4.2.11. Tuberculosis of breath organs combined with dust occupational lung diseases (coniotuberculosis)


The term coniotuberculosis (Greek – conia or conis – dust, ashes) means dustiness and tuberculosis. This group consists of from all forms of lung tuberculosis combined with dust occupational diseases: silicosis, asbestosis etc. At the formulation of the diagnosis, it is necessary in the beginning to write “Coniotuberculosis”, then to give the detailed characteristic of coniosis – “antracosis”, “silicosis” etc., and detailed description of tubercular process.

Coniotuberculosis refer to big group of lung diseases – pneumoconiosis. Pneumoconiosis is caused by continuous inhalation of certain types of dust particles over long periods which may result in peribronchial fibrosis, causing disability, and even death. The picture is entirely different from that produced by inhalation of irritating chemical materials.

Classification dust occupational lung diseases

Depending on character of an inhaled dust allocate various kinds of pneumoconiosis. Up to six kinds of pneumoconiosis are classified.

  • Silicosis – disease caused by inhalation of a dust, containing free silica (SiO2).
  • Silicatosis. Silicatosis arise at inhalation of silicate dust, containing bounded SiO2.
  • Metalloconiosis arise at inhalation of dust containing metals and metal alloys.
  • Carboconiosis occurs from inhalation of coal dust.
  • Pneumoconiosis is caused by inhalation of the mixed dust containing free SiO2 and metallic alloys not containing SiO2.
  • Pneumoconiosis is caused by inhalation of an organic dust (cotton, grain, cork, reed).

Pneumoconiosis produces similar changes in the lungs. Host prominent among these is silicosis. There is no distinctive difference between this and other types of silica involvement. The pneumoconiosis nodules detected microscopically in the lung. So the cause of certain pneumoconiosis could be determined with special diagnostics means. Using short description of silicosis pathogenesis, clinic and diagnostics general signs of pneumoconiosis are submitted.

The most common causative agent of pneumoconiosis is silica and that any dust is harmful in direct proportion to the silica which it contains. Organic dust causes irritation; chemical dust may cause toxicity but neither causes the same degree of fibrosis and lasting damage to the lung. Only the smallest particles of silica, 10 microns or less in size are harmful. Once these dust particles become deposited in the alveoli they cannot escape except by phagocytosis and elimination through the lymphatics.

The most often complication of silicosis is the tuberculosis – silicotuberculosis.

Incidence of tuberculosis in persons with silicosis three to seven times higher compared to those without silicosis among persons working at the same place. Overall, it appears that tuberculosis occurs in as many as 20 to 25 per cent of all silicosis patients in their lifetime. Tuberculosis is one of the important predictors of mortality in patients with silicosis. For the same radiological extent of silicosis, the mortality risk is higher than expected if tuberculosis develops. It appears that the relative risk of death from tuberculosis is three to six-fold greater in patients with silicosis than in the general population. Epidemiological and experimental studies also suggest that the exposure to silica dust, even in the absence of radiological silicosis, may be responsible for the increased rate of pulmonary tuberculosis. Better control of tuberculosis in a population has an important influence on decreasing the risk of tuberculosis in patients with silicosis.

Several pathogenetic processes are common to tuberculosis and silicosis which may be synergistic in producing more fibrosis and in enhancing susceptibility to mycobacterial infection or reactivation of a latent focus of infection. The silica particles are phagocytosed by the alveolar macrophages. Inside these cells, silica particles are engulfed in phago-lysosomes. Silica has the capacity to cause damage to the cell membranes which leads to the death of the macrophages with re-exposure of the other macrophages to the same particles. It has been postulated that both humoral and cell-mediated immune responses are inhibited in silicosis. Cell-mediated immunity is important to contain the mycobacteria, and its alteration could facilitate infection with mycobacteria. Lung flbrosis occurs in both diseases and may interfere with the clearance of dust-laden alveolar macrophages or mycobacteria-laden material from the lung. Lymphatic obstruction causes macrophages to accumulate in the interstitial tissues resulting in local fibrosis.

If the process procedes `mall rounded, nodules or whorls of collagen develop along the lymphatic channels. As the disease progresses this beaded appearance gives place to large blotchy areas of fibrosis or collagen deposits throughout the lungs. These large collagen deposits are frequently in the apices of the lower lobes. Not all individuals exposed to hazardous dust inhalation contract the disease. Ordinary 5 to 10 years are required to develop the disease; rarely does it develop under two years of heavy dust exposure.

Clinical Features.
The manifestations of tuberculosis in patients with silicosis are similar to those in general population. However, since malaise, fatiguability, dyspnoea and night sweats occur in silicosis also, at times, it may be difficult to detect superimposed tuberculosis clinically. Disability in silicosis is due to the inadequate oxygen supply. Gas exchange is hampered by the thickening and rigidity of the alveolar walls due to collagen deposits and associated emphysematous changes (alveolar elasticity loosing). Capillary engorgement and edema of the air sacs and terminal bronchioles result causing inadequate aeration of the blood. The degree of disability cannot be estimated from the radiographic appearance, but is most reliably determined by respiratory function tests.

Focus, disseminated tuberculosis and tuberculoma most often are met at silicosis.
The diagnosis of active tuberculosis in patients with silicosis demands a high degree of suspicion.. Tuberculosis can be suspected in patients with silicosis when the radiographic abnormalities are seen in the apical area of either of the lungs. These abnormalities include poorly demarcated infiltrates of variable size that do not cross the lung fissures. These opacities may surround pre-existing silicotic nodules. Presence of a cavity in a nodule is usually indicative of tuberculosis. Cavity formation without associated tuberculosis is so rare that from a practical standpoint any evidence of lung destruction accepted as indication of tuberculous disease.

Features suggestive of tuberculosis in patients with siiicosis:

  1. Apical location;
  2. Cavitation;
  3. Rapidly changing opacities;
  4. Pleural effusion.

Establishing the diagnosis of pulmonary tuberculosis in a patient with silicosis by bacteriological methods is often difficult. Therefore, more frequent sputum examination for acid-fast bacilli is recommended. The bronchopulmonary with smear investigation are indicated.


Presently, a closely supervised eight to nine months treatment is recommended. For the initial two months, a combination of rifampicin, isoniazid, pyrazinamide, and ethambutol or streptomycin are given which is followed by two or three drugs for another six to seven months. Long-term follow-up is recommended to diagnose possible relapse after the completion of treat-ment.

As tuberculosis is quite common in patients with silicosis, there is a strong case for considering antituberculosis chemoprophylaxis in patients with silicosis. The currently accepted regimen of administering isoniazid for six to twelve months. At present it is recommended isoniazid prophylaxis for one year to all patients with silicosis who are tuberculin positive. Any complications such as tuberculosis, emphysema, spontaneous pneumothorax, or cardiac enlargement give a very unfavorable prognosis to tuberculosis patients.

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