General Medicine

Clinical Medicine: Clinical medicine is a branch of medicine which deals with the diagnosis,
treatment, prognosis and observation of individual diseased animal.

Preventive Medicine: Preventive medicine is a branch of medicine which deals with

prevention and control of diseases in population.

General Medicine: It deals with the non-specific conditions of diseases in different host like
fever, dehydration, toxemia, septicemia, acidosis, alkalosis, anorexia, pica etc.

Toxemia: Toxemia is a clinical systemic state caused by widespread activation of host

defense mechanisms to the presence of toxins produced by bacteria or injury to tissue cells.
Theoretically, a diagnosis of toxemia can be made only if toxins are demonstrable in the
blood stream. But, practically toxemia is often diagnosed when syndrome is present.
Marked abnormalities for toxemia include-
 Marked abnormalities in cardiopulmonary function
 Abnormalities in blood cellular elements leading to coagulopathies
 Changes in vascular integrity
 Decrease organ blood flow and metabolism leads to heart and renal failure
 Major changes in gastrointestinal function especially motility
 Decreased perfusion of peripheral tissues leading to shock
 Need for intensive and complex therapy
 A high case fatality rate
Etiology
 Antigenic toxin
 Exotoxin: Produced by bacteria (Clostridium sp; Escherichia coli)
 Endotoxin: LPS of gram –ve bacterial cell wall (coliform mastitis and
septicemia) produce endotoxemia
 Metabolic toxins: Ketonemia (abnormal fat metabolism), acidosis
accompanied with hepatic dysfunction.

Toxin accumulates in blood and produce toxemia.

Clinical findings
 Acute endotoxemia
 Dullness, depression and anorexia
 Tachycardia and decreased cardiac output
 Decreased systemic blood pressure
 Muscle weakness and recumbency
 Collapse, death, coma and convulsion
 Hyperthermia followed by hypothermia
 Cold skin and extremities
 Congested mucosa with increase capillary refill time
 Scant feces but diarrhea may occur
 Chronic toxemia
 Lethargy and inappetance
 Separation from group
 Emaciation
 Decrease production
Diagnosis
 History and clinical findings
 Laboratory diagnosis: It is required for confirmatory diagnosis
Treatment
 Treatment should include removal of causal agent (foci of infection)
 Antimicrobials (broad spectrum antibiotics)
 Non steroidal anti inflammatory drugs:
 Flunixin meglumine 1.1 to 2.2 mg/kg bw for 24 hrs I.M or I.V
 Ketoprofen 3 mg/kg b.w I.M or I.V
 Steroid anti inflammatory drugs
 Glucocorticoid: Dexamethasone 1.0 mg/kg b.w every 24 hours. Experimentally
it has been shown that glucocorticoids are beneficial for the following reasons.
o Organelle and cell membrane stabilization
o Improved cellular metabolism and gluconeogenesis
o Mininmum reticuloendothelial depression
o Decrease leukocyte degranulation

 Fluid and electrolytes therapy: Large volume of isotonic fluid should be infused IV
and beneficial response is noted by the followings
 Correction of peripheral vasoconstriction
 Restoration of an acceptable pulse quality
 Return of urine output
 Increase arterial blood pressure
 Restoration of oxygen delivery to acceptable levels

Body temperature

Mammals are homeothermal i.e. they maintain their body temperature independently by
thermoregulatory center in the hypothalamus. Thermoregulatory mechanism consists of
neural and hormonal components. Decrease body temperature stimulates to increase
secretion of ACTH and TSH from the pituitary gland and increase metabolic activity in the
body.

Thermoregulatory mechanism
a) Heat loss
 Convection
 Coduction
 Radiation
 Vaporization
 Excretion through feces and urine

b) Heat production
 Food digestion
 Metabolic activity
 Absorption from environment
 Skeletal muscle movement
c) Chemical pathway

Hypothalamus

ACTH TSH
 Increase metabolic rate
Increase metabolic activity
d) Autonomic system pathway

Rostral part Caudal part

Heat dissipation Heat conservation

Maintain heat

Hypothermia

Hypothermia is lower than normal body temperature which occurs when excess heat is lost or
insufficient is produced. Neonatal hypothermia is a major cause of morbidity and mortality in
newborn farm animals within first few days of life.
Etiology
1. Excessive heat loss: Exposure to excessive cold air causing excessive heat loss from
the body, if increase metabolic activity, muscle tone and peripheral vasoconstriction
unable to compensate.
2. Insufficient heat production: Due to lack of feed intake and starvation increases the
susceptibility of insufficient heat production. Some secondary disease also causes
decrease heat production in the body like parturient paresis, ruminal impaction, during
anesthesia and sedation, decrease cardiac output, shock etc.
3. Combination of excessive heat loss and insufficient heat production

Epidemiology
 Susceptibility: Neonatal farm animals are very much susceptibility to hypothermia.
 Thermoregulation in newborn: In newborn animals, heat regulating centre of
hypothalamus is not well developed. So, newborn calves, lambs and kids are
susceptible to hypothermia.
 Cold induced thermogenesis
 Shivering thermogenesis: muscle tonacity
 Non shivering thermogenesis: Common in 40% of newborn lambs. Because
they have brown subcutaneous fat tissues.
 Tissue insulation: It is usually influenced by subcutaneous deep fat, which is
absent in newborn. So, they are susceptible to hypothermia.
 External insulation: Skin and hair coat play an important role as heat insulating agent
during cold exposure.
 Colostrum feeding: Deprived colostrum feeding increase the risk factor for cold
stress.
 Environment condition: Cold and humid weather increase the prevalence of cold
shock in newborn farm animals.
Clinical findings
  Decrease body temperature less than 370 C
 Weakness, decreased activity and cold extremities
 Bradycardia, varying degree of shock
 Collapse of major vein are characteristics
 Poor venous return
 Decrease suckling reflex
Diagnosis
 History and clinical finding
 Clinical examination
Treatment
 Specific treatment should be made according to causal agent
 Supplemental heat should be provided to the affected individual
 Animals should be kept in enclosed box and provide blanket convering
 5% or 10% Dextrose saline should be infused in acute condition
 Drinking warm water and colostrums feeding to the affected animals
 Temperature should be checked in every 30 minutes interval.

Hyperthermia (Heat stroke)

Hyperthermia is the elevation of body temperature due to excessive heat production or
absorption or to deficient heat loss.
Etiology
 High environmental temperature
 Diminished air current which impairs cooling the body
 Inadequate sweating or no sweating
 Thick body coat of the animal
 Defects in thermoregulatory mechanism (damage to hypothalamus)
 Dehydration - insufficient tissue fluids to accommodate heat loss by evaporation
(dehydration hyperthermia)
 Excessive muscular activity. e.g. strychnine poisoning
 Iodism
 Specific mycotoxins. e.g. Claviceps purpura

Epidemiology
 Environmental temperature: High environmental temperature. Hot and humid
climate increase the susceptibility to heat stroke.
 Health status: Fatty animals are more susceptible to heat stroke as compared with
lean animals
 External insulation: Heavy hair coat of animals increase the risk factor for heat
stroke. e.g. Angora goat
 Age: Young animals are more susceptible than adult.
Factors responsible for heat stroke
 A hot day, especially in summer season
 High humidity in the environment
 Keeping animals in ill-ventilated stuffy room
 Too much overcrowding of animals
 Exposure to unaccustomed heat during transportation of animals
 Limited supply of water in hot weather
 Too much covering of body with warm clothing
 Less capabilities of heat tolerance in young and old age group of animals

Clinical findings
 Dullness, depression
  Rapid breathing
 Open mouth breathing (panting)
 Protrusion of tongue
 Frothy discharge from mouth and nostrils
 Congested mucus membrane of conjunctiva
 Tachycardia
 Temperature as high as 106-1100F
 Convulsion
 Paralysis of the respiratory centre
 Coma
 Death
Diagnosis
 History and clinical findings
 Clinical examination

Management of heat stroke

 The animals should be kept in a well ventilated shady place
 All the door and windows should be kept open
 Fixing fan if possible
 Animal should be given cold bath with ice cold water
 Cold drinking water should be provided
 Ice cold normal saline or 5% dextrose should be infused IV , if animals become
dehydrated
 Tranquilizer may be given to sedate the centre
 Rectal temperature should be checked at every 10 minutes interval.

Fever (Pyrexia)
Fever is a pathological state of hyperthermia due to increased heat production and decreased
heat loss. It is a syndrome in which hyperthermia and toxemia are produced by substances in
the blood stream.
Etology: Two groups of etiology are involved and causing fever
 Septic fever
 Localized infection such as abscess, cellulitis (dermis and subcut fat.) and
empyema (pus accumulation in the body cavity)
 Intermittently systemic as in bacteremia and endocarditis
 Consistently systemic as in septisemia
 Aseptic fever
 Chemical fever caused by injection of foreign protein, intake of dinitrophenol
 Surgical fever due to breakdown of tissue and blood
 Fever from tissue necrosis. e.g. breakdown of muscle following injection with
necrotizing material
 Severe hemolytic crisis
 Extensive infarction
 Immune reaction
 Anaphylaxis
 Drug induced-the prolonged use antimicrobials may cause a cryptic
fever(mysterious unknown)
Pathogenesis
1. Endogenous pyrogens: Endogenous pyrogens initiate the release of arachidonic
acid, which subsequently synthesis of prostaglandin. It acts on heat regulatory centre
of hypothalamus and produce fever.
 2. Protein released from monocytes (monokines and lymphokines). The cytokines
IL-1 stimulate the production of PGE2, which acts on hypothalamus and produce
febrile response in the body.
3. Exogenous pyrogens (bacteria, virus): Febrile response initiated by exogenous
pyrogen with endogenous pyrogen/ Exogenous and endogenous pyrogens jointly
performed febrile response in the body.
Beneficial response of fever
 Stimulate T-cell proliferation
 Increase body temperature in the body causes-
 Leukocytic mobility
 Bacteriocidal action
 Phagocytic activation
 Lymphocyte trasnsformation
 Enhance the effect of interferon and IL-1
Adverse effect of fever
 Prolonged fever

Anorexia and excessive catabolism in the body

 Pyrexia effects on central nervous system causes convulsion
 Disseminated intravascular coagulation

Stages of fever: Fever is usually considered to occur in three main stages

1. Increment or onset
 Cutaneous capillaries are constricted with resulting coldness and dryness of
skin
 Respiration is reduced, shivering of muscle and decrease urine production
2. The fastigium
 When the demand for heat production subside and rate of heat loss increases
 Cutaneous and mucosal vasodilation with dieresis
3. The decrement
 Temperature decreased in this stage
 Stored heat become dissipated
 Fall down body temperature
Clinical findings
 Elevation of body temperature more than 1030F, accompanied with increase thirst,
anorexia, dullness and depression
 Constipation, muscle weakness, erection of hair and disinclination to move
 Clinical examination
 Increase rectal temperature, breathing and heart rate
 Mucous membrane of nose, mouth, vagina are often viscid or sticky
 Dry muzzle
 Feverish eye
Degree of fever
 Mild fever: Body temperature up to 400 C (10C above or normal)
 Moderate fever: Body temperature 40-410C (1.7-2.20C above normal)
 High fever: more than 420C (2.8-3.30C above normal)

Types of fever
a) Simple fever: The body temperature rises and remains elevated with 10F variation
more than normal and then subsided temperature and animal recover or collapse prior
to death. e.g. Bovine ephemeral fever
 b) Continuous fever: The body temperature remains elevated for a longer period of time
than simple fever. e.g. Tick born fever (Babesiosis)
c) Remittant fever: In this type of fever, temperature does not touch the normal limit in
24 hrs and variation of temperature is more than 10C in 24 hrs. e.g. Septicemia,
bronchopneumonia.
d) Intermittent fever: High temperature for several hours followed by a drop to normal
temperature and again rises to temperature, so on. e.g. Malaria, Chronic surra in
horse.
e) Induced fever: Injection of prepared products of bacterial origin (tuberculin,
paratubercullin, mullein etc.) for diagnostic purpose induces febrile response in the
body.
Diagnosis
 History and clinical findings
 Laboratory diagnosis: marked changes in TLC and DLC, isolation and
identification of pathogen form excreta
Treatment
Principles of treatment
 To remove the source of toxin and causal agent
 To treat the toxemia and hyperthermia
 To stimulate circulation and respiration
Specific treatment
 Antimicrobial drug to control infection
 Specific antibodies and antitoxin to control and reduce the effect of toxins
 Removal of necrotic material in aseptic fever and local infection
 Diuretics: remove exudates or transudates from the body
 Non specific treatment
 Antipyretic agent: Sodium salicylate, paracetamol,
 Nonsteroidal anti inflammatory agents: Ketoprofen, flunixin meglumine,
meloxicam, which inhibit prostaglandin synthesis in the body.

Septicemia/Viremia

Septicemia: Septicemia is the acute invasion of the systemic circulation by pathogenic

bacteria, which may cause sepsis or septic shock with possible localization in various body
systems or organs if the animal survives.

Viremia: Viremia is the invasion of the systemic circulation by pathogenic viruses with
localization in various body tissues and in which lesions produced are characteristics of the
specific virus.

 Although rickettsia, protozoa and fungi are also spread hematogeously, but they
could not make systemic infection.

Bacterimia Septicemia
Bacteria present in blood for Pathogen present throughout the
only transitory periods and course of disease and is directly
don’t produce clinical signs responsible for initiation of disease
process

All species: Anthrax, Pateurellosis and Salmonellosis are found in all species of food animals
 Neonatal septicemia
Gram –ve bacterial infection in calves: E. coli, Salmonella sp.
Foals: E. coli, Klebsiella penumoniae.
 Secondary septicemia
  Radiation injury: Injury to bone marrow and loss of leukocyte production
 Congenital defect in immune system
 Corticosteroid therapy in older animals
 Bracken fern poisoning
Epidemiology
1. Animal risk factor: Colostrum deprived new born animals are highly susceptible to
septicemia
2. Environmental factor
 Poor hygiene condition (soiling animal house with feces and urine)
3. Pathogen risk factor
E. coli, Pasteurella multocida
Pathogenesis
 Pathogens on monocyte and lymphocyte initiates systemic inflammatory response
 Transplacental infection (abortion, infertility)
 Disseminated intravascular coagulation (bacterial cell wall, ag-ab complex and
endotoxin)

Adhere to platelets and consumed by macrophage

Haemorrhagic condition throughout the body

Clinical findings
 Toxemia and fever
 Submucosal and subepidermal hemorrhages (petichial and occasionally echymotic):
Hemorrhages are best seen in conjunctiva, mucosa of the mouth and vulva
 Tachycardia and tachypnea
 Cardiovascular hypotension
 Myocardial asthenia (lack of energy)
 Respiratory distress
 Localization of infection in various organ: valves, meninges, eye and other organs
 Neonatal septicemia: Fever, diarrhea, dehydration, recumbency, depression,
congested mucus membrane, weakness and rapid death

Diagnosis
 History
 Clinical findings
 Laboratory examination
 Blood culture
 Necropsy findings (submucosal hemorrhage is a characteristic finding)
 Immunoglobulin status (low level of Ig)

Treatment

 Treatment should include removal of causal agent (foci of infection)

 Antimicrobials (broad spectrum antibiotics)
 Non steroidal anti inflammatory drugs:
 Flunixin meglumine 1.1 to 2.2 mg/kg bw for 24 hrs I.M or I.V
 Ketoprofen 3 mg/kg b.w I.M or I.V
 Steroid anti inflammatory drugs
 Glucocorticoid: Dexamethasone 1.0 mg/kg b.w every 24 hours. Experimentally
it has been shown that glucocorticoids are beneficial for the following reasons.
o Organelle and cell membrane stabilization
o Improved cellular metabolism and gluconeogenesis
o Mininmum reticuloendothelial depression
 o Decrease leukocyte degranulation
 Fluid and electrolytes therapy: Large volume of isotonic fluid should be infused IV
and beneficial response is noted by the followings
 Correction of peripheral vasoconstriction
 Restoration of an acceptable pulse quality
 Return of urine output
 Increase arterial blood pressure
 Restoration of oxygen delivery to acceptable levels
Pain
Pain is a distressing sensation arising from stimulation of specific end-organs (terminal end
of nerve conduction pathway) in particular parts of the body and perceived in the thalamus
and cerebral cortex. It is basically a protective mechanism to ensure that the animal moves
away from damaging influences.

The detrimental effects of pain

1. Stress induction resulting delayed healing process
2. Increased catabolism and decrease feed intake
3. Prolonged recovery and longer recumbency with a greater risk of postoperative
complication
4. Ineffective respiratory ventilation with the development of respiratory process
5. Self-mutilation
6. Potential of acute pain can lead to chronic pain

Etiology
a) Cutaneous or superficial pain: This type of pain usually caused by agent or process
which damage skin such as burning, freezing, cutting and crushing. e.g. severe
dermatitis, acute mastitis, laminitis, infected surgical wounds, foot rot, crushing by
trauma, conjunctivitis etc.
b) Visceral pain: Pain originated from visceral organ. e.g. inflammation in serous
surfaces, as in pleurisy, peritonitis or pericarditis.
 Distension of viscera including the stomach, intestine, uterus and bladder
 Swelling of organs. e.g. hepatomegaly, splenomegaly
 Stretching of the mesentery and mediastinum
 Inflammation as in nephritis, peripelvic cellulitis and enteritis
c) Somatic or musculoskeletal pain: Muscular pain can be caused by lacerations and
hematomas of muscle, myositis and space-occupying lesions of muscle
 Osteomyelitis, fracture, arthritis, joint dislocations, sprains of ligaments and
tendons also causes severe pain. e.g. deep penetrating injury in limbs, extension of
infection from foot root, amputation of digit, laminitis and septic arthritis.

Clinical findings
Physiological response to pain are manifested by the following signs-
 Tachycardia
 Polypnea
 Pupillary dilatation
Hyperthermia
 Sweating
 Abnormal posture and gait when pain is musculoskeletal
 Lameness
 Other responses to pain includes rolling, pawing or crouching (knees are bent
and upper body move forward)
 Moaning, grunting and grinding of the teeth
 If vocalization arises from each respiration or rumination: pain arises from
thoracic or abdominal cavity
Diagnosis
 History and clinical findings
 Elicitation of pain by the veterinarian: palpation and percussion to detect the pain
response
 Movement of animal (active or passive movement)
 Detection of cortisol in saliva and blood
Treatment
 Analgesia
 Salicylate (effective for pain): 100 mg/kg b.w. orally every 12 hours, which has
limited absorption from small intestine
 Phenylbutazone: Phenylbutazone used in horse in case of musculoskeletal
pain; Horse-4.4 mg/kg bw orally or IV routes, cattle-10-20 mg/kg bw initially
followed by 2.5-5.0 mg/kg. This drug should not be used in case of preexisting
GI ulcer
 Xylazine
 NSAID : Flunixin meglumine 1.1 mg/kg bw at 12 hrs interval, carprofen,
ketoprofen
 Supportive therapy: Application of moist heat locally to relive pain
 Provide adequate soft bedding for animals which are recumbent for longer period
of time.

Stress
Stress is a systemic state, which develops as a result of the long term application of stressors.
Stressors are environmental factors, which stimulate homeostatic, physiological and
behavioral responses in excess of normal. Adrenal corticosteroid is the only acceptable
measurement of stress in blood.
Effect of stress
 Lead to the development of psychosomatic disease
 Increase susceptibility to infection
 Reduce the efficiency of production
 Represent an unacceptable level of consideration for the welfare of animals
Etiology of stress
 Road transportation for prolonged period of time, especially during inclement weather
or overcrowded
 Climate: excessive heat or cold climate
 Excessive physical effort-endurance rides for horses, struggling in restrained animals,
fear and excitement
 Pain-dehorning, castration, severe colic (horse)
 Overcrowding-temperature, humidity and physical exhaustion associated with
standing for long period time
 Presence or absence of bedding
 Housing-comfort as well as that of maintaining moderate temperature
 Nutritional deficiency-lack of energy, bullk and fluid
 Quietness versus excitemen-harassment by man or other animals sufficient to cause
fear does elicit stress response e.g. transportation, fear and shows
 Herding and flocking instinct-if the herding or flocking species are separated from the
group may be distressed

Stress in any stimulus (physical, chemical, emotional, internal or external)

Excite hypothalamus
 Pituitary gland

ACTH

Secretion of cortisol
Non carbohydrate source

Increase glucose
Clinical findings
 Stress induces psychosomatic disorders
 Stress and animal welfare
 Increase susceptibility to infection
 Heat stress reduces milk production
 Infertility and mastitis associated with stress disorders
 Stress induces metabolic disorders: hypocalcemia, hypomagnesemia in cold weather

Management of stress
 Animal should be free from abuse or adverse exploitation
 Prolonged deprivation of feed and water during transportation should be avoided
 Should follow the guidelines dealing with codes of practice for livestock production
 Stocking density, temperature, humidity, noise should be maintained according to
requirements

Sudden death: When an animal is found dead or died suddenly without showing any clinical
signs is called sudden death of animal.

Etiology
 Single animals
 Spontaneous internal hemorrhage: rupture of internal carotid artery
 Peracute endeogenous toxemia: ruptutre of stomach of horse , abomasums of
cows and colon in mares during foaling
 Peracute exogenous toxemia: snake biting (poisonous)
 Toxemia: Internal hemorrhage or damage to CNS
 Gastro-intestinal rupture in the horse: overeating of highly fermentable food,
adding excess amount of fluid by nasogastric tube, torsion or gastrointestinal accident,
bloat and impaction in goat and cattle
 Iatrogenic death: overdose calcium injection IV in excited animal, IV injection of
ivermectin in horse, IV injection of procaine penicillin suspension, too rapid IV
infusion of fluid with pulmonary edema
 Group of animals
 Lightning strike or electrocution
 Nutritional deficiency and poisoning
 Cyanide or nitrite plant poisoning
 Acute cardiomyopathy in young animals deficient with vitamin E and
Selenium.
 Falling disease in cattle with copper deficiency
 Acute to potent poisons: cyanide poisoning, organophosphate, lead
poisoning in young animals
 Diseases caused by infectious agents: BQ, anthrax, hemorrhagic
septicemia, enterotoxemia etc.
  Neonatal animals: hypothyroidism, toxemia, colibacillosis etc.
 Anaphylaxis: administration of vaccine and sera, iron injection in piglet
with low vitamin E and selenium.
Diagnosis
 History of changes feed or exposure to poisons
 Examinaton of dead animals: struggling, frothy nasal discharge, bloat, release
unclotted blood through natural orifice, burn marks on body surface and signs of
trachea
 Post mortem examination of dead animals and suspected sample should be collected
for laboratory diagnosis.

Dehydration
The term dehydration is derived from Latin word ‘de’ means away and Greek word ‘hydor’
means water, that is loss or removal of fluid from the body.

Etiology
There are two major causes of dehydration a) Failure of water intake b) Excessive fluid loss
a) Failure of water intake
 Deprivation of water
 Lack of thirst due to toxemia
 Inability to drink water as in esophageal obstruction
b) Excessive fluid loss
 Diarrhea, vomiting, polypnea, extensive skin wound, copious sweating, acute
carbohydrate engorgement of ruminants, acute intestinal or gastric obstruction, dilation
and torsion of abomasum
Pathogenesis
a) Lack of fluid intake
Catabolism of fat, protein and carbohydrate

Acidosis and Blood urea nitrogen

b) Excessive loss of fluid
Fluid loss from the body is compensated by dry feces, decreased urine and sweating

Renal ischemia

Oliguria, concentrated urine and exacerbation of acidosis

Both lack of fluid intake and excessive loss of fluid combinedly causes andydremia: Increase
blood viscosity, oligemia and hemoconcentration
c) Depression of tissue fluid : Interfere tissue metabolism causing muscle weakness,
hypothermia and anorexia

Clinical findings
 Dryness and wrinkling of the skin
 Rapid weight loss
 Reduce elasticity of skin
 Dry mucous membrane
 Eye recede into the socket
 Fluid loss more than 10-15% is fatal condition for the body
Diagnosis
  History and clinical findings
 Clinical examination: Folding corrugation of skin in opposite direction of upper
eyelid and neck to diagnose the degree of severity of dehydration.

Assessment for degree of severity and dehydration

Loss of body Sunken eyes and Skin fold test PCV% Fluid
weight face persist for second requirement
ml/kg b.w
<5 Not specific --- 40-45% 20-25
6-8 ++ 2-4 50% 30-50
>8-10 +++ 6-10 55% 50-80
>10-12 ++++ 20-45 60% 80-120

Treatment
 Treatment should be provided on the basis of etiology
 Saline and dextrose should be administered as per requirement

Acid-base imbalance
The pH of the blood is maintained within the normal range of 7.35-7.45 by its buffere system,
which is maintained by bicarbonate carbonic acid system (buffer). The proportion of the
dissolve carbon dioxide and bicarbonate ion which from the component of the buffer system
is maintained at a constant level either by increased pulmonary ventilation or by increased
urinary excretion of the bicarbonate radical.
Acidosis: Depletion of the body’s alkali reserve with resulting disturbances of the acid-base
balance is called acidosis
Etiology
The general cause of acidosis can be divided into three categories on the basis of
pathogenesis
1. Excessive loss of base
2. Accumulation of endogenous or exogenous acid
3. Combination of both of the above process
 Excessive loss of HCO3 + ion in acute enteritis
 Absorption of large quantities of fixed acids as in carbohydrate engorgement in
ruminants, grain engorgement in horse, ketosis in ruminants.
 Retention of CO2 in blood due to interference with respiratory exchange in
pneumonia, severe pulmonary emphysema, prolonged parturation causing asphyxia in
newborn
 Shock and peripheral circulatory failure leading to anaerobic oxidation
 Overtreatment with acidifying solution in alkalosis
 Retention of acid metabolites due to renal disease-renal insufficiency and renal failure

Pathogenesis
Uncompensated e.g. when respiratory centre depressed by hypovolemic shock or
enterotoxigenic colibacillosis

Hypoventilation

Respiratory rate slow and shallow. Increase pCO2

Weakness, lassitude (lack of energy), terminal coma, tachycardia, decreased blood pressure
and pulse amplitude

Compensated
Increase rate and depth of respiration

Hyperventilation
Decrease in blood pCO2 & H+. Compensatory movement of K+ out of the cell into
extracellular space

Hyperkalemia

Bradycardia
Diagnosis
 History and clinical findings
 Laboratory findings
 Reduced venous blood pH , pCO2 and HCO3- concentration
 Increased neurtophilic leukocytosis with left shift
Treatment
Sodium bicarbonate isotonic solution 1.3% 2.5-4.5 liter depends on severity of lesion.

Alkalosis
Increased plasma bicarbonate concentration (HCO3-) and a fall in blood acid (H+)
concentration is known as alkalosis
Etiology
 Increased absorption of alkali (overdose with HCO3-)
 Excessive loss of acid
 Deficit of CO2
Pathogenesis
Excessive loss of acid

Abomasal atony due to dilatation, impaction and trosion

Continuous secretion of HCl and K+ in the abomasum

Failure to evacuate abomasal contents into duodenum

Reflux in to rumen

K + shift from the extracellular to intracellular

Alkalosis

Clinical findings
  Slow, shallow respiration, because lack of CO2 stimulaiton
 Depression of ionized fraction of serum calcium may lead to muscle tremor and
tetany with tonic and clonic convulsion
 Hyperpnea and dyspnea in terminal cases
Diagnosis
 History and clinical findings
 Laboratory analysis of blood samples include increased venous blood pH and
bicarbonate ion concentration
Treatment
 Treatment should be directed according to cause
 Correction of alkalosis by oral administration of vinegar (5% acetic acid) in
ruminants

Pica/ Allotriophagia
Ingestion of materials which are not considered as food.
Coprophagia: Eating of its own or other animal’s feces
Osteophagia: Chewing of bones
Geophagia: Eating of soil
Infantophagia: Eating of its own infant
Pilophagia: Licking of hairs and body coat
Iron mongering: Lick or chew iron or metallic substances

Etiology
 Vitamin B deficiency
 Mineral deficiency (phosphorum, sodium chloride, cobalt etc)
 Lack of fibrous food in the diet
 Lack of protein
 Chronic endoparasitism
 Chronic pancreatitis, gastritis, peritonitis
Treatment
 Primary cause should be corrected
 Deficiency of vitamin and mineral should be supplemented
 In ruminants, yeast powder and cud transplantation may be beneficial.

Ill thrift
Ill thrift is a syndrome of weight loss or failure to gain weight in the presence of adequate
food supply and a normal appetite. It is also called thin sow syndrome or weak calf syndrome
Etiology
 Nutritional cause
 Deficiency of essential trace elements in diet
 Inadequate intake of adequate supply of food
 Other factors which reduce the animal food intake includes anxiety, the
excitement of estrus, new surroundings, loss of newborn, bad weather,
ectoparasitim etc.
 Excessive loss of protein and carbohydrate
 Glucose loss in urine (Diabetes mellitus)
 Protein loss in feces
 Ulcerative lesion
 Proteinuria for long time (Chronic renal disease)
 Faulty digestion, absorption and metabolism
 Diarrhea cause faulty digestion and absorption
 Abnormal physical function of the gastrointestinal tract
 Vagus indigestion
  Chronic liver disease (inadequate utilization of absorbed nutrients)
 Neoplasia of any organ
 Chronic disease like TB and Para TB
 Congestive heart failure (lack of oxygenation of tissues causing loss of body
weight)

Diagnosis
 History and clinical findings
Treatment
Treatment should be provided according to the merit of etiology.

Digestive System

Principles of alimentary tract dysfunction

The primary functions of the digestive system includes prehension of feed and water,
mastication, ensalivation, swallowing of feed, digestion of feed and absorption of nutrients,
maintenance of fluid and electrolyte balance and evacuation of waste products.
There are four major function of alimentary tract dysfunction
1. Abnormal motility of GI tract: Normally peristaltic movement of the alimentary
tract moves ingesta and feces from esophagus to the rectum. Motility activity
controlled by vagus and autonomic nerve.
Disruption of GI tract motility due to-
a) Hypermotility: Increase in intestinal muscular activity due to gastroenteritis lead to
diarrhea
b) Hypomotility: Debility and weakness of the muscle lead to constipation
c) Distension of the segment of intestinal tract
d) Accumulaiton or inefficient expulsion of gas
e) Occlusion of the lumen of intestine due to pyloric or ileocecal valve obstruction
f) Abnormal pain due to stretching and inflammation of serous membrane
g) Dehydration and shock

2. Abnormality of secretion
This type of abnormality is not recognized in farm animals. Human and monogastric
animals usually suffer with this problem.
 Hyposecretion: Maldigestion
 Hypersecretion: Enterotoxigenic colibacillosis
 Lactose deficiency in intestine in case of neonates (calves, foals)
3. Abnormality of digestion: Digestion in carnivores depends on motor and secretory
functions. In herbivores, digestion depends on ruminal microflora. Ruminal flora
capable of digesting cellulose and fermenting to volatile fatty acid and converting
nitrogenous substance to ammonia and protein. Ruminal flora can be modified by
following conditions-
 Failure to provide correct diet
 Grain overload
 Inappetance
 Prolong starvation
 Long time administration of oral antibiotic and sulphonamide (alter p H of
rumen)
4. Abnormality of absorption: Defects in intestinal villous absorptive cells causing
abnormal absorption of water and nutrients in intestine.
Principles of diagnosis of alimentary tract diseases
The history, epidemiology, clinical findings and laboratory examination are the important
methods to diagnose the diseases of digestive system.
1. History
 Feed history-nature of feed, amount, composition etc
 In case of calf, time of feeding, milk substitute and amount of drinking water
should be monitored properly.
2. General examination
 Appetite , feeding
 Thirstiness, fluid intake
 Rumination , eructation
 Vomition
 Nature of defecation
3. Special examination
a) Examination of different organs
b) Rectal examination
c) Examination of gastrointestinal fluid
d) Feces examination

a) Examination of different organs

 Examination of oral cavity and pharynx

 External inspection
o Profuse salivation
o Swelling and injuries in check, jaw and pharynx
o Excessive ptyalism may be caused by FMD, bovine malignant catarrh,
bovine viral diarrhea
o Difficulty in swallowing of saliva due to organophosphorus poisoning
and choke
o Palpation of swelling to detect consistency-edema, cellulitis, abscess,
actinomycosis etc.
 Internal inspection
o For internal inspection, mouth should be open by mouth gag and holding
tongue with towel
o Oral mucosa is checked for redness, swelling injury, ulceration etc.
o Teeth, jaw, tongue are checked for abnormal injury and lesion
o Unswallowed food may be present in the check pouch
 Mouth odor
o Normal odor: Slight sweetish and stale
o Foul odor: Purulent infection and necrosis of pharynx and esophagus
o Decomposing contents of rumen
o Lung gangrene
o Ketosis: Aromatic smell
 Examination of esophagus: Length of the esophagus normally 110-125 cm long
 Only cervical part of the esophagus can be palpated
 Palpation is carried out by placing one hand on each side of the neck and examine
jugular furrow
 Swelling within the lumen : esophageal tumor
 Choke due to swelling at the surroundings of esophagus: abscess, edema ,
emphysema and cellulitis
 Examination of ruminant stomach: Ratio of rumen and abomasums is 9:1
 Dorsal and ventral sac of rumen occupy the entire left half of the abdominal cavity
  Rumen-villi or papillae, Reticulum-honey comb, Omasum-Leaf like and
Abomasum-Spiral fold
 Observe degree of fullness of rumen at the paralumbar fossa (left side)
o Hollow flank-Not full
o Tensed-Normal
o Bulging-Overfull (gas formation)
o Palpation
o To detect ruminal contraction
o To detect consistency of rumen: Tympany-gas, Firm-overloaded, Soft or
doughy-roughage feed
o Auscultation
o Rumen sound: 5-12/minute
o Hypermotility: foamy bloat
o Hypomotility: impaction of rumen
o Percussion
o Examination of rumen fluid: Puncture paralumbar fossa with 20 cm long syringe.
After sample collection, stored at room temperature and should be examine within 9 hr
o Color of rumen fluid: Green-grazing grass, straw-eating straw, milky grey-acidosis
and greenish black-stasis with decomposed food
o Consistency: normally viscous, bubble-foamy bloat
o Odor: Normal- hay, grass odor ; sour odor-ruminal acidosis and foul odor-protein
decomopostion
o PH of rumen 5.5-7.0; rumen feeding pH 6-7 and concentrate feeding 5.5-6
o Examination of reticulum
o Ventral ends of 6th or 7th ribs
o Palpation: grunting sound in traumatic reticulo peritonitis
o Auscultation: left side of the reticulum
 Examination of omasum
o Right side between 7th and 9th ribs
 Examination of abomasums
o Make an imaginary line from umbilicus to xyphoid region and puncture at the
middle of line (4 to 8 cm long)
o Color: normal grayish, yellow green or olive green
o PH : Stale acidic smell 2 to 4.
 Examination of intestine: Enteritis, intestinal accident
o Rectal palpation: intestinal abnormality, genital organ, urinary bladder, kidney
 Examination of feces
o Unweaned calf: yellowish-brown
o Adult cattle: Dark green
o Colibacillosis: Whitish color diarrhea
o Salmonellosis: Olive grey color
o Tary color feces (melena): Abomasal abnormality
o Light red/dark red color-blood from posterior part of intestine
o Foamy, yellowish-brown-lactic acidosis
 Smell: Acidic smell-ruminal acidosis, Bad smell-necrotic enteritis (feces contain pus)

Principles of treatment of alimentary tract diseases

1. Supportive and symptomatic treatment
 Incrase GI tract motility: Atropine sulphate 0.2 mg/kg b.w
 Decrease GI tract motility: purgative, parasympathomimetic durg
 Diarrhea and dehydration: Fluid and electrolytes therapy
 Distension with ingesta and gas: antizymotic durg, surgical treatment
  Prolong indigestion and inappetance: Cud transplantation with stomach tube
 Excessive feeding concentrate diet: alkaline drugs
 Excessive feeding alkaline diet: acidifying drugs
2. Specific treatment
 Microbial infection: antibiotics
 Parasitic infestation: anthelmintic drugs
 Protozoal infection: antiprotozoal drugs
 Poisoning: Specific antidote
If conservative therapy is not effective, then go for surgical operation

Respiratory system

Pathophysiology of respiratory system

Hypoxia: Diminished amount of oxygen in the tissues is called hypoxia

 Anemic hypoxia: Deficiency of Hb per unit volume of blood
 Hypoxic anoxia: Resulting from defective oxygenation of blood in the pulmonary
circuit, pneumonia, pulmonary edema, chronic congestion etc.
 Stagnant hypoxia: The rate of blood flow through capillaries is reduced e.g.
congestive heart failure, peripheral circulatory failure
 Histotoxic hypoxia: Interference with the cells in their utilization of oxygen e.g.
cyanide poisoning.
 Respiratory failure: Respiratory failure is defined as respiratory insufficiency
resulting in abnormalities of oxygenation or elimination of CO 2 severe enough to
impair or threaten the functions of vital signs.
 Asphyxial failure
o Pnumonia, pulmonary edema, respiratory obstruction
o Hypoxia: Hypercapnia Treatment: oxygen supply
o Paralytic failure: acute heart failure, poisoning with respiratory centre
depressant. Treatment- respiratory centre stimulant
o Tachypneic failure: Hypoxia, but no CO 2 retention. Treatment: O2 and CO2
provided.
 Hypercapnia
Hyper-above and Kapnos-smoke. Excess CO2 in blood is called hypercapnia

Principles of diagnosis of the diseases of respiratory system

1. History
a) Clinical history
 Nasal discharge
 Coughing
 Abnormal sound associated with breathing
 Abnormal vocalization
 Respiratory distress
 Increase respiratory rate
b) General history
 Outbreak of tuberculosis
 Rearing healthy cattle with diseased cattle
c) Management history
 Housing environment
 Light and air movement
 Hygienic environment of animal house
 Adequate ventilation
 d) General clinical examination: Breathing is best observed from behind and to one
side of the animal without disturbing the animal by movement of costal arch and
flank.
 Faster respiratory rate: Fever, anger, sexual excitement, after violent
exercise, very cold or hot weather
 Slower respiratory rate: Lying, sleeping or unconsciousness condition
slowing the respiratory rate
 Types of breathing
o Costo-abdominal type breathing eg. cattle, sheep and goat etc.
o Costal breathing: Problem in diaphragm, space occupying lesion in
the abodominal cavity
o Abdominal breathing: painful chest wall, pulmonary emphysema
e) Respiratory depth/ intensity of respiration
 Eupnea: normal breathing
 Hyperpnea: Increase or decrease depth of respiration
 Polypnea: Increase rate and depth respiration
 Oligopnea: Decrease respiratory rate
 Apnea: Stop breathing
 Dyspnea: Difficult breathing. Inspiratory and expiratory dyspnea
f) Abnormal lung and thoracic sound
 Bronchial lumen remain normal, but lung tissue become consolidated
 Crackles: Dry and moist rale.
 Wheezes: Inspiratory and expiratory wheezes
 Absense of lung sound: Hydatid cyst in lung, tumor, neoplastic growth etc.
g) Examination of respiratory organ
 Examination of muzzle and nose
 Examination of breath: Breath odor- putrefactive odor, ammonia odor,
sweet odor
 Examination of nasal discharge: amount,color, odor, consistency
 Examination of pharynx and larynx
 Examination of trachea
 Examination of lung and pleura
h) Special examination of the respiratory system
 X-ray, tracheo-bronchial aspiration
 Pleural paracentesis ( 6th or 7th intercostals space)
 Examination of feces for lung worm
 Tuberculosis: Tuberculin test
 Serological test: Specific organism detection

Principles of treatment of respiratory diseases

1. Antibiotic therapy: Selection of antibiotic by antibiotic sensitivity test
2. Environmental alteration: Keep the animal in well ventilated house, provide
adequate amount of drinking water
3. Oxygen therapy: Provide oxygen therapy in anoxic anoxia cases
4. Respiratory stimulant: Use respiratory stimulant in case of respiratory center
suppression cases e.g. caffeine, amphetamine sulfate, picrotoxin, metrazol,
coramine etc.
5. Expectorant
 Unproductive coughing
 Chronic coughing
Treatment: Ammonium and potassium salt, anodyne expectorant, morphin,
belladonna, codeine etc.
6. Bronchodilator: aminophylline, theophyline
 7. Relief of respiratory obstruction e.g. Tracheotomy relief respiratory
obstruction.

Skin and appendages

Principle of diagnosis of skin disease

a) Case history
 Previous infection
 Number of affected animals
 Skin care and management
b) General clinical examination (skin is the mirror of health)
c) Examination of hair
 Consistency of hair related to presence or absence of zinc
 Chronic digestive and respiratory diseases
 Seborrhea dew drop like fat over the hair
 Examination of hair color
 Pale hair: Jhone’s disease
 Spectacles around the eyes: Hypocuporosis, Molybdenosis
 Parakeratosis: zinc deficiency
 Examination of absent or defective hair formation (atrichia, hypotrichia)
 Examination of skin
 Dry skin: Asteatosis
 Seborrhea: Vitamin A and essential fatty acid deficiency
 Skin color: pale-jaundice, red-hyperemia and cyanosis-poisoning
 Examination of skin temperature: Normally extremity of the body
having lower temperature than body trunk
 Examination of skin odor: sweet-ketosis, foul-putrefactive lesion on skin
 Examination of pruritus and itching
 Peripheral itching : allergy or external paretic infestation
 Central itching: Medulla control itching sensation of the body,
psudorabies, scrapie, liver disease and chronic kidney disease
o Treatement should be according to etiology
 Examination of skin lesions
 Discrete skin lesion
o Macule- discolration of skin due to ectoparasitic infestation
o Papule L. Papula-pimple pea like growth on the skin
o Noudule L Noudus- knot size more than papule
o Vesicle L. vesicular
o Pustule
o Wheal
 Diffuse lesion
o Scale: shedding of the external layer of skin
o Excoriation: Abrasion or scratches
o Fissure: Lesion extend up to subcutaneous tissue
o Gangrene
o Ulcer
o Crust
o Scar
 Examination of thickness of skin
 Elasticity of skin
 Examination of increase size of the skin: edema, abscess, hematoma and
emphysema
 Special clinical examination
  Inspection: abnormal hair or skin, sebaceous secretion, discrete or
diffuse skin lesion etc.
 Palpation: Detection of abnormality of skin size e.g. edema, abscess,
emphysema, hematoma etc.
 Wood’s lamp: Detection of dermatophytes
 Laboratory examination
 Collection of samples: hair, skin swab, scrapings and biopsy
sample of skin
 Isolation and identification of causative agents
 Skin swab: Bacteriological examination
 Skin scrapings: Dermatophytes and metazoan protozoa
 Biopsy sample: Histopathological examination

Principles of treatment of the disease of skin

a) Specific treatment: Isolation of specific microbes and selection of antibiotics
 Local treatment
 Systemic treatment
b) Non-specific treatment
 Application of antiseptic ointment and proper dressing can prevent infection
 Topically applicable anesthetic ointment and systemic sedative injection can
prevent scratching or self inflicted injury
 Infuse saline to prevent fluid loss from the skin
 Provide adequate amount of sulphur (methionine and cysteine) containing acid
hasten skin healing.

Principles of diagnosis of the diseases of musculo-skeletal system

1. History
a) General history
 Location of illness
 Number of same cases affected every year and causes fall in production
 Any preference for a particular age group of animals or production group-
pregnancy , fattening cattle and lactation
 Nutritional history
 Oysteodystrophies and myopathies are nutritional origin
 Check the balanced nutrition in feed
 Environment and housing: Quality of floor evaluate the state of injuries
b) General examination
I) Observation of recumbent animals (cattle): lame or paralysed animals
 Sternal recumbency, lateral recumbency-milk fever
 Frog like posture (one or both hind legs are extended forwards is
the sign of obturator nerve paralysis)
 Legs are stretch out infront-myositis/muscle degeneration
 Torticollis (permanent abnormal twist of neck)-diseases of cervical
vertebrae, muscles, tendon
II) Observation of the process of standing up
 Normally cattle take weight on the hind legs, then fore legs and
swinging their head and neck
 If animal starts taking weight on forelegs-excessive body weight,
disorder of hindlegs.
 If taking weight on flexed carpi (kneeling)-osteomalacia, fluorosis
and calcinosis, foot pain, fracture of 3rd phalanx, abscess
III) Observation of standing animals
 Patient should be walk on hard or soft surface to detect
abnormalities in gait and lameness
 Inspection of the gait to localize the site of illness
 If any of the limb is neither lifted or brought forward-animal walk
on three legs
 If animal keep the limb away from the body-Lesion probably on
the outer claw
 Limb held inwards (adduction)-inner claw
 Sudden lameness-trauma, accident, injury
IV) Physical examination
a) Examination of limb
 Physical examination of the affected area to localize the illness
 Passive movement of limbs to indentify fractures, dislocation and
pain on movement
b) Examination of muscle: muscle can be palpated for evidence of
µenlargement, pain or atrophy
c) Examination of joints
 Inspection of joint structure
 Palpation of the joint cavity
d) Examination of claws
 Dirt of the claws should be scraped off by brush and water
before examination
 Coronet, heel and inter digital space should be examined
 Manual palpation of the claws
V) Radiographic examination: Radiography of foot in latero-medial and dorso-
planter planes showing lesions in phalanges, joints and sessamoid bones
VI) Muscle biopsy: Histopathological or histochemical examination-
Inflammatory degeneration of traumatic muscles
VII) Arthrocentesis
 Joint fluid is collected by needle puncture and examined for the
presence of biochemical changes in joint fluid and presence of
infectious agents.
 Needle size: 1.5 to 2.00 mm size.
 Normally synovial fluids clear, colorless or with a yellowish
opalescence and without smell and <10 neutrophil/µl
 Septic synovitis: 85-100% neutrophils and > 1 lac nucleated cell
IV) Serum biochemistry and enzymology
 Creatinine phosphokinase (CPK), SGOT (AST)-sensitive indicator for
muscle degeneration
 Serum level of calcium, phosphorus, alkaline phosphatase is the
sensitive indicator for bone diseases.