THE LABORATORY DIAGNOSIS OF LEPROSY

I t is now more than three-quarters of a century since Armauer Hansen, in 1874, first made public his finding of the leprosy bacillus. Hansen was seeking an extrinsic agent, a contagia, as the cause of leprosy, in order to remove this malady from the category of hereditary diseases, where it has been so firmly intrenched by the authority of Danielssen and Boeck in 1847. He was convinced, on the basis of his investigations of syphilis, with which he was prone to compare leprosy, that leprosy was a contagious disease. In considering fixed films of leprous tissue examined microscopically, he states in the original report, “In some cells one finds bunches of rods and some cells are, as it were, packed with them.” Having made this preliminary announcement, Hansen carried on with sedulous zeal his study of the nature and distribution of the rods, and proved that, in lepromatous leprosy, they were to be found in all typical nodules, in the spleen, the liver, and particularly the lymph nodes. They were never present in healthy individuals or in patients with other diseases. He therefore concluded that these rods were the cause of leprosy. Coming as it did during the prelude to the acceptance of the germ nature of disease, his belief was shared by a relatively small number of leprologists. In connection with the discovery of the tubercle bacillus by Koch in 1882, a staining technique was developed which differentiated Hansen’s bacillus and Koch’s bacillus from other microorganisms. The stain could be applied directly to tissue films and the two germs detected if present in sufficient numbers. Thus, to the clinical signs and symptoms, there was now added the microscopic search for Hansen’s bacillus in the diagnosis of leprosy. Koch, however, promptly discerned the limitations of identifying an organism as the etiological agent in a suspected infectious disease by differential staining, because of possible contamination with extraneous saprophytic forms. He insisted, before any such relationship be advanced, that the germ seen in the stained film be grown in pure culture on artificial media, and that the inoculation of a susceptible laboratory animal with a suspension of the pure culture induce an infection identical with the natural occurring disease. These steps, later designated as “Koch’s Postulates,” were implemented and became the dogma to be fulfilled before sponsoring a specific germ as the cause of a specific disease. With the passage of time and the increases in knowledge of changes occurring in the host as a result of infection, two additional diagnostic approaches were developed : (1) serological reactions employing the serum of the patient in such tests as agglutination, precipitation, and complementfixation, noting particularly increases or decreases in the titer of the serum in successive samples; and (2) immunological reactions, i.e., the failure to induce disease in specifically immunized animals by the injection of suspensions of homologous virulent organisms or their toxic products. Un-