Treatments

Antibiotics for Hidradenitis Suppurativa: Why They Are Used and What to Know

HS is not primarily a bacterial infection, yet antibiotics remain one of its most common treatments. Here is why that isn't a contradiction, how doxycycline, clindamycin and rifampicin are actually used, and why antibiotic resistance deserves its own conversation.

60-second summary

If you only remember five things, remember these:

  • HS is a chronic inflammatory disease, not primarily a bacterial infection — antibiotics remain common because some work through anti-inflammatory as well as antimicrobial effects.
  • Systemic antibiotic courses for HS are commonly used for around 12 weeks, not the 5–10 days people associate with treating an acute infection.
  • In the largest prospective comparison, tetracyclines and clindamycin/rifampicin produced similar 12-week response rates (40.1% vs. 48.2% HiSCR).
  • Antibiotics reduce inflammatory activity; they do not reliably dissolve established structural tunnels or scar tissue.
  • Long antibiotic courses, and repeated ones, can contribute to antimicrobial resistance — current European guidance treats this as a genuine stewardship issue, not a footnote.

Being prescribed an antibiotic for HS does not mean an untreated infection is suspected. It usually means a specific anti-inflammatory and/or antimicrobial strategy, tried for a defined period with a plan to review it.

How much benefit comes from anti-inflammatory action versus effect on bacteria isn't fully settled and may differ by drug. Resistance rates reported in HS lesions vary substantially between studies.

Before starting or repeating a course, ask what the antibiotic is meant to achieve, how long it will run, and what happens if it doesn't help enough.

This summary is written and updated together with the full text. The evidence, limitations and sources stay unchanged in the article below.

Continue to the detailed explanation

“We’ll try doxycycline for three months.” For a lot of people newly living with HS, that sentence is the first moment the disease stops making sense. HS isn’t caused by poor hygiene. It isn’t contagious. Bacteria aren’t considered the underlying cause. So why does treatment so often start with an antibiotic — and why does it run for months rather than the week or two most people associate with clearing an infection?

The short answer is that antibiotics in HS are rarely doing only one job. Several of the antibiotics used for HS have real anti-inflammatory effects, separate from their ability to act against bacteria, and that anti-inflammatory action is a major reason they’re prescribed for a chronic inflammatory disease. Bacteria can still matter — HS lesions and tunnelsSinus Tract: A tunnel-like channel under the skin that forms between abscesses or nodules. Sinus tracts indicate more advanced disease and can chronically drain fluid. They are associated with Hurley Stages II and III. can host a complex bacterial community, and secondary infectionSecondary Bacterial Infection: A bacterial infection that develops in skin already affected or damaged by another condition. Open or draining HS lesions can sometimes become secondarily infected. This is a possible complication of HS, not the underlying cause of the disease. does happen — but “you’re on an antibiotic” does not mean “your dermatologist thinks this is fundamentally an infection.”

Educational content only. This article explains the antibiotic strategies commonly discussed in HS care and the evidence behind them. It does not recommend a specific antibiotic, a dose, or a duration for you, and it is not a substitute for individualized medical advice. Never start, stop, or change a prescribed antibiotic course based on this page.

Key takeaways

  • HS is a chronic inflammatory disease of the hair follicleHair Follicle: The tube-shaped pocket in the skin from which a hair grows. In Acne Inversa, the follicle becomes plugged and eventually ruptures, spilling its contents into surrounding tissue and triggering the inflammatory cascade that defines the disease., not primarily a bacterial infection — but some antibiotics are still useful because of anti-inflammatory as well as antimicrobial effects.
  • Systemic antibiotic strategies (tetracyclines; clindamycin plus rifampicinRifampicin (Rifampin): An antibiotic used for Acne Inversa, including as part of the clindamycin-rifampicin combination regimen. Rifampicin is a strong enzyme inducer and can reduce the effectiveness of several hormonal contraceptive methods. Anyone prescribed rifampicin who uses hormonal contraception should discuss this with whoever manages their contraceptive care.) are typically run for around 12 weeks before their effect is assessed. That length reflects the treatment plan, not months of untreated infection.
  • The largest prospective comparison found broadly similar 12-week response rates between tetracyclines and clindamycin/rifampicin — the combination is not automatically the stronger choice.
  • Antibiotics can calm active inflammation; they are not expected to dissolve an established, epithelialized tunnel or remove scar tissue.
  • Long or repeated antibiotic courses carry a real antimicrobial-resistance cost. Current European guidance treats that explicitly as a reason for a deliberate, reviewed treatment plan rather than an open-ended prescription.

Why are antibiotics used for HS if it isn’t an infection?

Antibiotics are used in HS because several of them combine anti-inflammatory activity with antimicrobial activity, and HS is fundamentally an inflammatory disease that can also involve a complex bacterial community within its lesions and tunnels. Depending on disease activity, clinicians may reach for topical clindamycinTopical Clindamycin: An antibiotic lotion or gel applied directly to the skin. First-line topical treatment for mild Acne Inversa in most guidelines., oral tetracyclines such as doxycycline, or oral clindamycin plus rifampicin — chosen less to “kill an infection” than to reduce inflammatory activity, with any antimicrobial effect as a secondary or contributing benefit.

That framing matters because it changes what a reasonable patient question looks like. “Is the antibiotic working” is a fair question. “Does this mean I have an infection” usually isn’t — and assuming so is where a lot of unnecessary anxiety, and a lot of unnecessary DIY antiseptic routines, come from.

Does pus or drainage from a lesion mean it’s infected?

Not by itself. HS lesions can drain, produce pus-like material, and look red, swollen and tender purely as features of inflammatory disease — that appearance alone can’t tell you whether a particular lesion has a clinically significant bacterial infection layered on top. Secondary infection is real and does happen, which is why it’s worth paying attention to features that are more specific to it: rapidly spreading redness, fast-increasing pain or swelling, fever, feeling generally unwell, or a wound behaving very differently from your usual pattern. Those are reasons to get assessed — not reasons to self-diagnose an infection from what a lesion looks like, and not reasons to reach for a home antiseptic regimen instead.

The main antibiotic strategies used in HS

The specific choice depends on things like how active and widespread the inflammation is, prior treatment, other medicines, pregnancy, allergies, and what the clinician is actually trying to achieve. Broadly, four categories come up in HS care:

StrategyTypical roleKey patient question
Topical clindamycinSelected mild-to-moderate inflammatory HS without draining tunnelsDraining Tunnel: A sinus tract or fistula actively leaking fluid (serous, purulent, or blood-tinged) to the surface. Draining tunnels carry the heaviest weight in modern HS severity scores because they signal long-standing, structurally damaged disease.Which lesions should this actually improve?
Tetracyclines (e.g. doxycycline)Systemic treatment across mild-to-severe inflammatory HSWhen will we review whether it’s helping?
Clindamycin + rifampicinClindamycin + Rifampicin: A 10-week oral combination antibiotic regimen that has been a standard second-line option for moderate Acne Inversa for years. Effective for some patients; tolerability (gastrointestinal upset, body-fluid discoloration from rifampicin) is a real limitation.Selected moderate-to-severe inflammatory HSWhat interactions and resistance issues matter here?
Specialist regimens (short-course IV clindamycin, others)Selected severe or treatment-resistant diseaseWhat is the plan after this course?

This is not a ladder to climb on your own, and it deliberately has no “which is best” column — as the evidence below shows, that framing doesn’t hold up well in HS.

Topical clindamycin

Topical clindamycin has the longest and clearest HS-specific study history of any topical antibiotic. A classic double-blind trial randomized 30 patients with HS to topical clindamycin or placeboPlacebo: An inactive substance, usually identical in appearance to the real drug, used in clinical trials to control for the meaningful placebo response in Acne Inversa. for three months; 27 completed it, and clindamycin was significantly more effective than placebo overall. But when the researchers broke that down by lesion type, the advantage over placebo held up clearly for pustules and superficial inflammation, while the effect on deeper inflammatory nodulesNodule: A firm, palpable lump deep in tissue. Nodules can be painful and may progress to abscesses. They are among the typical early signs of Acne Inversa. and abscessesAbscess: An inflamed cavity or swelling containing pus or fluid. In hidradenitis suppurativa, abscesses can form as part of the inflammatory disease process and do not automatically mean that a bacterial infection is present. Secondary bacterial infection can occur and may require separate medical assessment. In Acne Inversa, abscesses occur mainly in the armpits, groin, and other skin folds. was considerably smaller (Clemmensen, 1983). That distinction has held up in how the treatment is used since: it’s positioned for milder, more superficial inflammatory disease without draining tunnels, not as a way to clear deep abscesses or established tunnels.

Worth asking: Which lesions is this meant to improve? How long should I try it, and applied how often? What irritation should make me stop?

Tetracyclines, including doxycycline

Tetracyclines — doxycycline is the name most people recognize, though lymecycline, minocycline and plain tetracycline are also used depending on country and practice — are one of the most common systemic antibiotic strategies in HS. Part of the reason is that this drug class has genuine anti-inflammatory properties on top of its antimicrobial ones, which is what makes it plausible as a treatment for a disease that is inflammatory rather than infectious at its core.

In the largest prospective comparison to date — a European cohort study of 283 patients treated with either tetracyclines or clindamycin/rifampicin — both groups showed a statistically significant reduction in disease severity (measured with the IHS4 scoreIHS4 Score: A validated, dynamic tool for measuring current inflammatory disease activity in Acne Inversa (unlike the mainly structural, static Hurley stage). The score is calculated from the number of inflammatory nodules, plus 2 points per abscess, plus 4 points per draining sinus tract; scores up to 3 are mild, 4–10 moderate, 11 or more severe. This allows objective tracking of treatment response over time.) after 12 weeks. Among patients on tetracyclines, 40.1% reached HiSCRHiSCR (Hidradenitis Suppurativa Clinical Response): The dichotomous response criterion that became the regulatory standard in the adalimumab trials. HiSCR50 is met when: (1) the combined count of abscesses and inflammatory nodules drops ≥50%, (2) the number of abscesses does not increase, and (3) the number of draining tunnels does not increase. HiSCR75, HiSCR90, and HiSCR100 apply the same logic at higher thresholds., a validated clinical-response threshold (van Straalen et al., 2021). That’s a genuinely useful number, and it cuts both ways: it shows tetracyclines can produce meaningful improvement, and it shows that roughly six in ten patients did not reach that response threshold within 12 weeks — which is exactly why a review point matters more than blind persistence.

What is HiSCR? Short for Hidradenitis Suppurativa Clinical Response, it’s a research and clinical-trial measure based on counting inflammatory lesions before and after treatment. It is not a synonym for “cured,” and not reaching it doesn’t mean nothing improved — it’s a threshold used to make studies comparable, not a verdict on an individual’s treatment.

Clindamycin plus rifampicin

Oral clindamycin combined with rifampicin (called rifampin in the US) is a long-standing HS treatment option, generally considered for selected patients with moderate-to-severe inflammatory disease.

Is it stronger than tetracyclines? This is where a lot of informal “treatment ladders” get it wrong. In the same 283-patient cohort study referenced above, clindamycin/rifampicin achieved HiSCR in 48.2% of patients at 12 weeks, compared with 40.1% for tetracyclines — and the authors reported this difference was not statistically significant (P = .26) (van Straalen et al., 2021). A 2023 study looking at adalimumabAdalimumab: A biologic drug from the class of TNF-α inhibitors and the first medication officially approved for treating moderate-to-severe Acne Inversa. It is marketed under the brand name Humira® and as biosimilars. paired with clindamycin/rifampicin versus adalimumab alone found the combination arm did significantly better on several measures, including a larger reduction in draining tunnels — but that’s a different comparison (add-on to a biologicBiologic: A class of medications derived from living cells that target specific components of the inflammatory process. For Acne Inversa, biologics such as adalimumab and secukinumab are used when other treatments are insufficient., not head-to-head against tetracyclines), and it was a retrospective, matched cohort rather than a randomized trial (Aarts et al., 2023). Neither study supports treating clindamycin/rifampicin as a simply “stronger” version of tetracycline-class treatment; it’s a different combination with a different tolerability and interaction profile, considered for somewhat different clinical situations.

Rifampicin’s interaction profile deserves real attention. Rifampicin strongly induces liver enzymes that metabolize many other drugs, which can reduce the effectiveness of hormonal contraception, among other medicines — see our contraception and HS guide for that specific interaction. It also causes harmless but sometimes alarming orange-red discoloration of urine, sweat, saliva and tears, and can stain soft contact lenses. Make sure whoever prescribes it knows your full medication list, including hormonal contraception and supplements.

Clindamycin’s own caution: clindamycin (topical or oral) is associated with gastrointestinal side effects and, notably, Clostridioides difficile infection, which can cause serious diarrhea and colitis. Significant or persistent diarrhea on clindamycin is a reason to contact your care team, not to wait it out.

Other, more specialist regimens

European HS guidance also describes other systemic strategies — a short, roughly five-day course of intravenous clindamycin to shorten overall antibiotic duration, and combinations involving agents like moxifloxacin or metronidazole for selected severe or treatment-resistant disease (Zouboulis et al., 2025). These belong in specialist decision-making, not a general patient menu: their existence in a guideline doesn’t make them routine options, and several are typically used as a bridge to another treatment approach — a biologic, a procedure, or surgery — rather than as a standalone long-term plan.

Can antibiotics get rid of tunnels?

Not reliably, and this boundary matters. Antibiotics — like most HS medicines — work primarily by reducing inflammatory activity. An established tunnel that has become epithelialized and fibrotic is a structural change in the skin, not simply “more inflammation,” and there’s no good evidence that antibiotic treatment removes that structure. Medication can quiet the inflammation around a tunnel; it generally can’t undo the tunnel itself. That’s a major reason contemporary HS care increasingly separates active inflammatory disease (where medical treatment is the main lever) from structural disease like tunnels and scars (where procedures or surgery become the relevant conversation) — see our guide to HS scars and the HS Surgery Planner for more on that distinction.

Why antibiotic resistance deserves its own conversation

This is the part general “which antibiotic is used for HS” articles tend to skip, and it shouldn’t be skipped.

What resistance actually means: antibiotic exposure creates selective pressure that favors bacteria able to survive it. Those bacteria — not the patient — become resistant, and they can then be genuinely harder to treat, in that patient and potentially in others. The current European S2k guideline for HS includes a dedicated discussion of bacterial resistance under long-term antibiotic treatment and states plainly that any antibiotic can select for resistance within a patient’s microbiome, calling this out specifically because antibiotic courses of roughly 10–12 weeks are so widely used in HS (Zouboulis et al., 2025).

Has resistance actually been found in HS lesions? Yes, though the numbers vary a great deal by study, population, bacterial species and how the sample was taken — which is exactly why this article won’t hand you a single scary percentage. A 2024 cross-sectional study of 103 HS patients found substantial resistance among cultured organisms, including clindamycin resistance in 61.5% of anaerobic isolates (Koumaki et al., 2024). A 2025 genomic and phenotypic study of bacteria isolated from HS lesions identified resistance genes for methicillin and macrolides alongside strong biofilm-forming capacity in several species (Cucu et al., 2025) — biofilms being a structural reason chronic tunnels can be so hard for antibiotics to reach at all. A more recent 2026 study of 123 patients, by contrast, found meaningfully lower resistance overall, with clindamycin resistance detected in roughly 30% of non-skin-flora isolates rather than the majority (Mentesoglu & Kartal, 2026). Put together, these studies support one confident conclusion — resistance in HS-associated bacteria is a real, documented phenomenon — and one important caution: there is no single “X% of HS is resistant” figure that applies broadly, so treat any source (including this one) that offers you one number with skepticism.

None of this is an argument against using antibiotics for HS. It’s an argument for using them deliberately, with a clear goal and an actual review date, rather than as an indefinite default.

Questions worth asking about any antibiotic course

  1. What specifically are we trying to achieve with this antibiotic?
  2. How long is the planned course, and why that length?
  3. When will we assess whether it’s helped enough, and by what measure?
  4. Which side effects or symptoms should make me contact you?
  5. Does this antibiotic interact with my other medicines or my contraception?
  6. How does antibiotic resistance factor into this particular decision?
  7. If symptoms come back after I stop, what’s the plan?
  8. How many similar courses have I already had, and does that change anything?
  9. Do I have tunnels or scarring that this antibiotic isn’t going to solve on its own?
  10. At what point would we consider a different treatment class — a biologic, a procedure, or surgery?

Should every HS lesion be cultured before starting antibiotics?

There’s no blanket requirement to culture every HS lesion before starting antibiotic treatment — in part because antibiotics are so often being used for an anti-inflammatory effect rather than to treat one specific identified organism. Culturing becomes more clinically relevant in particular circumstances: suspected secondary infection, an unusual or recurrent infection, or treatment that isn’t working the way it should, where resistant bacteria are a live possibility. That’s a decision for your clinician to make based on the specific clinical picture, not something to request reflexively — and not something to interpret on your own if you do have a result in hand.

Antibiotics alongside biologic treatment

Antibiotics and biologics aren’t mutually exclusive categories. A 2023 retrospective, matched cohort study compared adalimumab started on its own against adalimumab started together with clindamycin and rifampicin, and found the combination group did significantly better on several measures after 12 weeks — including a larger reduction in disease severity (IHS4) and, notably, a larger reduction in draining tunnels, an area where adalimumab alone often underdelivers (Aarts et al., 2023). That’s a genuinely interesting finding, and worth knowing about if you’re starting a biologic — but it’s one retrospective study of a specific drug pairing (adalimumab specifically), not a general instruction that everyone starting a biologic should also take antibiotics. Whether it’s relevant to you is a conversation for whoever is managing your biologic treatment.

A note on pregnancy

Antibiotic choice changes in pregnancy — tetracyclines, for example, are not used during pregnancy because of effects on fetal bone and teeth development, and other antibiotics used for HS carry their own pregnancy and breastfeeding considerations that don’t generalize from one drug to the next. If pregnancy is possible or planned, raise it before an antibiotic course starts, not after. See HS, Pregnancy & Family Planning for the broader picture.

Turning a course into something you can actually review

If you use the Symptom Tracker, creating a Treatment Checkpoint when an antibiotic course starts gives you something more useful than a memory of “I think it helped.” Recording the same symptoms you’d normally track — pain, drainage, flare days, sleep — lets you look at the period before and after side by side when it’s time to reassess, without the tool ever telling you whether the treatment “worked.” That judgment stays with you and your clinician; the tool just keeps the record honest.

Create a Treatment Checkpoint →

When to contact your treatment team sooner than a routine review

  • A suspected significant reaction to the medicine
  • Severe or persistent diarrhea, particularly on clindamycin
  • Rapidly worsening skin symptoms, or a wound behaving very differently from usual
  • Fever or feeling generally unwell
  • Any other symptom you were specifically told to watch for

See when to get medical help for HS for the fuller picture of what warrants urgent versus routine contact.

The bottom line

Antibiotics are a genuinely important part of HS treatment, but the reason they work is more layered than “HS is a bacterial infection.” Several act on inflammation as well as on bacteria, courses commonly run around 12 weeks rather than days, and response is real but far from universal — roughly four in ten patients reach a formal clinical-response threshold with tetracyclines, and not quite half with clindamycin/rifampicin, in the best comparative data available. Antibiotics can meaningfully calm active inflammatory disease. They are not expected to dissolve an established tunnel, and they are not a cure. And because repeated or prolonged antibiotic exposure carries a real resistance cost, the antibiotics conversation worth having with your dermatologist isn’t just “which one” — it’s what this particular course is for, how long it will run, and what happens next if it isn’t enough.

Choose the next step:

Terms explained in this article

Quick definitions of the key medical terms. Select any term for its full glossary entry.

Sinus Tract
A tunnel-like channel under the skin that forms between abscesses or nodules. Sinus tracts indicate more advanced disease and can chronically drain fluid. They are associated with Hurley Stages II and III.
Secondary Bacterial Infection
A bacterial infection that develops in skin already affected or damaged by another condition. Open or draining HS lesions can sometimes become secondarily infected. This is a possible complication of HS, not the underlying cause of the disease.
Hair Follicle
The tube-shaped pocket in the skin from which a hair grows. In Acne Inversa, the follicle becomes plugged and eventually ruptures, spilling its contents into surrounding tissue and triggering the inflammatory cascade that defines the disease.
Rifampicin (Rifampin)
An antibiotic used for Acne Inversa, including as part of the clindamycin-rifampicin combination regimen. Rifampicin is a strong enzyme inducer and can reduce the effectiveness of several hormonal contraceptive methods. Anyone prescribed rifampicin who uses hormonal contraception should discuss this with whoever manages their contraceptive care.
Topical Clindamycin
An antibiotic lotion or gel applied directly to the skin. First-line topical treatment for mild Acne Inversa in most guidelines.
Draining Tunnel
A sinus tract or fistula actively leaking fluid (serous, purulent, or blood-tinged) to the surface. Draining tunnels carry the heaviest weight in modern HS severity scores because they signal long-standing, structurally damaged disease.
Clindamycin + Rifampicin
A 10-week oral combination antibiotic regimen that has been a standard second-line option for moderate Acne Inversa for years. Effective for some patients; tolerability (gastrointestinal upset, body-fluid discoloration from rifampicin) is a real limitation.
Placebo
An inactive substance, usually identical in appearance to the real drug, used in clinical trials to control for the meaningful placebo response in Acne Inversa.
Nodule
A firm, palpable lump deep in tissue. Nodules can be painful and may progress to abscesses. They are among the typical early signs of Acne Inversa.
Abscess
An inflamed cavity or swelling containing pus or fluid. In hidradenitis suppurativa, abscesses can form as part of the inflammatory disease process and do not automatically mean that a bacterial infection is present. Secondary bacterial infection can occur and may require separate medical assessment. In Acne Inversa, abscesses occur mainly in the armpits, groin, and other skin folds.
IHS4 Score
A validated, dynamic tool for measuring current inflammatory disease activity in Acne Inversa (unlike the mainly structural, static Hurley stage). The score is calculated from the number of inflammatory nodules, plus 2 points per abscess, plus 4 points per draining sinus tract; scores up to 3 are mild, 4–10 moderate, 11 or more severe. This allows objective tracking of treatment response over time.
HiSCR (Hidradenitis Suppurativa Clinical Response)
The dichotomous response criterion that became the regulatory standard in the adalimumab trials. HiSCR50 is met when: (1) the combined count of abscesses and inflammatory nodules drops ≥50%, (2) the number of abscesses does not increase, and (3) the number of draining tunnels does not increase. HiSCR75, HiSCR90, and HiSCR100 apply the same logic at higher thresholds.
Adalimumab
A biologic drug from the class of TNF-α inhibitors and the first medication officially approved for treating moderate-to-severe Acne Inversa. It is marketed under the brand name Humira® and as biosimilars.
Biologic
A class of medications derived from living cells that target specific components of the inflammatory process. For Acne Inversa, biologics such as adalimumab and secukinumab are used when other treatments are insufficient.
Biofilm
A structured, slime-encased community of bacteria that attaches to surfaces (including tunnel walls) and is highly resistant to antibiotics. Biofilms inside Acne Inversa tunnels are one reason oral antibiotics often fail to clear chronic disease.
Flare
A period of acute worsening in a chronic condition. In Acne Inversa, a flare may be triggered by stress, hormonal changes, friction, or other factors and can manifest as new nodules, abscesses, or increased pain.

FAQ

Why do doctors prescribe antibiotics for HS if it isn't an infection?

Because some antibiotics, particularly tetracyclines, have anti-inflammatory effects in addition to activity against bacteria. HS lesions can also contain a complex bacterial community and, sometimes, secondary infection, so an antimicrobial effect can matter too. Current European HS guidance explicitly recognizes both mechanisms rather than treating antibiotics as proof that HS is an infection.

How long are antibiotics usually taken for HS?

Systemic strategies such as tetracyclines or clindamycin plus rifampicin are commonly used for around 12 weeks before response is assessed — much longer than the short courses used for an acute infection. That reflects a planned treatment strategy for chronic inflammatory disease, not evidence of an ongoing untreated infection.

Is doxycycline used for HS?

Yes. Doxycycline belongs to the tetracycline class, which is commonly used as a systemic treatment for inflammatory HS and is considered broadly comparable in effectiveness to clindamycin plus rifampicin in the largest prospective comparison to date.

Is clindamycin plus rifampicin stronger than doxycycline or other tetracyclines?

Not established as such. In a prospective European cohort of 283 patients, 12-week HiSCR response was 40.1% with tetracyclines and 48.2% with clindamycin/rifampicin — a difference that was not statistically significant. Treating the combination as automatically the 'stronger' next step oversimplifies the evidence.

Can antibiotics cure hidradenitis suppurativa?

No. HS is a chronic disease with no cure. Antibiotics can meaningfully reduce inflammatory activity in some people for a period of time, but they do not eliminate the underlying disease process.

Can antibiotics get rid of HS tunnels?

Not reliably. Antibiotics can reduce inflammation around active disease, but an established, epithelialized tunnel is a structural change in the skin. Persistent tunnels are generally a question for procedural or surgical assessment, not something a course of antibiotics is expected to resolve.

Does drainage or pus from an HS lesion mean I need antibiotics?

Not automatically. HS can produce drainage and pus-like material as part of inflammatory disease without every episode representing a bacterial infection that needs treating. Rapidly spreading redness, fever, or a wound behaving very differently from usual are more specific reasons to seek assessment.

Can repeated antibiotic use for HS cause antibiotic resistance?

Antibiotic exposure of any kind can select for resistant bacteria, and current European HS guidelines specifically flag antimicrobial resistance as a concern with long-term antibiotic treatment. This doesn't mean antibiotics shouldn't be used — it means each course is worth having a clear purpose, duration and review point.

Should every HS lesion be cultured before starting antibiotics?

No. There's no blanket rule requiring a culture before HS-directed antibiotic treatment, partly because antibiotics are often used for their anti-inflammatory effect rather than to treat one identified organism. Culturing becomes more relevant when a clinician specifically suspects secondary infection, an unusual pathogen, or resistance-driven treatment failure.

What should I ask if I've already had several antibiotic courses for HS?

Ask what the longer-term treatment strategy is, how this course will be evaluated, how many similar courses you've already had, and at what point another treatment class — such as a biologic or a procedure — might be considered instead.

References

  1. van Straalen KR, Tzellos T, Guillem P, et al. The efficacy and tolerability of tetracyclines and clindamycin plus rifampicin for the treatment of hidradenitis suppurativa: Results of a prospective European cohort study. Journal of the American Academy of Dermatology, 2021
  2. Zouboulis CC, Bechara FG, Benhadou F, et al. European S2k guidelines for hidradenitis suppurativa/acne inversa part 2: Treatment. Journal of the European Academy of Dermatology and Venereology, 2025
  3. Clemmensen OJ. Topical treatment of hidradenitis suppurativa with clindamycin. International Journal of Dermatology, 1983
  4. Aarts P, van Huijstee JC, van der Zee HH, van Straalen KR, Prens EP. Improved clinical effectiveness of adalimumab when initiated with clindamycin and rifampicin in hidradenitis suppurativa. Journal of the European Academy of Dermatology and Venereology, 2024
  5. Koumaki D, Evangelou G, Maraki S, et al. Antimicrobial Resistance Trends in Hidradenitis Suppurativa Lesions. Journal of Clinical Medicine, 2024
  6. Cucu CI, Giurcăneanu C, Poenaru E, et al. Phenotypic and Genotypic Bacterial Virulence and Resistance Profiles in Hidradenitis Suppurativa. International Journal of Molecular Sciences, 2025
  7. Mentesoglu D, Kartal SP. Antibiotic and Microbiological Profiles in Hidradenitis Suppurativa. Journal of the College of Physicians and Surgeons Pakistan, 2026
  8. American Academy of Dermatology. Hidradenitis Suppurativa: Diagnosis and Treatment. Patient information
  9. NHS. Hidradenitis suppurativa. Patient information
  10. gesund.bund.de (German Federal Ministry of Health portal). Acne inversa. Public health information