The host parasite relationship in tuberculous infection

Abstract

My partners in this research, Dr Honor B. Fell of the Strangeways Research Laboratory, Cambridge, and Dr V. E. Cosslett of the Cavendish Laboratory, Cambridge, appreciate with me this opportunity to report on experiments which we have made jointly in order to examine certain problems in the mechanism of tuberculous infection, which hitherto have resisted the single-handed attempts of pathologists unaided by research workers of other branches of Science. I consider myself very fortunate that Professor Boyd is in the Chair, because I shall take the text of my lecture from his 'Textbook of Pathology', where he gives a most concise description of one of the crucial problems in tuberculous infection: 'The epithelioid cell may be regarded as a large mononuclear which has partially digested tubercle bacilli, and its distinctive cytoplasmic state seems to be the result of destruction of many bacilli with progressive emulsification of their lipoid (Long, Lurie). It is evident that by the time the mononuclears have become transformed into epithelioid cells the bacilli have undergone extensive destruction. This explains the difficulty which is experienced in demonstrating bacilli in the ordinary type of lesion in man, in which they are few and far between and may only be found after prolonged search, although in acute fulminating lesions such as tuberculous caseous pneumonia they may be present in great numbers. The mononudears do not always have the power of destroying the bacilli which they engulf. Thus, in the rat the bacilli thrive and multiply within the phagocytes, and the latter also multiply with the remorselessness of a malignant growth, until finally the animal succumbs to the cellular accumulation.' With these words the ambiguous nature of the phenomenon known as 'Phagocytosis' is expressed as far as the mononuclear macrophages the mother cells of the epithelioid t u b e r c l e a r e concerned. There are two