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 ULCERATIVE STOMATITIS IN SOLIPEDS.

Causes. Apart from the ulcerations and erosions of specific

diseases (glanders, horsepox, pustulous stomatitis, aphthous fever,
etc.,) this condition is especially liable to appear in anæmic and
debilitated subjects (Cauvet), as in rachitis (Friedberger and
Fröhner), cancer (Cadeac) chronic internal abscess (Cadeac), etc. As
an exciting cause and as a means of furnishing an infection atrium
for the microbes of ulceration all conditions of simple lesion of the
mucous membrane—mechanical, chemical, thermic, venomous, etc.,
are operative. Dieckerhoff has described it in connection with
diphtheritic rhinitis, Friedberger with a nasal and conjunctival
catarrh, Zeilinger and Kohler with aphthous fever, Mobius and
Hackbarth with trefoil poisoning.
Lesions and Symptoms. There is the usual dainty feeding and
disposition to masticate imperfectly or even to drop the partly
insalivated morsels, working of the lips, the formation of froth on
their margins, and the drivelling of saliva in long strings or filaments.
As the disease advances this becomes bloody and fœtid. The local
lesions may be at first like white pulpy spots of softened and
degenerating epithelium, which is exceptionally, raised in blisters.
This is followed by desquamation and the formation of open sores
which are indolent, and show a disposition to further erosion and
extension. They may be rounded or irregularly indented in their
borders, and contain a brownish, blackish or greenish viscid debris.
They vary widely, however, in general appearance and in their
disposition to speedy or sluggish healing, being apparently
influenced by the nature of the pathogenic microbe and the
susceptibility of the subject. In some cases the molecular
degeneration extends deeply into the mucosa, and even over the
edges of the lips into the adjacent skin. Recovery and complete
cicatrization may take place in one week, or successive outbreaks
may take place in the same animal lasting in all for months as in
Cadeac’s case associated with chronic abscess of the mesentery.
Treatment. The first consideration is to correct the debility on
which the affection is based. Iron and bitter tonics, mineral acids,
and nourishing food given in the form of soft mashes, pulped roots,
or farinas, which will require little mastication, and the antiseptic
cleansing of the mouth after each meal are the main features of the
treatment. As antiseptics, vinegar is inimical to the microbes of the
mouth, which affect alkaline media, borax, boric acid, carbolic acid,
sulphurous acid, the sulphites and hyposulphites, permanganate of
potash, chlorate of potash, creolin, and sulphate or chloride of iron
furnish a sufficient choice of comparatively nontoxic agents. Ulcers
may be touched with tincture of iodine, lunar caustic, or sulphate of
copper.
 ULCERATIVE STOMATITIS (DIPHTHERIA)
IN CALVES.
Accessory causes. Infection. Experimental inoculation. Bacillus, grows on blood
serum. Lesions in mouth, nose, air passages, intestines, digits. Symptoms: difficult
sucking, fever, swollen, whitish spots on buccal mucosa, phagadenic sores, fœtor,
symptoms of extending disease, anorexia, debility, prostration. Duration.
Diagnosis from foot and mouth disease, from actinomycosis, from tuberculosis.
Prevention: cleanliness, antisepsis, segregation, diet of dam, sterilized milk.
Treatment: antiseptic and eliminating: locally antiseptic.
This has been observed at frequent intervals in calves, as a serious,
fatal, communicable disorder occurring in the first few weeks of life.
Causes. It has been attributed to unhygienic conditions of the
dams, close, damp, impure stables, unwholesome or spoiled food,
and privations of various kinds, and these, in all probability, increase
the susceptibility. The congestion and traumatism connected with
the cutting of the teeth is another predisposing cause. The ultimate
cause is, however, the contagious element and the disease has been
conveyed to healthy lambs by the introduction into their mouths of
the necrotic products from the diseased subjects (Dammann). Sheep
inoculated in the conjunctiva presented violent conjunctivitis in
forty-eight hours. Inoculated rabbits died of septicæmia. Mice
showed the same symptoms as calves, while guinea pigs showed an
abscess only at the seat of inoculation (Löffler).
The identity of the germ has not been fully demonstrated.
Dammann found a micrococcus, but testimony from the inoculation
of its pure cultures is wanting, and the buccal mucosa of the sucking
calf is full of varied germs some of which are irritating and
pathogenic to an injured mucosa.
Löffler found in the epithelial concretions (false membranes) of
the mouth and intestines, a bacillus of half the thickness of the
bacillus of malignant œdema, five times as long as broad and usually
connected with its fellows to form filaments. He failed to obtain
cultures of this in nutrient gelatine, but grew it successfully in blood
serum from a calf. Transferred to fresh serum the culture failed. The
pure culture does not seem to have been tried on the calf.
According to Dammann the lesions occur indiscriminately in the
mouth, the nose, the larynx, trachea, lungs, the intestinal canal and
the interdigital space.
It has been suggested that the mouth of the calf rendered
susceptible by the congestion caused by suction, is infected by licking
the previously infected umbilicus.
Symptoms. There are the usual symptoms of indisposition to suck,
salivation, redness of the buccal mucosa, and general indisposition.
In two or three days the mucosa shows raised, pulpy, white or
grayish patches about a line in diameter. These gradually soften and
break down and in four or five days leave dark red angry sores one-
sixth to one-third inch in diameter dotted with grayish points and
surrounded by a congested areola. These exhale an offensive odor
and tend to extend in superficial area and in depth, invading
indiscriminately the various subjacent tissues. The lips may be
perforated, the muscles, cartilages, periosteum, and periodontal
membrane invaded, the teeth may be shed, and the alveoli filled with
the offensive debris of ulceration. Swelling of the throat may follow
from implication of the pharynx and its lymph glands, symptoms of
laryngitis, bronchitis, and pneumonia may succeed, also infective
gastritis and enteritis. These various parts may be infected by the
direct transference of the infecting saliva, but the germ is also held to
be transmitted through the blood to implicate distant organs.
Appetite is gradually lost, a blackish, fœtid diarrhœa, sets in and
the calf is sunk in a profound prostration and debility due partly to
the enforced abstinence and colliquative diarrhœa, but much more to
the absorption of toxic matters. Death may ensue from the sixth to
the twelfth day. In case of recovery a month may be requisite for the
completion of convalescence.
Diagnosis. This has to be distinguished especially from aphthous
fever by the absence of the large, and clearly defined vesicles of that
disease, by the fact that the mammary region and interdigital spaces
usually escape, and especially by the immunity of the dam and of
other more mature animals. From actinomycosis of the tongue it is
diagnosed by its more rapid progress, by the marked constitutional
depression, and prostration, and by the absence of the marked
induration of the actinomycotic organ (holzzunge) and by the
sulphur yellow pin head-like nodules of actinomyces. Tuberculosis is
rare in the first weeks after birth in calves, and never makes the rapid
progress nor causes the profound depression of this disorder.
Prevention. The first object must be to destroy the infection, and
the second to obviate the susceptibility of the young animal. The
clearing away of all accumulations of litter, filth, and even fodder
from the stable proper, including the stalls where the dams lie,
should be followed by a thorough whitewashing or disinfection, with
sulphate of copper or of iron, or even mercuric chloride, (1:500.) If
the disease has already appeared in a stable the calves should be
penned singly to avoid the possibility of infection through sucking
each others navels. In all cases an antiseptic (tannin, carbolic acid)
should be applied to the navel of the new born. The food of the dam
and nurse should be nutritive and free from any suspicion of
mustiness or decomposition, and when possible the calf should be
allowed to draw its own milk from the teat. When this cannot be
allowed, artificial feeding should be surrounded by all the
safeguards, named under acute indigestion of calves.
Treatment. Cadeac strongly recommends ½ oz. common salt daily
with the food, or alcohol ¾ oz., or a strong infusion of coffee mixed
with the milk. Lenglen advises quinoa in the form of tincture, ½ to 1
oz. McGillivray sulphate of soda. Tincture of chloride of iron 30
drops in an ounce of water with each meal would be an excellent
resort.
Locally antiseptics are our main reliance. Naphthol, naphthalin,
salicylic acid, or salicylate of soda, may be applied directly to the
diseased mucous membrane. Tincture of chloride of iron in water
(1:2) is one of the best agents (James). Carbolic acid 1 drachm in 6
oz. water, and 1 oz. alcohol has been used safely and with excellent
results (Lenglen). Like most other antiseptics, however, this latter
must be used with caution as regards the amount. No actively
poisonous antiseptic is admissible. The antiseptic should be swabbed
over the whole interior of the mouth after each meal.
In case of deep gangrenous masses excision and antiseptics are
demanded.
 ULCERATIVE STOMATITIS IN LAMBS AND
KIDS.
Causes: Accessory, locality, youth, debility, unsuitable food, impure air,
parasitism, contagion. Bacteria. Symptoms: difficult sucking, frothing, salivation,
buccal redness and swelling, white, softened patches, suppuration, granulation,
fœtor, emaciation, debility, bowel symptoms, respiratory. Duration. Treatment:
Artificial feeding, antisepsis, disinfection, mild caustics, etc.
Causes. This has been noticed as an enzootic affection in young
and debilitated animals, while the mature and more robust ones
escape. Anæmic lambs, those that are fed on watery, innutritious
materials (potatoes, grains, waste of sugar factories), those kept in
close confinement, indoors, and those that suffer from distomatosis
show the disease. Impure air, damp, dark places and impure water
have their influence. The disease is manifestly contagious, but the
infecting microbe has not been demonstrated. It was formerly
supposed to be the oidium albicans, the fungus of muguet, but
Neumann demonstrated its absence, and though he found leptothrix
buccalis, bacilli, spirochcæte and micrococci he failed to show that
any one of these in pure culture would cause the disease. Rivolta
charged it on bacterium subtile agnorum and Berdt on the
polydesmus exitiosus which according to him the sheep contract
from eating rape cake. The withdrawal of the cake led to a rapid
recovery.
Symptoms. The disease may begin insidiously without at first very
marked symptoms. Sucking is painful and infrequent, an acid froth
collects about the mouth, and white patches appear on the gums or
other part of the buccal mucosa, with at times redness and swelling,
and the separation of the gums from the teeth. The white epithelial
patches soften and are easily detached, leaving bright red patches,
which bleed easily, and tend to extension and coalescence. These are
covered by a viscid mucopurulent matter, and may become the seat
of granulations, or they may involve the subjacent tissues in
ulceration causing evulsion of the teeth, or necrosis of the jaw bone.
The odor of the mouth is fœtid. Prostration and emaciation set in,
and often bear a ratio to the extension of the disease to the digestive
and respiratory organs. This is manifested by uneasy movements of
the hind feet, shaking of the tail, frequent lying down and rising,
constipation or diarrhœa: or by cough, snuffling breathing, swelling
of the submaxillary and pharyngeal glands, and hurried, oppressed
breathing. The complication of vesicular and pustular eruption has
been noticed. Death may occur in eight or ten days, or more
commonly recovery ensues.
Treatment must proceed on the same lines as in the calf. Artificial
feeding on gruels, with antiseptic washes for the mouth at each meal
are indicated. Chlorate of potash, chloride of lime, borax, sulphites
and hyposulphites of soda, carbolic acid, and the salts of iron afford
an ample field for selection. For ulcers, a pointed stick of nitrate of
silver, or a solution of muriatic acid in three times its volume of
water, applied by means of a glass rod or pledget of cotton will serve
a good purpose.
 ULCERATIVE STOMATITIS IN SWINE.

Causes: improper food; filthy pens; debility; toxins of specific diseases;

microbian infection. Symptoms: inappetence; grinding teeth; champing jaws;
salivation; fœtor; buccal swelling and redness; pulpy spots; desquamation; ulcers;
pharyngeal, enteric and osseous complications. Treatment: Segregation;
disinfection; local antiseptic washes; tonics.

This is the Scorbutus of Friedberger and Fröhner, the gloss-

anthrax of Benion.
Causes. It has been attributed to insufficient or irritant food, to
damp, close pens, and to chronic debilitating diseases and all these
act as predisposing causes. In gastritis and in infectious fevers like
hog cholera, swine plague, and rouget (hog erysipelas) the spots of
congestion and petechiæ on the buccal mucous membrane may
become the starting points for ulcerative inflammations. These
conditions appear, however, to be supplemented by infection from
bacteria present in the mouth or introduced in food and water, and
as in the case of other domestic animals the most successful
treatment partakes largely of disinfectant applications.
Symptoms. Loss of appetite, grinding of the teeth, champing of the
jaws, the formation of froth round the lips, fœtor of the breath,
redness of the gums and tongue, and the formation of vesicles or
white patches which fall off leaving red angry sores. These may
extend forming deep unhealthy ulcers, with increasing salivation and
fœtor. As the disease advances the initial dullness and prostration
become more profound, and debility and emaciation advance
rapidly. Unless there is early improvement an infective pharyngitis,
or enteritis sets in, manifestly determined by the swallowing of
virulent matters from the mouth, and swelling, redness and
tenderness of the throat, or colics and offensive black diarrhœa
hasten a fatal issue. Rachitis may be a prominent complication, as it
seems in some instances to be a predisposing cause.
Treatment. Isolate the healthy from the diseased and apply
disinfection to all exposed articles and places. Employ local
antiseptics as on the other animals. Sulphuric or hydrochloric acids
in 50 times their volume of water, or tincture of iron, chlorate of
potash, or chloride of ammonia, or borax have been used
successfully. Bitters and aromatics have also been strongly
recommended.
 ULCERATIVE STOMATITIS IN CARNIVORA.
Causes: dietary causes; constitutional debilitating diseases; dental disorders;
microbian infection; microbes. Symptoms: difficult sucking or mastication;
salivation; dullness; prostration; mucosa red with gray patches, erosions, and
ulcers; fœtor; loose teeth; excess of tartar. Extensions to face, throat, lymphatics,
nose, eyes, stomach, liver, bowels. Duration. Treatment: clean teeth; antiseptics;
mild caustics; stimulants.
Causes. This affection is more common in this class of animals
than in the herbivora, being apparently dependent in great part on
their artificial habits of life, the sweet and stimulating diet and the
derangement of the digestive organs. The lowering of the general
health in connection with privation or disease and especially canine
distemper, rachitism or indigestion must be recognized as
predisposing causes, while the accumulation of tartar on the teeth, or
the decay of the teeth themselves, constitutes a potent exciting local
cause. In connection with such cretaceous deposits the decomposing
elements of the food collect, and the irritant products of their
fermentation lead to disease of the gums, congestion and ulceration.
Superadded to this is the bacteridian infection of such diseased
parts, through which the ulceration is started, maintained and
extended. This infection is not that of a specific microbe, but usually
of a multiplicity of germs, one or more of the bacteria that live
habitually in the healthy mouth, taking the occasion of the existence
of a wound, or of a reduction of vitality to colonize the mucosa which
would otherwise have remained sound. The microbes actually found
in the ulcers are very varied. Pasteur isolated a spirillum, Fiocca the
bacillus salivarius septicus, others have found pus bacilli, and in
sucking kittens the bacillus coli communis.
But the attempts made to convey the disease to healthy mouths by
the transfer of the microbes have usually failed (Pasteur, Netter,
Cadeac). To establish their pathogenic action therefore, it appears to
be necessary to furnish a susceptible mucosa as well as an infecting
microbe. This explains why the disease does not spread as an
infection, the average mouth is immune and it is only when it
becomes the seat of a wound, bruise or other injury, or when the
general system has become so reduced that the resisting power is a
minor quantity, that the hitherto harmless germ becomes actually
pathogenic.
Symptoms. There is indisposition to suck or eat, the patient leaves
the teat or the food, and looks dull, depressed and disposed to lie
down apart. There is evident salivation and on opening the mouth we
may find the offensive odor, the tartar covered teeth with red or
ulcerated gums, and on the cheeks, lips and tongue dark red patches
of congestion, or whitish or yellowish gray, soft, pulpy spots of
disintegrating epithelium. This is followed by shedding of these
epithelial patches, and the formation of rounded ulcers of a line in
diameter or less. These are tender, and bleed readily. They may
extend to the skin of the lips, or deeply into the mucosa, the muscles
or bones, and the attendant morbid process may cause loosening and
evulsion of the teeth. There may be implication of the pharynx, the
lymph glands, the nose, the eyes, the stomach, the liver, or the
intestines with corresponding symptoms. Death may supervene in
from six to thirty days, or a more or less speedy recovery may take
place.
Treatment. The first step as a rule is to remove the tartar from the
teeth. This is often done with a wooden spud dipped in a weak
solution of hydrochloric acid. A steel scraper will usually act well and
without the solvent action of the acid.
Next will come the removal of all diseased teeth which are
operating as local irritants and as centres for infectious microbes and
their hurtful products.
Then antiseptics in the form of liquids applied as in the other
animals with each meal, will be necessary to counteract infective
action, and give the tissues an opportunity to re-establish their
integrity. Cadeac recommends a 10 per cent. solution of oil of thyme,
as a safe and efficient application. Boric acid, borax, salol, salicylic
acid, tannic acid, sulphurous acid, or carbolic acid largely diluted
may be substituted. Internally iron tonics and bitters are of great
value in improving the tone of the system and securing antisepsis of
the intestinal canal. The sulphites too may be given with advantage
internally. In depressed conditions alcoholic stimulants may be used
both as local antiseptics and general stimulants. As in other animals
ulcers may be touched with a rod dipped in tincture of iodine, or a
strong solution of chloride of zinc, or nitrate of silver.
 MERCURIAL STOMATITIS.
Animals suffering. Causes: mercurial baths, ointments, blisters and surgical
dressings; mercurial vapors; deposits on vegetation; rat poisons; malicious
poisoning. Lethal dose in horse, ox, sheep and goat. Mature and old eliminate
more slowly. Symptoms; Salivation; red, swollen buccal mucosa; gingivitis;
loosening of teeth; fœtor; ulceration; anorexia; gastro-intestinal tympany; loose,
fœtid stools; fever; weakness; dyspnœa; langor; blood extravasation in nose,
mouth, throat, bowels, womb, skin; abortion; skin eruptions. Lesions in mouth,
stomach, intestines, serosæ, kidneys, muscles, encephalon. Treatment; stop the
introduction of mercury; as antidote potassium sulphide; emetic; cathartic;
mucilaginous and albuminous antidotes; potassium iodide as an eliminating agent.
Locally potassium sulphide or chlorate. Iron tonics.
This has been especially seen in the sheep, dog and ox, and less
frequently in other domestic animals.
Causes. In sheep the use of baths containing corrosive sublimate,
or of mercurial ointment for acariasis or other cutaneous parasitism.
In other animals it comes mostly from licking mercurial dressings
applied to the skin—calomel, red precipitate, mercurial ointment,
protoiodide of mercury. The red iodide being more irritating is less
frequently taken in. The modern extensive usage of mercuric
chloride solutions as surgical antiseptics opens up a new channel of
infection. In the injection of the uterus or of large abscesses, or in the
daily irrigation of large wounds a dangerous amount may be
absorbed. The application of this agent as a caustic in cases of
tumors is correspondingly dangerous. Vapors from metallic mercury
in confined spaces as in ships’ holds, or from fires on which the
mercurial compounds have been thrown, are ready means of
poisoning, acting primarily on the air passages and lungs and later
on the mouth. The condensation of mercury on vegetation and other
food products in the vicinity of factories where mercury is handled
(Idria) affects domestic animals directly. Finally the small animals
are poisoned by eating the mercurial rat poisons, and all animals are
subject to malicious mercurial poisoning, with sublimate especially.
Stomatitis with fatal pharyngitis and enteritis will result in the
horse from 2 drs. of corrosive sublimate. About one-half of this may
poison the ox, and one-fourth the sheep or goat. Ruminants are more
susceptible to the toxic action of mercury than monogastric animals,
one evident reason being the long delay of the successive doses in the
first three stomachs, so that finally a large quantity passes over at
once into the fourth stomach and duodenum for absorption. The old
too are more readily poisoned than the young, as the functions of the
kidneys are more impaired in age and the poison is not eliminated
with the same rapidity.
Symptoms. Mercurial stomatitis is a local manifestation of a
general poisoning. Salivation is one of the most prominent
phenomena, the watery saliva falling in streams from the angles of
the mouth. The buccal mucosa generally becomes red and swollen
and the tongue becomes indented at the edges by pressure against
the molars. The gums especially suffer and the teeth raised in their
sockets by the swelling of the periodontal membrane, become loose,
and easily detached. The mucosa of the gums becomes soft and
spongy, bleeds readily under pressure and soon shows erosions and
ulcers. This condition extends to the lips, cheeks and lower surface of
the tongue while the upper surface of the latter organ, the fauces and
pharynx commonly escape. The breath and buccal exhalations are
very offensive, and the animal loathes food, and has little power of
mastication or deglutition. Sometimes the ulcers extend even to the
bones.
Along with these local symptoms there are usually gastro-
intestinal irritation, tympany, inappetence, continuous rumbling in
the belly; badly digested fœtid stools, often diarrhœa, small weak
pulse, hyperthermia, accelerated breathing, cough, and great langor
and prostration. A tendency to blood extravasation is shown in
sanguineous fæces, epistaxis, bleeding from the mouth, the throat or
the womb and even into the skin. Pregnant females may abort. The
eyes are dull and sunken, and the conjunctiva yellow. Eczematous or
pustular eruptions may appear on the skin on the nose, lips, neck,
back, loins, croup or perineum.
Lesions. In addition to the lesions described above, there are
usually gastro-intestinal inflammation, œdema of the peritoneum
and pleura, in the lung as well as in the serosæ, (pneumonia is not
uncommon especially in sheep), intestines, kidneys and muscles,
hæmorrhagic spots are not uncommon, the blood forms a loose black
coagulum, and the encephalon is anæmic and softened.
 Treatment. The first consideration is to cut off the supply of
mercury. Mercurial applications on the skin should be washed off
with tepid water and if necessary soap. An application of sulphide of
potassium will precipitate the mercury in an insoluble form. For
mercurial agents in the alimentary canal an emetic may be given (if
the animal is one susceptible to emesis) followed by a saline laxative.
This may be combined with or followed by raw eggs, mucilage, wheat
gluten or other albuminoid, sulphide of potash or sulphur, to
precipitate the mercury and prevent its absorption. Later, when the
bowels have been cleared, iodide of potassium in small doses will
serve to dissolve and remove what mercury may be lodged in the
tissues.
Locally one of the best applications is chlorate of potash as a
mouth wash, 2 drs. to the quart of water. To this may be added
tannic acid or other vegetable astringent and even alcohol.
Finally a course of iron and bitter tonics will serve a good purpose
in restoring the general tone.
 STOMATITIS FROM CAUSTICS.

Caustic Alkalies; symptoms, lesions and antidotes. Caustic Acids; symptoms,

lesions and antidotes. Caustic salts; symptoms, lesions and antidotes.

Caustic Alkalies (soda, potash, ammonia and their carbonates)

often cause stomatitis. What is supposed to be weak lye, given to
counteract indigestions, colics, and tympanies often proves
dangerously irritating, and some of the worst forms of stomatitis we
have ever seen in the horse originated in this way. As the animal
refused to swallow, the caustic liquid lay in the mouth and virtually
dissolved the epithelium and surface layers of the fibrous mucosa.
The surface in such a case is usually of a deep red, and where the
cuticular covering remains, it is white and corrugated. The antidote
is a weak, non-irritant acid, such as vinegar, boric, citric, or salicylic
acid. When the caustic alkali has been thoroughly neutralized in this
way the ordinary treatment for catarrhal stomatitis may be followed.
The attendant gastritis must receive its special treatment.
Caustic Acids. Sulphuric, nitric and hydrochloric acids act by
abstracting liquids and charring the tissues. The lesions from strong
sulphuric acid turn black, those due to nitric acid, yellow,
(zanthoproteic acid,) and those due to muriatic acid are white, with
the characteristic odor of chlorine. The antidote in such cases is a
non-irritant basic agent, such as chalk, lime water, soapsuds,
calcined magnesia, and mucilaginous liquids, albumen, gluten, flax
seed, with opium. The same agents are applicable to the attendant
gastritis and when the acids are thoroughly neutralized the treatment
is as for simple inflammation.
Caustic Salts. Among caustic salts may be named mercuric
chloride, sulphates of copper and iron, chlorides of iron and zinc,
tartar emetic. These may be treated by albumen, blood, white of egg,
milk, gluten, mucilage and other sheathing, protecting agents which
will form with the salts insoluble and harmless coagula. The
subsequent treatment will follow the lines marked out for simple
stomatitis. To prevent infection of the raw surface Cadeac
recommends: tannic acid 1 oz., benzo-naphthol 3 drachms,
powdered gentian 6 drachms, honey, sufficient to make an electuary.
 MYCOTIC STOMATITIS IN FOALS, CALVES
AND BIRDS. THRUSH. MUGUET.

Oidium (saccharomyces) albicans; a parasite of the young; cultures. Symptoms

in foals and calves; congested buccal mucosa; curd-like concretions; erosions.
Diagnosis from rinderpest. Treatment; disinfection; sunshine; open air; exercise;
locally antiseptics.

This is a form of stomatitis manifested by a raised white patch on

the mucous membrane and determined by the presence of the
oidium albicans (saccharomyces albicans), a cryptogam
discovered by Berg in 1842 in thrush in children. It is closely allied to
the mucor, and attacks only the young and feeble. The white crust
consists of epithelial cells intermingled with an abundance of the
white mycelium and oval spores of the fungus. Andry in his artificial
cultures found that it was pearly white when grown on gelatine, dirty
white on potato, and snow white on carrot.
Foals and Calves. Symptoms. The buccal mucosa red, congested
and tender, shows here and there white curdy looking elevations, or
red erosions caused by the detachment of such masses. These bear a
strong resemblance to the concretions seen on this mucosa in
rinderpest, but are easily recognized by the absence of the attendant
fever, and by the discovery, under the microscope, of the specific
microphyte. The eruption may extend to the pharynx and œsophagus
and interfere fatally with deglutition, but usually it merely renders
sucking painful and is not serious.
Treatment. It is always well to destroy floating germs by cleansing
and whitewashing the stable, and to invigorate the young animals by
sunshine, free air and exercise. Locally the most effective agent is the
old favorite remedy borax which arrests the growth of the parasite
whether in artificial cultures, or in the mouth. The powder may be
rubbed into the sores or it may be mixed with honey or molasses and
used as an electuary. As substitutes boric acid, salol, thymol, chlorate
of potash, or permanganate of potash may be used.
Birds. The affection has been twice observed as occurring in the
œsophagus and crop of two chickens. Martin tried in vain to
inoculate it on other fowls, and Neumann failed to convey it from
child to chicken by feeding. The element of individual susceptibility
was manifestly lacking. From its seat in the crop the malady passed
unnoticed during life. In cases that can be recognized, treatment
would be the same as in young mammals.
 PARALYSIS OF THE TONGUE.
GLOSSOPLEGIA.
Causes: Nervous lesions—central or peripheral, parasitic, inflammatory,
infectious, traumatic or degenerative. Symptoms: unilateral and bilateral.
Treatment: remove cause; use nerve stimulants, embrocations, blisters, frictions,
galvanism, suspension of tongue.
Paralysis of the tongue depends on a lesion of the medulla
oblongata, or of the 7th or 12th cranial nerve. The central lesions may
be connected with cœnurus or other parasites in the brain,
hydrocephalus, meningitis, cerebro spinal meningitis, infectious
pneumonia, abscess (strangles), and tumors. The distal or nerve
lesions may be due to neuroma, tumors, traumas, lacerations,
bruises, or violent distension of the tongue. Parotitis, abscess of the
guttural pouch and tubercle may be added as occasional causes. As
direct traumatic injuries those caused by wearing a poke by a
habitual fence-breaker, excessive dragging on the tongue in
operations on the mouth, and compression of the tongue by a loop of
rope passed over it, require mention.
Symptoms. In unilateral paralysis the affected half of the tongue
remains soft and flaccid and is liable to be crushed between the
teeth, the active muscles of the opposite half pushing the organ over
to the paralyzed side. In bilateral paralysis the tongue hangs out of
the mouth, and being crushed and torn by the teeth, it swells up, and
may even become gangrenous.
Treatment. Will vary according to the cause. After removal of the
central or nervous lesions, the remaining functional paralysis may be
treated by strychnia, internally or hypodermically, by frictions or
stimulating embrocations to the intermaxillary region, or by
electricity. The tongue must be suspended in a sling to prevent
œdema, inflammation and wounds by the teeth. In bad cases of
bilateral traumatic glossoplegia in meat producing animals it has
been advised to have the subject butchered.