Coexistence of mycobacterial infections – Mycobacterium tuberculosis and Mycobacterium leprae – in Sri Lanka: a case series

A 57-year-old Sinhalese woman presented to the dermatology unit of the National Hospital of Sri Lanka with extensive seborrheic dermatitis and tender facial induration (Fig. 1) of 1-year duration. She was a homemaker from an urban area with poor social background. She did not have diabetes or hypertension. She had received a Bacillus Calmette–Guérin (BCG) vaccination. She did not smoke tobacco or drink alcohol. A skin biopsy taken from indurated facial plaque revealed evidence of borderline tuberculoid leprosy with type 1 reaction. She did not have hypopigmented anesthetic patches or thickened peripheral nerves in the rest of her body. She was commenced on multibacillary treatment for leprosy. A year later, she developed fever, loss of appetite, loss of weight, and widespread skin abscesses all over her body. Her body mass index (BMI) was within normal range and the rest of the general examination was normal. A respiratory examination revealed bilateral (B/L) coarse crepitations; a neurological examination was normal. Her erythrocyte sedimentation rate (ESR) remained persistently elevated at more than 120 mm/hour. She had inflammatory shadows in a chest X-ray (CXR). A sputum examination for AFB was positive and GeneXpert confirmed rifampicin resistance. At that time, she revealed a diagnosis of human immunodeficiency virus (HIV) infection and tuberculous lymphadenitis, which was made 5 years back, where she had taken 6-month TB treatment but had defaulted on antiretroviral therapy. During this presentation, her CD4+ count was 57/μL. The rest of the investigations are summarized in Table 1. There was no contact history of leprosy or TB. She was started on a multidrug treatment regime, which included intravenously administered kanamycin (15 mg/kg per day), orally administered ethambutol (800 mg/day), orally administered levofloxacin (750 mg/day), isoniazid (300 mg/day), orally administered ethionamide (500 mg/day), orally administered cycloserine (750 mg/day), and orally administered pyridoxine (10 mg/day). A repeated split skin smear was negative and she continued with multidrug treatment-multibacillary therapy (dapsone 100 mg/day and clofazimine 50 mg/day and 300 mg/once a month) for leprosy without rifampicin. Highly active antiretroviral treatment was restarted subsequently. At 6 months she had clinically, hematologically, and radiologically improved.

A 47-year-old Tamil woman with poorly controlled long-standing diabetes mellitus presented with facial infiltration, multiple ichthyotic patches, and peripheral neuropathy associated with Charcot joints and trophic ulcers (Fig. 2). She was a homemaker with poor social background and there was no contact history of TB or leprosy. She did not smoke tobacco or drink alcohol. She had received a BCG vaccination. She had a low BMI and a respiratory examination revealed B/L coarse crepitations. There was no peripheral neuropathy. A clinical diagnosis of lepromatous leprosy was made which was later confirmed with histology and slit-skin smears: bacteriological index (BI) of 5; morphological index (MI) of 2%. Initial investigations revealed persistently elevated ESR (100–122 mm/hour) and inflammatory shadows in a CXR. Two consecutive sputum smears were positive for AFB and the result of a Mantoux test was positive (18 mm). Her liver and renal functions were normal (Table 1). She was negative for HIV screening. She was commenced on both TB (isoniazid 300 mg/day, rifampicin 450 mg/day, ethambutol 800 mg/day, and pyrazinamide 1500 mg/day) and multibacillary leprosy treatment (dapsone 100 mg/day and clofazimine 50 mg/day and 300 mg/once a month) without a monthly loading dose of rifampicin. She had poor compliance and defaulted treatment several times and ultimately succumbed to the illness. An autopsy was not performed.

A 72-year-old Tamil man presented with a 2-year history of trophic ulcers, auto-amputated fingers, and facial infiltration (Fig. 3). He was a retired mason from a poor social back ground with low income and did not have any other medical diseases. A general examination and neurological examination was normal. There was no significant contact history of leprosy or TB. He had received a BCG vaccination. He was an ex-smoker of tobacco and an ex-drinker of alcohol. His evaluation confirmed the clinical diagnosis of leprosy with highly positive slit-skin smears and histological evidence of lepromatous leprosy. He also gave a history of constitutional symptoms, evening pyrexia, and loss of weight and appetite. His ESR was 113 mm/hour and a sputum examination revealed AFB along with positive Mantoux test of 14 mm and CXR evidence of pulmonary TB. Basic investigations are given in Table 1. He was evaluated for both congenital and acquired immunodeficiency status, which did not reveal any abnormality. Although treatment for both conditions was commenced (isoniazid 300 mg/day, rifampicin 450 mg/day, ethambutol 800 mg/day, and pyrazinamide 1500 mg/day and dapsone 100 mg/day and clofazimine 50 mg/day and 300 mg/once a month) in liaison with a respiratory team, he was lost to follow up.

A 59-year-old Sinhalese man presented with nonhealing ulcers and deformities of both upper and lower limbs and indurations of his face (Fig. 4) for many years. He was clinically diagnosed to have borderline lepromatous leprosy, which was subsequently confirmed with slit-skin smears and histology. He was a laborer from poor social background and did not have a significant past medical history. He was emaciated with low BMI; a neurological examination did not reveal neuropathy. There was no contact history of leprosy or TB. He had received a BCG vaccination. He did not smoke tobacco and he drank alcohol occasionally. During his initial evaluation he was also found to have high ESR (> 100 mm/hour) with positive Mantoux test (21 mm) and sputum was positive for AFB. A CXR and contrast-enhanced computer tomography scan of his chest revealed the focus of pulmonary TB; bronchoalveolar lavage for TB culture revealed growth of AFB, but GeneXpert did not reveal rifampicin resistance. His HIV status was negative and repeated blood sugar levels remained within normal range. Other basic investigations are given in Table 1. He was commenced on multibacillary leprosy treatment (dapsone 100 mg/day and clofazimine 50 mg/day and 300 mg/once a month) and subsequently added TB treatment (isoniazid 300 mg/day, rifampicin 450 mg/day, ethambutol 800 mg/day, and pyrazinamide 1500 mg/day) for 6 months. At 6 months, his ESR came down, sputum was negative for AFB, and skin lesions and ulcers improved.

A 54-year-old Sinhalese man, an intravenous substance abuser, a tobacco smoker, and alcoholic, who was a garbage truck worker by occupation, with a close contact history of leprosy (his daughter), presented with leonine face and asymptomatic infiltrated papules and plaques over his earlobes of 5 months’ duration and hypopigmented hypoanesthetic patches all over his body for a similar duration (Fig. 5). His skin smear and skin biopsy were compatible with borderline lepromatous leprosy. He had a normal BMI; a neurological examination was normal. He had received a BCG vaccination. He was commenced on multibacillary treatment for leprosy (dapsone 100 mg/day, clofazimine 50 mg/day and 300 mg/once a month and rifampicin 600 mg/month) with tailing-off of dose of prednisolone starting from 40 mg daily. Six months later, he presented with productive cough with nocturnal pyrexia; an evaluation revealed high ESR (130 mm/hour), CXR evidence of active pulmonary TB, and positive sputum smear for AFB. Immune function studies carried out to evaluate his immunodeficiency status did not reveal any congenital or acquired immunodeficiency conditions, including diabetes and HIV. Table 1 gives the basic investigations. He was commenced on TB (isoniazid 300 mg/day, rifampicin 450 mg/day, ethambutol 800 mg/day, and pyrazinamide 1500 mg/day) treatment. He defaulted treatment several times with regards to both leprosy and TB and later died due to TB. An autopsy was not performed.

A 50-year-old Sinhalese man with poorly controlled diabetes mellitus presented with facial infiltration (Fig. 6) and erythematous painful nodules over his lower limbs and trunk suggestive of lepromatous leprosy with erythema nodosum leprosum. He was a manual laborer with low BMI. The rest of the general and neurological examination was normal. He had received a BCG vaccination. He did not smoke tobacco and drank alcohol occasionally. A skin biopsy revealed evidence of foamy macrophages with well-developed grenz zone. He was commenced on multidrug treatment-multibacillary treatment for leprosy (dapsone 100 mg/day, clofazimine 50 mg/day and 300 mg/once a month, and rifampicin 600 mg/month) with prednisolone 40 mg daily for type 2 reaction. Twelve months later he developed generalized lymphadenopathy with low-grade evening pyrexia and elevated ESR (80–100 mm/hour). Both Mantoux and QuantiFERON Gold test were positive. A CXR remained persistently normal. He was negative for HIV and diabetes. Basic investigations are given in Table 1. A lymph node excision biopsy revealed suppurative inflammation with focal foamy histiocytes; a TB culture from the lymph node biopsy later showed growth of AFB. GeneXpert did not reveal rifampicin resistance. Therefore, he was started on TB treatment (isoniazid 300 mg/day, rifampicin 450 mg/day, ethambutol 800 mg/day, and pyrazinamide 1500 mg/day) by the respiratory physician for the treatment of extrapulmonary TB. At 6 months, he had improved clinically and biochemically.