Mycobacterium kansasii infection

 

                                      Mycobacterium kansasii infection

                                         PKGhatak, MD

Mycobacterium kansasii is a harmless mycobacterium for healthy people. It is a different picture for people with long standing chronic lung diseases like cystic fibrosis, alpha1 antitrypsin deficiency and immune depressed people because of HIV infection, autoimmune diseases, or under medical treatment for cancer, etc.

Mycobacterium kasasii (M.kansasii) belongs to a group of mycobacteria known as NMB (non-mycobacteria tuberculosis) which is distinct from MTB responsible for Pulmonary tuberculosis.

Mycobacterium kansasii.

M.kanasasii are acid fast, slow growing NMB. The colony produces an orange colored smooth colony when grown on solid media and exposed to light. In the dark, the colony is colorless and rough. It tests negative for niacin and positive for catalase and has other similar biochemical features of NTBs. M. kansasii, unlike other NTM, is not universally present in soil and water, and colonization of the respiratory tract in healthy adults is a rare event. In addition to infection of the lungs, M. kansasii also infects vertebrae, bone marrow, spleen, liver, muscles, and skin.

In the USA, the incidences of new cases of M. kansasii are increasing as the mycobacteria tuberculosis infections are declining.

Texas recorded the most new cases of M.kansaii followed by Louisiana and Florida. As the name implies, M.kansasii is prevalent in Kansas and also seen in the adjoining mid-central states. White populations are more susceptible to M. kansasii infection.

Globally - the miners in South Africa have high rates of new infections, and also in Wales, UK.

Two groups are commonly infected -adults with underlying conditions and children between 4 and 6 years old, along with young adults.

Pulmonary diseases due to M. kansasii.

Three distinct clinical presentations are recognized

 1. Cavitary pulmonary tuberculosis.

 2. Nodular bronchiectasis.

 3. Disseminated infection.

The incidence of hemoptysis is 30%, weight loss is about 50%, and chest pain is seen in 25% of cases. Other symptoms like cough, production of sputum, fever, etc. have no specificity to this infection. Children and young adults present with cervical adenopathy in addition to pulmonary infections.

X-ray features. A single or multiple thin walled cavities in the apical portion of the lungs and hilar lymph node enlargement in association with bilateral pulmonary infiltrates are seen. In patients with severely depressed CD4 cell count, localization of the infection or cavity formation does not happen and dissemination of disease is usual. These findings along with a positive acid-fast organism in the sputum nearly clinch a clinical diagnosis of NMB infection.

Nodular bronchiectasis.

Inflammatory reactions and tissue destruction produce a weakened wall of smaller size bronchial tubes result in the development of multiple nodule shaped bronchiectasis in the central lung field. Frequent bouts of productive cough with streaks of blood along with other symptoms of infection are usually present. Secondary fungal and bacterial infections are frequent occurrences.

Disseminated infection.

Disseminated infection is mostly present in severely immunosuppressed patients. Bides lungs, bones, spleen, subcutaneous tissues, and kidneys are infected.

The sputum and bronchial washings should not be treated with KOH in the laboratory (a normal practice), because KOH kills M. kansasii and no growth will result in culture. Rapid liquid culture media should be used in growing M. kasasii, a growth in 2 weeks is expected. Newer techniques of species identification should be done. These tests are the Molecular hybridization test, PCR restriction analysis, Nucleic acid amplification test, Restriction fragment length polymorphism, Polymorphic tandem repeats, DNA genomics probe, etc.

Species identification not only speeds up identification but is also used as a guide in the selection of anti-tubercular drugs.

Non-pulmonary M.kasasii infection.

Cervical lymphadenitis in children is primarily due to M. tuberculosis followed by M. bovis. Of the NTM, the M. avium complex infection predominates. M. Kansasii cervical adenitis is the next common cause of childhood cervical adenopathy. The submandibular, submaxillary nodes are primarily involved but the submental, preauricular and periauricular glands are also infected. The skin over the enlarged glands appears glossy, the glands feel rubbery to touch. Often the swollen glands rupture and produce chronic discharging sinus tracts. Many children have a low grade fever, anorexia and fail to gain weight.

Osteomyelitis of the spine and sacroiliac.

The flat bones are susceptible to infection due to a rich blood supply. Often pain and fever are followed by abscess formation. In lower thoracic and lumbar vertebra osteomyelitis the abscess drains down the psoas fascia to the groin and can rupture producing a pus draining sinus tract.

When the spleen is infected, generally an abscess forms and patients can present as a fever of unknown origin. Liver, bone marrow granulomas and skin lesions are seen. Rarely, a meningoencephalitis develops.

Non-pulmonary infections are more common following a hematogenous spread and HIV infected people with CD4 cell counts below 50 are susceptible to these complications.

Diagnosis.

Biopsy tissues. All biopsied tissues should be stained for acid fast and cultured. Identification should be augmented by the newer methods listed above. Fungal and bacterial cultures are done at the same time.

Lymph nodes and bone marrow typically show several noncaseating granulomas with variable numbers of acid-fast organisms.

In disseminated M.kasasii infection blood culture, urine and bone marrow cultures usually show growth in 2 weeks. All positive cultures are tested for drug resistance.

Treatment.

M.kansasii are resistant to pyrazinamide and resistance to INH & Rifampin is increasing. The initial anti-tubercular medications include INH, Rifampin, and Ethambutol. If M.kansasii is resistant to any 1^st line drugs, then Azithromycin, Fluoroquinolones, Sulfamethoxazole, and Streptomycin are added in various combinations.

Complications. Pleural effusion is a rarity, pneumothorax is occasionally seen.

Treatment of cervical adenitis.

Early surgery should be done and is a very effective way to cure. In advanced cases with draining sinus tracts, treated with anti-tubercular medications for 3 to 6 months, followed by surgery.

Mortality and morbidity vary according to the extent of the disease at the time of presentation and the immunological status of patients.

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Clinical Presentation of Pulmonary Tuberculosis

                                    Clinical Presentation of Pulmonary Tuberculosis

                                                PKGhatak, MD

Pulmonary Tuberculosis presents in multiple ways.

Pulmonary tuberculosis is a very old disease. Evidence of tuberculosis was detected in 4,000 old Egyptian mummies. Description of TB like disease was recorded in 3,500 old Sanskrit literature, and still, older evidence was uncovered in Israel in a skeleton found in an old grave. Currently, pulmonary tuberculosis is still very much prevalent globally and is a curse for people of Southeast Asian and Northern African countries. 10,000 new cases were detected worldwide and 1.5 million people died of tuberculosis in 2018.

Pulmonary tuberculosis has several modes of presentation. The clinical presentations of clinical illness due to TB vary according to the prevailing standard of sanitation and public health of countries.

Latent Tuberculosis in Western countries.

Immigrants coming to Western countries require a negative chest x-ray as a prerequisite for a visa. Tuberculosis (TB) tests are mandatory in many countries for employment in schools, universities, hospitals, healthcare, nursing homes, and would be new nursing home residents and workers in the retail business. Some of the applicants react positively to the Interferon gamma release blood test or the old fashioned TB skin test.

These positive TB-tested people are completely symptom free, have no indication of prior TB infection, and are unable to recall coming in contact with an infectious TB patient.

Recently, a new method has been described to identify active tuberculosis from latent infection by determination of IL-8.IL-18, and IL-33 in TB-antigen stimulated of the whole blood with 85 % accuracy.

A careful review of a recent chest x-ray or CT chest will identify a small nodule in the upper part of the lungs, and also occasionally a small regional calcified lymph node. Induced sputum smears and cultures are done routinely and are negative.

The Public Health Department (PHD) must be notified and state mandated treatment protocol and follow up are taken up by the PHD.

Reactivation of Latent TB.

Two ways the reactivation of latent TB presents

 1. Local spread,

 2. Pleural effusion.

Local spread.

Many immigrants from countries where TB is prevalent may not be subjected to TB surveillance upon arrival in the new country. They remain symptoms free for a very long time until the cellular immunity is reduced by an infection like HIV, and immunosuppressed conditions due to Diabetes mellitus, prolonged use of corticosteroids, immunosuppressed drug therapy in organ transplants, and cancer chemotherapy. The dormant TB bacteria residing within the macrophage cells wake up and become metabolically active and begin to multiply. Eventually, TB bacteria break up the cellular barrier and invade adjoining tissues.

As TB becomes an active disease the patient may experience profuse night sweats, unproductive cough, evening chills and a low grade fever and loss of weight.

The clinical examination, followed by laboratory tests, reveals a positive Interferon gamma release assay (IGRA) and a single pulmonary nodule in the upper zone of the lung in the CT chest. These abnormal shadows often show two distinct densities - a denser central core and a lighter peripheral cellular infiltrate zone 

The major concern at this stage is – it is cancer or granuloma. TB bacteria are one of the few other microscopic organisms that produce granulomas.

The most direct way to distinguish between the two is to obtain tissue by a skinny needle biopsy with ultrasound/ fluoroscopic guidance.

But if the granuloma is due to TB infection, that might contaminate the path of the needle and might help to spread TB to the pleura and subcutaneous tissues.

The alternative is to wait 3 to 6 months and obtain a repeat CT scan and then evaluate the activity of the lesion and then decide when to biopsy.

This decision must depend on the best judgment of the attending physician and the patient. There are risks both ways.

Induced sputum for cytology for cancer, fungal, and TB is also performed as a part of the initial evaluation. Depending on the culture media used for TB culture, positive growth may or may not be available in 4 to 6 weeks. Bronchoscopic brushing and washings are examined for cancer and infectious agents. The success rate of identifying cancer/ infection is better by examining the bronchoscopy materials, but the success rate is not 100 %. The IGRS test of bronchial brushing and wash fluid containing mononuclear cells has a much higher rate of positivity of IGRS compared to peripheral blood lymphocytes.

Pleurisy and Pleural Effusion.

Clinical presentation.

The onset of chest pain, fever, and mild non-productive cough suddenly occurs in young apparently young healthy individuals. Pleural space TB inflammation takes place in one of the two ways - hypersensitive reaction and direct infection.

Hypersensitive reaction.

It is the usual mode. The initial symptom is a sudden onset of chest pain aggravated by breathing. The two layers of pleura, rubbing against each other during inhalation and produce chest pain. A few days or weeks later the pain suddenly diminishes once the pleural fluid begins to accumulate. Then the patient feels heaviness in one side of the chest and may develop a low grade persistent fever.

In the pleuritic state, audible friction rubs on auscultation are diagnostic of pleurisy but not diagnostic of TB pleurisy only. The right sided pleural effusion is usually seen and less than 10 % of cases of TB pleural effusion may be bilateral. The pleural fluid is easily obtained by bedside thoracentesis, at the same time pleural biopsy is performed by a special needle (Abram's needle). A pleural biopsy is safe because the lung is separated from the pleura by a layer of fluid and the chance of pneumothorax is minimal.

The TB pleural fluid is light yellow in color, the protein content is over 3 gm/dL, cell count 100 to 1000 /ml and predominantly lymphocytic, glucose content is less than 40 mg/dL, ADL (adenosine deaminase) test on T-lymphocytes is typically over 45U/L but below 200U/L. The ADL is the most sensitive (93%) and specific test (94%) for TB pleural effusion. IGRA assays are specific, but sensitivity is 70% in the peripheral blood and 97% in pleural fluid lymphocytes. TB culture grown in liquid media is in the 50 % range. TB bacteria in smears are rarely seen in hypersensitive TB pleurisy/pleural effusion. In hypersensitive pleural effusion, a pleural biopsy may or may not show caseating granuloma. If granuloma is present, then a few TB bacteria can be identified in pleural TB infection.

TB infection of Pleura.

A subpleural TB nodule ruptures in the pleural space. The escaped TB bacteria infect the pleura. Occasionally the TB bacteria are carried into the pleural space by the lymphatics. The contamination of the pleura in one way or another results in pleurisy and pleural effusion. The clinical presentation, however, is a bit different. Here, any age group of people may be infected, except children. The patients are ill if they have progressive primary pulmonary TB infection. In latent TB patients, most patients are symptom free prior to pleural effusion. A short period of pleuritic chest pain followed by pleural effusion occurs, like the hypersensitive pleural effusion.

Chest X-ray reveals, in addition to pleural effusion, the site of latent TB infection.  The character of pleural fluid is no different from the hypersensitive pleural effusion and additionally, RBCs in variable numbers are present. The pleural biopsy reveals caseating granulomas and TB bacteria are generally identified in the granuloma. The smear of the fluid may not show TB bacteria, but cultures in liquid media are always positive. If the TB bacteria are scanty, they can be identified by Nucleic Acid Amplification Test (NAAT)

Primary Pulmonary Tuberculosis.

Primary pulmonary tuberculosis is a global health problem. People in every country of the globe are contracting pulmonary tuberculosis every year.

Two factors have made tuberculosis eradication a daunting task. 1. TB bacterial survival resiliency. 2. Handicapped immune system to fight TB infection. Human TB bacteria that produce primary pulmonary tuberculosis are called Mycobacteria Tuberculosis, in short MTB.

MTB survival resiliency.

MTB are rod shaped, nonmotile, slow growing bacteria and need oxygen to grow. It lives inside Macrophages and multiplies under favorable conditions. MTB has a three-layered cell wall. The multilayered cell wall blocks TB drugs to enter the bacterial body in sufficient concentration to kill the MTB.

Handicapped Immunity.

In any infection, both the Cellular and Humoral immune systems are activated. But in MTB infection the Humoral immunity remains largely inactive. The CD4 cells, macrophages and other immune T-cells collectively fight against MTB invasion.

Mode of MTB primary pulmonary infection.

 MTB is a respiratory pathogen, human to human transmission occurs via infected droplets. Causal contact with an open MTB case (TB bacteria in sputum) does not cause infection; prolonged contact and repeated exposures over months are necessary. Overcrowded prisons, sailors in submarines, residents in dormitories, hostels and nursing homes are ideal places for MTB transmission.

A majority of inhaled droplets are caught by the mucociliary escalator and are eliminated. A few MTB reaches the alveoli. MTB penetrates the alveolar wall and enters the interstitial tissues and is promptly caught and swallowed by the tissue macrophages. Macrophages are unable to digest the MTB due to the presence of enzymes in bacteria that neutralize the digestive enzymes of macrophages, and the bacterial wall is indigestible. Additional macrophages and lymphocytes accumulate around the infected macrophage and a nodule is formed. 85 % of the initial infections are contained and confined locally. But MTB remains dormant inside the infected macrophages. This infected nodule becomes Latent TB.

Progressive Pulmonary TB.

People with suppressed cellular immunity are unable to limit the initial infection. The MTB multiplies and break out of macrophages and infect the adjoining areas, some of the infected macrophages carry the bacteria to the regional lymph follicles/nodes and these two infected areas are collectively called the primary complex. Further growth and progression of infection continue. 6 to 9 months after the initial infection the patient starts to experience symptoms.

In advanced countries, only 1/3 of newly diagnosed cases are due to fresh infections and the rest 2/3 are due to the reactivation of latent TB.

Symptoms are - lack of energy, easy fatigue, anorexia, loss of weight, short but successive unproductive coughs and profuse night sweats are common.

Further progression of the disease produces: 1. Wide areas of Pulmonary infection and is known as primary progressive Tuberculosis. 2. Hemoptysis. 3. Miliary TB.

Primary Progressive Pulmonary Tuberculosis.

These patients are sick and weak. Persistent low grade fever, wasting of muscles, anemia, cough productive mucopurulent sputum and occasional streaks of blood in sputum is present. Confirmation of pneumonia is not difficult but there are no special clinical features of MTB pneumonia.

Chest x-ray shows infiltration in the upper zone of the lung, usually on the right side and spread of the disease in the adjoining lobes. In some cases, thick walled cavity is seen in the upper lobe or apical portion of the middle lobe. In nursing home patients, middle lobe and lower lobe infiltrations are common.

Sputum smears and cultures are the cornerstones of MTB diagnosis. IGRA assay of peripheral blood is both sensitive and specific. In occasional cases, NAAT (Nucleic acid amplification) test may be necessary.

Hemoptysis. Blood-streaked sputum is an indication of the progression of disease and destruction of the lungs. That leads to bringing up frank red blood.

Almost all patients present with hemoptysis undergo bronchoscopic examination. It not only helps to diagnose MTB but also eliminates the possibility of lung cancer and fungal infection.

Miliary Tuberculosis.

MTB not only destroys the lung parenchymal tissues but also penetrates blood vessels and spreads far and wide. MTB can also spread via lymphatics. The tissues rich in oxygen support further MTB growth. Lungs, meninges, bone marrow, and kidneys are common sites of extrapulmonary TB infection.

The patients are very malnourished, very weak and unable to cough properly. Sputum production is generally absent or minimal. Patients are febrile and may show abnormal liver, renal functions and electrolyte imbalance. Both acute and chronic phase reactants are positive. In severely immunosuppressed patients with low CD4 cell count, the TB skin tests and IGRS test may be negative.

The chest x-ray is virtually diagnostic, and a bone marrow biopsy showing granulomas and MTB are easily demonstrated. Bone marrow cultures are necessary for the final diagnosis and also for the detection of drug resistance. Concurrent HIV infection must be eliminated by proper tests.

All Pulmonary MTB cases must be reported to the local Public Health Department (PHD). PHD use approved treatment protocol, makes sure of TB drug delivery and compliance of patient in taking TB drugs, and performs contact tracing and chemoprophylaxis of appropriate people.

In addition to these modes of presentation of MTB pulmonary infections, some unusual presentations are also identified in unsuspected patients on bronchoscopy. The use of more advanced tests helps to identify MTB infections. That part is not discussed here.

Non-MTB mycobacterial pulmonary infections are less common but the number of new cases is growing. This subject is discussed in a separate place.

edited May 2025

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Metal Fumes and Lung Diseases

 

                                              Metal Fumes and Lung Diseases

                                                 PKGhatak, MD

People do not encounter metal fumes every day, and many may be completely unaware of them. It is a different story for factory workers, foundry workers, ironworkers, and workers in many other workplaces where exposure to metal fume inhalation is a daily occurrence.

Lungs are exposed to the environment directly; whatever is in the air it finds its way eventually into the lungs. The gastrointestinal tract is very well protected by a layer of very strong acid secreted by the stomach, the skin is impervious to most agents to a certain degree, and the eyes are partially protected by tear secretion.

Reactions of the lung to metal fumes.

Metals used in industries and household products come in several forms. The metals may be in the pure metallic form, combined with other elements like oxide, sulfide, nitrite, halide, carbide and also combined with organic compounds. For these discussions, all are simplified as metals. Also, important to point out that the toxicities not only vary from compound to compound but also in the frequency of exposure and concentration in the air. The solubility of metal compounds influences pulmonary reactions; poorly soluble compounds are caught and eliminated by the mucociliary escalator, and soluble compounds react with tissues directly and produce more intense reactions.

Certain metal fumes produce only minimal fibrosis in the lung; the metal merely fills up the lung. An example is iron.

The inhalation of nickel and beryllium produces intense inflammation, leading to extensive fibrosis of the lungs.

Many other metals may produce reactions between these two reactions.

In some cases, the metals combine with the protein of the body and become antigenic and producing immune reactions. These metals act as Heptane, for example, platinum, chromium, cobalt, etc.

Some metals produce only one type of pulmonary disease, others, like chromium, produce several different clinical diseases.

Clinical conditions produced by metal fumes.

1. Cadmium, Lead, Zinc, and Chromium:

2. Nickel, Chromium, and Cobalt:

Acute bronchitis, chronic bronchitis, and sinusitis are common occurrences.

Occupational asthma.

3. Platinum:

Hypersensitive pneumonitis.

4. Iron, Tin, and Barium:

Pneumonitis without fibrosis.

5. Beryllium, and occasionally Tin and Aluminum'

6. Barium and Antimony.

Pneumonitis with fibrosis.

7. Cadmium:

Pulmonary emphysema.

8. Baetllium, Tin and Aluminium:

Granulomatous lung disease is similar to sarcoidosis.

9. Cobalt:

Desquamative giant cell interstitial pneumonitis.

10. Radium and Iron:

Lung cancer.

11. Lithium, Zinc, and Lead:

Pulmonary edema.

12. Zinc and Lead:

Chronic obstructive pulmonary disease.

13. Aluminum:

Alveolar Proteinosis .

In addition to lung diseases, metals also produce liver, kidney, and other organ damage. Those are not discussed here.

Professions outside metal manufacturing are susceptible to pulmonary diseases.

Diamond polisher – exposure to cobalt.

Aerospace industries – exposure to beryllium.

Electronic, computer, and ceramic – exposure to beryllium.

Dental technicians – exposure to align, beryllium.

Housewife/spouse (workers bringing home) - beryllium dust in their clothing.

Painters – pigments containing various metal compounds.

Boilermakers and Oil tanker cleaners - exposure to vanadium.

Firework and explosive makers - exposure to aluminum.

Hard metal toolmakers and users - exposure to tungsten

Chrome plating – exposure to chrome.

Glass polishers and lens makers - exposure to cerium (rare earth).

How metals act in tissues:

1. Metals like iron, copper, magnesium, cobalt, and zinc are coenzymes in many enzyme systems.  2. Many transport proteins are compounds of metals. 3. Some metals readily combine with proteins and sensitize immune cells. 4. Metals combined with macromolecules hinder DNA repair.

2. The incidence of inhaled metal compounds and pure metal fumes is increasing due to the expansion of manufacturing facilities near residential districts and the relaxation of air quality standards in recent years.

3. The lung diseases caused by metal fumes have no easily distinguished features from usual chronic lung conditions like chronic bronchitis or pneumonitis, and pneumonia. People are well aware that lung cancer and COPD are related to cigarette smoking. However, many nonsmokers develop COPD and lung cancer, and they are baffled and ask their doctors what caused their illness.

It is only by a careful and detailed history of occupation, home environment, recreation, and hobby habits that a cause can be identified.

Tests for the identification of metals:

1. High Performance Liquid Chromatography. And Gas Chromatography.

The final identification depends on the demonstration of that metal in the respiratory tissues or secretions, or bronchial washing fluid, by one of the two tests mentioned above.

2. Immunoassays.

3. The specific antibodies against the suspected metal tests are available, but are not as sensitive and specific as chromatography.

 edited May 2025.

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Black Lung Disease

 

                              Black Lung Disease / Coal Miners Pneumoconiosis

                                           PKGhatak,MD

Coal dust was thought to be inert particles, but now it is well established that inhaled coal dust is responsible for black lung disease. The accumulation of coal dust in the lungs and the tissue reactions to its presence produce black lung disease.

Coal dust of 4 μm size or smaller can easily reach the alveoli, bypassing the mucociliary defense of airways. The small dust particles penetrate the alveolar membrane and travel via lymphatics to the local lymph nodes. Macrophages in the interstitial tissue of the lung engulf coal particles, but macrophages can not digest coal. Coal laden macrophages release cytokines. The cytokines cause inflammatory reactions. The accumulated macrophages form a small, tiny flat collection of cells called macules. The macules are found in the upper lobes of the lungs. Later the macules coalesce to form nodules due to fibrosis. The fibrous tissues distort bronchioles and result in focal emphysema. Initially, the fibrosis may be localized but becomes diffuse when coal dust exposure continues.

The incidence of back lung disease is increasing in the USA due primarily to the relaxation of laws and regulations, over the years, limiting coal dust exposure to miners. Because of the wider use of coal in developing countries for electricity generation, global incidence is on the rise.

This is a major setback for those physicians, attorneys, social workers, researchers and others who worked so hard for so many years in hostile environments, created and financially supported by the management/investors, at the cost of the health and welfare of miners and their families.

In the USA, the incidence of Black Lung Disease among coal miners is -

In 1975 - 32 cases / 1000 miners were diagnosed with black lung disease.

In 1980 - 13 cases / 1000.

In 1990 - 25 /1000.

In 2000 - 3.7 / 1000.

In 2010 - 19 /1000.

In 2015 - 51 / 1000.

Types of Coal and Black Lung Disease.

Anthracite coal is hard coal, it has 84 % of carbon and contains less volatile compounds. It is also the worst coal for the development of black lung disease. In Pennsylvania coal towns -Scranton and Wilkes-Barre area, where coal mines were the main employers, the incidence of black lung was 10 % in miners exposed to coal dust over 25 years. Since anthracite coal is exhausted from this area, the mining companies switched to Bituminous coal mining. Bituminous coal is abundant in West Virginia, Kentucky, and Pennsylvania. Bituminous coal is soft, and it is less harmful to the lungs.

Cigarette smoking does not directly exacerbate fibrosis but chronic bronchitis and emphysema secondary to smoking worsen the coal miners' symptoms.

The inhalation of coal dust is usually accompanied by the inhalation of silica dust. The coal seams are embedded in between the layers of hard rocks and had to be blasted off. That generates a cloud of dust in the underground mines due to poor ventilation. The silica and coal dust in large quantities are inhaled. At present, the practice of blasting off the top of mountains to reach the coal seams is also causing huge dust clouds. That is not only inhaled by miners but also by their children and other family members.

  

               Black lung.

Clinical presentation.

In early cases, the patients may have no symptoms but chest X-rays show multiple small lung nodules in the upper lobes of the lungs. In more advanced cases the apical portion of the middle lobe is also involved and the shows become more profuse. As the disease advances further the fibrosis becomes more diffuse. And lower lobes also show changes. In addition, pulmonary emphysema and cavities of different sizes may be present. This stage of the illness is called Progressive pulmonary Fibrosis.

In patients with Rheumatoid arthritis, subpleural cavitary nodules are seen. This is known as Caplan syndrome

Symptoms.

There are no specific symptoms of back lung disease. Cough, and sputum production containing black dust may be present. Shortness of breath, exhaustion and weight loss and limitation of physical activities are usual and at this stage patients are disabled.

Disability Determination.

Federal and State laws developed over years, and their criteria are well described in publications. The criteria were developed based on

    1. Type and size of shadows in the x-rays.

    2. The percentage of lung area affected in relation to the whole lung.

3. The degree of pulmonary function test abnormality

4. Under saturation of Oxygen detected during a standard exercise. A detailed description of this subject can be obtained in the State Coal miners disability acts.

Complications.

Pulmonary hypertension and right heart failure and cardiac arrhythmia eventually develop. The lung cavities invite bacteria. Mycobacterial tuberculosis infections often coexist. Mycobacteria tuberculosis and atypical mycobacterial infections produce accelerated fibrosis.

Treatment.

Once the black lung disease is well established, the reversal of the disease is not possible. Treatment is directed toward controlling the secondary complications. The standard therapy for pulmonary emphysema and chronic bronchitis, heart failure and respiratory insufficiency are undertaken depending on the cases.

Prognosis.

In the USA 1,500 die each year from black lung disease and 25,000 globally.

[ Nomenclature:

Pneumoconiosis is a Greek word meaning dust disease of the lung. Pneuma= wind, kons= dust.

Black lung disease is known as Anthracosis in Greek / medical literature. Anthraco means coal.]

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