is a non-motile, acid-fast staining, obligate aerobe normally suppressed by cell-mediated immunity in the normal host. There has been a recent increase in TB incidence in the US because of HIV/AIDS.
Epidemiology
an old disease, affects 1.7 billion people worldwide, 8 million active cases/year
Pathophysiology
spread by inhalation of aerosolized droplets containing the organism. UV light and desiccation kills it.
Most individuals infected with M tuberculosis have an adequate immune response and do not develop evident disease.
In those individuals that do have clinically significant disease it is either:
(1) Primary Tuberculosis pulmonary infiltrates are present in the middle or lower lobes of the lungs, the organisms multiply in the lungs and spread to regional lymph nodes. An enlarged hilar lymph node is called a Ghon complex. From the lymph nodes the organism may disseminate via the bloodstream to extrapulmonary sites. Within 3-6 weeks lymphocytes and monocytes have formed tubercles. Tubercules contain Langerhans Giant cells surrounded by fibroblasts, lymphocytes, and monocytes to form Granulomas. As the granulomas heal they may calcify.
(2) Reactivation tuberculosis 10% lifetime risk but the majority reactivate within 2 years of initial infection. This occurs with reactivation of bacilli in previously healed granulomas. The bacilli are aerobic so they tend to localize in the lung apices (higher pO2).
Clinical features
most patients with primary tuberculosis have mild nonspecific symptoms of transient lower resp. infection
upper lobe apical infiltrates and pleural effusions (effusions are usually a reaction to rupture of a tubercle into the pleural and organisms are only cultured in 20-40% of cases)
diagnosis established by identifying the organism in sputum or culture.
Treatment: multiple drugs for at least ½ a year. (INH, rifampin, pyrazinamide, and ethanbutol) for active cases.
Prophylaxis for individuals with asymptomatic infection (+PPD) who are at risk to develop active disease. INH is given for 6-12 months. A positive PPD signifies that the host has developed an immune response to Mycoplasma.
Fungal Pulmonary Diseases
Lungs are the primary site of entry for fungus into the body. Immuno-competent people are able to contain the organisms.
T-cells are needed to contain Histoplasmosis, Blastomycosis, and Coccidioidomycosis. B-cells are needed for Aspergillus.
(1) Histoplasmosis
endemic to the Ohio and Mississippi river valleys, Histoplasma capsulatum grows in soil enriched with bird and bat droppings. When the soil is disturbed, the fungi are aerosolized and inhaled. Once inhaled the fungi are converted into the yeast form and spread to the hilar lymph nodes. From there they can disseminate throughout the body.
Primary infection
in normal hosts, looks like "flu". Hilar adenopathy and patchy infiltrates on CXR.
Progressive Disseminated Histoplasmosis
fever, weight loss, hepatosplenomegaly, and bone marrow involvement. Seen in patients with
ß cell-mediated immunity.
Diffuse micronodular histoplasmosis
seen in patients who have a large innoculum or in COPD patients. This may progress to fibrocavitary disease.
Progressive Mediastinal fibrosis
seen in genetically susceptible patients. Exaggerated immune response to a small innoculum leads to inflammation that compresses hilar structures. Very poor prognosis, no effective treatment.
Diagnosis and Treatment
diagnosis by Ý in antibody titers, no treatment needed unless severe pulmonary or disseminated disease.
(2) Blastomycosis
endemic to the northern and central Midwestern states (Wisconsin and Minnesota). Infection acquired by inhalation. The organism exists in areas irrigated by streams. An initial pulmonary infection gives rise to a progressive chronic disease with skin and bone lesions. Acute pulmonary blastomycosis is a severe febrile illness with a productive cough. Diagnosis is made by culture of sputum after digestion with KOH. IV amphotericin is used to treat. Although it will often resolve on its own, Blastomycosis is always treated to avoid disseminated disease.
(3) Coccidioidomycosis
endemic to the Southwestern US. Present in soil. Epidemics after earthquakes because of aerosolization of the spores. Inhaled, migrates to hilar lymph nodes, disseminates around body (trophic for the meninges) primary infection is flu-like, CXR shows multiple densities with hilar enlargement. 60% of patients will asymptomatic. 1/200 will get symptomatic extrapulmonary disease (meningitis, skin, joints).
Diagnosis and Treatment
serological test (because culture is dangerous to lab personnel) Treat with amphotericin.
Meningeal involvement requires lifelong therapy.
(4) Cryptococcus
worldwide distribution, found in bird droppings, acquired by inhalation. Chronic meningitis is its usual presentation. Respiratory symptoms are uncommon but patient will still have an abnormal CXR.
Diagnosis and Treatment
culture, visualization, + Ag (in disseminated disease). Need to do an LP to rule out menigitis.
(5) Aspergillosis
present in decomposing organic matter. Aspergillus fumigatus is the main culprit. Neutrophils are needed to contain these little guys. Three forms of the disease:
(1) Allergic Bronchopulmonary aspergillosis occurs primarily in asthmatics, a reactive airway disease.
(2) Aspergillomas fungus grows in previously existing lesions from old TB or COPD problems. Occasionally locally invasive and causing necrotizing pneumonia.
(3) Invasive Aspergillosis most often in immunosuppressed patients. High fevers, a rapidly progressive disease that invades blood vessels
Þ hemorrhagic infarts. Poor prognosis; as immune system recovers, lesions cavitate.
Diagnosis and Treatment
lung biopsy required for definitive diagnosis. Treatment is with steroid. Life-threatening hemoptysis requires surgical resection of the aspergilloma.