J. F. SHIRLAW 351
posterior incoordination only and a temperature of 106° before death, after
three days illness. The only lesions were slight enlargement of the spleen,
slight gastro-enteritis and slight congestion of the bladder, which contained
blood-stained urine. Filly 8545 was the most severely affected case and was
found down in the paddock unable to rise. Kept in slings, it survived for two
months and was finally destroyed. The only symptom noted was grave poste-
rior incoordination and marked swelling of the vulva and sexual excitement.
Hæmoglobinuria was noticed. At post-mortem, the only lesion found was a
chronic indurative cystitis, much blood in the urine and fibrous thickening
of the blood vessels in the parenchymatous tissues. Filly 9020 was a case of
paraplegia and showed loss of sensation in the quarters and perineum. Brain
symptoms were present and the temperature rose to 106.8° before death, after
five days illness. The blood was tarry, the intestines showed slight gastro-
enteritis, the blood vessels of the brain and cord were markedly prominent,
hæmorrhages were seen within the endocardium, the spleen was normal and
the bladder was thickened and full of blood.
The remaining fillies simply showed symptoms of posterior incoordina-
tion, the majority with loss of sensation in the perineal region, paralysis of the
tail muscles, sinking of the loins, a straggling gait and vesical and rectal paraly-
sis. It will be seen therefore that there was no constant symptomatology in
these cases, which would lead one to a solution of the etiological factors.
VI.—HISTOPATHOLOGICAL STUDIES
Histopathologically, the lesions are centered in (a) the brain and spinal
cord, (b) the arterial system and (c) the kidney.
The essentially infiltrative, non-exudative lesions of the meninges have
been commented upon but occasionally cases of exudative meningitis have
been encountered, the brain and spinal meninges being covered with a thick
gelatinous exudate.
The lesions affecting the nervous tissues are perivascular ' cuffing'
and degeneration of the nerve cells of the grey matter, that is, a true polioen-
cephalomyelitis. The vascular sheaths are densely infiltrated by monocytes
and dense aggregation of these cells occur around the vessels, infiltrating
into the neuroglial tissue proper. In some cases perivascular " cuffing "
is not so prominent and in these cases there exists a diffuse monocytic in-
filtration of the neuroglia which is equally characteristic. Polymorphonu-
clear cells have never been seen. Coincident with this process a considerable
degree of proliferation of the glial cells (cells of Cajal) occurs, indicating a
response of the fixed " connective tissue " elements to the stimulus of what
is obviously a chronic inflammatory process.
The earliest change affecting the nerve cells (as seen in the cortex of the
parietal area and the cord) is a loss of Nissl granules rapidly succeeded by
a shrinkage of the dendrite processes with a consequent rounding of the cell.
The cytoplasm becomes granular and changes in the nucleus (pyknosis)
are evident. Karyorrhexis and karyolysis ensue and the degenerate cell is
quickly invaded by monocytes, and engulfed, the cell spaces then existing
as lacunae in which the monocytes remain. This process of neuronophagia
is frequently so complete that no trace of viable cells can be determined. The