Synonyms. Definition: Acute, infectious, microbian disease, often
localized in lymph glands and plexuses of nose and air passages,
etc.; with hyperplasia, degeneration, necrosis, liquefaction.
Affects solipeds, and, by inoculation, man and all domestic animals
save cattle, chickens and (usually) swine. Geographical distribution
and historic notes: known in Ancient Greece; now where solipeds live
and fresh subjects are exposed; Central Europe; great horse trade
and movement; war, Franco-German, Napoleonic, Afghanistan, American
Civil War, Boer War. Unknown in Australia. Susceptibility: solipeds,
Guinea-pig, rabbit, goat, cat, dog, pigeon, sheep, and swine in low
condition. Cattle, chickens, white and house mice, linnets,
chaffinches, and frog immune. Microbe lives in frog in water at 86°
F. Cause: Bacillus mallei. Accessory causes: trade in solipeds,
mingling of sound and sick, crowding, common feeding and drinking
troughs or buckets and racks, debility, low condition, starvation,
overwork, damp, dark, draughty stables, carriage in transports or
cars. Insular quarantined lands—Australia, Tasmania, and New Zealand
exempt. Bacteriology: Bacillus Mallei; 2 to 5μ by 0.5 to 1.4μ,
nonmotile, ærobic grows in ordinary culture media, stains tardily
but is easily bleached. Spores uncertain, easily killed by
disinfectants, preserved in stables, does not grow in infusion of
hay, straw or horse manure, lives 15 to 20 days in water; infection
by coitus, and through placenta, by ingestion, by blood transfusion,
through dust; microbe in all lesions and discharges, (unless
sometimes in milk, sperm, etc.). Infection-atria: skin wound,
mucosa, hair follicles, lungs. Forms: Acute, chronic, nasal,
pulmonary, cutaneous (farcy), orchitic, arthritic, abdominal,
occult. Symptoms: nasal; incubation, 3 to 5 days, languor,
weariness, stiffness, horripilation, tremors, inappetence, thirst,
hyperthermia, epiphora, snuffling, nasal discharge, serous, viscid,
agglutinating, purulent, swollen alæ, violet mucosa, elevated spots
and patches with central ulceration, may become confluent, and
involve submucous tissues; submaxillary lymph glands swollen,
nodular, not tender, non-suppurating, swollen (corded) facial
lymphatics, from nose, eye or lymph glands; swellings, cutaneous and
lymphatic in skin of limb or body, ulcers (farcy buds), deposits in
throat or lungs; chronic cases; slow, indolent, persistent, nasal
discharge—unilateral (or bilateral), viscid or not, nodules on
mucosa with whitish centres or points; red areolæ, later ulceration,
puckered white cicatricial lesions, submaxillary swelling, nodular,
large or small, insensible; cutaneous cases; arthritis with
lymphangitis, skin engorgement, corded lymphatics with ulcerating
nodules, sanious discharge, intermuscular abscesses. Occult cases:
lesions in internal organ;—cough, leucorrhœa, enlarged testicle, low
condition, weakness, lack of endurance. Diagnosis: inoculation of
male Guinea-pig in flank or peritoneum,—ulcer and orchitis, cat,
dog, old soliped; mallein test,—swelling, involving lymphatics,
fever, 1.5° to 2.5 F. and upward above normal, at 10th to 18th hour,
lasting two days. Lesions: cell proliferation in nests in fibrous
stroma, pea upward, central degeneration, fatty debris, ulcer or
abscess, hyperplasia of lymph vessels, on nasal mucosa like
sand-grains, peas, patches, centre grayish or yellowish, blood
extravasation, necrotic degeneration, ulcer with ragged edges;
fibroid degeneration—cicatricial lesion; lesions in guttural pouch
or tube, larynx, trachea, bronchia; lungs—peribronchial, lobular or
interlobular inflammation, cell proliferation in foci,
degeneration—nodules—and caseation; skin,—cell proliferation,
degeneration, rupture, fibroid hyperplasia of lymphatics, exudates
in connective tissue; dependent lymph glands congested,
hypertrophied, cell proliferation, caseation; lesions in pharynx,
spleen, kidney, heart, brain, testicle, scrotum, mammæ, vagina,
uterus, joints, bones; bone fragility. Glanders in swine, sheep,
goat, rodent, dog, cat.
_Synonyms._ Malleus, Equinia, Farcy.
_Definition._ An acute infectious disease caused by the bacillus mallei,
which tends to localize itself in the lymphatic glands and plexuses,
especially of the nose and upper air passages but also in other parts of
the body, where it produces a progressive hyperplasia, with a strong
tendency to degeneration, necrosis, and liquefaction. It occurs casually
in horses, asses, mules and other solipeds, and is communicable to man
and all domestic animals except the bovine races, chickens, and, under
ordinary circumstances, swine.
_Geographical Distribution._ Glanders (Malis) appears to have prevailed
in asses in Greece as noted by Aristotle. Its contagious prevalence in
horses is recorded by Absyrtus in the time of Constantine, and again by
Vegetius Renatus in 381 A.D. At the present time its existence is almost
coextensive with the equine family, but its prevalence is in a direct
ratio with the facilities for the infection of fresh subjects. In the
central countries of Europe where the equine population is greatest and
where there is the most extensive trade and movement among horses it
secures the greatest relative number of victims. War with its constant
opportunities for infection, in crowded cavalry and artillery stables
and the successive changing of place, tends greatly to enhance its
ravages. Thus in the German army it rose from 966 to 2058 per 100,000
per annum in the year of the Franco-German war; in Spain it was
practically unknown until the Napoleonic war in the Peninsula, but after
this it proved a veritable scourge; in Hindostan it was hardly known
until the Sepoy rebellion yet its ravages greatly hampered the army
movement in Afghanistan in 1879; and in the United States it became very
prevalent in the armies during the Civil War of 1861–4, and was widely
scattered over the whole country on the sale of the army horses and
mules. Since that time, as before, it has been most prevalent in the car
stables of the great cities, though it has also gained a wide extension
in many great horsebreeding establishments in the Rocky Mountain region,
where however it proves much less destructive than in the East.
It is unknown in Australia, whence it is excluded by a rigid system of
quarantine.
_Susceptibility of Different Animals._ Horses, asses and mules are the
most susceptible, and it is only exceptionally that the disease is
contracted casually outside the class of solipeds. The Guinea pig and
rabbit are susceptible to glanders in the order named and the former is
especially available for experimental diagnostic inoculations. The goat,
cat and dog sometimes contract the disease from living in stables with
glandered horses, but infection is much more certain when they are
inoculated. The pigeon is also susceptible. In the dog the disease is
rarely fatal, but the ulcerations tend to heal in 14 days and recovery
ensues. In sheep and goats too, many cases recover though in other cases
an internal infection takes place followed by death. Swine are
comparatively insusceptible, but they may be successfully inoculated
when in ill health and low condition. (Spinola, Cadeac and Malet).
Cattle and chickens have uniformly proved refractory even on
inoculation. White and house mice and rats, have proved immune, also
linnets and chaffinches and the frog at ordinary temperature. If however
the frog is placed in water at 30° C., he may be successfully inoculated
and, though it does not prove fatal, the bacillus may be found in the
blood and tissues after a lapse of 50 days.
_Etiology._ As already stated this disease is due to the presence of a
microörganism, the _bacillus mallei_. Many secondary causes, however,
contribute to its propagation. The activity of movement and commingling
of horses has been already noticed. Crowding in close yards where the
animals bite each other, snort out the virulent discharges on each other
and eat and drink from the same troughs, leads to a rapid extension.
Even on the western ranges where the disease tends to be mild, Billings
observed a deadly extension when yarded during winter storms. Debility
from chronic ill health, starvation, overwork and damp, dark, draughty
stables, is so conducive to the disease that it was at one time
considered as the sole cause. Close confinement in impure air is at once
a cause of increased susceptibility and a means of concentration and
transmission of the poison. Hence confinement, between decks, of
military and other horses, carried by sea, is a source of wide
extensions. On the other hand insular places from which strange horses
are excluded or into which they are admitted under careful inspection
and quarantine have succeeded in preserving immunity. Australia,
Tasmania and New Zealand are examples.
_Bacillus Mallei._ Christot and Kiener claimed to have found a bacillus
in the lesions of glanders in 1868. In 1881 bacilli were found by
Bouchard in a glander abscess in man, and these were cultivated _in
vitro_ and inoculated in a number of animals, by Capitan and Charrin in
1882. Independently in the same year (1882) Löffler and Schütz
discovered the bacillus, cultivated it _in vitro_, and successfully
inoculated it on animals. The microbe is rod-shaped, 2 to 5μ long, by
0.5 to 1.4μ thick, the same length as the bacillus tuberculosis but
thicker. It is nonmotile, ærobic (facultative anærobic) and grows
readily in a variety of culture media at a temperature of 37° C. On
neutral bouillon of the flesh of horse, ox, calf or chicken with or
without peptone, it grows readily, producing cloudiness in one or two
days. In peptonized gelatine it forms a whitish flocculent mass. On
glycerine agar with milk it forms in 48 hours a milk white layer,
changing to yellowish brown. On potato it forms long slender filaments,
in yellow, viscous, glistening colonies, changing to fawn and darker. It
grows best at 35° to 39° C. and growth ceases below 25° C., and above
42° C. It stains tardily in aniline colors, and not at all by Gram’s or
Weigert’s, but will readily take Kuhne’s stain prepared as follows: take
of phenic acid in solution (5:100) 50cc., absolute alcohol 10cc., and 1
to 2 grammes methylin blue. The stain is very easily bleached by acid,
differing in this from the bacillus tuberculosis. For decolorizing
Löffler recommends 10cc. distilled water, 2 drops of strong sulphuric
acid, and 1 drop of a 5 per cent. solution of oxalic acid. Sections
should be left in this not longer than 5 seconds. The bacillus often
appears granular, and unequally stained in its different parts. It may
be difficult of discovery in old standing lesions of horses, but comes
out clearly in recent lesions of experimental cases in Guinea pigs and
donkeys.
Baumgarten claims sporulation but this is uncertain.
The bacillus has only limited power of resistance to destructive
physical and chemical agents. It is killed in 10 minutes at 55° C., in 2
minutes at 100° C., or by mercuric chloride solution (1:5000), or by
phenol (5:100), or by permanganate of potass (1:100). In warm dry air
and sunshine it is sterilized, in thick layers in 2 months (Peuch), in
moderate layers in 4 to 15 days (Galtier), and in very thin layers in 3
days (Cadeac and Malet). In moist, cool air and in the shade it is much
more resistant. In stables it may remain virulent for three or four
months, and thus the disease has often reappeared among the newly
introduced horses after a stable has been abandoned for a length of
time. The microbe does not grow in infusions of hay, straw or horse
manure, and it is doubtful if it can maintain an active saprophytic
existence. Its vitality and virulence, however, persists in putrefying
materials for 14 to 24 days, and in water from 15 to 20 days. Hence it
is largely propagated through drinking troughs and occasionally through
ponds, lakes and sluggish streams. Again the virus is likely to be
preserved in and transmitted by rotten or even sound woodwork, as of
mangers, racks, buckets, shafts and poles, and by harness, halters,
blankets, combs, brushes and rubbers. Sometimes direct transmission
takes place in snorting or coughing, or by the animals biting or licking
each other. As the virus is spattered on surrounding objects, the walls,
stable utensils, soiled fodder and feed, and even the attendant’s
clothes may be the medium of transmission. Contagion during copulation
is not unknown, nor infection of the fœtus _in utero_ from a diseased
mother. Carnivora (dog, cat, lion) fed on the diseased carcasses have
become infected. Experimentally infection has been conveyed by
administering, by the mouth, balls containing the virus (Renault,
Coleman, etc.), and again by transfusing the blood from a bad case of
glanders into the veins of a sound horse (Viborg, Coleman, Renault,
Hering, Chauveau, Nocard). Transmission through the air on dust is
counteracted by the speedy destruction of virulence on dust, and horses
often stand side by side in adjacent stalls for months without
communicating the infection. Such escapes may, however, in some of these
cases, be attributed to the immunity secured by a previous exposure and
slight attack. That the germs may be exceptionally conveyed through the
air appears to have been proved by Viborg and Gerlach, who collected the
floating dust in a stable containing infected animals and successfully
inoculated with it.
The microbes are especially found in the visible lesions of glanders, in
the mucous, cutaneous and subcutaneous swellings and abscesses, in the
swollen lymph glands, in the nodules and ulcers of the mucous membranes
and skin, in the morbid discharges, from the nose, eyes, pharynx,
guttural pouches, larynx, trachea and bronchia, and in the discharge of
farcy buds and abscesses. They are not necessarily distributed through
all the tissues, and in chronic cases, with strictly local lesions, the
infection appears to be often confined to these or nearly so, and the
contamination of other animals is slow and uncertain. When, however, the
disease is acute and advanced, or generalized, every part must be looked
upon as probably infecting. Thus virulence has been shown in the blood,
the exhalations of the serous membranes, saliva, the aqueous humor
(Cadeac and Malet), the tears, (Viborg), the muscles, and the bones.
Galtier says the milk, sperm, bile and intestinal mucous are
non-virulent, also the vaccine lymph raised on glandered animals, but
much must depend on the grade and stage of the disease and no one would
care to run unnecessary risks with these liquids.
_Infection Atria._ Inoculation on a skin wound or abrasion, is a most
effective mode of transmission, but the virus undoubtedly enters in
certain cases with the air, food or water, or by accidental lodgment of
a speck of the virus on the mucosa of the nose or eye or other natural
opening. Through the healthy mucosa the bacillus may enter by
penetrating the soft epithelium, or entering the mucous follicles, but
it will find the way smoothed for it, if there has been friction,
abrasion, desquamation or congestion. The skin in its healthy state is
usually resistant, but Babes has conveyed infection by rubbing on the
virus mixed with vaseline, and without displacing the epithelium. The
channel of entrance was the hair follicles. Injected into the blood,
intravenously, or into a serous cavity, the bacillus infects with great
certainty and promptitude.
There is ample evidence that primary lesions appear not only in the skin
and nasal mucosa, but also in the bronchia, intestines, and other parts.
Much time and ink have been wasted in attempts to prove that pulmonary
lesions are always secondary, and doubtless many are so, but the cases
in which the lesions are confined to the bronchia or parenchyma, and the
many parallel cases of direct infection of the lungs by other diseases
(tuberculosis, lung plague, contagious pneumonia, influenza, etc.,)
furnish conclusive enough evidence that the germ may be inhaled and
colonize this part first. Cases of inhalation bronchitis, are equally
corroborative, and not only may the grosser solids be aspired, but
infection droplets can easily gravitate down when from congestion or
inflammation the action of the tracheal and bronchial cilia, is
suspended.