ABSTRACT
In 1941, Ansgar Kviem reported a clinical study in which lymph node tissue
obtained from a patient with sarcoidosis produced a granulomatous reac-
tion when injected subcutaneously in other patients with sarcoidosis but
not in controls (1). Using the same technique in a much larger cohort of
patients, Louis Sitlzbach demonstrated the sensitivity of what has become
known as the Kveim-Siltzbach test in the diagnosis of patients with the disease (2). Two important hypotheses in the search for a potential pathogen in
sarcoidosis arise from these early observations. First, a transmissible agent
or antigen may be present in the lymph node or spleen tissues of patients
suffering with the disease and is capable of inciting a granulomatous
response when transferred to another patient. Second, since not all patients
respond to the Kveim-Siltzbach test, the ability of the agent to incite gran-
ulomatous inflammation depends on individual patient characteristics and
inherent susceptibility to the development of the disease. The essential criteria of any potential pathogen in sarcoidosis should include characteristics
which allow for the dual observations of transmissibility and variation in
disease phenotype. The potential pathogen, or perhaps pathogens, should
account for the wide range of observed epidemiological and clinical varia-
bility of sarcoidosis. As in the Kveim test reaction, the sarcoid pathogen or
antigen should produce the characteristic disease phenotypes only in those
individuals who are at risk for disease development.
