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'm sure I've posted about this before trying to trace where people got the idea that Hidradenitis suppurativa doesn't involve infection, but it never hurts to go over things again to double-check. Please note that this is not intended as a recommendation for antibiotic therapy; the best recommendation in the case of antibiotic therapy for HS may be very careful, specifically targeted antibiotic therapy (especially if things like biofilm may be involved) - which is NOT something we might expect to get from a physician who doesn't see any need for it, because they don't believe that infection is a significant part of the disease even when numerous common symptoms of infection may be present.
If anyone wishes to contact the Mayo Clinic or their own microbiologist Robin Patel (to whom we are so grateful for her outstanding work on the treatment of Staphylococcus lugdunensis infections, which may be one of the best things that's ever happened to HS patients), and alert them that their webpage on HS may be unnecessarily misleading, please feel free - there is no telling how many of us might stand to be helped by this. (I have yet to do so myself since I'm still trying to put together something more detailed for them with more references in case it helps to sort things out, but I now have so many medical articles in my collection that it's often very hard to re-locate a number of important ones. The past year I was forced to take a break from medical research before I could complete this still unfinished task on my part).
http://www.mayo.edu/research/faculty/patel-robin-m-d/bio-00026595
One more important note I might make is about whether or not we are actually contagious if we turn out to typically have infectious diseases as part of HS. Both experience (my wife has never "caught HS" from me in the 12 years since my diagnosis) and research (it might generally take both a genetic predisposition and some significant breach of the skin to be at high risk of "catching HS" from someone with the diagnosis) suggest that we may not ordinarily be contagious. Likewise, a number of the microbes in discussion (at least by species) are thought to already be normal residents of the human skin, which should also help reduce concerns about spreading a number of the infections associated with HS.
(For what it's worth, it's hard to feel absolutely certain without additional HS studies, but after considerable research of the diagnosis and some related ones, I myself am still very much inclined to believe that a microbial model of HS may go the furthest by far toward explaining a great many otherwise mysterious aspects of the disease, from why we seem to see so few genuine reports of Staphylococcus aureus in the disease, to why symptoms and remedy responses can vary from patient to patient, to the presence of many of the "biomarkers" tentatively associated with the diagnosis, to the meaning of commonly detected "Hidradenitis genes").
-----------------------------------
THE STERILE SWAB, AND OTHER MYTHS? (A Brief History of What May Be Just a HS Rumor)
The Mayo Clinics' page on HS continues to inform doctors and patients that the disease "is not caused by an infection and can't be transmitted sexually. It's not contagious and is not due to poor hygiene" https://www.mayoclinic.org/diseases-conditions/hidradenitis-suppurativa/symptoms-causes/syc-20352306
This despite decades of accumulated bacteriological studies which illustrate the prevalence of infection in the diagnosis and the statistical likelihood of patients having at least one infection of clinical significance, and despite the frequency with which antibiotics are employed to produce improvements in severity of disease symptoms in the diagnosis.
The individuals who assemble this information for the Mayo Clinic or similar sources need only to have consulted authoritative textbooks on HS and have adopted the summaries of research therein in order have arrived at what may be an erroneous conclusion appearing on their webpage for the diagnosis.
Hindrik Van der Zee, writing in the textbook Hidradentis Suppurativa: Pathogenesis and Treatment (2011), informs us that
"At first sight, the signs of clinical aspects of HS do suggest infection. But result of bacterial cultures, despite the volume of discharge, are often negative or do only yield skin commensal microbiota [67,68]. In a retrospective study, axillary bacterial cultures from HS patients demonstrated that the most prevalent aerobic species were Staphylococcus aureus, Streptococcus pyraogenes, and Pseudomonas aeruginosa, the most frequent anaerobic bacterial were Peptostrepotoccus species, Prevotella species, microaerophilic streptococci, Fusobacterium species, and Bacteroides species [67]. 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 lesions [68]. Using this method, bacteria were collected in only half the samples [68].
(The references in question):
67. Jemec GB, Faber M, Gutschik E et al. The bacteriology of hidradenitis suppurativa. Dermatology 1996; 193: 203-6.
68. Lapins J, Jarstrand C, Emtestam L. 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. Br J Dermatol 1999; 140: 90-5.
In summary, (1) Van der Zee cites studies by both Lapins, et al [68] and Jemec, et al [67] in stating that "bacterial cultures, despite the volume of discharge, are often negative or do only yield skin commensal microbiota," (2) cites Jemec, et al in describing the detection of numerous bacteria, including some organisms of considerable clinical significance, while suggesting that these cultures obtained by Jemec, et al may have been contaminated with skin surface flora, and (3) implies that the results of Lapins, et al are more reliable because of the precautions taken against contamination by commensal flora, and that Lapins, et al, using more careful methods, "bacteria were collected in only half the samples"
What do the studies cited by Van der Zee ACTUALLY say?
Jemec, et al report (the actual bacteriological methods do not seem to appear in the article abstract)
RESULTS: Bacteria were found in 49% (20/41) of all lesions... CONCLUSION:... bacteria are only found in approximately 50% of all active hidradenitis lesions.
https://www.ncbi.nlm.nih.gov/pubmed/8944341
While Lapins, et al report
"In this study, 22 women and three men with a mean age of 35.3 years and a mean HS duration of 10.6 years were treated with this CO2 laser surgical method. Aerobic and anaerobic cultures from superficial and deep levels were taken during surgery... 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."
https://www.ncbi.nlm.nih.gov/pubmed/10215774
Thus, in contrast to Van der Zee's apparent summation of Lapins' study as finding infection in only 50% of samples (which actually appears to apply only to the lower-quality study by Jemec, et al), the study by Lapins, et al actually seems to report that
100% of 25 (25/25 = 100%) exhibited infection at either deep or superficial levels
All but three cases (23/25 = 92%) exhibited infection at deep levels, two showing Staphylococcus only)
21 of 25 patients (25/21 = 84%) exhibited coagulase-negative Staphylococci (CNS)
16 of 21 findings (16/21 = 76%) of CNS detected came from deep levels, with
16 of 25 cases (16/25 = 64%) patients in total exhibiting coagulase-negative Staphylococci (CNS) from deep levels
In other words, even when doing more reliable work using deep samples to assure against contamination with normal surface flora from the skin, infection still seems to have been reported in a stunning 92% of cases by Lapins, et al, even when examining deep levels.
Similar prevalence of infection may be seen in the more recent and more careful microbiological studies by the Pasteur Institute affiliates (Olivier F. Join-Lambert and co-authors).
In another possible case of misrepresentation of data in a what is most likely another valued and frequently-consulted clinical textbook on the diagnosis, Cristina Oprica, writing in
Bacteriology of Hidradenitis Suppurativa (Chapter 11 in the book Hidradenitis Suppurativa by Jemec, et al, 2006), http://eknygos.lsmuni.lt/springer/197/86-94.pdf
quotes the very same two studies by Lapins, et al and Jemec, et al to inform us that
"Despite the volume of the discharge the HS lesions are often found to be sterile [29, 33]"
(The references in question):
29. Jemec GB, Faber M, Gutschik E, et al (1996) The bacteriology of hidradenitis suppurativa. Dermatology
193:203–206
33. Lapins J, Jarstrand C, Emtestam L (1999) 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. Br J Dermatol 140:90–95
Whereas summarization of the higher quality study by Lapins, et al specifically seemingly finds lesions to be infected with an actual frequency of 92%-100%. These numbers are not only remarkable in their own right, but may be even more so in light of the possibility of the involvement of microbes whose presence can sometimes be difficult to verify. Vlassova et al, for example, have suggested the possible participatory role of fastidious organisms, with other studies suggesting the possible frequent involvement of bacterial biofilms in the disease.
N Vlassova, O Olowoyeye and G Hinds Dermatology, Johns Hopkins Hospital, Baltimore, MD, Analysis of bacterial communities in hidradenitis suppurativa lesions
"Over the years a large number of microorganisms have been cultured from the HS lesions with Staphylococcus and Streptococcus species being the most commonly isolated species. However standard cultures often overestimate the importance of bacteria that are easily cultured while underestimating the importance of fastidious organisms which require more specialized tests."
http://www.nature.com/jid/journal/v132/n1s/full/jid201288a.html
Potentially misleading summarizations may have resulted in doctors and their mistrusted sources believing HS to rarely involve infection, thus allowing even potentially dangerous infections such as Staphylococcus or Streptococcus, to be overlooked even when observed by the attending physician.
In the following instance too, we find the declaration of "frequently sterile" swabs traceable back to works by Jemec and Oprica already cited
Guideline on Hidradenitis suppurativa (Developed by the Guideline Subcommittee of the European Dermatology Forum)
http://www.euroderm.org/edf/index.php/edf-guidelines/category/5-guidelines-miscellaneous?download=45:guideline-hidradenitis-suppurativa
"4.4.Bacteria
HS is not a «classic» infectious disease: there is no unique bacterial agent but a polymorphic flora; it is a chronic disease with or without acute flares. Bacterial sampling of suppurations are frequently negative i.e. sterile. Several members of the normal skin flora are found in the HS lesions (50,51)....
The absence of Staphylococcus aureus, whatever the level of sampling is striking. A recently reported study (55) has partially confirmed these results showing the predominance of Staphylococcus lugdunensis in low severity grade lesions (Hurley I). In more severe lesions anaerobic bacteria, actinomycetes and streptococci of the Milleri group were present. Staphylococcus aureus was only found in superficial samples, which may indicate a clinically irrelevant colonization. Hence, CNS and anaerobic bacteria are the main bacteria recovered from HS lesions.
Most CNS infections have a slow, subacute evolution. CNS are able to form biofilms on medical devices and hence escape an immune reaction. S. lugdunensis has special features in the group of CNS: as a frequent resident of the perineum it can be responsible for infections e.g. abscesses and wound infections. Clinically, infections caused by S. lugdunensis are similar to those caused by S. aureus rather than those caused by other CNS (56)."
(The references in question):
50. Jemec GB, Faber M, Gutschik E, et al. The bacteriology of hidradenitis suppurativa. Dermatology 1996;193:203-206.
51. Oprica C, Nord CE. Bacteriology of Hidradenitis Suppurativa In: Jemec GBE, Revuz J, Leyden J, eds. Hidradenitis suppurativa. Berlin: Springer Verlag; 2006:86-94.
Such possible mangled information as seen in these sources might have also contributed to inappropriate approval of certain pharmaceuticals for the condition. The anti-inflammatory, anti-TNF-a biologic Humira has been approved in some countries for HS even while the manufacturer continues to warn, "Do not start Humira if you have a pre-existing infection," in spite of the great likelihood indicated by a broader body of research (especially studies done by affiliates of the Pasteur Institute) of pre-existing infections in patients otherwise approved to receive the treatment.
Whether, therefore, patients are in fact approved to receive this treatment may remain a largely unanswered question for patients (as may questions concerning patients' rights and recourse in the event of incidence while thus using a medication in a manner contrary to manufacturers' instructions).
Meanwhile, personal experience with caregivers indicates that they may often somehow be unaware of the inflammatory potential of infection and the possibility that palliatives for the condition such as Humira (or others, including retinoids, 5-alpha-reductase inhibitors, and other medications) are unknowingly dampening symptoms of infections that may be much more appropriately treated with targeted antimicrobial therapies. Patients may be informed that their condition is being caused or significantly aggravated by inflammation associated with factors such as obesity or tobacco use, with sheer disregard for the inflammatory potential of even well-known bacterial factors themselves.
Misinformation or misconception about the disease may also tempt caregivers or patients into constructing and acting on invalid etiologies of the disease. Discouraged from interpreting the disease or its symptoms as infection by trusted sources, and in the absence of any other clear proposals of causative factors, caregivers or patients may misuse or misinterpret statistical information as a causal statement regarding the disease.
Inappropriate emphasis may thus be placed on amendments to lifestyle factors at the expense of recommended microbiological investigations and services which may be urgently needed. (Ultimately, patients may sometimes even be "blamed" for their condition or considered guilty of patient non-compliance should they fail to enact these same lifestyle modifications).
Likewise, it may be difficult and even greatly discouraging for patients who independently research their own diagnoses, to share such experimental etiological models (or the sometimes voluminous amounts of microbiological research on which they may be based) with caregivers who may be devoted to preconceived or misleading ideas or sources concerning these conditions, and unable to attend to the task of wading through the literature themselves - an environment in which misconceptions may flourish.
With the possible difficulty in treating some cases of the disease with antibiotic therapies that lack specific targets, and even the possibility of cases having been further complicated by previous antibiotic therapy lacking specific targeting, less than ideal outcomes of less than ideal antibiotic therapies may be misinterpreted as further evidence against a microbial model being relevant to the disease. It may be often posited by authors or caregivers that antibiotic use lends improvement in many cases because of possible beneficial "side effects" of antibiotics rather than antibiotic activity itself.
With considerable focus on inflammatory aspects of the disease, a number of authors have suggested that antibiotics have earned a reputation for causing improvement in management of the disease by exerting anti-inflammatory effects, yet researchers involved in the Pasteur Institute studies have pointed out that the same effects can be seen even in the case of antibiotics lacking in known anti-inflammatory effects:
Study Suggests New Treatment for Hidradenitis Suppurativa, Kate Johnson, Medscape Medical News, March 19, 2012
"It is the first time an antibiotic with no recognized anti-inflammatory activity has shown a real efficiency in HS, which raises the question of an infectious participation," said Dr. Nassif, who is from the Institut Pasteur in Paris, France."
https://www.medscape.com/viewarticle/760502
--------------------------------------------------------
In closing (for now), I would like to express my gratitude to the authors of
Guideline on Hidradenitis suppurativa (Developed by the Guideline Subcommittee of the European Dermatology Forum)
1), for acknowledging the 2012 study by Sartorius, et al, which reports finding infection of 10/10 (100%) of HS patients examined
Bacteriology of hidradenitis suppurativa exacerbations and deep tissue cultures obtained during carbon dioxide laser treatment.
Br J Dermatol. 2012 Apr;166(4):879-83. doi: 10.1111/j.1365-2133.2011.10747.x. Epub 2012 Mar 2.
Sartorius K1, Killasli H, Oprica C, Sullivan A, Lapins J.
https://www.ncbi.nlm.nih.gov/pubmed/22098253
"Bacterial samples for aerobic and anaerobic cultures were taken from the skin surface (before surgery) and then from the deeper layers (during surgery) of the lesions. At each level two samples were taken, one with a punch biopsy and one by pressing a soft agar gel against the skin. The bacterial findings were typed and quantified... RESULTS: A total of 10 patients (eight women and two men), with a mean age of 37·2 years and a mean HS duration of 14·5 years, were included. All of them had an ongoing exacerbation (mean duration 5·6 days) of their HS, with one inflamed lesion that was treated by carbon dioxide laser vaporization. Coagulase-negative staphylococci (CNS) were found in the deep layers in all 10 patients."
And 2). for advising us that
"Anaerobes are frequently responsible for soft tissue infections: cellulitis, dermo-hypodermitis, myonecrosis; in HS their presence should be systematically suspected. It becomes self evident in case of foul odour of exudates. The absence of positive bacterial culture in spite of abundant flora on direct examination is a clue to their responsibility; “sterile pus”.
As a whole, bacterial infection in HS is mainly due to CNS and anaerobes and is polymicrobial, a usual feature of anaerobic infections. "
Which seems to inform us that malodor in HS case may itself be evidence of infection, and that samples from HS which culture negative (i.e., the "mythical" sterile swabs) may nonetheless still show bacteria on "direct examination" - both of which seem to be very important points.
Bacterial pathogens associated with hidradenitis suppurativa, France.
Guet-Revillet H, Coignard-Biehler H, Jais JP, Quesne G, Frapy E, Poirée S, Le Guern AS, Le Flèche-Matéos A, Hovnanian A, Consigny PH, Lortholary O, Nassif X, Nassif A, Join-Lambert O.
Emerg Infect Dis. 2014 Dec;20(12):1990-8. doi: 10.3201/eid2012.140064.
Abstract: http://www.ncbi.nlm.nih.gov/pubmed/25418454
Free full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4257786
Free full text: https://wwwnc.cdc.gov/eid/article/20/12/pdfs/14-0064.pdf
Comments: Seminal high-quality metagenomic microbiological study of HS giving a highly detailed view of the bacteriology of some individual cases, perhaps most notably showing very strong associations between Stage 1 HS and Staphylococcus lugdunensis, and a considerable prevalence of Prevotella bivia in higher stage cases. If Prevotella bivia is able to dominate the bacteriological landscape of HS in vivo the way it is seemingly able to dominate it in vitro here, it may prove to be a major architect some of the more severe symptoms or characteristics of HS.
Microbiologic profiles of hidradenitis suppurativa lesions
Olivier Join-Lambert, MD, PhD; Aude Nassif, MD; Hélène Guet-Revillet, MD; Xavier Nassif, MD, PhD
Journal of the American Academy of Dermatology
Volume 66, Issue 4, Supplement 1, Page AB110, April 2012
NOT free full text (?): http://www.jaad.org/article/S0190-9622(11)01696-3/fulltext
Bacteriology of hidradenitis suppurativa exacerbations and deep tissue cultures obtained during carbon dioxide laser treatment.
Sartorius K1, Killasli H, Oprica C, Sullivan A, Lapins J.
Br J Dermatol. 2012 Apr;166(4):879-83. doi: 10.1111/j.1365-2133.2011.10747.x. Epub 2012 Mar 2.
"Coagulase-negative staphylococci (CNS) were found in the deep layers in all 10 patients. Nine of the patients carried Corynebacterium spp. and two alpha-haemolytic streptococci at various levels. Among the anaerobic microorganisms, Gram-positive cocci were the most common bacteria.
CONCLUSIONS: As found in a previous study, CNS were the most common bacteria, but contrary to what we expected, Staphylococcus aureus was not found in any cultures from acute inflammatory nodules of HS exacerbations."
Abstract: http://www.ncbi.nlm.nih.gov/pubmed/22098253
The bacteriology of hidradenitis suppurativa: a systematic review.
Ring HC1, Riis Mikkelsen P1, Miller IM1, Jenssen H2, Fuursted K3, Saunte DM1, Jemec GB1.
Exp Dermatol. 2015 Oct;24(10):727-31. doi: 10.1111/exd.12793. Epub 2015 Aug 21.
"Studies have isolated an array of different bacteria specimens. Consistent findings of Gram-positive cocci and Gram-positive rods including Staphylococus aureus, coagulase-negative staphylococci (CoNS) and Corynebacterium species in deep tissue samples have been demonstrated in HS and may constitute a central target for the immune system. Efficacy of antibiotics, that is rifampicin, clindamycin or tetracycline, supports a microbial role in disease pathogenesis."
Abstract: http://www.ncbi.nlm.nih.gov/pubmed/26119625
Free Full Text: http://onlinelibrary.wiley.com/doi/10.1111/exd.12793/pdf
The Microbiology of Hidradenitis Suppurativa.
Ring HC1, Emtestam L2.
Dermatol Clin. 2016 Jan;34(1):29-35. doi: 10.1016/j.det.2015.08.010.
"Although the clinical presentation of Hidradenitis Suppurativa (HS) is strongly reminiscent of bacterial infection, the role of bacteria remains controversial. Studies have isolated an array of different bacterial specimens as well as biofilm formation in lesional HS skin. Consistent findings of Gram-positive cocci and -rods including Staphylococus aureus, Coagulase-negative staphylococci (CoNS) and Corynebacterium species (spp) in deep tissue samples have been demonstrated in HS. Although efficacy of antibiotics, i.e., rifampicin, clindamycin or tetracycline may support a microbial role in disease pathogenesis, the most often isolated bacterial specimens are commensal bacteria (CoNS)."
Abstract: http://www.ncbi.nlm.nih.gov/pubmed/26119625
Free Full Text: https://www.researchgate.net/publication/284811951_The_Microbiology_of_Hidradenitis_Suppurativa
Several references on Biofilm in Hidradenitis suppurativa
(Antibiotic treatment failure related to unusual populations of bacteria such as biofilms or SCVs (Small Colony Variants) may also contribute to a false impression that the disease is non-microbial in nature due to the frequent failure of antibiotics to resolve symptoms beyond the period of antibiotic administration.
Considering hidradenitis suppurativa as a bacterial biofilm disease.
Kathju S1, Lasko LA, Stoodley P.
FEMS Immunol Med Microbiol. 2012 Jul;65(2):385-9. doi: 10.1111/j.1574-695X.2012.00946.x. Epub 2012 Mar 12.
"...The clinical characteristics of HS as an infectious disease are all highly suggestive of other bacterial biofilm-based disorders (although HS has never been recognized as such): a chronic course punctuated by acute exacerbations, localized to specific anatomic regions, and temporarily responsive, but ultimately refractory to conventional antibiotic therapy. We hypothesized that HS bacteria exist in biofilm configuration, which would explain the clinical features of HS and have implications for the development of adequate therapies."
Abstract: http://www.ncbi.nlm.nih.gov/pubmed/22353357
Free Full Text: http://femsim.oxfordjournals.org/content/65/2/385.long
Bacterial Biofilm in Acute Lesions of Hidradenitis Suppurativa.
Okoye GA1, Vlassova N2, Olowoyeye O1, Agostinho A3, James G3, Stewart PS3, Leung S1, Lazarus G1.
Br J Dermatol. 2016 Jun 13. doi: 10.1111/bjd.14805.
PMID: 27291084 DOI: 10.1111/bjd.14805
No abstract available. Pubmed entry: http://www.ncbi.nlm.nih.gov/pubmed/27291084
I continue to encourage others in joining me in contacting the Mayo Clinic and/or Dr. Patel, or other sources of caregiver guidance which may overlook the microbial studies that we patients have been blessed to have had take place, and letting these sources know that you'd appreciate their reconsidering whether including some reference to microbiological studies in their materials on HS might not be appropriate, considering the accumulating data on the presence of infections in HS.
Remember, this could turn out to be a great help to any and all of our fellow patients if we can get the right people's attention.
If you can't find hope, try and make a little every now and then, and never forget that you can. :-)
This is the paper for which we are indebted to Dr. Patel and colleagues, it should hopefully still give doctors a lot of help in dealing with Staphylococcus lugdunensis, as long as they are aware of a high likelihood of it being part of HS cases.
In vitro effects of antimicrobial agents on planktonic and biofilm forms of Staphylococcus lugdunensis clinical isolates.
Frank KL1, Reichert EJ, Piper KE, Patel R.
Antimicrob Agents Chemother. 2007 Mar;51(3):888-95. Epub 2006 Dec 11.
Abstract - Staphylococcus lugdunensis is an atypically virulent coagulase-negative staphylococcal species associated with acute and destructive infections that often resemble Staphylococcus aureus infections. Several types of infection caused by S. lugdunensis (e.g., native valve endocarditis, prosthetic joint infection, and intravascular catheter infection) are associated with biofilm formation, which may lead to an inability to eradicate the infection due to the intrinsic nature of biofilms to resist high levels of antibiotics. In this study, planktonic MICs and MBCs and biofilm bactericidal concentrations of 10 antistaphylococcal antimicrobial agents were measured for 15 S. lugdunensis isolates collected from patients with endocarditis, medical device infections, or skin and soft tissue infections. Planktonic isolates were susceptible to all agents studied, but biofilms were resistant to high concentrations of most of the drugs. However, moxifloxacin was able to kill 73% of isolates growing in biofilms at < /=0.5 mug/ml. Relative to the effect on cell density, subinhibitory concentrations of nafcillin substantially stimulated biofilm formation of most isolates, whereas tetracycline and linezolid significantly decreased biofilm formation in 93 and 80% of isolates, respectively. An unexpected outcome of MBC testing was the observation that vancomycin was not bactericidal against 93% of S. lugdunensis isolates, suggesting widespread vancomycin tolerance in this species. These data provide insights into the response of S. lugdunensis isolates when challenged with various levels of antimicrobial agents in clinical use.
PMID: 17158933 PMCID: PMC1803120 DOI: 10.1128/AAC.01052-06 [PubMed - indexed for MEDLINE] Free PMC Article
http://www.ncbi.nlm.nih.gov/pubmed/17158933
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1803120
http://pubmedcentralcanada.ca/articlerender.cgi?artid=538398
If the research is laid out in chronological order, it may show that it started with the observation that HS may be an amyloid disease, although apparently NOT a B-amyloidosis like Alzheimer's or Parkinson's.
One may have to go out a bit on a limb to find a missing link, but there could be one in be some research that suggests that B-amyloid is one of the human body's antimicrobial peptides and may be part of the body's natural response to infection. The best evidence is that Rudy Tanzi and colleagues killed a number of microbes with it in Petrie dishes. B-amyloid seems to have showed activity against a number of them, and it might just turn out that these HS genetics mean lacking what may be an important defense against certain infections, possibly Staphylococcus (compare this to all the reports of certain Staph species in HS), or Candida.
It may mean that we could benefit from being a little bit extra mindful of circumstances that might pose a risk of infection - using toilet gaskets in shared facilities, avoiding contact between vulnerable areas and surfaces that might be prone to germ growth like the walls of shower stalls, being mindful to try to keep bodily fluids away from HS prone areas, and other mainly common sense measures?
The bottom line, though, may be that you can have whatever genes you want, but you may still require certain infections to produce certain symptoms of HS and that genetics may only be a predisposing factor in HS - not a cause.
A lot remains to be considered about the possibility of a genetically related bactericidal defect in HS - better known and accepted human antimicrobial peptides may need to be accounted for also, although we have seen irregular levels of a number of them in HS studies. In some cases this might indicate that certain microbes have found a way around them, we already know some of the tools that bugs can use to get past some of these defenses. Some of them can produce enzymes that can just chew up these antimicrobial proteins.
I haven't seen much in the realm of dermatology that might suggest a definitive cause of HS that I'm able to tell - follicular defects and so forth could promote HS, but infections may be able to promote some of these same defects themselves, In fact, HS used to be called "acne inversa" because of similarities to ordinary acne (acne vulgaris) - in acne, the contributions that bacteria (like Propionibacterium acnes and others) can make to dermatological events and symptoms, seem to be rather well known.
I'm actually surprised there haven't been more confident statements about a possible role for infections in HS on that basis alone, but again there are enough possible things that could wrong with antibiotic therapies to all too easily give doctors a false impression about a possible role for infection in HS. It can still be a very confusing disease.
HS isn't specific to underarms and groin as far I know, although these may be some of the areas worst affected, presumably because of perspiration. HS has been reported on the buttocks, thighs, neck, back, and face.
You may be over-generalizing quite a bit about antibiotics and infections both here, but If antibiotics are having zero effect, then a person may have resistant infections. The other end of that stick is that we often DO see benefits from antibiotics but not a lot of complete "cures" so far - quite possibly because only part of the population of microbes may be susceptible to the particular antibiotic(s) used.
A person doesn't have to have immune issues to have HS, infections, or biofilm infections (these can be particularly good at thwarting the human immune system). I'm still able to beat what is probably the occasional Streptococcus viridans group infection or the occasional E coli infection even when they get right in my lesions - the ones I can't fight off seem to be a couple of particularly stubborn species.
Even the tiny spots of facial HS I have are likely to last years. Once a sore takes on that familiar HS-like character, I can't fight it off. I recently got a sliver which I normally don't have troubles with but it looks to have picked up this infection now and seems to think it's incurable.
One of the particularly nasty boils on my groin got out of hand and resulted in an urgent care situation where they were talking about sawing me in half if the antibiotics didn't work - they appear to have gotteb most of it but not all of it, so it came back - but they don't seem to think so unless it escapes from a cyst and is trying to do me in again.
Anyway, seriously - we have 20-30 years of microbiological studies attesting to the history of infection discovered in HS - the better, more modern and more careful the study, the fewer uninfected patients seem to be found, but findings of 92%-100% of patients studied having infection go some way back now.
A quick note to people about biofilm - if you start looking that up, you might find some glowing claims or promises about "biofilm busters" and I am just not sure what to think of these. For myself, I think I'm going to beware of them so I certainly couldn't recommend them to others.
Twice just in the last two days I've read in medical journal articles where the result of breaking up a biofilm infection very clearly sounds like it may be to simply further spread the infective organisms contained in the biofilm, whereas we already have antibiotics like rifampicin (rifampin) that don't seem to care all that much whether their target is a biofilm Staph infection or not
There's been some talk about combining anti-biofilm agents with antibiotics but I'm not sure how far that research has actually gotten. It makes sense, though, because there's also a fair amount of discussion about how when microbes leave a biofilm they can tend to switch back to their more aggressive, more virulent tendencies.
http://www.hstrust.org/Hidradenitis%20Suppurativa%20Research%202017.pdf
I don't quite know how useful this will actually be. It may overgeneralize whereas I'm tempted to think that the best course of antibiotic therapy in HS is going to be more individualized and aimed as specifically as possible at what a particular patient is actually infected with...
But I found this article especially interesting as it may point to more common sources of antibiotic treatment failure in HS (there seem to be many ways to get it wrong somehow, probably all of them leading to infections returning because not all of the bugs were successfully killed).
Patterns of antimicrobial resistance in lesions of hidradenitis suppurativa.
Fischer AH1, Haskin A2, Okoye GA3.
J Am Acad Dermatol. 2017 Feb;76(2):309-313.e2. doi: 10.1016/j.jaad.2016.08.001. Epub 2016 Oct 11.
Abstract
BACKGROUND: Antibiotic therapy is commonly used to treat hidradenitis suppurativa (HS). Although concern for antibiotic resistance exists, data examining the association between antibiotics and antimicrobial resistance in HS lesions are limited.
OBJECTIVE: We sought to determine the frequency of antimicrobial resistance in HS lesions from patients on antibiotic therapy.
METHODOLOGY: A cross-sectional analysis was conducted on 239 patients with HS seen at the Johns Hopkins Medical Institutions from 2010 through 2015.
RESULTS: Patients using topical clindamycin were more likely to grow clindamycin-resistant Staphylococcus aureus compared with patients using no antibiotics (63% vs 17%; P = .03). Patients taking ciprofloxacin were more likely to grow ciprofloxacin-resistant methicillin-resistant S aureus compared with patients using no antibiotics (100% vs 10%; P = .045). Patients taking trimethoprim/sulfamethoxazole were more likely to grow trimethoprim/sulfamethoxazole-resistant Proteus species compared with patients using no antibiotics (88% vs 0%; P < .001). No significant antimicrobial resistance was observed with tetracyclines or oral clindamycin.
LIMITATIONS: Data on disease characteristics and antimicrobial susceptibilities for certain bacteria were limited.
CONCLUSIONS: Antibiotic therapy for HS treatment may be inducing antibiotic resistance. These findings highlight the importance of stewardship in antibiotic therapy for HS and raise questions regarding the balance of antibiotic use versus potential harms associated with antibiotic resistance.
KEYWORDS: acne inversa; antibiotics; antimicrobial resistance; hidradenitis suppurativa
PMID: 27742173 DOI: 10.1016/j.jaad.2016.08.001 [Indexed for MEDLINE]
https://www.ncbi.nlm.nih.gov/pubmed/27742173
Perhaps the good news is that since both resistant superbugs and recurring infections such as seen in HS may involve a failure to kill all of the bugs, all those brilliant people out there who are hard at work on how to get rid of superbugs (kill 'em all) may also be hard at work on how to get rid of HS infections (kill 'em all). Wow, that's a lotta people working on Hidradenitis - about 10 times as much HS research going on as anybody thought there was? :-)
In the five years I've been studying biology (in the context of HS and several other diagnoses specifically), one of the most nagging questions has over been antibiotic failures with HS. Antibiotics routinely give improvements, yet the improvements are usually lost when the antibiotics run out. Thus antibiotics have such a poor track record for creating permanent improvements that it's apparently easy for a lot of people in medicine to think that HS isn't about infection. They've often proposed we're benefiting from antibiotics because of anti-inflammatory or sometimes immunosuppressive side effects rather than antimicrobial activity, although as Dr. Nassif reminded us it's increasingly less likely that the growing list of helpful but diverse antibiotics could all have these same beneficial side effects.
The Pasteur Institute got impressive results with combinations of powerful broad-spectrum antibiotics, yet relapses seem to be all too common, Since they've help demonstrate Staphylococcus lugdunensis as having a high prevalence in HS and a monopoly on the bacteriology of the first stage of the disease in their studies, I consider this Staph a cornerstone of the disease with a high likelihood of being present in the relapses, and tend to interpret these relapses as indicating a failure to permanently eradicate it. What has always been remarkable is they used rifampin, which seemed to have such a sterling reputation for being effective against Staph even as biofilm, that for the first year I studied HS I couldn't believe it was a biofilm disease simply because they're used rifampin.
In contrast, my physician managed to get rid of my Staphylococcus lugdunesis for good ten years ago. It didn't cure my HS because there are other infections that haven't been dealt with, but it seems to constitute major improvement without relapse. So the big question is, what is happening here? Did the Pasteur Institute somehow do something that isn't particular effective, did my doctor happen to do something that IS particularly effective, or both?
Again, we are greatly indebted to Dr. Patel for her work on the antibiotic susceptibilities of S. lugdunensis, which may be the "signature" Staph of HS. Her study has hopefully made a "no-brainer" out of treating S, lugdunensis infections / Stage 1 HS and gives the possibility of nipping stage 1 HS in the bud before the typical anaerobes that seem to complicate HS into Stages 2-3 can get involved. The remarkable thing they found is that S. lugdunensis doesn't seem to have much in the way of acquired resistance and can still be killed with just about anything but vancomycin, which makes what my doctor did look rather ordinary and puts the focus back on whether combining antibiotics against HS may not be a good idea.
I'm going to back up a minute and talk about biofilms, because some basic questions turned out to be of possible great importance here... What is biofilm, and what are biofilms?
Biofilms are communities of bacteria (often or possibly even always made of mixed species) that can behave very differently from the ordinary bacteria in infections as we normally think of them. Rather than floating or swimming around, they're glued in place and encased in some sticky junk called biofilm which they secrete, and they have a nasty reputation for being hard to get rid of with antibiotics.
I'm using the term "biofilm" to mean this sticky junk itself, "biofilms" to mean both this sticky junk and the microbial communities that live in it, and "biofilm microbes" to refer to microbes that have the same metabolic and reproductive profile of microbes found within the biofilm community, whether or not they may be secreting biofilm goop at a given moment. We can probably safely for intents and purposes here, lump together a number of different descriptions of bacteria expressing similar traits: Biofilm, persisters, small colony variants (SCVs); sessile, stationary phase, dormant or dormant-like microbes...(Microbes as we normally think of them are referred to as being in a "planktonic" state).
Many microbes can switch back and forth between planktonic and biofilm states, which is a hugely important point about biofilms. Another is that for intents and purposes here, biofilm microbes are avirulent and non-replicative. They are not very active at protein synthesis hence they are not very active at producing virulence factors which are proteins, such as tissue- or cell-destructive enzymes like proteases or hemolysins, and they are not actively reproducing. By themselves, they can therefore lack the "clinical drama" or severity of symptoms associated with planktonic infections and may therefore complicate diagnosis by failing to show the classic signs or severity normally required for diagnosis.
Even though they almost sound tame here, biofilms can still switch back to their destructive and rapidly dividing behavior under suitable conditions - this may be what some HS triggers do is put our biofilm microbes back on the warpath, back into the virulent planktonic state. Biofilms can go on to become the parents of whole new generations of destructive, virulent offspring, and the emerging picture may be that they may at least in some cases be the parents of superbugs.
If you've been reading up on biofilms or listening to lectures, you're probably aware of their reputation for being difficult to kill with antibiotics, which is very much the same reputation as HS. Some of the information actually makes things sound pretty hopeless at present for getting rid of them. However, this may be because they are still not well understood (and in fact antibiotics themselves may not be terribly well understood at present, which may not help much). Many articles give biofilm credit for being able to pose a physical barrier to the penetration of antibiotics into the target microbe, although this may have been disproven by multiple studies that showed that lethal doses of antibiotics can still make into the target microbes encased in biofilms, in a matter of minutes.
The best explanation for the peculiar antibiotic resistance of biofilms may be that because they are the next thing to dormant, they have temporarily suspended the growth processes that are targeted by antibiotics. For example, penicillins target actively diving bacteria, and because biofilm bacteria are not actively dividing, they manage to dodge the bullet. If they're not actively synthesizing DNA while being biofilm, then biofilm microbes may not be terribly impressed by DNA synthesis inhibitors like flouroquinolones - and so forth.
This antibiotic resistance they get just by switching into biofilms is called "phenotypic" resistance and it's not the same as the acquired resistance of superbugs - microbes don't get to keep it when they switch back to their normal planktonic form. (Often biofilm microbes are stated to be antibiotic tolerant rather than antibiotic resistant, requiring larger doses to eradicate).
To go back to the question of what my doctor did vs. what the Pasteur Institute did, it should be easy to spot that combining antibiotics may not always be the best idea if it failed to kill a Staph you can kill with just about anything. In one of their antibiotic trails the Pasteur Institute researchers combined rifampin with clindamycin and in the following paper ended up reporting that when these two are combined, rifampin can kick clindamycin out of blood plasma. I have other independent research which shows other antibiotics kicking rifampin out of blood plasma when combined, and etc. Just when a maximum dose may be needed to overcome the antibiotic tolerance of a biofilm, combination antibiotic therapies may get in each others way and prevent the maximum dose of key antibiotics from getting to their intended targets.
As I said, it's easy to not see much that's special about what my doctor did, just about anything will kill this S. lugdunensis except vancomycin... But wait... Remember that one of the key characteristics of biofilms is that they AREN'T actively growing and dividing? My sinus tracts had stopped expanding by the time I got the fateful dose of erythromycin, which implies that the bacteria inside them may have run out of key nutrients and reverted to the biofilm state.
Right, my doctor killed a biofilm, With erythromycin. With a protein synthesis inhibitor that isn't even supposed to be able to have killed anything - protein synthesis inhibitors are generally classified as bacteriostatics which slow down bacterial growth, rather than as bacteriocides which kill bacteria. My doctor killed something we are not supposed to be able to kill, with something that isn't supposed to kill anything. Furthermore, a microbe that has already almost completely shut down its protein synthesis isn't supposed to be impressed with protein synthesis inhibitors, and it's hard to think the immune system gets credit for finishing the job of killing when sinus tracts or cysts or abscesses containing biofilm may be immunologically priveleged areas where immune cells cannot go because of the immunosuppressive spew coming from the biofilm microbes inside them.
So we can already see where our ordinary classifications of antibiotics and our models of how they work may be in some serious trouble. I'm not the only one to notice this, some researchers are going back to the drawing board over how antibiotics actually work, and some of the work they've done may have helped me to complete a first draft of a model that might help explain exactly what my doctor managed to do. They propose that many bactericidal antibiotics may have a common killing mode similar to that of metronidazole, in which microbicide results from free radical damage inflicted on the microbe's DNA. Small problem here...
Biofilms tend to be using anaerobic respiration, and biofilms tend to be anaerobic environments, and it's already a known resistance mechanism in some anaerobes to produce a DNA repair protein that can not only undo the DNA damage caused by metronidazole, but while it's in there tinkering with the DNA, can insert acquired resistance DNA into the microbe's genome, so that all its descendants henceforth will be superbugs that have this newly acquired resistance. Futhermore, it's the free radical stress on the DNA that is supposed to sound the alarm to trigger the synthesis of the DNA repair proteins that may ensure the microbe's survival.
I'm going take a minute to emphasize that we need to learn to think of microbial populations as planktonic + biofilm. When we talk about an antibiotic losing its effectiveness, we generally mean against planktonic bacteria. Biofilms may be another subject altogether, and we need to get better at recognizing that and separate the two even if they're little more than than the same microbes in different moods - and I think I might be able to demonstrate why this is so imporant here.
The emerging picture may be something like that when we are talking about biofilms - the powerful microbicidal antibiotics may charge in like a bull in a china shop with a metronidazole-like activity that sets off the alarm to make the DNA repair protein...
Whereas antibiotics that are only microbistatic politely knock on the door, announce that they're the china shop inspector come to inspect, and before anyone is wiser, they cut the alarm wire before the alarm can go off by directly inhibiting the DNA repair protein from ever being produced should the signal to produce it sound..
But if this is so, how do protein synthesis inhibitor kills biofilm microbes? I am indebted to the work of Dr. Phil Stewart here, who worked on Pseudomonas aeruginosa biofilms, with a lot of the findings likely applicable to other species of biofilm microbes. They studied the gene expression profiles of Pseudomonas when in biofilm mode compared to planktonic mode to see what changes were taking place. Naturally as you'd expect for a microbe whose activity can be described as dormant-like, the biofilms had turned down the expression of most of their genes and their protein products, and had turned up the expression of very few, but I found something curious - there was the increased expression of genes which produce antioxidant proteins.
It's an easy one to explain away - I've said that microbes when in biofilm mode can be expected to be anaerobic, and anerobes are sensitive to oxygen, so naturally it would make sense for them to turn up their production of antioxidant proteins to protect themselves.
One small problem - biofilm microbes don't seem to see a lot of oxygen in their natural habitat which is anerobic, oxygen poor and CO2-rich, and when they do leave it and encounter oxygen, they tend to switch back to their planktonic forms, at which point we can expect them to turn their production of antioxidant proteins back DOWN! What?!? So what do they need with more antioxidant proteins if they never seem to get near oxygen?
Once I asked that question, two minutes Googling found an answer - they think biofilm bacteria need to increase production of antioxidant proteins to protect themselves from the free radical by-products of their own respiration. Without them, they would apparently do a metronidazole-like number on themselves - and one class of antibiotics we presume can block the synthesis of antioxidant proteins, and that's protein synthesis inhibitors.
So in theory, protein synthesis inhibitors can prevent DNA repair and DNA protection (antioxidant) proteins from being made so that DNA damage begins to happen just because of them breathing, and the damage can't get fixed - end of microbe story. Also rather like metronidazole, only more of a slow burn and it serves 'em right...
I'm sure I"ve been saying for four years around here that maybe there is something special about protein synthesis inhibitors because of what my doctor accomplished, but this is the first time I've had anything that much resembles an actual model or mechanism to explain it.
I have just enough peripheral support to start to take stock in all this - work done in Japan using erythomycin against biofilms with results that imply that it may be getting rid of biofilm the safe way by killing the microbes living in the biofilm who need to work at maintaining it (I learned about this from Dr. Wolcott's video lecture on biofilms Youtube), and an article on HS from last year trying to see how many superbugs are being made using antibiotics they way they are typically used for HS, that showed that oral clindamycin (another protein synthesis inhibitor) was not associated with the appearance of superbugs (although topical clindamycin use was).
All three of these instances (these two studies and my own case) all hint at the possibility of achieving final results against biofilm with protein synthesis inhibitor antibiotics. There may be more such evidence if I had the chance to look harder, and there certainly are at least scattered claims of killing microbes with biofilm characteristics with protein synthesis inhibitors.
Thus I've attempted to contact a few biofilm researchers to try to make certain they are aware of the possibility that the "Holy Grail" against biofilm that we all seem to be looking for might just have been spotted, of all places, at my doctor's office.
Something that gave me some confidence that this might be worth speaking up about, is when we get around to the question of "Where do biofilms come from? Did they crash-land their spaceship here ten years ago?" because the consensus seems to be that biofilms are a FACT OF LIFE. They roamed the earth with dinosaurs, they're in the puddle in your backyard, they're in the plaque on your teeth - in fact their discovery is often credited to van Leeuwenhoek who studied dental plaques in very early experiments with microscopy. The National Institute of Health asserts that 60% of the infections seen in clinical practice may involve biofilm (the numbers may be similar thus far for findings of biofilm in HS) and one expert has raised the ante to 80%, so in these terms too they are beginning to look like a fact of life, rather than anything new...
So if they're part of so many infections, why have we been able to have the successes with antibiotics that we have in the past, if they're so hard to kill? From where I'm sitting, the answer begins to look like there have always been a few of these bad apples in every barrel. THEY don't seem to be doing anything different, so what are WE doing different?
Moving away from protein synthesis inhibitors, with some authors having already given up on them because of rapidly growing resistance to them - yes, growing resistance in PLANKTONIC bacteria, but that is not the same thing as BIOFILM bacteria! - and moving more toward the proposed "bull in a china shop" antibiotics that may be brilliant to use against PLANKTONIC infections, but possibly not such a good idea normally to use against BIOFILM infections. We may also be moving more toward combinations of these antibiotics in emergencies or in order to try to prevent superbugs, but these combinations may be even worse for getting rid of BIOFILM infections because of antagonism between different antibiotics - different ways they can interfere with each other and decrease the effective dose being delivered.
Curiously, I'm having trouble thinking of any evidence that BIOFILMS have ever become more resistant to protein synthesis inhibitors. We continue to have recent evidence that hints at their useful properties, which one might assume they have always had since they were first introduced.
So that is essentially the hypothesis I submitted to the experts, sans the many references, It's based on as much research as possible, particularly research that seems to fit together particularly well, and as much as possible it's based on actual reported clinical events. I could ask my doctor to test it out on me, but he already did without me asking, and it worked great.
This of course says that we should be able to get lasting results against the Staph with oral clindamycin, so if that is not happening routinely we may need a closer look at why. Certainly if someone thought they were giving antibiotics as anti-inflammatories, they might give the kind of conservative doses like my doctor gave me of doxycycline for "non-antibiotic" reasons, to give just one example of something that might have given less than the desired results from clindamycin used as a monotherapy.
Again, I think what my doctor did demonstrated well enough that we can go after one key organism at a time in HS instead of trying to eradicate every microbe present all at once. Synergy between Staphylococcus and Prevotella has already been reported - the two bringing out the worst (virulence) in each other - thus it may be plausible that by eradicating the Staph, that Prevotella that may have been participating in sinus tract formation may have been tamed even if not killed. Any Bacteroides and Streptococci still standing after this may also be high value targets in attempting to decrease disease severity, I think these two are what is most likely holding my own case of HS together at this point.
I could be wrong about all of this, I could be wrong about my own name and often am, but case I don't get further opportunities in the near future, I thought I'd share it as-is. (It is just a first draft after all, and probably has plenty of room for improvement). If it actually turns out to be a viable model, I think there could be considerable cause for optimism, rather than pessimism, about our ability to get rid of biofilms for good.
Timing is key for bacteria surviving antibiotics
By Molly Sharlach
June 29, 2018
https://engineering.princeton.edu/news/2018/06/29/timing-key-bacteria-surviving-antibiotics
You'll note the focus on DNA repair proteins, They're not the only ones starting to focus there, there are actually a number of related research articles, Let's hope we are all barking up the right tree with that. Mainly once they get into the mechanics, they start talking about searching for new medicines, but hopefully it will dawn on more researchers soon to start asking if our ever-increasing understanding of the sneaky games that microbes play can allow us to put new life in the medicines that we already have so that we don't have to stand around waiting.
Just to show off my amazing powers of stating the obvious, I want to say that while we may still have a number of researchers who are skeptical about the role of infection in HS, who do sound smart for objecting that "If it's infection, why can't we get lasting results from antibiotics?" yet might not sound quite as smart if they said the same thing about biofilm. Biofilm is obviously infection according to virtually everyone. Like HS, it too can be tremendously refractory to antibiotics, but that's no indicator that biofilm isn't infection.
Biofilm is tricky stuff though, and we may even have set ourselves back 10 or 20 years by not being more careful to recognize that biofilms aren't homogenous in their makeup and that microbes in different layers of a biofilm can behave in different ways, and to talk about them accordingly for clarity's sake. There are countless statements in literature of how a biofilm did this, or a biofilm did that, and when I go to ask "Which part of the biofilm did that?" I usually have to try and deduce it. The good news is that biofilm isn't getting any smarter, but we are.
So anyway, that link is fresh news that gives me cause for considerable optimism, since in my opinion it's probably getting very close to striking at what may be at the very heart of HS.
Also, for what it's worth, I'm referring to Mark Brynildsen who is featured in that article as "The Fourth Musketeer" since I noticed he has co-authored a number of papers with JJ Collins. I frequently refer to Michael A Kohanski, Daniel J Dwyer, and James J Collins as "The Three Musketeers" because these frequent co-authors have collectively produced a remarkable number of works that I think (I hope) have been a great boon to my understanding of what I'm dealing with as a Hidradenitis patient.
We are all still struggling a bit with the subject and stumbling over some probably outdated ideas, but I think they are helping us all to have much better insights into how antibiotics may actually work so that we can make better choices with them and get better results. I'm very grateful to all of them for the hope this has given me the past six months while staring in the face of another year of the same misery and uncertainty with HS.
It's probably a lot easier to grapple with than a lot of what I've posted.
Sadly, the article is from way back in 2007, but it's still one of the best single articles I've seen on this subject - short, sweet and to the point, about how all antibiotics are NOT created equal, and why. It isn't perfect, and it's still stumbling over a couple of antiquated ideas about infections and antibiotics, but it can go a long way to explain why, for example, clindamycin has been spoken highly of regarding Hidradenitis.
It's a brilliant example of exactly what I mean when I say that one reason it may be so hard to get lasting results for HS with antibiotics, is because most doctors may not even really understand how antibiotics work - that was a very hard thing for me to believe myself. (Other basic reasons for less ideal results, may be that doctors may not realize they are likely to be dealing with a relatively unusual species of Staph, or that they are likely to be dealing with multiple infections in later stages of HS).
I'm up to Six "Musketeers" right now, Karl Dlrica and Xilin Zhao are also among a half-dozen researchers who are probably still hauling the whole world's weight on this subject of things that we never knew about antibiotics, and what it may mean to doctors' success rates dealing with diseases like HS that have become very closely associated with infection.
Open-minded people like these six researchers (and the people at the Pasteur Institute) and the wonderful work they do fill me with hope, they are one of the main reasons I still try to get up in the morning. They give me good reason to keep hoping for a cure, sooner than later.
BTW, if anyone is still in disbelief about how so many doctors and even their trusted sources could get things so wrong so often as they seem to have with HS or antibiotics, consider reading a few paragraphs about Barry Marshall and what he had to go through to get doctors to seriously consider whether infection with H, pylori bacteria could cause stomach ulcers. Doctors used to walk out of his lectures because "everyone knew" ulcers were "caused by stress and spicy food". A little over 20 years later, his discovery earned him a 2005 Nobel Prize in Medicine.