Key points
- Hidradenitis suppurativa (HS) is a chronic inflammatory disease of the skin folds — painful nodules, abscesses and sinus tracts — affecting around 1% of people[3].
- HS skin shows a consistent dysbiosis: reduced microbial diversity, depletion of commensals like Cutibacterium, and overgrowth of anaerobes such as Prevotella, Porphyromonas and Finegoldia[1][2].
- Lesions are frequently sterile to ordinary culture — antibiotics often help by anti-inflammatory and community effects, not by treating a simple infection[1].
- Biofilms in the tunnels appear to sustain inflammation and resist clearance[2].
What HS is
Hidradenitis suppurativa develops in apocrine-gland-rich, friction-prone folds — armpits, groin, under the breasts, buttocks — as recurrent painful nodules that can progress to abscesses, draining sinus tracts and scarring. It is one of the more painful and under-recognized dermatologic conditions, with a heavy quality-of-life burden[3]. Its pathogenesis weaves together follicular occlusion, a dysregulated immune response, genetics and the microbiome.
The microbial signature: diversity lost, anaerobes gained
Across studies, HS lesional skin shows a reproducible pattern: overall microbial diversity falls, protective commensals such as Cutibacterium are depleted, and anaerobic and opportunistic bacteria expand — Prevotella, Porphyromonas, Peptoniphilus, Finegoldia magna and certain Corynebacterium[1][2]. The shift is more pronounced in advanced, tunnel-forming disease. Some of these anaerobes are potent immune activators, which links the dysbiosis directly to the inflammation rather than leaving it a bystander[2].
| Overall diversity | richness of community |
| Cutibacterium (commensal) | depleted |
| Prevotella / Porphyromonas (anaerobes) | enriched |
| Finegoldia magna | immunogenic, enriched |
| Biofilm formation | in sinus tracts/tunnels |
More pronounced with higher Hurley stage. Many lesions are sterile to routine culture, underscoring dysbiosis-plus-immune-dysregulation over classic infection.
Why “it’s not just an infection” matters
A defining and counterintuitive feature of HS is that lesions are often sterile when cultured the ordinary way[1]. Antibiotics are still widely used and can help — but increasingly that benefit is understood as anti-inflammatory and community-modulating rather than the clearing of a single pathogen. Meanwhile, biofilms within the tunnels shelter bacteria from both immune attack and drugs, helping explain why HS is so persistent and relapsing[2]. This is dysbiosis interacting with a primed immune system, not a wound infection.
Where the field is heading
Because HS reflects lost diversity and anaerobe overgrowth feeding an aberrant immune response, interest is moving toward microbiome-aware strategies — understanding each person’s lesional community, addressing biofilms, and pairing that with the immune-targeted biologics that have reshaped HS care[2]. Measuring the community in affected areas is the entry point to that more precise picture.
Common questions
Is hidradenitis suppurativa an infection?
Not in the classic sense — HS lesions are frequently sterile when cultured the ordinary way. It is a chronic inflammatory disease in which a disturbed skin microbiome (lost diversity, anaerobe overgrowth) interacts with an over-reactive immune system. Antibiotics can help, but largely through anti-inflammatory and community effects rather than by clearing a single infecting organism.
What bacteria are involved in HS?
HS lesional skin shows depletion of protective commensals like Cutibacterium and overgrowth of anaerobes — Prevotella, Porphyromonas, Peptoniphilus and Finegoldia magna among them — with Staphylococcus and Corynebacterium species also present. Several of these anaerobes are strong immune activators, linking the microbial shift to the inflammation.
Why does HS keep coming back even after antibiotics?
Two reasons stand out. The underlying dysbiosis and immune dysregulation persist after a course ends, and biofilms within the sinus tracts shelter bacteria from both the immune system and drugs. Together these make HS chronic and relapsing, which is why long-term, often multi-pronged management is the norm.
Can testing my skin microbiome help with HS?
Mapping the microbial community in affected areas can show the diversity loss and anaerobe overgrowth characteristic of HS, adding detail beyond ordinary culture (which often reads sterile). It does not replace clinical care — HS warrants a clinician and often biologic therapy — but it can inform a more precise, microbiome-aware picture.
Map an affected area
Ordinary cultures often read HS lesions as sterile, missing the anaerobe overgrowth and diversity loss underneath. Parallel’s Body Spot Test sequences a problem area quantitatively, so you and a provider can see the community that culture misses.
Explore HS solutions →Offered by Parallel Health. Educational and wellness use; HS is a medical condition that should be managed with a licensed clinician. Not a substitute for diagnosis or treatment.
References
- Schell SL, et al. Yin and Yang: a disrupted skin microbiome and an aberrant host immune response in hidradenitis suppurativa. Exp Dermatol. 2021;30(10):1453-1470. https://onlinelibrary.wiley.com/doi/full/10.1111/exd.14398
- The skin microbiome in hidradenitis suppurativa: pathogenic insights, therapeutic implications, and future directions. Dermato. 2026;6(2):15. https://doi.org/10.3390/dermato6020015
- Hidradenitis suppurativa: consequences of microbiome dysbiosis on immune dysregulation and disease severity (review). https://pmc.ncbi.nlm.nih.gov/articles/PMC10043647/