Tuberculosis is mainly an inherited constitutional disease rather than a contagious infection.

Tuberculosis often ran through families. In an era before germ theory, that pattern made heredity a plausible explanation: perhaps “consumption” reflected a constitutional weakness passed from parent to child.

The disease also had a long, variable course. Some exposed people never became visibly ill, while others wasted away over months or years, reinforcing the idea that individual constitution was central.

Robert Koch changed the causal framework in 1882 by identifying the bacterium that causes tuberculosis, Mycobacterium tuberculosis. It was historically called the tubercle bacillus.

That did not make heredity irrelevant. Genetic variation strongly influences immune responses to Mycobacterium tuberculosis, and host factors help determine whether infection remains latent or progresses to active disease.

The mistake was treating inherited susceptibility as the disease’s primary cause rather than as one modifier of an infection.

Family clustering can now be understood through both shared exposure and shared biology. The bacterium is necessary for tuberculosis, while genes, immunity, nutrition, living conditions, and other factors shape the outcome after exposure.