pISSN : 3058-423X eISSN: 3058-4302
Open Access, Peer-reviewed
pISSN : 3058-423X eISSN: 3058-4302
Open Access, Peer-reviewed
Minah Cho,Juan Yang,Won Hee Jung,Hei Sung Kim
10.17966/JMI.2024.29.1.7 Epub 2024 March 28
Abstract
A 20-year-old female patient presented with localized erythematous scaly lichenified plaques on her right lower leg. Despite traditional treatments, the lesions consistently recurred in previously affected anatomical locations. Bacterial culture was performed, and Staphylococcus simulans was identified on both lesional and nonlesional skin. Histopathological examination revealed parakeratosis, Munro microabscess, hypogranulosis and regular acanthosis with an elongated rete. Based on clinical and histological findings, the patient was finally diagnosed with possible psoriasis. Although S. simulans is a common livestock colonizer, it rarely colonizes human skin. Herein, we report the first case of S. simulans colonization in a recurrent psoriatic lesion in previously affected anatomical locations.
Keywords
Psoriasis Staphylococcus simulans
Psoriasis is an immune-mediated chronic inflammatory disease characterized by skin symptoms, articular symptoms, and other systemic symptoms. Although the pathogenesis of psoriasis has not been fully elucidated, it is a multifactorial disease driven by both genetic predisposition and exposure to diverse environmental factors. Triggering factors include biomechanical stress, diet, drugs, alcohol, smoking, and in- fection1. Staphylococcus simulans (S. simulans) is a common livestock colonizer and a rare human colonizer. In this report, we present the case of S. simulans colonization in a recurring psoriatic lesion in anatomical areas previously affected.
A 20-year-old female patient presented with localized erythematous scaly lichenified plaques on the right lower leg (Fig. 1A). These lesions first appeared nine months ago and spread as she scratched herself constantly because of severe pruritus. She had no relevant personal or family history, and she also had no history of close contact with animals. The potassium hydroxide (KOH) smear was negative. The lesional and nonlesional skin of the right lower leg was rubbed 20 times (10 times in one direction and 10 times perpendicular to this direction) with a cotton stick for bacterial culture. For molecular identification of bacteria, a single colony was inocu- lated in tryptic soy broth (TSB; 1.7% casein peptone, 0.3% soybean peptone, 0.25% glucose, 0.5% sodium chloride, 0.25% dipotassium phosphate, and 1.5% agar) and cultured at 37℃2. Genomic DNA was extracted following the method described in a previous study3. The 16S rDNA region was identified using the universal primers 27F (5'- GAGTTTGA- TCMTGGCTCAG -3') and 1492R (5'- TACGGYTACCTTGTT- ACGACTT -3')4. The PCR product was sequenced for species identification. The resulting sequence was blasted against the nucleotide sequence database of the National Center for Biotechnology Information. The susceptibility tests were performed using the Muller-Hinton broth (MHB) medium and minimal inhibitory concentrations (MICs) were determined per the Clinical and Laboratory Standards Institute guidelines5. S. simulans was identified on lesional and nonlesional skin. MICs of vancomycin for both isolated strains were 2 μg/ml. MICs of methicillin for both strains were found to be in the 2~4 μg/ml range, indicating that the isolate showed slightly decreased susceptibility to vancomycin and methicillin.
With a clinical impression of lichen simplex chronicus sec- ondary to severe pruritus, we prescribed oral cyclosporine (200 mg/day) and oral antihistamine. After two months of cyclosporine treatment, the lesions improved significantly, leaving postinflammatory hyperpigmentation (Fig. 1B). How- ever, erythematous scaly plaques repeatedly recurred on the same area (Fig. 1C), and punch biopsy was performed. Histopathological evaluation revealed parakeratosis, Munro microabscess, hypogranulosis, and regular acanthosis with an elongated rete (Figs. 2A and 2B). Mild perivascular lympho- cytic infiltration was observed in the dermis. Periodic acid-Schiff (PAS) staining was negative. Per our clinical and histo- logical findings, the patient was finally diagnosed with possible psoriasis.
It has been suggested that infection may play a role in trig- gering and maintaining psoriasis. In particular, the association between streptococcal throat infections and guttate psoriasis is well-established. Additionally, a possible link has been suggested between exacerbations of existing plaque psoriasis and streptococcal infections6. Streptococcal infections can act as both inducing and aggravating factors of psoriasis, possibly by stimulating T-cell proliferation through superantigens and promoting the migration of skin-homing T cells via molecular mimicry between streptococcal and skin-specific epitopes7,8. Among Staphylococcus species, Staphylococcus aureus (S. aureus) infection have been found to be implicated in the disease activity of psoriasis. Its superantigens (particularly staphylococcal enterotoxin-A) play a role in the pathogenesis of psoriasis by stimulating T-cell signaling and interferon-gamma production9. In addition, bacteria such as Helicobacter pylori, Escherichia coli, and Pseudomonas aeruginosa, viruses such as the human immunodeficiency virus and hepatitis virus, and fungi such as Malassezia and Candida may play a role in the pathogenesis and exacerbation of psoriasis10. Further research is needed to determine their exact roles and the mechanisms involved.
To date, there have been no reported associations between S. simulans and psoriasis. S. simulans is a coagulase-negative Staphylococcus that is usually identified in animals such as cattle, sheep, and goats11. However, unlike its common occur- rence in livestock, it rarely colonizes human skin, and there have been only a few cases in which it has acted as a human pathogen causing skin infections11,12, toxic shock syndrome13, osteoarticular infections14,15, native valve endocarditis16, urinary tract infections17,18, and pleural empyema19. On the other hand, S. simulans may function as commensal bacteria, contributing to the maintenance of skin homeostasis rather than acting as a pathogen by producing auto-inducing peptides that block colonization and acute infection by methicillin-resistant S. aureus20. In our case, the use of immunosuppressants such as cyclosporine, along with repeated hand irritation on the lesion, may have affected the skin microbiome or rendered the lesion vulnerable to secondary infection by S. simulans. However, because S. simulans colonization was observed in both lesional and nonlesional skin, it is unlikely to be solely attributable to secondary infection from the external environment. Herein, to the best of our knowledge, we report the first case of S. simulans, a rare human skin colonizer and common livestock colonizer, in a recurrent psoriatic lesion in previously affected anatomical locations. Whether or not the colonization of S. simulans has pathophysiological significance in the pathogenesis and recurrence of psoriasis in this patient remains undetermined. Further research is needed to eluci- date the underlying mechanisms and the significance of the results.
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