GEORGE
H.
HART
83
ight be hereditary. Moore, Huffman
and Duncan [1935] described 24 cases of
is condition in calves and growing dairy
animals but concluded that it was different
from blindness due to deficiency of
vitamin A.
Hart and Guilbert [1937] experiment-
ly produced cases of blindness in vitamin
deficiency. In these cases the pupils
were widely dilated and there was a charac-
teristic greenish colouration inside the
eyeball when viewed through the cornea
with the animal facing the light. There
was pinching off and degeneration of the
ptic nerves where they pass through the
ptic canals in the sphenoid bone from
tenosis of the walls of these canals.
These authors regarded the bone changes
s secondary, but, in view of the experi-
ments of Mellanby [1938], this opinion
ay need revision. Kuhlman, Gallup and
Weaver [1936] reported both xerophthal-
-ia and the above permanent type of
blindness in their calves on a diet low in
vitamin A.
Mellanby [1938] produced deafness in
young puppies by withholding vitamin A.
There was nerve degeneration of the
ochlear neurons and new bony growth in
the modiolus, with degenerative altera-
tions in the organ of Corti and the sensory
epithelium of the semicircular canals.
He regarded the overgrowth of bone of the
abyrinthine capsule through pressure and
stretching, to be the most probable cause
of the nerve degeneration. New macros-
copic bone formation was also found at
the base of the skull. This author con-
cluded that nipping in the various foramina
was the cause of the degeneration found
in the optic, trigeminal and facial nerves.
A report by Moore [1939], on blindness
due to constriction of the optic nerve,
papillary oedema and nyctalopia in calves
deprived of carotene, has recently appeared.
Papillary oedma was noted in 19 calves
and 8 mature cows on low vitamin A
rations, as well as in 3 calves at birth
from dams receiving low intake of this
factor. The night blindness was cured by
the addition to the diet of carotene in the
form of alfalfa hay. In none of these
cases was xerophthalmia or keratitis
observed. The blindness was attributed
to intracranial pressure. It is presumed
that permanent blindness occurs only in
young animals because mature cows have
the optic canal fully developed and calcified.
Mucous membranes
Vitamin A deficiency may affect
epithelial structures in any part of the
body as well as peripheral nerves and the
central nervous system. Mason and
Ellison [1935] suggest that vitamin A
plays a part in protein metabolism within
the epithelial cell. In deprivation the
formation of glycoproteins or mucin seems
to be retarded and that of albumenoids or
keratin to be increased.
The respiratory tract is commonly affec-
ted and pneumonia is usually the terminal
condition, causing death. This is frequent-
ly a subacute pneumonia with nodules the
size of a pea or larger scattered through
the hepatised areas and containing a mix-
ture of air and pus cells. Lung abscess
is another condition developing late in the
deficiency. The legs are sometimes swollen
and oedematous and this may be due to
presence of parenchymatous nephritis.
HORSES
Vitamin A deficiency in horses has been
reviewed by Edwards [1937] and the
literature from widely scattered parts of
the world cited. Mitchell [1930; 1931;
1933; 1935; 1936] considers roaring,
stringhalt, navicular disease and bony
exostoses to be manifestations of nutri-
tional deficiencies, including deficiency of
vitamin A as well as Ca and P imbalance.
In Finland Klemola [1933] showed that
faulty hoops in the army horses were due
to vitamin A deficiency. The scaly secre-
tion of the peri-oplic band, which in places
formed a thick spongy crust, changed to
a normal, thin shiny, varnish like layer
when vitamin A or carotene was supplied.
The rations of horses as ordinarily
made up in many parts of the world are