TB

Primary Pulmonary Tuberculosis

• Parenchyma     

§       Upper lobes affected slightly more than lower

§       Alveolar infiltrate

§       Cavitation is rare

§       Lobar pneumonia is almost always associated with lymphadenopathy—therefore, lobar pneumonia associated with hilar or mediastinal adenopathy at any age should strongly suggest TB

• Lymph node

§       Mostly unilateral hilar and/or paratracheal, usually  right sided, rarely bilateral Differentiates primary from postprimary TB—it does not occur in postprimaryTB
Much more common in children

·       Airway

·       Atelectasis classically affects the anterior segments of the upper lobes or the medial segment of the RML

·       Pleura

§       Pleural effusion as a manifestation of primary TB occurs more often in adults than children

§       With appropriate treatment, it carries the best prognosis of all patterns of TB and is the least likely to develop complications

§       The fluid accumulates slowly and painlessly—therefore, patients with TB are seldom seen with a small amount of pleural fluid

§       Parenchymal disease will almost never be present with a pleural effusion although lymphadenopathy may

§       Apical pleural scarring is rarely tuberculous in origin

• Calcification in the primary complex is relatively rare.

• Very few patients with primary TB have clinical manifestations

Postprimary Tuberculosis  (“Reactivation TB”)

• Most cases in adults occur as reactivation of a primary focus of infection acquired in childhood

• Limited mainly to the apical and posterior segments of the upper lobes and the superior segments of the lower lobe

• Caseous necrosis and the tubercle (accumulations of mononuclear macrophages, Langerhan's giant cells surrounded by lymphocytes and fibroblasts) are the pathologic hallmarks of postprimary TB

• Healing occurs with fibrosis and contraction; calcification is rarer than in    primary

Patterns of distribution

§       Almost always affect the apical or posterior segments of the upper lobes or the superior segments of the lower lobes—bilateral upper lobe disease is very common

§       May present as pneumonia

§       Cavitation may result: the cavity is usually thin-walled, smooth on the inner margin with no air-fluid level

§       Transbronchial spread may occur—from one upper lobe to opposite lower or to another lobe

§       Miliary spread (below)

§       Bronchiectasis—usually asymptomatic

§       Bronchostenosis due to fibrosis and stricture: fibrosis may cause distortion of a bronchus and atelectasis many years after the initial      infection—“middle lobe syndrome”

§       Solitary pulmonary nodule—the tuberculoma—may occur in either primary or postprimary disease; round or oval lesions with small, discrete shadows in the immediate vicinity of the lesion—the “satellite” lesion

• Formation of a pleural effusion in postprimary TB almost always means direct spread of the disease into the pleural cavity and should be regarded as an empyema—this carries a graver prognosis than the pleural effusion of the primary form

• Direct extension into the ribs or sternoclavicular joints is uncommon

Miliary Tuberculosis

• Older men, Blacks and pregnant women are susceptible

• Onset is insidious

• Fever, chills, night sweats are common

• Takes weeks between the time of dissemination and the radiographic appearance of disease

• Considered to be a manifestation of primary TB–although clinical appearance of miliary TB may not occur for many years after initial infection

• When first visible, they measure about 1 mm in size; they can grow to 2-3mm if left untreated

• When treated, clearing is rapid—miliary TB seldom, if ever, produces calcification

TB and Other Diseases

• There is an association between TB and silicosis, TB and HIV

• There may be an association between TB and sarcoid

• There is no association between TB and bronchogenic carcinoma

HIV and TB

• No matter what form of TB the patient has, it tends to look like 1° TB

• Hilar and mediastinal adenopathy are common

• Cavitation is less common

• There is no predilection for the apices

• MAI (mycobacterium avium-intracellulare) is more common in HIV than TB

http://www.learningradiology.com
 

Minor infection with no symptoms - occurs in most cases
Most people in good health who breathe in TB bacteria do not develop active TB disease. The bacteria that are inhaled begin to multiply in the lung. This stimulates your immune system to activate. The TB bacteria are killed or made inactive by the immune system (white blood cells etc). There may be mild or no symptoms, and the infection is halted.

This is the end of the matter for most infected people. You are usually not aware if you have had this mild infection. A small scar on the lung may be seen on a chest X-ray. This shows that a 'battle' had occurred between the TB bacteria and the immune system.

Infection progressing into active disease
Active TB disease with symptoms occurs in about 1 in 20 people who breathe in some TB bacteria. In these people the immune system does not win the battle and halt the invading bacteria. The TB bacteria multiply further and spread to other parts of the lung and body. Symptoms of active TB then develop about 6-8 weeks after first breathing in some bacteria.

TB infection which progresses to active disease can occur in anybody who is infected with TB bacteria. But, it is more likely if you are already in poor health. For example, it is common in malnourished children in developing countries.

Re-activated (secondary) infection causing active disease
Some people develop active TB months or years after a minor TB infection had been halted. The body's immune system at first stops the bacteria from multiplying (described above). However, not all the bacteria may be killed. Some bacteria may be 'walled off' in the scar tissue of the initial minor infection. They are stopped from multiplying by the immune system. They do no harm but can remain dormant (inactive) for many years. Dormant TB bacteria may start to multiply and cause active TB if the body's immune system begins to fail later in life. A failing immune system and re-activated TB is more likely to occur if you:

• are elderly or frail.
• are malnourished.
• have diabetes.
• take steroids or immunosuppressant medication.
• have kidney failure.
• are alcohol dependent ('alcoholic').
• have AIDS

Treatment principles
An effective anti-TB regimen must contain multiple drugs to which the organism is susceptible and must be continued for a sufficient period of time. The American Thoracic Society and US Centers for Diseases Control and Prevention have established guidelines for treatment of TB 

• Perform drug-susceptibility studies on all isolates of Mycobacterium tuberculosis.
• Select drugs and treatment duration on the basis of results of susceptibility studies.
• Repeat susceptibility testing whenever clinical worsening occurs or new drug resistance is suspected.
• Never add a single drug to a failing regimen.
• Isolate all patients with suspected or proven active TB until the disease is excluded or effective therapy has been initiated.
• Initiate directly observed therapy in all cases of active TB.
• Perform HIV testing in all newly diagnosed cases of active TB.
• Monitor patients for adverse drug effects and drug interactions.
• Consult a specialist early, especially in cases of multidrug-resistant (MDR) TB, pregnancy, and HIV infection.
• Promptly report all cases of confirmed active TB, as well as the patient's HIV status, to the state department of health. Department of health clinics can provide both consultative and ongoing care through a team of physicians, nurses, social workers, and outreach specialists free of charge.

In selecting an effective regimen, physicians should take into account any coexisting conditions (eg, diabetes, renal disease, hepatic disease, seizure disorder, alcoholism, substance abuse) and concurrent medication needs. In a patient with previous episodes of TB, thorough history taking regarding treatment and susceptibility-testing results is critical to the assessment of potential drug resistance. Often, initial treatment is started before findings of drug-susceptibility studies are available. Therefore, all regimens should be reviewed when these results have been obtained (2).

Oral-treatment approaches

MDR TB
MDR TB refers to M tuberculosis that is resistant to at least two drugs, usually isoniazid and rifampin. Although the incidence of MDR TB in the United States has been declining in the last 5 years, there has been an increase worldwide. In the United States, MDR TB has been noted mainly among immigrants from countries with high MDR-TB rates, HIV-infected patients, the homeless, and injecting drug users. Healthcare workers were found to be at high risk because of delays in diagnosis and inadequate respiratory isolation procedures. The most common cause of emergence of drug resistance is previous inadequate or incomplete treatment (6,7).

The principles of treatment for MDR TB are similar to those listed for susceptible organisms. Treatment regimens should contain multiple bactericidal drugs not previously used and to which the organism is sensitive. Bacteriostatic drugs can also be used (7,8). Susceptibility testing allows determination of effective regimens,

Duration of treatment for MDR TB depends on the response. In general, treatment with at least three effective drugs should be continued until the culture becomes negative, and then a regimen of at least two drugs should be continued for 12 to 24 months (2,7,8). Consultation with an experienced specialist should be considered for management of all cases of MDR TB.

An earlier report by Goble and associates (9) showed a treatment-failure rate of 44% and a TB-associated mortality rate of 22% among 171 patients with MDR TB between 1973 and 1983. Fortunately, a more recent study by Telzak and colleagues (10) reported better results, with a 96% clinical response rate among 25 HIV-negative patients between 1991 and 1994.

Evaluating response to treatment
The efficacy of a regimen is determined by the rate of bacteriologic conversion during therapy and the rate of relapse during or after completion of therapy. Patients should be closely observed during therapy and for the first 12 to 24 months after its completion

Monitoring should consist of sputum smears and cultures at biweekly or monthly intervals until cultures become negative or therapy is completed. A follow-up chest film is indicated if sputum smears remain positive after 2 months of therapy or if new symptoms develop. Chest films at regular intervals are not necessary if there is bacteriologic improvement, but one should be obtained on completion of therapy.

In treatment of drug-resistant TB, frequent follow-up with sputum studies and chest films is indicated. In the case of MDR TB, sputum smears and cultures should be checked quarterly after conversion, to monitor for relapse.

Treatment failure
A finding on acid-fast smear or culture of the sputum after 5 months of treatment is considered a treatment failure. Failure can result from prescription of an inappropriate dosage or inadequate number of drugs, patient noncompliance, malabsorption, or organism resistance (2).

Relapse
Occasionally, active TB develops within the first 2 years after successful completion of therapy. In such cases of relapse, the organism often has a susceptibility pattern that is similar to that of the initial infection. The possibility of a new infection with M tuberculosis should also be considered (2,15).

Role of surgery in active TB
In general, M tuberculosis thrives best in a high-oxygen-level environment. Surgical techniques in the early 20th century included artificial pneumothorax, plombage (ie, placing lucite balls or paraffin in pleural spaces),

and pneumoplasty to collapse the upper lobes and minimize oxygen availability. Advances in thoracic surgery led to lobar resection or pneumonectomy in some cases.

With the availability of effective drugs, surgery is rarely used today. However, in carefully selected patients with MDR TB who have a poor response or an unfavorable prognosis with use of medical therapy alone, surgical therapy has had cure rates exceeding 90% (16). Antibiotic activity should be adequate to permit healing of the bronchial stump and prevent development of bronchopleural fistulas.

TB and pregnancy
No increase in morbidity or mortality from TB has been noted during pregnancy if treatment is adequate (2,17). In the United States, pyrazinamide is not recommended for use in pregnant women; however, it has been used outside the United States for MDR TB during pregnancy. The aminoglycosides and all of the second-line anti-TB medications except para-aminosalicylic acid should be avoided during pregnancy (2,17). Breast-feeding is safe during anti-TB therapy. Consultation with a specialist in TB is strongly recommended when initiating treatment in pregnant women, especially those with MDR TB. After initial radiographic imaging, follow-up x-ray monitoring during pregnancy, with proper shielding, is recommended only if no clinical improvement is noted.

Extrapulmonary TB

Dissemination of tuberculosis outside of lungs can lead to the appearance of a number of uncommon findings with characteristic patterns:

Skeletal Tuberculosis: Tuberculous osteomyelitis involves mainly the thoracic and lumbar vertebrae (known as Pott's disease) followed by knee and hip. There is extensive necrosis and bony destruction with compressed fractures (with kyphosis) and extension to soft tissues, including psoas "cold" abscess.

Genital Tract Tuberculosis: Tuberculous salpingitis and endometritis result from dissemination of tuberculosis to the fallopian tube that leads to granulomatous salpingitis, which can drain into the endometrial cavity and cause a granulomatous endometritis with irregular menstrual bleeding and infertility. In the male, tuberculosis involves prostate and epididymis most often with non-tender induration and infertility.

Urinary Tract Tuberculosis: A "sterile pyuria" with WBC's present in urine but a negative routine bacterial culture may suggest the diagnosis of renal tuberculosis. Progressive destruction of renal parenchyma occurs if not treated. Drainage to the ureters can lead to inflammation with ureteral stricture.

CNS Tuberculosis: A meningeal pattern of spread can occur, and the cerebrospinal fluid typically shows a high protein, low glucose, and lymphocytosis. The base of the brain is often involved, so that various cranial nerve signs may be present. Rarely, a solitary granuloma, or "tuberculoma", may form and manifest with seizures.

Gastrointestinal Tuberculosis: This is uncommon today because routine pasteurization of milk has eliminated Mycobacterium bovis infections. However, M. tuberculosis organisms coughed up in sputum may be swallowed into the GI tract. The classic lesions are circumferential ulcerations with stricture of the small intestine. There is a predilection for ileocecal involvement because of the abundant lymphoid tissue and slower rate of passage of lumenal contents.

Adrenal Tuberculosis: Spread of tuberculosis to adrenals is usually bilateral, so that both adrenals are markedly enlarged. Destruction of cortex leads to Addison's disease.

Scrofula: Tuberculous lymphadenitis of the cervical nodes may produce a mass of firm, matted nodes just under the mandible. There can be chronic draining fistulous tracts to overlying skin. This complication may appear in children, and Mycobacterium scrofulaceum may be cultured.

Cardiac Tuberculosis: The pericardium is the usual site for tuberculous infection of heart. The result is a granulomatous pericarditis that can be hemorrhagic. If extensive and chronic, there can be fibrosis with calcification, leading to a constrictive pericarditis.

The incidence of extrapulmonary TB is about 10% to 14% of newly diagnosed cases of TB in non-HIV-infected patients and up to 50% in HIV-infected patients. Occurrences most commonly are pleural (26.5%), genitourinary (17.9%), miliary (10.6%), bones or joint (8.8%), central nervous system (4.7%), abdominal (3.8%), or pericardial (0.9%).

The treatment regimen for extrapulmonary TB is similar to that for pulmonary TB. In selected cases (eg, bone or joint TB, tuberculous meningitis, children with miliary TB), the recommended duration of treatment is 12 months. Use of adjunctive methods (eg, addition of corticosteroids in initial management, surgery) has proved to be beneficial in decreasing morbidity and mortality (2,20).

Recent treatment advances
Several established drugs not listed in the tables are being evaluated as possible second-line agents for TB. These include isoniazid given in high doses (16 to 20 mg/kg), clarithromycin (Biaxin), clofazimine (Lamprene), metronidazole (Flagyl, Metric 21, Protostat), and amoxicillin-clavulanate potassium (Augmentin). Use of fluoroquinolones has increased in treatment of MDR TB. Although some fluoroquinolones may be as potent as the first-line drugs, they are still considered second-line agents (2,3,8).

Studies of alternative therapies are under way, including gene therapy and immunotherapy with aerosolized interferon-gamma or Mycobacterium vaccae at initiation of treatment. The benefits of these approaches are not yet established, but such research gives hope for future development of more effective treatment strategies.

Summary
Management of active TB requires a team approach. All patients newly diagnosed with TB should be tested for HIV infection. Currently available anti-TB drug regimens are well tolerated and highly effective. Directly observed therapy has shown improved survival and decline in the rate of new cases of active TB. In suspected or proven drug-resistant TB, the regimen should be individualized in consultation with a specialist experienced in MDR TB. Primary care physicians play a pivotal role in reducing morbidity and emergence of drug resistance through early diagnosis and prompt initiation of an effective regimen under directly observed therapy.

(http://www.postgradmed.com/issues/2000/08_00/lazarus.htm)

Mass mini Tb screening result card 1976