giving rise to an _inflammatory œdema_, or, if the inflammation is on a
free surface, forming an _inflammatory exudate_. The quantity and
characters of this exudate vary in different parts of the body, and
according to the nature, virulence, and location of the organisms
causing the inflammation. Thus it may be _serous_, as in some forms of
synovitis; _sero-fibrinous_, as in certain varieties of peritonitis, the
fibrin tending to limit the spread of the inflammation by forming
adhesions; _croupous_, when it coagulates on a free surface and forms a
false membrane, as in diphtheria; _hæmorrhagic_ when mixed with blood;
or _purulent_, when suppuration has occurred. The protective effects of
the inflammatory reaction depend for the most part upon the transudation
of lymph and the emigration of leucocytes. The lymph contains the
opsonins which act on the bacteria and render them less able to resist
the attack of the phagocytes, as well as the various protective
antibodies which neutralise the toxins. The polymorph leucocytes are the
principal agents in the process of phagocytosis (p. 22), and together
with the other forms of phagocytes they ingest and destroy the bacteria.

If the attempt to repel the invading organisms is successful, the
irritant effects are overcome, the inflammation is arrested, and
_resolution_ is said to take place.

Certain of the vascular and cellular changes are now utilised to restore
the condition to the normal, and _repair_ ensues after the manner
already described. In certain situations, notably in tendon sheaths, in
the cavities of joints, and in the interior of serous cavities, for
example the pleura and peritoneum, the restoration to the normal is not
perfect, adhesions forming between the opposing surfaces.

If, however, the reaction induced by the infection is insufficient to