Synonyms. Definition: infectious, cattle fever, with long incubation,
insidious onset, excessive pulmonary exudation, infarctions and
sequestra. History: ancient, modern; England, Norway, Sweden, Denmark,
United States,—its extinction in 1887 to 1892—Massachusetts, New
Jersey, S. Africa, Australia, Tasmania, New Zealand. Causes: contagion
only. Bacteriology: Nocard’s organism cultivated in collodion capsules
_in vivo_, as actively motile refrangent points, morphology uncertain.
Modes of transmission, exhalations from sick inhaled by susceptible,
ingestion of infected food, pastures, watering troughs, ponds,
commingling of herds, attendants, dealers, stables, manure,
unrestricted commerce, convalescent cattle, breed, hot seasons.
Lesions: profuse exudation in lymph networks of lungs, marbling,
parenchymatous cell proliferation, compression and gangrene of
lobulets, thrombi, sequestra, infarction, fibroid sac, or
stalactite-like fibroid peribronchial formations, hepatization,
pleural effusions and false membranes, pericardial, bronchial, lymph
glands congested. Incubation: 6 to 30 days, protracted cases, bearing
on quarantine. Symptoms: conditions affecting gravity, breed,
excitement, heat, chill, susceptibility, usually insidious, infrequent
cough, roused by cold water, dusty food, exertion, etc., hurried
breathing when driven, slight auscultation râles, hyperthermia (103°
to 108° F.), dulness, anorexia, suppression of milk, stiffness, no
pandiculation, troubled breathing, auscultation, and percussion signs
of extensive consolidation, tenderness of chest walls, in bad cases
stands obstinately, head extended, mouth open, tongue protruded,
grunts with expiration, heavy breath, nostrils dilated, nasal and
buccal discharge, rapid emaciation, fœtid diarrhœa, erect hair, pale,
scurfy, adherent skin, varied chest râles, abortion. Mild in winter,
severe in summer. Loss of one-third or one-half weight in one week.
Chronic cases, fibroid and necrotic changes, sequestra. Diagnosis:
Anamnesis, inoculation: from _tuberculosis_ by high fever, rapid,
extensive infiltration, early succession of new cases, failure to
react under tuberculin, absence of tubercles; from _bronchitis_ and
_pulmonary strongylosis_, by the succession of cases in place of many
at once, the extensive exudation, the evident cause (exposure or
infected place), and by the lesions; from _fibrinous pneumonia_, by
absence of climatic cause, the more extensive consolidation, more
troubled breathing, and coexistence of old and recent lesions; from
_infectious pneumonia_ by the greater area consolidated, more exalted
hyperthermia, more marked dyspnœa, the absence of white points of
alveolar cell proliferation, and by the old and recent lesions; from
_septicæmia_ hæmorrhagica, by its occurrence at all seasons, on all
soils, by the absence of sanguineous swellings at other parts, by the
absence of cocco-bacillus from the exudate, and by its
non-inoculability on sheep, horses, pigs and rodents; from _needle in
pericardium_, by its epizoötic prevalence, fever, and the absence of
preliminary gastric and later cardiac, morbid phenomena; from
_emphysema_ by the fever, absence of drumlike tympany, and presence of
consolidation; from _aspergillosis of the lung_ by the fever, more
rapid progress and extended consolidation, by the harmlessness to
birds, by the absence of aspergillus from expectoration and lung; from
_insolation_ by the absence of the causes of heat stroke, of the
implication at once of a number of exposed animals, of the excessive
hyperthermia, the brain symptoms and sudden deaths. Treatment: a poor
economy, to be punished when extinction is attempted. Prevention:
importation under three months quarantine, surveillance of three
months more in case of single animals; applied to lung plague
countries and those adjoining; disinfect cars and boats that have been
used in lung plague country; exclude hay and fodder from lung plague
country; also litter, bags, head ropes, horns, hoofs, hides, hair. To
extirpate: stop all ingress of possibly infected cattle, stop movement
of cattle, prohibit common or unfenced pasturage, kill without
indemnity in case of violation, record all cattle, make necropsy of
all dead, kill and pay for all infected herds, disinfect all infected
premises and things, use horses in removing and plowing under manure.
Unaided owner may: breed all his stock, in buying bull quarantine him,
allow no intercourse between his herd and others, get new cattle from
herds only that have had no illness nor losses for a year, and no
exposure, and bring by thoroughly safe route, in disinfected cars or
boats, then quarantine, under special attendants. Immunization; by a
first attack, inoculation in tail, intravenous, of sterilized exudate.
Conditions permitting and forbidding immunization.
_Synonyms._ Bovine Pleuro-Pneumonia, Contagious Pleuro-Pneumonia,
Peripneumonie (Fr.), Lungenseuche Vieseuche (Ger.), Pneumosarcia,
Peripneumonia Exudativa, Epizoötic Pleuro-Pneumonia, Pulmonary Murrain,
Slijmlongziekte (Dutch), Pulmonea dei Bovina (Ital.), Phush phush
pirdaho, Pheepree (Bengalee).
_Definition._ An infectious febrile disease, occurring casually in
cattle only, so far as known, and characterized by a prolonged
incubation (10 to 90 days), a tardy insidious onset, inflammation of the
bronchia, lungs and pleuræ, a profuse exudation into the interlobular
connective tissue and chest, a very extensive area of consolidation,
pulmonary infarction, and sequestra.
_History._ It is difficult or impossible to identify this disease among
the various animal plagues in ancient times. Yet when lesions are given
it may be admitted in different cases. Aristotle, writing 350 years
before Christ says “the cattle that live in herds are subject to a
malady which causes the breathing to become hot and frequent. The ears
droop and they cannot eat. They die rapidly and the lungs are found
spoiled.” Here the facts that cattle alone suffered, that large herds
suffered most, that the lungs were the seat of very marked lesions, and
that fever and mortality were both marked, point forcibly toward lung
plague. Valentini’s description of a fatal lung disease in cattle also
stands out prominently in the obscure records. The first full and
definite report is that given by Bourgelat of its prevalence in
Franche-Compté in 1769. Later the records are frequent and from all over
Europe, indicating its general prevalence before as well as after
Bourgelat.
Much more important are its definite extensions into new countries after
a long interval of immunity as showing that with trustworthy records
such invasions can always be satisfactorily accounted for by the
introduction of cattle or their fresh products from a previously
infected area. Into Holland it was imported from Germany in 1835 by
Vanderbosch a Guelderland distiller and spread over the whole country.
Attempts were made in Friesland, and at first successfully, to stamp it
out by slaughter and disinfection, but the demands of the trade toward
England grew so enormously that it was being constantly introduced anew
and the measure was abandoned. The British Consul at the Hague, in 1839
sent some Dutch cows to a friend in County Cork, Ireland, which led to
the general infection of that island and indirectly of Great Britain. In
1842, under the Free Trade Act, England became at once deluged with lung
plague cattle from Holland, Belgium and France on the one side, and
Ireland on the other. Soon the whole island had been infected except
exclusively breeding districts (Welsh and Scottish Highlands, etc.) into
which no cattle were ever introduced from outside.
In 1847 an importation of English cattle into Sweden conveyed the
disease, where it prevailed for some time and even infected Denmark
through shipments of cattle, but was finally extirpated by the pole axe
and disinfectants.
In 1860, Norway imported infected Ayrshire cattle for the Royal
Agricultural College at Aas, but the imported and exposed stock were
promptly destroyed and the previous immunity of the country has been
maintained up to the present.
Denmark was infected in 1848 by importation from Sweden, and on
different other occasions from Germany and England, but by prompt and
rigid suppressive measures, stamped out the disease on each occasion.
This was true also of Schleswig so long as it remained a part of
Denmark, but the infection entered in the commisariat parks of the
German army in 1864, and the principality remaining in German hands, the
lung plague became permanently established.
Mecklenburg-Schwerin and Oldenburg also maintained vigorous suppressive
measures and for long kept clear of the infection.
Into Brooklyn, lung plague was introduced in 1843 through the purchase
of an English ship cow by a dairyman (Peter Dunn). From this centre the
infection spread until it prevailed in Connecticut, New York, New
Jersey, Rhode Island, Pennsylvania, Maryland, Virginia, District of
Columbia, Ohio, Indiana and Illinois.
In 1879, measures were taken in New York and New Jersey to extirpate the
disease but failed to receive the requisite continued support and were
practically abandoned. It was only in 1887 when the infection had
reached Chicago, the largest cattle market in the world, that the
National and State Governments were aroused to the gravity of the
danger, and, the Federal Government supplying the funds and the Illinois
Government the authority, the beginning of a real attempt at extinction
was seriously undertaken. The author acted as chief of the national
veterinary force in Illinois in 1887, and takes great pleasure in
recording that at the end of three months from the date of his arrival,
the last acute case of the disease had been disposed of and the
frightful danger that had threatened the nation through the Chicago
stock yards had been removed. The supervision was maintained for a year
later, and some old sequestra were later found in the lungs of cattle
slaughtered, but no acute nor dangerous cases of the disease. This was
followed by vigorous suppressive work in other infected states and by
September, 1892, the quarantine was raised and the nation pronounced
free from lung plague. The last cases were met with in New Jersey, early
in 1892. In this last anti-lung-plague crusade the National Government
inspected 1,605,721 cattle in 166,951 herds, made 356,404 necropsies,
purchased 21,961 head of cattle, and disinfected 4,128 premises. 7,438
cattle were found affected at the necropsy.
Another line of infection was started by 4 Dutch cows, landed at Boston
in 1859, and before the end of the year the infection had extended into
20 different townships in Mass. In 1860, a State Commission was created,
with Dr. E. F. Thayer as veterinary commissioner, and in the next few
years they destroyed 1,164 cattle, and stamped out the plague at a total
cost of $77,511.07.
An importation of infected cattle into New Jersey was made in 1847, by
Mr. Richardson, who on discovering the nature of the disease, made an
end of that particular contagious centre, by slaughtering his whole herd
at a cost of $10,000.
South Africa was infected in 1854 by the landing of a Dutch bull at Cape
Town. As there were no railroads and all inland carriage was conducted
by ox-wagons, it soon spread over the colonies and extended thence into
the native states, and has continued to the present time.
Australia was infected in 1859 through an English cow landed at
Melbourne. When the disease was identified, the whole herd was
slaughtered and paid for, and the farm quarantined. But the quarantine
was broken by a teamster turning his work oxen into the pastures under
cover of night, and the infection escaped and has prevailed over
Australia to the present day.
Later the disease extended in a similar manner, to Tasmania and New
Zealand.
_Causes._ The one essential cause of lung plague is contagion from a
preëxisting case. Before the days of bacteriology, this had been
demonstrated as conclusively as any truth can be. All extensions into a
new country or district could be traced to direct importation from a
preëxisting area of infection. Until such importation such lands have
been immune from time immemorial; at once after, the infection has
spread from the imported animals as a centre; if the stock is divided up
and scattered, several primary centres are formed from each of which the
plague makes extension. Again, isolated islands (Channel Islands) and
purely breeding districts (Scottish Highlands) into the herds of which
no store cattle from outside are admitted, remain immune through
centuries, no matter how prevalent lung plague may be in the countries
immediately around. The immemorial immunity of the Western Continent, up
to the date of the arrival of the now famous Dunn cow, the continued
immunity of Canada and Mexico after the infection of the Eastern United
States, and the immunity of the United States since the last infected
cattle were destroyed in 1892, are equally conclusive in this respect.
_Bacteriology._ The history of lung plague forcibly illustrates how
harmless microbes of large size, that may be easily discovered, and
which existing in the environment, readily find their way into diseased
and susceptible parts (in this case into the bronchia), may be held to
be the pathogenic cause. Willems and Van Kempen, in 1852, found microbes
in the exudate. Lustig in 1885 found four separate microbes in the
lesions, 1st, a short, thick, liquefying bacillus to which he attributed
the disease; and 2d, 3d, and 4th, three forms of micrococcus. Poels and
Nolen, in 1886, demonstrated bacilli of variable size (0.9μ), solitary,
in pairs and chains, cultivable in different media, and inoculable by
injecting such cultures into the lungs, but the resulting lesions were
not marked by the full lung plague exudate. Arloing, in 1887, separated
from the exudate the _bacillus liquefaciens bovis_, a very short,
slender bacillus, often in pairs with flagella, motile, staining easily
in anilin but not in Gram’s solution, quickly liquefying gelatine as a
culture medium and assuming a form that might be taken for micrococci,
quickly obscuring peptonized bouillon, and growing on potato. The
exudate placed in a thermostat at 95° F. encreases in potency. The
bouillon cultures injected under the skin or into the lung, produced
characteristic lesions of lung plague.
In the light of the later experiments of Nocard and Roux in 1897–8, it
would appear that Arloing’s bouillon cultures were probably complex,
containing not only the _bacillus liquefaciens bovis_, but also, the
infinitesimal microbe which is the true cause of the lung plague. In
seeding culture media with the exudate taken with all possible
precaution against contamination, from the interlobular pulmonary
connective tissue, they and others constantly failed to obtain results.
Better success attended their efforts with Martin’s culture bouillon for
producing diphtheritic toxin. Five pigs’ stomachs are minced, pounded to
pulp, mixed as follows: stomach 200 grs., pure muriatic acid 10 grs.,
water 50° C., 1000 grs., left in a thermostat at 50° C. for 12 hours,
(to 24), then heated to 100°C. to destroy the action of the pepsin, then
lowered to 80° C., alkalized, filtered from flocculi that formed, heated
to 120° C., and filtered. This is then mixed with peptonized meat juice
prepared as follows: fresh beef or veal, minced and pulped, 500 grs.,
and water, 1 litre, are kept for 20 hours at 35° C., the liquid
expressed, 5 grs. common salt added, mixed in equal proportions with the
peptonized liquid from the pig’s stomach, heated to 70° C. to coagulate
albuminoids, filtered, alkalized and sterilized. To this mixture is
added ¹⁄₂₅th part of blood serum (sterile) from the rabbit or cow.
This bouillon was inoculated with the pulmonary interlobular exudate,
enclosed in collodion capsules, having very thin walls, and inserted
aseptically into the abdomen of the rabbit. In 15 days the rabbit was
sacrificed, and the capsules enucleated from their envelopes of exudate
and cells. The contents showed the slightest possible shade of opacity,
but they contained neither cells nor any other definite organism. Under
a magnifying power of 2000 diameters the liquid contents were found to
be full of brilliantly refrangent points, actively mobile, but so minute
that their form could not be made out even when staining was resorted
to. The contents of these capsules when inoculated on cattle produced
the unequivocal phenomena of lung plague infection in a period of from 8
to 15 days. Other collodion culture cases inoculated from this produced
the same cultures in the peritoneum of the rabbit. Collodion cases
charged with the uninoculated peptonized bouillon, and placed in the
rabbit’s peritoneum remained absolutely clear, with no refrangency nor
motility under high powers and with no infectivity when inoculated. The
rabbits used for the infective cultures often became emaciated to the
last degree and even died, but their tissues proved in no respect
infecting to culture media nor when inoculated. The attempt to cultivate
the germs in collodion cases in Guinea pigs completely failed.
This ingenious form of culture devised by Metchnikoff for experiments on
the more delicate organisms, has been used by Nocard to accustom the
tubercle bacillus of mammals to grow in the bird and opens up great
possibilities for future investigators. The collodion, being impermeable
to leucocytes and bacteria, allows these to grow almost together, only
on the opposite sides of the collodion wall, restrains phagocytosis, and
protects the microbe against the destruction which would otherwise
overtake it.
_Modes of transmission._ The exhalations from the sick convey the
infection to susceptible healthy cattle. Yet even this was denied by one
veterinary teacher in Great Britain in the latter half of the 19th
century. The transmission of the disease by mediate contagion was denied
by those in authority in Great Britain up to the end of the century and
this delusion contributed largely to the loss of many millions by the
nation. Experiments made at Brown Institution were held to sustain this,
but not an atom of evidence was furnished to show that the exposed
animals were susceptible ones. Diseased lungs kept for a year at 21° F.
proved infecting when inoculated (Laguerriere).
_Contagion through the air_ in the same stable was admitted even by the
English sceptics. It may be carried in this way for forty yards, or if
dried on dust or light materials to a great distance.
_Infection through food_ soiled by breath or nasal defluxion is a common
cause. In our great swill stables during the prevalence of the plague,
it was notorious that the disease advanced rapidly along the line of a
feeding trough to the sixty or more animals using it, and that the
rapidity of the advance was determined largely by the fact that the
first animal was at the higher end of the trough. If at the lower end
there was no upward current to carry infection to the others. _Open
pastures_ where the sick have fed and _watering troughs_ or _ponds_ are
common sources of infection. The permanence of infection in and around
large cities is largely due to the common pasturage by different herds
in succession on the same unfenced lots waiting to be purchased for
building. For this reason the plague always extended in summer when the
cattle frequented these lots, and diminished in winter when they were
strictly confined to stables and yards.
_Mingling of different herds_ on _great unfenced areas_ has been the
main cause of the maintenance of the infection from time immemorial in
the hills and forests of central Europe and on the boundless Steppes of
Europe and Asia. This alone is chargeable with the permanence of the
affection, in spite of all efforts for its extinction, in South Africa,
Australia, Tasmania and New Zealand.
_Contagion carried by attendants_, _cattle dealers_ and even _dogs_, is
generally recognized, I have elsewhere quoted the case, in E. Lothian,
Scotland, in which the son of the steward, who was cattleman on an
infected farm, was the means of infecting first, his father’s cow, and
later the whole of the stock on the place; also the case at Quincy,
Mass., in which a farmer coming straight from the slaughter of sick
cattle, infected his own herd; also the case of Mr. Jewell, of Long
Island, who carried the infection from the herds visited, to his own
family cow in a thoroughly secluded stable.
_Infection through infected and emptied stables_, was a common
experience in dealing with the lung plague in America. Cows kept alone
and only introduced after the predecessor had died habitually contracted
the disease, though brought, through the most carefully guarded
stockyards, from healthy districts. Stables have continued infecting for
a year after having been vacated, (Friedberger and Fröhner).
_Infection through manure_ spread on ground to which susceptible cattle
had access was an occasional occurrence.
An _active, unrestricted commerce_ is however the most prolific means of
infection in cultivated countries. Slow as the disease progresses, and
long as the animal diffuses infection, it soon attacks and kills or
immunizes all the susceptible animals in the single herd, and if no
other susceptible animal is bought or born into the herd, the germ in
due time loses its pathogenic potency and infection is at an end. In
this way many centres of infection started in herds on well fenced farms
have worn themselves out. But the case was far otherwise in the city
dairies and swill stables. The trade demanded that the stalls emptied by
deaths should be filled up to consume the swill, or supply the milk
route and thus fresh susceptible cattle were constantly exposed in the
infected stable. The dairy cows were supplied by dealers who charged
exorbitant prices for them and held a chattel mortgage for the amount.
They had come through the infected dealer’s stable, and if they did not
come up to the milk yield promised, they were either passed on to
another dairy or returned to the dealer’s stable carrying back a new
load of infection. The wagons used to carry the cows through the city
were constantly infected and infecting. The swill stables became the
final destination of the surviving cows that had gone dry and thus
infection constantly gravitated into them.
In Europe where the great cattle and meat trade with England and the
constant demand for cattle to consume the marc of the beet sugar and
other factories, cause a continuous draught upon the infected districts
the great western centres of enterprise and commerce have found it
impossible to exterminate the plague.
In the country districts in England outbreaks were almost exclusively
confined to the times when fresh cattle were purchased at one of the
great fairs. Hence the late autumn, the period of laying in feeding
cattle, witnessed the greatest extensions.
In Ireland, as shown by Ferguson, the whole cattle trade seemed to be
arranged as if for the speedy and universal diffusion of infection.
Calves, bought by jobbers from all sources, were bunched together with
every opportunity for intercommunication and infection. As soon as they
were a little further matured, they were assorted in lots and sent to a
fair, where they were sold, and found their way to great common
pastures, and this process was repeated again and again until they had
reached full maturity. On the way to and from each market they were
quartered over night in a public yard which had just been vacated by
other animals, often diseased, traversed the same roads, and drank and
fed from the same troughs which diseased ones had just used.
The _introduction of apparently recovered cattle_ is generally credited
with the infection of a fresh herd and Friedberger and Fröhner quote
with approval Walley’s assertion that a recovered animal with a
sequestrum in the lung can infect a herd into which it is taken. I have
failed to produce even local exudate, subcutem or in the lung, from
sequestra which were much more recent, but the animals operated on were
rendered immune and inspired me to carry out a system of immunization by
the use of the sterilized fresh exudate. The actual date of the
expiration of virulence in the necrotic lung tissue has never been
demonstrated and probably varies in different cases.
The _receptivity_ of different breeds has been discussed and the
Holsteins and Shorthorns have been thought to show the greatest
susceptibility. These are among the cattle that are most prized, bought
and sold, and exposed to infection. The Shorthorn especially has a great
development of the circulatory system, including the connective tissue
with its great lymph sacs and channels, and the microbe we are dealing
with shows a marked preference for the lymph system, in which it finds
its appropriate field of development. Susceptibility is greatly
encreased by a _warm climate_ or _hot season_, under which large herds
may die without a single exception, the disease running a fatal course
in two or three days. In cooler climates 20 per cent. will often escape
at first (French Commission Experiments, 1849).
_Lesions._ If death has taken place early, the lesions are usually
essentially pulmonary, though they may implicate the pleuræ and
mediastinum. In many cases the lung alone is involved, yet even then the
predilection of the microbe for the lymph network of the interlobular
tissue is strongly manifested in the serous infiltration of that, rather
than of the lung structure proper. This determines the much talked of
marbled lung, the pulmonary lobules standing out at first as a more or
less deep red brown or black, while the marbling is caused by the
yellowish or grayish infiltrated tissue surrounding each pulmonary
lobulette which appear set in, as in mosaic on the surface of a section.
Sometimes a blood extravasation discolors the interlobular exudate as
well, yet it retains its soft liquid appearance which sufficiently
distinguishes it from the firmer lung tissue. These yellowish
interlobular markings vary much in thickness, but in acute cases this
may be up to half an inch or even more. In the lesions of longer
standing the interlobular exudate has usually coagulated, or even
undergone fibroid organization, so that it compresses and condenses the
lobules which it surrounds.
The pulmonary lobules may show the earliest changes of the alveolar and
lobular capillaries, with formation of an exudate, and an active
proliferation of small round cells in and around the alveoli. Later the
exudate coagulates, forming the familiar red hepatization, and this in
its turn may pass into the gray, or it may liquefy and undergo
absorption and resolution. Other changes are not uncommon. The excess of
interlobular exudate will compress the pulmonary lobules so as to reduce
their size and expel the blood from their structure, giving them a pale
color, or this compression becomes still greater, completely arresting
the circulation and inducing lobular gangrene. Thrombi in the afferent
and efferent vessels contribute to the necrotic change, and sequestra of
varying size, from that of a nut to that of an infant’s head or larger,
are formed. The earliest stage of this necrosis is usually infarction of
the lung, a definite area of which becomes saturated with dark blood
cells so that in contrast with the rest of even the hepatized lung, it
is almost as characteristic as the marbling. The further progress of
this necrosis is varied. Most commonly the exudate surrounding the
necrotic mass becomes organized into white fibrous tissue and forms an
investing sac in the interior of which is the dead lung tissue, showing
for a time distinctly, the bronchia, blood vessels, lobulettes, and
interlobular tissue. This gradually becomes detached and floating in a
liquid debris, slowly undergoes solution, and is absorbed, the sac
meanwhile closing in on the cavity. A large sequestrum may be a year or
sixteen months in undergoing complete solution. In other cases the
pulmonary lobulettes undergo an individual softening while the
interlobular tissue becomes organized and when cut across, the lung
presents a distinct honeycombed appearance. In still other cases a
considerable area of both lobulettes and interlobular tissue is necrosed
and liquefied, while the exudate, around the bronchial tubes, that
supplied it, becomes organized, and on the necropsy the latter are found
to constitute a thick branching mass of a very characteristic
appearance.
The newly affected lobulettes have a watery or gelatinoid or dropsical
appearance and if freely incised give out a large amount of serum and
flatten down in doing so. When hepatized the cut surface is granular,
and microscopic examination shows the terminal bronchia and alveoli
filled with a fibrinous exudate containing great quantities of red blood
globules and leucocytes. The distension of the lung is enormous, so that
when the entire organ is infiltrated it may weigh from 50 to 100 pounds.
In recent cases the lung may be extensively affected without affecting
the _pleuræ_; in other cases both are early involved. In advanced cases
the pleuræ are always implicated. First there is the subpleural
infiltration over the affected part of the lung; later the pleural
surface has reddened arborescent patches, with a slight solid exudate,
and a yellowish (sometimes blood-stained) serum collects in the bottom
of the cavity; later still the affected portion of the lung is covered
more or less thickly with false membranes, while others cover the organ
or the parietal pleura below this level, and hang in shreds or bind the
lung to the ribs. In old standing and recovered cases these may be
largely represented by dense, white fibrous investments covering the
lung or the rib, or establishing permanent adhesions. The amount of
pleural effusion may be about two gallons in bad cases, and like the
invasion is either unilateral or bilateral. The _pericardium_ is usually
more or less involved in pleuritic cases.
The _larger bronchia_ sometimes contain false membranes.
The _bronchial_, _prepectoral_ and _mediastinal lymph_ glands are often
enlarged, congested and infiltrated with an abundant exudate.
Similar infiltration of the lymph glands of the pharynx, mesenteries.
sublumbar region and groin are described, together with hypertrophy and
congestion of the intestinal follicles, and congestion of the muscles
and intermuscular tissue, of the articular and tendinous synovial sacs,
and even of the meninges of the brain and cord. I know of no facts to
show that these conditions result from anything else than the toxins and
the general constitutional disorder. The indications are that the
microbes are speedily destroyed in the circulating blood, and
intravenous injections and caudal inoculations alike fail to cause the
characteristic lesions in the lung, their favorite point of casual
election.
_Incubation._ This usually lasts from 6 to 30 days, being greatly
abridged by hot weather and often prolonged in the cold. Delamotte
claims to have seen it extend to 5 months, and in one case a calf turned
out on Montauk Point, L,. I., from an infected place was noticed ill on
the 104th day. Australia, South Africa and Norway were each infected by
cattle that had been three months out of their native infected land. I
have seen cattle pass three or four months after purchase in an
unthrifty condition, yet without cough or other recognized diagnostic
symptom and then come down with lung plague. Such doubtless explain the
alleged protracted incubations, the system has been invaded, ill health
ensues, but the lungs are only slightly affected for a length of time.
In other cases one animal in a herd has had a mild attack, which escaped
notice, and it was only later that the disease was recognized in a
second victim, infected from this first.
The bearing of this on imported animals is evident. An animal imported
alone should be kept under surveillance for a month or two after
quarantine, while in any considerable herd the disease would certainly
manifest itself during the prescribed three months detention.
_Symptoms._ These vary greatly with the animal and its environment.
Other things being equal it may develop more suddenly and violently in
the obese Shorthorn, Angus, Hereford, Ayrshire or Dutch, and less so in
the spare Brittany or Jersey. In very hot weather the attack is very
sudden and severe. A chill from exposure, an attack of bronchitis or
pneumonia, the excitement attendant on parturition, on travelling by
rail or driving may precipitate and aggravate the seizure. Under some
such conditions there may be sudden and extreme hyperthermia, rapid
pulse, oppressed breathing, percussion and auscultation evidence of
extensive pulmonary consolidation and death in two or three days, while
the body is still plump and fat.
Individual susceptibility appears to have influence, the same stable
presenting simultaneously cases of acute and fatal type and others that
are slow, and insidiously progressive. In newly invaded countries and in
bovine families that have not been exposed to the infection for many
generations the tendency is to a higher proportion of severe and fatal
cases, while in herds native to districts that have been continuously or
frequently exposed, mild cases tend to predominate. The more susceptible
strains of blood have been killed out, and the surviving strains show a
greater power of resistance.
Apart from the predisposing environment the tendency of lung plague is
to set in slowly, insidiously, and for a time almost without outward
symptom. For a week, fortnight, month or more there may be a slight
cough heard only at rare intervals and neither painful nor specially
troublesome. Though sometimes hard, it is more commonly small, weak,
short and husky, noticed only when the animal rises, drinks cold water,
goes out to the cold air, or eats dusty or fibrous fodder, and is
usually attended by arching of the back, extension of the head, opening
of the mouth and protrusion of the tongue. For weeks there may be no
indication of constitutional disorder, appetite, rumination, milking,
and other functions appearing to be normal. Driving the animal may
unduly accelerate the breathing, and a careful auscultation may detect
an unusually loud blowing sound behind the middle of the shoulder, a
mucous râle, or a wheeze. In some cases the disease never advances
farther, the trouble subsides and the subject is thereafter immune.
Cases of this kind occurring as the first in a herd, explain some
instances of what are claimed to be specially prolonged incubations.
In the great majority of cases further symptoms appear, hyperthermia
sets in, varying in different animals from 103° to 108° F., the animal
becomes dull, depressed, loses in appetite, rumination and milking,
omits pandiculation on rising, shows stiffness of the hind limbs,
sometimes knuckles forward at the fetlocks, wanders apart from the herd,
is found lying apart, shows extra thirst, bloats slightly, and shows
some constipation. Pulse and breathing are accelerated, auscultation
signs are more marked, and on percussion, areas of flatness may indicate
lobular consolidation, usually more extended than in ordinary pneumonia
with the same grade of constitutional disturbance. The muzzle becomes
hot and dry, the roots of the ears and horns hot, and the hair stands
erect along the dorsal aspect or in patches over the body. Pinching of
the dorsal spines, sternum or intercostal spaces, may cause marked
wincing and a deep groan. The eye is dull, lacking in prominence and
clearness, and the lids are often partially closed. At this stage
improvement sometimes ensues and after inappetence and suppression of
milk for one or two days, the patient may take to feeding and milking as
before, and apparently recover, though with a large pulmonary
sequestrum.
In the continuous and violent cases all the symptoms are aggravated.
Fever may run to its extreme height, there is complete anorexia and
suspension of rumination, pulse and breathing are rapid, the victim no
longer lies down but stands with feet apart, arms and elbows turned out,
head extended nearly on a line with the neck, mouth open, tip of the
tongue projecting, and each expiration accompanied by a moan, so loud
that it may be heard at a distance (often 50 yards). The breath is
heavy, feverish, mawkish. The flanks heave violently, the nostrils are
widely dilated and discharge muco-purulent, often bloody liquid, strings
of fœtid saliva drivel from the open mouth, there may be tympany or even
colic, the eyes are sunken, and the conjunctiva and nasal and buccal
mucosæ are of a dull brownish and yellowish red. Emaciation advances at
a rapid rate, and the constipation may be superseded by a profuse, fœtid
diarrhœa which wears out the animal. The skin is dry, scurfy, withered,
pale, and clings firmly to the bones, and the interior of the vulva may
show the pallor of anæmia. The spine, sternum and intercostals are more
than ever tender, and pressure on the tender areas may detect a lack of
movement of the lung which is felt on the healthy parts.
On percussion very extensive areas of consolidation are revealed by the
dulness and flatness. If pleuritic effusion exists the resulting
flatness is extreme below and up to a given horizontal level, the line
of which may, however, be elevated at points by consolidation of the
lung at such parts. Auscultation may reveal almost any of the abnormal
sounds of pneumonia or pleurisy. Absence of respiratory murmur over
large areas, with blowing, heart or abdominal sounds in unwonted
situations (where the murmur is absent), and abnormally loud murmur
where the lungs are still pervious; crepitation around the margins of
the consolidated portions; the creaking sound of stretched false
membranes, scarcely distinguishable from crepitation; mucous râles;
wheezing sounds of various pitches; exceptionally splashing sounds, and
if the animal has just risen, the metallic tinkling sound. In other
cases the pleural friction sound is prominent.
Abortions are common in pregnant animals.
_Course._ This varies greatly. In our northern states in winter, many
would seem to recover after a few days illness; in summer, many died in
a few days with excessive exudate, dyspnœa, and prostration. Others died
early from tympany of the rumen. In others still, profuse, fœtid,
colliquative scouring led to an early death. In extreme cases there
would be a loss of one-third or one-half the weight in a single week. In
the less rapidly fatal cases all the symptoms became aggravated, the
emaciation progressed, and a liquid pultaceous condition of the bowels
continued for two, three, four, or even six weeks, the animal finally
dying in a state of marasmus. In such cases the shrunken, pallid skin
and mucosæ bespoke an extreme degree of anæmia.
Recoveries may take place from comparatively advanced stages, but they
are liable to be slow and imperfect, the animal remaining unthrifty for
a length of time. In some of the more favorable cases, when the recovery
is less interrupted or retarded, fattening may take place rapidly, so
that it would appear as if the loss of a portion of lung, and the
lessened consumption of hydrocarbonaceous matter contributed to the
deposition of fat.
In some cases the active morbid processes subside, but are not quite
arrested and the malady assumes a chronic form, the exudates become
organized, causing a sclerotic or fibroid condition of the lung and
especially of the interlobular tissue, which compresses and carnifies
the lung tissue, or leads to necrotic changes and the formation of
sequestra, or again to liquefaction and the formation of vomicæ. Here
the proliferation of the germ may go on, though little new tissue is
invaded, and the animal may remain infecting for a long period. The
patient remains thin, and weak, is easily blown under exercise, has a
small, accelerated pulse, little power of digestion or assimilation,
shows frequent tympanies, and may have profuse diuresis or diarrhœa. The
cough is frequent, often paroxysmal, easily roused, loose, mucous,
painful and may be attended by muco-purulent discharge. Such animals are
liable to die in the end in marasmus.
In some cases the malady is complicated by other infections, leading to
the formation of abscesses in the lungs, pleuræ, chest walls, bronchial
glands, joints or elsewhere, or tuberculous deposits may complicate the
lung plague, and there may be an early death or a long drawn out
decline.
_Diagnosis._ So many different affections resemble lung plague closely
during life, that a certain means of diagnosis is a great desideratum.
Yet many points help one to reach a reasonably certain diagnosis:
1. Does lung plague exist in the country? If not the presumption is very
strongly against it.
2. Have the suspected animals been recently imported from a lung plague
infected country? or have they been in contact with animals recently
imported from such a country?