Tuberculosis
Tuberculosis: Excerpt from Professional Guide to Diseases (Eighth Edition)
An acute or chronic infection caused by Mycobacterium tuberculosis, tuberculosis (TB) is characterized by pulmonary infiltrates, formation of granulomas with caseation, fibrosis, and cavitation. People who live in crowded, poorly ventilated conditions and those who are immunocompromised are most likely to become infected. In patients with strains that are sensitive to the usual antitubercular agents, the prognosis is excellent with correct treatment. However, in those with strains that are resistant to two or more of the major antitubercular agents, mortality is 50%.
Causes and incidence
After exposure to M. tuberculosis, roughly 5% of infected people develop active TB within 1 year; in the remainder, microorganisms cause a latent infection. The host’s immune system usually controls the tubercle bacillus by enclosing it in a tiny nodule (tubercle). The bacillus may lie dormant within the tubercle for years and later reactivate and spread.
Although the primary infection site is the lungs, mycobacteria commonly exist in other parts of the body. Several factors increase the risk of infection reactivation: gastrectomy, uncontrolled diabetes mellitus, Hodgkin’s disease, leukemia, silicosis, acquired immunodeficiency syndrome, treatment with corticosteroids or immunosuppressants, and advanced age.
Transmission is by droplet nuclei produced when infected persons cough or sneeze. Persons with a cavitary lesion are particularly infectious because their sputum usually contains 1 to 100 million bacilli per milliliter. If an inhaled tubercle bacillus settles in an alveolus, infection occurs, with alveolocapillary dilation and endothelial cell swelling. Alveolitis results, with replication of tubercle bacilli and influx of polymorphonuclear leukocytes. These organisms spread through the lymph system to the circulatory system and then through the body.
Cell-mediated immunity to the mycobacteria, which develops 3 to 6 weeks later, usually contains the infection and arrests the disease. If the infection reactivates, the body’s response characteristically leads to caseation — the conversion of necrotic tissue to a cheeselike material. The caseum may localize, undergo fibrosis, or excavate and form cavities, the walls of which are studded with multiplying tubercle bacilli. If this happens, infected caseous debris may spread throughout the lungs by the tracheobronchial tree. Sites of extrapulmonary TB include the pleurae, meninges, joints, lymph nodes, peritoneum, genitourinary tract, and bowel.
The incidence of TB has been increasing in the United States secondary to homelessness, drug abuse, and human immunodeficiency virus infection. Globally, TB is the leading infectious cause of morbidity and mortality, generating 8 to 10 million new cases each year.
Signs and symptoms
After an incubation period of 4 to 8 weeks, TB is usually asymptomatic in primary infection but may produce nonspecific symptoms, such as fatigue, weakness, anorexia, weight loss, night sweats, and low-grade fever.
ELDER TIP Fever and night sweats, the typical hallmarks of TB, may not be present in elderly patients, who instead may exhibit a change in activity or weight. Assess older patients carefully.
In reactivation, symptoms may include a cough that produces mucopurulent sputum, occasional hemoptysis, and chest pains.
Diagnosis
CONFIRMING DIAGNOSIS Diagnostic tests include chest X-rays, a tuberculin skin test, and sputum smears and cultures to identify M. tuberculosis. The diagnosis must be precise because several other diseases (such as lung cancer, lung abscess, pneumoconiosis, and bronchiectasis) may mimic TB.
These procedures aid in diagnosis:
❑ Auscultation detects crepitant crackles, bronchial breath sounds, wheezing, and whispered pectoriloquy.
❑ Chest percussion detects dullness over the affected area, indicating consolidation or pleural fluid.
❑ Chest X-ray shows nodular lesions, patchy infiltrates (mainly in upper lobes), cavity formation, scar tissue, and calcium deposits; however, it may not be able to distinguish active from inactive TB.
❑ Tuberculin skin test detects TB infection. Intermediate-strength purified protein derivative or 5 tuberculin units (0.1 ml) are injected intracutaneously on the forearm. The test results are read in 48 to 72 hours; a positive reaction (induration of 5 to 15 mm or more, depending on risk factors) develops 2 to 10 weeks after infection in active and inactive TB. However, severely immunosuppressed patients may never develop a positive reaction.
CONFIRMING DIAGNOSIS Stains and cultures (of sputum, cerebrospinal fluid, urine, drainage from abscess, or pleural fluid) show heat-sensitive, nonmotile, aerobic, acid-fast bacilli.
Treatment
First-line agents for the treatment of TB are isoniazid (INH), rifampin (RIF), ethambutol (EMB), and pyrazinamide. Latent TB is usually treated with daily INH for 9 months. RIF daily for 4 months may be used for people with latent TB whose contacts are INH resistant. For most adults with active TB, the recommended dosing includes the administration of all four drugs daily for 2 months, followed by 4 months of INH and RIF. Drug therapy must be selected according to patient condition and organism susceptibility. Another first-line drug used for TB is rifapentine. Second-line agents, such as cycloserine, ethionamide, p-Aminosalicylic acid, streptomycin, and capreomycin, are reserved for special circumstances or drug-resistant strains. Interruption of drug therapy may require initiation of therapy from the beginning of the regimen or additional treatment.
Directly observed therapy (DOT) may be selected or required. In this therapy, an assigned caregiver directly observes the administration of the drug. The goal of DOT is to monitor the treatment regimen and reduce the development of resistant organisms.
Special considerations
❑ Initiate acid-fast bacillus (AFB) isolation precautions immediately for all patients suspected or confirmed to have TB. AFB isolation precautions include the use of a private room with negative pressure in relation to surrounding areas and a minimum of six air exchanges per hour (air exhausted should be exhausted directly to the outside).
❑ Continue AFB isolation until there’s clinical evidence of reduced infectiousness (substantially decreased cough, fewer organisms on sequential sputum smears).
❑ Teach the infectious patient to cough and sneeze into tissues and to dispose of all secretions properly. Place a covered trash can nearby or tape a lined bag to the side of the bed to dispose of used tissues.
❑ Instruct the patient to wear a mask when outside his room.
❑ Visitors and staff members should wear particulate respirators that fit closely around the face when they’re in the patient’s room.
❑ Remind the patient to get plenty of rest. Stress the importance of eating balanced meals to promote recovery. If the patient is anorexic, urge him to eat small meals frequently. Record weight weekly.
❑ Be alert for adverse effects of medications. Because INH sometimes leads to hepatitis or peripheral neuritis, monitor aspartate aminotransferase and alanine aminotransferase levels. To prevent or treat peripheral neuritis, give pyridoxine (vitamin B6), as ordered. If the patient receives EMB, watch for optic neuritis; if it develops, discontinue the drug. If he receives RIF, watch for hepatitis and purpura. Observe the patient for other complications such as hemoptysis.
❑ Before discharge, advise the patient to watch for adverse effects from the medication and report them immediately. Emphasize the importance of regular follow-up examinations. Instruct the patient and his family concerning the signs and symptoms of recurring TB. Stress the need to follow long-term treatment faithfully.
❑ Advise staff members and other persons who have been exposed to infected patients to receive tuberculin tests; chest X-rays and prophylactic INH may also be ordered.
❑ Emphasize to the patient the importance of taking the medications daily as prescribed. He may enroll in a supervised administration program to avoid the development of drug-resistant organisms.
Book Source Details
- Book Title: Professional Guide to Diseases (Eighth Edition)
- Author(s): Springhouse
- Year of Publication: 2005
- Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2005 Lippincott Williams & Wilkins.
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