Overview.
Pulmonary mycobacteriosis, also known as Gilkes disease or North American mycobacteriosis, is a chronic granulomatous and pyogenic disease caused by infection with the bacterium Bacillus dermatitidis or known as the North American mycobacterium, which can attack any part of the body, primarily involving the skin, lungs, and bones. Botrytis cinerea is also a biphasic fungus found in the soil. It usually develops in young adults and is more common in males than females. The clinical picture may include high fever, chills, and cough. Some patients are asymptomatic, often with concomitant dermatitis lesions.
Etiology
It is caused by dermatophyte infection.
Symptoms
The disease can be divided into four types: primary pulmonary mycobacteriosis, chronic cutaneous and skeletal mycobacteriosis, systemic mycobacteriosis, and inoculative mycobacteriosis. Primary pulmonary mycobacteriosis is similar to tuberculosis or histoplasmosis, the symptoms are not specific, some cases are very similar to primary tuberculosis, most of them can be cured by themselves, a few of them become subacute or chronic or even spread to the whole body, T-cell dysfunction, the infection is often very serious, difficult to cure, easy to spread to multiple organs, extensive bilateral pulmonary infiltration and high incidence of meningeal dissemination are its clinical characteristics.
Examination
Most cases are diagnosed by smear, culture and histopathologic methods.
1. Direct microscopic examination
Direct microscopic examination of blood, pleural fluid, sputum or other secretions is the easiest and fastest diagnostic method; histopathologic examination of biopsy specimens can also establish the diagnosis.
2. Bacterial culture
Easier to grow, but the growth is slow, the routine culture needs several weeks.
3. Skin test
Mainly used for epidemiologic investigation.
4. Serologic tests
Complement binding test, immunodiffusion method and enzyme immunoassay, etc. High specificity, poor sensitivity.
5. X-ray chest examination
There may be lung lesions and/or enlarged hilar and mediastinal lymph nodes.
Diagnosis
Diagnosis can be made on the basis of history, clinical manifestations, histopathologic examination and microscopic findings.
Treatment
1. Immunocompetent hosts
Patients with acute pulmonary dermatophytosis with extensive pulmonary lesions and severe hypoxemia should be treated immediately with amphotericin B (AMB). It is now advocated that antifungal therapy not be given to patients who present with acute pneumonia, have relatively mild first symptoms, and are significantly improved at the time the diagnosis is established. Itraconazole is effective in the vast majority of patients with pulmonary dermatophytosis, including acute, subacute, chronic, and nonmeningeal dissemination. Occasionally a longer course of therapy is required. Fluconazole may be used in patients who cannot tolerate or do not absorb itraconazole. In addition, fluconazole’s ability to cross the blood-cerebrospinal fluid barrier makes high-dose fluconazole potentially effective in CNS dermatophytosis.AMB is used only in a limited number of patients with severe disease, including diffuse pulmonary infiltrates, severe signs of toxicity, severe gas-exchange deficits, and those with rapid dissemination. For severe infections, sequential therapy may be used. Treatment with AMB first to achieve clinical improvement, followed by itraconazole.
2. Patients with acquired immunodeficiency syndrome (AIDS)
The prognosis for this group of patients is not encouraging. Even if the patient responds well to the initial induction therapy there is no permanent cure. In severe cases, death may occur early. A sequential treatment program may be used. Induction therapy with AMB until clinical control, followed by lifelong maintenance therapy with itraconazole. Certain mild-to-moderate patients with less severe immunosuppression may be treated with itraconazole from the onset of the disease.
3. Other immunosuppressed patients
Ultimate cure can be achieved in less severely immunosuppressed individuals (including glucocorticoid-treated and organ transplant recipients). The treatment regimen is usually AMB and itraconazole for at least 12 months, or AMB until clinical improvement and continuation of itraconazole for 6 to 12 months.