The passage of this material causes violent straining, which becomes more and more common, and is accompanied by very pronounced rectal tenesmus. The animals stand with their backs arched for one or two minutes, sometimes longer, and the liquid escapes in large quantities, soiling the quarters and hocks. The animals are dull, show a certain degree of colic, and frequently grind the teeth. Appetite is lost, thirst is severe, and rumination ceases. Wasting makes rapid strides, the coat stares, the animals have difficulty in standing on account of their weakness, fever sets in, and the temperature rises to 40° C. This condition may last from five to ten days and terminate either in recovery or death. Recovery is frequently rapid in animals which have continued to eat, and in which the acute period has been of short duration—five to seven days at most. On the other hand, it is slow if the appetite has disappeared and the acute period has been prolonged beyond ten days.
The diarrhœa, which has lost its sanguinolent character towards the sixth or eighth day, may continue for somewhat longer. The attacks of straining become rare, and cease between the tenth and fifteenth days. The appetite remains capricious for a long time.
Convalescence is marked by alternate improvement and retrogression. The animals are weak, and only recover quickly under energetic treatment and forced feeding with concentrated digestible foods like milk, soup, cooked grain, etc., administered for three weeks or more.
Death may occur towards the tenth or fifteenth day from exhaustion. The patients become very anæmic and thin, the eyes are withdrawn into the orbits, and the animals appear indifferent to what goes on about them. They still groan feebly, occasionally grind the teeth, and lie continually on the chest with the head extended. The body temperature falls and death follows.
In well-bred animals in good condition the disease sometimes assumes a much graver and more rapidly progressive form, with peracute symptoms, and makes as many, if not more, victims than that previously described.
The process is as follows: After suffering for a day from serous diarrhœa, to which the owners pay little attention, the animals show sanguinolent diarrhœa and pass blood clots. This is almost immediately followed by very violent convulsive attacks—true eclampsia. The animals are then unable to stand, lie on the side with the head outstretched and resting on the ground, the eyes withdrawn into the sockets and often showing pirouetting movements (nystagmus), the neck drawn upwards and backwards (opisthotonos), and the limbs rigidly extended. From time to time the whole body is shaken by extremely violent convulsive movements.
This condition, which is sometimes preceded by weakness of the hind quarters and symptoms of locomotor ataxia and inco-ordination, may continue from six to thirty-six hours; in nine cases out of ten it terminates in death.
Causation. On microscopic examination of the serous dejections one finds distributed throughout the liquid mass very small numbers of ovoid corpuscles having a double outline, and contents of varied appearance; these are the coccidia.
When the diarrhœa has become sanguinolent and muco-fibrinous, the fluid contains these coccidia in considerable quantities, and large numbers of them may be found in the mucus, where they are mixed with epithelial débris, blood corpuscles, and lymphatic cells, etc. They are rarer in the clots. Coccidia cannot be found in the fæces of healthy animals, even in those occupying the same pastures with the diseased. Should the clinical symptoms be thought insufficient of themselves clearly to identify the disease, a simple microscopic examination of the fæces will remove any doubt.
Lesions. Post-mortem examination immediately after death enables one exactly to identify the habitat of the parasite and the lesions it produces. These lesions are to be found throughout the large intestine, from the cæcum to the anus.