sanitary agents. Formalin is the commercial name for the 40 per cent
solution of formaldehyde gas in water, and is one of the most powerful
antiseptic and disinfectants that we possess. Solutions of this strength
are manufactured by different commercial houses and sold by the drug trade
under the name of "formalose" and "formal." In this connection it should be
mentioned that while the 40 per cent solution of formaldehyde gas and
formalin are exactly the same thing, the former can be purchased at 33-1/3
to 64 per cent less than the latter. Formalin, diluted with water in the
proportion of 1 pint to 30 parts of water, or 4 ounces to each gallon of
water, may be applied, and it may thus be used as a wash or as a spray on
all paints, metals, and woodwork, as well as on clothing and other fabrics,
without injuring them. It may also be applied to floors, walls, and
woodwork in whitewash by mixing 1 part to 30 parts of limewash, or 4 ounces
to each gallon of limewash. Formalin has the appearance of water and in the
strong solution is poisonous, but when diluted as recommended above it is
not dangerous. The fumes given off by it, however, are very disagreeable
and irritating to the eyes and nasal mucous membranes. One and one-half
ounces of formalin added to 1 gallon of water is a valuable agent for the
disinfection of the skin or septic wounds, but is somewhat painful and
irritating to raw surfaces.
Formaldehyde is a gas which is soluble in 2-1/2 parts of water (40 parts of
formaldehyde gas to 100 parts of water); this solution constitutes the
formalin of commerce. The use of formaldehyde gas is in most cases
impracticable for stable disinfection. In case the stable is not too large
and can be made almost air-tight the generation of formaldehyde gas, after
removing all the animals, will be found very serviceable. It penetrates all
parts of the stable--the walls, crevices, floors, ceiling--and is probably
the best fumigating disinfectant that we have.
Probably one of the most simple and practical methods of liberating this
gas is by means of the chemical reaction which takes place when formalin is
poured upon permanganate of potassium. For each 1,000 cubic feet of air
space, 16-2/3 ounces of crystallized or powdered permanganate of potassium
is placed in a wide-surfaced pan; 20 ounces of formalin is then poured upon
it, and the stable immediately closed for a period of 12 hours or longer.
This method is efficient only when it is possible to seal tightly the place
to be disinfected, and should be used only by experienced persons.
(6) Some coal-tar products are cheap, effective, and easily applied
disinfectants, their action being due to the carbolic acid and creosote in
their composition. They may be used in 3 to 5 per cent solution. As a rule
they form a milky solution in water.
(7) Compound solution of cresol (liquor cresolis compositus), now
recognized as an official preparation, is composed of equal parts of cresol
and linseed-oil-potash soap. The mixture is a thick, dark, amber-colored
fluid which mixes readily with water in all proportions to form a clear,
soap solution. It is an efficient disinfectant in a 3 or 4 per cent
solution, and in this strength it may be applied in the same manner as a 5
per cent solution of carbolic acid.
When it is desired to apply one of these above-mentioned agents to the
stable or barnyard, a preliminary cleaning up of all dÈbris and litter is
advisable, together with the scraping of the floor, mangers, and walls of
the stable with hoes; also the removal of all dust and filth. This should
be followed by the burning of all such accumulations, inasmuch as this
material likewise contains the infectious principle and is best destroyed
by heat. Heat may be applied to the surface of the affected pen, byre, or
barnyard by means of a cyclone burner, which consists of a tank, pump,
hose, and cyclone nozzle for spraying with paraffin (gas oil). The latter
is ejected in the form of spray, which when ignited gives a very hot and
effective flame to be applied to the infected ground. Where such burning is
impracticable the surface soil of the yard and surroundings should be
removed to a depth of 5 or 6 inches and then placed in a heap and
thoroughly mixed with air-slaked lime. The fresh surface of the soil thus
exposed may then be sprinkled with the disinfectant.
In addition to these artificial substances there are several natural
sanitary agents of great importance as destroyers of virus. These are
cleanliness, ventilation, drying, and sunshine. All virus, excepting such
as may live in the soil, is killed sooner or later by drying and sunshine,
and the importance of these factors in the daily life of animals need not
be insisted on here. Finally, all sanitary measures which contribute to the
healthfulness of animal surroundings are directly or indirectly inimical to
disease germs, and all carelessness in the keeping of animals may be
regarded as an ally of these destructive organisms.
CONTAGIOUS PLEUROPNEUMONIA.
[Pls. XXIX-XXXII.]
_Definition and history._--This disease has been eradicated from the United
States, and it is not probable that it will ever be seen in this country
again. As, however, much interest was manifested in regard to it for a
number of years, and as our cattle are still prohibited from some foreign
markets on account of its previous existence here, the subject is treated
at greater length than would otherwise be necessary.
The contagious pleuropneumonia of cattle is a specific, epizootic disease
which affects bovine animals, and from which other species are exempt. It
is characterized, when the disease results from exposure in the usual
manner, by an inflammation of the lungs and pleurÊ, which is generally
extensive, and which has a tendency to invade portions of these organs not
primarily affected and to cause death of the diseased portion of the lung.
This disease is frequently called the lung plague, which corresponds to its
German name of Lungenseuche. In French it is spoken of as the pÈripneumonie
contagieuse.
The history of the contagious pleuropneumonia of cattle can not be traced
with any certainty to a period earlier than the beginning of the eighteenth
century. No doubt it existed and ravaged the herds of Europe for many years
and perhaps centuries before that time, but veterinary knowledge was so
limited that the descriptions of the symptoms and post-mortem appearance
are too vague and too limited to admit of the identification of the
maladies to which they refer. It has been supposed by some writers that
certain passages in the writings of Aristotle, Livy, and Virgil show the
existence of pleuropneumonia at the time that their works were composed,
but their references are too indefinite to be seriously accepted as
indicating this rather than some other disease.
It seems quite plain that as early as 1713 and 1714 pleuropneumonia existed
in Swabia and several Cantons of Switzerland. There are even clearer
accounts of its prevalence in Switzerland in 1732, 1743, and 1765. In 1769
a disease called murie was investigated in Franche-ComtÈ by Bourgelat which
undoubtedly was identical with the pleuropneumonia of to-day. From that
period we have frequent and well-authenticated accounts of its existence in
various parts of Europe. During the period from 1790 to 1812 it was spread
throughout a large portion of the Continent of Europe by the cattle driven
for the subsistence of the armies, which marched and countermarched in all
directions. It was generally prevalent in Italy in 1800. It appears to have
been unknown, however, in the Department of the Nord, France, until 1826,
but during the years from 1820 to 1840 it penetrated into most parts of
that country. During the same period it was introduced into and allowed to
spread over Belgium and Holland.
This contagion is said to have been carried to Ireland from Holland in
1839, and is reported as existing in England in 1842. The disease was
brought to the United States at several different times. Probably its first
introduction was with a diseased cow sold in Brooklyn, N. Y., in 1843. It
came to New Jersey by importing affected animals in 1847. Massachusetts was
infected in the same way in 1859.
South Africa was infected by a bull brought from Holland in 1854, and
Australia likewise received the contagion with an English cow in 1858. It
is also reported as existing in various parts of the Continent of Asia, but
the time of its first appearance and the extent of its distribution are
very uncertain.
Some countries, such as Norway, Sweden, and Denmark, which had been
infected for only a short time, have succeeded in eradicating the disease
without much difficulty by slaughtering all affected and exposed animals.
Other countries long infected and in which the contagion was thoroughly
established, like Australia, South Africa, Italy, France, Belgium, and
parts of Germany, have labored long, in some cases making no progress and
in others being only partially successful. Holland was one of the first of
the thoroughly infected countries to free itself from the contagion.
In the United States, Massachusetts eradicated pleuropneumonia during the
period from 1860 to 1866. New York and New Jersey made an attempt to
eradicate it in 1879, but were not successful. Late in 1883 the contagion
was carried to Ohio, probably by Jersey cattle purchased in the vicinity of
Baltimore, Md., to which place it had extended before 1868. From the herd
then infected it was spread by the sale of cattle during 1884 to a limited
number of herds in Illinois, to one herd in Missouri, and to two in
Kentucky. The alarm caused among the stock owners of the United States by
this widespread dissemination of a disease so much dreaded led to the
adoption of active measures for its control and eradication. By cooperation
between the United States Department of Agriculture and the authorities of
the affected States it was found possible to prevent the further spread of
the contagion and to eradicate it after a few months' delay.
In 1886 pleuropneumonia was discovered in some of the large distillery
stables of Chicago and among cows on neighboring lots. This led to renewed
efforts for the complete extirpation of this disease from the country.
Congress in 1887 enlarged the appropriation available for this purpose and
gave more extended authority. During the same year the disease was stamped
out of Chicago, and has not since appeared in any district west of the
Allegheny Mountains.
The work of eradication was at the same time commenced in all the infected
States. Before the end of the year 1889 Pennsylvania, Delaware, Maryland,
the District of Columbia, and Virginia had been freed from the disease.
More difficulties, however, were encountered in the States of New York and
New Jersey, on account of the larger territory infected and the density of
the population. The long struggle was successful, however, and the last
animal in which the disease appeared in the State of New York was
slaughtered early in 1891, and the last one affected in New Jersey met the
same fate early in the spring of 1892.
[Illustration: PLATE XXIX.
Haines del. ZEESE-WILKINSON CO., INC., N.Y.
UPPER OR DORSAL SURFACE OF THE LUNGS OF THE OX.
(ONE-TWELFTH NATURAL SIZE.)]
[Illustration: PLATE XXX.
Haines del. ZEESE-WILKINSON CO., INC., N.Y.
BRONCHOPNEUMONIA.]
[Illustration: Plate XXXI.
Fig. 1
Fig. 2
Haines del. ZEESE-WILKINSON CO., INC., N.Y.
CONTAGIOUS PLEUROPNEUMONIA.]
[Illustration: PLATE XXXII.
Haines del. ZEESE-WILKINSON CO., INC., N.Y.
CONTAGIOUS PLEUROPNEUMONIA.]
During these same years a supreme effort had been made to stamp out this
lung plague from Great Britain. From the official reports it appears that
the number of infected districts and of diseased animals had rapidly
diminished, but it was not until 1898 that the infection was finally
eradicated.
The other infected European countries, though they maintain a veterinary
sanitary service, are not making satisfactory progress in eradicating the
disease. This is owing partly to delays in carrying out the provisions of
the laws and partly to mistaken ideas as to the measures which are
necessary to accomplish the object. The United States was the last of the
countries having old infected districts which undertook to stamp out this
contagion, and, except Holland, it was the first to reach success.
_The cause (etiology) of pleuropneumonia._--This is a contagious disease,
and arises only by contagion from a previously affected animal;
consequently it can never be seen here except as the result of importing
affected animals from the Old World. When thoroughly stamped out it does
not reappear; and if imported animals continue to be properly inspected and
quarantined, we have every reason to believe that pleuropneumonia will
never again be seen in this country.
The exact nature of the virus or contagion of lung plague has never been
determined. Various investigators have from time to time claimed the
discovery of the specific organism of the disease, but it was not until
1898 that Nocard and Roux, by an ingenious method of cultivation, succeeded
in obtaining a very feeble growth of an exceedingly minute microorganism.
With these cultures the disease was produced in cattle.
Some investigators and writers are of the opinion that the disease can be
contracted only by an animal coming near enough to a living diseased one to
receive the contagion directly from it. They hold that the contagion is
expired with the air from the affected lungs, and that it must be almost
immediately inspired by another animal in order to produce the disease.
Some experimental attempts to infect animals by placing them in stables
where diseased animals have been, and by placing the diseased lungs of
slaughtered animals in their feeding troughs have failed, and,
consequently, apparently confirm this view.
* * * * *
CONTAGIOUS PLEUROPNEUMONIA.
DESCRIPTION OF PLATES.
PLATE XXIX. Upper or dorsal surface of the lungs of the ox, reduced to
one-twelfth of the natural size: _a_, _a'_, the right and left principal
lobes. These are the largest and are situated posteriorly, resting upon
the diaphragm; _b_, _b'_, the ventral lobes, situated between the principal
lobes; and _c_, _c'_, _c''_ the most anterior, or cephalic, lobes. The
right anterior is divided into two lobes (_c_, _c'_), the left is single
(_c''_); _d_, trachea, or windpipe.
In the majority of the lungs examined in the laboratory of the bureau which
were affected with contagious pleuropneumonia the principal lobes (_a_,
_a'_) were primarily affected.
PLATE XXX. Bronchopneumonia. The ventral or middle lobe of the right lung
affected with collapse and beginning bronchopneumonia. The light yellowish
portions represent healthy lung tissue; the red represents the disease. It
will be noticed that the lines between the lobules are quite faint,
indicating little or no inflammation of the connective tissue between the
lobules. The healthy lung tissue is seen to be raised above the level of
the diseased portion. In contagious pleuropneumonia the exact reverse is
the case, the diseased portions being very much larger than the healthy.
PLATE XXXI. Contagious pleuropneumonia. Appearance of a cow's lung affected
with contagious pleuropneumonia when sections or slices are made of it and
cut surfaces examined.
Fig. 1. Transverse section through the right principal lobe in a case of
acute pleuropneumonia. The area drawn includes the air tubes, veins, and
arteries, and illustrates the great thickening of the interlobular
connective tissue into broad whitish bands and of the walls of the air
tubes, veins, and arteries: _a_, air tube cut obliquely; _a'_, air tube cut
directly across; _b_, arteries cut across; _c_, large vein completely
occluded by a thrombus or plug formed during life. The great thickening of
the walls of the artery and vein in this disease is especially brought out
by stating that in the healthy lung they are so thin as to be easily
overlooked.
Fig. 2. Transverse section of the principal lobe in a case of acute
pleuropneumonia, illustrating the different kinds of hepatization or
consolidation of the lung. These are indicated by the different colors from
dark red to reddish yellow. This variation of color is regarded by some as
the real marbling characteristic of pleuropneumonia, while the whitish
bands penetrating the lung tissue in all directions constitute the true
marbling according to other observers.
PLATE XXXII. Contagious pleuropneumonia. This illustrates what are called
infarctions. The right half of the figure shows nearly normal lung tissue.
The left represents a blackish mass, in which the lung tissue is filled
with blood and solidified. This is caused by the plugging of the vein
carrying away the blood from this portion. The heart forces the blood
through the artery into the tissue at considerable pressure, but owing to
the fact that its return is prevented, the minute blood vessels rupture and
the air vesicles become distended with blood, which coagulates and causes
the firmness of the tissue.
* * * * *
On the other hand, it is known that the serum from affected lungs retains
its virulence and may be used successfully for inoculation weeks or months
after the death of the animal from which it was taken. This is
particularly the case when this liquid is hermetically sealed in glass
tubes. Other investigators state that they have successfully infected
cattle by placing, in the nostrils, sponges or pledgets of cotton saturated
with such serum. Cattle have also, according to the best evidence
obtainable, been infected from the clothing of attendants, from horns used
in drenching, and from smelling about wagons which have been used to
transport affected carcasses. In the work of eradicating pleuropneumonia
from the United States many stables were found in which the disease would
appear and reappear after the slaughter of affected herds, and in spite of
any precautions which were adopted. These were always old stables, with
woodwork in a decaying condition and with floors underlaid with filth which
could not be thoroughly removed or disinfected. In every one of these cases
the destruction of the stable, the burning of the lumber of which it was
constructed, the removal of the accumulations beneath the floors, and
thorough disinfection, prevented the recurrence of the plague in new
stables built upon the same premises. This experience conclusively shows
that under certain conditions, at least, stables may retain the infection
for a considerable time, and that when restocked the disease may break out
again from such infection.
As a rule, however, the disease is acquired by a healthy animal being near
an affected one and receiving the contagion direct. Affected animals may
give off the contagion in the early stages of the disease before the
symptoms are apparent to the observer; also, they may retain this
infectious character, if they survive the attack, for six months and
probably for a year after all symptoms of the disease have disappeared.
_Incubation._--The time which elapses between exposure to the contagion of
pleuropneumonia and the first appearance of the symptoms of this disease
varies greatly with different individuals and with different outbreaks of
the disease. Ordinarily the symptoms of disease make their appearance
within three to six weeks after exposure; they may be observed, however,
within two weeks or they may not become apparent until nearly or quite
three months. It is this long period of incubation and the great length of
time that an animal may disseminate the contagion after apparent recovery
which give the plague that insidious character so often spoken of, and
which greatly increase the difficulties of eradication.
_Symptoms._--The symptoms are such as would be expected with inflammation
of the lungs and pleurÊ, but they vary considerably, according to the type
which the disease manifests. If the attack is an acute one, as is
frequently seen in hot weather, the symptoms appear suddenly; the breathing
becomes rapid and difficult, the animal grunts or moans with each
expiration, the shoulders stand out from the chest, the head is extended on
the neck, the back is arched, the temperature is 104∞ to 107∞ F., the milk
secretion is suspended, there is no appetite, rumination is stopped, the
animal may bloat and later be affected with a severe diarrhea. Such cases
are generally fatal in 7 to 20 days.
Very often the attack comes on slowly and the symptoms are much less clear.
In the mildest cases there is a cough for a week or two, but no appreciable
loss of appetite or elevation of temperature. The lungs are but slightly
affected and recovery soon follows. Such animals may disseminate the
contagion for a long time without being suspected, and for that reason are
the most dangerous of all.
A more severe type of the plague is the most frequently seen. In these
cases the cough is frequent, more or less painful, the back somewhat
arched, and the milk secretion diminished. The prominence of these symptoms
increases, the appetite is affected, the animal loses flesh, the breathing
becomes more rapid, the cough more painful, pressure of the fingers between
the ribs shows tenderness, the hair loses its gloss and stands erect, the
skin becomes adherent, little, if any, milk is secreted, and the
temperature rises, varying in different animals from 103∞ to 107∞ F.
Animals thus affected may continue to grow worse and die in from three to
eight weeks, or they may after a time begin to improve and make an apparent
recovery. The inflammation of the lung does not, as a rule, subside and the
organ return to its normal condition, as is the case in ordinary pneumonia,
but with this disease the life of the affected portion of the lung is
destroyed, the tissue dies, and a fibrous wall is formed around it to shut
it away from the living parts. The tissue, thus encysted, gradually
softens, becomes disintegrated, and breaks down into pus. The recovery,
therefore, is not complete; it is only apparent and partial.
To those accustomed to examining the lungs of cattle, other and extremely
important symptoms may be apparent during the course of the disease. By
applying the ear over the walls of the chest an area of a certain extent
may be found in which the natural breathing sound is diminished or entirely
lost. This represents the diseased portion of the lungs. In other cases a
loud blowing sound may be heard, quite different from any sound produced
when the lung is in a healthy condition. In some cases crepitation is heard
near the border line of the diseased area and friction sounds produced by
the roughened pleura; these can be appreciated, however, only by those
whose ears have been trained to distinguish between the different sounds
which reach the ear when applied to the chest wall. By percussion--that is,
by pressing the fingers of the left hand firmly against the wall of the
chest and tapping upon the middle finger with the ends of the fingers of
the right hand--an area of dullness may be discovered corresponding to the
portion from which the respiratory murmur has disappeared. This loss of
respiration detected by auscultation, and the dullness brought out by
percussion, are the most important evidences of an inflamed or consolidated
lung.
Seriously affected animals remain standing if they have sufficient
strength, but those which lie down always lie on the affected side.