Abstract

A BRIEF review of present concepts of the fate of the primary complex may serve as a useful introduction to the problem of treating the infant or child with asymptomatic primary tuberculosis. The primary lesion persists for months and gradually disappears, usually leaving calcification in the site of the primary focus and the corresponding lymph nodes. In most instances recovery is uneventful despite the almost universal occurrence of a hematogenous or lympho-hematogenous spread of tubercle bacilli, but this accounts for most of the severe complications of primary tuberculosis such as tuberculous meningitis and skeletal tuberculosis. The spread may be of various types and degrees but is usually an occult hematogenous dissemination from the primary lesion, which may take place during the incubation period or during the first few months after the appearance of the primary complex. Hematogenous spread also may be massive, resulting in miliary tuberculosis. Tubercle bacilli in the tracheo-bronchial lymph nodes may spread to other lymph nodes or other areas of the body through lympho-hematogenous dissemination. Common sites of invasion are the cervical lymph nodes and tonsils. The primary lesion may progress locally by excavation and by bronchogenic dissemination; it is then often called locally progressive primary tuberculosis. The majority of the complications appear within the first year of infection in an infant or a child who has previously been asymptomatic. In children, reinfection or chronic, adult type of tuberculosis is most common in adolescence. It may be of exogenous or endogenous origin. The endogenous type might be considered a distant complication of primary tuberculosis, since it is believed to occur as a result of activation of a dormant focus.

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