Association Between Hidradenitis Suppurativa and Recurrent Skin Infections
Hidradenitis suppurativa (HS) is fundamentally a chronic inflammatory disease of follicular occlusion, not an immunodeficiency disorder, and recurrent skin infections like cellulitis represent local complications of the disease process rather than evidence of systemic immune dysfunction. 1
Understanding the Relationship
HS is Not an Immunodeficiency
Adult patients with HS do not require evaluation for neutrophil function disorders or immunodeficiency, as the Infectious Diseases Society of America explicitly states that patients who develop abscesses during adulthood do not need neutrophil function testing. 1
Neutrophil dysfunction evaluation is only indicated if recurrent abscesses began in early childhood, not in typical adult-onset HS. 1
The pathophysiology of HS centers on follicular occlusion, aberrant immune response to commensal bacteria, and inflammatory dysregulation—not primary immune deficiency. 2, 3
Local Factors Drive Recurrent Infections
Recurrent abscesses at sites of previous infection should prompt a search for local causes, specifically hidradenitis suppurativa, pilonidal cysts, or foreign material, as these structural abnormalities are the primary drivers of recurrence. 1
When cellulitis develops around HS lesions, the appropriate terminology is "HS with surrounding inflammation" rather than "cellulitis," because the primary pathology is the suppurative focus itself, not a spreading skin infection. 1
The distinction is clinically crucial: primary cellulitis requires antimicrobial therapy as the main treatment, whereas HS with surrounding inflammation requires drainage of purulent collections as the primary intervention, with antibiotics playing a subsidiary role. 1
Microbiologic Considerations
Microbiologic screening has limited utility in HS, as mixed normal flora and skin commensals are the main bacteria cultured from suppurative discharge, though gram-negative organisms can be abundant in some lesions. 1
Biofilms have been described in most HS skin samples, especially in sinus tracts, which may explain persistent bacterial colonization without representing true immunodeficiency. 1
Culture is not recommended in clinical practice unless signs of secondary infection such as surrounding cellulitis or fever are present. 1
Clinical Algorithm for Distinguishing HS from True Infection
When to Suspect HS Rather Than Primary Infection:
Chronicity and recurrence at the same anatomic sites (axillae, groin, inframammary, perianal regions) rather than random locations. 1, 4
Typical lesions including painful nodules, abscesses, sinus tracts, bridged scars, or open comedones (double comedones are pathognomonic). 1, 5
Post-pubertal onset with female predominance, rather than infections beginning in early childhood. 1, 5
Absence of systemic toxicity despite impressive local suppuration—patients with HS typically lack high fever, hypotension, or severe systemic symptoms unless secondary infection supervenes. 1, 4
When to Suspect True Secondary Infection:
Rapidly spreading erythema, warmth, and tenderness extending beyond the typical HS nodule or abscess. 1
Systemic manifestations including fever, tachycardia, confusion, hypotension, or leukocytosis occurring acutely. 1
Crepitus, necrotic tissue, or rapid progression suggesting Fournier gangrene, which is a surgical emergency with high mortality risk. 5
Management Approach:
For typical HS flares without surrounding cellulitis: Incision and drainage is the primary treatment; systemic antibiotics are usually unnecessary unless fever or systemic infection is present. 1, 4
For HS with surrounding cellulitis: Obtain cultures, provide drainage, and treat with antibiotics active against streptococci (for mild cases) or add MRSA coverage (vancomycin or alternatives) if there is penetrating trauma, purulent drainage, or systemic inflammatory response syndrome. 1
For recurrent HS abscesses: Consider a 5-day decolonization regimen with intranasal mupirocin twice daily, daily chlorhexidine washes, and decontamination of personal items, though efficacy data are sparse. 1
Common Pitfalls to Avoid
Do not misinterpret chronic HS suppuration as evidence of immunodeficiency—the disease mechanism is inflammatory and structural, not immunologic. 1
Do not routinely culture HS lesions unless signs of secondary infection are present, as mixed flora will confuse rather than clarify management. 1
Do not use the term "cellulitis" for inflammation surrounding an HS abscess, as this implies the wrong primary treatment (antibiotics rather than drainage). 1
Do not perform immunodeficiency workup in adult-onset HS—reserve neutrophil function testing only for patients with recurrent abscesses beginning in early childhood. 1
Screening for True Comorbidities
While HS is not associated with immunodeficiency, routine screening should focus on metabolic and inflammatory comorbidities that genuinely co-occur with HS:
Type 2 diabetes (1.5- to 3-fold increased risk, up to 30% prevalence)—screen with hemoglobin A1c or fasting glucose in patients with signs of diabetes, hypertension, obesity, or hyperlipidemia. 1
Depression and anxiety (up to 26% prevalence of depression, 1.3 to 4.8 times higher odds)—screen routinely given substantial impact on quality of life. 1
Follicular occlusion tetrad components: acne conglobata (4.5-15.2% prevalence), dissecting cellulitis of scalp (9.2% prevalence), and pilonidal disease (1.4-2.3% prevalence). 1, 6
Squamous cell carcinoma in chronic HS-affected skin, particularly perineum and buttocks—perform periodic skin examination of long-standing lesions. 1