Summary
A forty-year-old man, an ex-smoker was admitted to Department of Respiratory Medicine, Yangon Specialty Hospital with low-grade fever and productive cough for a month. He has chronic history of pulmonary TB (although smear negative) and treated as drug-sensitive tuberculosis. The current condition looked like bacterial chest infection and sputum culture revealed Klebsiella pneumoniae. He responded well to appropriate antibiotics and other supportive management. Since his Chest X-Ray was not typical of tuberculosis alone plus Klebsiella infection and because of his previous occupational history and frequent episodes of lithoptysis (coughing up of broncholiths), we proceeded to further investigations.
Introduction
Silicosis is the world’s most prevalent occupational lung disease associated with gold mining, abrasive blasting, denim jean manufacture, artificial stone production, brickwork, pottery, porcelain work, tunneling and structural construction and demolition. Silica particles in the lower respiratory tract are phagocytosed by alveolar macrophages that undergo apoptotic cell death. Toxic silica particles are released and repeating the process after they are reingested by other macrophages eventually perpetuating alveolitis, eventually leading to development of fibrosis. Pathologically, around the respiratory bronchioles but eventually becoming more diffuse seen throughout the parenchyma resulting in characteristic acellular nodules called silicotic nodules.
There are two main clinical forms 1 Acute silicosis: alveolar silico-proteinosis and 2 Classic silicosis: chronic interstitial reticulonodular disease which is more common than the acute form and further classified as simple or complicated classic silicosis. In some situations, there is a rapid progression of the disease which is sometimes termed accelerated silicosis.
Lithoptysis presents with coughing up of small, hard, white-to-brown particles (broncholiths or “spiculated” silica-containing material) is a rare but highly specific sign of silicosis, where calcified nodes erode into the airways1.
Silico-tuberculosis is defined as the combination of silicosis and active TB and/or post-tuberculous lung disease (PTLD) and covers all temporal sequences of occurrence.
The persistence in high tuberculosis burden countries of hazardous occupational exposure to silica underlies the continuing importance of combined diseases. Silicosis increases the risk of TB fourfold, with a strong disease severity-response gradient2. In co-pathogenesis, damage by silica particles to the macrophage, in the frontline of innate defense against silica and M. tuberculosis, has been established in vitro and in vivo3.
Clinical and radiological abnormalities due to silicosis and/or PTLD, consequently fade the specificity for active TB especially in high TB burden countries with large silica-exposed populations. Coexisting conditions warrants to consider the accuracy of microbiological tests for TB but silicosis did not reduce the sensitivity of sputum microscopy and culture for active TB, nor the specificity of smear.
High rates of empirical treatment of silico-tuberculosis may follow either from lack of access to confirmatory tests or the clinical presentation of symptoms and an abnormal chest radiograph with a negative sputum smear or X-pert MTB/RIF test. Over-treatment of tuberculosis in silicosis is common and causes unnecessary side effects.
Clinical acumens and consideration of radiological similarities and differences in two diseases are main points in accurate diagnosis. The following table describes radiological presentations of silicosis and tuberculosis4 5 6.
Treatment of tuberculosis in patients with silicosis is difficult due to impairment of macrophage function by free silica and/or poor drug penetration into fibrotic nodules. Usual anti-tuberculosis drugs with an extended duration of at least eight months are probably needed, to reduce the chances of relapse. Risk of TB relapse in patients with silicosis was 1.55 times higher than in patients without silicosis. In India study, co-prevalent silicosis significantly raised the odds of drug resistance and retreatment among patients with TB7.
Case presentation
A forty-year-old man, ex-smoker with 2.8 pack years, was admitted to Department of Respiratory Medicine, Yangon Specialty Hospital on 8th September 2025 with the complaints of low-grade intermittent fever and productive cough for one month. He denied chest and back pain, coughing up of blood, breathlessness on exertion and on lying flat, swelling of lower limbs and face, noisy breathing and weight and appetite change.
On examination, he appeared a middle-aged man with BMI 22 kg/m2, SpO2 97% on air, without clubbing and palpable cervical lymph nodes. There were vesicular breath sounds with bi-basal fine crackles and few rhonchi. Features of respiratory failure and cor pulmonale were not present.
He had consulted at Thingangyun General Hospital, Respiratory Medicine Department in March 2024. His Chest X-ray (Fig 1) at that time showed small nodules with irregular margins scattered on both lung fields with fibrotic areas in the pulmonary upper lobes and near both hilar. MTB was not detected in sputum for X-pert/MTB RIF testing. Bilateral upper lobe bronchi had mucopurulent secretion and mucosae were inflamed on bronchoscopy. Bronchoalveolar fluid from both upper lobes were negative for malignancy.
He was given anti-tuberculosis retreatment regime which was later changed to modified regime including Rifampicin, Ethambutol and Levofloxacin due to drug-induced liver injury for 9 months until November 2024. This is his third anti-tuberculosis treatment, first time for 6 months in 2007 and the second time for 8 months in 2017. Recheck chest X-rays in May and September 2024 showed persistent multiple nodules throughout the lungs with fibrosis in both perihilar areas.
Chest X-ray (Fig 2) in recent admission in September 2025 revealed persistent extensive, widespread diffuse reticulonodular opacities of varying sizes throughout both lungs and perihilar fibrosis. Sputum for AFB was negative. Neutrophil leucocytosis with increased C-reactive protein were noted with Klebsiella pneumoniae on culture of sputum. He was clinically improved after a course of antibiotics according to sensitivity.
Further questioning revealed that he had been exposed to dust during working in a gold mine for 12 years from 2013 up to 2024, with working hours of 8 hours per day without protective mask or equipment. In the last 8 years, he had been occasionally coughing up of small, spiculated, hard, white to brown colored particles, sized from 1 to 3 mm broncholiths (Fig); a phenomenon called lithoptysis.
High resolution computerized tomography of the chest followed by contrast enhanced computerized tomography of the chest in September 2025 (Fig 4) showed numerous small, discrete, cebtrilobular micronodules (silicotic nodules) , paracicatricial emphysema ajacent to fibrosis and (2.7 x 2.8 cm) cavity in right upper pulmonary area and eggshell calcifications: enlarged bilateral paratracheal, perivascular, AP window, subcarinal and both hilar lymph nodes with peripheral ring of calcium. There were also multiple splenic calcification in visualized upper abdomen. Conglomerate masses: irregularly shaped bilateral symmetric masses in upper lobes, represent coalescence of smaller silicotic nodules into progressive massive fibrosis.
Spirometric parameters of the patient were consistent with obstructive patterns. Marked reduced in forced vital capacity in comparison with previous values 16 months ago reflected the progression of lung fibrosis.
He was advised to halt further exposure to silica and given appropriate treatment including chest physiotherapy and arranged to monitor clinically, radiologically and functionally with spirometry.
Discussion
This gentleman has been suffering from classic complicated silicosis as well as silico-tuberculosis. Clinical judgement with non-invasive ways of confirming activity of tuberculosis such as sputum or broncho-alveolar fluid for gene X-pert testing and judicious prescription of anti-tuberculosis treatment are pillars in the management of a patient with silico-tuberculosis. Confirmation of tuberculosis by microbiological methods such as culture from lung biopsy or finding of silicotic nodules or granuloma are invasive and in-practical in our current practice. Prescribing retreatment regimens of anti-tuberculosis treatment in chronic silicosis should be cautious as the clinical presentations and radiological manifestations are difficult to differentiate especially in countries where both silicosis and tuberculosis are highly prevalent. Silicosis is a well-known TB mimic because of upper-lobe cavities and nodules in both conditions and silicotic nodules can undergo necrosis, causing fever and productive cough that looks like an infection.
Secondary bacterial respiratory infections in such structurally damaged lungs are also frequent. The “multiple nodules” and “perihilar fibrosis” represent progressive massive fibrosis that typically occur in the upper and middle zones and can appear nearly identical to TB or carcinoma. The tiny echogenic splenic nodules found on CT are consistent with extrapulmonary silicosis which derived from thoracic silicosis via lymphohematogenous spread to the liver, spleen, bone marrow, and extra-thoracic lymph nodes. Combined clinical proof such as lithoptysis, history of prolonged unprotected occupational exposure to silica with radiological manifestations like progressive massive fibrosis and splenic calcifications leaded to classic complicated silicosis in this gentle man whose final diagnosis was silico-tubercul
Fig. 1 – Chest X-ray showed small nodules with irregular margins scattering on both lungs fields with fibrotic areas in the pulmonary upper lobes and near both hilar.
Fig. 2 – Chest X-ray revealed extensive, widespread diffuse reticulonodular opacities varying sizes throughout both lungs and perihilar fibrosis.
Fig. 3 – Small, spiculated, hard, white to brown colored particles sized from 1 to 3 mm broncholiths.
Fig. 4 HRCT and CECT chest (a) and (b) Numerous small, discrete, cebtrilobular micronodules, paracicatricial emphysema ajacent to fibrosis and a cavity in right upper pulmonary area. (c) Eggshell calcifications: enlarged bilateral paratracheal, perivascular, AP window, subcarinal and both hilar lymph nodes with peripheral ring of calcium. (d) Conglomerate masses; irregularly shaped bilateral symmetric masses in upper lobes, representing coalescence of smaller silicotic nodules into progressive massive fibrosis.
References
- Antão VCS, Pinheiro GA, Jansen JM. (2002) Broncholithiasis and lithoptysis associated with silicosis. European Respiratory Journal. Oct 1;20(4):1057–9.
- Ehrlich R, Akugizibwe P, Siegfried N, Rees D. (2021) The association between silica exposure, silicosis and tuberculosis: a systematic review and meta-analysis. BMC Public Health. May 20;21(1):953.
- Pasula R, Britigan BE, Turner J, Martin WJ. (2009 ) Airway Delivery of Silica Increases Susceptibility to Mycobacterial Infection in Mice: Potential Role of Repopulating Macrophages. J Immunol. Jun 1;182(11):7102–9.
- Solomon A. (2001) Silicosis and tuberculosis: Part 2–a radiographic presentation of nodular tuberculosis and silicosis. Int J Occup Environ Health.;7(1):54–7.
- Leung AN. (1999) Pulmonary tuberculosis: the essentials. Radiology. Feb;210(2):307–22.
- Maboso B, Te Water Naude J, Rees D, Goodman H, Ehrlich R. (2023) Difficulties in distinguishing silicosis and pulmonary tuberculosis in silica-exposed gold miners: A report of four cases. Am J Ind Med. Apr;66(4):339–48.
- Rupani MP. (2024) Silicosis predicts drug resistance and retreatment among tuberculosis patients in India: a secondary data analysis from Khambhat, Gujarat (2006-2022). BMC Pulm Med.Oct 18;24(1):522.
Author Information
Khaing Pwint Wai1, Win Win Myint2, Yin Mon Thant3
- Consultant Physician, Department of Respiratory Medicine, Yangon Specialty Hospital
- Senior Consultant Chest Physician, Department of Respiratory Medicine, Yangon Specialty Hospital
- Professor and Head, Department of Respiratory Medicine, Yangon Specialty Hospital/University of Medicine 1, Yangon
