Main Metabolic and Deficiency Diseases Found in Animals

List of seven main metabolic and deficiency diseases found in animals:- 1. Parturient Apoplexy 2. Rickets 3. Pica or Malacia or Aphosphorosis 4. Dystrophic Diseases 5. Osteodystrophia fibrosa, Osteofibrosis or Osteoporosis 6. Scurvy 7. Anhydrosis.

Metabolic and Deficiency Disease # 1. Parturient Apoplexy:

Synonym:

Milk Fever, Dropping after calv­ing.

This is a disease of cows occurring usually shortly after parturition in which chief symptoms are loss of power and loss of consciousness. It is a disease which has been mostly noted in cows but has been noted in milch goats and in ewes after lambing. In cows, it usually develops first shortly after third calving and it may reappear subsequent to each calving while the full milking powers are retained.

It has also been occasionally met with after the second calving and rarely after the first. Cows most susceptible to milk fever are good milkers. The disease appears after an easy parturition. The symptoms develop usually on the 2nd or 3rd day after calving, occasionally a few hours before calving but sometimes it is de­layed for 1 week or even 2 weeks.

Etiology:

Direct cause of the disease is not yet known.

The following are a few of the more modern theories regarding causation:

1. Hypocalcemia:

The generally accepted theory as to the cause and essential nature of milk fever attributes it to an acute calcium deficiency in the blood stream. In milk fever in cows, the blood calcium drops from a normal of 10 mg per 100 ml of serum to 3.0 mg per 100 ml. The cause of the reduction has yet to be determined.

It has been attributed to:

(a) Some defect in the secretion of Parathy­roids but in milk fever, there is also a reduction in phosphorus content of the blood.

(b) Rapid removal of the calcium from the blood stream, first of all to meet the requirements of the calves and secondly during rapid produc­tion of milk. There is no decrease of calcium in other tissues. It is only in the blood stream that the lack of soluble calcium is evident. The most probable reason is that mobilisation of calcium from storage in skeleton may not be sufficiently rapid to maintain normal serum levels.

2. Anaemia (Cerebral):

In which it is taken that the symptoms are due to rapid passage of large quantities of blood to the vessels of the abdomen after parturition and to the udder dur­ing early stages of lactation.

3. Udder intoxication theory:

According to this theory, some toxic agents—either in the form of ptomaines or bacterial leucomaines prod­ucts—are absorbed from the udder into the blood stream and act upon the brain. It is surmised that the blood calcium content is reduced by these agents.

Symptoms:

Very rapidly and the initial and premonitory symptoms are—the cow paddles with her hind legs, has staggering gait, takes no interest in its calf, occasionally moans and the milk supply if develops is decreased. Sometimes, the animal goes down and makes several at­tempts to rise before the symptoms set in. These are called ‘premonitory symptoms’.

When the case is developed, the animal is down frequently lying on its briskets and generally with its head turned towards its sides and close to the chest wall. If the head is straightened and released, it will return immediately to its previous position. Occasionally, it will be found lying flat on its side.

In such cases, tympanitis rapidly develops and if that becomes marked, death may result from asphyxia. The pupils are dilated and the eyes are staring, sometimes, there is a discharge of tears, there is profound coma and the animal pays no attention to its surroundings or manipu­lation. There may be shaking of head, protrusion of the tongue and grinding of the teeth.

Another stage is one of sternal recumbency. The muzzle is dry, the skin and extremities cold, and the rectal temperature subnormal (97° F to 101° F 36.2°C to 38.6°C). The pupils are dilated. The pulse, in most cases, is impalpable, the heart sounds inaudible and increased in rate up to 120 per minute, but it may be impossible to raise the jugular vein.

Faeces are retained, peristaltic movements being in abey­ance. The urine may also be retained and it con­tains lactose. The udder is relaxed and flabby and the secretion is very slight. The surface of the body is cold.

With modern treatment, 95% of animals re­cover provided the treatment is adopted early.

Complication which may arise include:

1. Foreign body pneumonia and Septic pneumonia from choking

2. Mastitis and uncommon complications

3. Paralysis of the hind limbs due to pres­sure upon some of the nerves of the limb and the cow has not been properly bedded down or has been allowed to remain on one side for a long time

4. Necrosis or Bed sores from prolonged pressure.

Treatment:

If the animal is down on its side and tympanitic, it should be immediately placed on its brisket. The tympany soon disappears and the use of trocar and canula is seldom required.

Two methods of modern treatment are now in vogue:

1. The injection of the four quarters of the udder with air or oxygen. For this purpose, a teat syphon attached to an oxygen cylinder for an injection is used. Injection of solutions containing either phosphorus, magnesium or dextrose may also be given. While injecting air or oxygen, the teat syphon must be sterilised before use and the syringe washed with an antiseptic solution.

The upper hind limb is drawn back and a clean cloth is placed under the udder. The teats are washed with an antiseptic. It is usually convenient to inject under teats first. If one quarter is infected with mastitis, it should be left to the last or its injection omitted altogether. The injection of each quarter is continued until the udder is moder­ately tense.

A broad piece of tape may be applied as a ligature with a moderate pressure over each teat to prevent the escape of the gas from the udder, but this tape must be removed in 2 to 3 hours, better in 2 hours. After the injection, mas­sage the udder. If the animal does not recover in 8 hours, a second injection should be given.

After the injection of the udder, a stimulant may be given hypodermically such as adrenaline. The animal should be properly bedded down and propped up on its brisket, with a truss or bag of straw against its shoulder or chest. Care must be taken that the animal is turned from one side to another every 4 hours. Instead of strychnine or Adrenaline, one may give gr. 1/2 (60 mg. to 1.20 mg) of atrophine subcut with advantage.

2. This method consists in subcutaneous or intravenous injection of Calcium gluconate—the percentage of solution commonly used is 10% and the quantity injected varies from 300 to 500 ml. The solution should be boiled and properly filtered. It has recently been found that the addi­tion of Boric acid to the solution will prevent the precipitation of salt and a tendency to necrosis of the skin and tissues in subcutaneous injection.

The solution is injected into Jugular vein if given intravenously or under the skin in front or behind the shoulder with the usual surgical precautions. It would be better if, out of 500 ml, 375 ml be given intravenously and 125 ml. be given subcutaneously in several places. To avoid danger of heart failure, from rapid administration, the intra­venous injection should be given slowly over a period of 15 to 30 minutes.

Because of the fre­quency of acetonemia in association with milk fever, many veterinarians often give an equal amount of 40% dextrose mixed with Calcium gluconate solution. If this injection is not suffi­cient to effect a cure, a second injection is given in 6 or 8 hours.

Both forms of treatment seem to be equally efficacious, frequently they are combined. Recovery usually takes place within a few hours. The animal should be put on half ration for a day or two and should not be milked out but only sufficient milk removed for a day or two required for the feeding of the calf. A laxative is sometimes given.

Prevention:

Various preventive measures have been recommended to avoid milk fever at subsequent parturitions and include:

1. Keeping the animal in only moderate condition by putting cows on bare pastures, re­ducing rations and exercise.

2. Giving a laxative before or after parturi­tion.

3. Allowing the calf to suck the cow for a few days after parturition. If premonitory symp­toms appear, the injection of air and oxygen into the udder or Calcium borogluconate should be given.

Metabolic and Deficiency Disease # 2. Rickets:

A condition only seen in young animals be­fore the development of bones is complete, in which deposition of calcium salts in the bones is deficient and the replacement of cartilage by bone irregular. The disease is most common in puppies and pigs but has occasionally been observed in lambs, kids, calves and foals.

The disease is usu­ally noted in single cases but is not uncommon in a number of animals which are kept under simi­lar conditions. It is most common when the ani­mals are only a few months old but earlier cases are occasionally noted.

1. Etiology:

The cause of the condition is not definitely established but the disease is due to number of factors including:

Want of Vitamin D in the food and defi­ciency of calcium or phosphorus, chiefly the former, and when sufficient minerals are pro­vided, rickets and osteomalacia will not appear. Vitamin D is absent to a large extent from carbo­hydrate diet, such as white bread or biscuits, vegetable oil and it is present in largest amount in Cod liver oil, Halibut liver oil, Shark liver oil, Milk of cows at grass and the yolk of eggs.

2. Want of sunlight:

The ultraviolet rays of the sunlight act upon cholesterols of the skin and tend to produce Vitamin D or Ergosterol.

3. Deficiency in lime salts in the food or drinking water or even in the milk of the dam. Food deficient in lime salts are potatoes, bread, biscuits etc.

4. Lack of exercise:

In dogs, rickets is most common in larger breads and in them the condi­tion is commonly associated with confinement. Other conditions which may predispose the ani­mals to rickets include cold floor, bad hygiene and dirty surroundings.

Symptoms:

Usually develop within a few months of birth. The animal is unthrifty and stunted, abdomen is pendulous and it is tender in its gait. The appetite is capricious or voracious and the mucosa pallid. The animal is pigeon- breasted. The long bones are shorter than usual and the ends are enlarged.

The chondro-costal joints are first affected and appear like so many beads on the side of the lower portion of the chest. Owing to want of rigidity and the effect of weight, the limbs become bent and the animal becomes Knock-kneed and the hind limbs Calf- hocked. Sometimes, carpus becomes abnormally flexed and the puppy may walk like a bear. The prognosis is doubtful in most cases unless the condition is detected early.

The effects of the disease remain, i.e. to say, there is always en­largement of joints etc. In severe cases, the verte­bral column may undergo unusual curvatures, more commonly seen in man—Scoliosis, Lordosis, Kyphosis i.e. lateral, downward and upward cur­vatures, respectively.

Treatment:

Apply bandages to give support to the limbs, when the latter are showing evi­dence of bending. Give exercise and plenty of Sunshine. A diet rich in Vitamin D, such as cows milk, cod liver oil is very essential with lime salts such as a large bone to grow, Calcium carbonate lime water or Calcium phosphate. Rickets are also treated by exposure to ultraviolet rays or artifi­cially prepared Vitamin D.

Metabolic and Deficiency Disease # 3. Pica or Malacia or Aphosphorosis:

It is noted in cattle in various countries in which the herbage is poor in phosphates. It is seen on pasture which has not been dressed or cultivated. It affects young stock, heifers and, particularly, calves. The—first change usually noted in curving of bones. The animal becomes very stiff and lame, has difficulty in rising, moves with quick steps and back arched.

The animal becomes unthrifty and some of the joints specially fetlocks—become enlarged. The claws also be­come deformed and may be turned upwards and inwards. The condition disappears to a large extent upon dressing the land grazing ground with fertilisers such as phosphates and improving the diet of the animals by adding bone-meal to the food. No treatment is of any value but pre­ventive measures now adopted are very efficient.

Metabolic and Deficiency Disease # 4. Dystrophic Diseases:

The three chief dystrophic diseases of the skeleton in animals are:

1. Rickets

2. Osteomalacia and

3. Osteodystrophic fibrosa or Osteoporosis or Osteofibrosis.

Rickets, a dystrophy of the young, is a well recognised pathological entity. Osteomalacia is, in short, adult rickets and as in the case of rickets, is characterised by the presence of excessive amount of Osteoid tissue. The formation of os­teoid tissue represents a stage in bone formation which is normally followed by lime salt impreg­nation. In rickets and Osteomalacia, the deposi­tion of calcium salt is defective and so bone for­mation is arrested at the stage of Osteoid tissue.

In rickets, osteoid tissue is prominent at the epi­physis of long bones. In osteomalacia, it makes its appearance in the diaphysis of the bones. It is not evident at the epiphysial junction because at the age when the osteomalacia occurs, growth of bone at the epiphysis has ceased and the junction has undergone ossification, as bone formation from the periosteum is more or less continuous throu­ghout life.

Osteoid tissue becomes prominent along the shaft under the periosteum. Osteoid tissue also makes its appearance in isolated areas within the bone. Apart from defective bone for­mation and the consequent accumulation of os­teoid tissue which occurs in osteomalacia, there occurs side by side with it atrophy of bone or osteoporosis. Osteoporosis occurs whenever there is an excessive drain on the mineral reserves in the skeleton and is the result of lime salt resorption.

Metabolic and Deficiency Disease # 5. Osteodystrophia fibrosa, Osteofibrosis or Osteoporosis:

This is a condition of adult animals in which first lime salts are removed from the bones, later becoming soft and secondly the bones of certain parts become enlarged. The bone tissue becomes replaced by osteoid tissue or fibroid tissue. This disease is met with a varying degree in different parts of the body. It is common in certain parts of Africa, Europe and in Australia. India and Sri Lanka. The disease affects not only equines but also cattle, goats, dogs and even wild animals such as bears and monkeys kept in confinement.

Etiology:

Causes are not well known and include:

1. Some defect in the proportion of mineral salts of the food, the ratio of lime and phosphoric acid being too low. The disease has also been noted in horses in the continent fed largely on bran and it was called Bran disease or Miller’s disease.

2. Want of Vitamin A or D, or both. This affection can be ascribed to animals kept in confinement.

Symptoms:

In horses, the first symptoms actually noted are those of an indefinite lameness or stiffness, sometimes rupture of ligaments and tendons takes place as fracture in bone in which later case, there is little attempt to repair. Later, the bones of the face become swollen. The swell­ing is symmetrical and confined to the lower and upper jaw bones largely.

The swelling is sym­metrical and the bones are softened, the rami become very broad and sub-maxillary space nar­row. The molar teeth become loose and mastication difficult and so the animal loses condition.

The thickening of the bones surrounding the na­sal chambers causes narrowing of the latter and even dyspnea and snoring. The urine contains large quantities of phosphates and the amount of phosphate is in direct proportion to the acuteness of the attack. The course varies very much but lasts usually for months, most cases are chronic and become worse.

Lesions:

They are confined to the bones and particularly to the bones of face or head. The affected bones are enlarged and softened and are of a pinkish colour, can be cut like a cartilage and resemble cartilage to the naked eye. When the bones are boiled, so as to remove all the organic tissues, they become very fragile and porous. In the fresh condition, the spaces left have been filled with a very firm fibrous tissue.

Treatment:

Send the animal to some other part of the country. Lime phosphates have been used in treatment but not very successful. In places, where the disease is common, bone meal given in the food each day has been very success­ful in preventing the occurrence of the condition. In cattle, the condition is similar but treatment with lime salt or bone meal has been more suc­cessful.

In goats, fractures of the limbs are not uncommon and the head is frequently affected. Sometimes, the condition may be mistaken for the fracture of the jaw as the animal cannot close the mouth and bone is flexible, the teeth are movable in the sockets. In dogs, the head is commonly affected and hence the term—Rubber nose. Re­coveries have been claimed where parathyroid extracts and lime salts have been given.

Iodine Deficiency (Goitre, Hairless pigs, weak foals and lamb)

It is characterised by an enlargement of the thyroid glands (simple goitre) in newborn calves and by a hairless condition of the skin of new­born pigs. A deficiency of iodine in the food or water supply of the dam is the sole cause.

Morbid Anatomy:

There is a marked swell­ing of the thyroid glands and the tissues around them are infiltrated with blood and serum. The thyroids are enlarged, soft and have the appear­ance of clotted blood.

Symptoms:

Calves are usually born alive but a few are aborts. There is marked weakness and the calf cannot rise. In swine, the deficiency causes a hairless condition in newborn pigs but majority of them die. Affected foals and lambs are weak and they often die.

Prevention:

The condition is readily pre­vented by giving the dam small amount of iodine during last three months of pregnancy. A conve­nient method of administration of iodine is to add Potassium iodide to the salt—1; 3,500.

Metabolic and Deficiency Disease # 6. Scurvy:

It is due to absence from the diet of a suffi­ciency of a specific accessory food factor—Vita­min C. It consists in a general disorder of nutri­tion characterised by debility, anaemia, sponginess of gums, ulceration of the mouth and a tendency to haemorrhage.

Etiology:

The disease results from a deficient intake of the Vitamin C. Bad hygienic condition appear to favour a development of the disease.

Symptoms:

The earliest symptoms are weak­ness, dizziness and bleeding from the gums on slight provocation. Pain in the limbs are noticed and there may be a characteristic hardness of certain group of muscles. There may be some changes in the mouth.

The gums begin to swell, specially around the teeth. The teeth becomes loosened in their sockets and may fall out. Haemorrhages into the skin and subcutaneous tissues are seen. As the disease progresses, anaemia becomes a marked feature. Appetite is not necessarily impaired. Constipation is present; the urine may be albuminous.

Diagnosis:

In all, the characteristic symp­toms are present. If the disease arises simulta­neously in a number of subjects, diagnosis is easy.

The disease which perhaps most closely resembles it is Purpura haemorrhagica but in this, the affec­tion of the gums is absent.

Treatment:

The essence of both of the pro­phylaxis and the active treatment of Scurvy is to supply a sufficiency of the vitamin C in the diet. With this object, fresh uncooked vegetables should be given freely. The juice of fresh lemons or oranges may be given. Germinated peas, beans, lentil have also some antiscorbutic powers. Drugs are of little help but iron may be given during convalescence. Peroxide wash will help to remove the foetor whilst Nitrate of Silver solution 2% to 3% may be painted on the affected gums.

Metabolic and Deficiency Disease # 7. Anhydrosis (Non-Sweating):

It is non-contagious affection of horses and is characterised by dry coat and dry sweat, noted in horses which are brought from temperate cli­mates to tropical countries. It is rarely noticed in Arab horses. The condition usually appears after some months resting and generally during hot weather. It starts by diminution in the amount of visible sweat and an absence of lather even with moderate exercise. The temperature of the af­fected horse may rise up to 107° F (41.5 °C) to 108° F (42.°C) and the respiration to 150 per minute.

Symptoms:

Non-sweating, signs of lassi­tude, dullness and staggering gait, accelerated respiration, polyuria, capricious appetite, rise of temperature, loss of condition etc. and, in many cases, an intense itching of the skin with sym­metrical loss of hair—particularly over the head, face, shoulder and legs.

Etiology:

It is unknown. It was one time believed due to thyroid deficiency.

Treatment:

90% of horses removed to hills at an altitude of 2,000 to 6,000 feet metres, 600 metres to 1,800 metres recover within a week. Some, however, may relapse 2 or 3 days after returning, about 10% never recover. For mild cases of dry coat, give

(a) Sodium chloride in drinking water; re­peat twice daily at least.

(b) Ratio of oats to bran should be 3: 1.

(c) 500 gms of germinated gram, morning and evening.

(d) The following recipe may be pre­scribed:

Sig:

One table spoonful over the food once daily in slight cases or twice in the more ad­vanced cases.

For advance cases of dry coat:

(a) If the treatment fails after some 10 days try, they give along with the above treatment — Ry Pulv. Adrenal Cortex—gr x.

Sig:

Carefully dust the powder over a small primary feed, morning and evening in the worst affected.

Sterility:

By sterility is meant the failure on the part of an animal—male or female—to procreate its spe­cies. Sterility is a disease or rather a symptom of disease of the reproductive organs which causes great continuous and increasing loss to agricul­ture and animal husbandry.

Etiology:

It is now recognised that many of the factors which limit or prevent fertility are merely predisposing or contributory causes, whilst the actual cause is often a definite diseased condi­tion of some part or parts of the genital organs. It is rare to find the male totally and permanently sterile although he may prove an indifferent stock getter or actually sterile at times.

That the female is much more affected than the male is not sur­prising when we consider the number and nature of the risks to which she is exposed, specially as the result of parturition. The female organs are also more complex than the male and they are, therefore, more liable to disease, the uterus in particular.

Sometimes, loss of function, rather than the structural changes—appears to be the cause of the trouble, e.g., the semen is weak or Oestrum is absent, irregular or excessive. The uterus may be quite healthy but the ovary fails to form or dis­charge the ova.

On the other hand, fertilization of healthy ovum is of no avail if the ovum cannot obtain a firm attachment to the uterus on account of the disease. A cure cannot be claimed if suc­cessful efforts to impregnate an animal are fol­lowed by early abortion. But it is common knowl­edge that abortion frequently leads to sterility.

What may be termed mismanagement is responsible for a certain number of infertile ani­mals. This includes errors in diet, work or exer­cise, overuse with holding the bull and possibly in breeding. Many bulls are blamed for causing sterility but the evidence is by no means convinc­ing.

Generally speaking, nitrogenous foods like peas, beans increase vigour, therefore, sexual de­sire; whilst grains, maize and similar material is less active in this respect. The fact is that constitu­ents of rational diet are of minor importance provided the diet is suited to the circumstances of the particular case.

It should be remembered that the presence of pronounced oestrum is no guide to female’s abil­ity to breed nor is the power to copulate any criterion of sexual soundness in the male. After all, it is the amount of food rather than the actual constituents of the diet which is important point. This depends upon the age, the amount of work and the number of services on the part of the male. Thus, a stallion serving, say, 80 mares or a bull, a hundred cows require generous diet, rich in protein.

With regard to exercise, there is general con­scientious opinion that confinement like over­feeding lessons fertility. Bulls in confinement be­comes easily lazy and heavy after 4 years age and their fertility rapidly diminishes. This problem has now been overcome by the introduction of artificial insemination in cattle. The powers of a male are overtaxed by too frequent use during a comparatively limited period. The semen becomes watery and less potent, the male sperms sluggish and few in number.

Age is seldom an obstacle to conception whilst it is true that the semen of very young males is of low fertilizing powers. Yet a young sire of breeding age is more prolific than an old animal, provided he has been properly fed and cared for.

Hormonal defects:

The internal secretions maintain a balance in metabolism and if that balance is broken down by a defect in one or several of the internal secretions, sterility may be one of the results. Such internal secretions would include those formed by interstitial cells of the Ovary, Thyroid and Parathyroid, Suprarenal and Pituitary bodies. On account of that, Thyroid and Ovarian extracts are sometimes used for the res­toration of fertility in the absence of gross lesions of genital organs.

Chronic inflammation of the uterus and cer­vix and cysts in the ovaries. These inflammations frequently cause abortion and, to a less extent, ordinary parturition owing to the fact that infec­tion of uterus readily takes place at such times. By infection we mean the invasion of microorganisms which occurs apart altogether from abortion when the genital passages are injured during the birth of the foetus. Retention of after birth is also a specific cause of infection and, therefore, of sterility.

Diagnosis:

The most important thing of all in dealing with the problem of sterility is early and accurate diagnosis. Let us take a typical case of a cow which has been over repeatedly to the bull and shows no signs of holding. She may have aborted or had a difficult calving. In either case, she probably retained her after birth and suffered from a discharge with slight straining occasion­ally for some weeks.

The fact that the uterus was diseased was, however, not recognised. The infec­tion which was invariably present in such cases was allowed to take its course until extensive and often incurable changes have taken place not only in the uterus but also in the ovaries and other parts.

Treatment:

Hormonal treatment is quite ef­fective if sterility is due to deficiency in hor­mones. Commonly, it is a chronic disease and it is well to remember that there is no specific treat­ment for cure. However, this has been properly dealt with in the chapter on Gynaecology.

Prevention:

Sterility is largely dependent on the accidents and diseases connected with partu­rition. At parturition, the chief point to remember is to avoid infection which is very apt to occur from even slight wounds inflicted during birth from dirty hands and instruments, ropes, syringes, dirty surroundings and from retention of after birth. An early and complete removal of after birth is always desirable. Vaginal and uterine injections are of the greatest importance in diffi­cult births.

Any of the following solutions may be employed at blood heat:

1. 1% Cresol solution or Jeye’s fluid—3 table spoonfuls to 5 litres of water.

2. Pot. permanganate—(1 in 1,000)

3. Perchloride of Mercury (1 in 8,000)

It should be supposed that douching the va­gina will suffice to control or prevent the infec­tion. They must be supplemented by irrigation of the vagina with warm solution is beneficial. Many good antiseptics are now available and interuterine douching may be done by modern antibi­otic medicines.

As a rule, what may be termed as combined treatment is necessary—briefly this con­sists in crushing cysts in the ovaries, massaging and cleansing the uterus, opening up the cervix and performing artificial insemination. Artificial insemination is now widely used to improve the breed and also when any obstruction exists in the cervix, vagina or vulva.

Semen from one service can be utilised to impregnate many. An antisterility fat soluble Vitamin ‘E’ has been discovered for the treatment of sterility. Wheat germ oil is particularly rich in Vitamin K and it is also found but in lesser degree in certain cereals and in green leaves and seeds.

Deficiency of salts in the food that would apply particularly to calcium salt and Iodine. Bone-meal and other calcium salts may be given. A change of food or climate may sometimes effect a cure.