general systemic states.ppt

There are several general systemic states
which contribute to the effect of many
diseases. toxemia, hyperthermia, fever and
septicemia are closely related in their
effects on the body.

I-TOXEMIA
Definition:
Toxemia means the presence of toxins,
deriving from bacteria or produced by body
cells, in the blood stream.
N.B.:
It does not include the diseases caused by
toxic substances produced by plants, or
insects or ingested organic or inorganic
poisons

Etiology:
Toxemia caused by 2 types of toxins:
1. Antigenic toxins: Which act as antigens (Ag) and
stimulate the development of antibodies (Ab), and
produced by bacteria and helminth parasites.
Antigenic toxins are divided into:
a. Exotoxins: Which are protein substances diffuse
into the surrounding medium produced by bacteria
such as clostridium spp. which causing: botulism –
black leg – black disease – enterotoxemia in calves
and lambs.
b- Endotoxins: These are lipopolysaccharides found in
the cell wall of the bacteria and find their way into
the medium or systemic circulation only in case of
breakdown of the bacterial wall. Liberation of the
toxins occur and not absorbed through the intestinal
mucosa except in case of damage as in : -enteritis –
acute intestinal obstruction.

In this case, the toxins absorbed and enter the
circulation causing systemic intoxication. Small
amount of endotoxins can be detoxified in the
liver. In cases of reduction of hepatic efficiency
or if the amount to toxins is large, endotoxemia
is produced.
Endotoxins may also be absorbed in large
amounts from sites other than intestine in cases
of: Mastitis. - Peritonitis. -Abscesses. - Large
areas of burns.
Examples of bacteria producing
endotoxins:
E. coli - Salmonella spp. - Corynebacterium spp.

2. Metabolic toxins:
These toxins are produced by body metabolism or by abnormal
metabolism.
a. In case of body metabolism: Normally, toxic products
produced in the alimentary tract or tissues are either:
Excreted in urine or feces or detoxified in the plasma and liver.
In obstruction of the lower alimentary tract, there may be
increased absorption of toxic phenols, cresols and amines,
which normally excreted with the feces, resulting in
autointoxication. Also, in hepatic dysfunction, the toxins
which normally detoxified in the liver, accumulate beyond a
critical point causing the appearance of toxemia syndrome.
b. In abnormal metabolism:
Toxins such as histamine and histamine-like substances are
produced in cases of:
• Ketonemia (due to defect in fat metabolism).
• Lacticacidemia (caused by acute ruminal impaction).

Etiology of toxemia can be summarized as follow:
Causes of toxemia
Toxins
Metabolic T
Antigenic T
Abnormal
metabolism
Histamine
Histamine-like subst.
* Produced in
ketonemia or
lacticacidemia
Body metabolism
Toxicphenols
Cresols
Toxic amines.
Excreted in feces or
urine or detoxified
by plasma and liver.
Intestinal obstructino
or hepatic
dysfunction causes
Autointoxication
Endotoxins
(lipopolysaccharides)
Produced by:
E. coli
Salmonella spp.
Corynebact. Spp.
Absorbed in:
Enteritis.
Intestinal obst.
Mastitis.
Peritonitis
Burns
Abscesses
Exotoxins
(protein substancs)
Produced by
clostridium spp.
Which causing:
Black leg
Black disease
Botulism
Enterotoxemia

Pathogenesis:
Toxemia affects carbohydrate, protein and also
mineral metabolism. It also has an effect on
tissues and body systems.
1.Carbohydrate metabolism:
• Fall in blood sugar.
• Disappearance of liver glycogen.
• Decreased glucose tolerance of tissue.
• Increased blood pyruvate and lactate levels.
Resulting in mental depression and poor survival.
2. Protein metabolism:
• Increased tissue breakdown.
• Increased blood non-protein nitrogen level.
• Increased total serum protein.
• Decreased albumins.
• Increased globulins.

3. Mineral metabolism:
Decreased in serum iron level.
Decreased in serum Zn level
Increased in blood Cu level.
Resulting in negative mineral balance
4- Effects on tissues: Toxemia causing damage of the
parenchyma of some organs or endocrine glands in
the body such as:
Liver.
- Anterior pituitary gland.
Kidney.
- Adrenal gland.
5- Effects on body systems:
Interference with tissue enzyme systems due
to the effect of hypoglycemia with high blood lactate
leading to:
a-Myocardial weakness.
b- Capillary wall damage.
c-Falling in blood pressure.

•Oral mucosa: darker in color.
•Liver: decrease in function.
•Kidney: damage of renal tubules and glomeruli
leading to rise in blood urea nitrogen and
albuminuria.
•Alimentary tract: reduction in tone and motility.
•Skeletal muscles: reduction in tone.
All previous effects resulting in:
a-Failure in appetite.
b- Impaired digestion.
c- Constipation.
d-Dullness.
e- Depression.
f- Coma.

Clinical findings:
The clinical signs depends mainly upon the speed
and the severity of the toxic processes.
1.Depression.
2.Lethargy.
3.Separation from the group.
4.Anorexia.
5.Failure to grow or produce.
6.Emaciation.
7.Constipation.
8.Weak pulse (but rapid and regular)
9.Albuminuria.

10. Increased heart rate with reduction in sound.
11. Bacterial toxins associated with fever.
12. Terminally, muscular weakness, collapse, coma
or convulsion, death.
13. Toxic shock:
which caused by E. coli and occurs due to the rapid
toxin formation with high toxicity to the degree of
causing cardiovascular signs such as:
Severe peripheral vasodialation.
- Fall in blood
pressure.
-Pale mucous membranes.
-Tachycardia.
-Hypothermia.
-Weak pulse.
-Muscle weakness.

Clinical pathology: Depends mainly on the
changes in blood and urine and also on
the isolation and identification of specific
toxins:
•Low blood sugar.
•High total serum protein.
•High level of serum albumin.
•High level of serum non protein nitrogen.
•Albuminuria.

Necropsy findings: Which mainly applied
by microscopical examination.
Degeneration of the parenchyma of the
liver and kidney (glomeruli and tubules)
and the myocardium.
Degeneration and necrosis in the adrenal
glands.
Diagnosis:
Mainly depends on laboratory
examination. Toxemia should be
differentiated from metal poisoning (e.g.
Arsenic poisoning) by the examination of
the outer environment for the source of
poison (food, gut content and tissues).

Treatment:
1.Removal of the origin of the toxin.
2.Give specific antitoxins with supportive treatment.
3.Intensive fluid and electrolyte therapy
intravenously until the animal begins to eat and
drink.
4.Parenteral nutrition may be indicated in cases of
impaired appetite and digestion (glucose, amino
acids and emulsions of fat with the fluid therapy).
5.Concentrated vitamin preparations which aid in
glucose utilization (vit. B complex group).
e.g.: Tri B (B1, B6 and B12)
(2-3 amp. In cattle , 1-2 amp.. in sheep) I.M injection.

6. In toxic shock, glucocorticoids given in large
doses intravenously. e.g. : Dexamethazone 1 mg/kg
B.W./12h.
7. Non-steroidal anti-inflammatory drugs (NSAIDs)
which have adreno-corticoid-like activity. (e.g.:
phenylbutazone). 15 mg/kg B.W. (initial dose), then
followed by (10 mg/kg B.W. at 6-12h).
8.Antibiotic therapy:
e.g.: (a) Ampiciillin 1-2 gm I.M. in cattle.
(b) Chloramphinicol 3-4 vial I.M in large animals,
one vial in small animals.
9- Sulfamethazine 33 1/3%. 0.2 gm/kg B.W.. I.V.
10- In non-specific toxemia, preparations containing
sodium thiosulphate and methylene blue are in
general use in veterinary practice.
N.B. If the endotoxin is likely to originate in the
intestine, the medication should be administered
orally.

II-HYPERTHERMIA, HYPOTHERMIA &
FEVER
Hyperthermia, hypothermia & fever are
symptoms complexes characterized by
significant changes in body temperature.
Body temperature:
It is a reflection of the balance between
heat gain and heat loss, which regulated
by the heat-regulating functions of the
hypothalamus.
Sources of heat gain:
High environmental temperature.
Muscular movement.
Metabolic activity.

Methods of heat loss:
1. Convection.
2- Conduction.
3- Radiation.
4- Evaporation of moisture.
Evaporation of moisture include:
1. Exaggerated respiration.
2- Salivation.
3- Sweating (especially in horses).

A-HYPERTHERMIA (HEAT STROKE)
Def.:
It is the elevation of body temperature due to
excessive heat production or absorption, or to
deficient heat loss when the causes of these
abnormalities are purely physical.
Etiology:
1.High environmental temperature.
2.Muscular excretion of prolonged and severe
character (with high humidity, heavy hair coat
and inadequate ventillation).
3.Neurogenic hyperthermia due to damage of the
hypothalamus.
4.Dehydration (insufficient T. fluids to compensate
heat loss by evaporation).
5.Excessive muscular activity as in strychnine
poisoning.
6.Poisoning including dinitrophenols.

High environmental temperature:
The tolerance between the animals to high
environmental temperature, exposure to
sunlight and exercise is depends upon:
1. Breads of the animals:
Water buffaloe is less tolerant than shorthorn
steers due to capacity to increase skin
evaporation under heat stress.
2. Lactation:
Lactating cows have a greater responses in
rectal temperature, heart and respiratory rates
when the environmental temperature is raised.
3. Rest and hydration:
Rested, hydrated horses are well able to
maintain body temperature in the hottest
environmental conditions

Pathogenesis:
* When the body temperature reaches a critical
point:
1.A short period of hyperthermia occurs with
activation of immune body production and
phagocytosis, also with impairment of the activity
of most invading organisms.
2.Metabolic rate increased (40-50%).
3.Depletion of liver glycogen.
4.Protein metabolism is increased causing extra-
energy.
5.Anorexia (due to dryness of the mouth).
6.Loss of body weight.

7. Lack of muscle tone leading to hypoglycemia and
uremia.
8.Increased thirst.
9.Increase in heart rate due to:
a. Directly: due to the rise in blood temperature.
b. Indirectly: due to decrease in blood pressure
resulting from peripheral vasodilatation.
10.Respiration increases in rate and depth.
12.Urine secretion is decreased due to the reduction
of the renal blood flow due to vasodialatation.

* When the critical temperature is exceeded:
Depression of both nervous and respiratory activities
which may leading to death due to respiratory
failure.
Circulatory failure due to myocardial weakness, the
heart rate becoming fast and irregular.
* If the period of hyperthermia is prolonged:
Extensive degenerative changes in most body tissues
occur due to increased endogenous metabolism.

Clinical findings:
1.An elevation of body temperature (exceeds
39.5°C).
2.Initially, sweating and salivation, followed by an
absence of sweating.
3.An increase in both heart and respiratory rates,
with a weak pulse.
4.Increased thirst which make the animal go to the
cool places, lying in water.
5.Restlessness, dullness, walking in unsteady
manner ends by lie down.
* When the body temperature reaches 41°C:
1.Respiration is labored.
2.General distress.
3.Respiration becomes shallow and irregular.
4.Rapid and weak pulse.
5.Collapse, convulsions and terminal coma.

* When the body temperature reaches 41.5-42.5°C:
Death occurs in most species.
N.B. Abortion may occur with high incidence of
embryonic mortality in prolonged hyperthermia
especially in sheep (3-6 week pregnancy).
P.M:
1.Peripheral vasodilatation.
2.Slowing in blood clotting.
3.Rapid putrifaction and rigor mortis.

Diagnosis:
It should be differentiated from:
1.Septicemia which characterized by: petechial
hemorrhages in the mucosae and skin with positive
reactions in bacterial blood culture.
2.Fever : temperature exceeds 40°C.
N.B. : In hyperthermia we should examine the
environment to know the causative factor.

Treatment:
1.Intravenous administration of fluids. e.g. : normal
saline or 5% dextrose.
2.Cold applications either by spraying, immersion,
cold packs or rectal enema.
3.Supportive treatment (glucose & protein).
4.Adequate drinking water.
5.Shelter alone is a most important factor.
6.Antipyritics, such as: Novalgin - Pyralgin -
Analgin

B-FEVER:
Def.:
Fever is the symptom complex in which hyperthermia
and toxemia are produced by substances
circulating in blood stream.
Etiology: Fever may be:
a. Septic (specific).
b. Aseptic (non specific).
I-Aseptic causes: (most common)
1. Bacteria.
2- Viruses.
4- Protozoa.
3- Fungi.
The infective process may be:
Localized: abscess or empyemia.
Generalized: bacteremia or septicemia.

II- septic causes:
1.Chemicals: foreign protein by injection, or
Intake of nitrophenols.
2.Surgical: due to breakdown of tissues and
blood.
3.Necrotic:
• Breakdown of muscles due to injection of
necrotizing agent.
• Severe intravascular hemolysis.
• Extensive infarction.
• Extensive necrosis in rapidly growing
neoplasms: (necrosis of tissues).
4. Ag-Ab reactions.

Pathogenesis:
A- In bacterial fever:
Bacteria produces endotoxins (exogenous
pyrogens) which are fever-producing
substances (within one hour) by causing the
release of endopyrogen from the leukocytes
(granulocytes, monocytes and macrophages). It
is thought that pyrogens act directly on the
hypothalamic temperature control center.
B- In other specific and non specific fever:
Agents capable of giving rise to fever are also
able to produce an exogenous-pyrogen-like
substances which causing the release of
endopyrogen from the granulocytes.

Stages of fever:
The reactions that occur as body temperature
is increased during fever usually consists of 3
stages:
1-Period of onset (or chill): which is manifested
by:
(a). Cutaneous vasoconstriction resulted in
coldness and dryness of the skin with absence
of sweating.
(b). Respiration is reduced.
(c). Muscular shivering.
(d). Urine formation is minimal.
(e). Elevated rectal temperature.
Increased pulse rate.

2-The period of maximum temperature
(fastigium):
• Constant body temperature.
• Shivering ceases.
• Ruminal motility decreased.
• Metabolism is increased.
3- The stage of decrement: (It occurs after
removal of the effect of pyrogenic substances).
1.Vasodilatation.
2.Sweating.
3.Muscle flaccidity.

N.B.: The body temperature falls by one of the
following manners:
1.A crisis: rapid reduction of fever (few hours).
2.A lysis: slow reduction of fever.
3.Collapse: falling in body temperature
accompanied by signs of approaching death
(cardiac failure).
In both crisis and lysis, the fall in temperature is
roughly paralleled by that of the pulse rate

Clinical findings:
The effects of fever are the combined effects of
toxemia and hyperthermia:
1. Systemic reaction which includes:
• Elevation of body temperature.
• Increase in pulse rate but weak.
• Increase respiratory rate.
2. Wasting.
3- Oligurea with albuminurea.
4. Increased thirst.
5- Anorexia.
6- Constipation.
7- Depression.
8- Muscle weakness.

Classification of fever:
1. According to the severity:
1.Mild (1°C above normal).
2.Moderate (pyrexia) 1.7-2.2°C.
3.Severe (hyperpyrexia) 2.8-3.3°C.
2. According to the course:
1.Simple fever: Temperature rises, remains high with
variations of less than 1°C for several days and
then falls as the animal recovers or collapses prior
to death.
2.Continuous fever: temperature remains high for a
longer period than in the simple fever.

3. Remittent fever: temperature rises and
falls by more than 1°C at short and
irregular intervals.
Intermittent fever: short attacks of fever
lasting for 2-3 days with non-febrile
intervals between them (usually
regular).
4. Recurrent fever: prolonged attacks of
fever with non-febrile periods of about
similar durations.
5. Atypical fever: it runs an irregular
course in many febrile diseases: e.g.
strangles and canine distemper.

Necropsy findings:
The findings are a combination of those
of hyperthermia and those of toxemia.
1. Hyperthermia: Vasodilatation – rapid
onset of rigormortis and putrifaction.
2. Toxemia: degeneration in
parenchymatous organs.

Diagnosis:
Fever should be differentiated from:
1.Hyperthermia: (no toxemia).
2.Septicemia: (infection in the blood stream).
The infectious fever characterized by:
• Sudden onset.
• High fever (39.5-41°C).
• Anorexia.
• Dullness, depression, unable to move.
• Splenomegaly.
• Isolation of pathogen from blood or excreta.
• Marked changes in total and differential
leukocytic counts.

Treatment:
It includes the treatment of toxemia and hyperthermia:
1.Remove the source of toxin by controlling the
infections by using antibacterial drugs, antibodies
or antitoxins.
2.Remove the necrotic material in aseptic fevers and
local infections.
3.Give anti-inflammatory drugs and antibiotics such
as adrinocortical hormones to facilitate repair
processes and alleviate inflammation, with great
caution & supported by large dose of broad-
spectrum antibiotics (because of the depression of
resistance to infection).
e.g.:
dexamethasone (1 mg/kg b.w. I.V every 24 h).

4.To avoid the previous side effects we can
use Non-Steroidal Anti-Inflammatory Drugs
(N.S.A.I.D), with anti-prostaglandins
(salycylates and phenylbutazon).
5.Diuretics: to remove transudates
(inflammatory fluids).
6.Glucocorticoids: e.g. : Betsolan soluble
(betamethasone) vials 20, 50 ml – Dose: 1-2
ml/100 lb B.W.. I.V with antibiotics.

C-HYPOTHERMIA
Def.:
Falling in body temperature due to excess heat loss
or insufficient heat production.
Causes:
1.Exposure to excessively cold air temperature and
the body can not able to prevent heat loss (by
increased metabolic activity, muscle tone and
peripheral vasoconstriction).
2.Decrease in muscle tone as in parturient paresis
(Hypocalcemia), acute ruminal impaction and
during anesthesia and sedation.
3.Peripheral vasodilatation in shock.

4. Reduction of metabolic activity in the terminal
stages of many diseases (pre-mortal fall in
temperature). It is a bad prognostic sign.
5.In sheep: post shearing mortality occurs due to
hypothermia especially it is proceeded by fall in
body weight.
N.B.
• Cattle and sheep during prolonged exposure to
cold environmental temperature, it needs more
diet to obtain the same amount of energy due
to the reduction in digestibility of diet.
• In calves: experimental exposure to severe
cold severely limits the intake of colostrum by
calves.

III-SEPTICEMIA / VIREMIA
Def. It is the disease state compounded of toxemia,
hyperthermia and the presence of large numbers
of infectious microorganisms (viruses, bacteria and
protozoa) in the blood stream.
Etiology:
1.Cattle, sheep and pigs:
• Pasteurella multocida.
• Pasteurella hemolytica.
• Pasteurella yersinia.
• Pseudotuberculosis.
2.Lambs:
• Histophilus ovis.
• Hemophilus agni.

3.Pigs:
• Hogcholera virus.
• Avian swine fever virus.
• Streptococcus zooepidemicus.
4.Horse, donkey and mules:
• Pasteurella haemolytica.
5- In all species:
• Anthrax
• Pasteurellosis.
• Salmonellosis.
• Rift valley fever.
• Leptospira interrogans.
• Neonatal septicemia.

Special septicemias:
It includes septicemia which resulting from:
1.Subacute radiation injury.: which leading to
death due to loss of leukocyte production from
injured bone marrow.
2.Congenital defect in the immune system.
3.Immuno-suppression in old animals due to:
• Corticosteroid therapy.
• Toxin.
• Infection (bovine viral diarrhea virus).

Pathogenesis: It includes two mechanisms
1.Production of toxins: By the infectious agents
(exotoxins or endotoxins) leading to toxemia and
fever due to the rapid multiply and spread to all
body tissues.
2.Localization of toxins: In many organs producing a
serious defects in animals (direct endothelial
damage and hemorrhages into tissues).
In viremia:
Virus

multiply

killed tissue cells

production of
toxins, from the killed cells.
N.B.
Viruses not produce toxins.
Vascular injury and partial rupture of the intema due
to the circulation of foreign materials.
Formation of platelet thrombi causing intravascular
coagulation (bacterial cell walls, Ag-Ab complexes,
endotoxins with platelets).
Hypocoagulation: due to the consumption of clotting

Clinical findings:
They are those of toxemia and
hyperthermia and include:
Fever.
Submucosal and subepidermal hemorrhages (usually
petechial or ecchymotic).
The hemorrhages are best seen under the vesible
mucous membranes (conjunctiva, oral mucosa and
valva).
Localizing signs may occur as the result of
localization of the infection in joints, heart valves,
meninges, eyes or other organs.

Clinical pathology:
Isolation of the causative agents from the blood
stream at the peak of the fever.
Presence of leukopenia or leukocytosis.
Falling in platelet counts and prothrombin and
fibrinogen values.
Post mortum: As in P.M of toxemia and hyperthermia
beside subserous and submucosal hemorrhages
with embolic foci of infection in various organs.

Diagnosis:
Only by the isolation of the causative agents
from the blood stream.
The presence of petechiae in mucosae and
conjunctivae may suggest septicemia.
High environmental temperature suggest
hyperthermia.
Treatment:
The same general recommendation for
treatment apply here as in fever.
I.V or parenteral treatment with antibacterial
drugs or sera and antitoxins.
Strict hygienic precautions to avoid spread of
diseases.

IV- DISTURBANCES OF APPETITE, FOOD
INTAKE AND NUTRITIONAL STATUS
I-POLYPHAGIA
Def.:
Polyphagia means increased food intake.
Causes:
Starvation.
Functional diarrhoea.
Internal parasitism.
Chronic gastritis.
Abnormalities of digestion due to pancreatic
deficiency.
Metabolic diseases which including diabetes
mellitus and hyperthyrodism in small species.

2-ANOPHAGIA (APHAGIA)
Def.:
Anophagia means decreased food intake.
Causes: Physical factors such as:
Painful conditions of the mouth (sharp teeth,
dental caries, stomatitis) and pharynx
(pharyngitis).
Lack of desire to food.
Decrease hunger contractions of the stomach
due to hyperthermia, toxemia and fever.
Deficiency of thiamin (in simple stomach
species) which causing atony of the gut.
Deficiency of cobalt in ruminants.
Heavy infestation with trichostrongylid
helminthes.
Alimentary tract stasis.
Some sensations, including severe pain,
excitement and fear.

Treatment:
Remove or treat the cause.
In cattle: intrarumenal administration of 10-20
liters of rumen juice (Fresh) from a normal cow
produce excellent results.
Strychnine (orally) or parasympathomimetic
drugs (by injection) for the stimulation of the
alimentary tract contraction.
Give the most palatable feed.
Fluid and electrolyte therapy orally or by
injection.
In severe cases: parenteral nutrition may be
indicated.

3- PICA (ALLOTRIOPHAGIA)
Def.:
Pica means the ingestion of materials
other than the normal food which varies from
licking to actual eating.
Causes:
dietary deficiency (salt, cobalt or phosphorus).
Chronic abdominal pain due to either peritonitis
or gastritis.
C.N.S. disturbances including rabies and
nervous acetonemia.

Types of pica:
Osteophagia: due to chewing bones.
Infantophagia: due to eating of young animals
especially in pigs.
Coprophagia: eating of feces.
Wool eating in sheep.
Salt hunger: licking coat, chewing leather, eating
earth (stones or sand) and drinking urine.
Cannibalism (biting) : in housed animals due to
protein, iron or bulk deficiency in the diet.
In pigs: bite one another's tail which controlled
by the following:
Removal of all tails during the first few days of life.
Using large pens or one pig in pen.
Removal of incisor teeth.
Avoidance of mixing animals of different sizes.

Serious consequences of pica:
Cannibalism leads to : Many deaths. - Lead
poisonings. - Botulism (dangerous form of food
poisoning).
Foreign bodies lodging in the alimentary tract.
Accumulation of wool, fiber or sand causing
obstruction of the alimentary tract.
Perforation of the oesophagus or stomach from
ingestion of sharp foreign bodies.
Grazing time is reduced, so, both the production
and reproduction efficiency is reduced.

4-STARVATION
Def.:
Complete deprivation of food causes rapid
depletion of glycogen stores and changeover in
metabolism to fat and protein.
Symptoms:
In early stages: hunger with increase in muscle
power and activity.
Loss of body weight.
In sheep: decrease in serum Ca levels leading to
clinical hypocalcemia.
Ketosis and acidosis due to increase in fat
utilization.
In mares: in late pregnancy highly fatal
hyperlipemia occurs.
In lactating cows: short period of starvation
depress glucose level and increases lipid
concentration in plasma, with drop in milk yield
by 70%.

5-INANITION (MALNUTRITION)
Def.:
Incomplete starvation which commonly occurs
in field conditions.
Causes: In sufficient diet in quantity (all essential
nutrients are present but in suboptimal amounts).
Clinical findings:
Ketosis.
2-Loss of body
weight.
3-Fall in metabolic rate leading to:
- Systemic reaction.
- Fall in body
temperature.
- Fall in resp. Rate.
- Fall in heart rate.
4-
Loss of muscular power.
5-Mental
depression.
6-
Increased susceptibility to infection.
7-
Increased susceptibility to some poisons (due to
the effect of starvation on hepatic function).
N.B.: in ruminants: The effects of starvation on the

Treatment:
Hygienic measures:
Affected animals must be brought indoors & kept
warm and well-bedded during treatment.
2- Medical treatment:
Nutritional fluid therapy (electrolyte solutions
containing glucose and amino acids).
Highly palatable digestible diet (high quality legume
hay, small amount of ground grain, daily
administration of multiple vitamin and mineral
mixture).
Young animals should receive skim-milk powder
(source of carbohydrate and protein).
Horses should receive green grass followed by good
quality hay (Alfalfa) with legume hay, or grains
mixed with molases.
In horses with broken jaws, should be prevented from
taking food per month and should be taken the

6-Thirst
Def.:
It is an increased desire for water
manifested by excessive water intake
(polydipsia).
Causes:
Dryness of the oral and pharyngeal mucosae
increases the desire for water.
Rising in blood osmotic pressure due to cellular
dehydration (due to vomiting, diarrhoea,
polyuria and excessive sweating.
In early fever due to changes in cell colloids
leading to increased water retention.
Salt deficiency in lactating cows leading to
polydipsia, polyuria with loss weight, decrease
in milk production and salt hunger (diagnosed
by determination of salivary sodium levels).
Clinical symptoms: It is not well defined.

On examination:
Hollow abdomen.
2-Sunken eyes.
3-Signs of dehydration.
4-Exitability.
5-Slight frothing at the mouth.
Stiff gait and incoordination, followed by
recumbency.
Abortion yielding decomposed calves, with dystokia.
P.M.:
Extensive liquifaction of the fat deposits +
dehydration.
The effect of experimental water deprivation on
some animals:
Camels: complete water deprivation can loss about
25% of its body weight and death occurred after 7-
9 days.
Lactating cows: When the animal receives only 50%
of their regular water supply, it becomes very
aggressive about water trough, spends more time
near it and lie down. After 4 days, milk yield

IV-DISTURBANCES IN BODY FLUIDS, BLOOD
ELECTROLYTES
AND ACID-BASE BALANCE
Body fluids consist of water and electrolytes.
Body fluids are divided between the intracellular and
the extracellular compartments. The intracellular
compartment contains about 2/3 of the body’s water
and the extracellular compartment about one-third.
Environmental stresses and diseases states
often increase losses, impair intake and otherwise
interfere with mechanisms that regulate body fluid
volume and composition.
The water constituents of the youngs are 75-
80% of the body weight whereas in adults are 60-
70%. The young animals are more likely to develop
fluid imbalances than the adults. This is because the
young has both a higher metabolic rate and a larger
surface area in relation to its body mass than the

Water requirements:
Approximately 100 ml of water/100 calories
metabolized.
A-Water gains:
The main source is that which is absorbed from the
gastrointestinal tract from:
a- Fluids.
b-
Ingested foods.
Water derived from cellular oxidation of feed stuffs.
B-Water losses:
Through the kidneys as urine.
Through the skin as sweat.
Through the lungs as water vapor.
Through gastrointestinal tract with feces.
There are many diseases of farm animals in which
there are disturbances of body fluids, electrolytes

I-DEHYDRATION
Definition:
Dehydration means a disturbance of
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.
Causes: There are two major causes of dehydration:
I- Decreased fluid intake.
II- Increased fluid losses.
I- Decreased fluid intake:
Deprivation of water.
2- Inability to express
thirst.
3-Impaired thirst mechanism.
4-Oral trauma or
inability to swallow.
5-With holding fluids for therapeutic purposes.
6-Obstruction of esophagous.
II-Increased fluid losses:

Pathogenesis:
The fluid is drained primarily from the intravascular
compartment and the interstitial fluid spaces
(major loss from C.T., M and skin) and little loss
from the essential organs such as C.N.S., heart and
skeleton. This loss leads to muscular weakness,
hypothermia and anorexia.
Reduction in the fluid content of the blood leading to
reduction in circulating blood volume (oligemia)
with increasing the concentration of the blood
(hemoconcentration) which leading to increasing
viscosity of the blood which impeded blood flow
ended by peripheral circulatory failure.
Compensatory reduction in fluid output occurs, the
kidneys decrease the urine flow, the intestines
reduced fecal output with increasing the
absorption of water (dry feces) and the skin
minimize the sweating.

Clinical findings:
The first and the most important sign in dehydration
is dryness and wrinkling of the skin, giving the
body and face shrunken appearance.
The eyeballs recede into the sockets (sunken eyes).
The skin subsides (returns) slowly after being picked
up into a fold, especially the skin of the upper
eyelids and of the neck and gives the best
indication of the degree of dehydration.

Peracute and acute losses not clinically detected
because major loss occurred from intravascular
compartment and minor loss from interstitial
spaces.
Loss of body weight.
Muscular weakness and fatigue.
Lack of appetite.
Thirst.
Urine excretion decreases and urine become more
concentrated.
Decreased plasma volume (increased serum
osmolality, increased PCV and increased BUN).
Decreased vascular volume indicated by
(Tachycardia, weak pulse, hypotension and shock).
In cattle on pasture with deprived water up to 9 days
and then given water

staggering, falling,
convulsion and sometimes death.
In dehydration secondary to enterities with severe

Diagnosis : depend on
Case history.
Clinical symptoms.
Laboratory examiantion:
Blood: increased PCV (40-60%).
Serum : increased serum urea nitrogen (more than
35% mg).
Increased total serum solids.
Imbalances of electrolytes.
Faeces: decrease moisture content.
Urine: decrease in volume, increase in concentration,
high in specific gravity.
Acid-base imbalance.

Treatment of dehydration:
The most important principles of fluid and
electrolyte therapy is to prevent or minimize
dehydration and electrolyte loss if possible by:
Give an adequate supply of water, adequate drinking
space with continuous salt supply with necessary
minerals.
Treat potential losses of fluids and electrolytes as
quickly as possible to minimize the degree of
dehydration and acid-base imbalance.

The major objectives in fluid and electrolyte therapy
are to:
Correct the abnormalities which occur (require 4-6
h.).
Provide maintenance therapy until the animal has
recovered (require 2-4 days).
The abnormalities which occur due to dehydration
are:
The volume of fluid lost.
Deficiency of the plasma osmolar.
Specific electrolyte imbalances.
Acid-base imbalance.

The amount of fluid required will depends on :
The degree of dehydration.
The amount of the continuous losses which
occurring during treatment.
The maintenance requirements of the animal during
treatment.
The fluids are usually given in 2 stages:
Hydration therapy in 4-6 h.
For the maintenance of the circulating blood
volume. The fluids given slowly I.V (10 ml/min) and
if acidosis or alkalosis occur, it should be treated
immediately. Clinical and laboratory improvement
indicated by urination of animal within 30-60 min.
While unfavorable responses include:
Dyspnoea (dut to pre-existing pneumonia, pulmonary
oedema because of rapid administratino).
Failure to urinate (due to renal failure, paralysis of
the bladder).

Maintenance therapy (losses and maintenance):
In the next 20-24 h. depending on the course and
severity of the disease and given I.V or orally (if no
digestive abnormalities is present), and calculated
on the basis of:
50-100 ml/kg b.w. over 24 h. period or 150 ml/kg
b.w. over 24 h period in cases of profuse diarrhoea.

Calculating fluid requirements:
To calculate the requirements based on the
body surface area according to the following
formula:
Surface area (m2) = 0.1 x body weight (kg)0.66
The surface area of a 50 kg foal is as follows:
Surface are (m2) = 0.1 x 50 kg0.66 = 1.32 m2
The maintenance requirement is 2 L/m2/day.
Fluid requirement = 1.32 m2x2 L/m2= 0.64 L or 53
ml/kg/day.
In a cow of 450 kg:
Surface area = 5.64 m2
Fluid requirement = 5.64 m2x2 L/m2
= 11.3 L or 25 ml/kg/day

The treatment summarized in:
To maintain circulating blood volume give 0.9%
sodium chloride (isotonic saline).
Dehydration and acidosis: give equal mixture of
isotonic saline + isotonic sodium bicarbonate
(1.3% sodium bicarbonate).
Dehydration and acid-base imbalance and
electrolyte losses: give balanced electrolyte
solution:
Na (138), K (12), Cl
(100),
Mg
(5), Ca (3)
and Acetate 50 in litre water.
fluid therapy (5% glucose saline solution) +
mother blood, give good results but it should be
warm and slowly injected,
50 ml/lb b.w in small animals & 12 ml /lb b.w. in
large animals.

N.B.
Blood transmission must be from the same
species, breed, age or from the dam (of the
same blood group). Whole blood or plasma
(50-100 ml injected initially) to avoid
anaphylactic shock. The rest amount should
be injected before 72 hours.
Routes of fluid administration:
Oral: It provides a safe, convenient, practical
and economical means of delivering fluids,
electrolytes & nutrients. Whole milk is the
most practical choice for neonates. Anorexic
or dysphagic animals will need to have the
fluids delivered by stomach tube.
Subcutaneous (S/C): Crystalloid solutions
(lactated Ringer’s solution) may be given S/C.
to maintain hydration but they are poorly

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