Page:Popular Science Monthly Volume 61.djvu/81

Rh modification insoluble: l-Tartaric acid; d-Methoxylsuccinic acid; d-Mandelic acid. Penicillium glaucum destroys: d-Tartaric acid; l-Æthoxysuccinic acid; l-Mandelic acid. Lewkowitch's schizomycetes destroy: l-Tartaric acid; d-Mandelic acid. Strychnine separates: l-Lactic acid; l-Æthoxysuccinic acid. Many other examples can be cited, the principal difference being that the alkaloids separate the insoluble optical isomer and the micro-organisms make use of one of the optical isomers to build up their own structure.

The bi-partic powers of the alkaloids are as limited as those of the micro-organisms; thus strychnine can bi-part lactic acid, cinchonine malic but not lactic acid, etc., and most likely two acids bi-parted by the same base have analogous configuration.

From these arguments, I take it that predisposition and immunity are intimately connected with stereo-chemical changes, i.e., where the configuration, according to Fischer, of the nutrient, on the one hand, and the ferments, enzymes, sporozoa, etc., on the other, must be to each other as lock and key. Moreover, I believe that infectious diseases are not caused by any one class of ferments, but by many acting synergetically. In line with these results it strikes me that predisposition is a condition well suited to act synergetically when the missing ferment presents itself. Immunity, on the other hand, betokens the absence of a number of active synergetic ferments, owing to lack of requisite configurations.

While this suggestion may seem to offer one hazy hypothesis for another equally hazy, it opens a broader field for investigation, it admits of better explanations of observed results, and it agrees with our ideas that the demolition of complex organic materials, such as blood and the tissues, takes place step-like and not abruptly.

Surely some day physiological chemistry will be sufficiently powerful to shed its light through the mist now surrounding the so-called vital processes—clearly define the differences between the healthy and the disease-disturbed systems—teach us how to preserve the former and counteract the latter, by other than merely empirical methods.

When that day comes, infectious diseases like tuberculosis will no longer rob the stricken patient of all hope and cause him to be a constant menace, dreaded even by those who love him most dearly. When that day comes, parents no longer need be haunted by the fear that predisposition be transmitted to their children born and unborn.