Definition: Acute, infectious, bacteridian disease of sheep, with
colic, enteritis, emphysematous swellings, dark, diffluent blood, and
after death rapid putrefaction. Geographical distribution: Iceland,
Norway, Faroe Islands, Scotland. Causes: inclement weather, exposed
localities, low condition, winter food, chill, frosted grass.
Bacteriology: Bacillus gastromycosis ovis: 2 to 6 μ by 1 μ, in pairs
or filaments, sporogenous, polar staining, anærobic liquefying,
gasogenic, found in the gastro-intestinal congested mucosa, serosa,
liver, kidneys, blood. Pure cultures by boiling five minutes.
Pathogenic to sheep, Guinea pig, mice, pigeons, hens and less
certainly rabbits. Symptoms: resemble blackquarter, sudden, rapid,
fatal, back arched, stiff hind parts, crepitating swellings on hind
parts or elsewhere, colics, tympany, anorexia, pulse and breathing
hurried, separation from flock, lying, drooping head, ears and eyelid.
Usually found dead in morning when apparently well previous night.
Lesions: early putrefaction, slight, transient rigor mortis, tympany,
fœtor, sero-sanguineous exudates under skin, on fourth stomach and
bowels, and elsewhere. Contents of large intestine dry, hard.
Effusions in serosa. Spleen enlarged or not. Liver and kidneys
congested, softened, small, pale necrotic areas containing bacillus.
Prevention: drainage and cultivation, winter feeding, abandon infected
pastures in late fall and winter as pasture for young, avoid
overstocking, burn old fibrous heather. Immunization by sterilized
kidney extract. Treatment.
_Definition._ An acute infectious disease of sheep, manifested by sudden
attack, colicy pains, inflammatory and sero-hæmorrhagic lesions of the
bowels, and sanguino-emphysematous swellings occurring subcutaneously
and especially in the hind quarters. The blood is dark, tarry and
comparatively incoagulable and after death putrefaction advances with
extraordinary rapidity.
_Geographical Distribution._ Braxy is generally prevalent in Iceland
where it was described over a century ago (1778) by Ketilson as
“vinstrarfár” or “vinstrarplága” (“Omasum disease”). In Norway it
prevails on the whole Atlantic border to as far north apparently as the
sheep industry extends (Stavanger to Tromso Amt). The Faroe Islands are
said to be affected throughout. In Scotland it prevails like louping-ill
along the west coast especially, and embraces Caithness, Ross, Cromarty,
Banff, Inverness, Aberdeen, Argyle, Bute, Ayrshire, Lanark, Galloway,
Dumfries, Peebles, Selkirk and Roxburgh.
_Causes._ Like louping-ill this affection is associated with inclement
seasons, exposed localities, and insufficient or indigestible food, but
it differs in being an affection of autumn and winter rather than
spring. It is rarely seen in summer. At a time when it was looked upon
as an acute indigestion, its coincidence with hard frost or deep snow,
was explained on the basis that the victim had been driven to eat dry,
fibrous, indigestible grasses, brakens and heather. W. Williams who
formerly identified the disease with anthrax, seemed to go back to this
theory of indigestion. Though that is no longer tenable, yet it would be
wrong to ignore the effect of inclement weather and unwholesome food in
predisposing the animal system, and robbing it of the healthy tone which
would otherwise have successfully resisted the infection in many cases.
The occurrence of deaths after frosty mornings more than during mild
weather, suggests at once the chill effected in the animal, the chilling
of the paunch by the frosted grass eaten producing a subsequent
congestive reaction, and the known facility with which frozen vegetables
undergo rapid fermentation.
Cowan and Borthwick, (Transactions of Highland Society 1863) agree that
the disease is especially prevalent when the land has been overstocked
in summer, or when there has been a drought which withered up the
pastures, and later a free growth of green herbage from the autumn
rains. This they attribute to the “foul and unwholesome” character of
the autumn growth, but it suggests no less the low condition of the
sheep on the overstocked lands and the soft, aqueous character of the
herbage grown rapidly in a comparatively cold season. Cowan quotes cases
in which the lambs, weaned early and put in a separate pasture (hogg
hirsel), suffered a mortality of 50 per cent., while in later years when
allowed to remain with the ewes until winter, the deaths were reduced to
10 or 15 per cent. Here the more rugged health and vigor were manifestly
strong prophylactic factors.
Both Cowan and Borthwick incriminate the withered heather and the dry,
fibrous (“tathy”) and innutritious tufts of grass which make up a large
proportion of many hill pastures in autumn and winter.
Cowan strongly condemns heavy smearing with tar, which he believes to
encrease the mortality, by lowering the general tone of the system:
“Hoggs are very dull and listless for some time after being smeared with
tar, more especially if heavily smeared; ... when the skin is taken off,
every shed or opening in the wool where the tar has been laid on, is as
distinctly visible upon the flesh as the stripes upon a piece of printed
calico.”
It has been further alleged that the deaths are especially common during
the full of the moon, the usual explanation being that the sheep are
tempted to feed in the night and overload the stomach. It may be added
that at such times the grass is taken in a cold—(often frosted)
condition so as to chill the stomach and cause a congestive reaction,
and that short of this, under the night dews the microbian ferments are
moist and ready to start into full activity, while the herbage if it has
been partly frosted is particularly susceptible to bacteridian attack.
_Bacteriology of Braxy._ The essential cause of braxy was revealed by
Ivar Nielson in 1888, who demonstrated on the local lesions of the
alimentary canal and the capillaries of various internal organs a
bacillus which he named _bacillus gastromycosis ovis_. This is 2 to 6μ
long by 1μ broad, occurring in pairs or filaments. The organism has an
elliptical form and stains deeply at the extremities, while the central,
bulging portion fails to take the color, is highly refrangent, and
represents the spore. The non-spore-bearing bacilli are long, uniform
rods with rounded ends. The germ is anærobic, grows readily in serum
glycerine agar, and is gas producing and foul smelling. Liquefies
gelatine. It is found abundantly in the congested parts of the abomasum
and to a less extent in the bowels, in the mucosa, and in the submucous
and subserous tissues. It was also found in the blood and in the small
areas of degeneration in the liver and kidneys. Jensen obtained pure
cultures through the survival of the spores when impure cultures were
boiled for a few minutes.
_Animals Susceptible._ Inoculation of the cultures subcutem produces an
affection resembling malignant œdema, or braxy, in sheep, Guinea pigs,
mice, pigeons and hens, and less certainly in rabbits. Inoculation of a
calf had no deleterious effect, while a second succumbed in forty-eight
hours. In its pathogenesis this microbe appears to be more closely
allied to that of malignant œdema than that of black quarter, as the
latter attacks cattle very readily and has little effect on rabbits,
pigeons and chickens.
_Symptoms._ The more obvious manifestations of braxy bear a resemblance
to those of black quarter, so that the two affections have been often
confounded. In both the attack is sudden, the course rapid and fatal,
the back arched, the step short, especially with the hind limbs, and
there are swellings which crepitate on pressure on the hind quarters or
some other part of the body. Symptoms of colic soon appear, the sheep
lying down and rising frequently and moving the hind limbs uneasily, and
the abdomen becomes distended, tympanitic and tender. Rumination and
feeding are promptly suspended, and as a rule defecation as well. Urine
may be passed frequently in small amounts and of a high color. The pulse
is rapid and often irregular and the breathing hurried and labored. In
some cases the abdominal pain is less acute, the animal standing apart
with drooping head, ears and eyelids and frothy lips, or lying by itself
at a distance from the flock. Sooner or later emphysematous swellings
appear on some part of the body, but most commonly on the hind quarter,
which have a soft, doughy feeling and crackle or gurgle on pressure. In
the great majority of cases, however, the disease runs a rapid course
and ends in death in a few hours, and as the attacks are mostly in the
cold of the night, the victim, which appeared well at night, is found
dead in the morning. Cowan has often noticed that those that stepped
short at night were dead next morning. In certain cases the sheep stood
obstinately to the end and fell dead as if shot. When death was deferred
for several days a common result was shedding of the wool.
_Pathological Anatomy._ A marked feature of braxy is the early
putrefaction of the carcass. The rigor mortis quickly passes and the
carcass bloats up and exhales a putrid odor. On removing the skin one
sees extensive sero-sanguineous exudations, mixed with bubbles of gas of
an offensive odor. The abdomen is tense and tympanitic and the anus
protrudes. Visceral lesions are especially marked in the fourth stomach,
the walls of which are thickened in patches or throughout by a
hæmorrhagic or sero-hæmorrhagic exudation of a dark purplish color. If
killed in the early stages this may be very restricted in area, but
becomes general in animals that have died of the disease. Similar
exudations are found on the walls of the first three stomachs, or on the
small or large intestines. The fourth stomach and duodenum are, as a
rule, empty of food, though containing a sanguineous liquid. The
contents of the large intestines are usually dry and hard. Some serous
exudate is usually present in the peritoneum, pleura and pericardium.
The spleen may be normal or slightly enlarged. The liver is pale, soft
and friable. The kidneys may be congested and swollen and usually show
brownish areas of necrosis in which the bacillus is readily found. The
blood is dark, and though it may be coagulated, the clot is usually soft
and diffluent.
_Prevention._ Much may be done in the way of drainage and above all
cultivation and liming of the braxy pastures, and again laying them down
in grass. Cowan found that braxy diminished largely in ratio with the
improvement and cultivation of the soil. A rotation of crops and the
free æration of the soil tends to destroy an anærobic microbe or to
render it non-virulent. Winter feeding is another well attested source
of protection. Hay with turnips, oats, linseed cake or oil cake seems to
encrease the tone and vigor, and to counteract the fermentations in the
digestive organs which lay the system open to attack. Wholesome and
nutritious food then must be a main stay whenever the health threatens
to be undermined by insufficient or unwholesome pasture, by dried or
withered grass, ferns or heather, by the watery grass of recent and
rapid growth, by frosted and partially decayed herbage, or by pasture
exhausted by overstocking or drought.
Fields and hills known to be infecting must be abandoned especially in
late fall and winter and in the case of the younger and more susceptible
sheep. Understocking is always better than overstocking as the flock is
kept better nourished, stronger and with a greater measure of tolerance
and resistance. Upon land covered with old, fibrous, astringent heather,
burning is often of great value. The new growth of young heather is much
more digestible and nutritious, and destitute of injurious astringency,
and maintains a stronger and healthier flock.
Finally the question of _immunization_ arises. Nielsen attempted this
by drying and heating to sterilization the diseased kidney and
injected small quantities of this suspended in water. Sheep treated in
this way in Norway and Iceland have had a circumscribed inflammatory
swelling and afterward appeared to resist casual infection when placed
on the braxy fields. Jensen carried the experiment a step farther and
inoculated his artificially immunized sheep with 2½ cc. of a virulent
serum-gelatine-agar culture. It was rather unwell for half a day and
walked lame but soon recovered. A dose of ¹⁄₃₀ cc. of the same culture
killed in fifteen hours a larger sheep that had not been artificially
immunized.
_Treatment._ Though some cases of braxy recover yet the treatment of the
disease can hardly be seriously considered as yet. A disorder which is
so rapid in its progress, so early associated with such great and
rapidly extending lesions of the most vital organs, and which proves
fatal so early and almost invariably, leaves little room for a
successful treatment. In the milder cases, likely to recover of their
own accord, this may be hastened by the internal use of antiseptics and
purgatives, and perhaps even by antitoxic serum from the blood of an
immunized animal.
SOUTH AFRICAN HORSE SICKNESS. ŒDEMA MYCOSIS. DUNPAARDZIEKTE.
DIKKOPZIEKTE.
Definition: Geographical distribution: S. Africa; enzoötic or
epizoötic on damp soils; damp, humid atmosphere. Pathogenesis: horses,
and more mildly mules and asses, quagga; (cattle and goats?). Causes:
green forage, from rich, damp lands, eaten dewy; cut and fed with dew
on; dried in sun safe; so of horses stabled or corralled; in hot
summer only; inoculable; penicillium; cultures cause the disease;
debility. Forms: lung sickness—head sickness—blue tongue. Symptoms:
incubation 8 days. Fulminant form asphyxiates in an hour. Acute lung
form has rigor; remittent hyperthermia; prostration; dyspnœa;
cyanosis; serous nasal discharge; frothing; gurgling breathing; cough;
death in 3 or 4 days. Head œdema; general swelling and oozing of
serum. Blue tongue: great lingual swelling; cyanosis; coldness;
projection from mouth; salivation; stertor; asphyxia. Three forms
combined. Mortality. Lesions: serous exudate coagulates with heat or
blood; intermuscular exudates; whole head densely infiltrated;
excessive bloody pleural effusion; punctiform petechiæ; lungs pale,
yellow, great interlobular infiltration; or, if worked, hepatization;
dark, congested mucosæ; blood diffluent; heart pale; spleen enlarged,
blood-gorged; kidneys infiltrated; gastro-intestinal congestions;
cerebro-spinal effusion. Prevention: keep indoors during summer and
autumn; allow no fresh damp forage; or cut only after dew is off;
check rein or muzzle; pastured horses must be stabled at night or in
damp weather. Immunization: by protective inoculations; recovered
horse is re-inoculated until a high grade of resistance is secured and
his blood used to immunize.
_Definition._ An ectogenous, infective disease of solipeds in South
Africa, characterized by intense vascular congestions, destructive
changes in the blood and the profuse exudation of liquor sanguinis into
the tissues of the affected parts.
_Geographical Distribution._ The affection is not known out of South
Africa, where it has been observed since 1780. It appears yearly in
certain areas in the Transvaal, Orange River Colony, Natal, and adjacent
States, but only in certain years in Cape Colony and especially in its
southern portion. In certain years it makes wide extensions so that it
has appeared to become epizoötic instead of enzoötic. The habitual
enzoötic prevalence is in the areas that are relatively lower, damper
and richer than the surrounding country, where the vegetation is
luxuriant and the surface of the ground moist. Thus it is a disease of
low meadows, basins, river bottoms, drying marshes or ponds, and the
Boers have been in the habit of protecting their horses by sending them
to high, dry tablelands, from the first appearance of the disease until
the first frost. Yet elevation in itself is no protection, thus
Johannisburg, 6000 feet above the sea, is habitually ravaged and
Rhodesia loses 90 per cent. annually. A humid atmosphere, mist, or rain
with a high temperature are directly connected with the outbreaks.
_Animals susceptible._ Horses take the disease in its most fatal form.
Mules suffer like horses, while in asses the disease is relatively
somewhat more benign, and the virus after having passed through the ass,
has lost part of its potency. A disease of a similar nature is seen in
cattle and goats. The quagga is also alleged to suffer (Edington).
_Causes._ The disease has been traced to the green forage, grown in
damp, hot seasons on the rich moist bottom lands, in basins, gullies,
etc., and which has been consumed while damp with night dews or fog. Few
suffer that are only turned out to pasture after the sun has dried up
the dew, and that are shut in the stable or kraal before sunset. Coley
who witnessed a loss of 60 per cent. of the stabled horses at Eshowe,
Zululand, found that the deaths were among horses that had been allowed
to eat their fodder wet. The Guinea or Ubaaba grass and Indian corn were
cut at night and fed to the horses next day. The horses that ate this
wet from the bundles were attacked, while those that had it only after
it had been opened and dried in the sun escaped. Race horses that
receive no green fodder very rarely suffer. Horses that are corralled
(in kraal) at night escape.
The hot season is the season of greatest prevalence, the disease
beginning in November and proving especially fatal from the end of
December to the first of March. It appears in a modified form until May
when the first frosts appear.
Though the disease can be fatally inoculated by transferring the blood
from one horse to another, it is the rarest possible occurrence to have
it propagated in this way. It can be absolutely prevented therefore by
attention to the diet.
The real cause of _horse sickness_ is a mold having the general
characters of a penicillium, and which enters the system with the moist,
dewy food. Edington, who discovered this cryptogam, has found it in the
blood in all his necropsies of horses dying of horse sickness. Why this
should be no longer infecting when dried does not clearly appear. It has
been alleged that the disease has gradually extended to the higher
grounds which were formerly free from it, and the introduction of
diseased or infected horses has been advanced as the cause, but in the
unfenced state of the veldt and the former abundance of wild animals
this should have ensured such extension long ago, if it is really a
permanent one. The deadly prevalence of the malady in particular areas
in given years, and its entire absence from such localities in others
may explain the instances of apparent extension. The dryness and cold of
winter is the factor which usually extinguishes the poison in a given
district. We have as yet no absolute proof of a progressive
acclimatisation of the germ in a colder and drier region. Wittshire
observes that it will prevail on one side of a narrow river, while the
other at an equal elevation is practically free from it. There is no
mention of shade which might have explained such a difference in the
growth of cryptogams on the right and left banks.
Such limitations, together with the activity of the infection in damp
seasons, and during damp hours of the day, and its inactivity in dry air
and vegetation, would strongly suggest a microbe which is conveyed in
the body of some invertebrate, but this appears to be nonessential
because Edington has cultivated his mold in vitro and inoculated its
products on horses so as to secure immunity.
Debility doubtless renders an animal more susceptible, yet the disease
usually kills nearly all horses attacked, excepting such as have been
immunized. This is the same for casual and inoculated cases. When,
however, the virulence has been lessened by culture or by passing
through the body of an unsuitable animal the results are very uncertain;
some horses it will kill, while in others it produces a slight and
harmless fever.
_Forms._ Two leading forms of the disease are known: 1st, the _lung
sickness_ (_Dunpaardziekte_), and 2nd, the _head sickness_
(_Dikkopziekte_). A variety of this last is _blue tongue_ (Blautong),
which has been confounded with gloss-anthrax.
_Symptoms._ The _lung sickness_ may appear as a fulminant affection
following on the usual _incubation_ of about eight days. Suddenly, in
the midst of apparently full health and vigor, the breathing becomes
accelerated and dyspnœic; this encreases for about an hour, then the
patient staggers, falls, ejects a mass of white froth from mouth and
nostrils and dies. When death is more delayed, there may be noted a
rigor, and in the evening a rise of temperature to 103° F., lowering a
little next morning and rising again toward night, yet making an
encrease day by day until near the end, when it becomes subnormal. Death
in such cases occurs on the third or fourth day, preceded by great
prostration, hurried, labored breathing, dark red or cyanosed mucosæ,
loud rattling over the large bronchia or lower end of the trachea,
coughing and dropping of a serous fluid from the nose, or accumulation
of white froth around nostrils and mouth. The froth soon condenses in
part into a straw-colored liquid, which collects in considerable
quantity. The abundance of froth blocking the air passages produces
death by suffocation.
In the _head œdema_, the muzzle, lips, head and neck become the seat of
excessive exudation, the swelling of the face drawing back the lips so
as to expose the teeth of the lower jaw. The skin is rendered tense and
exudes the straw-colored serum, as do also the buccal and pituitary
mucosæ.
In _blue tongue_ the exudate is concentrated in the lingual organ, which
swells to an enormous size, forcing the jaws and lips apart, and hanging
out as a dark blue, cold mass. A foul, liquid mixture of saliva and
exudate drivels from the mouth. The pressure on the larynx may cause
marked stertor, advancing to asphyxia.
While these three types may seem to be distinct and uncomplicated in
some cases, more commonly the exudation appears to a slight extent in
all three situations, and it is only the predominance of the symptoms in
one particular part that assigns the attack to one type rather than
another. All are very fatal, but the lung sickness is preëminently so,
very few such surviving.
_Lesions._ There is usually a mass of white froth around the mouth and
nostrils. The serous exudate coagulates readily in the presence of
minute traces of blood, and forms a solid mass of clot when heated. A
yellow gelatinoid exudate is found in streaks or patches, subcutaneously
and between the muscles, but especially along the jugular furrow. In the
_head sickness_ the whole subcutaneous and intermuscular tissue in the
head and neck are infiltrated, and the straw-colored liquid escapes
abundantly when the part is scarified. The same is true of the tongue,
which is stained throughout with blood that has gravitated into it.
The pleuræ contain an abundant exudate more or less deeply stained with
blood. The same is true of the pericardium. In the latter Edington has
found 140 fluid ounces. On the surface of the lungs and pericardium are
extensive yellowish exudates. They are covered with petechiæ mostly
small or punctiform. If the horse has stood at rest throughout the
illness the lungs seem pale, yellowish, yet swollen and indisposed to
collapse. The interlobular tissue especially is infiltrated with serum
so that toward the free margin the lobules may be separated by intervals
of half an inch in breadth as in lung plague of cattle. In horses that
have been worked during the illness the whole organ is congested and
firm, resembling the condition of croupous pneumonia. The trachea and
bronchia show dark congestion of the mucosæ and a mixture of froth and
serous exudate. The large blood vessels contain diffluent blood clots of
an intensely dark color. In the vascular furrows of the heart and along
the large vessels are yellow exudates or blood extravasations. The
muscular tissue of the heart appears normal or rather pale, and under
the microscope the striæ are found to be obscured by cloudy swelling,
and minute blood extravasations and hæmatin are met with. The
endocardium is cloudy, with blood extravasations, and exceptionally
ante-mortem clots are found. The spleen is usually swollen, very dark,
blood gorged and covered with petechiæ. On section there are found
extensive extravasations, with masses of blood pigment and crystals. The
kidneys are enlarged, the capsule easily detached, the epithelium of the
glomeruli and convoluted tubes swollen and their nuclei multiplied. A
gelatinoid exudate is usually present in the renal pelvis. Congestions
have been found in the right gastric _cul-de-sac_ and less frequently in
the intestines. Exudations have also been found in the cerebro-spinal
nervous system, the laryngeal mucosa and the conjunctiva. The latter is
usually cyanosed.
_Prevention._ The first consideration is to keep work horses indoors or
in a kraal during the summer or sickly season. Here they must be fed on
dry hay and grain only, grass being strictly withheld. If it becomes
absolutely necessary to feed green fodder of any kind it should not be
cut until all dew or rain has completely dried off in the heat of the
sun, and if kept over night should be kept under cover and again dried
before feeding. When taken out to work the animal should wear a check
rein or muzzle so that he cannot by any chance reach the green
vegetation. This rule must be most strictly adhered to at night or
during damp weather.
For horses turned to pasture a fair amount of protection may be secured
by shutting them in a stable or kraal before sundown, and until the
vegetation has been thoroughly dried by the sun the next morning.
_Immunization._ A horse that has recovered from the _sickness_ has been
long held to be immune and will bring from six to ten times its former
price. As any disease is liable to be called the sickness this enhanced
value is too often insubstantial. Wiltshire even says that all “salted”
horses eventually die of _horse sickness_ if allowed to live long
enough. Be this as it may Edington appears to have established a
reasonable measure of immunity by his protective inoculations. He takes
a recovered (‘salted’) animal and reinoculates it at intervals with
encreased doses of virulent blood. After the last of these inoculations
the subject is allowed to rest for a long period of time, and is then
re-inoculated with a small dose of virulent blood. A definite amount of
this horse’s virulent blood is mixed with 50cc. of serum and injected
subcutaneously; some days later 30cc. of the same serum with the same
dose of blood is injected; at a later date the procedure is repeated,
with a reduced dose of serum, and fourteen days later pure virulent
blood is injected.” The result has been perfectly satisfactory.