The role of bacteria in the pathogenesis of hidradenitis suppurativa (HS) remains controversial. Firmicutes is the largest bacterial phylum, and it contains several important and well-known genera, such as Staphylococcus and Streptococcus. Studies1,2 have consistently reported bacteria from this phylum, such as Staphylococcus aureus, coagulase-negative staphylococci, and Enterococcus species, in tissue samples and cultures of purulent drainage from HS lesions. The association between obesity and HS is well known, and obesity has also been linked to an increase in bacteria from the Firmicutes phylum in gut microflora.3-5 We hypothesized that this change in the microbial milieu that occurs with increasing body mass index (BMI) may expose patients to different bacterial species that promote a more robust inflammatory response in the skin or hair follicles of patients with HS. This study aimed to examine the prevalence of Firmicutes in bacterial cultures of purulent drainage from HS lesions and to explore its potential association with BMI.
This study was approved by the Johns Hopkins Medicine Institutional Review Boards. A waiver of informed consent was granted given the retrospective nature of the study. We conducted a cross-sectional analysis of 632 patients diagnosed as having HS between January 5, 2010, and August 27, 2015, at The Johns Hopkins Medical Institutions. The results of the first recorded bacterial cultures of purulent drainage from HS lesions were compared between nonobese (BMI <30) and obese (BMI ≥30) patients (BMI was calculated as weight in kilograms divided by height in meters squared). We examined the association between obesity and bacterial culture results (by phyla) using χ2 or Fisher exact tests. The adjusted prevalence odds ratios (aPORs) for bacterial phyla were computed according to obesity status using multivariable logistic regression with robust variance estimation, adjusting for variables (age and ethnicity) known to be a priori predictors of obesity.
The Figure shows the distribution of bacteria cultured from HS lesions by phyla. Of the 239 patients with bacterial culture data, 189 patients (79.1%) had available BMI data. Of these 189 patients, 142 patients (75.1%) were obese. After adjusting for age and ethnicity, the odds of culturing Firmicutes from HS lesions of obese patients was 3.1 (95% CI, 1.3-7.1) times higher than in nonobese patients (Table) and remained significant after additional separate adjustments for oral tetracycline use (aPOR, 1.35; 95% CI, 1.07-1.70) and topical clindamycin use (aPOR, 1.38; 95% CI, 1.11-1.73). A larger proportion of obese patients with HS grew S aureus and Enterococcus (Table). The proportion of cultures that grew bacteria from Bacteroidetes, Proteobacteria, or Actinobacteria phyla showed no significant differences among obese and nonobese patients.
The results of this study reveal important differences in the microbiota of HS lesions in obese vs nonobese patients. Gut flora alterations are seen in obese patients,4,5 and HS has been associated with obesity. It is possible that altered gut or skin flora could have a pathogenic role in HS.
Some of the limitations of the present study include the use of retrospective data and the lack of a control group consisting of patients with no history of HS. Although these cultures were obtained from purulence extruding from HS lesions, the bacterial culture results could represent skin or gut flora contamination. Information about the specific anatomic locations of HS cultures was not available. Because only the first recorded culture of each patient was analyzed, it is unknown if the culture results would change with time and further antibiotic therapy. The use of data obtained from swab-based cultures may also represent a potential limitation because DNA-based approaches to microbial analysis may yield more information and lead to identification of organisms that are not cultivable. The use of more advanced microbiome techniques may be an important consideration for future studies. These data indicate that further research is needed to elucidate the role of specific bacterial species in the pathogenesis of HS and may suggest a role for targeted treatment of specific bacterial species in this disorder.
Accepted for Publication: May 26, 2016.
Corresponding Author: Ginette A. Okoye, MD, Department of Dermatology, The Johns Hopkins School of Medicine, Johns Hopkins Bayview Medical Center, 5200 Eastern Ave, Ste 2500, Baltimore, MD 21224.
Published Online: July 20, 2016. doi:10.1001/jamadermatol.2016.2337.
Author Contributions: Ms Haskin and Dr Okoye had full access to all the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.
Study concept and design: Haskin, Okoye.
Acquisition, analysis, or interpretation of data: All authors.
Drafting of the manuscript: All authors.
Statistical analysis: Fischer.
Conflict of Interest Disclosures: None reported.
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