Streptococcal infection as trigger for psoriasis

Key Points

THE CASE

DIAGNOSIS: Perianal group A β-hemolytic streptococcal infection and acute guttate psoriasis

PATHOPHYSIOLOGY

It is widely accepted that psoriasis is caused by T-cell mediated abnormal keratinocyte proliferation. Although the exact mechanism by which GABS triggers the appearance of psoriasis is not fully understood, it has been proposed that the exotoxin produced by GABS acts as a superantigen, which stimulates specific T cells.⁴

These T cells react with both streptococcal M protein and a keratin-like skin determinant, causing the psoriatic lesions to persist.⁵

GABS AND PSORIASIS

The original case report of an association between psoriasis and streptococcal infection was published in 1916,⁶ and the association between GABS and psoriasis has been well documented since then.

A 2-year prospective study was conducted in which ASO titers were measured as a marker of recent streptococcal infection in patients presenting with AGP and patients with chronic plaque psoriasis.⁸

Researchers found that 17 of 20 (85%) patients with AGP had elevated ASO titers (>200 Todd units) and that less than 5% of patients with chronic psoriasis had elevated ASO levels.

Similar results were found in a study that looked at patients presenting with AGP over a 15-month period. In that study, elevated ASO titers were found in 58% of patients with AGP compared with 26% of patients with exacerbations of chronic psoriasis (P<.02).⁹

Although the association between streptococcal infection and AGP is perhaps the most well described,^8,10 strep infection has been shown to be associated with plaque¹¹ as well as with pustular psoriasis.⁴

In addition to streptococcal pharyngitis, GABS infections of the perianal and genitourinary regions have also been more recently recognized as triggers. Several case reports describe children with perianal streptococcal dermatitis presenting with plaque or guttate psoriasis.^11-14