The irritation caused by infection with bacteria, on the other hand, is cumulative, as the organisms not only multiply in the tissues, but in addition produce chemical poisons (toxins) which aggravate the irritative effects.  The resulting reaction is correspondingly progressive, and has as its primary object the expulsion of the irritant and the limitation of its action.  If the natural protective effort is successful, the resulting tissue changes subserve the process of repair, but if the bacteria gain the upper hand in the struggle, the inflammatory reaction becomes more intense, certain of the tissue elements succumb, and the process for the time being is a destructive one.  During the stage of bacterial inflammation, reparative processes are in abeyance, and it is only after the inflammation has been allayed, either by natural means or by the aid of the surgeon, that repair takes place.

In applying the antiseptic principle to the treatment of wounds, our main object is to exclude or to eliminate the bacterial factor, and so to prevent the inflammatory reaction going beyond the stage in which it is protective, and just in proportion as we succeed in attaining this object, do we favour the occurrence of ideal repair.

#Sequence of Changes in Bacterial Inflammation.#—­As the form of inflammation with which we are most concerned is that due to the action of bacteria, in describing the process by which the protective influence of the inflammatory reaction is brought into play, we shall assume the presence of a bacterial irritant.

The introduction of a colony of micro-organisms is quickly followed by an accumulation of wandering cells, and proliferation of connective-tissue cells in the tissues at the site of infection.  The various cells are attracted to the bacteria by a peculiar chemical or biological power known as chemotaxis, which seems to result from variations in the surface tension of different varieties of cells, probably caused by some substance produced by the micro-organisms.  Changes in the blood vessels then ensue, the arteries becoming dilated and the rate of the current in them being for a time increased—­active hyperaemia.  Soon, however, the rate of the blood flow becomes slower than normal, and in course of time the current may cease (stasis), and the blood in the vessels may even coagulate (thrombosis).  Coincidently with these changes in the vessels, the leucocytes in the blood of the inflamed part rapidly increase in number, and they become viscous and adhere to the vessel wall, where they may accumulate in large numbers.  In course of time the leucocytes pass through the vessel wall—­emigration of leucocytes—­and move towards the seat of infection, giving rise to a marked degree of local leucocytosis.  Through the openings by which the leucocytes have escaped from the vessels, red corpuscles may be passively extruded—­diapedesis of red corpuscles.