CLINICAL PRESENTATIONS AND DIAGNOSTIC CRITERIA
Chronic pulmonary disease is the most common clinical manifestation of NTM. MAC, M. kansasii, and M. abscessus, in that order, were the most frequent NTM pulmonary pathogens in the United States between 1981 and 1983.
In that study, there was a predominance of males with NTM pulmonary disease in general and in disease caused by all species except M. chelonae (probably M. abscessus) and M. simiae. The mean age of patients with NTM pulmonary disease was 57 years.
In the CDC report from the mid-1990s, MAC, M. kansasii, and M. fortuitum were the most frequent pulmonary pathogens in the United States between 1993 and 1996. Males predominated in disease caused by all species except M. abscessus and the majority of isolates were from patients 50 years of age or older.
In light of more recent information that reflects a post-menopausal female patient predominance for MAC lung disease, it is likely that these epidemiologic estimates are not currently valid.
Symptoms and signs
The symptoms of NTM pulmonary disease are variable and nonspecific. However, virtually all patients have chronic or recurring cough. Other symptoms variably include sputum production, fatigue, malaise, dyspnea, fever, hemoptysis, chest pain and weight loss. Constitutional symptoms are progressively more prevalent with advancing NTM lung disease.
Evaluation is often complicated by symptoms caused by coexisting lung diseases, such as bronchiectasis, chronic obstructive airway disease associated with smoking, cystic fibrosis and pneumoconiosis.
Physical findings are nonspecific and reflect underlying pulmonary pathology, such as bronchiectasis and chronic obstructive lung disease.
On chest auscultation, findings may include bronchi, crackles, wheezes and squeaks. Patients with nodular/bronchiectatic MAC disease tend to be postmenopausal women, many of whom also have a characteristic morphotype with a thin body habitus and may also have scoliosis, pectus excavatum and mitral valve prolapse.
Mycobacterium and Sarcoidosis
Sarcoidosis is an inflammatory disease that can affect almost any organ in the body. It causes heightened immunity, which means that a person's immune system, which normally protects the body from infection and disease, overreacts resulting in damage to the body's own tissues. The disease is mediated by either or both Th1 and Th2 T cells.
The classic feature of sarcoidosis is the formation of granulomas--microscopic clumps of inflammatory cells that group together (and look like granules, hence the name). When too many of these clumps form in an organ, they can interfere with how that organ functions.
In people in the United States, sarcoidosis most commonly targets the lungs and lymph nodes, but the disease can and usually does affect others organs, too, including (but not limited to) the skin, eyes, liver, salivary glands, sinuses, kidneys, heart, the muscles and bones, and the brain and nervous system.
Evidence from several lines indicates that Mycobacterium spp are involved in the disease process. The evidence includes:
(1) demonstration of Mycobacterium DNA in granulomas (Drake et al, 2002; Saboor et al, 1992);
(2) the induction of interferon gamma of patient lymphocytes by antigens of Mycobacterium (Carlisle et al, 2007; Allen et al, 2008) and
(3) and epidemiological evidence that have an etiological role in the disease (Gupta et al, 2007).
Finally, HLA phenotypes appear to increase the risk for developing sarcoidosis in both Caucasians and Afro-Americans (Rossman et al, 2003; 2008).
From these data, it can be concluded that Mycobacterium spp have an etiological role in some cases of Sarcoidosis and that certain HLA phenotypes increase the risk of the disease.
Mycobacterium and Hypersensitivity Pneumonitis
Hypersensitivity pneumonitis (also known as Hot Tub Fever or Farmer's Lung disease) is a granulomatous disease of the lungs caused by Mycobacterium avium complex. The disease is characterized by reactive airways, inflammation, nodular infiltrates (granulomas), and bronchiectasis. The intracellulare form is increasingly recognized as a pulmonary pathogen.
For more information, see: Waller et al, 2006; Sood et al, 2006; Hanak et al, 2007; Embil et al, 1997.
Several species of Mycobacterium avium complex have been identified in damp indoor spaces.
Skin Lesions and Lymphoadenopathy
M. Ulcerans is endemic to the tropical regions of the world. It produces Mycolactone which is immunosuppressive and cytotoxic.
M. marinum and liflandii have been identified as two other species that produce this toxin. These organisms are present in fresh and salt water. Ulcerans and marinum have been noted to cause skin lesions in humans that ulcerate and can cause necrosis of underlying muscle.
Inflammation is found in the lesions that include neutrophils and lymphocytes. Usually, the lesions are not painful because mycolactone suppresses pain reception. Infections may occur in individuals who handle fish, e.g., aquarium fish or fisherman who are exposed to the organisms.
Marinum has a worldwide distribution and has been identified off the Florida Coast, Gulf of Mexico an California Coast. These conditions are noted here since the spectrum of mycolactone producing Mycobacterium has not been completely investigated.
For more information, see Pidot et al, 2008; Ang et al, 2000; Tran et al, 2008; Williamson et al, 2008; Simmonds et al, 2009; Sarfo et al, 2020).