MENINGITIS IN HORSES 463 
and adjacent tissue. In a later epizootic they failed to find the brain 
lesion but did detect the vascular changes. 
McCarthy and Ravenel in a study of fifteen animals found certain 
lesions in the upper gastro-intestinal tract and in the central nervous 
system. These were (1) in the intervertebral and Gasserian ganglia 
where a peri-capsular, small round cell accumulation was present. 
‘The cells were all of the same type, the nucleus and protoplasm being 
about the size of a red corpuscle. There was no evidence that these 
cells were the result of proliferation of the original layer of capsular 
cells. (2) Cortical lesions. These consisted of congestion of the 
cerebellar and cerebral cortex. There were also capillary hemor- 
rhages. The meninges were normal. (3) Changes in the choroid 
plexus. In three cases the choroid plexus was changed into a triangu- 
Jar, tumor-like mass, of a yellowish red color and of a firm consistency. 
‘The increase in size was found to be due to a proliferation of the elastic 
tissue surrounding the vessels. (4) Changes in the peripheral nerves. 
‘There was a distinct degeneration of the nerves supplying the larynx 
and neck. This was present in the nerve up to the ganglion, but was 
not found in the posterior roots. Other slight changes were detected. 
These authors conclude that this disease is not a true meningitis, 
but that the evidence goes to show that it is caused by some poisonous 
substance contained in the forage. They propose the name “forage 
poisoning” for ‘“‘cerebro-spinal meningitis” and leucoencephalitis 
suggested by MacCallum and Buckley. It is highly probable that 
up to the present time, cases of uncomplicated meningitis and possibly 
werebritis have been confused with the disease in question. The entire 
subject must await the results of further investigation. 
Williams investigated an outbreak at Idaho Falls and Milks one 
jn Louisiana. They concluded that the cause was not forage poison- 
ing. 
The lesions described by Joest for Borna disease and found by Udall in 
the outbreak in Kansas and Nebraska in 1912 were similar and different 
from those heretofore described. There were no macroscopic character- 
istic lesions visible on post-mortem. Joest found: ‘“The principal seat of 
the lesion is the brain, acute encephalitis being present; slight meningitis 
is also found, which is probably a secondary condition. The lesions 
in the spinal cord are less extensive and not so well marked. The 
vessels of the brain, and to a less extent those of the spinal cord, 
usually show a marked inflammatory infiltration of their external 
coats; the perivascular lymph spaces are partly involved. The 
