eMedicine Specialties > Pediatrics: General Medicine > Infectious Disease
Tuberculosis
Updated: Oct 30, 2008
Introduction
Background
Tuberculosis (TB) is the most common cause of infection-related death worldwide. In 1993, the World Health Organization (WHO) declared tuberculosis to be a global public health emergency. Mycobacterium tuberculosis is the most common cause of tuberculosis. Other rare causes include Mycobacterium bovis and Mycobacterium africanum. Tubercle bacilli belong to the family Mycobacteriaceae and order Actinomycetales. The acid-fast characteristic of the mycobacteria is their unique feature. M tuberculosis is an aerobic, non–spore-forming, nonmotile, slow-growing bacillus with a curved and beaded rod-shaped morphology. It is a very hardy bacillus that can survive under adverse environmental conditions. Humans are the only known reservoirs for M tuberculosis.
Pathophysiology
Tuberculosis occurs when individuals inhale bacteria aerosolized by infected persons. The organism is slow growing and tolerates the intracellular environment, where it may remain metabolically inert for years before reactivation and disease. The main determinant of the pathogenicity of tuberculosis is its ability to escape host defense mechanisms, including macrophages and delayed hypersensitivity responses.
Among the several virulence factors in the mycobacterial cell wall are the cord factor, lipoarabinomannan (LAM), and a highly immunogenic 65-kd M tuberculosis heat shock protein. Cord factor is a surface glycolipid present only in virulent strains that causes M tuberculosis to grow in serpentine cords in vitro. LAM is a heteropolysaccharide that inhibits macrophage activation by interferon-gamma and induces macrophages to secrete tumor necrosis factor-alpha, which causes fever, weight loss, and tissue damage.
The infective droplet nucleus is very small, measuring 5 micrometers or less, and may contain approximately 1-10 bacilli. Although a single organism may cause disease, 5-200 inhaled bacilli are usually necessary for infection. The small size of the droplets allows them to remain suspended in the air for a prolonged period of time. Primary infection of the respiratory tract occurs as a result of inhalation of these aerosols. The risk of infection is increased in small enclosed areas and in areas with poor ventilation. Upon inhalation, the bacilli are deposited (usually in the midlung zone) into the distal respiratory bronchiole or alveoli, which are subpleural in location. Subsequently, the alveolar macrophages phagocytose the inhaled bacilli. However, these naïve macrophages are unable to kill the mycobacteria, and the bacilli continue to multiply unimpeded.
Thereafter, transportation of the infected macrophages to the regional lymph nodes occurs. Lymphohematogenous dissemination of the mycobacteria to other lymph nodes, the kidney, epiphyses of long bones, vertebral bodies, juxtaependymal meninges adjacent to the subarachnoid space, and, occasionally, to the apical posterior areas of the lungs. In addition, chemotactic factors released by the macrophages attract circulating monocytes to the site of infection, leading to differentiation of the monocytes into macrophages and ingestion of free bacilli. Logarithmic multiplication of the mycobacteria occurs within the macrophage at the primary site of infection.
A cell-mediated immune (CMI) response terminates the unimpeded growth of the M tuberculosis 2-3 weeks after initial infection. CD4 helper T cells activate the macrophages to kill the intracellular bacteria with resultant epithelioid granuloma formation. CD8 suppressor T cells lyse the macrophages infected with the mycobacteria, resulting in the formation of caseating granulomas. Mycobacteria cannot continue to grow in the acidic extracellular environment, so most infections are controlled. The only evidence of infection is a positive tuberculin skin test (TST) result. However, the initial pulmonary site of infection and its adjacent lymph nodes (ie, primary complex or Ghon focus) sometimes reach sufficient size to develop necrosis and subsequent radiographic calcification.
Most persons infected with M tuberculosis do not develop active disease. In healthy individuals, the lifetime risk of developing disease is 5-10%. In certain instances, such as extremes of age or defects in CMI (eg, human immunodeficiency virus [HIV] infection, malnutrition, administration of chemotherapy, prolonged steroid use), tuberculosis may develop. For patients with HIV infection, the risk of developing tuberculosis is 7-10% per year.
Progression of the primary complex may lead to enlargement of hilar and mediastinal nodes with resultant bronchial collapse. Progressive primary tuberculosis may develop when the primary focus cavitates and organisms spread through contiguous bronchi. Lymphohematogenous dissemination, especially in young patients, may lead to miliary tuberculosis when caseous material reaches the bloodstream from a primary focus or a caseating metastatic focus in the wall of a pulmonary vein (Weigert focus). Tubercular meningitis may also result from hematogenous dissemination. Bacilli may remain dormant in the apical posterior areas of the lung for several months or years, with later progression of disease resulting in the development of reactivation-type tuberculosis (ie, endogenous re-infection tuberculosis).
Frequency
United States
Approximately 15 million people are infected with M tuberculosis in the United States. The number of tuberculosis cases reported annually in the United States dropped 74% between 1953 and 1985 (84,304 to 22,201). Subsequently, resurgence in the number of tuberculosis cases was reported, with a peak of 26,673 cases in 1992. Although the incidence increased by approximately 13% in all ages from 1985-1994, the rate among children younger than 15 years increased by 33%. This resurgence was attributed to the HIV epidemic, which increased the risk of developing active tuberculosis among persons with HIV and latent tuberculosis infection. Other contributory factors included emigration from developing countries and transmission in settings such as endemic hospitals and prisons.
Development of multidrug-resistant (MDR) organisms and deterioration of the public health infrastructure for TB services further contributed to the rise in the number of cases.
The incidence of tuberculosis in the United States decreased 44% from 1993-2003, with the lowest number of cases reported in 2003 (14,874). The decline in case numbers since 1992 has been attributed to increased awareness of the disease, the institution of more aggressive preventive measures, improvement in health care strategies (eg, prompt identification and treatment of patients with tuberculosis), and highly active antiretroviral therapy for individuals with HIV. Although the case rate has declined since 1992, a huge reservoir of individuals who are infected with M tuberculosis remains.
According to the Centers for Disease Control and Prevention (CDC), a total of 13,767 new cases were reported in the United States in 2006.1 This represents a rate of 4.6 cases per 100,000 population, and the incidence of tuberculosis in 2006 is the lowest since 1953. However, the rate of the decline has slowed since 2000.1,2 This is influenced by the rate of tuberculosis of foreign origin; incidence of tuberculosis of foreign origin increased 5% from 1993-2004, whereas the rate of US-born individuals declined 62% over the same period.International
According to the WHO, more than 8 million new cases of tuberculosis occur each year. Currently, 19-43.5% of the world's population is infected with M tuberculosis.3 Tuberculosis occurs disproportionately among disadvantaged populations, such as homeless individuals, malnourished individuals, and those living in crowded areas. According to the WHO, developing countries including India, China, Pakistan, Philippines, Thailand, Indonesia, Bangladesh, and the Democratic Republic of Congo account for nearly 75% of all cases of tuberculosis.
Mortality/Morbidity
The mortality rate from tuberculosis in the United States is currently 0.6 deaths per 100,000 individuals, which represents approximately 1,700 deaths per year and an annual mortality rate of approximately 7% per newly identified case. In 1953, the mortality rate was 12.5 deaths per 100,000 individuals. This decrease in mortality is attributed to improved health care and prompt initiation of therapy. MDR-tuberculosis cases have a reported fatality rate of greater than 70%. Worldwide, deaths due to tuberculosis are estimated to be 3 million per year.
Race
According to the CDC, rates of tuberculosis are 10 times higher among Asians and Pacific Islanders, 8 times higher among non-Hispanic blacks, and 5 times higher among Hispanics, Native Americans, and Native Alaskans compared to non-Hispanic whites. However, race may not be an independent risk factor, and risk is best defined on the basis of social, economic, and medical factors as well.
Sex
TB equally affects females and males.
Age
An increased risk of mortality from tuberculosis is noted at the extremes of age.
Clinical
History
- Staging: Although the natural history of tuberculosis (TB) in children follows a continuum, the American Thoracic Society (ATS) definition of stages is useful:4,5,6,7,8
- Stage 1: Exposure has occurred, implying that the child has had recent contact with an adult who has contagious tuberculosis. The child has no physical signs or symptoms and has a negative tuberculin skin test (TST) result. The chest radiography does not reveal any changes at this stage. Not all patients who are exposed become infected, the TST result may not be positive for 3 months. Unfortunately, children younger than 5 years may develop disseminated tuberculosis in the form of miliary disease or tubercular meningitis before the TST result becomes positive. Thus, a very high index of suspicion is required when a young patient has a history of contact.
- Stage 2: This stage is heralded by a positive TST result. No signs and symptoms occur, although an incidental chest radiography may reveal the primary complex.
- Stage 3: Tuberculous disease occurs and is characterized by the appearance of signs and symptoms depending on the location of the disease. Radiographic abnormalities may also be seen.
- Stage 4: This stage is defined as tuberculosis with no current disease. This implies that the patient has a history of previous episodes of tuberculosis or abnormal, stable radiographic findings with a significant reaction to the TST and negative bacteriologic studies. No clinical findings suggesting current disease are present.
- Stage 5: Tuberculosis is suspected, and the diagnosis is pending.
- Asymptomatic infection: Patients with asymptomatic infection have a positive TST result but do not have any clinical or radiographic manifestations. Children with asymptomatic infection may be identified on a routine well-child physical examination, or they may be identified subsequent to tuberculosis diagnosis in household or other contacts (eg, children who recently have immigrated, adopted children).
- Disease evaluation: Any patient with pneumonia, pleural effusion, or a cavitary or mass lesion in the lung that does not improve with standard antibacterial therapy should be evaluated for tuberculosis. Also, patients with fever of unknown origin, failure to thrive, significant weight loss, or unexplained lymphadenopathy should be evaluated for tuberculosis.
- Pulmonary tuberculosis may manifest itself in several forms, including endobronchial tuberculosis with focal lymphadenopathy, progressive pulmonary disease, pleural involvement, and reactivated pulmonary disease. Symptoms of primary pulmonary disease in the pediatric population are often meager. Fever, night sweats, anorexia, nonproductive cough, failure to thrive, and difficulty gaining weight may occur.
- Endobronchial tuberculosis with enlargement of lymph nodes: This is the most common variety of pulmonary tuberculosis. Symptoms are the result of impingement on various structures by the enlarged lymph nodes. Persistent cough may be indicative of bronchial obstruction, whereas difficulty swallowing may result from esophageal compression. Vocal cord paralysis may be suggested by hoarseness or difficulty breathing.
- Tubercular pleural effusion: Pleural effusions due to tuberculosis usually occur in older children and are rarely associated with miliary disease. Typical history reveals an acute onset of fever, chest pain that increases in intensity on deep inspiration, and shortness of breath. Fever usually persists for 14-21 days.
- Progressive primary tuberculosis: Progression of the pulmonary parenchymal component leads to enlargement of the caseous area and may lead to pneumonia, atelectasis, and air trapping. This is more likely to occur in young children than in adolescents. The child usually appears ill with symptoms of fever, cough, malaise, and weight loss.
- Reactivation tuberculosis: This condition usually has a subacute presentation with weight loss, fever, cough, and, rarely, hemoptysis. Reactivation tuberculosis typically occurs in older children and adolescents. The condition is more common in patients who acquire tuberculosis when aged 7 years and older.
- Extrapulmonary tuberculosis includes peripheral lymphadenopathy, tubercular meningitis, miliary tuberculosis, skeletal tuberculosis, and other organ involvement.
- Lymphadenopathy: Patients with lymphadenopathy (ie, scrofula) may have a history of enlarged nodes. Fever, weight loss, fatigue, and malaise are usually absent or minimal. Lymph node involvement typically occurs 6-9 months following initial infection by the tubercle bacilli. More superficial lymph nodes commonly are involved. Frequent sites of involvement include the anterior cervical, submandibular, and supraclavicular nodes. Tuberculosis of the skeletal system may lead to involvement of the inguinal, epitrochlear, or axillary lymph nodes.
- Tubercular meningitis: One of the most severe complications of tuberculosis is tubercular meningitis. Tubercular meningitis develops in 5-10% of children younger than 2 years; thereafter, the frequency drops to less than 1%. A very high index of suspicion is required to make a timely diagnosis because of the insidious onset of the disease. A subacute presentation usually occurs within 3-6 months after the initial infection. Nonspecific symptoms such as anorexia, weight loss, and fever may be present. After 1-2 weeks, patients may experience vomiting and seizures or alteration in the sensorium. Deterioration of mental status, coma, and death may occur despite prompt diagnosis and early intervention.
- Miliary tuberculosis: This is a complication of primary tuberculosis in young children. It may manifest subacutely with low-grade fever, malaise, weight loss, and fatigue. A rapid onset of fever and associated symptoms may also be observed. History of cough and respiratory distress may be obtained.
- Bone or joint tuberculosis: This may present acutely or subacutely. Vertebral tuberculosis may go unrecognized for months to years because of its indolent nature.
- Additional sites: Other unusual sites for tuberculosis include the middle ear, GI tract, skin, kidneys, and ocular structures.
- Congenital tuberculosis is rare. Symptoms typically develop during the second or third week of life and include poor feeding, poor weight gain, cough, lethargy, and irritability. Other symptoms include fever, ear discharge, and skin lesions. To make a diagnosis of congenital tuberculosis, the infant should have proven tuberculosis lesions and at least one of the following:
- Skin lesions during the first week of life, including papular lesions or petechiae
- Documentation of tuberculosis infection of the placenta or the maternal genital tract
- Presence of a primary complex in the liver
- Exclusion of the possibility of postnatal transmission
- Pulmonary tuberculosis may manifest itself in several forms, including endobronchial tuberculosis with focal lymphadenopathy, progressive pulmonary disease, pleural involvement, and reactivated pulmonary disease. Symptoms of primary pulmonary disease in the pediatric population are often meager. Fever, night sweats, anorexia, nonproductive cough, failure to thrive, and difficulty gaining weight may occur.
Physical
- Primary tuberculosis is characterized by the absence of any signs on clinical evaluation. These patients are identified by a positive TST result. Tuberculin hypersensitivity may be associated with erythema nodosum and phlyctenular conjunctivitis.
- Signs of disease depend on the site involved (pulmonary or extrapulmonary).
- Pulmonary disease may manifest itself in several forms, including endobronchial tuberculosis with focal lymphadenopathy, progressive pulmonary disease, pleural involvement, and reactivated pulmonary disease.
- Endobronchial disease: Enlargement of lymph nodes may result in signs suggestive of bronchial obstruction or hemidiaphragmatic paralysis. Vocal cord paralysis may occur as a result of local nerve compression. Dysphagia due to esophageal compression also may be observed.
- Progressive primary pulmonary tuberculosis: This condition presents with classic signs of pneumonia, including tachypnea, nasal flaring, grunting, dullness to percussion, egophony, decreased breath sounds, and crackles.
- Pleural effusion: Signs include tachypnea, respiratory distress, dullness to percussion, decreased breath sounds, and, occasionally, features of mediastinal shift.
- Reactivation tuberculosis: Physical examination results may be normal or may reveal posttussive crackles.
- Manifestations of extrapulmonary tuberculosis include peripheral lymphadenopathy, tubercular meningitis, miliary tuberculosis, skeletal tuberculosis, and other organ involvement.
- Lymphadenopathy: This usually involves the anterior or posterior cervical and supraclavicular nodes. Less-commonly involved lymph nodes include: submandibular, submental, axillary, and inguinal lymph nodes. Typically, infected lymph nodes are firm and nontender with nonerythematous overlying skin. The nodes are initially nonfluctuant. Suppuration and spontaneous drainage of the lymph nodes may occur with caseation and the development of necrosis.
- Tubercular meningitis: Three stages of tubercular meningitis have been identified.
- Stage 1: No focal or generalized neurologic signs are present. Possibly, only nonspecific behavioral abnormalities are found.
- Stage 2: This stage is characterized by the presence of nuchal rigidity, altered deep tendon reflexes, lethargy, and/or cranial nerve palsies. Tubercular meningitis most often affects the sixth cranial nerve, resulting in lateral rectus palsy. This is due to the pressure of the thick basilar inflammatory exudates on the cranial nerves or to hydrocephalus. The third, fourth, and seventh cranial nerves may also be affected. Funduscopic changes may include papilledema and the presence of choroid tubercles, which should be carefully sought.
- Stage 3: This final stage comprises major neurologic defects, including coma, seizures, and abnormal movements (eg, choreoathetosis, paresis, paralysis of one or more extremities). In the terminal phase, decerebrate or decorticate posturing, opisthotonus, and/or death may occur. Patients with tuberculomas or tubercular brain abscesses may present with focal neurologic signs. Spinal cord disease may result in the acute development of spinal block or a transverse myelitis–like syndrome. A slowly ascending paralysis may develop over several months to years.
- Miliary tuberculosis: Physical examination includes lymphadenopathy, hepatosplenomegaly, and systemic signs including fever. Respiratory signs may evolve to include tachypnea, cyanosis, and respiratory distress. Other signs, which are subtle and should be carefully sought in the physical examination, include papular, necrotic, or purpuric lesions on the skin or choroidal tubercles in the retina.
- Bone tuberculosis: Common sites involved include the large weightbearing bones or joints, including the vertebrae (50%), hip (15%), and knee (15%). Destruction of the bones with deformity is a late sign of tuberculosis. Manifestations may include angulation of the spine (gibbus deformity) and/or Pott disease (severe kyphosis with destruction of the vertebral bodies). Cervical spine involvement may result in atlantoaxial subluxation, which may lead to paraplegia or quadriplegia.
- Signs of congenital tuberculosis include failure to thrive, icterus, hepatosplenomegaly, tachypnea, and lymphadenopathy.
Causes
Risk factors for the acquisition of tuberculosis are usually exogenous to the patient. Thus, likelihood of being infected depends on the environment and the features of the index case. However, the development of tuberculosis disease depends on inherent immunologic status of the host.
- Infection
- The number of bacilli in the inoculum and the relative virulence of the organism are the major factors determining transmission of the disease. Tuberculosis is transmitted by inhaling the tubercle bacilli.
- The infectiousness of the source case is of vital importance in determining likelihood of transmission. Bacillary population of tuberculosis lesions varies and depends on the morphology of the lesion. Nodular lesions have 100-10,000 organisms, whereas cavitary lesions have 10 million to 1 billion bacilli. Thus, persons with cavitary lesions are highly infectious. Also, contacts of persons with sputum-positive smears have an increased prevalence of infection as opposed to contacts of those with sputum-negative smears.
- Persons who have received antituberculosis drugs are much less infectious than those who have not received any treatment. This decline in infectiousness is due primarily to reduction in the bacillary population in the lungs.
- Environmental factors also contribute to the likelihood of acquiring the infection. The concentration of bacilli depends on the ventilation of the surroundings and exposure to ultraviolet light. Thus, overcrowding, congregation in prison settings, poor housing, and inadequate ventilation predispose individuals to the development of tuberculosis.
- Disease
- Defects in cell-mediated immunity and level of immunocompetence are major determinants for development of disease.
- HIV infection is one of the most significant risk factors for tuberculosis infection. Case rates for persons who are dually infected with HIV and M tuberculosis exceed the lifetime risk of persons with tuberculosis infection who are not infected with HIV.
- Steroid therapy, cancer chemotherapy, and hematologic malignancies increase the risk of tuberculosis.
- Malnutrition interferes with the cell-mediated immune (CMI) response and therefore accounts for much of the increased frequency of tuberculosis in impoverished patients.
- Nontuberculosis infections, such as measles, varicella, and pertussis, may activate quiescent tuberculosis.
- Individuals with certain human leukocyte antigen (HLA) types have a predisposition to tuberculosis. Hereditary factors, including the presence of a Bcg gene, have been implicated in susceptibility to acquisition of tuberculosis.
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Further Reading
Keywords
tuberculosis, TB, consumption, mycobacterial infection, Mycobacterium tuberculosis, M tuberculosis, primary tuberculosis, primary TB, miliary tuberculosis, miliary TB, tubercular meningitis, multidrug-resistant tuberculosis, MDR-TB, multidrug-resistant TB, pulmonary tuberculosis, pulmonary TB, endobronchial tuberculosis, endobronchial TB, reactivation tuberculosis, reactivation TB, extrapulmonary tuberculosis, extrapulmonary TB, lymphadenopathy, scrofula, vertebral tuberculosis, vertebral TB, bone tuberculosis, bone TB, joint tuberculosis, joint TB, congenital tuberculosis, congenital TB, skeletal tuberculosis, skeletal TB, Pott disease, tuberculous spondylitis, human immunodeficiency virus, HIV, pneumonia, pleural effusion, fever of unknown origin, failure to thrive, atelectasis, respiratory distress, measles, varicella, pertussis
