The Bacteriology of Skin Lesions in Patients with Hidradenitis Suppurativa Is Associated with Previous Antibiotic Treatment in the Community Setting: A Referral Center Experience

Abstract

<b><i>Background:</i></b> Hidradenitis suppurativa (HS) is a chronic skin disease characterized by inflammatory nodules and abscesses. The pathogenic role of bacteria is not fully understood. As the diagnosis is usually delayed, patients are often treated with several lines of antibiotics in a nonstandardized fashion. The aim of the study was to investigate and compare the bacteriology of active HS lesions in patients treated or not treated with antibiotics in the community setting before referral to a dedicated HS clinic. <b><i>Methods:</i></b> Purulent skin lesions of patients with HS referred to the HS Clinic of Rabin Medical Center in 2009–2020 were cultured. Data were collected from the patients’ medical files and microbiology reports. The correlation between the location of the skin lesion and the bacteriologic profile was analyzed, and the effects of previous antibiotic treatment on the bacteriologic profile of the lesions and susceptibility patterns of the cultured bacteria were evaluated. <b><i>Results:</i></b> Pus (or tissue) from inflammatory lesions of 97 patients with HS was cultured. Mean (SD) patient age was 39.5 (13.0) years, and mean delay in diagnosis was 7.3 (8.3) years. Most patients (57.7%) had dominant involvement of one location, with the most active lesions concentrated in the genitalia, gluteal/perineal area, and axilla. Enterobacterales species were the most frequent isolates detected in all locations except the face and scalp. Seventy-eight patients (80.4%) had been treated in the community setting prior to referral with a median (range) of 2 (1–8) lines of antibiotics. The most commonly prescribed antibiotics were amoxicillin/clavulanate (22.0%), doxycycline/minocycline (16.8%), clindamycin (16.2%; monotherapy 8.1%, clindamycin with rifampicin 8.1%), and cephalexin (13.9%). Compared to the previously untreated patients, cultures of lesions from the previously treated patients yielded a higher percentage of gram-negative Enterobacterales (the most common isolates in this group) (31.3% vs. 10.3%) and a significantly higher median number of isolates per culture (2 vs. 1, <i>p</i> < 0.0001). Gram-positive bacteria, usually considered contaminants (mainly coagulase-negative staphylococci<i>)</i> accounted for 31.0% of the isolates in the previously treated group. Susceptibility testing for the entire cohort revealed 100% bacterial sensitivity to ciprofloxacin<i>. Staphylococcus</i> spp. were 100% sensitive to rifampicin. Both gram-positive and gram-negative bacteria had high sensitivity to trimethoprim and sulfamethoxazole. <b><i>Conclusion:</i></b> Nonstandardized antibiotic treatment of HS in the community setting can skew the microbiology of skin lesions toward gram-negative bacteria. Therefore, treatment with trimethoprim and sulfamethoxazole or ciprofloxacin, either alone or combined with rifampicin, may be considered.

Obstacles to Early Diagnosis and Treatment of Hidradenitis Suppurativa: Current Perspectives on Improving Clinical Management

“…Across eleven studies, the diagnosis of HS after initial presentation of symptoms ranged from 3 to 10 years with most studies finding a delay of 6 to 10 years. [18][19][20][21][22][23][24][25][26][27][28] Two studies that focused only on patients diagnosed prior to 2013 found the average delay also around 7 years. 18,19 Recent studies from 2017 to 2020 showed similar findings, with an average delay of 10 years, indicating that diagnostic delay remains an ongoing barrier to care for patients with HS.…”

Phytotherapeuthics Affecting the IL-1/IL-17/G-CSF Axis: A Complementary Treatment Option for Hidradenitis Suppurativa?

“…In HS lesions, the limited epidermal upregulation of antibacterial proteins enables the propagation of the microbes in the skin [ 20 , 41 , 42 ]. The persistent presence of bacterial components supports the chronic inflammation through the stimulation of monocytes/macrophages/dendritic cells via their innate immune receptors (i.e., pattern recognition receptors, PRRs) [ 41 , 43 ].…”