(1) The development of anthrax in guinea pigs is slowed down if an acute inflammation accompanied by an oedema is provoked elsewhere in the
body. Thus the injection of saponin into a fore-limb or into the peritoneal
cavity retards an anthrax inoculum in the hind-limb. Tissue destruction
with inconsiderable oedema, as caused by concentrated salt solution, does
not have this effect.
(2) Large doses of anthrax injected into inflamed areas are retarded and often completely inhibited. However, the killing power of fractions
of a lethal dose are enhanced if injected into early inflammatory, oedematous
lesions, although the onset of deaths may be delayed. The effects of injecting
large inocula into necrosed non-oedematous areas are neither increased nor
diminished, while the killing power of small inocula is markedly increased.
(3) Excipients such as saponin which cause tissue destruction accompanied by considerable oedema may slow down the development of large doses of anthrax. Small doses, fractions of a lethal dose, are, however, stimulated
and their killing power greatly increased, although the onset of deaths is
somewhat delayed. Excipients such as concentrated salt, which cause
necrosis with little oedema, have no apparent effect on large anthrax inocula,
but increase the killing power of fractions of a lethal dose, without delaying
the onset of deaths.
(4) The apparently anomalous action of inflammation on small and on
large inocula is explained by the fact that if stimulation raises say a fifth
of a lethal dose to a full lethal dose, the effect is very obvious, whereas
the raising of a hundred lethal doses an equivalent amount will be virtually undetectable.
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