Prominent symptoms, asthenia and vertigo. Vary with cryptogam, merge
into zymotic diseases. Causes: grain harvested damp and moulded,
bluish or greenish, hay greenish white, brown or black, clover
reddish, musty fodder, and diuresis, indigestion, gastric intestinal
and systemic paresis, somnolence, delirium. Rusts, spring and summer,
their evolution. Bunt, smut, produce fever and paralysis, spasms,
abortions and dry gangrene, buccal erosions; evolution of ergot, honey
dew on leguminous plants causing skin disease, bacterial ferments,
diplococcus, streptococcus from foul water, causing enteritis.
Symptoms: _adynamic_, dullness, blunted sense, pendent head, ears,
eyelids, congested, yellow, ecchymosed conjunctiva, fever, tympany,
colic, constipation, dung small, round, coated masses, vertigo,
sometimes fatal diarrhœa, or colliquative diuresis; _vertiginous_:
fever, anorexia, yellow mucosæ, tardy breathing, costiveness colics,
stupor, somnolence, giddiness, heavy steps, stumbling, delirium, push
head against wall, clinch jaws, grind teeth, make walking or trotting
or plunging motions, or pull on halter and fall, amaurosis, paralysis,
coma. Remissions. Death in one day or upward. Resumption of functions
and recovery. Diagnosis: from meningo-encephalitis. Lesions:
gastro-intestinal congestion, infiltration, ecchymosis, fermenting
ingesta, congestion of mesenteric glands, liver, brain and meninges.
Leucin and tyrosin in urine. Treatment: stomach pump, antiferments,
potassium iodide, purgatives, enemata; for brain, bleeding, sedatives,
ice, snow, elevation, derivatives, prevent mechanical injury.
The most prominent features of cryptogamic poisoning in these animals
are asthenia and vertigo. In dealing with such poisoning, however, we
must bear in mind that we have in hand, not one particular disease but a
group, differing among themselves according to the cryptogam and its
products which may be present:—a group moreover which overlaps more or
less the true zymotic diseases.
_Causes._ Oats, barley and other grain or fodder which has been put up
damp, and especially ground feed, becomes speedily overgrown and
permeated with moulds, especially =penicillium glaucus=, =aspergillus
flavus= and =glaucus=, =mucor racemosus=, and =ascophora mucedo= which
give a bluish or greenish color and heavy odor, rob it of its nutritive
constituents and charge it with toxic products. On mouldy hay it is
common to find =aspergillus candidus=, =botrytis grisea=, =torula
herbariorum=, and =eurotium herbarium= which form a greenish white or
brownish dust. The =spœria herbarium= is characterized by small black or
brown spots with yellowish, brown or black spores. The peronspora
trifolium attacks growing clover (clover sickness) and =isaria
fuciformis= the fescue grasses. The latter has a red color and mucous
consistency and is charged with producing fatal poisoning in cattle.
=Mouldy= or =musty= oats, or other grain or fodder have long been
notorious for producing diuresis in horses with excessive elimination of
phosphates, extreme emaciation, weakness and death. In other seasons,
and probably because of a difference in the fungi or their products they
have caused widespread enzootics of indigestion with paresis of stomach
and bowels, and of the systemic muscles. Paraplegia is a common
manifestation, suggesting lesions of the spinal cord, and in other cases
there are general paresis, somnolence and delirium suggesting cerebral
lesions, (Staggers).
Gillespie records an enzootic of gastro-intestinal indigestion and
tympany among the horses of a battery of artillery in Afghanistan from
eating mouldy grass. Fröhner, Martin and Varnell have seen cases of
poisoning by moulds without digestive, urinary or febrile troubles.
Of =rusts= growing on grain crops there are two chief varieties; the
=spring rust= (_uredo rubigo vera_) which commences as light yellow
patches on the leaves and stems, which change to black as the fungus
approaches maturity; and the =summer rust= (_uredo linearis_) which
grows to a larger size and assumes a browner color. Each of these passes
through an evolutionary cycle, the small preliminary patches (=uredo=)
passing into the mature fungus (=puccinia rubigo vera= and =puccinia
graminis=.) Then it must pass through an alternate generation on another
family of plants before it can again grow on the gramineæ.
=Bunt= produced by the _tilletia caries_ attacks the grasses and small
grains. The growing seed (wheat especially) is changed into a black or
olive colored powder, having a fishy odor. If the stems are attacked the
leaves become pale, withered and dry. It can only be detected by
carefully examining the individual seeds.
Other forms of smut are the =ustilago carbo= and =ustilago maidis= the
familiar black smuts of small grains and maize. These develop by
preference in the growing seeds, but also in the stem and leaves. The
_tilletia caries_ is as a rule more poisonous than the _ustilago_ the
effects being mainly hyperthermia and paralysis. There is, however, a
tendency to spasmodic contractions, and abortions, and dry gangrene will
occur from smut. The author has seen a large herd of cattle attacked
with gangrenous sores around the coronet, which were promptly stopped
when the light, smutty ears of corn were no longer given. In other cases
the hoof was in part separated from the quick and creaked when the
animal walked.
In connection with the gangrenous ergotism of cattle, the author has
found on the same farms and feed, horses with ulcers on the buccal
mucosa and gastro-intestinal indigestion. =Ergot= affects the seeds in
nearly all the small graminaeæ and is produced by the _claviceps
purpurea_ which first attacks the ovary of the seed (_sphacelia_ stage),
then it invades the whole seed which grows out from the glumes as a
hard, dark or purple spur-like process (_ergot_ stage), then falling on
the ground it grows up as a minute stalk with rounded head containing
spores.
=Honey dew= growing on leguminous plants is reputed to cause skin
disease in white horses and on the white spots of dark horses, from
which those not eating the diseased plants escaped.
_Bacterial ferments_ have an equally bad reputation. Bastin records the
poisoning of five foals by fermented rye; Dieckerhoff describes an acute
gastro-enteritis with congestion and swelling of liver, spleen and
kidneys, as the result of microbes and their products in the fodders.
Galtier traced a pneumoenteritis in the horse to two cocci, a motile
_diplococcus_ and non-motile _streptococcus_. Both stained in aniline
colors, and were bleached by iodine. They grew in ordinary culture media
above 50° F. but most freely at 98° F. The animals were infected by
drinking putrid water or spoiled fodders in which the microbes were
contained. The change to boiled water in the former case led to their
prompt disappearance. Reynal, Cailleux and Foucher have also adduced
instances of severe enteritis in the horse from drinking putrid water.
These animals showed active congestion of the intestinal mucosa with
abundant infiltration of the submucosa.
Bouley found 14 cases in one stable, the owner of which had marketed the
good fodder and kept the spoiled for home use. Barthelemy, Alasonniere,
Lombroso and Hausmann, Clichy, Rey, Gamgee and others give similar
examples.
A large number of observations show the dangerous results on the horse
of mouldy bread, inducing colics, vertigo, profuse sweating.
_Symptoms_. When =Adynamia= prevails there is great dullness and
depression, the senses are blunted, the head depressed resting on the
manger, the eyes sunken, weeping and half covered by the drooping upper
lid, the conjunctiva is congested, sometimes yellow or marked by
petechiæ. The mouth is hot, the lower lips pendent, the tongue furred,
the abdomen somewhat tympanitic, with slight colics, but with little
rumbling or indication of peristalsis. There is a primary constipation,
a few small, hard pellets being passed with effort. The temperature may
be 102° to 104°, breathing short, pulse small, weak; the walk unsteady,
the animal preferring to stand, completely apathetic. In some cases a
profuse diarrhœa sets in and may prove fatal.
In the cases attended by diuresis, the weakness is extreme, emaciation
advancing rapidly, but the other symptoms of nervous depression are less
marked, the poisons being apparently eliminated by the kidneys (see
_diuresis_).
In the =Vertiginous form= the disease may set in with more or less
hyperthermia, anorexia, a dislike particularly of the spoiled fodder,
yellowness of the visible mucosæ, slow breathing, small accelerated
pulse, costiveness, tympany, colics more or less intense, tenderness of
the belly, and sooner or later marked nervous disorder. This may be in
the form of stupor, the head resting in the manger, the senses are
manifestly clouded, the animal walks unsteadily, staggers, steps
heavily, striking the feet against obstacles, and stumbling. At the end
of a variable number of hours (2 to 6 or 8 after feeding) nervous
excitability and vertigo may supervene. He may push the head against the
wall, the jaws clenched, grinding the teeth, the eyes fixed, pupils
dilated, facial muscles contracted, respirations hurried, heart
palpitating and the skin perspiring. He may continue in this position,
moving his feet as if walking, or he may rear plunging his feet into the
manger or fall back over, and rising push anew against any object he may
come in contact with. Coulbaux speaks of rabiform symptoms such as
attempts to bite but any such deliberate purpose is rare.
There may follow complete amaurosis, insensibility to pricking of the
skin, and even paralysis or coma. Hyperæsthesia may also be temporarily
present.
_Course._ Remissions and exacerbations usually alternate, the duration
of the former furnishing some criterion by which to establish a
favorable prognosis. Death may take place in 24 hours or it may be
delayed for several days. Recovery is usually heralded by the resumption
of defecation and urination, and the return of appetite. It is liable to
be at first only partial, some of the senses remaining dull, or a
general stupor persisting.
_Diagnosis._ In all such forms of poisoning there is the history of
the ingestion of the toxic matters, and in any suspicious looking
cases a careful examination of the food should be made. From
meningo-encephalitis the presence of the abdominal disorder will serve
to identify and to incriminate the food.
_Lesions._ These vary much with the poison. There is always, however,
inflammation of the gastro-intestinal mucous membrane, usually with
ecchymosis, and infiltration of the submucosa. The contents of the
bowels are imperfectly digested, the mesenteric glands congested and
enlarged, the liver congested and softened, and the brain and its
meninges hyperæmic or infiltrated. The leucine and tyrosine present in
the urine during the acute attack is said to disappear when improvement
sets in (Pellagi, Azzaroli).
_Treatment._ The first object must be the removal or neutralizing of the
poison. In some instances the stomach pump or tube might be tried.
Usually one must fall back on antiferments such as naphthol, naphthalin,
salol, salicylic acid, and above all iodide of potassium. The last
checks the growth of the fungi or bacteria and favors elimination of the
toxins. It may be given freely to act on the kidneys. Creolin, 1¼
drachm, repeated three times a day has been found effective (Albrecht).
In addition the action of the bowels may be solicited by full doses of
sulphate of soda and abundance of water.
When the brain is implicated Cadeac recommends bleeding as an
eliminating as well as a sedative measure. In any case use cold water,
snow or ice to the head, elevation of the head, and purgatives which may
as a rule be doubled. Potassium iodide or other antiseptics should be
pushed, and diuresis as well as a relaxed condition of the bowels
maintained. Counter-irritants such as mustard may be applied to the
abdomen, and enemata used at frequent intervals. It is important to fix
the patient to a ring in the centre of a box stall or barn to keep him
from injuring himself.