according to the virulence of the outbreak, the susceptibility of the
animals, and the length of time during which exposure is continued.
Sometimes not more than 15, 20, or 30 per cent will contract the disease
when a large herd is exposed; on the other hand, however, 80 or 90 per cent
may be affected. The proportion of cases in which the disease proves fatal
also varies greatly--it may not exceed 10 and it may reach 50 per cent. In
general, it may be said that about 40 per cent of the exposed animals will
contract the disease and about one-half of these cases will prove fatal.
_Post-mortem appearances._--Owing to the complexity of the structure of the
lung tissue, its ramifications of bronchial tubes and blood vessels, and
its abundant supply of lymphatics, the pathological changes in
pleuropneumonia are interpreted with great difficulty. Furthermore, there
are certain kinds of pneumonia which present some resemblances to
pleuropneumonia and which may therefore be confused with it in some of its
phases.
If we kill an animal affected with acute pleuropneumonia and examine the
cavity of the chest and lungs, the following appearances will be noted:
The thorax may contain more or less serum, which may be clear or clouded.
There may be firm adhesions of different parts of the lungs to the chest
wall, the extent of which depends on the stage and severity of the disease.
The diseased lobes are unusually large and exceedingly firm to the touch.
The weight of a single large lobe may reach 40 pounds. Usually only one
side is affected, often but a single lobe, and this most commonly the large
or principal lobe. The pleura may be covered with one or more layers of a
firm, elastic, grayish membrane, which varies in thickness and which
sometimes may be pulled away entirely. Sometimes it is absent. The pleura,
however, is opaque and apparently very much thickened. This is owing to the
diseased condition of the connective tissue beneath the pleura, as will be
explained later. When an affected lobe is cut through at right angles to
its long diameter, the cut surface presents a variety of interesting
changes. In the first place the spaces between the small subdivisions of
the lung (the lobules), which in the healthy lung are barely visible, are
distended with a yellowish-white, usually quite firm, substance, which is
coagulated fibrin. The cut surface thus appears divided into small fields
by yellowish-white bands of varying thickness running in various directions
through the lung tissue and beneath the pleura. (Pl. XXXI.) These bands may
appear honeycombed and the spaces filled with yellowish fluid (serum) or
they may be uniformly solid. It will also be noticed that the space
immediately outside of and around the artery, vein, and air tube is
similarly broadened by fibrinous deposits. Some authorities look upon these
bands as constituting the so-called "marbling" of pleuropneumonia.
In addition to these changes which have taken place in the connective
tissue between the lobules, the lung tissue itself may be markedly altered.
Certain areas of the cut surface may be very firm in texture and of a
brownish-red color. The cut surface is granular or roughened, not smooth to
the eye. Other areas equally firm may be more grayish yellow and still
others may be blackish. (Pl. XXXII.) Besides these areas which represent
solidified (hepatized) lung tissue there may be others which approach the
normal lung tissue in color, are soft, and float in water. From these a
milky, purulent fluid may often be expressed. These different shades are
represented in Plate XXXI, fig. 2, within a small compass. Some authorities
are inclined to consider these variations in color on the same cut surface
as the so-called marbling of pleuropneumonia. It matters not whether we
regard the bands between the lobules or the varying shades of the lobules
themselves as the marbling, provided either or both are peculiar to
contagious pleuropneumonia. If we examine the blood vessels appearing on
such cut surface they will usually be found plugged within the firmly
hepatized regions. The artery contains a dark, soft, removable clot, the
vein a grayish-pink, granular, fragile plug (thrombus), which adheres
firmly to the wall of the vein, and if this is slit open, indications of a
diseased condition of the inner coat will be readily detected. When large
regions of the lung tissues are hepatized, the main air tube and its
branches are usually filled with grayish, cylindrical branched masses of
fibrin that are easily removed, as they do not adhere to the mucous
membrane.
The views of pathologists differ as to the nature of the earliest changes
in pleuropneumonia, and it is not within the scope of this work to present
controverted or imperfectly developed theories. In the foregoing
description we have taken as a type the acute pleuropneumonia in its fully
developed phase, which can scarcely be mistaken for any other disease. We
have seen that there is an inflammatory condition of the connective tissue
between the lobules, resulting in the exudation of coagulable lymph. This
inflammation is equally marked around the blood vessels and air tubes. It
leads to inflammatory changes in the inner wall of the veins, and these
cause the deposition of thrombi or plugs in the vessels, which prevent the
return of the blood. The blood pumped into the lung tissue through the
artery, but unable to get out by way of the vein, leaves the mesh-work of
capillaries around the air vesicles, enters the latter, and produces the
firm, hepatized condition so characteristic of this disease. If we bear in
mind that the veins in different parts of the lung tissue are plugged at
different times, and that, therefore, the affected regions are in different
stages of disease, it will be easily understood how the different shades of
color from dark red to grayish or yellowish red are produced.
The complete plugging of the veins may lead to the death of circumscribed
masses of lung tissue. A line of separation forms between the living and
the dead tissue and a thick cyst wall of fibrous tissue forms around the
latter. The dead tissue for a time preserves the appearance of lung tissue,
then undergoes disintegration and liquefaction. The softened mass is
finally absorbed, and the walls of the cyst, or capsule around it,
gradually collapse and form a cicatrix. This favorable termination takes
place only when the dead mass is not too large. It may, however, involve
over half of one of the large lobes. Under such circumstances recovery is
improbable. A more favorable termination is the abundant growth of fibrous
tissue around and into the hepatized masses. The formation of fibrous
tissue may extend to the pleura, or lung covering, and cause firm adhesion
of the lungs to the chest wall and to the pericardium, or heart case.
The same peculiar, inflammatory changes which take place between the
lobules of the lung and around the bronchi and vessels may invade the
pleural cavity, cause extensive membranous and spongy deposits on the
pleura and firm deposits around the heart and large arteries, the gullet,
and windpipe.
These are the main features of the lung disease caused by contagious
pleuropneumonia. In the typical, acute cases there are a sufficient
number of peculiarities to enable us to make a positive diagnosis. There
are, however, many cases in which the disease is restricted to small areas,
or to the interlobular tissue, or in which the changes are still
imperfectly developed, or else so far advanced that doubts may arise as to
the true nature of the affection. In such cases all obtainable facts,
including the history of the case, the symptoms during life, and the
pathological changes observed on post-mortem examination must be taken into
consideration. Only one who has made a careful study of the disease is
fitted to decide in such cases.
Other kinds of lung disease, because of certain features common to most
lung diseases of cattle, may be confounded with pleuropneumonia. The
inflammation of the connective tissue between the lobules is not
infrequently observed in so-called interstitial pneumonia and may lead to
the formation of whitish bands intersecting the lung tissues in various
directions. On the cut surface these bands may give rise to a decidedly
marbled appearance. Again, in traumatic pneumonia, caused, as its name
implies, by the entrance of foreign bodies into the lung tissue, generally
from the paunch, the connective tissue around the place of disease becomes
inflamed and thickened, and the disease itself may simulate pleuropneumonia
in its retrogressive stages when it is confined to a small portion of lung
tissue. The filling up of the interlobular spaces with fibrin and
connective tissue of inflammatory origin is not thus limited to
pleuropneumonia, but may appear in a marked degree in other lung diseases.
It must not be inferred from this statement that these interlobular changes
are necessarily the same as those in pleuropneumonia, although to the naked
eye they may appear the same. We simply note their presence without
discussing their nature.
In general, the distinction between pleuropneumonia and bronchopneumonia is
not difficult to make. In the latter disease the pneumonia generally
invades certain lobes. The disease attacks the smaller lobes in their
lowest portions first and gradually extends upward, i. e., toward the root
of the lung or the back of the animal and backward into the large principal
lobes. Again, both lungs in advanced cases are often symmetrically
affected. In contagious pleuropneumonia the large principal lobe of one
side is most frequently affected, and a symmetrical disease of both lungs
is very rare, if, in fact, it has ever been observed. The lung tissue in
bronchopneumonia is not enlarged, but rather more contracted than the
normal tissue around it. This is well illustrated in Plate XXX. Normal,
air-containing lobules may be scattered among and around the hepatized
portion in an irregular manner. In pleuropneumonia the diseased and healthy
portions are either sharply divided off, one from the other, or else they
shade into each other by intermediate stages.
The hepatized lung tissue in bronchopneumonia when the cut surface is
examined is visually of a more or less dark flesh color with paler
grayish-yellow dots regularly interspersed, giving it a peculiar, mottled
appearance. In the more advanced stages it becomes more firm, and may
contain nodular and firmer masses disseminated through it. The air tubes
usually contain more or less soft, creamy, or cheesy pus or a turbid fluid
quite different from the loose, fibrinous casts of acute pleuropneumonia.
The interlobular tissue may or may not be affected. It sometimes contains
loose, fibrinous plugs, or it may be greatly distended with air, especially
in the still normal portions of the lung. The pleura is seldom seriously
diseased. If we contrast with these features the firm dark-red
hepatizations, the plugging of the veins, the extensive interlobular
deposits, and the well-marked pleuritis in pleuropneumonia, there is little
chance for confusion between well-developed cases of these two lung
diseases.
It should not be forgotten, however, that the lesions of the disease known
as contagious pleuropneumonia may be confined to the serous membranes of
the thorax, or they may be confined to the parenchyma of the lungs; they
may affect a whole lobe, or only a small portion of it; they may or may not
cause the so-called marbled appearance. In the same way bronchopneumonia
may vary as to the parts of the lung affected, the extent of the lesions,
the degree and kind of pathological changes in the interlobular tissue, the
color of the lung on cross section and the amount of hepatization. In
individual cases, therefore, it is often necessary to take into account the
history of the animal, the course of the disease, and the communicability
of the affection before a diagnosis can be made between the two diseases.
_Prevention and treatment._--The prevention of pleuropneumonia, as of other
contagious diseases, consists in keeping animals so that they will not be
exposed to the contagion. As the disease arises only by contagion, there is
no possibility of an animal becoming affected with it unless it has been
exposed. If, therefore, pleuropneumonia exists in a locality the owner of
healthy cattle should make every effort to keep his animals from coming
near affected ones or which have been exposed. He should be equally
particular not to allow persons who have been on the infected premises to
visit his own pastures, stables, or cattle.
If pleuropneumonia breaks out in a herd, every animal in it should be
slaughtered, the stables thoroughly cleaned and disinfected, and no other
cattle allowed on the premises until a period of 90 days has elapsed.
Medical treatment of affected animals is unavailing and should not be
attempted. No matter how valuable the diseased animals may have been before
they contracted the disease, they should at once be destroyed and the
contagion eradicated. This is the best policy for the individual as well as
for the community.
The eradication of this disease by local or National Governments can be
successful only when the same principles are adopted and carried out as
here recommended for individual stables. It is then a difficult
undertaking, simply because the contagion is generally widely disseminated
before any measures are adopted, and because a great majority of cattle
owners will never report the existence of the disease. Regulations must
therefore be enforced which will insure the prompt discovery of every herd
in which the disease appears, as well as the destruction of all diseased
and exposed animals and the thorough disinfection of the premises.
To discover pleuropneumonia sufficiently early for this purpose, the
district supposed to be infected should be clearly defined and inspectors
should be constantly employed to inspect every herd in it at least once in
two weeks, or, better, once a week. No bovine animal should be allowed to
go out of the defined district alive, and all which enter it should be
carefully inspected to insure their freedom from disease. As an assistance
to the discovery of diseased herds, every animal which, from any cause,
dies in the infected district and every animal which is slaughtered, even
if apparently in good health, should be the subject of a careful
post-mortem examination. Many affected herds will be found in this way.
In addition to these measures it is also necessary to guard against the
removal of animals from one stable to another and the mixing of herds upon
common pastures or in the public highways. The object must be to isolate
every individual's cattle as completely as possible, or otherwise a single
affected animal may infect a dozen or more herds. To prevent surreptitious
sale or trading of cattle, each animal must in some way be numbered and
recorded in the books kept by the official in charge of the district. In
the work of the United States Department of Agriculture a numbered metal
tag was fastened to each animal's ear and index books were so arranged that
with a number given the owner could be at once ascertained, or from the
owner's name the cattle for which he was responsible could be at once
learned. In this way, if an animal was missing from a stable, the fact
became apparent at once, or if one too many was found in a stable the
number in its ear would indicate where it came from.
When pleuropneumonia is discovered by these means, the entire herd should
be slaughtered as soon as the formalities of appraisement can be arranged.
In country districts the carcasses should be buried, as it is generally
impracticable to dispose of them in any other way. In city districts the
animals may be taken to a slaughterhouse, with such precautions as are
possible to prevent dissemination of the contagion. The animals should be
slaughtered under the supervision of an inspector. The healthy carcasses
may be utilized for food, but the blood, entrails, and all diseased
carcasses should be heated to a temperature equal to that of boiling water
or above, and then used for the manufacture of fertilizers.
The disinfection of premises should be thorough and should be carried out
by a trained corps of men employed for the purpose. The floors of stables
should be removed, the accumulations removed from beneath them, the
contents of haylofts should be destroyed, and the woodwork and soil beneath
the stables should be thoroughly drenched with a solution of bichlorid of
mercury, 1 part to 2,000 of water. After the flooring is replaced the
woodwork should be coated with limewash, containing one-fourth pound of
chlorid of lime to the gallon of mixture.
Usually in these cases the owners are dependent upon their herd of cows for
a living, and consequently it is difficult or impossible to hold the
stables vacant for any considerable period. In a majority of instances
cattle may be admitted at once to stables so disinfected, without the
reappearance of the disease. Occasionally, however, it will reappear
without apparent cause. For this reason the inspection and other measures
must be maintained in the infected district for six months or a year after
the last case of disease has been disposed of.
Many people have objected to the slaughter of diseased and exposed animals
as an unscientific and expensive method of eradicating the disease. To
these it may be answered that it is the only method which has ever proved
successful, and that in the end it is much more economical than temporizing
measures.
Inoculation has been adopted in many countries, and has undoubtedly
lessened the death rate, but where this practice is allowed the disease is
kept up and spreads. For this reason it should be prohibited wherever there
is a possibility and disposition to eradicate the contagion.
RINDERPEST.
Rinderpest, also known as cattle plague, is an acute, infectious disease of
cattle, in which the digestive organs are mainly involved. Though unknown
in this country, the importance of having near at hand a few definite facts
concerning this disease, should it ever reach our shores, will be at once
appreciated. A knowledge of such facts may aid in an early recognition of
the disease. It must not be forgotten, on the other hand, that a
superficial knowledge of diseases, such as the layman may gain through
reading, not infrequently leads to confounding comparatively harmless,
noninfectious maladies with such as are truly dangerous (foot-and-mouth
disease, rinderpest, etc), and causes temporary panics among stock owners.
According to some authorities, rinderpest has its home in the territory
around the Black Sea and the Volga River in Russia; according to others, in
Central Asia. Thence it has been conveyed at various times by cattle to
nearly every country of Europe and Asia, where it has proved to be a
veritable bovine scourge. It probably visited Europe as early as the
beginning of the Christian era, and since then the migrations of the people
from the Far East have from time to time introduced the disease. Especially
during the eighteenth century it was more or less prevalent in Europe,
owing to the frequent wars, during which herds of cattle were brought from
eastern Europe and Asia to supply the demands of the armies. It prevailed
in Europe during the Franco-Prussian War. At present it exists in eastern
Europe and in portions of Asia and Africa.
The virus is conveyed from one country to another chiefly by means of
infected cattle, although infected hides, wool, and feed may play an
important part in its dissemination. The railroad facilities of the
present, which furnish the means of such rapid communication, are
particularly liable to aid in the spread of the disease.
In the past rinderpest has been supposed to be identical with various human
diseases, among them smallpox and typhoid fever. These suppositions are
unfounded, and the view of authorities to-day is that it is a disease of a
peculiar kind, not identical with any other known infectious disease.
_The contagion of rinderpest._--The cause of rinderpest must be looked for
among microorganisms--most likely bacteria. The investigations made thus
far for this causal factor have been fruitless. However, certain recent
experiments would indicate that the unseen microbe is of such dimensions
that it is withheld by the dense bacterial filters, but passes through the
more porous ones. Formerly it was supposed by various authorities that
rinderpest virus appeared spontaneously under the influence of deteriorated
feed and long and exhausting drives; also during unusual meteorological
conditions. This view, however, is no longer maintained. It is probable
that in its home in Asia the disease is perpetuated by continual infection
of fresh animals, and some authorities go even so far as to believe that
the disease would be entirely stamped out, even in its native haunts, by a
destruction of all sick and infected herds. However this may be, the
success of such an undertaking would largely depend on the nature of the
cause. If a strictly parasitic organism, like the contagion of
pleuropneumonia, it might be completely extirpated in this way. If,
however, the germs or bacteria may live and multiply outside of the bovine
body, in the soil, water, or in some other animal, extirpation would be
impossible.
The virus may be transmitted in a variety of ways, both direct and
indirect, from sick to healthy animals. It is said to be present in the
various excreta, such as the discharges from the nose, and the saliva, the
urine, and the manure, of the diseased. For months it retains its vitality
in a moist state outside the body, and the disease is reported to have
developed after feeding hay a year after it had lain in an infected stable;
hence manure and the fodder and bedding soiled with discharges may convey
it. Persons may carry the virus on their shoes, clothing, or implements.
Even small animals, such as cats and rats, which frequent barns and
stables, have been looked upon as carriers of the virus.
Cattle are very susceptible to the disease, and in its virulent type all
those exposed are said to become infected. Buffaloes, sheep, and goats are
likewise susceptible, but in a less degree.
It is also claimed that animals after having passed through one attack
successfully resist future attacks. Inoculation with virus is said to
produce immunity, but in many cases the process of inoculation itself is
followed by death.
_Symptoms._--The symptoms of rinderpest are not very characteristic, and
hence the diagnosis of a suspected case in the beginning of an invasion is
attended with difficulties. Certain appearances which are characteristic of
one epizootic may be absent in another. Different observers are not quite
agreed as to the most constant and important.
The period of incubation, i. e., the time between the exposure to infection
and the earliest outward symptoms, varies from three to nine days. The
first sign is a very high fever, which may reach 107∞ F. The heat of the
skin varies in different parts of the body, and may be felt at the base of
the ears and horns. Repeated chills are frequently observed. The pulse
reaches 50 to 60 beats a minute, and in very severe attacks may rise to 90
or 100.
The animal manifests great debility. The head droops and rests on some
object of support. One or both ears may droop. The coat is staring and the
muzzle dry. The secretion of milk diminishes very rapidly. Within twelve to
twenty hours the usual quantity may have become reduced one-half or
two-thirds. The back is arched, and the four limbs are brought together
under the body.