_Last week of September, 1872._ Toronto, _Ontario_; (30th) and
neighborhood.
_First 2 Weeks of October._ Barrie, Collingwood, Owen Sound, Guelph,
_Ont._; St. John, _N. B._ (13th); Niagara Falls, (11th), _N. Y._;
Montreal (8), Ottawa (12th), Stratford, Brantford, London, _Can._;
Buffalo, _N. Y._ (14th); Detroit, _Mich._ (13th).
_Third Week in October._ Goodrich, Kingston, (19th), _Ont._; Rochester
(18th), Syracuse, Lockport, Canandaigua, Geneva, Albany, (19th),
Ogdensburg, (21st), New York, (21st) _N. Y._; Bangor, _Me._; Port Huron,
_Mich._
_After Third Week in October._ Quebec, (28th) _Can._; Utica, (29th),
Watertown, Oswego, Schenectady, Saratoga Springs, Poughkeepsie (28th),
Elmira, Binghamton, (28th), Jamestown, Ithaca, (31st), Port Jervis
(29th), Nyack, _N. Y._, (30th); Revere, (22d); Springfield, (23d),
Worcester, (27th), Fall River, New Bedford, _Mass._; Waterbury, (27th),
Norwich, (23d), New Haven, Hartford, _Conn._; Providence, (23d),
Newport, _R. I._; Burlington, (26th), St. Albans, _Vt._; Concord,
Nashua, Portsmouth, (23d), _N. H._; Bath, (28th), Portland, _Me._;
Philadelphia, (26th), Harrisburg, Lancaster, York, Erie, Corry,
Titusville, (28th), Pittsburg, (29th), _Pa._; Baltimore, (25th), _Md._;
Washington, _D. C._, (28th); Norfolk, (31st), Richmond, _Va._;
Cleveland, _O._; Chicago, (29th) _Ill._
_First Week of November._ Kingston, _N. Y._, (1st); Rutland, _Vt._,
(3d); Meadville, (2d), Pottsville, Williamsport, (6th), Reading, Easton,
Bethlehem, _Pa._; Trenton, _N. J._, (2d); Wilmington, _Del._, (6th);
Jackson, _Mich._, (7th); Milwaukee, _Wis._; Raleigh, _N. C._;
Charleston, _S. C._, (4th).
_Second Week in November._ Scranton, _Pa._, (13th); Lynchburg, _Va._,
(11th); Wheeling, (13th), Parkersburg, _W. Va._; Dayton, Sandusky,
Toledo, _O._; Adrian, Kalamazoo, (9th), Grand Haven, _Mich._ (8th);
Davenport, _Ia._, (14th); Janesville, Green Bay, _Wis._; Louisville,
_Ky._, (9th); Wilmington, _N. C._, (12th); Columbia, _S.C._; Savannah,
_Ga._
_Third Week in November._ Steubenville, (15th), Columbus, (16th),
Zanesville, (16th), Springfield, _O._; Indianapolis, (17th), Fort Wayne,
Lafayette, Evansville, (21st), _Ind._; Bloomington, Galena, (21st),
_Ill._; Dubuque, Iowa City, _Ia._; Madison, Fond du Lac, _Wis._; St.
Paul, _Minn._; Memphis, Nashville, Chatanooga, _Tenn._; Augusta,
Atlanta, _Ga._; Helena, Fort Smith, _Ark._; Havana, _Cuba_, (20th).
_In November after third Week._ Terre Haute, Madison, _Ind._; Peoria,
Galesburg, _Ill._; Keokuk, Muscatine, Des Moines, _Ia._; Paducah, _Ky._;
Knoxville, _Tenn._; Charlotte, New Berne, _N.C._; Macon, Rome, Columbus,
_Ga._; Jacksonville, Lake City, _Fla._; Mobile, Montgomery, Selma,
_Ala._; Natchez, Vicksburg, _Miss._; New Orleans, (25th), _La._;
Galveston, (29th), Houston, (28th), _Tex._; Little Rock, _Ark._
_First week in December._ Cairo, _Ill._; Lincoln, Omaha, Nebraska City,
_Neb._; Yankton, (5th), Vermilion, _Dak._; Tallahassee, _Fla._; Camden,
_Ark._; St. Louis, Kansas City, _Mo._
_Second Week in December._ Quincy, _Ill._ (8th); Shreveport, _La._;
Hanibal, _Mo._; Fort Scott, Lawrence, Leavenworth, Topeka, _Kan._
_December after the Second Week._ Denver, Central City, _Col._;
Cienfuegos, _Cuba_.
_January 1873._ San Antonio (3d) _Tex._; Cheyenne, _Wyo._; Cimarron,
(1st week), Elizabeth City (2d week), Alberquerque (4th week), _N. M._;
Salt Lake City, (2d week), Corrinne (3d week), _Utah_; Santiago, _Cuba_.
_February._ Brownsville (3d week) _Tex._; Winnemucca, _Nev._; Monterey
(1st week), _Mex._
_March._ Prescott (1st week), Tucson (2d week), Yuma (4th week) _Ariz._;
Boise City, (3d week), _Ida._; Helena (4th week) _Mont._; Virginia City,
(1st week), _Nev._; Carson City, _Nev._, Santa Barbara, Visalia, _Cal._;
Guaymas, Mazatlau, Manzanillo, _Mex._
_April._ San Diego (1st week), Mariposa, Stockton, San José, Oakland,
Sacramento, Marysville and Shasta (2d week), San Francisco, Vallejo,
Nevada City and Weaverville (3d week), and Lava Beds, _Cal._ (4th week);
Baker City (2d week), Jacksonville, _Ore._ (4th week); Walla Walla,
_Wash._ (4th week); Acapulco (1st week), _Mex._
_May._ Eugene City, (3d week), Dallas and Portland, _Ore._ (4th week);
Olympia, _Wash._
_June._ Seattle, _Wash._ (3d week).
_July._ Guatemala City, Guatemala (2d week), Victoria, _B. C._
_August._ La Union, _San Salvador_ (1st).
Among the deductions from this record are:
1. The affection advanced gradually from Toronto over the whole
continent of North America, where horses are kept, taking full ten
months to accomplish this. Nothing checked its advance, over lowland and
highland, swamp and arid land, in summer as in winter, with a
temperature at 0° or at 100° F., in country pasture or in city street or
stable, idle or overworked, on all kinds of soils and geological
formations, under all successive conditions of meteoric and terrestrial
electricity, in all conditions of the air—pure, impure, dense, light,
moist and dry. No one condition of the environment operating on the
animal system, can be conceived of that could advance as this disease
did from place to place in regular sequence for this length of time.
2d. The rapidity of its progress was manifestly subordinate to the
activity of the movement of the equine races from points already
infected. Its most rapid advance was along the lines of railway while
the back districts shut out from railway traffic were much later in
being invaded. The larger cities situated on the through railroad routes
suffered earlier than the smaller places on the same lines. The outbreak
was several days earlier in Montreal than in the nearer and smaller
cities of Kingston, Ottawa, Belleville, Port Hope, Peterboro, Stratford,
Brantford, Guelph, London and Owen Sound. The important port of St.
John, N. B., suffered two weeks earlier than Quebec. Along the N. Y.
Central and Erie Railways etc., Boston and New York suffered nearly a
week earlier than Utica, Poughkeepsie, Binghampton, Elmira, and
Jamestown, while the smaller places like Kingston, Nyack, Ithaca, etc.,
were later still. In Baltimore the disease was seen a day earlier than
in Philadelphia, and in these cities and Washington over a fortnight
before it was seen in Scranton, Pa. So it was almost everywhere and in
these large cities the outbreak could in nearly every case be traced to
horses just arrived from a pre-existing centre of infection. In Detroit,
Syracuse and Chicago it spread first in stables that had just received
Canadian horses, in Ithaca in one which had received horses from an
infected centre in Northern New York and in Pittsburgh and Washington in
stables that had just admitted horses from infected New York.
3d. It advanced with much greater rapidity eastward than westward, being
in the line of greatest horse traffic, the animals being mainly raised
and fitted in the West and shipped in large numbers to the great cities
near the Atlantic seaboard.
4th. In the absence of this active railway traffic In horses, the
advance was most rapid through other lines. In Pa., in a number of
valleys opening to the south, the disease reversed its general
direction, and extended northward up these valleys. In Lehigh Co., Pa.,
it followed the course of the canal, being carried by horses and mules
employed on the towpath. In Davidson and Sumner Cos., Tenn., it followed
the track of a circus which came through an infected locality. It
reached the Pacific coast at Santa Barbara (not at the railway terminus
at San Francisco) having followed a mule stage route in the absence of
an active, westward progress of horses by rail.
5th. The affection failed to overstep any serious gap over which there
was no movement of equine animals. It prevailed in Victoria, B. C., in
July, but, owing to a strict quarantine on horses and mules, it failed
to reach Vancouver Island. It ravaged New Brunswick and Nova Scotia in
November but failed to reach Prince Edward Island which was then ice
bound and shut off from all traffic with the mainland. It ravaged Cuba
to which it was brought by American horses landed at Havana, but no
other West Indian island was attacked. Its southward course was finally
arrested at Central America, where horses are few and horse traffic
nearly unknown.
Every fact in connection with its eruption and progress agrees perfectly
with the hypothesis of transmission by contagion alone, and taken
altogether the history excludes all other causes from being anything
more than accessory. Before the days of modern bacteriology we had ample
proof that glanders, rabies, sheeppox, lung plague, and Rinderpest were
due to contagion alone as an essential cause, and so now we have the
same evidence concerning equine influenza.
_Other testimonies to Contagion._ Trasbot says the virulence is “almost
equal to that of Rinderpest or aphthous fever,” and adds “all
practitioners have become assured that the bringing of an affected
animal into a stable constantly introduces the malady to the others.”
Cadeac says “the diseased or infected animals are the main channel of
propagation of the malady” and again the disease is “essentially
infectious.” Friedberger and Fröhner are more definite—“influenza which
is as highly infectious as any other disease can be produced only by
infection.” Cadeac implies nearly as much in saying: “in all the
epizoötics that have invaded Paris, the disease has been carried into
the four quarters of France by horses bought in this city. In most
regiments the malady shows itself after the arrival of horses from
remounts where it was prevailing. At Sibourne it is through horses from
St. Jean d’Angely. At Lyons it is by a horse from Cæn. At Bourges the
source was not traced but it spread from the garrison to the whole
surrounding country. The Omnibus stables in the Rue d’Ulm were invaded
when a horse was introduced from Clichy where influenza raged.”
_Stables_ are fruitful sources of infection hence dealers’ horses and
horses travelling from place to place have long been objects of just
suspicion (Trasbot, etc.).
_Cars_ are often infected, and spread the disease widely. (Poucet,
Salle, Trasbot, etc.).
_Manure_ is especially dangerous. Trasbot gives a number of cases of the
infection of farms, by the manure taken from the Alfort Veterinary
College, and other infected stables in Paris. Friedberger conveyed the
disease experimentally in the manure.
The conveyance of the virus on the _clothes of attendants_ has been
alleged by Friedberger and Fröhner, and considering that it has been
noted to pass over intervals of about half a mile without the
intervention of any horse, it must have been wafted on the air, or
conveyed on the surface of man or non-equine beast.
Jensen and Clark allege that the contagium may be conveyed to mares by
_coition, for months_ after the stallion has shown all outward signs of
recovery. This would be entirely in keeping with the analogous fact in
swine plague.
_Inoculation._ Experimental inoculations have transmitted the disease
with difficulty and uncertainty. Those of Hertwig, Nocard, Arloing,
Labat, Friedberger, Trasbot, Pasteur and others came to naught. Even the
transfusion of the blood of the sick, proved as harmless as the
inoculation of the serous exudate. A probable explanation is found in
the extreme diffusibility of the germ of equine influenza, which spreads
over a city or county in a few days, attacking practically all equine
animals. Inoculation is necessarily made at the time of the prevalence
of influenza and at such a time all horses in a wide area are likely to
be suffering from the affection. Those that are unaffected and therefore
apparently available for experiment, are the immune animals. If they
were susceptible the probability is that they would speedily show the
disease through infection drawn from another source than the
inoculation. If the inoculated animal failed to contract the disease,
and yet very shortly afterward became infected by simple exposure, there
would be some basis for alleging that inoculation was always
inoperative. Dieckerhoff, on the other hand, transmitted the disease to
healthy horses by subcutaneous and intravenous inoculation of the blood
of the sick, and the same seems to be true of inoculations of the
cultures of the cocco-bacillus by Lignieres.
_Bacteriology._ Our knowledge of the bacteria of equine influenza is as
yet very imperfect and uncertain. Galtier and Violet found streptococci
and diplococci in the blood and tissues of cases showing intestinal
lesions, and held that they were derived from musty fodder. Injections
of infusions of such fodder into the trachea of the horse produced
broncho-pneumonia, double pleuro-pneumonia, and at times intestinal or
meningeal congestion. But there is no proof that the malady so caused,
passed with the certainty and rapidity of equine influenza from horse to
horse in the same stable.
The _cocco-bacillus_ found by Lignieres in the blood and exudate of the
patients has more plausible claims to being the specific germ. This is
an ovoid bacterium, somewhat smaller than that of chicken cholera, and
like it pigmented at the poles and clear in the central part, a
characteristic feature of the group of Pasteurella of Trevisan. This
group includes the nonmotile germs of swine plague, the septicæmic
pneumo-enteritis of sheep, wildeseuche, and septicæmia of rabbits and
chickens, as well as that of fowl cholera; all stain easily in gentian
violet and fuchsin, and all cause some form of hemorrhagic septicæmia.
The germ is ærobic and grows best in peptonized bouillon to which a
little serum has been added. It forms, in peptonized gelatin, round
colonies, at first transparent and later opaque or milky, and without
liquefaction. The cultures when inoculated subcutaneously proved fatal
to Guinea pig, rabbit, rat, mouse, dog, cat, sheep, pig, ox, ass, pigeon
and chicken.
Intravenous inoculation on the horse of 1 to 2cc. of the culture kills
in a few hours, the temperature having risen to 104° F., the mucosæ
acquire a dull brown tint, the eyes are swollen and weeping, enteritic
colics appear, the limbs may swell and there may be painful arthritis
and jaundice. At the necropsy the blood is black and incoagulable, the
muscles as if parboiled, the liver a deep violet, the intestinal mucosa
congested, a yellowish or reddish effusion in the pericardium and
numerous petechiæ on the serosæ.
Subcutaneous inoculation causes an enormous inflammatory œdema resulting
in a sanguinolent abscess, in case the subject survives. There are also
hyperthermia (106° F.), dulness, stupor, weakness, staggering, and
congested, swollen, weeping eyes.
Intratracheal injection is harmless to the horse.
Lignieres finds his cocco-bacillus in the expectoration at the outset
and in the nasal and guttural forms of the disease later, but not in the
blood nor lungs after death, as it is then replaced by streptococci, the
great reproduction of which is favored by its presence. In ordinary
cases of equine influenza it is often impossible to find the
cocco-bacillus in the lung or other organs after an illness of 8, 10 or
15 days. (Lignieres).
Lignieres appears to have omitted the obvious test of the infection of
other horses in the same stable, from the cases produced by his
experimental cultures, so that we must still call for more confirmatory
proof. Cadeac, indeed, assures us that cultures of cocco-bacilli taken
from cases of equine influenza, are often innocuous. Deadly as the germ
cultures of Lignieres prove, they appear to lack that element of extreme
infectiousness shown by equine influenza when the susceptible animals
come into proximity with the sick.
_Accessory Causes._ The recognition of the one essential cause in the
microbian invasion, need not exclude as accessory factors the many
unwholesome conditions which have long been recognized as contributing
to the severity of epizoötics. As the seed requires the rich field, the
rain and sunshine to bring it to an abundant harvest so the microbe of
equine influenza flourishes best where the conditions are most favorable
and the antagonisms least.
The _chill_ which comes from a sudden extreme fall of temperature, or
the standing in a cold draught when wet or perspiring, lays the system
open to this as to other microbian invasions.
The _electric tension_ preceding a thunderstorm, to which many of the
lower animals are excessively susceptible equally prepares the system to
succumb to the germs. It may here be noted that September 1872, the last
days of which witnessed the start of the great epizoötic, had no less
than eleven thunderstorms, while in September of the previous year there
were but two in the vicinity of Toronto. It is just possible that the
great and frequent electric tension, lowered the animal vitality,
allowing a violent invasion by the hitherto slumbering germ, and gave to
the latter that encreased potency which sent it forth on that year of
almost unparalleled epizoötic record.
The _high barometer_ and _low dew point_ similarly affect the animal
economy and encrease receptivity to disease. Rain fell at Toronto 16
days in September 1872 and but 8 days in September 1871.
_Impurities in the air_ whether originating in volcanic eruptions,
telluric emanations, close, filthy overcrowded buildings or compartments
or large collections of decomposing organic matter, impair the animal
vigor and lay the system open to a more violent attack. For this among
other reasons epizoötics of equine influenza are nearly always more
deadly in the closely packed city stables than in the pure country air.
_Overwork_ and _poor irregular feeding_ and _watering_ pave the way for
debility, prostration and severe invasion.
_Sudden vicissitudes of temperature_, which are so common in _spring_
and _autumn_, associated as they are with the _shedding and growth of
the coat_, materially encrease susceptibility and sometimes determine an
encreased severity in the attack.
_Youth_ has its influence, even if it means only that the system that
has never before been exposed to the poison, retains all its native
susceptibility, and has none of that acquired immunity which comes from
a previous exposure to the virus and successful resistance.
_Acquired immunity_ must of course be reckoned with. After a non-fatal
attack this is usually to be relied on for several years or even for the
rest of the lifetime, yet it varies with the individual animals, and,
under the baleful combination of a specially potent germ and strongly
conducive accessory causes, it may become worn out in a year. Yet the
older horses can always be trusted to show a large measure of this
immunity, so that in the absence of extraordinary epizoötics it is
mainly the young that suffer, and it is only when a country has had no
general invasion for a length of time, or when the germ has acquired an
unusual pathogenic potency, or when these two conditions conjoin, that
the invasion of the equine population becomes universal, as it virtually
was in the United States and Canada in 1872–3. Under other circumstances
the germ, temporarily shorn of its power, lingers in city and dealers
stables, biding its time until circumstances become more favorable for a
new general outbreak.
Immunity largely explains the comparative mildness of the last cases in
any particular locality. The more susceptible animals are attacked first
and most severely, while the partially immune ones, which for a time
resist, throw off the disease with greater readiness. The explanation
has been sought in a lessening potency of the germ, but though this may
hold true of some cases, it manifestly does not apply when slight
lingering cases only are left in one locality, and the disease is
advancing over the neighboring state with all its original force and
vigor.
_Incubation._ This appears to vary within certain limits. When during an
epizoötic a sick horse is brought into a new locality and stable, other
cases usually develope in from one to three days. Trasbot gives examples
of one day, Salle, Cadeac and others of two, others claim four, seven
and even, exceptionally, fifteen days. One reason for an apparently
prolonged incubation may be found in the seclusion of the germs in the
alimentary canal, so that they escape only when passed with the fæces.
The pathogenic potency of individual germs, and the varying
susceptibility of the animals exposed must also be taken into account.
_Symptoms._ Equine influenza is liable to show a special predilection
for a given set of organs in different epizoötics, so that we find
descriptions of the different forms as independent types or even
separate diseases: as the _catarrhal form_, _thoracic form_, _abdominal
form_, _bilious form_, _nervous form_, _pink eye_, _infectious
cellulitis_, and _rheumatic influenza_. These forms may, however, appear
in different subjects in the same epizoötic, and when they are not due
to complications, may be looked on as a concentration of the morbid
processes on one class of organs rather than another.
_Initial pathognomonic symptoms._ Certain prominent and striking
symptoms are so constantly present in the earlier part of the disease
that they may be held as virtually diagnostic. These are the _suddenness
of attack_, the _anorexia_, the _profound early prostration and
weakness_, the _high temperature_, _the swelling and watering of the
eyes_, and the specially _brownish red coloration of the conjunctiva and
other visible mucosæ_. The attack may come on with almost lightning
rapidity. The animal which yesterday, or it may be but an hour or two
ago, appeared to be in the most vigorous health and spirits, is found
with pendant head, resting perhaps on the manger, ears drooping, eyelids
swollen and half closed, epiphora, conjunctiva of a brownish red or
violet, lips loose and drooping, and one or two legs partially flexed,
while the body is balanced on the others. The patient is indisposed to
move, and when compelled to walk may sway and stagger from nervous and
muscular weakness. The arched back, cracking limbs, and their stiff,
rigid movement further indicate the suffering in muscles or joints or
both. Appetite is greatly impaired or lost, thirst marked, and
hyperthermia 102° to 105° or upward. Sneezing, cough or symptoms of some
other special localization may be present, but the above occurring in a
number of horses at once, without appreciable climatic cause, when one
or two new horses have been very recently acquired, or when influenza
has been prevailing in the vicinity or in a neighboring place, will
usually stamp the nature of the attack.
Cadeac considers the sudden attack, high fever, and profound nervous
prostration and stupor as the manifestations of the uncomplicated
disease, while the localizations in the lungs, bronchia, pleura, liver,
bowels, etc., are indications of complications by germs of other
diseases, which find the debilitated influenza system especially open to
attack. The _fever_ which always sets in early may be little above the
normal in mild cases, and may reach 107° or 108° F. in the more severe
ones. It may last thus for five or six days and then rather suddenly
descend to near the normal. In other cases it descends a little daily,
the lowest temperature for the day being seen in the morning. Shivering
is often nonexistent or passes unperceived.
The _pulse_ does not usually encrease in ratio with the temperature. It
may be at first only 40 or 50 per minute, though later, and especially
with extensive disease of important organs, it may reach 60, 70, 80 or
even 100. It usually lacks in firmness and force, even when the heart
beats forcibly, being soft, somewhat compressible, and often irregular
in successive beats, the weakest corresponding to the last part of the
inspiratory act, or when the lungs are full and the heart compressed.
The _heart_ impulse behind the left elbow is usually forcible and may
show variation in rhythm or even intermissions.
Mild _catarrhal symptoms of the nose and throat_ are usually present,
the discharge being at first serous and later muco-purulent. As a rule
this is complicated with more or less bronchitis, but this does not
indicate anything serious. Acceleration of the breathing, sneezing, and
cough are present. Cough may be at first nervous, husky and paroxysmal,
but later as the discharge is established it assumes a looser, mucous
character. It is liable to be roused by excitement, by drinking cold
water, by inhalation of dust, or by giving medicine. In connection with
these symptoms there are some indications that the digestive organs are
involved. The pharyngeal and submaxillary glands may be swollen and
tender. If the subject has been seized just after a full meal, there may
be slight tympany, and in any case, the fæces are passed in small balls,
a few at a time, hard and with a baked or glistening surface. These may
have an unusually strong or heavy odor, and laxatives are liable to act
with dangerous energy. The urine is scanty and high colored, sometimes
icteric.
In such mild attacks, which constitute the majority, improvement may be
noted as early as the fourth day, and a prompt recovery follows.
With extensive _thoracic lesions_, the symptoms are much more severe and
the danger greatly enhanced. These may occur in any patient, but there
appears to be a special predisposition in the young and still very
susceptible animals, in those crowded together in close, badly aired
buildings, in the overworked, poorly fed or in any way debilitated
subject, and in horses that have been especially excited and exposed, as
by railway travel.
In exceptional cases _congestion of the lungs_ may be so acute as to
lead to speedy death, and the objective symptoms do not differ greatly
from those of ordinary cases of this condition, if we except the very
high temperature in influenza, associated as it is with the fact of the
epizoötic prevalence of the disease.
In _pneumonic_ cases the lesions are usually double and have a tendency
to develop toward the lower borders of the lungs, just behind the elbow
or farther back, and less frequently in the centre of the organ. It may
be impossible to detect crepitation, but sounds of distant organs (heart
beats, bronchial blowing, intestinal rumbling) are heard with unwonted
clearness over the consolidated parts. A mucous râle can usually be
detected behind the shoulder blade, along the line of the larger
bronchia. Percussion sounds may be indefinite, as the area of
consolidated lung is usually small in ratio with the hyperthermia. The
area of flatness in ordinary fibrinous pneumonia is usually much greater
with a high fever, and if the lesions are on one side only, right or
left, it is still more suggestive. The crepitation too in pneumonia is
significant. When the pulmonary lesions are extensive by reason of
œdema, a marked infiltration may often be noted on the lower surface of
the trunk or in the limbs as well.
_Pleuritic_ symptoms may show in the same connection. The breathing
becomes more hurried and shorter, friction sound may be heard but it is
very transient and soon superseded by an absolute flatness on
percussion, rising to a definite horizontal line, representing the
boundary of the effusion in the lower third or half of the chest, and
usually rising to the same height on both sides. Tenderness of the
intercostal spaces may or may not be present. As the disease advances
creaking sounds may be heard from the stretching of the consolidated
false membranes. The combination of double pleuro-pneumonia constitutes
a very fatal type of the disease.
The symptoms of _pericarditis_ and of cardiac disorder usually accompany
those of pleurisy. The tumultuous heart beats, often associated with
soft, weak or even rapid pulse, and later, a deadening or muffling of
heart sounds, as in hydropericardium are characteristic when present.
With _endocarditis_ the early tumultuous heart beats, with small weak
pulse, irregular and sometimes intermittent, become complicated by a
blowing or hissing murmur with the first heart-sound. In such cases
clots of blood are liable to form in connection with the valves, and may
cause sudden and early death. When the heart is involved the tendency to
extensive infiltration of limbs and lower aspect of the trunk is much
enhanced. (See _diagnosis_ for table of phenomena in influenza,
fibrinous pneumonia and contagious pneumonia respectively).
_Symptoms_ of digestive disorder are usually in evidence. Even in the
thoracic forms the mouth is dry, hot, and has an offensive odor; the
tongue coated above, has often red margins and tip; it may even be
yellowish; the gums may be swollen and dark red or violet especially
around the incisors; mastication may be slow and unwilling; the pharynx
maybe swollen; the pharyngeal and submaxillary lymph glands may be tumid
and tender; and swallowing may be difficult.
Congestions of the stomach and intestines are indicated by inappetence,
sometimes flatulence, passage of flatus, constipation with small, round,
mucous-coated balls passed in small numbers, and by slight transient
colics, pawing, looking at the flanks, and retraction of the abdomen.
The retention of bile and destruction of blood elements are indicated in
a deeper yellow of the conjunctiva and visible mucosæ, and in a yellow,
brown or red color of the urine. There may be tenderness of the abdomen,
but this, like the colics, is moderate, the senses being blunted by the
attendant stupor which is usually even greater than in the thoracic
forms. Urination may become frequent with straining, and the urine may
become turbid, opaque, with flocculi of cystic epithelium and mucus, and
even albumen. In from three to five days diarrhœa supervenes, the fæces
becoming soft, pulpy, watery, glairy or bloody, and escaping through a
permanently dilated sphincter. The diarrhœa may alternate with periods
of torpor or complete inactivity, otherwise tenesmus of the rectum is
marked. The exposed rectal mucosa is congested, of a deep red or it may
be of a dark violet hue. Eversion is not unknown.
In the worst cases death may ensue by the third or fourth day, but in
others the diarrhœa is critical and heralds an improvement which goes on
to a speedy recovery. In still other cases the bowel troubles continue,
the fever does not give way and the privation of food and rapid
metamorphosis of tissue produce steady emaciation and fatal marasmus.
A striking feature of the gastro-intestinal disease is the extraordinary
susceptibility to laxatives. So much is this the case that I have known
of two drachms of aloes proving fatal by superpurgation in a large,
mature Percheron horse. It is never safe to use laxatives in equine
influenza until one has ascertained whether in the special form of the
epizoötic in question the gastro-intestinal organs are or are not
especially involved.
_Disorders of the eye_ are so common or constant as to have procured for
certain epizoötics the name of _pink eye_. They set in suddenly, and
equally in both eyes, with infiltration of the lids and particularly of
the mucosa which is of a more or less deep red, and may bulge between
the margins of the eyelids, (chemosis). The flow of tears is profuse,
seropurulent matter accumulates at the canthi and in the lachrymal sacs,
vision is impaired and there is intolerance of light. The cornea becomes
bluish, cloudy or milky white, with a red zone around its margin and,
above all, on the adjacent sclerotic. In some cases the aqueous humor
becomes turbid or flocculent, and the iris changes its clear, healthy
dark lustre for a dull brown or yellow tint. The tension of the globe
may be materially encreased. They are readily distinguished from
recurrent ophthalmia by the attendant weakness, stupor and hyperthermia,
and by their non-recurrence in case the patient survives.
The _nervous symptoms_ are especially manifest in the sudden seizure,
great prostration, extreme weakness, profound stupor or lassitude, the
staggering gait, in bad cases, insensibility to voice, slap or, it may
be, even to the whip, the rigidity of the loins, their insensibility to
pinching, the difficulty of turning in a short circle, or of backing.
The high fever, disproportionate to the appreciable local lesions, and
its sudden improvement at the critical period, the excessive weariness
and the disposition to lie down contrary to the habit of other
inflammatory chest diseases are further indications.
This may go on to coma, there may be more or less complete anorexia,
muscular trembling, paresis, especially of the hind limbs, or delirious
manifestations indicating meningitis.
_Rheumatoid attacks of the muscles and joints_ usually appear in the
advanced stages of the disease, but may appear earlier. They may occur
in any latitude but seem to be especially common in cold, damp,
inclement northern regions, and at seasons when climatic vicissitudes
are sudden and extreme. These may appear suddenly and disappear with
equal rapidity, or they may last for a time during and even after an
apparent recovery in other respects. When the joints are involved they
usually become engorged with exudates in the synovial membranes.
_Lameness_ in either _fore_ or _hind limb_ may assume an _intermittent
type_ developed by exercise and subsiding with rest, evidently
bespeaking local arterial embolism, and in such cases it is likely to
persist for months.
A tendency to _transudations_ and _dropsical effusions_ is common in
severe cases, showing especially in the filling of the legs, but in
certain epizoötics, these become strikingly prevalent and have secured
for such a special name (_epizoötic cellulitis_). Apart from the limbs
these affect particularly the inferior surface of the chest and abdomen.
The swellings are not necessarily hot nor painful nor petechiated as in
petechial fever, yet they may merge into that affection or they may
become phlegmonous and develop abscess.
_Complications_ of many kinds are to be looked for, pregnant mares may
_abort_; _laminitis_ may set in; the microbes of _strangles_,
_contagious pneumonia_, _cerebro-spinal meningitis_, _septicæmia_,
_pyæmia_, etc., may take occasion to attack the debilitated system, and
thus complex diseases and manifestations are developed.
_Morbid Anatomy._ The lesions may predominate in different organs in
different subjects and successive epizoötics. It is a protean disease
and may expend its main energy on any one of a number of different
organs or systems of organs.
In the slighter cases the lesions are often largely confined to the
anterior part of the respiratory organs. The _fauces_, _pharynx_,
_larynx_, _guttural pouches_ and _nasal mucosa_ are tumified, congested,
red and covered with mucous, and this condition may extend down to the
bronchia. In such cases the _blood_ is normal or may coagulate with
undue readiness and firmness. The pharyngeal and intermaxillary lymph
glands are red and congested in their outer zone.
In the more severe cases the _alterations in the blood_ are perhaps the
most constant of the morbid features. The blood is fluid and
incoagulable, or the clot is soft, diffluent and black, the red globules
are crenated or broken up, and show little tendency to adhere in
rouleaux. The escaped hæmatoidin accumulates in masses in the serum in
crystalline forms, giving it a high staining power when a line is drawn
with it on white paper. Fatty globules also float in the mass. The
leucocytes are relatively very much encreased and the red globules
diminished. Dieckerhoff found 30,000 and Trasbot 40,000 leucocytes in a
cubic millimetre.
The diffluence is not constant. Blood drawn in the earlier stages of the
disease, coagulates with extraordinary firmness, influenced, doubtless,
by the encrease of the leucocytes, the disintegration of the blood
globules, and the liberation of globulins. This serves also to partially
explain the early and sudden deaths from coagula in the heart and large
vessels, which are occasionally met with. Such clots in the heart are
often found adherent to the valvular or ventricular endocardium which at
such points shows cloudy swelling, thickening, cell proliferation and
even encreased vascularity and granular elevations.
In advanced cases, however, the prominent features are usually acidity,
blackness, and incoagulability of the blood, its resistance to oxygen,
altered and broken down red globules, free coloring matter, relative
encrease of white cells, and, if necropsy has been delayed, the
abundance of septic microbes (cocci and bacilli). Petechiæ are abundant
on the serosæ especially on the pericardium.
_Lesions of the alimentary mucosa_ are very constant. There may be
stomatitis, with tumid follicles and even ulcers (Kowalavsky). In the
_stomach_ the _right sac_ has its mucosa thickened, softened, red,
congested, petechiated and discolored. The summits of the folds may be
ulcerated (Labat). Similar lesions are presented in the _small
intestines_. The agminated glands may show many rounded elevations, with
or without open discharging follicles. The mucosa is covered with a
muco-purulent material. Otherwise, the small intestines, like the
stomach, are usually empty. The _large intestines_ present similar
lesions, the nodular elevations often representing the solitary glands,
and the masses of ingesta are likely to be dry and indurated, in the
earlier stages or semiliquid in old standing cases. The _peritoneum_ may
be congested, petechiated and at points infiltrated and usually contains
a reddish serum in variable quantity. The _mesenteric glands_ are more
or less enlarged and congested.
The _liver_ shows more or less congestion as in other infectious
diseases localized in the bowels. It usually has a parboiled appearance,
and yellowish gray areas of necrosis may be manifest, or again, fatty
degeneration may be present. Petechiæ, and even small blood clots may be
found on or beneath the capsule. The _pancreas_, and, still more, the
_spleen_ may be the seat of congestion or engorgement but this is far
from constant.
The capsule of the _kidney_ may be petechiated or elevated at points by
serous exudate or extravasation. The surface of the organ and of
sections show a mottling with darker and lighter areas, and petechiæ and
patches of congestion may be found on the bladder and urethra.
The _nervous centres_ exceptionally show meningeal congestions, and
exudations, and petechiæ as has been noted of other serosæ.
Lesions of the _eye_ may be confined to the mucosa, or they may extend
to the membrane of the aqueous humor, the iris, or even the deeper
structures.
Other lesions such as _laminitis_, _bursitis_, _arthritis_, like those
attendant on _abortion_ need no special description.
When _pulmonary lesions_ are extensive, the bronchial mucosa is not only
softened, opaque and covered with a serous, or muco-purulent discharge,
but deeply congested and petechiated. When the chest is opened there is
usually an effusion, pale straw, red or bloody and more abundant than in
contagious pneumonia. False membranes may exist and show a blackish tint
from extravasated blood. The lung fails to collapse and shows on the
surface and throughout its substance petechiæ and small black
infarctions. In some instances the whole lung is blood gorged, black,
almost jelly like, as in acute congestion. In others these are limited
infiltrations, concentrated especially in the anterior and lower parts,
and almost invariably affecting both right and left lungs. The
infiltration is circumscribed in area in comparison with the attendant
fever and constitutional disturbance, resembling in this respect, the
lesions of contagious pneumonia. It differs however in having a greater
tendency to liquid infiltration of the connective tissue, and but for
the lack of such tissues in the horse’s lung it would tend to
approximate to the lesions of lung plague in cattle. It shows a distinct
thickening of the interlobular septa, a tendency to extension to the
pleura, and to issue in pleural and subpleural infiltration, and to a
more copious effusion into the pleural cavity than in either fibrinous
or contagious pneumonia. The lung tissue may be granular and hepatized,
but far more frequently it is only splenized, the lung being the seat of
a bloody infiltration, yet retaining much of its elasticity and
coherence. Portions may be infarcted and black and large areas may have
a pale or parboiled appearance, and gangrene is by no means uncommon.
_Diagnosis._ This is based largely on the suddenness of the attack, its
epizoötic character, the numbers attacked in rapid succession, and over
a large area as contrasted with contagious pneumonia, the sudden and
extreme prostration and weakness, the swelling, watering and
discoloration of the eyes, the mildness of the average case, the
congestion of the upper air passages, and in the mild cases a
comparative immunity of the lungs, the irritability or congestion of the
gastro-intestinal mucosa, and the history of the case:—the arrival of
the infected horses within a few days from an infected place, or coming
through infected channels, or the attack of new arrivals in a previously
infected stable, or the known advance of the disease towards the place
where the patients are, will usually serve to mark the true nature of
the affection.
As a help to correct diagnosis we give below some of the prominent
conditions and phenomena of the three forms of lung disease known as
_fibrinous pneumonia_, _contagious pneumonia_, and the _pneumonia of
equine influenza_:
=Pneumonia=: =Pneumonia=: =Pneumonia=:
_Croupous Fibrinous._ _Contagious, of Equine _of Equine Influenza_.
Animals._
From climatic Slow succession of Rapid succession of
vicissitude, cases in the same cases in the same
exposure, etc. stable, irrespective stable or locality,
Attacks exposed of climate or irrespective of
animals only, and all exposure climate or exposure
at once
Prevails in inclement Any season: worse in Any season: worse in
seasons, spring, inclement season inclement season
autumn, (Winter)
Infection from close Infection spreads
proximity, contact, widely and rapidly
stall, manger, rack, through the air.
bucket, trough, etc.: Spread rapid and
Spread slow often general
Carried in manure, on Carried in manure, on
harness, wagons, harness, wagons,
clothes, etc. clothes, etc.