Do Bacterial Infections Cause Guttate Psoriasis?

Guttate psoriasis is not an infection itself but may result when the immune system becomes dysfunctional following an infection.

Psoriasis is a chronic and often relapsing inflammatory skin condition that can produce a wide spectrum of different rashes.[1] The most common type of psoriasis, called plaque psoriasis, affects the skin with pink plaques that have silvery scales that can be itchy and painful. Guttate psoriasis is another type of psoriasis that usually occurs suddenly in children and teenagers. “Guttate,” derived from a Latin word for “drop,” describes the scattered, smaller, “drop-like” shaped scaly pink plaques that are usually scattered on the trunk and extremities.[2] Interestingly, guttate psoriasis usually develops following infection with a group of bacteria called streptococci.[3]


Guttate Psoriasis Often Occurs After a Streptococcal Infection

Guttate Psoriasis Often Occurs After a Streptococcal Infection 

Many people who developed guttate psoriasis often had a recent bacterial streptococcal infection. In fact, up to 97% of patients with new onset guttate psoriasis have been reported to have had a recent history of streptococcal infection.[4] Interestingly, there are a few case reports of children who have developed guttate psoriasis after having a streptococcal infection in the perianal area.[5,6]


It Is Not Known If Infections Actually Cause Psoriasis

The association between new onset guttate psoriasis and a history of streptococcal infection appears strong. However, the mechanism of how psoriasis caused by staph bacteria occurs is not fully understood. Most likely, guttate psoriasis occurs as a result of multiple factors, including genetics and the environment, leading to abnormal immune system response.[7] Rather than streptococcal infections being the direct culprits of guttate psoriasis, they might be responsible for a phenomenon referred to as “molecular mimicry.” Streptococcal bacteria are speckled with proteins (called “M proteins”) that appear structurally similar to keratin proteins in the skin. In molecular mimicry, our immune cells are programmed to attack streptococcal “M proteins” and instead, they accidentally attack our own keratin proteins in the skin, leading to the inflammation seen in psoriasis. 

Guttate psoriasis is not an infection itself but may result when the immune system becomes dysfunctional following an infection. In addition, guttate psoriasis can also occur in the absence of any known infection, which shows the importance of the many contributing factors involved in the development of psoriasis. 

In many people, guttate psoriasis caused by bacteria will resolve spontaneously in weeks to months. First-line treatment is phototherapy, which is usually more effective for guttate psoriasis compared to the treatment of chronic plaque psoriasis.[8]



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  2. Ko HC, Jwa SW, Song M, et al. Clinical course of guttate psoriasis: long-term follow-up study. J Dermatol.2010;37(10):894-899; PMID: 20860740 Link to research.
  3. Mallbris L, Larsson P, Bergqvist S, et al. Psoriasis phenotype at disease onset: clinical characterization of 400 adult cases. J Invest Dermatol.2005;124(3):499-504; PMID: 15737189 Link to research.
  5. Patrizi A, Costa AM, Fiorillo L, et al. Perianal streptococcal dermatitis associated with guttate psoriasis and/or balanoposthitis: a study of five cases. Pediatr Dermatol.1994;11(2):168-171; PMID: 8041660 Link to research.
  6. Herbst RA, Hoch O, Kapp A, et al. Guttate psoriasis triggered by perianal streptococcal dermatitis in a four-year-old boy. J Am Acad Dermatol.2000;42(5 Pt 2):885-887; PMID: 10767696 Link to research.
  7. Valdimarsson H, Thorleifsdottir RH, Sigurdardottir SL, et al. Psoriasis--as an autoimmune disease caused by molecular mimicry. Trends Immunol.2009;30(10):494-501; PMID: 19781993 Link to research.
  8. Gokdemir G, Kivanc-Altunay I, Koslu A. Narrow-band ultraviolet B phototherapy in patients with psoriasis: for which types of psoriasis is it more effective? J Dermatol.2005;32(6):436-441; PMID: 16043915 Link to research.