Lectures on the etiology of typhoid fever / by Robert King.

  • King, Robert.
Date:
1879
Catalogue details

Licence: Public Domain Mark

Credit: Lectures on the etiology of typhoid fever / by Robert King. 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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    all be absorbed by water, and can all be expelled from tbeir aqueous solution by prolonged boiling. Nor is this all, for animal charcoal, which possesses such extraordinary power of disinfecting and sweetening the atmosphere of a sick-room by absorbing and oxidising putrid organic effluvia, is also capable of absorbing an almost unlimited quantity of gaseous ammonia, while many of the vegetable alkaloids, if mixed with it in sufficient quantity, are wholly irrecoverable by chemical means. With regard to other disinfectants and so- called germicides, it will generally be found that their anti- septic power is in direct proportion to their albuminoid affinities; and the fact that meat may be preserved from putrefaction for some time by the agency of carbolic acid, salicylic acid, thymol, and a host of other substances, admits of a ready explanation when we consider that the antiseptics in question form with albumen very insoluble, and therefore comparatively stable, compounds. Perhaps the weightiest ai’gument which can be adduced in favour of the theory that the specific fever-poisons consist of living particles or germs, is based upon the undoubted multiplication of these poisons in the system of the infected person; but I think that even this fact admits of a different explanation: for if the poison consist of some product of albuminoid decomposi- tion, gifted with the power of affectinrg those particular elements of tissue from which it was derived, it is only natural to suppose that the process thus started, possibly in some one constituent of a single cell, would be liable to spread to similar constituents of adjoining cells, in much the same mannei: as the ordinary inflammation of a serous mem- brane, for example, is known to spread. The combined pro- ducts of the decomposition of the mass of tissue thus finally involved would of course supply abundant material for an enormous increase on the amount of poison originally employed. Thus the multiplication of the poison may pos- sibly represent the waste of tissue instead of marking the extent and progress of bacterial growth. This is well illus- trated in the case of specific inflammatory diseases, such as gonorrhoea, for example. A very minute portion of the gonorrhoeal pus is sufficient to occasion the disease; and no