A 32-year-old man was first seen in 1989, when he had a 1-year history
of a reddish-brown, nonscaling elevated, soft plaque with telangiecta
ses on his nose (lesion A) (Fig. 1) and a 9-year history of slowly adv
ancing, asymptomatic, multiple, hyperkeratotic, purple-brown, infiltra
ted nodular lesions on the left lateral aspect of the leg and the heel
(lesions B) (Pig. 2). The patient was an official and did not describ
e any wound or abrasion. Multiple punch biopsy specimens had been take
n from lesion B beginning in 1989 and on histologic Acid-fast stains f
ailed to reveal organisms in any of the specimens taken from lesions A
or B. Cultures, using the BACTEC radiometric system and Lowenstein-Je
nsen medium, and inoculations into animals were negative. Routine labo
ratory values were within normal limits. Chest roentgenograms were rep
eatedly negative and no acid-fast bacilli were detected in the sputum.
The tuberculin test was positive. The patient had been treated with s
ystemic antimicrobials and a variety of topical medications for lesion
A, but with no response. Antituberculosis chemotherapy, consisting of
isoniazid (300 mg daily), rifampicin (600 mg daily), ethambutol (1000
mg daily), and pyrazinamide (1500 mg daily), was initiated for lesion
8. After 2 months of treatment, pyrazinamide and ethambutol were disc
ontinued because of toxic optic neuropathy. Isoniazid and rifampicin w
ere continued for 4 more months. The lesion B did not regress and the
therapy was stopped in 1990. The patient was treated conservatively fr
om 1991 to 1994. Polymerase chain reaction (PCR) became available in o
ur unit in 1993. Tissue biopsies were performed for histologic diagnos
is again and PCR was carried out to investigate the presence of mycoba
cterial DNA in lesions of both locations in order to evaluate the diag
nosis of lupus vulgaris.