J. F. SHIRLAW 363
streptococcal infection (Strep. melanogenes). The part played by this organism
in equine encephalomyelitis is one that has given rise to much discussion.
It is generally conceded that this organism is of no etiological significance and
the fact that it was found in only four cases in spite of strict bacteriological
examination must rule it out as a possible pathogenic factor, thus lending
additional proof, if that were necessary, to the general consensus of opinion.
In three experiments, which are not recorded in the text, attempts were
made to reproduce disease in horses by the intrathecal inoculation (two
cases) of freshly isolated broth cultures of the organism. One experimental
horse received 5 c. c. of the culture intravenously. In none of the cases was any
reaction noted.
What, therefore, is the explanation of ' septicaemic ' cases, if a bacterial
infection is found incapable of proof ? The writer has pointed out that, in
certain cases, lesions occur around the hypothalamic area, in which is found
the heat regulating centre. Interference in the conducting paths then results
in an uncontrolled rise of body temperature and a condition approaching
heat stroke. It is interesting to note that, as in heat stroke, the temperature
of some of these cases has been observed to rise after death, and the post-
mortem lesions, with the severe internal haemorrhage, tarry fluid blood, and
rapid decomposition are not dissimilar to those encountered in heat stroke
cases at post-mortem. These haemorrhages are not to be confused, however,
with those found at post-mortem in which fully clotted extravasations are
seen within the brain pulp, around the cord and in the kidney, spleen and
liver. These develop, apparently, from venous haemorrhage consequent
on a sclerotic arteriole system. Nicolau and Galloway say, when mentioning
the areas of haemorrhage in the kidneys of inoculated rabbits, that they appear
to develop from compression of the arteries, an opinion with which the writer
is in full accord, although it is strange that these writers do not comment on
structural dysfunction of the arterial system, if this be a suitable explana-
tion.
Generally speaking, the severe, acute forms of equine encephalomyelitis
in India are associated with severe haemorrhage. In mild cases which
progress to paralysis necessitating destruction, extensive haemorrhage is
absent and the only vascular abnormality noted is an over-fullness of the
veins, both of the central nervous system and the internal tissues.
It is impossible to account for the generalized arterial sclerosis and it is
peculiar that it has never been observed by writers on the disease in other
countries. The writer has frequently observed that in normal Indian horses,
there is a decided tendency to arterial sclerosis, and this is ascribed to the
general massive helminthic infection, with the absorption of toxins, to which
the Indian horse is normally subject. It may be, therefore, that the degree of
arterial sclerosis noted in cases of equine encephalomyelitis is not a specific
lesion of that disease, although it may be a lesion aggravated by the disease
through trophic influences resulting from the impairment of the vaso-motor
centre which is one peculiarly susceptible to neuron destruction.
It appears fairly certain that, if the intensity of the lesions and their
irregular distribution throughout the brain are a criterion, variations in
symtomatology owe their origin to this factor. The ultimate elucidation of