Large neck ulcer in an immunocompetent adult male.

Tuberculosis is a global health burden. It can affect the pulmonary as well as extrapulmonary organs. Rarely, it can cause persistent ulcers on the skin, without any systemic involvement.[1] With a large incidence of infective ulcers in tropical countries, tuberculosis should be considered an etiology of nonhealing ulcers.[2] Herein, we report a case of primary cutaneous tubercular ulcer in an immunocompetent adult male.

A 41-year-old male presented with a progressive ulcer over the back of his neck. It started as multiple asymptomatic flesh-colored papules. Over the next 4 months, the papules coalesced to form a si?ngle annular plaque. Gradually, the plaque was ulcerated in the center. The patient was diagnosed as discoid lupus erythematosus (DLE) and was treated with topical and systemic steroids. The ulcer grew in size to the present status in the next 6 weeks. On examination, there was a shallow well-defined ulcer of size 10 × 5 cm with an undermined margin. The floor of the ulcer was covered with hemorrhagic crusting with bleeding at few places. The surrounding skin showed infiltrated papules [Figure 1a]. The ulcer base was not indurated or fixed to the underlying structures. Peripheral lymph nodes were not enlarged. The patient had no constitutional symptoms. Clinically, respiratory and other systemic examination showed no detectable abnormality. Routine laboratory examinations were within normal limits except for mild leukocytosis. The chest X-ray and ultrasonography of the abdomen were normal. The patient tested negative for HIV, his sputum did not yield any acid-fast bacillus (AFB), and his tuberculin skin test was also negative. Punch biopsy from the ulcer margin showed multiple epithelioid cells, histiocytes, lymphocytes, distinct Langhans giant cells with areas of caseous necrosis [Figure 2a]. Ziehl-Neelsen (ZN) stain for AFB was positive [Figure 2b]. The patient was started on antitubercular therapy (ATT) and the ulcer showed complete resolution at 3-months follow-up [Figure 1b].

Figure 1

(a) Ulcer over the posterior aspect of the neck (10 cm × 5 cm) on presentation; (b) Complete resolution of ulcer within 3 months of antitubercular therapy.

Figure 2

(a) Punch biopsy from ulcer margin showing presence of characteristic Langhans giant cells (black arrow) and caseous necrosis (blue arrow) (hematoxylin and eosin stain, 10×); (b) Positive Ziehl-Neelsen stain for acid-fast bacilli (100×, oil immersion field).

Cutaneous tuberculosis constitutes 1–2% of all tuberculosis cases.[1] It varies in its morphological presentation according to the host immunity and mode of spread. Primary inoculation tuberculosis is caused by direct entry of the bacillus into the skin of a person who has no natural or acquired immunity to the organism.[3] It has been reported with the Bacillus Calmette-Guerin vaccine, needle stick injury, and intralesional steroid injection.[4] Our patient had no history of trauma at the ulcer site, but minor trauma may have gone unnoticed. Classically, primary inoculation tuberculosis starts as inflammatory papules, evolves into the firm, shallow, non-tender ulcer with undermined margins and granulomatous base.[3] Our patient's evolution of disease was similar to the classical description, however, the ulcer's final morphology caused a clinical dilemma. This could be explained by the prolonged application of high-potent steroids. Clinical confusion was compounded by the ulcer site, which is an uncommon site for trauma. Our differentials included pyoderma gangrenosum, leishmaniasis, ulcerated DLE, ulcerated basal cell carcinoma, atypical mycobacterial infection, alongside cutaneous tuberculosis. Based on histopathology and positive ZN stain for AFB, with excellent response to ATT, primary cutaneous tuberculosis was diagnosed.[5] Primary cutaneous tuberculosis is a rare entity that should be considered in isolated nonhealing ulcers in the absence of other symptoms suggestive of tuberculosis. Indiscriminate steroid use is rampant in India and often distorts the classical presentation. The atypical presentation in our case illustrates the need for considering cutaneous tuberculosis, a differential while evaluating nonhealing ulcers in endemic countries.

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Conflicts of interest

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