in february 2013 , a 70-year - old man sought care at the university of amsterdam department of dermatology for a neuropathic ulcer on his left foot .
it was determined that he had a neuropathic ulcer , a complication of nerve damage caused by leprosy , for which he was treated successfully .
he was a native of suriname , where he lived until he moved to the netherlands 1977 .
he had multiple instances of treatment for skin infections , beginning with a diagnosis of leprosy ( hansen disease , caused by the mycobacterium m. leprae ) when he was 10 years of age .  
, he moved to groningen , the netherlands , and clofazimine was added to his treatment for leprosy for 6 months . in february 1982 , he moved to amsterdam and sought routine follow - up care for leprosy at the university of amsterdam department of dermatology , and quiescent borderline lepromatous leprosy was diagnosed .
he was treated during february 1982february 1983 with a triple therapy  consisting of  rifampin , dapsone , and clofazimine . in 1984
, the man traveled to paramaribo and coronie in suriname , where he stayed for 4 weeks during the spring season . during that time
, he fished in creeks . in december 1984 , he sought treatment again at the university of amsterdam department of dermatology for a painful red swelling on the dorsal side of the right wrist after he had scratched it on a rough wall 5 weeks earlier , in mid - november .
beginning in february 1985 , the patient had signs of infection of the wound , including conspicuous edematous swelling of the hand .
however , during april 26may 11 , 1985 , the patient experienced recurrent infection with abscess formation .
a biopsy was taken , and an acid - fast bacilli ( afb ) smear and culture for nontuberculous mycobacteria were done .
the histopathology report indicated scarring dermis and mixed cell infiltrate , leucocytoclastic vasculitis , fibrinoid changes , and some diffusely spread histiocytes .
on june 3 , partly dry wounds , 1 deep ulcer , fistula formation , and spontaneous drainage of another lesion were documented .
the wound was cultured , and amoxicillin and clavulinic acid 4 times daily for 3 weeks was prescribed ; after that time , the patient s treatment for related conditions consisted of local wound care .
after 6 weeks incubation , the mycobacterial culture was positive at 30c but negative at 37c and 45c . in august , ulcers were still present , and multiple nodules at the underarm and an enlarged lymph node at the elbow were palpable .
, the isolate was sent to the institute of tropical medicine of antwerp and was identified as m. ulcerans itm 842 according to phenotypic characteristics ( 3 ) .
the isolate was further analyzed by several genotypic methods ( 36 ) . by april 7 , 1986 ,
phenotypic characteristics of isolates from suriname and french guiana are identical , whereas isolates originating in africa , australia , and asia have different phenotypic characteristics ( 3 ) .
variable - number tandem - repeat genotypic analysis had been shown to discriminate the suriname isolate from french guiana isolates and from mycolactone - producing m. marinum ( 4,5 ) .
results confirmed that this isolate was different from m. ulcerans isolates from other geographic origins , albeit closely related to m. ulcerans strains from french guiana by genetic characteristics ( 4,5 ) .
the incubation period of primary bu is estimated to be 23 months , but latency of the disease can span years .
persons who were in an area to which bu is endemic months to years earlier can manifest bu in a traumatized body site ( 6,7 ) .
co - infections with leprosy and bu have been described , but rarely ( 8) . during 19521977 ,
the patient was treated with dapsone monotherapy . additionally , he received clofazimine for 6 months upon his arrival in the netherlands .
subsequently , during february 1982february 1983 , he was treated with a triple therapy consisting of rifampin , dapsone , and clofazimine .
treatment of bu patients with dapsone has not been properly evaluated in humans ( 9 ) , and clofazimine is not indicated in the treatment of patients with bu ( 10 ) ; however , rifampin is highly bactericidal against this organism ( 11 ) .
if the patient was infected with m. ulcerans before his arrival in the netherlands in 1977 , it is unlikely that the dapsone and clofazimine that he received for treatment of leprosy could have controlled the infection . whether or not he had been infected with m. ulcerans when he first arrived in the netherlands , treatment for 1 year with rifampin and dapsone before he returned to suriname for 4 weeks in 1984 would have been expected to have killed any m. ulcerans .
thus , the most likely hypothesis is that he acquired bu infection during the 4 weeks he spent in suriname in 1984 , and that the scratch obtained against a rough wall in november 1984 in the netherlands reactivated a latent infection .
it is unlikely that the rough wall was contaminated by m. ulcerans , because bu is not considered prevalent in europe .  
there are many similarities between this case and that reported by lindo and daniels ( 7 ) .
both patients manifested symptoms of bu after having left a disease - endemic area , and in both patients , the lesion developed at the site of a trauma that occurred in a non  disease - endemic country .
correct laboratory confirmation remains essential to confirm the discovery of new foci of bu , and the use of genetic mapping can provide additional information about the geographical location in which patients were infected . the importance of laboratory confirmation of bu has been emphasized by the world health organization s manual for the laboratory diagnosis of bu ( 12).the study of imported cases , and in particular this case from suriname , has enabled us to acquire more knowledge regarding latency and reactivation of the disease , and the existence of new foci . as in the report by meyers
et al ( 13 ) , this case report emphasizes the role of trauma to the skin in the delayed manifestation of this disease caused by m. ulcerans . reports from european countries , canada , america , and australia describe travelers visiting friends or relatives in bu - endemic countries who manifested bu upon return to a non  disease - endemic area ( 14,15 ) .
thus , bu may be diagnosed in patients late , or not diagnosed , in non  disease - endemic countries , where health care professionals are usually not familiar with the condition or its causal organism .
the clinician s consideration of the patient s recent travel history and awareness of cutaneous and bone lesions of bu are needed for accurate testing , diagnosis , and treatment of the patient .
 we report buruli ulcer in a man in the netherlands . 
 phenotyping of samples indicate the buruli pathogen was acquired in suriname and activated by trauma on return to the netherlands . 
 awareness of this disease by clinicians in non  
 buruli ulcer  
 endemic areas is critical for identification . 
The Case-Patient
Conclusions