Leprosy: cause, transmission, and a new theory of pathogenesis.

Leprosy is generally accepted as being caused by Mycobacterium leprae, an acid-fast organism often present in great numbers in certain forms of leprosy. However, it has not been possible to confirm with scientifically acceptable evidence that this entity is the cause of leprosy; laboratory cultivation, an essential factor in the proof, has not been accomplished with the acid-fast bodies seen in leprotic tissue. The mechanisms of transmission of the disease also remain conjectural; prolonged, close contact and transmission by nasal droplet have both been proposed, and, while the latter fits the pattern of disease, both remain unproved. It is proposed that the causative agent of leprosy is not a difficult-to-transmit agent but, rather, an organism that has evolved a highly efficient state of parasitism in stable types of populations and that everyone in the population harbors the leprosy parasite at some time. The majority of the population incubate subclinical infections at various levels; clinical leprosy arises from within the pool of subclinical infection in the endemic population rather than by transmission from an index case. A theory of complete infection of endemic populations is consistent with the rate of development and distribution of positive lepromin reactions among healthy persons in endemic regions and provides an explanation for the difficulty in controlling leprosy in endemic populations by isolation of patients or by therapy for clinical cases.

Evaluation of a new blood test for its potential to indicate leprosy infection prior to the appearance of clinical symptoms.

A test is described that utilized a laser nephelometric measure of the interaction between human serum and a leprosy biopsy suspension to demonstrate household contact with a leprosy index case. None of the test sera was from persons with clinical evidence of the disease. There was a 5:1 ratio of higher level reactors in sera from household contacts vs high level reactors in sera from persons in the surrounding community. This did not appear to be a result of age, sex, family relationship to the index case, or clinical character of the index case. Some index cases had high level serum reactors among their contacts; others did not. This phenomenon was not a function of the clinical classification of the index case. The reason is unknown. This test should provide another practical means to study leprosy.

Rapid effective measure of a humoral substance(s) reacting specifically with Mycobacterium leprae antigens.

Leprosy-specific humoral reactants were demonstrated by light scatter. Of 132 lepromatous leprosy sera, 70% gave more extensive reactions than 99% of 100 normal sera.