Disease of blood and blood-formation organs
HAEMORRHAGE
The rapid loss of whole blood from the vascular system causes peripheral circulatory failure
and anaemia.
Aetiology
Spontaneous rupture or traumatic injury to large blood vessels are the common
causes of severe haemorrhage but rapid blood loss may occur by bleeding from the
mucous surfaces or by massive infestation by blood-sucking nematodes. Severe
haemorrhage can thus occur in coccidiosis and salmonellosis. An important
occurrence of nasal haemorrhage is in horses while racing. Extensive blood loss into
tissues may also occur when there are defects of vessel walls or the clotting
mechanism.
Pathogenesis
The major effects of haemorrhage are loss of blood volume, loss of plasma protein
and loss of erythrocytes. If the rate of blood loss is rapid the loss of circulating blood
volume results in peripheral circulatory failure and anaemic anoxia results from the
loss of erythrocytes.
Clinical Findings
Pallor of the mucosae is the outstanding sign but there is in addition, weakness,
staggering and recumbency, a rapid heart rate and a subnormal temperature. The
respirations are deep but not dyspnoeic.
Clinical Pathology
Examination of the blood for haemoglobin and haematocrit levels, and the
erythrocyte count are of value in indicating the severity of the blood loss and provide
an index to the progress of the disease. Estimation of clotting and prothrombin times
should be undertaken in cases in which unexplained spontaneous haemorrhages
occur.
Necropsy Findings
Extreme pallor of all tissues and a thin watery appearance of the blood may be accompanied
by large extravasations of blood if the haemorrhage has been internal. Where the
haemorrhage has been chronic anaemia and oedema are characteristic findings.
Diagnosis
Other forms of peripheral circulatory failure include shock and dehydration but they can
usually be differentiated on history alone. Anaemia due to other causes is not accompanied
by signs of peripheral circulatory failure.
Treatment
All elements of the blood should be replaced and in severe cases blood transfusion is the
most satisfactory treatment (1, 2, 3, 9). In large animal practice donors are usually readily
available and the need for storing blood does not arise.
SHOCK
Secondary or surgical shock occurs some hours after trauma and is manifested by peripheral
circulatory failure without evidence of fluid or blood loss.
Aetiology
Shock follows severe injury to tissues caused by accidental trauma, surgery, especially when
the abdominal viscera are roughly handled, and occurs also after prolapse of the uterus, and
when large quantities of fluid are released from body cavities. Acute infections including
particularly septicaemias and peritonitis may have a similar effect.
Pathogenesis
Although there need be no actual blood loss there is an appreciable fall in circulating blood
volume (CBV) and peripheral circulatory failure is manifested. The reason for this depression
of CBV is the subject of many hypotheses. Exhaustion of adrenal cortical activity, liberation
of histamine from damaged tissues resulting in peripheral vasodilatation, and
overstimulation of the adrenal-sympathetic system have all been advanced as causes of
traumatic shock but complete evidence is lacking to support any of them as other than
contributory factors..
Clinical Findings
Coldness of the skin, a subnormal temperature, rapid, shallow breathing, and a rapid heart
rate accompanied by a weak pulse of small amplitude and low pressures are characteristic of
shock. Venous blood pressure is greatly reduced and the veins are difficult to raise. The
condition is fatal, dies in a coma.
Clinical Pathology
Measurement of the CBV is possible by the use of dyes or radioactive substances but the
techniques are unlikely to be used in clinical practice. Haemoconcentration may or may not
occur depending on whether the fluid loss is in the form of plasma or whole blood, but
measurement of the haematocrit may be of value in individual cases to determine the
progress of the disease..
Necropsy Findings
There may be evidence of trauma and the capillaries and small vessels of the splanchnic area
may be congested.
Diagnosis
Shock is usually anticipated when severe trauma occurs, and is diagnosed when peripheral
circulatory failure is present without evidence of haemorrhage or dehydration.
Treatment
The primary aim in the treatment of shock is to restore the circulating blood volume,
preferably by blood transfusion although the use of plasma or plasma expanders is of much
greater value than in severe blood loss.
OEDEMA
Oedema is the excessive accumulation of fluid in tissue spaces caused by a disturbance in
the mechanism of fluid interchange between capillaries, the tissue spaces and the lymphatic
vessels.
Aetiology
Oedema results mainly from an increase in hydrostatic pressure in the capillaries, from a fall
in osmotic pressure of the blood, from obstruction to lymphatic drainage or from damage to
capillary walls. Increased hydrostatic pressure occurs mainly as a result of congestive heart
failure but it may also occur in more limited regions such as in the portal circuit when there
is hepatic fibrosis. Oedema of the udder and ventral abdominal wall occurs commonly in late
pregnancy in cows and to a less extent in mares and is caused largely by foetal compression
of venous drainage, although hypoproteinaemia is also thought to play a part in this form of
oedema.
Decreased plasma osmotic pressure is caused in most instances by a reduction in the
concentration of plasma protein. Continuous haemorrhage, especially in heavy parasitic
infestations, often leads to oedema.
Obstruction of lymphatic flow plays a part in the production of most local oedemas
caused by tumours and inflammatory swellings. Congenital lymphatic obstruction of
calves and pigs and sporadic lymphangitis of horses are typical examples of
obstructive oedema. Allergic oedema, manifested by urticaria, angioneurotic
oedema and purpura haemorrhagica occur as a result of capillary dilation and
damage caused by the local or general liberation of histamine. Fog fever probably
has a similar basis. Damage to small vessels by toxins or infectious agents may also
result in oedema. The oedema of septicaemic pasteurellosis of cattle, anthrax,
blackleg, malignant oedema, gut oedema and mulberry heart disease of pigs and of
infectious equine rhinopneumonitis, equine viral arteritis and infectious equine
anaemia originates in this way.
Pathogenesis
At the arterial end of the capillaries the hydrostatic pressure of the blood is sufficient
to overcome its osmotic pressure and fluid tends to pass into the tissue spaces. At
the venous end of the capillaries the position is reversed and fluid tends to return to
the vascular system. The pressure differences are not great and a small increase in
hydrostatic pressure or decrease in osmotic pressure leads to failure of the fluid to
return to the capillaries
Clinical Findings
Accumulations of oedematous transudate in subcutaneous tissues are referred to as
anasarca, in the peritoneal cavity as ascites, in the pleural cavities as hydrothorax
and in the pericardial sac as hydropericardium. Anasarca in large animals is usually
confined to the ventral wall of the abdomen and thorax, the brisket and, if the
animal is grazing, the intermandibular space. Intermandibular oedema may be less
evident in animals which do not have to lower their heads to graze. Oedema of the
limbs is uncommon in cattle, sheep and pigs but occurs in horses quite commonly
when the venous return is obstructed or there is a lack of muscular movement.
Oedematous swellings are soft, painless and pit on pressure. In ascites there is
distension of the abdomen and the fluid can be detected by a fluid thrill on tactile
percussion, fluid sounds on succussion and by paracentesis. A level top line of fluid
may be detectable by any of these means.
In the pleural cavities and pericardial sac the clinical signs produced by the fluid
accumulation include restriction of cardiac movements, embarrassment of respiration and
collapse of the ventral parts of the lungs. The heart sounds and respiratory sounds are
muffled and the presence of fluid may be ascertained by percussion, succussion and
paracentesis.
Clinical Pathology
Examination of a sample of fluid reveals an absence of signs of inflammation. In some
instances the transudate is free of protein but in advanced cases much protein may be
present because of the capillary damage which has occurred. The fluid may clot, have a high
specific gravity and even contain free blood, particularly if the oedema is caused by
increased hydrostatic pressure.
Necropsy Findings
The cause of the accumulation of fluid is obvious in many cases but estimations of the
concentration of protein in the plasma may be necessary if hypoproteinaemia is thought to
be the cause. If the primary cause is endothelial damage this will probably be detectable
only on histological examination.
Diagnosis
Differentiation of the specific causes of oedema listed in aetiology above depends upon
identification of the primary disease. Subcutaneous and peritoneal accumulations of urine
occur when the urethra or bladder ruptures after urethral obstruction by calculi. Peritonitis,
pleurisy and pericarditis are also characterized by local accumulations of fluid but toxaemia
and other signs of inflammation are usually present.
Treatment
The treatment of oedema should be aimed at correcting the primary disease. Myocardial
asthenia should be relieved by the use of digitalis, pericarditis by drainage of the sac, and
hypoproteinaemia by the administration of plasma or plasma substitutes and the feeding of
high quality protein. Ancillary measures include restriction of water intake and the amount
of salt in the diet, the use of diuretics and aspiration of fluid. Diuretics
Diseases Characterized by Abnormalities of the Cellular
Elements of the Blood
ANAEMIA
Anaemia is defined as a deficiency of erythrocytes, or haemoglobin, per unit volume of
blood. It is manifested by pallor of the mucosae, an increase in the rate and force of the
heart beat and by muscle weakness. Dyspnoea at rest is not a common sign, a feature which
helps to distinguish it from uncompensated heart failure.
Aetiology
Anaemia may be caused by excessive loss of blood by haemorrhage, or by increased
destruction or the inefficient production of erythrocytes. Anaemias are therefore
usually classified as haemorrhagic or haemolytic anaemia, or anaemia due to
decreased production of erythrocytes.
Haemorrhagic anaemia may occur after acute haemorrhage or with chronic blood
loss as it occurs in parasitism, particularly haemonchosis in ruminants (1) and
strongylosis in horses (2). The cause is unknown and the disease closely resembles
sweet clover poisoning of newborn calves.
Haemolytic anaemia is a manifestation of many infectious and non-infectious
diseases. Protozoan diseases in which haemolytic anaemia occurs include babesiasis
which occurs in all species, anaplasmosis of ruminants and eperythrozoonosis of
swine and ruminants. In cattle other common causes are leptospirosis, bacillary
haemoglobinuria, poisoning by onions or by rape and other cruciferous plants and
postparturient haemoglobinuria. Calves which drink large quantities of cold water
may also suffer an acute haemolytic episode and this may also occur as part of a
transfusion reaction. In horses equine infectious anaemia, phenothiazine poisoning
and iso-immunization haemolytic anaemia of foals are the common causes. Although
uncommon, haemolytic disease of the newborn occurs also in pigs and cattle.
Chronic copper poisoning in sheep causes severe haemolytic anaemia and is a major
factor in the production of the clinical signs of toxaemic jaundice in this species. The
same effect may be produced in cattle.
Anaemia due to decreased production of erythrocytes or haemoglobin. These
comprise the bulk of the naturally occurring anaemias of animals and are due in
most cases to nutritional deficiency, although toxic depression of the erythropoietic
activity of bone marrow may also be a cause. Nutritional deficiencies of cobalt and
copper cause anaemia in ruminants and although these elements are probably
necessary for erythropoiesis in other species, the requirement of them does not
seem to be so great and clinical anaemia does not occur under natural conditions. A
deficiency of iron in the diet causes anaemia in piglets but under natural conditions
does not appear to be of major importance in the other species.
Pathogenesis
Irrespective of the cause of anaemia the primary abnormality of function is the
anaemic anoxia which follows. In acute haemorrhagic anaemia there is in addition a
loss of circulating blood volume and plasma proteins. The fluid loss is quickly
repaired by equilibration with tissue fluids and by absorption and, provided
haemorrhage does not continue, the plasma proteins are quickly restored to normal
by synthesis in the liver. However erythropoiesis requires a longer time interval to
alleviate the anaemia. Haemolytic anaemia is often sufficiently severe to cause
haemoglobinuria and may result in haemoglobinuric nephrosis and depression of
renal function.
The primary responses to tissue anoxia caused by anaemia are an increase in cardiac
output due to increases in stroke volume and heart rate, and a decrease in
circulation time.
Clinical Findings
Pallor of the mucosae is the outstanding clinical sign but appreciable degrees of
anaemia can occur without clinically visible change in mucosal or skin colour. These
degrees of anaemia are usually not sufficient to cause signs of illness but they may
interfere with performance, particularly in racehorses, and this aspect of equine
medicine has come into prominence in recent years (5). Many horses suffer from
moderate anaemia, due probably in most cases to strongylosis, and respond
spectacularly to treatment with haematinic drugs.
In clinical cases of anaemia there are signs of pallor, muscular weakness, depression
and anorexia. The heart rate is increased, the pulse has a large amplitude and the
absolute intensity of the heart sounds is markedly increased. Terminally the
moderate tachycardia of the compensatory phase is replaced by a severe
tachycardia, a decrease in the intensity of the heart sounds .and a weak pulse. The
initial increase in intensity of heart sounds is caused by cardiac dilatation and an
increase in blood pressure.
Clinical Pathology
Clinical signs do not appear until the haemoglobin level of the blood falls below
about 50 per cent of normal. The erythrocyte count and the haematocrit are usually
depressed. In haemorrhagic and haemolytic anaemias there is an increase in the
number of immature red cells in the blood. The characteristic finding in anaemia
caused by a deficiency of iron is hypochromasia caused by a reduction in mean
corpuscular haemoglobin concentration; the haemoglobin level is low but the
erythrocyte count may be normal.
Necropsy Findings
Necropsy findings include those specific to the primary cause. Findings indicative of
anaemia include pallor of tissues, thin, watery blood and contraction of the spleen.
Centrilobular hepatic necrosis is commonly present in cattle, and probably in other
animals, if the anaemia has existed for some time (9).
Diagnosis
A diagnosis of anaemia is usually suggested by the obvious clinical signs. Differentiation
between haemorrhagic and haemolytic anaemias and those caused by deficient production
of erythrocytes or haemoglobin depends upon the history of haemorrhage,
haemoglobinuria, jaundice, or diet, and upon clinical evidence of these signs.
Treatment
Treatment of the primary cause of the anaemia is essential. Non-specific treatment includes
blood transfusion in acute haemorrhage and even in chronic anaemia of severe degree.
Haematinic preparations are used in less severe cases and as supportive treatment after
transfusion. Iron administered by mouth or parenterally is in common use. Preparations
injected intravenously give a rapid response and intramuscular injections of organic-iron
preparations give less rapid but more prolonged results. Vitamin B12 is widely used as a non-
specific haematinic, particularly in horses. In extreme cases of anaemia irreversible changes
caused by anoxia of kidneys and heart muscle may prevent complete recovery in spite of
adequate treatment.
LEUKAEMIA
Leukaemia is manifested by abnormal proliferation of myelogenous or lymphatic tissues
causing a marked increase in the number of circulating leucocytes. The disease is probably
neoplastic in origin and is usually accompanied by enlargement of the spleen, lymph nodes
and bone marrow, singly or in combination. There is sufficient evidence that some
leukaemias are transmissible by means of viruses to suggest that some of those which occur
commonly in livestock have a similar cause. There is as yet no concrete evidence that this is
so.
In leukaemic leukaemia immature leucocytes appear in the blood, in aleukaemic leukaemia
the total leucocyte count may or may not be increased. In leukaemia the differential
leucocyte count may be distorted, a preponderance of immature granulocytes occurring in
myelogenous leukaemia and a relative increase in lymphocytes occurring in lymphatic
leukaemia. There may be an accompanying aplastic anaemia if erythropoiesis is depressed
by expansion of myeloid tissue in the bone marrow—a myelophthisic anaemia. Examination
of smears of bone marrow has become commonplace in cases of leukaemia in large animals.
Samples of bone marrow contents are easily obtained from the sternum of animals in the
standing position. In the horse specimens can be readily obtained from the ilium, entrance
being made through the tuber coxae (1). Bone marrow biopsy techniques have also been
described for cows (3, 4) and goats (5).
In farm animals the only common form of leukaemia is lymphomatosis. Myelogenous
leukaemia is rare but has been recorded in all species. Erythroblastic and plasma cell
tumours and monocytic leukaemia are still less frequent. Information on haemopoietic
tissue tumours has been reviewed recently (2) and is not recapitulated here. When the
leukaemia is leukaemic there is usually no difficulty in making a diagnosis because of the
very high total white cell count, the distortion of the differential count, and the presence of
immature cells. Most cases of Jymphomatosis in farm animals are subleukaemic, at least
when the disease is clinically recognizable, and the differentiation from lymphadenitis may
be difficult. In lymphadenitis enlargement of the nodes usually occurs rapidly and asymmetrically and the ‘enlargement may
fluctuate or completely regress.
The leucocytosis associated with local or generalized infections is usually less severe in
degree than that of leukaemic leukaemia and the distortion of the differential count is not so
marked, following a standard pattern. There is a neutrophilia with a relative increase in band
forms in acute generalized or local inflammatory processes, and a lymphocytosis or
monocytosis in chronic suppurative infections.
LEUCOPENIA
Leucopenia does not occur as a specific disease entity but is a common manifestation of a
number of diseases. Virus diseases, particularly hog cholera, are frequently accompanied by
a panleucopenia in the early acute stages. Leucopenia has also been observed in
leptospirosis in cattle although bacterial infections are usually accompanied by a
leucocytosis.
Acute local inflammations may cause a transient fall in the leucocyte count because of
withdrawal of the circulating cells to the septic focus.
Leucopenia may also occur as part of a pancytopenia in which all cellular elements of the
blood are depressed. Agents which depress the activity of the bone marrow, spleen and
lymph nodes and result in pancytopenia occur in trichloroethyleneextracted soya bean meal
and bracken fern. Pancytopenia occurs also in radiation disease. Chronic arsenical poisoning,
and poisoning by sulphonamides, chlorpromazine and chloramphenicol cause similar blood
dyscrasias in man but do not appear to have this effect in animals.
The importance of leucopenia is that it reduces the resistance of the animal to bacterial
infection and may be followed by a highly fatal, fulminating septicaemia. Treatment of the
condition should include the administration of broad spectrum antibiotics to prevent
bacterial invasion. Drugs, including pentnucleotide, which have been used to stimulate
leucopoietic activity, have not been shown to materially affect most leucopenias.
Diseases of the spleen and lymph nodes
- Splenomegaly
- Splenic Abscess
- Elargement OF THE LYMPH NODES