Tuberculosis
Tuberculosis: Excerpt from Handbook of Diseases
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 living in crowded, poorly ventilated conditions 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
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 killing it or walling it up in a tiny nodule (tubercle). However, the bacillus may lie dormant within the tubercle for years and later reactivate and spread. Those at higher risk for disease progression or reactivation of dormant disease include infants, the elderly, and individuals who are immunocompromised (such as those with acquired immunodeficiency syndrome [AIDS], those undergoing chemotherapy, or transplant recipients taking antirejection medications).
A person’s risk of contracting TB increases if he has frequent contact with people who have the disease, if he lives in crowded or unsanitary living conditions, or if he has poor nutrition. There has been an increase of incidence of TB in the United States due to the increase of human immunodeficiency virus infection, the increasing number of homeless individuals (poor environment and poor nutrition), and the appearance of drug-resistant strains of TB.
Reactivation risk factors
Although the lungs are the primary infection site, mycobacteria commonly exist in other parts of the body. A number of factors increase the risk of infection reactivation: gastrectomy, uncontrolled diabetes mellitus, Hodgkin’s disease, leukemia, silicosis, AIDS, and treatment with corticosteroids or immunosuppressants.
Mode of transmission
TB is transmitted by droplet nuclei produced when infected persons cough or sneeze. After inhalation, if a tubercle bacillus settles in an alveolus, infection occurs. Cell-mediated immunity to the mycobacteria, which develops about 3 to 6 weeks later, usually contains the infection and arrests the disease.
Response to reactivation
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 pleura, meninges, joints, lymph nodes, peritoneum, genitourinary tract, and bowel.
Signs and symptoms
❑ In primary infection, after an incubation period of 4 to 8 weeks, TB is usually asymptomatic but may produce nonspecific symptoms, such as fatigue, weakness, anorexia, weight loss, night sweats, and low-grade fever.
❑ In reactivation, symptoms may include a cough that produces mucopurulent sputum, occasional hemoptysis, and chest pains.
Diagnosis
Diagnostic tests include chest X-rays, a tuberculin skin test, and sputum smears and cultures to identify M. tuberculosis. The following procedures aid diagnosis:
❑ Auscultation detects crepitant rales, bronchial breath sounds, wheezes, and whispered pectoriloquy.
❑ Chest percussion detects a 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.
❑ Stains and cultures (of sputum, cerebrospinal fluid, urine, drainage from abscess, or pleural fluid) show heat-sensitive, nonmotile, aerobic, acid-fast bacilli.
UNDER STUDY: Newer testing uses deoxyribonucleic acid probes to confirm disease in days rather than weeks. A novel heminested IS6110 polymerase chain reaction assay shows promise as a rapid and sensitive method for early diagnosis of pediatric TB.
Treatment
Treatment includes antitubercular therapy with daily oral doses of isoniazid, rifampin, and pyrazinamide (and sometimes ethambutol) for at least 6 months. Longer courses may be required for patients with AIDS or for patients who respond slowly. After 2 to 4 weeks, the disease generally is no longer infectious. The patient can resume his normal lifestyle while taking medication.
Patients with atypical mycobacterial disease or drug-resistant TB may require treatment with second-line drugs, such as capreomycin, streptomycin, para-aminosalicylic acid, cycloserine, amikacin, and quinolone drugs.
Special considerations
❑ Isolate the infectious patient in a quiet, well-ventilated room until he’s no longer contagious.
❑ Teach the patient to cough and sneeze into tissues and to dispose of all secretions properly. Place a covered trash can nearby or tape a waxed bag to the side of the bed for used tissues.
❑ Instruct the patient to wear a mask when outside his room. Visitors and hospital personnel should wear masks when they’re in the patient’s room.
❑ Remind the patient to get plenty of rest and to eat balanced meals. If the patient is anorexic, urge him to eat small meals throughout the day. Record weight weekly.
❑ Be alert for adverse effects of medications. Because isoniazid sometimes leads to hepatitis or peripheral neuritis, monitor aspartate aminotransferase and alanine aminotransferase levels. To prevent or treat peripheral neuritis, give pyridoxine (vitamin B6).
CLINICAL TIP: If the patient receives ethambutol, watch for optic neuritis; if it develops, discontinue the drug. If he receives rifampin, watch for hepatitis and purpura. Also observe the patient for other complications such as hemoptysis.
❑ Emphasize the importance of regular follow-up examinations, and instruct the patient and his family concerning the signs and symptoms of recurring TB.
❑ Advise persons who have been exposed to infected patients to receive tuberculin tests and, if necessary, chest X-rays and prophylactic isoniazid.
Book Source Details
- Book Title: Handbook of Diseases
- Author(s): Springhouse
- Year of Publication: 2003
- Copyright Details: Handbook of Diseases, Copyright © 2003 Lippincott Williams & Wilkins.
More About Arachnoiditis
More Medical Textbooks Online about Arachnoiditis
Review other book chapters online related to Arachnoiditis:
Medical Books Excerpts
- Meningitis
- "Professional Guide to Diseases (Eighth Edition)" (2005)
- [ read ]
- Kernig's sign
- "Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series" (2007)
- [ read ]
Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
|
|
More About This Book:
Title: Handbook of Diseases
Authors: Springhouse
Publisher: Lippincott Williams & Wilkins
Copyright: 2003
ISBN: 1-58255-266-5
|
|
» Next page: Encephalitis (Handbook of Diseases)
Rate This Website
What do you think about the features of this website?
Take our user survey and have your say:
Website User Survey
Medical Tools & Articles:
Next articles:
Tools & Services:
Medical Articles:
Forums & Message Boards
- Ask or answer a question at the Boards:
