Psoriasis is a chronic, auto-inflammatory disease affecting millions of individuals worldwide.  In addition to classic cutaneous manifestations, the condition is linked to significant co-morbidities including cardiovascular disease, metabolic syndrome, melanoma and non-melanoma skin cancer, and psychiatric disease [1,2].  Therefore, more aggressive treatment and multi-disciplinary care is critical.   Measures of disease burden (quantified by anatomic location, body surface area (BSA) of involvement, and impact on daily life) assist in determining the severity of disease and have been integral in objective assessment of treatment regimens and new drug therapies [1].  Biologic agents have entered the clinical armamentarium as treatment options for patients with moderate-to-severe psoriasis who have failed traditional systemic therapies.  Three of the four FDA-approved biologic agents for psoriasis suppress TNFa mediated pathways [2], which are essential for granuloma formation and maintenance, key components of host defenses against intracellular pathogens [3].  Subsequently, the increased use of these agents is accompanied by increased reporting of granulomatous infectious diseases such as tuberculosis, histoplasmosis, nocardia, and nontuberculous mycobacteria [4].  Report of any unusual infection is therefore vitally important in the care of this immune suppressed patient population.