On latent and recurrent infection, and on subinfection / J. George Adami.

  • John George Adami
Date:
1912
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Licence: In copyright

Credit: On latent and recurrent infection, and on subinfection / J. George Adami. Source: Wellcome Collection.

Provider: This material has been provided by The Royal College of Surgeons of England. The original may be consulted at The Royal College of Surgeons of England.

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    properties of the B. coli, opened by Dr. Rolleston, and here one speaker after another—including Dock, Woods Hutchison, Sims Woodhead, and others—expressed themselves as favorable to the idea of subinfection. Indeed since the admirable experimental work of Opie upon the production of hepatic cirrhosis, it is difficult to hold any other opinion. While I have repeatedly been able to obtain the cultures of organisms of the B. coli type from cases of cirrhosis in man, I have been unable to reproduce the disease by inoculation of the growths of the same. Both Weaver and Hektoen of Chicago have, it is true, announced the isolation of strains of B. coli which would produce cirrhosis in the liver of animals. I think I am right in saving that both of these observers were unable to obtain these constantly or indeed other than in occasional cases, and other work- ers have had the same experience. On the other hand as everyone knows, the common form of cirrhosis as known in man is associated with alcoholism; but observer after observer, with it is true some exceptions, has found that the long continued treatment of animals with alcohol by inoculation or through the digestive tract does not. save in exceptional cases, lead to hepatic cirrhosis. There is a stronger narcotic than alcohol, namely chloroform, which has pronounced effects upon the hepatic cells ^causing necro- sis and destruction of, more particularly, the cells of the centre of the lobules. Opie found that employing chloroform alone, this destruction is not followed by fibrosis or cirrhosis; instead of this where the dose given has/been the means of death, the dead cells undergo regeneration and in a few weeks the organ assumes its normal appearance. But now he found that if he combined the two processes and treated the animals of the laboratory with chlo- roform and then made an intraperitoneal or intravenous inocula- tion of a growth of a culture of B. coli he could with certainty produce well-pronounced cirrhosis resembling that seen in man. The simplest view, therefore, of the etiology of “gin-drinker's liver” in man, is that alcohol or some other irritant taken into the alimentary canal/absorbed therefrom has a deleterious action upon the hepatic parenchyma and at the same time causes inflammatory conditions of the intestinal mucosa; that by the entrance of the B. coli and other organisms into the portal vessels these organisms are carried to the liver and there destroyed, their toxins* setting up that low form of irritation which leads to the simultaneous de- generation and destruction of the hepatic cells and overgrowth* of the connective tissues of the organ. We do not deal with infection but with subinfection. The liver of hepatic cirrhosis does not show indications of active growth of the bacilli, there are no local foci of bacterial proliferation, no abscess production or diffuse puru-
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