A 17-month-old Hispanic boy presented to the emergency department with a 2-week history of cough, wheezing, fever, and weight loss. The child was born in the US and lives with his dad and uncle, both employed as migrant farm workers. He was admitted to the hospital with the diagnosis of bacterial pneumonia and asthma exacerbation. His initial chest radiograph (CXR) showed right upper and lower lobe infiltrates (Figure 186-1). He continued to have high grade fever despite intravenous antibiotics. After further history revealed that his mother recently died of tuberculosis (TB), he was immediately placed in respiratory isolation. A tuberculin skin test (TST) was positive with a 17 mm of induration, and a computed tomography (CT) of the chest showed a large lymph node compressing the trachea and the right main bronchus (Figure 186-2). Gastric aspirates for acid fast bacilli (AFB) stain and culture were obtained and he was started on anti-TB medications. The culture was positive for Mycobacterium tuberculosis. His father, sister and uncle all had a positive TST and evidence of active pulmonary TB. They were referred expeditiously for evaluation and treatment.
FIGURE 186-2
Compression of the trachea and right main stem bronchus due to an enlarged and necrotic lymph node on chest CT of the boy in Figure 186-1 with primary pulmonary tuberculosis. (Used with permission from Nazha Abughali, MD.)
Despite the significant decrease in TB rates in the US and other developed countries, tuberculosis continues to be a major cause of morbidity in developing countries. It is estimated that one third of the world’s population is currently infected with TB, with 90 percent occurring in developing countries. Diagnosis of TB in children can be very challenging due to its non-specific clinical presentation and its paucibacillary nature coupled with the decrease in TB expertise among practitioners in developed countries. Without timely diagnosis and prompt institution of appropriate antituberculous therapy, TB in children can be associated with significant morbidity as well as mortality.
Worldwide, around 9 million new cases of tuberculosis and approximately 1.5 million deaths are annually reported by the world health organization (WHO), with an estimated 500,000 cases and 64,000 deaths occurring among children <15 years of age.1
In spite of the steady decrease in TB rates in the US among adults and children, tuberculosis continues to occur especially among certain ethnic and racial groups as well as among foreign-born individuals.
Currently, more than 60 percent of the total TB cases occur among the foreign born persons in the US.2
In children, specific groups with greater TB infection and disease rates include immigrants, international adoptees, and refugees from or travelers to high-prevalence regions.
Tuberculosis is caused by aerobic, fastidious, acid fast bacilli belonging to the M. tuberculosis complex group, which is composed of multiple species.
The most important species include Mycobacterium tuberculosis (M.tb) that causes the majority of human tuberculosis and Mycobacterium bovis that could causes disease in humans by consumption of unpasteurized milk.3
Mainly airborne with inhalation of droplet nuclei containing tubercle bacilli.
Transmission to a pediatric patient occurs from an adult or adolescent with active TB disease.
Occurs during coughing, sneezing, and singing.
Young children are rarely contagious.
Infection is usually transmitted from a close adult contact.
Tubercle bacilli are deposited in the alveoli where they multiply forming the initial pulmonary focus or the “Ghon focus.” Infection is spread to the regional lymph nodes (hilar, mediastinal, paratracheal, or subcarinal). The initial pulmonary focus and the draining regional nodes forms what is known as the “primary complex” that is more likely to be seen radiographically in children compared to adults.
Occult mycobacterial lymphohematogenous spread could occur at this initial phase of infection with possible dissemination throughout the body, including the lymph nodes, kidneys, bones, brain, and the lungs. This provides a nidus for subsequent progressive disease or reactivation disease.
The incubation period from the initial infection to the development of tuberculin hypersensitivity is around 2 to 10 weeks and can be demonstrated by either a positive tuberculin skin test (TST) or interferon γ release assay (IGRA) blood test.
The ultimate risk for TB infection in a child is contact with an adult with untreated or inadequately treated pulmonary TB.
Epidemiologic risk factors—Foreign birth, history of travel to high TB prevalent areas or history of incarceration. Also, history of exposure to adults with the following risk factors: foreign birth, abuse of intravenous drugs, dwellers of homeless shelters, and migrant farm workers.
Recent infection—Risk for progression to TB in immunocompetent individuals is 5 to 10 percent during their whole life spans with 50 percent of this risk occurring within the first two years after infection.
Age—Young infants and adolescents are especially at risk for TB progression. Children <1 year of age with TB infection have 40 percent risk of progression to disease.
Immunosuppressive conditions—HIV infection, prolonged use of high dose steroids, and use of tumor necrosis factor-alpha (TNF-alpha) antagonists.
Chronic conditions—Diabetes, renal failure, malnutrition, lymphoma.
Tuberculosis Exposure—Patient with history of exposure to suspected contagious TB case, with negative IGRA and negative TST, with no clinical, physical or radiological findings that are consistent with TB.
Latent TB infection (LTBI)—Patient with a positive IGRA and/or TST, with no clinical, physical or radiological findings that are consistent with TB. These patients are non-contagious. The onset of the hypersensitivity reaction could be associated with erythema nodosum (Figure 186-3) or phlyctenular keratoconjunctivitis.
Tuberculosis disease (Tuberculosis)—Patient with a positive TST and/or IGRA with clinical symptoms or signs (physical, radiological, bacteriologic, or histological examination) that are consistent with tuberculosis.
In general, pulmonary disease predominates in both adults and children.
TB can develop in any organ system; however, both the frequency and severity of extrapulmonary TB are increased among children. Different manifestations of TB disease tend to occur after different periods of latency in children (Figure 186-4).4
Signs and symptoms of TB in children depend on the organ of involvement.
FIGURE 186-4
The clinical manifestations of tuberculosis occur at different times in the disease course in children. Renal involvement is the last manifestation to occur typically. (Adapted from Marais, BJ, Gie, RP, Schaaf, HS, et al. The natural history of childhood intra-thoracic tuberculosis: A critical review of the pre-chemotherapy literature. Int. J. Tuberc. Lung Dis. 8:392-402, 2004. “Reprinted with permission of the International Union Against Tuberculosis and Lung Disease. Copyright © The Union.”)
The most common type of TB in children.
Children are mostly asymptomatic, but could present with fever, persistent cough, and weight loss.
Typically diagnosed in an asymptomatic child who has a positive TST/IGRA and an abnormal CXR, which shows intrathoracic lymph node enlargement especially of the hilar or mediastinal nodes (Figures 186-1, 186-2, and 186-5).
Bronchial compression and Endobronchial disease—Enlarged nodes may cause compression or obstruction of adjoining airways (Figure 186-2). In addition, bronchial obstruction may be caused by severe tuberculous disease secondary to invasion by an infected node into the bronchus (Figure 186-6). Children may present with persistent cough, wheezing or recurrent localized bacterial pneumonia.
Diagnosis—Mainly clinical and epidemiological based on history of exposure to TB. AFB smear and culture are best obtained from early morning gastric aspirates.
The primary parenchymal focus may enlarge and caseate. This may drain into adjacent bronchi, resulting in local cavitation and spread into other areas of the lung (Figure 186-7).
Children are quite ill with productive cough, weight loss, fever, and malaise.
Progressive primary TB develops more frequently in infants and immunosuppressed patients.
AFB cultures can be obtained from sputum, gastric aspirates, or bronchoalveolar lavage.
Pleural effusions are more often seen in older children and appear within 6 to 9 months after the primary infection (Figure 186-8).
Presentation is sudden onset of fever, cough, chest pain, and shortness of breath.
The majority of pleural effusions are believed to be secondary to hypersensitivity reaction to mycobacterial antigens in the pleural space.
Pleurocentesis shows pleocytosis with lymphocytic predominance. AFB stain is usually negative. Pleural biopsy may show caseating granulomas with positive AFB culture.
FIGURE 186-8
Right-sided pleural effusion following primary tuberculous infection. (Used with permission from Nazha Abughali, MD.)
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