this risk must also be considered for patients who are using these medications for off - label inflammatory skin conditions .
we present the first patient with treatment - refractory sweet 's syndrome who developed disseminated nocardia brasilienses whilst on methylprednisolone and infliximab .
a 62-year - old white male with a 10-year history of treatment - refractory sweet 's syndrome was admitted to the hospital with purpuric skin lesions .
the patient had myelodysplastic disease that was under treatment with intravenous immunoglobulin ( ivig ) infusions , and also diabetes mellitus , peripheral neuropathy , chronic corticosteroid - induced adrenal suppression .
as sweet 's syndrome proved refractory to dapsone , methotrexate , etanercept , lenalidomide , rituximab , cyclosporine , mycophenolate mofetil , and cyclophosphamide , methylprednisolone and infliximab infusions were administered .
after the second infusion of infliximab , he presented with new purpuric , painful lesions , and subjective fever . on examination , a 6 cm indurated erythematous and purpuric plaque with overlying pustules was noted on the left flank of abdomen , with similar smaller plaques located distally over both lower extremities [ figure 1 ] .
subsequently , the patient developed pulmonary involvement and was diagnosed with disseminated nocardia infection . during the course of his prolonged hospitalization , trimethoprim  sulfamethoxazole
( tmp - smx ) , imipenem , minocycline , and amikacin were administered for nocardia infection .
seven months later , after mistakenly receiving infliximab during a scheduled ivig infusion , the patient experienced a recurrence of nocardia infection with both cutaneous and systemic involvement .
the patient was hospitalized for over 5 months in three separate hospitals and was transferred to our care with widely disseminated nocardia .
multiple antibiotics were administered during his treatment , but the patient eventually succumbed to respiratory failure .
indurated , erythematous , and purpuric plaque on the distal lower extremity branching , filamentous organism on gomori methenamine silver stain consistent with nocardia , 40
as more patients are being treated with immunosuppressive medications such as tnf- inhibitors , the rates of infectious complications , especially with atypical pathogens , are increasing . in the literature ,
most cases of tnf- inhibitor - related nocardia infections have been reported in patients with psoriasis , rheumatoid arthritis , or inflammatory bowel disease .
however , patients being treated with tnf- inhibitors for off - label inflammatory skin disorders are also at risk .
to our knowledge , this case represents the only nocardia infection reported in a patient being treated with a tnf- inhibitor for sweet 's syndrome .
nocardia asteroides causes most cases of disseminated nocardiosis with skin involvement ; however , most cutaneous nocardiosis is caused by n. brasiliensis .
clinically , cutaneous nocardiosis may present as nodules , pustules , ulcerative lesions , bullae , or abscesses .
disseminated infection can occur rarely from primary cutaneous infection but more commonly causes secondary skin involvement .
mortality rate for patients with central nervous system or disseminated nocardiosis has been estimated to be as high as 50% .
culture is the gold - standard for diagnosis of nocardia , but it may also be identified on histologic evaluation as characteristic filamentous organisms .
other antimicrobial agents that have been used successfully alone or in combination with tmp - smx include amikacin , imipenem , minocycline , tetracycline , dapsone , streptomycin , linezolid , cycloserine , amoxicillin 
several tnf- inhibitors , including infliximab , have been reported to be associated with nontuberculosis opportunistic infections , such as nocardia.467 it is hypothesized that infliximab 's high peak drug levels , high - affinity tnf- binding , as well as macrophage and t - cell death lead to more significant immunosuppression when compared with other tnf- inhibitors .
a french ratio study demonstrated higher rates of opportunistic infection in patients on monoclonal - type tnf- inhibitors , such as infliximab , versus the soluble - type tnf inhibitor , etanercept .
this study also found that one - third of these opportunistic infections were caused by bacterial pathogens , such as nocardia .
infliximab binds both soluble and transmembrane tnf- , thereby inducing apoptosis of macrophages and t cells , which are essential for cell - mediated immunity .
this impairment of cell - mediated immunity is implicated in the susceptibility to granulomatous infections , such as nocardiosis . in all patients on tnf- inhibitors , including patients being treated for inflammatory skin disorders , such as sweet 's syndrome , the slow - growing types of bacteria should be considered in the differential diagnosis when presenting with signs of cutaneous or systemic infection .
cultures must be maintained for at least 23 weeks to detect the presence of such bacteria .
it is important for dermatologists to adequately inform patients on tnf- inhibitors about the risk of opportunistic infections and to maintain a higher index of suspicion while culturing such patients .
 a 62-year - old white man with a 10-year history of treatment - refractory sweet 's syndrome was admitted to the hospital with the onset of purpuric lesions . 
 methylprednisolone and infliximab were administered . our patient developed disseminated nocardia infection and eventually succumbed . 
 opportunistic infections such as nocardia have been associated with infliximab and other tumour necrosis factor ( tnf)- inhibitors . 
 the astute clinician should be aware of the risk of rare opportunistic infections , particularly in patients on tnf- inhibitors and systemic corticosteroids . 
INTRODUCTION
CASE REPORT
DISCUSSION