Like rheumatic fever, glomerulonephritis, toxic shock syndrome, PANDAS and erythema nodosum, guttate psoriasis is a nonsuppurative complication of Streptococcus pyogenes (Group A Strep) infection [2,3,4]. It is specifically associated with acute pharyngitis and 20-97% of patients with acute guttate psoriasis will be culture-positive for S.pyogenes [4]. Patients with a family history of psoriasis are at higher risk. It is usually self-limited, although approximately one third of patients will develop chronic psoriasis following a single episode [5]. It is thought that guttate psoriasis is mediated by a secreted streptococcal superantigen (pyrogenic exotoxin C) that causes proliferation and accumulation of Vß2+T-cells in psoriatic lesions. In turn, these T-cells secrete growth factors that induce keratinocyte proliferation [6].

Despite the association with streptococcal infection, there is no convincing evidence that antibiotic therapy has a role in the management of guttate psoriasis. In the only blinded randomized control trial of antibiotics vs. placebo, 43 patients with guttate psoriasis who had culture or serologic evidence of Group A strep infection were randomized to receive no treatment, oral erythromycin or oral penicillin x 14 days. No statistically significant or qualitative improvement was found between groups at 14 days or 6 weeks of follow-up [7]. Current recommendations for treatment of guttate psoriasis are therefore limited to topical steroids or various forms of tar in conjunction with Ultraviolet B phototherapy [8].

Case Conclusion by Maia Dorsett (@maiadorsett)

References