Abstract:
1. In the dikkop form of horse-sickness:
(a) sedimentation of red corpuscles is much accelerated in the later stages of the disease, owing to clumping of the cells. This clumping is due to a property acquired by the plasma;
(b) at the time of the fever acme and for some time thereafter, the jugular blood becomes poor in red cells, probably mainly on account of the tendency towards clumping and the weak action of the heart. These favour erythrocyte retention in the capillary system. It is possible that water retention and decreased formation of red cells also play some subsidiary part in the production of this phenomenon;
(c) the decreased erythrocyte content of venous blood decreases peripheral resistance considerably, and allows the heart to maintain a fairly bulky circulation in spite of mechanical interference with its action (hydropericardium) and weakening of the myocardium;
(d) the dyspnoea which is noted in some cases is due not so much to the decreased oxygen carrying capacity of the blood, as to the inability of the heart to maintain a sufficiently bulky circulation and so ensure the efficient removal of wastes;
(e) if oedema formation is rapid and extensive and if complications such as paralysis of the oesophagus or pharynx persist for a long time, jugular blood may again become rich in red cells. This increases peripheral resistance and favours sudden cardiac failure.
2. In peracute and very mild cases of horse-sickness no marked or constant changes in erythrocyte content of jugular blood are noted – probably because there is no time for the formation of haemagglutinins, or because these are formed only to a very slight extent.
3. In all cases of horse-sickness, leucocytes disappear progressively from the jugular blood during the incremental stages of the disease; the rate at which leucocytes disappear is an index of the severity of the disease, but the extent of disappearance is to some extent also dependent upon the duration of the disease.
