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complicated with lymphadenitis: hence the grouping of these different morbid conditions under the heading of lymphogenic diathesis.
Investigations have now thrown more light on the subject because of the more perfect recognition of the varieties of white blood corpuscles, and the above-mentioned morbid conditions may be defined as follows:—
(1.) The first variety consists of a more or less marked adenitis or lymphadenitis without leucæmia (aleucæmic lymphadenitis).
(2.) The second variety, consisting of leucæmic lymphadenitis, or leucocythæmia, is a lymphatic lucæmia or lympho-cythæmia, the anatomical characteristic of which is enlargement of lymphatic glands, and the histological characteristic increase in number of the large and small lymphocytes.
(3.) A third variety, formerly regarded as simple leucæmia without lymphadenitis, is myelogenic leucæmia or myelo-cythæmia, the anatomico-pathological characteristic of which is to be found in myeloid hypertrophy of the bone marrow, giving to the bone marrow on post-mortem examination a puriform appearance, and in the myeloid condition of the spleen.
Histologically this variety is characterised by an absolute increase in numbers of the large mono- and poly-nuclear eosinophile leucocytes.
Symptoms. Simple lymphadenitis begins in an insidious manner, and is characterised by weakness, anæmia, paleness of the mucous membranes, and wasting without apparent reason, although the appetite is preserved. It is only at a later stage that the glandular enlargements are discovered (adenitis), and often this discovery is not made until the veterinary surgeon is called in.
The existence of the disease is indicated by enlargement of the superficial glands, and this enlargement, which may commence at any point, extends along the course of the lymphatic vessels to the neighbouring glands, until in a shorter or longer time it involves all the lymphatic glands in the body.
The enlargement of the glands is usually symmetrical, and on clinical examination it is sometimes easy to detect at the outset an
increase in size of the retro-pharyngeal glands, the glands of the neck, the prescapular glands, the glands of the flank, etc.
Rectal exploration reveals hypertrophy of the glands of the pelvis and of the sublumbar region, etc. The animals waste very rapidly, and sometimes in a few months become incapable of standing. They develop cachexia, and die in a state of exhaustion, with no other lesions than those of lymphatic hypertrophy. Neither do they exhibit any marked increase in the number of white corpuscles in the blood.
In lympho-cythæmia the beginning of the disease is often identical with that of simple lymphadenitis, the increase in the number of white blood corpuscles not occurring until later. In other cases, on the contrary, leucæmia appears first, and the enlargement of the lymphatic gland follows; but what characterises this form and allows of it being distinguished from myelo-cythæmia is the great increase in the number of large or small lymphocytes. The development is identical with, and sometimes much more rapid than, that of the preceding form. The animals waste away and become anæmic and cachectic, dying at last in a state of absolute exhaustion.
Post-mortem examination reveals, as in the previous condition, symmetrical hypertrophy of all the lymphatic glands; the spleen is very often enormous, and the liver is sometimes affected, as are also, in exceptional cases, the kidneys.
It may happen that the spleen alone appears affected, or at least that it has been first attacked, a fact which explains the existence of leucæmia before any enlargement of the lymphatic glands.
Causation. The causes of lymphadenitis and of lympho-cythæmia are unknown in veterinary as in human medicine. Apparently these diseases are more common in adults than in young animals. Some regard them as infectious in character, but this can hardly be the case, as all experimental attempts to transmit the diseases have failed. It is more plausible to compare the development of these morbid conditions with that of malignant tumours, and although some doubt still exists, simple lymphadenitis may be described as an aleucæmic lymphoma or lympho-cytoma, which has gradually become generalised, spreading by way of the lymphatic channels from the gland first affected through the surrounding glandular system. Lympho-cythæmia, on the other hand, may be said to be a leucæmic lympho-cytoma, which spreads both by the blood
circulation and by the lymphatic paths (spleen, hæmatopoietic glands and organs).
This view of the development of the lesions enables us to class lympho-sarcomata with lymphomata and lympho-cytomata. The malignant character and extremely rapid development of lymphosarcomata appear due to its extending by contiguity of tissue, and simultaneously by the lymphatic paths.
This new grouping would consequently place on one side myelogenic leucæmia, also called myelo-cythæmia, which is perhaps a different morbid species. This would destroy the unity implied in Jaccoud’s theory of the lymphogenic diathesis; but for all that this method of grouping might be justified by reference to specific cellular characteristics. In myelo-cythæmia the disease appears to commence as a lympho-cythæmia, i.e., it is unaccompanied by enlargement of lymphatic glands or hypertrophy of the spleen or liver, though the blood appears leucæmic. The condition is not a leucæmia due to lymphocytes, but rather a leucæmia produced by mono- and poly-nuclear eosinophile leucocytes, i.e., leucocytes derived from the bone marrow.
The patients are carried off rapidly after persistent wasting, decline and cachexia, whilst on post-mortem examination the puriform aspect of the bone marrow is an extremely striking characteristic.
Diagnosis. There is rarely much difficulty as regards the diagnosis. The enlargement of the lymphatic glands, for instance, can readily be detected, and the only disease with which this can possibly be confounded is tubercular enlargement.
With the means at present available for diagnosing tuberculosis, such as microscopic examination of the discharge, inoculation with discharge, examination of material from the glands, injection of tuberculin, etc., the nature of the disease can always be placed beyond doubt.
In lympho-cythæmia and in myelo-cythæmia, the whitish-violet lactescent appearance of the blood is of unmistakable significance, particularly when the manifest progressive wasting of the whole system is taken into account.
Histological examination of the blood after fixation and staining will in the former cases reveal the presence of very large numbers of lymphocytes, and in the latter an absolute increase in the number of the mono- and poly-nuclear lymphocytes. It should be easy, therefore, to distinguish the two diseases, especially as other symptoms vary.
In the early stages leucæmia may be mistaken for the leucocytosis seen in infectious diseases. These forms of leucocytosis are very common in animals of the bovine species. They occur in certain forms of tuberculosis, in uterine infections, in cases of internal suppuration, in tumour of the heart, the rumen, etc., and vary in so far as one style or another of white blood corpuscle predominates. The diagnosis, therefore, necessitates that the white blood corpuscles should be counted, and whenever it is found that their variations in number are no more than between 5,000 and 15,000 per cubic millimètre, the case may be regarded as one of temporary leucocytosis.
If, on the other hand, those corpuscles number more than from 15,000 to 20,000, or, as may sometimes happen, they attain to from 200,000 to 300,000 per cubic millimètre (one white to two or three red blood corpuscles), the case is one of leucæmia, and, according to the predominance of the particular type of cell, it is a lymphocythæmia or a myelo-cythæmia.
In leucæmic conditions the red blood corpuscles are also present in fewer than the normal numbers. They are more irregular, assume giant and dwarf forms (macrocytes and microcytes), sometimes exhibit lacunæ, and are always polychromatophile, i.e., without special affinity for any particular constituent of double or triple stains.
Prognosis. The prognosis of diseases included in the lymphogenic diathesis is extremely grave, and in the present state of our knowledge it may be assumed that sooner or later death is inevitable.
Treatment. Treatment can scarcely be considered to exist, for at the best it can only delay the development of the disease. Nevertheless, and with this reservation, it is certain that preparations of iron, iodine and arsenic have a certain effect, probably by acting on the hæmatopoiesis.
CASEOUS LYMPHADENITIS OF THE SHEEP.
In the sheep the lymphatic glands are sometimes the seat of peculiar changes, which do not appear to have any marked effect on the general condition. Thus a post-mortem examination or an examination of animals in the slaughter-house sometimes shows a certain number of isolated or symmetrical glands, such as the mediastinal, tracheal, inguinal, pelvic or sublumbar glands, to be greatly enlarged and completely degenerated. The precrural, prescapular, and popliteal glands are said to be most frequently affected. Their contents are caseous and yellowish, enveloped in a fibrous sheath, and show no signs of peripheral inflammation. The other organs and viscera may either be healthy or exhibit caseous lesions identical with those found in caseous broncho-pneumonia.
The causes of this disease are imperfectly understood, although Cherry and Bull (1899, the Veterinarian, Vol. LXXII., No. 860, p. 523) have isolated from the lesions an organism identical with Preisz’s bacillus and with the microbe of ulcerative lymphangitis in the horse.
Norgaard and Mohler (Annual Report, United States Bureau of Agriculture, 1899, p. 638) have studied the disease. In June, 1897, Turski, at Danzig, found about 150 breeding ewes, from eight to twelve years old, suffering from nodules or abscesses the size of a child’s fist in the inguinal and prescapular regions. They had been sold for slaughter, and many were in very poor condition. The disease occurs in Europe, Western America, South America, and Australia. Several thousand cases are annually seen in the slaughterhouses of the United States.
The symptoms generally escape notice, and it is only by accident that one sometimes detects marked enlargement of the lymphatic glands of the neck or of the superficial inguinal glands. The patients, moreover, may remain in very good bodily condition, so that the lesions are only discovered on the meat being inspected.
Having regard to our imperfect knowledge of this disease, it is impossible to express an opinion as to its importance or treatment.
GOITRE IN CALVES AND LAMBS.
Although not strictly relevant to the foregoing matter, a few remarks may here be made on the subject of goitre.
True goitre consists in hyperplasia of the follicles of the thyroid gland, with colloid change of their contents, which are chiefly albuminous. The swelling is mainly due to enlargement of the follicles, and is termed struma follicularis. It may attack the entire organ or only one-half; less frequently it is confined to certain sections. Other varieties of goitre are recognised, such as fibrous, varicose and cystic goitre. (For fuller details see Möller and Dollar’s “Regional Surgery,” p. 149.)
Treatment by injection of thyroid juice or by feeding on thyroid extract has given better results than drugs.
The following account of an outbreak in New Zealand is summarised from the Annual Report of the Chief Veterinarian of New Zealand, 1901:—
The calves affected were born with enlarged thyroids. The farm is of rich alluvial deposit, and rather below the level of the river, which
F . 213. Calf showing swelling due to goitre.
it borders. The land has been in occupation, however, for many years, and no similar condition had been previously noted. At first, as calves only were affected, it was thought possibly to be due to the bull, a two-year-old animal, but when a foal was born suffering from a similar malformation this theory naturally fell to the ground.
The land had been ploughed with a special plough 20 inches deep, but this is no uncommon practice in the island.
About the same time, a similar disease was discovered affecting lambs at a farm near Outram. From 450 ewes, 150 lambs had been lost, the glands being enlarged to the size of a cricket ball. A few had been born dead, many only lived a few hours, others lived several days, and a considerable number recovered. There was no connection, directly or indirectly, between the two farms, they being at least fifty miles apart. A few of the calves died or were killed, the remainder recovered, and the foal grew rapidly better. The land on both farms is very similar in composition.
Mr. Wilkie states, from observation of previous cases in lambs, that “it appears to be always associated with malnutrition and a condition of anæmia in the parent, induced in most cases by feeding with watery, innutritious foods.”
Specimens were forwarded, from a calf and from a lamb, of enlarged glands. The gland of the calf was enormously enlarged, being at least twice the size of an orange, dark in colour, flabby in consistency, and on section a mucous material exuded copiously from the cut surface. Micro-examination showed the acini to be larger than normal, filled with the usual mucous material, and lined with cubical epithelium. The connective tissue surrounding the alveoli was, however, crowded with round-cells, so much so that the whole parenchyma seemed to be practically composed of these cells.
A specimen of an enlarged thyroid from the lamb was about the size of a sheep’s kidney, and very much the same shape and colour. Sections microscopically examined showed a different condition to that of the calf’s thyroid. Here the acini were filled with epithelial cells loosely arranged as if the lining epithelium had been proliferating rapidly, while the connective tissue surrounding the acini was fairly normal. The section had a somewhat adenomatous appearance.
SECTION V. NERVOUS SYSTEM.
CEREBRAL CONGESTION.
According to Cruzel, cerebral congestion is somewhat frequent in working oxen subject to continued concussion from the yoke, especially among animals working on a rocky soil. The condition may also be produced by prolonged exposure to the sun, as well as by sudden and intense cold.
Passive cerebral congestion by stasis may be produced by any cause markedly interfering with the return circulation (pericarditis due to foreign bodies). Clinically it is of no importance.
The animals, previously in good health, suddenly appear comatose. They are insensible to stimulation of any kind, the head is rested on any convenient object or is held stationary, the animal looks drowsy, the gait is hesitating or vacillating, the respiration slow or irregular. Left at liberty, the animal does not seem to know where it is going; indeed, sometimes it is absolutely blind and strikes against any obstacle in its path, or falls and suffers from epileptiform convulsions. The cranial region is abnormally warm. The course of the attack is rapid, and the animal either dies in a state of coma or convulsions or else recovers rapidly.
Diagnosis. The diagnosis is decidedly difficult; and the prognosis should be reserved.
Treatment commences with free bleeding, the amount of blood drawn being proportioned to the animal’s size. The sides of the body may then be stimulated and a purgative administered.
MENINGITIS.
The generic term “meningitis” includes all inflammations of the arachnoid, pia mater and internal surface of the dura mater.
These forms of inflammation occur in diseases such as tuberculosis and in parasitic diseases of the brain. Under other circumstances, they are rare, and may be produced by very varying causes.
An epizootic cerebro-spinal meningitis of the bovine species has also been described, principally in Germany. It seems almost unknown in France, and French literature contains no wellauthenticated case.
Furthermore, an epizootic cerebro-spinal meningitis of sheep, or rather of lambs, has been described in Germany, in Italy, and in France. These descriptions are all open to many objections. It seems that under the term “cerebro-spinal meningitis” have been grouped cases of enzootic tetanus, doubtful cases of poisoning, and particularly cases of cœnurosis in the first stage of development. We therefore discard these descriptions, which differ too much among themselves to be of any value.
Causation. Meningitis occurs in the ox and sheep as a complication of wounds in the cranial region, accompanied by fissuring of the bone, periostitis, abscess formation, etc.
It is also seen as a complication of fractures of the horns, and oldstanding catarrh of the facial sinuses. In the sheep it follows parasitic catarrh due to the larvæ of œstridæ.
The meningitis appears, according to circumstances, in the forms of local meningitis, anterior frontal meningitis, basilar meningitis, etc. Finally, it may develop as a complication of different diseases, such as gangrenous coryza, purulent infection, subparotid abscess, suppurative phlebitis, suppuration of the eye or of the orbit, etc.
Symptoms. It is difficult to detect and interpret the first symptoms shown, because these chiefly consist in dulness, want of appetite and constipation, without any particular fever. At a later
stage, excessive excitability is produced by noises, by changes of light, or by handling. Careful examination of the patients shows a change in their expression, rapidly followed by contraction and inequality of the pupils or deviation of the visual axis (strabismus, squinting). The pulse becomes irregular, as also the respiration. The appetite is entirely lost, and it is not uncommon to note a contraction of the muscles of the neck and jaws, as well as inability to move about and symptoms similar to those of dropsy of the cerebral ventricles.
The chronic form is rare.
Lesions. The lesions comprise local or general hyperæmia and exudative inflammation of the pia mater and arachnoid, together with the formation of false membranes or of pus in the subdural space. The meninges are partially adherent, and the superficial layers of the brain are also inflamed by contiguity of tissue.
Diagnosis. The diagnosis must be based on the disturbance of vision, movement, and appetite, and on the course of the symptoms, as well as on the external signs in the case of such diseases as are prone to become complicated with meningitis.
Prognosis. Sooner or later the case is likely to end fatally, and there is no practical use in treating the patient.
Treatment. If in exceptional cases slaughter is objected to, setons and blisters may be applied to the poll or the parotid region, or the parts may be enveloped in ice bags or compresses of iced water frequently renewed.
ENCEPHALITIS.
Encephalitis, i.e., inflammation of the cerebral substance, is very closely allied to meningitis; in a great number of cases meningitis and encephalitis co-exist. In other cases encephalitis may be found apart from meningitis, and vice versâ. Moreover, many of the symptoms of meningitis are to be found in cases of encephalitis.
Encephalitis may develop as a complication of meningitis. Encephalitis may also follow abundant parasitic infestation, as in cœnurosis (which will be particularly studied as it affects sheep), or microbic infection, the commonest form of which in the ox is tuberculosis. The encephalitis may be diffuse or circumscribed, according to the cause, while the symptoms are varied and numerous. Very frequently, particularly in cases of tuberculosis, encephalitis assumes a chronic form.
Symptoms. The earliest symptoms are extremely difficult to detect, because they are scarcely characteristic and because it is impossible to ascertain the sensations of the animal.
It is only when the disturbances in walking, in the eyesight, in swallowing, etc., are noted that suspicion is aroused.
The symptoms may appear suddenly. Nevertheless it is beyond doubt that there are certain slightly marked prodromata, indicated by diminution of appetite, wasting, and changes in vision. Soon afterwards occur other forms of disturbance, which may be classified under the heading of “motor, visual, nervous, and impulsive.” The patients appear stunned, their movements are slow and hesitating, they partially lose control over their limbs and display lameness, with spasmodic movements of one or two limbs. Examination of the joints shows no injury. The lameness may simultaneously affect two diagonal limbs or two fore and two hind limbs, or even three limbs. This lameness is of central origin.
The ocular disturbance is marked by diminution or loss of vision, by strabismus, or by frequent unconscious movements of the eyes and eyelids, and also more particularly by inequality, contraction or dilatation of the pupils.
Nervous, impulsive disturbance is most readily noted when the animals are at liberty. Even when the sight remains, they seem quite incapable of avoiding obstacles or as though absolutely forced to move to the right or left, etc.
Attacks of giddiness, moreover, are not unusual under the influence of the slightest excitement. During such attacks the animals thrust the head against a wall, or they involuntarily recoil or make lateral movements. In many cases these vertiginous attacks end by the animal falling and showing epileptiform convulsions, during which it may die.
The symptoms are never the same in two different animals, but they may easily be classed according to the above indications. The indications furnished by the condition of the eyes and by the peculiar impulsive movements are particularly significant.
On the other hand, there are modifications in breathing without apparent local cause, and difficulty or even impossibility of swallowing, etc., although there exists no material obstacle.
Diagnosis. The condition is often confused with meningitis, and the mistake is not serious, because meningitis and encephalitis frequently accompany one another.
Prognosis. The prognosis must be regarded as fatal. The patients very seldom recover, and there is no reason for keeping them alive.
Treatment. Here, again, blisters may be applied to the upper extremity of the neck, or setons may be passed. Cooling applications to the cranial region have also been suggested. None of these methods produces more than a temporary palliative effect.
CEREBRAL TUMOURS.
The brain may be injured and compressed by various tumours of other than parasitic origin. Such tumours may originate in the bones, the meninges or the choroid plexus, or they may simply be due to generalisation of a previously existing tumour. Whilst of very varied origin and nature, all tumours of the cranial cavity have one common effect, viz., to compress the brain. This continuous compression causes progressive atrophy of the brain, but its existence is not always suspected, because the lesions may not give rise to any marked symptoms.
The hind portions of the hemispheres and the white substance are generally very tolerant. The front portions, on the other hand—the frontal lobes and the grey substance—resent compression, which provokes various symptoms in consequence.
The symptoms of compression and atrophy of the brain differ greatly, a fact which is easily understood, inasmuch as the seat of the change may vary, and therefore it is possible only to trace the chief manifestations, which suggest the existence of a cerebral tumour.
The general changes are indicated by signs precisely similar to those so common in horses with dropsy of the ventricles (general depression, inability to back, long intervals between the prehension of successive mouthfuls of food, sudden cessation of mastication, etc.), by an impulsive or automatic gait, and by the assumption of strange attitudes (kneeling down in front, etc.). When at rest the animals appear to be in a state of continual torpor.
Special symptoms sometimes occur, which enable the seat of the injury to be localised in more or less exact fashion. These symptoms affect the vision (amblyopia, amaurosis, strabismus, nystagmus), general sensibility (hyperæsthesia, anæsthesia, etc.), and the power of movement (total, partial or crossed hemiplegia, want of coordination of movements, etc.).
Trifling stimuli almost always lead to marked and even epileptiform attacks.
The diagnosis of cerebral tumours is very difficult, particularly when attempts are made to indicate their exact seat, but that of other cerebral lesions is somewhat easier.
The prognosis is very grave, and in the case of domestic animals nothing can be done. In the ox intra-cranial operations are difficult, by reason of the presence of the sinuses which obstruct the approach to the brain cavity; economically surgical treatment is seldom advisable.
INSOLATION.
Insolation is an exceptional accident in animals of the bovine, ovine, or porcine species. If at liberty these animals move about, and always seek shelter when the sun is fierce. If, on the contrary, they are harnessed and kept standing for long, exposed to the full midday sun during June, July or August, they may suffer from insolation.
During the International Cattle Show attached to the Exhibition of 1900 in Paris, a considerable number of cases of insolation occurred in animals of one class, exposed to the full midday sun, in an illventilated spot. The other classes only received sunlight from the sides, and in them not a single case occurred.
Death may follow in a few hours; it is difficult to say precisely how it is brought about, but it is always accompanied by congestion of the cerebro-spinal centres and general blood stasis.
The symptoms of the development of insolation occur very rapidly. In animals of the bovine species there is accelerated respiration, which soon amounts to dyspnœa. The mucous membranes then become cyanotic. The animals attacked seem anxious, although not agitated, and soon afterwards the eyes water, the mucous membrane and the lips of the vulva display œdematus infiltration and congestion, and areas of cutaneous congestion, closely resembling mud fever in the horse, appear over the mammæ. At this stage the animals move with difficulty, and show all the symptoms seen at the outset of gangrenous coryza.
All these symptoms develop in one, two, or three hours, and death may follow if nothing is done. They disappear, however, as rapidly as they appear. In an hour or less we have seen in some cases a complete return to the normal condition. Given the facts, the diagnosis is extremely easy.
Treatment. Treatment should be commenced by immediately removing the animal to a cool, airy, shady place. It may then be bled, and the head and neck should be freely drenched with cold water. The symptoms generally disappear as though by magic.
For a great part of the following short account we are indebted to an excellent report by J. J. Repp, V.M.D., in the Journal of Comp. Medicine and Veterinary Archives, September, 1901:—
The word “fever” in connection with the terminology of this disease is not very appropriate, because in the majority of cases fever is not present, but the animal has a subnormal temperature. The term milk fever is very misleading and indefinite, as it is also used by the laity to designate other diseases, such as parturient septicæmia and the various forms of mammitis. Parturient paralysis must be clearly differentiated from parturient septicæmia, which is a disease of an entirely different character and which may occur in any of the domestic species, whereas parturient paralysis occurs only in the cow.
Distribution. Parturient paralysis occurs wherever milch cows are kept. It is more prevalent in dairy districts, because it is the heavy milking strains of cows that are most subject to the disease.
Cause. No definite cause can be assigned for this disease. Schmidt’s theory is that parturient paralysis is caused by the evolution in the mammary gland of a poisonous substance through the over-activity of the epithelial cells of this gland excited by the determination to the udder after birth of large quantities of blood which was supplied to the uterus and the fœtus before birth, but which now goes to the udder because of the natural demand for milk secretion. This poisonous substance being carried in the circulation to various parts of the body, brings on the symptoms which characterise the disease. It is well recognised that living cells may, under certain circumstances, produce poisonous substances. Schmidt’s theory, therefore, is in accord with an established principle.
Pathogenesis, or generation, of the disease. Parturient paralysis, as a rule, occurs in cows which give a heavy flow of milk and which are in a high state of nutrition. It may develop at any age, but is extremely rare in cows before they have reached adult age and have given birth to several calves. It is also rare in old cows. It occurs, then, in cows which are of middle age and in the full height of their activity as milk producers. The disease attacks the cow after she has given birth to a calf, usually within twenty-four hours thereafter, but in some cases not until a week or even a month after parturition. In a few cases the disease has its inception a short time before parturition. Cows which are stabled and deprived of exercise are said to be more prone to the disease than those which are permitted to exercise at will. There are many exceptions to this statement, although it is the usual teaching. Further observation may show that it is not correct. In Iowa more cows take this disease while at pasture than in any other circumstance. This doubtless arises from the fact that in Iowa cows are given more freedom than is customary in older dairy States. The disease may arise at any time in the year, but, on account of the fact that spring-time is pre-eminently the calving season, most cases originate at this season.
Morbid anatomy. The morbid alterations are limited and variable, and offer nothing characteristic. The blood is irregularly distributed, a condition which probably indicates marked vasomotor disturbance resulting from the profound interference with the nervous functions which accompanies the disease. The abdominal organs are usually filled with blood. The brain may be anæmic, œdematous, easily torn, and yellowish in colour. In other cases it shows hyperæmia of the meninges and of the brain substance.
Symptoms. The disease usually appears within twenty-four to forty-eight hours after parturition. In extreme cases it may not occur until two months or even six months after parturition. It may rarely occur before birth. It usually follows an easy birth. At the onset of the disease the cow manifests some uneasiness; it moves about in a restless manner, stamps, strikes the abdomen with its hind legs, perhaps bellows, grinds the teeth, and may have spasms of groups of muscles or even a general convulsion. After this period, which may be unnoticed, the symptoms of paralysis come on. The cow shows weakness, staggers, and at last falls. As the paralysis advances it
stretches on the ground, lying on its side usually with the neck bent to one side so as to bring the nose into the flank or the costal region. This is the characteristic position in parturient paralysis. If the head is brought into the normal position, it at once returns to the unnatural position in which it was found. The animal is in a state of partial or complete unconsciousness, does not respond to blows or calls, and takes no note of its surroundings. The eye is dull and not sensitive to the finger touch, sunken, pupil dilated, and the upper lid is drooping; the tongue is paralysed, saliva runs from the mouth, the pharynx and œsophagus have lost the power of motion, so that the animal is unable to swallow; the peristalsis of the stomachs and intestines is in abeyance, and as a result digestion is arrested, fermentation sets in, and the animal becomes tympanitic; the contents of the rectum and colon are hard and dry, and may be covered with mucus or blood, urination is suspended; the os uteri is almost invariably dilated if the disease occurs within a day of parturition; pulse small, often imperceptible, 60 to 120 per minute; temperature, usually normal or below normal, may be as low as 95° Fahr., in some cases may be as high as 105° Fahr. Such a high temperature probably does not occur in a case of pure parturient paralysis, but only when there is a complication of parturient septicæmia. The extremities are cold. The after-birth is sometimes retained. There may be accompanying prolapse of the uterus.
Course. Without treatment, and, indeed, with most kinds of treatment which have been applied in the past, the disease usually runs rapidly to a fatal issue. It lasts two to three days, and in some cases longer, the condition gradually becoming more and more aggravated. Death results from sudden failure of the heart or brain, and is often preceded by profuse diarrhœa. In milder cases the cow may linger as long as two to four weeks and then die of pneumonia, which results from the inhalation, or introduction through attempts at medication, of foreign substances into the lungs during the period of paralysis of the pharynx and œsophagus. If recovery occurs, the animal is entirely well in two to five days. In rare cases paralysis of the hind parts may persist for a long while.
Diagnosis. This is made by a study of the history and symptoms. It is comparatively easy.
Differential diagnosis. It must be distinguished from antepartum paralysis, broken-back, parturient septicæmia; but one familiar with the character of these diseases will find no difficulty in making this differentiation.
Treatment. This may be considered under two distinct subdivisions, viz., preventive treatment and curative treatment.
(a) Preventive treatment.—By considering what has been said under the head of “generation of the disease,” one can easily infer what measures should be adopted to prevent the disease. Cows in the later stage of gestation should be fed moderately, grain especially being given sparingly or entirely withheld; the animals should be given an opportunity to take plenty of exercise; the bowels should be kept in good condition by the administration of such salines as magnesium sulphate, sodium chloride, and sodium bicarbonate. The after-birth should be removed soon after parturition and several uterine douches administered.
(b) Curative treatment.—The older methods of treatment comprised: warmth and friction to the mammary gland; the administration of sedatives, such as opium, chloral and bromide of potassium; stimulants, including ammonia, ether, turpentine and alcohol; washing out the uterus with water or disinfectant solutions; the relief of tympany by the use of the trocar and canula (by which instrument medicines may also be injected directly into the rumen); the removal of fæces from the rectum; warm clothing of the body and general attention to the animal’s comfort, and to the teachings of hygiene. For all these widely diversified methods good results have been claimed, and, we may add, bad ones at times recorded. F. T. Harvey (Cornwall) estimates the average mortality at from 40 to 66 per cent., though he claims for his more recent practice a lessened mortality of only 20 per cent.
Schmidt does not claim that his method of treatment disposes bodily of the morbid condition, but that it does measurably assist Nature in her efforts to restore the animal to the normal physiological state. It is well known that after the beginning of the attack the animal, if left to itself, rapidly grows worse until the crisis of the disease is reached, at which time death occurs or convalescence begins, usually the former. It has been observed, however, that if the treatment is applied within a few hours after the
inception of the disease its progress is modified in such a way that convalescence at once begins, as a rule, and the animal hastily recovers its health, usually within twelve hours, although in extreme cases it may be as late as forty-eight hours. The following is an outline of the plan of treatment of parturient paralysis suggested by Schmidt. The operator should disinfect his hands and the udder and teats of the cow by washing with a 5 per cent. solution of carbolic acid or creolin, or a 1½ per cent. solution of lysol or trikresol. The apparatus needed for the treatment consists of a small glass funnel, a rubber hose three feet long and one-eighth inch in calibre into which the funnel fits, and an ordinary milking tube over which the rubber hose fits. This apparatus should be sterilised immediately before it is used by boiling or soaking in such a solution as recommended for washing the udder. Dissolve from 2 to 2½ drachms of potassium iodide—the size of the dose depending upon the size of the cow and the character of the attack—in about one quart of clean water previously boiled to sterilise it, and allow the solution to cool to a little above body temperature, or 40° C. or 104° Fahr. The temperature may be determined with the clinical thermometer. Withdraw all the colostrum or milk from the udder. Then insert the milking tube, with hose and funnel attached, into one of the teats, elevate the funnel about two feet above the teat and slowly pour in one-fourth of the solution, allowing the funnel and hose to become empty several times during the process in order to permit the entrance of a liberal quantity of air. Repeat this infusion with the other three quarters of the udder. After all is introduced, knead the udder carefully so as to cause the solution to permeate the ducts and acini as much as possible.
As the condition of the cow is usually such as to call for additional treatment, the veterinarian should not be content with injecting the potassium iodide solution, but should resort to any and all other measures which promise assistance.
As the cow is usually unable to urinate, the bladder will be found filled with urine. This should be removed with the catheter, and its removal accomplished at intervals until the recovery of the cow renders this procedure no longer needful.
It may be advisable that catharsis be brought about. As the cow is usually unable to swallow, it is dangerous to attempt to give
medicines by the mouth. This may be done if assurance that the cow can swallow is obtained. Some have given medicines successfully through a probang inserted into the stomach. The plan is feasible. Schmidt says that he usually resorted to an aloe powder. If this is done 1 ounce to 1½ ounces of aloes may be given. It would seem preferable to give the aloes in a bolus, capsule, or drench. Some have given linseed oil or Epsom salts. If the animal cannot swallow and a probang is not at hand, one may administer 1½ to 2 grains of physostigmine salicylate subcutaneously, repeating the dose in about three hours if purgation is not produced. Rectal injections should be given at short intervals in order to get rid of the accumulation of hard, dry fæces in the rectum. These injections may be of linseed oil, cotton-seed oil, or warm soap solution. Schmidt recommends, also, enemata of sodium chloride solution. Meanwhile the cow should be kept propped up on the sternum by means of bags of straw or pieces of wood. If the temperature is below normal, as it usually is, the cow should be thickly clothed with blankets and straw heaped up about it. Schmidt used powdered digitalis given by the mouth when the heart was rapid and weak. It would seem much better in every way to give the tincture of digitalis subcutaneously. He has also resorted to subcutaneous injections of camphor and caffeine. This is good treatment. If the cow does not show marked improvement within eight hours the potassium iodide infusion may be repeated. Schmidt has found that as much as 6 drachms may be injected into the udder without harm to the cow. Schmidt, in his first report, made in 1898, recorded 50 cases treated for parturient paralysis by this method with but two deaths from the disease. There were, however, only 46 recoveries, as two cows were slaughtered for beef during the first day of convalescence. A short time later a report was made by Jensen showing that in Denmark up to that time sixty-five veterinarians of that country had treated 412 cases by the Schmidt method, 90 per cent. of which recovered. Such results seem to indicate this as the treatment par excellence for parturient paralysis. It still remained to secure the introduction of this treatment into the United States and to determine what results could be obtained. In all 166 cases were reported; of these 166, 119 resulted in recovery, while 47 were fatal. Of the fatal cases, in eight of the cows death may be traced to some complication, such as prolapse of the uterus, foreign-body pneumonia, etc. In these cases the Schmidt treatment cannot be said
to have failed, for it is not in any way intended that it shall be able to overcome such accidental conditions. If the cow has recovered from its condition of paralysis as a result of the Schmidt treatment far enough to be out of danger from that source and to promise recovery, but later falls a victim to some complication that is in no measure a part of parturient paralysis, but only a result of that disease, it may with justice be said that the Schmidt treatment was a success so far as the malady against which it was directed is concerned. Looking at the reports from this generous point of view, in 127 cases out of 166, or 76·5 per cent., the Schmidt treatment was successful so far as the parturient paralysis was concerned.
In a paper published in the Berliner Thierärztliche Wochenschrift in August, 1902, Schmidt reviews the results of his treatment as evinced by 914 patients treated by thirty-one different practitioners: 884, or 96·7 per cent., recovered, twelve died and six were slaughtered during the course of the disease. Twelve others were slaughtered at a later period in consequence of complications. Jensen reported the results of 1,744 cases.
Schmidt also found that the simple injection of air was in many cases sufficient to produce recovery, and subsequent observation tends to show that the fluid injected is of less importance than was first anticipated. A large number of unirritating solutions may be employed. Schmidt, however, still counsels the use of a quart of 1 per cent. solution of iodide of potassium, in which can be dissolved 5 grammes of caffein sodio-salicylate if the heart’s action is weak. About 10 ounces of this solution are injected into each quarter, and are followed by a liberal injection of air. The parts should afterwards be freely massaged.
CŒNUROSIS (GID, STURDY, TURN-SICK).
Cœnurosis is a disease due to invasion of the animal body by embryos of larvæ of the Tænia cœnurus of dogs and wolves. These embryos only develop freely in the brain substance (Cœnurus cerebralis) and medulla oblongata. The hosts of the larvæ include the calf, sheep, goat, roedeer, reindeer and horse.
The disease was formerly erroneously called “turn-sick,” for the turning is only a manifestation, and even a tardy manifestation, of the disease, while in addition it is not invariably present.
Cœnurosis principally attacks lambs of from three to six months, although it occurs up to eighteen months, and sometimes even two years. It is exceptional, however, in adults. Similarly in the bovine species it usually affects young animals up to the fourth or fifth year.
Cœnurosis with diffuse parasitic encephalitis often remains unrecognised, the animals being regarded as affected with epizootic meningitis of unknown cause or septic intoxication, and when they die the owners are ignorant as to the cause of death. The stage corresponding to turn-sick, which is an advanced phase of the disease, is only seen in animals which have been infested to a slight extent, and in which three or four parasites only, sometimes only one, have attained the brain and developed there. Such cases exhibit all the classic symptoms of turn-sick, viz., turning movements, heaviness, vertigo, etc.
Causation. Cœnurosis is due solely to one cause, viz., the ingestion of eggs or embryos in feeding or drinking.
The Tænia cœnurus lives in the dog, and fertilised segments are passed with the fæces in yards, pastures and fields, and on the margins of roads, ditches and ponds. Amongst damp grass or in water the eggs, which contain more or less well-developed embryos, may retain their vitality for several weeks, and when swallowed the embryos are set at liberty in the intestine.
The six-hooked embryos perforate the walls of the intestine, pass into the blood stream or chyle ducts, and from these points are carried in all directions. Those which gain the nervous centres, the
brain or spinal cord, continue to develop; the others, dispersed through different tissues, degenerate and disappear.
Experimental infection with these parasites shows that the brain is invaded after about a week’s time. From the twentieth day the presence of embryos can easily be detected in the superficial layers of the convolutions. They make their way through the grey substance, leaving behind them greenish-yellow sinuous tracts with caseous contents.
The cyst or finn undergoing development can be found at the end of one of these tracts in the form of a little transparent bladder, of a size varying between that of a pin’s head and that of a lentil or a small hazel-nut.
Later the tracts, with their caseous contents, disappear, and the development of many of the vesicles proves abortive. At the end of a month the vesicles, continuing to develop regularly, attain to about the size of a pea. Between the fiftieth and sixtieth days heads or scolices appear in the interior of the vesicle, which then reaches the dimensions of a hazel-nut. From this time the vesicles continue to increase in size until the death of the patient. Usually they become as large as a walnut, or even larger, and the interior contains hundreds of scolices, each showing a head.
F . 214. Brain of sheep. Cœnurosis of the left hemisphere. Œstrus larvæ exposed by trepanation.
The cystic phase only develops completely in animals whose brains contain a limited number of cysts, and in such the signs of turn-sick are well developed. In others, where the numbers are large (ten to fifteen embryos or more), death occurs during the primary stage, usually towards the end of the first month, in consequence of acute encephalitis and without any of the symptoms of turn-sick.
F . 215. Skull of a sheep showing the brain infested with a gid bladder-worm (Cœnurus cerebralis). Two-thirds natural size.
The number of animals attacked is sometimes enormous. Moussu has recorded cases where fifty, one hundred, and even four hundred lambs of one flock were affected. The enormous mortality in such cases is very apt to cause errors in diagnosis. Cœnurosis occurs most frequently during rainy seasons, moisture favouring the preservation of the eggs. Young animals become infected, particularly during the spring and autumn, more rarely in the summer, as prolonged desiccation, say for a period of twelve to fifteen days, destroys the vitality of the eggs, but animals may become infested at any time through drinking contaminated water. Moussu has seen cœnurosis (acute encephalitis) from the last-named cause in the middle of January.
Symptoms. First phase. Disseminated encephalitis.—The symptoms vary with the phases of evolution of the parasite and of the disease which it causes. After the six-hooked embryos have penetrated to the brain, the animals affected lose appetite and show a certain degree of dulness, which is all the more marked inasmuch as the animals usually affected are young, and therefore should appear bright and alert. Then follow wasting and depression; the animals remain stationary for whole hours together, the head being carried low or inclined to one side. At this stage disturbance in vision and irregularities in movement may appear.
F . 216.—An adult gid tapeworm (Tænia
cœnurus). Natural size. (After Railliet.)
The eyesight is almost always affected, but the symptoms may vary widely. In some cases the patients seem to be absolutely blind, and strike against any obstacle in their way; in others the power of vision seems to be lost only on one side. All that can be discerned objectively is an inequality in the pupils, together with retraction or dilatation, convergent or divergent strabismus, nystagmus, etc. The humours of the eye appear infected, but examination with the ophthalmoscope reveals lesions of more or less extensive neuro-retinitis.
The visual disturbance is of central origin. The powers of movement may be affected in numerous ways, which at times are extremely difficult to estimate with accuracy. Sometimes the gait is uncertain, inco-ordinated, and hesitant; at others the animal shows lameness or loss of control over a front or hind limb, or over two limbs simultaneously (either the two front or hind limbs or the diagonal limbs), or it may be absolutely unable to stand.
It walks obliquely, or the front or hind limbs collapse; or again, it may persistently lie down, a fact which makes the shepherd think it is suffering from paralysis. On examination, however, no true indications of paralysis can be found; sensation and motor power are both preserved in a modified form.
Death is very frequent at this stage of the disease; the animals eat little or nothing, refuse drink, and die of exhaustion.
All this general disturbance is of central origin, and is due to disseminated parasitic encephalitis, but up to this point the seat of the disease is not yet clearly apparent.
F . 217.—Sexually mature segment of the gid tapeworm (Tænia cœnurus). cp, Cirrus pouch; gp, genital pore; n, nerve; ov, ovary; sg, shell gland; t, testicles; tc, transverse canal; ut, uterus; v, vagina; vc, ventral canal; vd, vas deferens; vg, vitellogene gland. × 20. (After Deffke.)
Second phase. Turn-sick.—The central symptoms are slow of development, and are due to the progressive growth of one or two, more rarely three or four, fertile vesicles. These are the true symptoms of turn-sick, and it is only after this phase of the disease has developed that the term becomes appropriate.
Left at liberty, the patient usually walks in a circle towards the right or left in an impulsive and irresponsible fashion. Sometimes it describes a circle, always of the same size. In other cases, on the
F . 218.—Brain of a lamb infested with young gid bladderworms (Cœnurus cerebralis). Natural size. (After Leuckart.)
contrary, it travels along a spiral track, getting further from or nearer to the centre as the case may be. The turning movement may become so accentuated that the animal appears to revolve as on a pivot, and if it is confined in a field or straw-yard its legs become caught in the litter and it falls to the ground.
Attempts have been made under these circumstances to discover the exact point of compression, i.e., the point at which the cyst exists, by noting the direction of the turning movement. The diagnosis, however arrived at in this way is frequently illusory, because it is not uncommon to find two or three vesicles, and in any case the most important information in regard to diagnosis is to be derived from the ocular symptoms.
When only one vesicle exists, the turning movement usually occurs towards the side on which it is situated, and the eye of the opposite side is affected with amaurosis.
F . 219. Sheep’s skull, the hind portion thin and perforated, due to the presence of gid bladderworms (Cœnurus cerebralis). (After Dewitz.)
If the cyst is situated near the olfactory lobes, the animal marches with a high-stepping movement and the head drawn back towards the body. If the cyst is in the cerebellum the animal is incapable of moving, because it can no longer co-ordinate its movements. Finally, if the cyst develops in the occipital region, animals turn towards the wind, with the neck raised and the head extended.
At the moment when they fall to the ground they sometimes have epileptiform convulsions, grind their teeth, and salivate profusely. In a severe attack even death may supervene at this point.
Cœnurosis of the Medulla. The embryos may develop in the medulla oblongata as well as on the brain itself. Compression and atrophy of the medulla then give rise to true paralysis.
