ON THE MECHANISM OF IMMUNITY IN TUBERCULOSIS : THE HOST-PARASITE RELATIONSHIP UNDER THE CONDITIONS OF A LOCALIZED AGAR FOCUS OF INFECTION AND THE GENERALIZATION OF THE DISEASE IN NORMAL AND IMMUNIZED RABBITS.
1. There is an extracellular factor which inhibits the growth of tubercle bacilli in immunized rabbits. 2. Extracellular factors localize carbon particles, trypan blue and tubercle bacilli at the site of introduction to a greater extent in the immunized than in the normal animal. 3. This greater fixation is brought about by an increase in the density and extent of the fibrin barrier formed about the focus of the immunized animal. The more pronounced in vivo agglutination of tubercle bacilli and carbon particles in the vaccinated or tuberculous rabbit also tends to immobilize them in the tissues. 4. The growth inhibitory and localizing agents are effective in the fixation of small doses on reinfection at the portal of entry. 5. With large doses on reinfection, the increased lymph flow resulting from the intensified inflammation in the immunized animal brings about a more rapid dissemination of the bacilli to the draining lymph nodes than in the normal animal. 6. The most significant factor in immunity is the increased capacity of the rapidly mobilized mononuclear phagocytes to destroy tubercle bacilli. The impotent polymorphonuclear leukocytes quickly disappear from the site of reinfection. 7. The invading bacilli that reach the draining lymph nodes of the immunized animal are retarded in multiplication or destroyed by these phagocytes. 8. Vaccination of rabbits with BCG brings into play the factors tending to immobilize the bacilli of reinfection, inhibit their growth and destroy them with a resulting significant immunity. 9. A virulent primary infection affords a greater immunity than one of low virulence and the host reactions are expressed by a quantitative increase in those immunity factors which operate in a vaccinated animal.
Lurie
M B
MB
The Henry Phipps Institute, University of Pennsylvania, Philadelphia.