Avascularity of Tuberculous Lesions

A Major Problem in Therapy

¹ Chief, Laboratory Service, Walter Reed Army Hospital., Office of the Surgeon General, Department of the Army.
² Office of the Surgeon General, Department of the Army.

The extensive thrombosis and obliterative endarteritis of vessels entering chronic tuberculous areas of disease produce essentially avascular lesions. Other closely associated pathological changes, ischemic (caseous) necrosis and fibrosis, further increase the avascularity. There is some evidence that streptomycin penetrates these pathological barriers; however, when it enters in less than therapeutic concentrations, it is neither tuberculostatic nor tuberculocidal, and the emergence of resistant tubercle bacilli results.

Efforts are presently being made to penetrate pathological barriers by various methods so as to allow drugs to come into direct contact with tubercle bacilli. The following methods have been tried: cavernostomy, potassium iodide, antihistaminics, detergents, streptokinase and tuberculin. Of these, tuberculin appears to revascularize tuberculous lesions, exposing tubercle bacilli to therapeutic levels of chemotherapeutic agents.

It appears that further effort must be made to penetrate pathological barriers of chronic tuberculosis, if the full effectiveness of present and future chemotherapeutic agents is to be obtained.