For the development of diphtheria it seems that much more [than the presence of the diphtheria bacillus] is necessary: (1) that the bacilli have attained a certain degree of virulence; (2) that these bacilli be borne in large numbers to the mucous membranes; (3) that the infected mucous membrane is at the time of infection in a condition which gives a footing to the bacilli and favors their increase, which condition is a not too acid reaction with a loosening or abrasion of the epithelium; (4) that the infected individual is in a general way receptive, having neither sufficient general resistance nor inherited nor acquired specific im munity, or at least only to an inadequate degree.
A potential predisposition may at times be increased or lessened, or it may first make itself known when the general vitality is lowered by an accidental sickness which in itself is quite insignificant.
Little that is positive is known about the special local predisposi tions. A lowered predisposition may be reasonably attributed to a mucosa of finn texture, and in infants during the early months of life to the acid reaction of the buccal cavity, especially. An increased tendency may possibly be found among individuals with hypertrophy of the lymphoid structures of the pharynx, which form in the majority of cases the starting point of the local process. In the same way all affections %vhich produce a loosening or inflammation of the pharyngeal mucous membrane, seem to favor the infection.
Numerous investigations point to the existence of an antitoxic state of the blood, not only in convalescents from diphtheria, but also in children, even up to the eleventh year, who, as far as known, have never had diphtheria. The transmission of an immune body in the milk of women convalescent from diphtheria to the infants nursed by them is doubtful (Auden).
in general, a disposition to contract diphtheria is present in rela tively few persons, probably because of congenital immunity; at least the figures for the morbidity appear rather low in proportion to the numerous opportunities for infection. The very frequent occurrence of the disease in early childhood can in part be attributed to the fact that children of this age are creeping on the floor and putting their soiled and infected fingers frequently into their mouths (Fees). The immunity of adults in spite of equal chances for infection [members of the same family] is not fully explained.
In the majority of cases, survival of an attack of diphtheria fur nishes an immunity for the rest of the individual's life, and yet instances of second and third attacks are not rare (according to Zucker in 9 to 13 per cent. of all cases).
the above-mentioned conditions the diph theria bacillus may act in a specific manner on the human system. It settles on a predisposed mucous membrane, especially the pharynx, and multiplies with rapidity. If the number of the bacilli and the toxin manufactured by them are sufficient, for which a varying length of time of from two to seven days is necessary, probably dependent on the• difference in the local predisposition and on the amount and intensity of the infecting virus, then there arise symptoms of a local process followed later by those of a general intoxication.
The next step consists in certain changes in the mucous membranes.
The poisonous metabolic products of the bacilli set up coagulation necro sis of the epithelium, which furnishes a still more favorable culture medium for the germs of the disease. At the same time the poisons dif fusing through the epithelium set up a decided inflammation of the lim iting layers of the mucosa. The blood vessels in the region become dilated and engorged and following the injury to their walls they pour out rapidly and richly an exudate of serum and fibrinogenous substance. The fibrin ferment set free by the death of the tissue-cells causes a coag ulation of this exudate pressing into the necrotic epithelial layers, and through constant repetition of the process a pseudomembrane is formed.
So long as only the superficial blood vessels are exposed to the ac tion of the poison, the exudative process is limited to the epithelial layer of the mucous membrane. The false membrane lies on the mucosa and can be easily removed. But when the vessels of the submucosa are af fected there then follows fibrinous exudation in the subepithelial layers also, and the false membrane is then formed intimate with the mucous membrane, so that it can be removed only with difficulty, its removal causing bleeding (croupous or diphtheritic process in the anatomical sense).
The compression of the vessels by the fibrinous exudate and the impeded circulation cause in addition a necrosis of the affected tissues so that after the spontaneous removal of the false membrane deep ulcers are left behind. If gangrenous processes set in, changing the mucous membrane into an offensive, dirty, liquefying mass or into a firmer blackish crust, there may then occur widespread destruction of the mucous membrane going on even to destruction of the underlying car tilages. Mention must also be made of the fact that degenerative pro cesses in the blood vessels occur not only at the site of the local processes but also in situations far removed, points of election being the lung, pleura and adrenals.