Download changes in blood

Chemical changes in blood
1) Dehydration
2) ACID BASE BALANCE DISEASES
- Alkalosis
- Acidosis
3) DISEASES OF BLOOD AND BLOOD-FORMATION ORGANS
- Haemorrhage
- Oedema
- Shock
4) DISEASES CHARACTERIZED BY ABNORMALITIES OF THE CELLULAR
ELEMENTS OF THE BLOOD
- Anemia
- Leukemia
- Leucopenia
5)DISEASES OF THE SPLEEN AND LYMPH NODES
- Splenomegaly
- Splenic Abscess
- Elargement Of The Lymph Nodes
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Dehydration:
It is disturbance of body water balance in which more fluid is lost from the body than is
absorbed results in reduction in circulating volume of the blood and in dehydration of tissues.
Etiology of dehydration:
1) Failure of water intake
- Deprivation of water, toxemia, and esophageal obstruction.
2) Excessive fluid loss
- Diarrhea is the most common reason, Vomiting, polyuria and loss of fluid from extensive skin,
Severe dehydration also occurs in acute carbohydrate and acute intestinal and abomasums.
Pathogenesis of dehydration:
Two factors are involved in the pathogenesis of dehydration:
1- Reduction of tissue fluid levels with resulting interference in tissue metabolism
2- Reduction in the fluid content of the blood.
- The initial response to negative water balance is the withdrawal of fluid from the tissues and
the maintenance of normal blood volume, From the intracellular and interstitial fluid spaces.
Essential organs including the central nervous system, heart and skeleton contribute little and
the major loss occurs from connective tissue, muscle and skin.
- The secondary response to continued negative water balance is a reduction in the fluid
content of the blood causing a reduction in circulating blood volume (volume depletion) and an
increase in the concentration of the blood (hemoconcentration).
Effects of dehydration on the body:
- Dehydration exerts some important effects on tissue metabolism. There is an increase in
breakdown of fat, then carbohydrate and finally protein, to produce water of metabolism.
- Urine formation decreases because of the restriction of blood flow and this, together with
the increased endogenous metabolism, causes a moderate increase in blood levels of nonprotein nitrogen.
- The body temperature may increase slightly initially in dehydration. Hyperthermia results
from insufficient fluid to maintain the loss of heat by evaporation.
- The death; especially in acute intestinal obstruction, vomiting and diarrhea.
Types of dehydration:
1)Hypotonic dehydration - Hyponatremia - ( Hyposmotic dehydration)2
- Sodium is the most abundant ion in the extracellular fluid and is chiefly responsible for
maintenance of the osmotic pressure of the ECF.
- The most common cause of hyponatremia is increased loss of sodium through the intestinal
tract in enteropathies, this is marked in cases of acute diarrhea and infection with
Enterotoxigenic E. coli which also cause diarrhea.
2)Hypertonic dehydration (True dehydration) (Hyperosmotic dehydration)- Desiccation
(drought).
Hypertonic dehydration Caused by Simple deprivation of water or water deficit due to
decreased intake, diabetes insipidus, diabetes mellitus, fever and through excessive
evaporation of the sweat from the skin.
3)Isotonic dehydration ( Isosmotic dehydration).
Isotonic dehydration occurs when there is a parallel loss or deprivation of water with losses or
deprivation of sodium. It is uncommon, can occur in animals which are unable to consume
water because of an esophageal obstruction and Losses of isotonic fluid.
Diagram compares between the different types of dehydration
Clinical findings of Dehydration: main points:
1. The dryness and wrinkling of the skin giving the body and face a shrunken appearance.
2. The eyes recede into the sockets and the skin subsides slowly after being picked up into a fold.
3. The elasticity of the skin of the upper eyelid and of the neck is one of the best indicators of the
degree of dehydration which on a clinical basis is commonly assessed as a percentage of body
weight.
4. The dehydration is usually much more marked if water and electrolyte losses have been
occurring over a period of several days.
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5. Peracute and acute losses may not be obvious clinically because major loss will have occurred
from the intravascular compartment and only minor shifts have occurred from the interstitial
spaces.
6. Sunken eyes and inelastic skin are not remarkable clinical findings of dehydration in horse. Loss
of body weight occurs rapidly in dehydration and muscular weakness and in appetence or
anorexia is common.
7. The degree of thirst present will depend on the presence or absence of other diseases causing
an inflammatory response or endotoxemia.
Clinical laboratory assessment of dehydration:
Dehydration is usually obvious clinically
Laboratory indices:
1- Packed cell volume (PCV) and total serum solids
Dehydration is characterized by an increase in the PCV and total serum solids. will indicate the
severity of water loss and improve the assessment of dehydration state. Anemic animals and
those affected with diseases causing hypoproteinemia may provide misleading value. The
range depends on the age and species of animal, pervious excitement and the presence of
anemia or hypoproteinemia.
-
-
Packed cell volume:
The normal range of PCV between 30-40% is considered normal. 50-60% fluids are necessary
for recovery. Above 60% intensive fluid therapy is necessary and the prognosis is unfavorable.
Total serum solids:
A total serum solid of 6-7.5 g/dL is usually considered normal.
Between 8-10 g/dL fluids are needed and the prognosis is favorable.
Above 12 g/dL the prognosis is unfavorable.
2- Serum electrolyte concentrations
The balance between sodium , potassium and chloride.
ACID BASE BALANCE
Physiology of Acid-Base Balance
Regulation of acid-base balance is closely linked to fluid and electrolyte balance.
Thus, fluid and electrolyte imbalances are often related to acid-base alterations and vice versa.
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Definition of pH
- The hydrogen ion concentration of the ECF is maintained within narrow limits and is normally about 40 nmol/liter. This is 40 x 10-6 mmol/liter or roughly one-millionth the
concentration of the other common electrolytes.
- The pH of a solution is equal to the negative logarithm of the hydrogen ion concentration:
pH = - log [H+]
- The pH varies inversely with hydrogen ion concentration. When hydrogen concentration
in the blood increases, pH decreases and the animal develops an acidosis. When the
hydrogen ion concentration in the blood decreases, the pH rises and the animal develops
an alkalosis.
Acidosis
Metabolic acidosis can be produced by the addition of hydrogen ions or a loss of bicarbonate
ions.
1- Metabolic acidosis
The body has accumulated too much acid and does not have enough bicarbonate toeffectively
neutralize the effects of the acid.
Causes of Metabolic Acidosis:
The most common causes of metabolic acidosis include Lactic acidosis, ketoacidosis,
Gastrointestinal losses (diarrhea), Renal failure , ingestion of certain drugs or toxic compounds.
2- Respiratory Acidosis
A respiratory acidosis is characterized by a decrease in pH and an increase in pCO 2
Causes of Respiratory Acidosis:
Any disorder that interferes with normal effective ventilation , acute upper respiratory
obstruction, pneumonia, and chronic obstructive lung disease, veterinary medicine closed
anesthesia system.
Under these conditions ventilation may be seriously reduced without producing hypoxia. The
high oxygen content of the gas mixture maintains high pO2 in the blood but depression of the
respiratory center may result in insufficient alveolar ventilation so that CO2 accumulates
Alkalosis
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1- Metabolic alkalosis
-
Metabolic alkalosis is characterized by an increase in pH and bicarbonate.
Metabolic alkalosis occurs with some frequency in domestic animals and is commonly seen in
association with digestive disturbances in ruminants.
Causes of Metabolic alkalosis
The most common causes of increased hydrogen loss are gastrointestinal losses due to
vomiting in small animals.Sequestration of fluid in the abomasums, Low chloride intake,
Excessive bicarbonate administration.
2- Respiratory alkalosis
Causes of Respiratory alkalosis
Respiratory alkalosis is due to hyperventilation which may be stimulated by hypoxemia
associated with pulmonary disease, congestive heart failure, or severe anemia.
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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
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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
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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
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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.
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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
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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
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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
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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
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