bacteria detected. These findings motivate a re-evaluation of the significance of bacteria in the progress of HS and in particular they suggest that CNS are true pathogens...
PMID: 10215774 [PubMed - indexed for MEDLINE]
THAT'S 13.5% NOT 50%... is that not correct?
And by the way, van der Zee doesn't seem to have noticed this article asserting that CNS Staph infections are troublemakers, being seemingly amazed at the thought of them causing the abscesses they are found in.
At least, the idea that our troubles come from commensal species of bacteria that are already everywhere provides that we probably don't need to worry about others catching HS from us, although given the laundry lists of bacteria that have been isolated from HS, I DO worry about contracting additional infections, which I seem to be good at.
And if one of these studies only used surface specimens from lesions as van der Zee states and it WASN'T Lapins et al?
It would be Jemec's study that only shows COMMENSAL, SKIN-SURFACE flora in only 50% of surface samples when they should probably be finding ordinary skin flora in up to 100% of samples, which could cast considerable doubt on the veracity of Jemec's study.
Unfortunately, I'm having trouble finding a free full text of Jemec's study
but if I can at least take that much of what van der Zee has to say seriously...?
It's just like those "sterile" swab results I've gotten - there's no way the swab has no bacteria on it - after being taken from the skin surface in my crack, it should offer at least a few commensal skin flora to culture, casting plenty of doubts on whether these results were worth wasting a swab. I have no idea what went wrong in Jemec's study but it certainly sounds like something did to judge by all this.
One other thing I could mention is that there are still bacteria which are "unculturable" and can't be grown in a dish from specimens (at least not until someone figures out what to feed them, all bacteria are "unculturable" until that happens obviously) and causal browsing of literature suggests there's good likelihood that these kind of organisms can come from the order of Bacteriodales that frequent isolates from HS like Bacteroides and Prevotella belong to, and they could be very similar in behavior and antibiotic response to the usually encountered types for all anyone knows.
Naturally if they can't get it to grow in a dish so they can try out different antibiotics to see what kills it instead of wasting antibiotics that aren't going to work, this poses a challenge, but nothing I've seen so far suggests that these elusive microbes could be at work in any more than about 10-15% of HS cases.
HS without bacteria? Is there such at thing? According to whom exactly?
As always my best advice to others with HS would be
1. Help your doctor to not underestimate the possible role of bacteria in causing your HS symptoms, and don't let them confuse an incurable disease with a treatable infection if you can possibly help it.
2. Encourage your doctor to be aware how common that problem-causing bacteria like Staphylococcus, Streptococcus and Bacteroides can be in HS, to do bacterial cultures, and if at all possible, to do susceptibility testing on cultures. The more stubborn someone's HS is, the more stubborn a bug they may have, the longer they've had it and the more antibiotics have failed them, the more likely it may become that they have something that could require these measures to find an antibiotic to successfully involve an infection.
I have an upcoming appointment where I intend to practice what I'm preaching here and see how it goes. It will be a new thing to get my doctor interested in my bacteriology outside of emergencies for once.
I could be wrong about all this stuff of course... but I do try not to be, because I hate this disease, I've had doctors threaten to saw me clean in half over this or obvious complications of it, the way it puts out a constant welcome mat for some of the scarier bacteria.
I know everyone else hates it too, I really wish I could come up with a "Treating HS for Dummies" for us all, but I wouldn't begin to know what advice to give someone without knowing their bacteriology, and if your doctor had that, they might not need some goofy patient like me to go and try to make it into a no-brainer for them.
This is another thing that may well have gone in my own bacteriological tests before.
Any bacterial infection is secondary only and really only treatable for isolated episodes for specific lesions and no long term advantage knowing whether you HS is inviting in invaders unless you treat the underlying cause. So definitely you want to treat an infection with antibiotics but it only really helps you for that episode/flare.
Diet is being attributed to the hormone and metabolism imbalances. prof William F Danby has written some very thorough papers on the cause and treatments... diet and metabolic management being number one... accompanied by immunosuppressives and retinoids.
For me it WAS diet. (In particular potato's being the trigger and dairy being the contributor as far as I can tell)
As far as I can tell Bill Danby is the leading expert
https://www.researchgate.net/profile/F_Danby/publications
I could have gone on to also point out that this study, probably the finest microbiological study of HS ever done, had a success rate similar to Lapins et al where only 13.5% of specimens failed to show bacteria; here 17% of specimens proved unculturable:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4257786
I stand corrected in learning that there is a third textbook on HS that came out this January,
Hidradenitis Suppurativa, An Issue of Dermatologic Clinics
Gregor B E Jemec
https://books.google.com/books?isbn=0323414508
The chapter on HS bacteriology isn't in the free preview but it looks like it may be the same as this recent article on HS bacteriology (same title and authors).
The Microbiology of Hidradenitis Suppurativa
Hans Christian Ring, MD, Lennart Emtestam,MD
https://www.researchgate.net/publication/284811951_The_Microbiology_of_Hidradenitis_Suppurativa
I don't know how much of the article I agree with but I think it's to be commended for this part, which may one of the bravest things any accredited author has ever had to say about HS:
"The recurring findings of skin commensals in the deeper layers of HS point to potential causal mechanisms of disease development."
In other words, those commensal bacteria they keep finding in HS then ignoring all this time might just turn out be the cause of this?
Well, there's a refreshing idea... That's... almost progress...
I can control mine by eliminating potato's and paprika and limiting tomato. I do eat a lot of dairy so I fall into the risk group... but alone it does not trigger my HS.
For me there's something in those vegatables whether it's calcitriol, selenium, starch... something triggers either causal mechanism. Whether that is bacterial or inflammatory first.... interesting.
When I had the pilonidal removed it included 10 days in hospital being pumped full if intravenous antibiotics. When I got out of hospital all of my lesions had flattened and I'd say full remission. Only then did I go on to discover the food triggers which kick it off again.
I suspected carrying around that pilonidal infection was making it very hard for my body to heal the lesions.
(True that most of my triggers weren't always triggers although I don't think I've become actually allergic to them, just sensitive to the inflammation they produce - whereas some of us do seem to be having to also deal with the inflammation from allergic reactions).
While I'm thinking of it, I must offer praise for these remarks from the Pasteur Institute also:
"These data show that bacteria known to cause soft tissue and skin infections are associated with HS lesions. Whether these pathogens are the cause of the lesions or are secondary infectious agents, these findings support targeted antimicrobial treatment of HS."
http://www.ncbi.nlm.nih.gov/pubmed/25418454
AMEN! Absolutely! We can debate until the cows come home whether these infections actually cause HS, but they're known troublemakers and should be treated. Thank you, Pasteur Institute!
Also, I think this link gets into a topic that might be worthwhile
https://www.researchgate.net/publication/284811951_The_Microbiology_of_Hidradenitis_Suppurativa
since it may be the subject of some confusion, which is "why do HS patients seem to be so prone to infection". I think researchers have tried to pin this on genetics and this that or the other thing, but it may not really take special susceptibility to infection to have the typical first microbe move in, and once it does it may be sufficient explanation in itself for increased susceptibility to infection.
Its efforts to subvert the immune system so that it can establish itself, may be sufficient to pave the way for other infections to also proceed more successfully.
In turn, other unrelated infections that strain the immune system might help a little to pave the way also.
I think it's also been tried before to frame the question as "why do these normal microbes of human skin suddenly turn on their hosts" but it may generally be a matter that the host is constantly working to keeping them in their place, and once any microbe successfully invades, it may interfere with that process - thus in at least some cases the susceptibility to additional infections may be more a matter of an immunocompromised host than normal human microbes suddenly behaving in an uncharacteristically aggressive manner.
There's also the matter of where the microbe actually is, though - microbes may behave one way in the gut or on the skin, and another way naturally if they've overstepped these boundaries, and no special susceptibility to infection on the patient's part or their genetics or lifestyle choices may be required for that to happen.
I think a lot of times though the impression of some inherent susceptibility to infection may be falsely implied simply by the tendency toward recurrence of symptoms. Caregivers may assume they've successfully killed the microbe and then assume it's recurring because the patient has been exposed to it again when it may be much more likely they just didn't get rid of all of it.
I wish I could help answer to that question for them (much) better than that, but it is a pretty complicated question. There may be a lot involved in keeping these normal human microbes in their proper place, for starters. Just giving it an awful lot of thought due to the constant burning reminders on your privates, hopefully helps a little to sort it all out eventually.
Staphylococcus aureus Small Colony Variants (SCVs): a road map for the metabolic pathways involved in persistent infections
Front Cell Infect Microbiol. 2014; 4: 99. PMCID: PMC4112797
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4112797
"Abstract - Persistent and relapsing infections, despite apparently adequate antibiotic therapy, occur frequently with many pathogens, but it is an especially prominent problem with Staphylococcus aureus infections...
Since 2006, it has been found that persistent organisms including SCVs are part of the normal life cycle of bacteria, and often they arise in response to harsh conditions, e.g., antibiotics, starvation, host cationic peptides...."
Antibiotic activity against small-colony variants of Staphylococcus aureus: review of in vitro, animal and clinical data
J. Antimicrob. Chemother. (2013)
http://jac.oxfordjournals.org/content/early/2013/03/13/jac.dkt072.full
"(Figure 1)... Electron-transport-deficient SCVs show alterations in the pathways leading to the synthesis of menadione or haemin (subsequent to mutations in biosynthetic enzymes), which causes a reduction in the amount of ATP produced. This leads to a reduced growth rate, which may affect the efficacy of antibiotics active against dividing bacteria, such as cell-wall-active agents..."
I'm not sure I understand this stuff at all, but would this help explain why HS/Staph is really starting to seem like it's difficult to clean up for good with beta-lactam antibiotics, even the carbapenems like ertapenem that seem to show so much promise for HS otherwise?
I ended up thinking along the same lines myself by wondering why there may be accounts of clindamycin successful treating HS without relapse, but none I can think of for carbapenems which otherwise often work wonders. Really not sure but what is quoted in this post does make me wonder if it wasn't a good question.
I have had HS for 50 years, did not know it had a name until this week.
What I know is one of my triggers is MILK CHOCOLATE.
I still get flareups at any time but I always get one when I eat MILK CHOCOLATE.