Metabolic, Nutritional and Reproductive Disoder Module Edited1 - 2

BARATON COLLEGE IN
COLLABORATION WITH UNISA
DEPARTMENT OF ANIMAL HEALTH AND PRODUCTION
E-LEARNING COURSE
METABOLIC, NUTRITIONAL AND REPRODUCTIVE DISODERS
00223 ANHP / 00223ANPR (Certificate)

0315 ANHP/ 0315 ANHPR (Diploma)
by
Dr. Machira D. N.
Machira.dickson@gmail.com
+254704670347
June 2020
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ANHE 0315/00223: Metabolic, Reproductive and nutritional disorders
MAIN INFORMATION PAGE
COURSE PRELIMINARIES
ANHP 0315/00223: Metabolic, Nutritional and Reproductive

disorders
Is this course for you?

This course has been designed for second year diploma and certificate
students pursuing a career as animal health professionals. To introduce the
learners to disorders associated with breakdown of metabolic processes in
various animal species, and the management and prevention of such
disorders. In addition to equip learners with knowledge and skills in the
recognition and management of reproductive disorders
You are expected to complete this course in 90 hours, 30 hours of which are
practical. Before starting this course, you are expected to have gone through
all courses in year 1.
Introduction to the course

This course aims to introduce students to Metabolic and nutritional disorders:
causes, pathogenesis, clinical signs, diagnosis, differential diagnosis,
treatment, prevention and control of: bloat, milk fever, pregnancy toxaemia,
grain overload and ketosis, grass tetany, water intoxication. Mineral
deficiencies and excesses, including iron, copper, zinc, phosphorous, selenium
and cobalt and their excesses. Vitamins A, D, E, K, and B complex. Define
infertility and sterility. Causes of infertility, non- specific causes of infertility,
nutritional, stress and intercurrent conditions, anatomical, physiological
dysfunction, managerial, hereditary causes and non- specific infections.
Specific infections – aetiology, signs, diagnosis, transmission, and treatment.
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Prevention and control of brucellosis, epivaginitis, campylobacteriosis and
trichomoniasis. Abortion and breeding records. Neo-natal diseases of cattle,
sheep, goats, pigs and camels. Normal parturition and neonatal care. Mastitis:
causes, transmission, morbidity, diagnosis treatment and prevention. There
will be a deliberate attempt to link all course content to what is happening in
the field through practical assignments as well as laboratory practicals. We
hope that you enjoy the course!
Course content
There are twelve (12) topics in this course, namely:
Topic 1: Introduction
Topic 2: Parturient paresis in cows
Topic 3: Lactic acidosis (grain overload)
Topic 4: Bloat
Topic 5: Hypomagnesaemic Tetanies
Topic 6: Ketosis of ruminants
Topic 7: Salt toxicity and water poisoning
Topic 8: Mineral and Vitamin Deficiencies and toxicities
Topic 9: Introduction to reproduction and obstetrics
Topic 10: Physiology of Parturition
Topic 10: Infertility and sterility
Topic 11: Neonatology
Topic 12: Mastitis
Topic 10: Breeding records
The course will also have the following practicals undertaken when schools
resume:
Course learning outcomes
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At the end of this course, the learner should be able to:
1. Explain general pathways that lead to metabolic, nutritional and
reproductive disorders
2. Describe animal metabolic, nutritional and reproductive disorders of
various animal species
3. Diagnose metabolic disorders in various animal species
4. Demonstrate skills and knowledge in clinical management of metabolic
disorders.
5. Describe the methods applied in control of metabolic disorders in
domestic animals.
6. Explain the causes of infertility, sterility and abortions in domestic
animals
7. Demonstrate skills in the management of parturating cows and their
newborns
Need Help?
This course was developed in June 2020 by Dr. Machira D.N. phone: +254
704 670 347, email Machira.dickson@gmail.com. Dr. Machira is a tutor at the
department of animal health and production. You may contact me between
Monday to Friday within normal working hours in the school portal chat and
discussion forums.
For technical support e.g. lost passwords, broken links etc. please contact
tech-support via e-mail baratonacademic@gmail.com
Assignments/Activities
Assignments/Activities are provided at the end of each topic. All assignments/
activities will require submission.
Course Learning Requirements
Timely submission of the assignments
2 CATs (30%).
Final Examination (70% of total score)
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Core Reading Materials for the Course
Core Textbooks
1. Mullei C.M. (2003) Metabolic and nutritional diseases of food animals
2. David Noakes Timothy Parkinson Gary England. (2018) Veterinary Reproduction and
obstetrics 10th edition
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Topic 1: Introduction to diseases (Certificate)
Definition of terminologies:
Disease: A state or condition brought about in animals/livestock by some micro-organisms or
parasites or unknown cause which is detrimental to health of that animal. The causes of a disease
also include mechanical or thermal injuries, nutritional deficiencies, poisons and hereditary causes
Health: Is the state in which cells remain intact and fully functional. However, health does not
mean absence of disease.
Aetiologv - Cause of disease e.g. bacteria, protozoa etc
Clinical signs - Signs Of disease e.g. coughing, diarrhoea, abnormal discharges
Necropsy/post mortem - Post mortem (after death) examination to establish the cause of
death
Predisposing/risk factors - These are factors which increase an animals vulnerability to a disease
e.g. starvation due to shortage of food, water etc.
Contributing factors - These are factors, which make an animal more sick e.g. nutritional
imbalances.
Contagious diseases: - these are diseases, which an animal gets through contact (direct or indirect
contact) between an infected and healthy but susceptible animal.
Infectious disease: disease caused by living organism that can multiply in the host.
Virulence: ability of an organism to attack a host, establish itself and cause disease.
Local infection: organisms stay in one place within body, e.g. CBPP in lungs.
Systemic infection- organisms spread throughout the body.
Toxaemia;- toxins in blood
Viraemia: virus in blood,
Bacteraemia: bacteria in blood
Dyspnoea: difficult breathing
Tachypnea – increased respiratory rate
Tachycardia – increased heart rate
Bradycardia – increase in the intensity of heart beat
Ataxia – Uncoordinated movements
Nystagamus - rapid involuntary movements of the eyes.
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Opisthotonos - spasm of the muscles causing backward arching of the head, neck, and spine
Anorexia: lack of appetite
Polydypsia – increase in water intake
Diagnosis: finding out the cause of disease.

Differential diagnosis – Diseases that exhibits some of the same clinical signs as the disease the
animal is showing
Clinical pathology – the examination of samples taken from an animal in the lab for disease
Specific treatment: here cause of disease is known and treatment is given. Symptomatic treatment:
here one treats what is seen, that is the presenting signs.
Prevention – Measures taken to prevent a disease from entering or establishing in a farm
Control – Measures taken to reduce the impact or eliminate a disease that has occurred in a farm
Causes of diseases
Mechanical injuries: Due to physical injuries or trauma e.g. simple cuts or breaks in skin or bone
or bruises etc.
Thermal injuries due to excess heat or cold applied to tissues may cause cell death eg burns,
freezing, heat
Poisons: substances that cause cell death e.g. lead, copper, nitrate and cyanide.
Hereditary conditions. Certain inherited genes are lethal and can be transmitted to offspring from
parents e.g. Dwarfism in calves, sickle cell anemia.
Nutritional/ metabolic disorders: Unless cells obtain all nutrients required by the body for survival-
Proteins, minerals, vitamins and energy they cannot function properly.
Infestation: this is due to parasites e.g. ticks, insects and worms. May be internal or external
infestations.
Infection: Due to microorganisms. They include bacteria, protozoa, fungi etc.
Nature of disease development
Disease usually progress in the following stages:
1. Transmission: Disease may get to animal through direct contact
Indirect contact -Sick animals graze on the pasture and saliva, urine, faeces etc from these animals
reach clean healthy animals
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Vectors - Flies, ticks, tsetse flies, and people. Living or non-living objects transmit livirg
organisms from sick to healthy animals.
We can prevent transmission of disease by
Quarantine - restriction of movement of animals and their products
Isolation of sick animals
Disinfecting of environments
2. Infection
Organisms get into healthy animals and start to multiply and grow.
Infection may be through the following routes:- ingestion, Inhalation, eyes, wounds and skin
penetration.
Incubation period
A few organisms may not make an animal sick so most organisms grow and multiply over a period
of 3— 10 days in order to make an animal sick. It is the period between infection and first
clinical signs.
Clinical manifestation
Peracute: - the disease progress very rapidly e.g. Anthrax. Mostly sudden death
Acute: - disease which is quick and short, lived
Sub-acute: - takes a bit longer. It is between acute and chronic
Chronic: - disease drags out for a long period of time or indefinitely.
Disease outcome
The outcome of the disease
Death - disease kills the animal
Recovery - total recovery
Partial recovery
Chronic illness
Carrier state
C. Disease control and treatment

Quarantine - restricting movement of animals and their products following an outbreak of a
notifiable disease. Objective is to prevent the organism from crossing a boundary.
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By keeping disease tolerant animals to the organism e.g. N'dama cattle tolerant to
Trypanosomiasis.
By keeping disease resistant animals. e.g. maintaining sheep in CBPP endemic areas.
By control of vectors e.g. mosquito to control in malaria endemic areas or ticks to control ECF
Vaccination
Vaccines — A fluid suspension of antigen, capable of stimulating the production of
corresponding antibodies.
Vaccination makes animal immune to a certain disease (Blackleg Infection)
Disinfection - disinfection refers to application of chemicals to the environment to kill
microorganisms.
Two types: physical disinfection, chemical disinfection
Physical disinfection e.g. boiling water — equipment, Incineration- carcass, Burning carcass, UV
light - chicken hatcheries
Chemical Disinfection e.g.: lysol — a phenol derivative, used at 3-5%, Chlorine bleaching powder,
for water treatment, Formaldehyde (methanol): microbes
D. Method of disease diagnosis
Needs careful observation; it is an art and science too; requires experience, good knowledge and
observation.
a) Clinical examination:
This involves the following: Case history: includes Number in herd involved; recent animal
movements; weather variations; time disease was first seen; treatment and control administered
amounts or doses. And finally the feeding and watering regimes.
i) Examination of the environment
Includes: Type of environment associated with disease e.g. liver flukes in marshy areas and Rift
Valley Fever in mosquito infested areas; presence of other animals —
e.g. wild animals which are reservoir hosts.
ii) Examination of the animals
Includes animal identification- ear tags etc; distance examination; close look examination; lonely
animals; gait, emaciation posture etc.
Close examination will include- temperature (rectally), RR (stethoscope), pulse rate (stethoscope).
(Know normal figures for the above parameters).
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Post Mortem Examination
Give detailed PM examination to confirm diagnosis, and this should show: Date, place, owner's
name, numbers affected, number dead, breed, sex, age, animal identification, time/date of death;
History, Results of clinical examination, results of environment examination, All these should be
done immediately.
Laboratory Diagnosis
Blood smears- Thin smears- identify ECF etc; Thick smears- Trypanosomiasis Gland smears- ECF
etc
Faecal samples — faecal examination e.g. worm eggs
Serological tests — look for antibodies like agglutination tests. Skin scrapings for mites, fleas, lice
and fungi.
Histological examinations
Tissue sections (normal and affected) for histology studies.
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Topic 2: Introduction to Metabolic and Nutritional Diseases
Metabolic diseases are diseases that arise out of improper functioning of the body’s internal
mechanisms and processes. This can be caused by external or internal factors.
Metabolic disorders relates to disturbances of one or more metabolic processes in the
animal/organisms whereas Nutritional disorders are diseases caused by lack of one or more
essential nutrients (deficiencies) or excessive levels of one or more nutrients (toxicities).
Metabolism is the sum of all physical and chemical processes by which living, organized substance
is produced and maintained. The word metabolism is derived from metaballein (Greek) which
means to turn about, change, or alter.
Metabolism is required to maintain homeostasis – stability in the normal body states of an
organism. Complex organisms such as mammals rely on the cells, tissues, and organs of the body
to work together to maintain homeostasis and a state of health.
Causes of Metabolic diseases
The various causes of abnormal metabolism are as diverse as the underlying diseases themselves.
These causes can disrupt specific metabolic pathways or can cause damage to specific organs or
tissues leading to secondary metabolic disease. These causes can be divided into:
a. Genetic defects – hereditary defects probably constitute the largest and most diverse
category. Many of these relate to faulty synthesis or deficiency of enzymes involved in
metabolic pathways.
b. Faulty nutrition can lead to abnormal metabolism by depriving the body of important
nutrients. Examples include vitamins and minerals as co-factors for many enzymes and
glucose for energy metabolism.
c. Hormonal deficiencies and imbalances participate in many metabolic processes. Examples
include deficiencies of insulin leading to diabetes mellitus, hyperparathyroidism as a cause
of metabolic bone disease and metastatic soft tissue mineralization, and the deficiency of
aldosterone in Addison’s disease.
d. Drugs / pharmaceuticals can inhibit enzymes or otherwise block important biochemical
pathways. Obviously, these effects can be the intended mode of action of the drug in the
treatment for disease but drugs may also have undesirable secondary effects. Cortisone is
used to block unwanted inflammation by inhibiting the enzyme phospholipase A2 in the
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synthetic pathway for prostaglandins and leukotrienes. Too much cortisone or related
compounds can cause Cushing’s disease. The diuretic Lasix blocks absorption of sodium
and water from the renal tubules and can lead to hyponatremia and dehydration.
e. Toxins / poisons often disrupt metabolic pathways or damage tissues leading to secondary
metabolic disease. The organophosphate compounds inhibit cholinesterase, the enzyme
necessary to metabolize the neurotransmitter acetylcholine leading to persistent neural
stimulation. A fungal toxin (mycotoxin) called aflatoxin B1 can damage the liver leading
to hepatic encephalopathy (covered later in this lecture).
f. Microorganisms can lead to metabolic disease in diverse ways. Parvovirus infection
damages the intestine in dogs and cats causing vomiting and diarrhoea that lead to
dehydration, ionic imbalances, and acid-base disturbances. Certain toxins produced by
strains of the bacterium Escherichia coli cause little to no overt morphological damage to
the intestine but stimulate active secretion of electrolytes and water from the intestinal
epithelium leading to a secretory diarrhoea, dehydration, electrolyte depletion, and acid-
base disturbances.
Nutritional Disorders
Nutrients in an animal are required for maintenance, growth, development, production and
reproduction. The six basic nutrients needed by an animal are:
a. Carbohydrates – The function of this nutrient is Growth, Body movement, basal
metabolism. Sources in the body include Metabolic breakdown of diet and Fat deposits.
Normal sources in the diet include Roughage and supplements. Some energy related
disorders which we are going to look at include fatty liver syndrome, ketosis (acetonemia),
lactic acidosis, bloat etc.
b. Fats / Lipids – These are considered sources of energy in the animal.
c. Proteins
d. Vitamins - Any of the organic elements, as that are essential to the functioning of the
human body and are obtained from foods. Important vitamins in animals include Vitamins
A, B complex, D, E, K among others. Metabolic disorders associated with imbalance in
vitamin content include white muscle disease among others.
e. Minerals - Any of the inorganic elements, as calcium, iron, magnesium, potassium, or
sodium, that are essential to the functioning of the human body and are obtained from
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foods. Some of the important minerals include calcium, phosphorus, iron, potassium etc.
Examples of metabolic/nutritional disorders associated with mineral imbalances include
milk fever, post parturient haemoglobinuria, piglet anemia etc.
f. Water – It is essential for the normal functioning of almost all metabolic processes in the
body. It is the medium in which chemical reactions take place, it is involved in transport
of substances within the body, temperature control among others. A metabolic/nutritional
disorder associated with water include water poisoning in calves.
When body fails to homeostatize over situation then it is called disorder and when problem
develops due to nutrition then it is called nutritional disorder. Causes of Nutritional Disorders are:
a. Quality of feed
b. Quantity of feed
c. Consistency of feeding
d. Constantibility of feeding
e. Regularity of feeding
Nutritional disorders are diseases caused by lack of one or more essential nutrients (deficiencies)
or excessive levels of one or more nutrients (toxicities).
Production diseases
The term "Production Diseases" referred traditionally to those diseases induced by management
practices, metabolic/ nutritional diseases being typical examples. These occur when the nutritional
demands of production exceed the supply of particular nutrients in the feed.
Recently, "Production related diseases" have been enhanced to include other traits, such as
infertility, and diseases such as mastitis and lameness (laminitis), retained placenta that might
involve infectious agents but exacerbated by nutritional or managemental factors.
They are at times the outcome of managemental mistakes brought about by the drive for higher
yields or genetic selection (hence man-made diseases). Some especially lameness, mastitis and
infertility are important constraint to the dairy industry (culling, low production, poor reproductive
performance).
Production diseases commonly occur in high yielding animals whereby the demand for production
exceeds the animal’s metabolic capacity. They are often multifactorial and appear at the same
stage of lactation i.e. have some interrelationships.
Diagnosis of metabolic, nutritional or production diseases
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Diagnosis of nutritional and Metabolic Diseases is achieved through:
a. History taking: Farmer’s description of what happened. This will include what signs the
farmer saw, when they started, events preceding the onset of the condition, any treatment
attempted, how many other animals in the herd affected, animal characteristics (age, sex,
pregnancy status)
b. General and Physical examination: The veterinarian will examine the animal generally
(demeanour, gait, temperament, posture and ambulation), physically (temperature, heart
rate, respiration rate, status of the mucus membranes, body condition and any other
abnormality)
c. Laboratory Examination – The veterinarian will take appropriate samples to confirm or
rule out any tentative diagnosis. These will include:
i. Whole blood for levels of packed cell volume (PCV), haemoglobin (HB), urea
nitrogen (BUN)
ii. Coagulated blood for Serum levels of inorganic phosphorus, magnesium, calcium,
potassium and sodium, total protein, albumin and globulin, copper, iron, plasma
and non stereatified free fatty acids.
iii. Milk contents (Physical and chemical).
iv. Urine analysis (Physical, chemical and microscopically).
v. Diet analysis (Quantity and quality).
Topic Assignment
Discuss the role of the following vitamins in an animal’s diet:
i. Vitamin A, D, E, K, B, C
ii. Minerals: Selenium, Sodium, Potassium, Magnesium, Iodine
iii. Water
What are their functions.
What happens when they lack?
What happens when they are in excess?
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Topic 4: BLOAT
It refers to distension of reticulorumen by gas by fermentation reaction that goes on in the
reticulorumen.
There are two types of bloat: primary (frothy) bloat and secondary (free gas) bloat.
Primary Bloat
Primary bloat is usually due to dietary and animal factors. Some pasture legumes like alfalfa and
clover are capable of causing this bloat especially when the legumes are immature. Grazing on
young cereal crops and young grasses can also lead to this type of bloat. This bloat is normally
found towards the end of the rainy season. Growing plants usually have high levels of protein.
When these proteins are released into rumen fluid gases will not diffuse from this fluid and a stable
froth is formed. The rumen will be distended by foam with bubbles of gas trapped and unavailable
for eructation.
Animal factors include such factors as the rate of saliva production. Saliva is essential in freeing
gas from ruminal fluid. There may also be differences between animals in the rate and extent of
physical breakdown of feed in the rumen, and the rate of passage of solids out of the rumen.
Secondary Bloat
It occurs when there is accumulation of free gas in the reticulorumen. It’ s due to failure of
eructation which can be due to obstruction of esophagus or stenosis of esophagus. Stenosis may
be due to injuries e.g. by stomach tube which leads to healing by fibrosis. Pressure may also come
from outside e.g. enlargement of lymph nodes of the chest region. Also tumors and hydatid cysts
may cause pressure.
Pathogenesis
Normally, gas bubbles produced in the rumen fluid coalesce, separate from the rumen contents to
form pockets of free gas above the level of contents, and are finally eliminated by eructation. In
frothy bloat, gas bubbles remain dispersed throughout the rumen contents, producing an abnormal
increase in the volume of rumino-reticular contents and consequently inhibiting eructation. The
characteristic frothiness is inadequate coalescence of gas bubbles.
In free gas bloat the gas bubbles coalesce and separate from the rumen fluid, but the animals cannot
eructate the pockets of free gas because of abnormalities of the esophagus.
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Clinical Signs
Bloat is a common cause of sudden death in cattle. Pastured beef cattle are usually more at risk
because they are not observed as regularly as dairy cattle. Feedlot cattle which die of bloat are
commonly found dead in the morning, which may be due to the relative inactivity during the night
or the lack of observation, detection and treatment.
Surviving animals have various degrees of abdominal distension, especially the left paralumbar
fossa. Abdominal distension is usually accompanied by restlessness, the animal may get up and
lie down frequently, dyspnea is marked and may be accompanied by mouth-breathing, protrusion
of the tongue, salivation and extension of the head.
Diagnosis
Diagnosis is fairly easily made from the signs seen, from the various degrees of abdominal
distension.
Treatment
Advise farmer to immediately remove the animal from pasture if bloat is seen. Emergency
treatment can be made by making incision with a sharp kitchen knife in the middle of the left
paralumbar fossa. Incision should be about 10 cm. The incision site is treated when a doctor has
arrived at the farm.
Anti-foaming agent such as poloxalene (Bloat guard) may be used to treat frothy bloat. It acts by
releasing gas from the fluid. Liquid paraffin can also act as anti-foaming agent. A solution of
sodium bicarbonate, 150 g in 1 liter of water administered by stomach tube is also useful.
In secondary bloat, trocar and canula can be used to relieve the free gas. The trocar and canula can
be left in place for several hours or days. However it’ s advisable to treat the primary cause of the
bloat.
Prevention
Frothy bloat can be prevented by limiting access to pasture and avoiding fine-milled feed. It’ s
advisable to feed the animals on dry hay to dilute the effects of dangerous pasture. The above
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drugs can also be given prophylactically. The anti-foaming agent can also be painted on the side
of the animal for it to lick.
MILK FEVER
It is also called parturient paresis or post parturient hypocalcaemia. It is a metabolic disease of
cattle occurring most commonly about the time of parturition in adult females (5-10 years) and is
characterized by hypocalcaemia, general muscular weakness, circulatory collapse and depression
of consciousness.
Aetiology
A depression in levels of ionized calcium in tissue fluids is the basic biochemical defect in the
disease. The levels fall because of loss of calcium and phosphorus in calostrum. The animal
cannot immediately compensate for the marked changes in calcium balance. Older animals for
instance are poor when it comes to mobilizing calcium from bone.
Insufficiency of parathyroid hormones (responsible for increasing blood calcium levels) can also
be an aetiological factor.
Malnutrition/starvation can also lead to low level of blood calcium and inorganic phosphorus.
Pathogenesis
Low calcium levels means there is reduced transmission of impulses in nerve-muscle junction.
There is also decreased muscle contraction and the animals exhibit muscle weakness.
Low calcium also leads to decreased stroke volume and hence decreased blood pressure. Muscles
will be poorly perfused and they become weak. They also experience hypothermia.
The animal eventually becomes unconscious.
Clinical Signs
There are three stages of the disease:
Stage one is a brief one of excitement and tetany with hypersensitiveness and muscle tremor of the
head and limbs. Temperature is normal.
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Stage two is characterized by sternal recumbency. Consciousness is depressed. The animal is dull
with staring eyes. There is lateral kinking of the neck. Temperature is subnormal and extremities
are cold. Intensity of heart sounds is diminished but there is increase in heart rate.
Muzzle is dry and rumen is quiet.
Stage three is characterized by lateral recumbency and the animal is almost completely comatose.
Depression is more marked and the animal is usually bloated. Mortality rate can reach 95% if
animal is untreated.
The three stages above occur within a few hours and death is within a few hours to two days.
Diagnosis
It is based on the occurrence of paresis and depression of consciousness in animals that have
recently given birth to young. Clinical signs such as kinking of neck, recumbency, dry muzzle,
staring of eyes, dilated pupils and lack of feces in area of recumbency help a lot in making
diagnosis.
Treatment
The parentral injection of Calcium salts is the standard practice. 25% solution of calcium
borogluconate is given at 400-800 ml, half the dose given intravenous while the other is given
subcutaneously, intramuscularly or intraperitoneally the salt should be given slowly. Signs of
response include shivering/muscle tremors, increase in intensity of heart sounds, moistness of
muzzle and the animal also defecates and urinates.
Prevention
Keep the animals on low calcium high phosphorus diet during the dry period i.e. later stages of
gestation. This makes the animal to learn to mobilize calcium. You can also do limited milking
in the first 72 hours after parturition.
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GRAIN OVERLOAD (IN RUMINANTS)
It is an acute disease of ruminants that is characterized by rumen hypomotility to atony,
dehydration, acidemia, diarrhea, toxemia, incoordination, collapse, and in severe cases, death.
Aetiology and Pathogenesis

The disease is common in cattle that accidentally gain access to large quantities of readily
digestible carbohydrates, especially grain. Grain overload is common in feedlot cattle when they
are introduced to heavy grain diets too quickly. Wheat, barley and corn are the most readily
digestible grains while oats are less digestible. The amount of feed required to produce acute
illnesss depends on the kind of grain, previous experience of the animal with that grain, the
nutritional status and condition of the animal, and the nature of the ruminal microflora. Adult
cattle accustomed to heavy grain diets may consume 15-20 kg grain and only develop moderate
illness, while others may be acutely ill and die after eating 10 kg grain.
Ingestion of toxic amount of these grains is followed within 2-6 hours by a change in the microbial
population of the rumen whereby the number of gram-positive bacteria (Streptococcus
bovis)increases markedly, which results in the production of large quantities of lactic acid. The
rumen pH falls to < 5, which destroys protozoa, cellulolytic organisms, and lactate utilizing
organisms, and impairs rumen motility. The low pH allows the lactobacilli to utilize the
carbohydrate and to produce excessive quantities of lactic acid. The lactic acid produced causes
causes increased osmotic pressure which results in the movement of excessive quantities of fluid
into the rumen, causing dehydration.
The low pH causes a chemical rumenitis, and the absorption of lactate causes lactic acidosis and
acidemia. There is also hemoconcentration, cardiovascular collapse, renal failure, muscular
weakness, shock and death.
(hemocencentration is increased concentration of cells and solids in the blood, usually resulting
from loss of fluids. Shock is a life-threatening condition occurring when body is not getting enough
blood flow, and is accompanied by signs like low blood pressure, weakness, shallow breathing)
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Clinical Findings
A few hours post-engorgement the only detectable abnormality may be an enlarged rumen and
some abdominal pain (manifest by belly-kicking or treading of hind limbs). In the mild form the
rumen movements are reduced but not entirely absent, the cattle are anorexic but bright and alert,
and diarrhea is common. Animals usually begin eating again 3-4 days later without any specific
treatment
Within 24-48 hours of onset of severe overload, some animals may be recumbent, some will be
staggering, and others will be standing quietly, and all will be completely off-feed. Immediately
after consuming large quantities of dry grain, cattle may engorge themselves on water, but once ill
they usually do not drink at all. The primary contractions of the rumen are completely lacking.
Rumen contents when palpated are firm and doughy. Severely a ffected animals stagger and may
bump into objects. Animals affected commonly lie quietly, often with the head turned to flank
(resembling parturient paresis)
Body temperature is usually below normal 36.5-38.5), but for animals exposed to the sun in hot
weather, it may increase to 410C. Respiration tends to be rapid and shallow 9up to 60-90/min).
heart rate is usually increased. Diarrhea is common, usually profuse and mal-odorous. Feces are
usually soft to liquid and invariably contains some undigested grains
Diagnosis
It is usually obvious if the history (of grain consumption) is available and multiple animals are
affected. Confirmation of diagnosis can be confirmed by a low rumen pH (< 5.5 in cattle
unaccustomed to high grain diet), and examining flora for presence of live protozoa. When only
one animal is involved and there is no history of engorgement, the diagnosis is less obvious, but
sighs such as static rumen, diarrhea, ataxia and normal temperature are characteristic. (in milk
fever, diarrhea and dehydration are not typical)
Treatment
Mild cases can be treated with purgatives (e.g. magnesium hydroxide 500g/450 kg body weight
added to warm water)
In severe cases gastric lavage can be done using stomach tube with warm saline solution.
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Rumenotomy can be done if lavage is unsuccessful.
Oral antibiotics can be given to stop fermentation
Isotonic physiological saline can be given in marked dehydration.
(Cathartics and laxatives/purgatives are drugs that increase motility of the intestine or increase
the bulk of feces. Examples are Caster Oil and Linseed oil for non-ruminants and Magnesium salts
for ruminants. Mineral oil is a common lubricant laxative in horses and ruminants)
Prevention
Avoid accidental exposure to concentrates especially if the animals are not accustomed to such
diets. Feedlot cattle should be introduced gradually to concentrate diets over a period of 2-3 weeks.
Beginning with a mixture of < 50% concentrate in the milled feed containing roughage.
PREGNANCY TOXEMIA
It is also called ovine ketosis, lumpy paralysis or pregnancy disease. It’ s common in overfed ewes
pregnant with twins or triplets or a large single lamb. It’ s characterized by hypoglycemia,
ketonemia, ketonuria, weight loss, depressed milk production and nervous signs. It commonly
occurs in last trimester of gestation, usually the last three weeks of pregnancy. It’ s highly fatal.
Aetiology and Pathogenesis

Primary disease is the under-nutrition in late pregnancy. This leads to hypoglycemia. If the animal
has less glucose it metabolizes fats and ketone bodies (acetoacetate, acetone, βhydroxybutyric
acid) will be formed.
Under ordinary circumstances ketone bodies are utilized for energy production provided there is
oxaloacetate (OAA). OAA is derived from carbohydrates (propionic acid). Therefore when the
animal is underfed or is anorexic there will be OAA deficiency and ketone bodies will accumulate.
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Clinical Signs
The ewe shows signs of restlessness and aimless walking. It knocks against objects as it walks.
Other signs include twitching of muscles of eye, ear and other body parts, blindness and sternal
recumbency. Terminal signs are coma and death.
Diagnosis
The disease is normally suspected in heavily pregnant ewes which show nervous signs and die
within a week.
Treatment
Ewes should be dosed at once with glucose, 60 g in 300 ml warm water. A Glucose solution plus
glucocorticoids may also be given intravenously.
An immediate caesarian section to remove lamb may also be done but results are not good.
Prevention
Ensure the plane of nutrition rises in the second half of pregnancy even if it means restricting diet
in the early stages. Keep the parasite load down and avoid stressing the animals.
KETOSIS
It is also called acetonemia. It is a metabolic disease of lactating cows within a few days to a few
weeks after calving. Its characterized also by hypoglycemia, ketonemia, ketonuria, inappetance,
lethargy, weight loss, depressed milk production and occasionally incoordination. Ketone bodies
will be accumulated in the body. Primary ketosis is due to carbohydrate deficiency or defect in
carbohydrate metabolism. Secondary ketosis is due to other diseases that cause anorexia.
Epidemiology
Disease occurs worldwide where high-producing dairy cattle are kept. Disease is common in older
cows producing more milk and it can occur at any time of the year. Usually one or two animals
are affected in a herd. Some animals are genetically more prone to the disease.
Pathogenesis
It is similar to pregnancy toxemia.
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Clinical Signs
There is usually a rapid loss of weight following a decrease in appetite. The feces are mucus coated
and there is acetone odor in breath. Central nervous system signs may be seen in other animals,
for instance, walking in circles, incoordination and blindness. This is called hypoglycemic
encephalopathy.
Diagnosis
It can be made from history of rapid weight loss following recent calving. Acetone breath and
retained fetal membranes can also aid in making diagnosis.
Treatment
50% glucose solution can be given at 500-700 cc intravenous. Glucose together with
glucocorticoids are very effective.
Chloral hydrate and CNS depressants can also be given when there are CNS signs.
Prevention
Cows susceptible to ketosis should be maintained on relatively high energy intake before calving.
The level should be increased substantially after calving.
Avoid unnecessary stresses to the animal e.g. abrupt changes to feed and complete milking of
animals.
LACTATION TETANY (GRASS TETANY, HYPOMAGNESEMIC TETANY, WHEAT

PASTURE POISONING DISEASE)
It is a highly fatal metabolic disease of ruminants, caused by hypomagnesemia and is characterized
by clonic and tonic muscular spasms and convulsions. Death is due to respiratory arrest.
(Spasm is an exaggerated contraction of muscle, usually associated with increase in tone. Tonic
spasm is a continuous contraction. Clonic spasm comes in bulks with relaxations in between.
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Tetany is a generalized tonic muscular spasm. Convulsions are violent muscular contractions
affecting part or all of the body )
The disease is worldwide but common in temperate countries. It usually occurs when there is grass
lash immediately after rains (usually within the first two weeks) This grass has low magnesium
levels. It is also common in pastures that have been top-dressed with fertilizers especially those
containing nitrogen and potassium which reduce availability of magnesium in soils. It occurs in
both beef and dairy cattle but can also affect sheep.
The disease also occurs when animals are fed on cereals like wheat, oat, barley grass (i.e. young,
green cereal crops)
Aetiology
Low magnesium levels can result from stresses such as lactation, reduced level of mineral intake
and assimilation. Animals fed on phytic-acid-containing plants can also suffer from the condition
because phytic acid combines with magnesium and calcium and makes them unavailable in
circulation.
Pathogenesis
Low magnesium levels facilitate increased transmission of nerve impulses across neuro-muscular
junctions
Clinical signs
In acute (convulsive) stage of disease there is sudden onset with severe hyperesthesia and there is
continuous twitching of muscles and ears. There will be a staggering gait and the animal falls
down when moving and there is tetany of all the limbs. The animal can die within one hour if not
treated. In most cases animals are found dead on pasture without any illness being observed.
In subacute form of disease the onset is gradual (3-4 days) there is slight inappetence and
exaggerated limb movements. The cow often resists being driven and throws her head about as
though expecting a blow. There is mild tetany and convulsions and frequent defecation. The
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animal can recover spontaneously without treatment or the animal may become recumbent as
disease progresses
In chronic form of disease many animals don’ t show clinical signs. A few animals can show
dullness, unthriftiness and indifferent appetite.
Diagnosis
History helps in achieving tentative diagnosis. It includes feeding of young pastures and cereal
crops within the first two weeks of rain.
Treatment
Give animals a solution of magnesium sulphate orally or intravenously. Give 200-300 ml of 20%
solution.
Control
Remove the animal from the pasture
Give animal mineral supplement containing magnesium and calcium Stop
using fertilizer containing nitrogen and potassium.
IRON
It is a trace mineral and in the animals body, more than 90% is found combined with proteins, the
most important being hemoglobin. Iron also occurs in blood serum in a protein called transferrin
which is concerned with the transport of iron from one part of the body to another. The storage
form of iron is ferritin and is found mostly present in liver, spleen, kidney and bone marrow. Iron
is also a component of many enzymes.
Deficiency Symptoms
A dietary deficiency of the element would affect hemoglobin since more than half the iron present
in the body is in the form of hemoglobin. Red blood cells are continually produced in the body to
replace those destroyed through catabolism. Anemia due to iron deficiency occurs most commonly
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in rapidly growing sucklings, since the iron content I milk is usually low. This is common in pigs
housed in pens without access to soil or pasture. The sow’ s milk is not able to produce as per the
demands of the piglets. Iron should be provided by dosing or injection with iron salts. Anemia in
piglets is characterized by poor appetite and growth and breathing is labored.
Sources of Iron
Good sources are green leafy materials, leguminous plants and seed coats. Feeds of animal origin
like meat, blood and fish meal are excellent sources. Milk is a poor source.
Iron toxicity
It is not a common problem in farm animals, but can result from prolonged oral administration of
the element. Chronic toxicity results in alimentary disturbances and reduced growth.
COPPER
A deficiency of copper impairs the animal’ s ability to absorb iron, mobilize it from the tissues and
utilize it in hemoglobin synthesis. Copper is a component of many proteins in the body e.g.
erythrocuprein which occurs in erythrocytes where it plays role in oxygen metabolism. Copper
also plays vital role in many enzyme systems e.g. it is a component of cytochrome oxidase which
is important in oxidative phosphorylation. Copper also occurs in certain pigments e.g. pigments
of feathers, hair, fur and wool. The liver acts as the main storage organ of copper in the body.
Deficiency Symptoms
Signs include anemia, poor growth, bone disorders, scouring, infertility, depigmentation of
hair/wool and gastrointestinal disturbances. Copper plays an important role in production of “
crimp” in wool. When there is deficiency the hair lacks crimp and is referred to as “ stringy” or “
steely” .
Sources of Copper
The copper content of crops is related to some extent to the soil copper content. Seeds and their
byproducts are usually rich in copper, but straws contain little. The milk copper content is low
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and therefore it is customary to include a trace of copper sulphate especially when dosing piglets
with an iron salt.
Copper Toxicity
Continuous ingestion of copper in excess of nutritional requirements leads to an accumulation of
the element in body tissues especially liver. Sheep are especially susceptible to chronic copper
poisoning. Poisoning has been known to occur in areas where the herbage contains copper at about
10-20 mg/kg DM. chronic poisoning results to necrosis of liver cells, jaundice, loss of appetite
and death from hepatic coma.
ZINC
It is found in every tissue of the animal. It tends to accumulate mostly in bone which is the main
storage organ. Several enzymes in the body contain zinc. Zinc also is an activator of several
enzyme systems.
Deficiency Symptoms
In pigs deficiency is characterized by subnormal growth, depressed appetite, poor feed conversion
and parakeratosis. Chicks exhibit retarded growth and foot abnormalities, parakeratosis and bone
abnormality called “ swollen hock syndrome” . In calves, deficiency signs include inflammation
of the nose and mouth, stiffness of joints, swollen feet and parakeratosis.
Sources of Zinc
Zinc is concentrated in the bran and germ of cereal grains, and animal byproducts such as meat
meal and fish meal are also rich sources compared to plant protein supplements.
Zinc Toxicity
Excessive amounts in the diet depress feed consumption
PHOSPHORUS
It has more functions in the body than any other mineral. It is closely associated with calcium in
bones. It occurs in phosphoproteins, nucleic acids and phospholipids. It plays a vital role in energy
metabolism in the formation of ADP and ATP.
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Deficiency Symptoms
Tropical and subtropical areas of the world are more prone to deficiency, and a deficiency of this
element can be regarded as the most widespread and economically important of all the mineral
disabilities affecting grazing livestock.
Like calcium, it is needed for bone formation and deficiency can cause rickets or osteomalacia.
Pica or depraved appetite has been noted in cattle where there is deficiency of phosphorus in their
diet. The animals have abnormal appetite and chew wood, bones, rags and other foreign material.
Low intakes of phosphorus have also been associated with poor fertility in adults and subnormal
growth in young deficiency is more common in cattle than sheep
Sources of Phosphorus
Milk, cereal grains, fish meal and meat products containing bone are good sources of phosphorus.
Hay and dry crop residues are generally very poor sources. Much of the element present in cereal
grains is in the form of phytates, which are salts of phytic acid, a phosphoric acid derivative.
Insoluble calcium and magnesium phytates occur in cereals and other plant products. Phytate
phosphorus can be utilized by ruminants because of the presence of bacterial phytases in the rumen.
SELENUIM AND VITAMIN E

Both selenium and Vitamin E are essential nutrients for animals and man. Each has a fundamental
role in maintenance of integrity of cells. They cooperate in protecting cellular membranes from
oxidative degradation.
Vitamin E occurs naturally in several forms, of which alpha-tocopherol is the most widely
distributed. Green fodders are good sources of the vitamin, as are young grasses. Cereal grains
are also good sources of the vitamin. Animal products are generally poor sources of the vitamin.
The level of selenium in foods of animal origin is extremely variable depending mainly on the soil
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conditions under which they are grown. Some species of plants which grow in seleniferous areas
contain very high levels of selenium and these can cause poisoning to animals with signs such as
respiratory failure.
Vitamin E, on its own, acts as a non-specific biological anti-oxidant. When it acts in association
with selenium, the vitamin protects vital phospholipids (found in membranes) from peroxidative
damage.
The vitamin (which is usually attached to cell membrane) also acts within the phospholipid
membrane of vital organelles in preventing formation of peroxides. These endogenous peroxides
(e.g. hydrogen peroxide and lipid peroxidases) which do form (in presence or absence of vitamin
E) are apparently destroyed by the enzyme glutathione peroxidase which contains selenium. The
peroxides are capable of causing irreversible denaturation of essential cellular proteins which leads
to degeneration and necrosis. The vitamin can therefore be regarded as the first line of defence in
preventing peroxide formation, with the selenium-containing enzyme acting as a second line of
defence in destroying any peroxides which are formed before they can damage the cell.
Deficiency Symptoms
Muscle degeneration (myopathy) is the most important manifestation of Vitamin E deficiency in
domestic animals. When heart muscles are affected there may be sudden death. When skeletal
muscles are affected there may be stiffness and un-natural postures. Pigs suffering from deficiency
show signs of muscular weakness and severe liver damage. In chicks the main muscles affected
are the pectoral muscles. “ Crazy chick disease” (encephalomalacia is a condition in which the
chick is unable to walk or stand, and is accompanied by hemorrhages and necrosis in brain.
Exudative diathesis is also a deficiency syndrome in chicks and it is a vascular disease
characterized by generalized edema of subcutaneous fatty tissue, associated with abnormal
permeability of capillary walls.
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COBALT
Cobalt is required by microorganisms in the rumen for the synthesis of Vitamin B12. If the element
is deficient in the diet the vitamin cannot be produced in sufficient to satisfy animal requirements.
The vitamin also has another role, that of activating certain enzyme reactions.
Sources
Most feeds including pastures contain traces of cobalt.
Deficiency Syndromes
Certain disorders noted in sheep and cattle include emaciation, anemia and listlessness. These
signs have collectively been known as “ pining” , and have been associated with dietary deficiency
caused by low concentration of cobalt in the soils and pasture.
Toxicity
It is extremely unlikely, as there is a wide margin of safety between nutritional requirement and
the toxic level.
VITAMIN A
It is a pale yellow crystalline solid, insoluble in water but soluble in fats and various fat solvents.
It is also known as retinol. The liver, egg yolk and milk fat are good sources of the vitamin Vitamin
A does not exist as such in plants, but is present as precursors or provitamins in the form of certain
carotenoids which can readily be concerted by the animals into the vitamin. At least 80
provitamins are known, but β-carotene is the most widely distributed in nature and also the most
active. Green feeds are excellent sources of β-carotene, and in dried crops the degree of greenness
is usually a good indication of the carotene content. Sun-drying of the crops therefore leads to
large losses of the vitamins. Yellow maize is also a good source of the provitamin (βcarotene) but
most concentrates used in animal feeding are devoid of the provitamin.
Conversion of carotene into vitamin A usually occurs in the intestinal wall and also in the liver.
Vitamin A is an important component of rhodopsin (visual purple) which is the photo-receptor for
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vision at low light intensities. Vitamin A is also involved in the formation and protection of
epithelial tissue and mucous membranes
Deficiency Symptoms
Animals have less ability to see in dim light, commonly known as “ night blindness” . In adult
cattle a mild deficiency is associated with rough hair and scaly skin. In breeding animals a
deficiency may lead to infertility, and in pregnant animals to abortion
In practice, severe deficiency symptoms are unlikely to occur in adult animals except after
prolonged deprivation. Grazing animals generally obtain more than adequate amounts of
provitamins from pasture grass. Cattle fed indoors on high cereal rations are prone to deficiency,
and should be given high vitamin supplement, as are pigs kept indoors.
In poultry, deficiency symptoms include retarded growth, weakness, ruffled feathers and a
staggering gait. Egg production and .hatchabilities are also reduced. Vitamin a concentrates can
be added to diet to address this problem since most concentrated feeds in poultry diets are poor in
Vitamin A
VITAMIN D
The two most important forms are ergocalciferol (D2) and cholecalciferol (D3). They are insoluble
in water but soluble in fats and organic solvents. Vitamin D is limited in distribution. Egg yolk is
a good source but cow’ s milk is a poor source. Calostrum is a good source. Clinical
manifestations of avitaminosis D are usually treated by injections of the vitamin into the animal.
Under natural conditions, animals can be able to synthesize vitamin D when exposed to irradiation
from the sun. under the influence of the sun, the two vitamin precursors present in the skin i.e.
ergosterol and 7-dehydocholesterol, are converted into calciferols before they are of any use to the
animal.
Together with parathyroid hormone and calcitonin, vitamin D is involved in calcium metabolism.
The three interact to maintain a constant concentration of calcium despite variations in intake and
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excretion. Vitamin D enhances intestinal absorption of calcium through the formation of calcium-
binding-protein.
Deficiency Symptoms
In young animals there will be rickets, in which deposition of calcium and phosphorus in growing
bone is interfered with. As a result the bones are weak and easily broken and the legs may be
bowed. In older animals deficiency causes osteomalacia, in which there is resorption of bone
already laid down. In poultry, deficiency causes bones and beaks to become soft and rubbery,
growth is retarded and legs may be bowed. Most feeds of pigs and poultry contain little or no
vitamin D and the vitamin is generally supplied in the form of synthetic preparations. The need to
supplement diets of cattle and sheep is not so great as that of pigs and poultry since adult ruminants
can receive adequate amounts from irradiation while grazing.
VITAMIN K
The two most important naturally occurring compounds of vitamin K are vitamin K1
(phylloquinone) found in green plants and vitamin K2 (menaquinone) which is a product of
bacterial growth. Vitamin k is present in most green leafy materials, Lucerne, cabbage and kale
being good sources. Egg yolk, liver and fish meal are good sources..
Vitamin k is necessary for the synthesis of prothrombin in the liver. Prothrombin is the inactive
precursor of thrombin, an enzyme that concerts the protein fibrinogen in blood plasma into fibrin,
the insoluble fibrous proten that holds blood clots together. Prothrombin normally must bind to
calcium before it can be activated.
Deficiency Symptoms
In ruminants and pigs, symptoms are rare under normal conditions because bacterial synthesis in
digestive tract supplies enough vitamins for the animal needs. In chicks, symptoms include anemia
and a delayed clotting time. Birds are easily injured and may bleed to death.
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SALT (SODIUM CHLORIDE POISONING) IN PIGS
Etiology
Salt poisoning (sodium chloride, NaCl), also called “water deprivation sodium ion toxicosis” can
result when excessive quantities of salt are ingested and intake of potable water is limited. The
toxicity is unlikely to occur as long as salt-regulating mechanisms are intact and fresh drinking
water is available. It has been reported in virtually all species of animals all over the world. It is
more common in swine (the most sensitive species), cattle, and poultry while the sheep are
relatively resistant.
The toxic doses for acute sodium chloride poisoning in pigs, horses and cattle is 2.2g/kg body
weight and 6g/kg for sheep. The toxicity is influenced by age and bodyweight. Salt toxicity is
directly related to water consumption. Water intake in animals can be reduced significantly or
abolished completely due to factors such as mechanical failure of waterers, overcrowding,
unpalatable medicated water, new surroundings, or frozen water.
The feeder pigs on feed containing only 0.25% salt have had salt poisoning when water intake
was limited, yet even 13% salt in feed may not produce poisoning when adequate fresh water is
consumed. Swine feed should contain 0.5-1% salt, and fresh drinking water should always be
available.
Epidemiology
Salt poisoning will mainly occur where borehole water is used for livestock drinking.
Sources of toxin
These include;
1. Saline drinking water when the animals are thirsty.
2. Water accumulating in salt troughs during drought periods
3. Salt deprived animals may eat excessive amounts if suddenly allowed access to unlimited
quantities
4. Where animals are confined and fed on prepared feeds containing much salt or salt is
provided intermittently or trough space is limited
5. Swill fed to pigs may contain a lot of salt especially from dough of bakers or brine from
butcher’s shops, salt whey from cheese factories or salted fish waste.
6. Excessive sodium sulfate given to pigs to treat gut edema it water intake is limited
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7. Environmental pollution by oil wells.
8. Temporary restriction of water supply to the pigs 8-12 weeks of age lambs and calves fed
prepared feeds containing the standard recommendation of 2% salt.
Pathogenesis
In acute poisoning, ingestion of excessive amounts of salt results in gastroenteritis due to

irritating effects of high salt concentration. This leads to dehydration and is exacerbated by
increased osmotic pressure of the alimentary tract contents. Absorbed salt may cause
involvement of the central nervous system as in chronic poisoning.
In chronic poisoning, there is decreased water but normal salt intake leading to accumulation of
sodium ions in tissues, including brain, within a period of several days. When water is made
available in unlimited quantities, it moves to the tissues to restore normal salt-water equilibrium.
This results to acute cerebral edema and sudden rise in intracranial pressure. In pigs, there is
accumulation of eosinophils in nervous tissues and the meninges. This form of salt poisoning is
chronic as the sodium ions accumulate gradually. The clinical syndrome however is acute. Most
outbreaks of polioencephalomalacia occur in circumstances which suggest chronic salt
poisoning.
Clinical findings
In pigs, chronic salt poisoning starts with appearance of constipation, thirst and pruritus 2-4
days after exposure. This is followed by a nervous syndrome 12-24 hours. There is blindness and
deafness, aimless wandering, bumping into objects and pressing the head. There may be circling
or pivotal standing on one front leg. Recovery may occur at this time or epileptic convulsions
begin, recurring every 7 minutes with tremor of the snout and neck. Clonic contractions of the
neck muscles cause jerky opisthotonus , head is almost vertical, pig moves backwards , sitting
posture, clonic convulsions, lateral recumbency, jaw champing, salivation and dyspnea, death
due to respiratory failure or coma which the animal may recover and starts the episode again.
Eosinophilic dermatitis has been observed at postmortem in pigs transported with salted trucks to
prevent slipping.
Diagnosis
1. Typical clinical signs- in pigs recently moved to new quarters, change of ration, lack of access
to water at all times suggest sodium salt poisoning
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Samples for confirmation
Toxicology-Samples for toxicology include; 50g liver, skeletal muscles, brain
Histology-formalin fixed half sectioned brain
Confirmation depends on detection of elevated levels of sodium chloride in blood or in tissues

and fluids and in pigs- presence of aggregations of eosinophils in the brain
Differential diagnosis
• Encephalitis
• Pseudorabies in suckling young pigs
• Viral encephalomyelitis
• Polioencephalomalacia in pigs
• Gut edema occurring in rapidly growing pigs in the same age group
• Mulberry heart disease
Treatment
Primary treatment- Immediate removal of toxic feed or water, restricted amounts of fresh water
at frequent interval
Supportive treatment- Alimentary tract sedatives if there is gastroenteritis, administration of
isotonic fluids in dehydration, administer sedatives if there is cerebral edema, diuretics or
hypertonic solutions injected parenterally.
Control
1. All drinking water of all livestock should not contain more than 0.5% sodium chloride or total
salts
2. Salt and water should be freely available at all times
3. Diets for pigs should not contain more than 1% salt.
Water Intoxication
INTRODUCTION
Water intoxication is a condition that occurs when excessive quantities of water are ingested by
very thirsty animals. It commonly occurs in animals that have been subjected to severe exercise
or high environmental temperatures.
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ANIMALS AFFECTED
In cattle, the condition has been reported to occur in all ages, but it is more common among calves
2–10 months of age and is most frequent in calves 3–5 months of age. All breeds of cattle are
affected. The condition has no sex predilection.
PREDISPOSING FACTORS
A number of factors predispose calves to water intoxication. Young bucket-fed calves usually
drink excessive quantities of water if it is offered to them in the manner in which they usually
receive their milk. Another predisposing factor is the high ruminal capacity to hold ingested water
as compared with total body size. Chronic subclinical dehydration accompanied by increased
environmental temperature, exercise or increased body water loss due to diarrhoea or fever also
predisposes calves to water intoxication.
HISTORY
Animals are exposed to a water source where they drink ad libitum after a long period of restriction
and they then start voiding ‘bloody’ urine. The farmer may report having raised calves on milk or
milk substitutes alone, without access to additional water, followed by either unlimited water
supply or an automatic water source. One or 2 calves are usually involved on small-holder farms,
while several may be involved on large beef and dairy farms. In adult cattle, the commonly
reported cases involve beef herds raised on rangelands that have had no water supply, followed by
excess supply.
CLINICAL SIGNS
In a group of calves, water intoxication may be manifested in all or only a few of theanimals.
Clinically, the condition is characterised by haemoglobinuria and nervous signs. The nervous signs
include hyperaesthesia, muscular tremors, nystagmus and lethargy. Mild cases recover in 3–4
hours. In severely affected animals, lethargy may progress to depression and coma, and death
occurs in 24–48 hours. In some cases haemoglobinuria is the only clinical sign observed; in others,
the nervous signs predominate and haemoglobinuria is not detected. Additional signs include
hypothermia, salivation, severe ruminal tympany, colic, diarrhoea, arrhythmia, oedema of the
eyelids and erection of body hair. In adult cattle, water intoxication is manifested clinically by
haemoglobinuria. Other signs present in calves are rare. Unlike camels27, bloody diarrhoea and
abortion have not been recorded in cattle.
PATHOGENESIS
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After drinking too much water, animals develop a state of positive water balance. The excess water
circulating in the body leads to haemodilution. In cases of water intoxication in both calves and
adult cattle under experimental conditions, a sharp drop in plasma Na+ concentration due to
haemodilution has been reported. This leads to increased absorption of water down a concentration
gradient into the cells. Cellular hydration occurs and in organised tissues, the cells increase in
turgidity; this is evident in the brain, where oedema occurs, causing nervous signs. In unorganized
tissues, particularly the erythrocytes, hypotonicity of the blood leads to lysis of the cells and the
resulting haemolysis may cause severe anaemia and haemoglobinuria. In calves, haemoglobinuria
has also been attributed to fragility of erythrocytes. The osmotic fragility of erythrocytes has been
found to be higher in calves suffering from water intoxication than those that do not suffer from
the condition. In adult cattle, fragility of erythrocytes has not been reported to play a role in the
pathogenesis of water intoxication.
DIAGNOSIS
Diagnosis of water intoxication is based on age incidence, history of free access to water after a
period of restriction, rapid onset of nervous signs and mortality, haemoglobinuria and the finding
of pulmonary oedema at necropsy. Confirmatory diagnosis is achieved by elimination of other
diseases that cause nervous signs and haemoglobinuria in cattle and, retrospectively, by response
to treatment.
DIFFERENTIAL DIAGNOSES
Water intoxication needs to be distinguished from other diseases that cause nervous signs and
haemoglobinuria. Numerous diseases and intoxications can cause nervous signs in cattle of various
ages. Babesiosisis the most usual cause of haemoglobinuria in adult cattle, and may sometimes be
observed in calves.
TREATMENT
Hypertonic saline (5 %) given intravenously has been recommended for treatment of water
intoxication. However, this is effective only in mild to moderate cases. In severe cases, use of both
5% dextrose saline solution intravenously and a tranquilliser such as acetylpromazine has been
found to achieve a better response in calves.
PREVENTION
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Prevention of water intoxication can be achieved by provision of salts and water ad libitum to
calves from as early as 2 weeks of age. The salts may be provided as blocks or powder licks for
the calves to lickadlibitum.
POISONOUS PLANTS
A variety of these plants have caused extensive loss to the livestock industry in many parts of the
world especially in the tropics and sub-tropics where drought and feed shortage force animals to
eat these plants.
Conditions For Eating The Plants
i) Most poisonous plants are unpalatable and remain green even if other plants have dried up.
They are also not attacked by insects and army worms. Drought kills regular grass and not
the poisonous plants. Animals will eat out of desperation
ii) When animals are transported over long distances without sufficient feed and water. When
they are later turned on pasture they eat indiscriminately and are likely to feed on these
plants.
iii) Sometimes poisonous plants are harvested together with hay. Most likely it’ s the seeds
that are included in the hay. iv) Overgrazing – animals eat everything available and
poisonous plants are left. Animals will have no other alternative.
Poisonous Principles Found in Plants

A variety of compounds produced in plants or absorbed by plants may cause toxic reactions when
ingested by animals. The poisonous principles include alkaloids, polypeptides, amines,
glycosides, oxalates, resins/resinoids, phytotoxins (toxalbumins), minerals, nitrogen compounds
and compounds causing photosensitivity.
BRACKENFERN POISONING
It has been seen in cattle, buffalo and sheep. Its characterized by persistent hematuria and anemia.
The outcome is usually fatal. The disease is worldwide and cattle over two years are commonly
affected. The disease is common in animals grazed on poor unimproved pasture.
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The disease is caused by feeding on low levels of Pteriduim aquilinium (Brackenfern) for long
periods. The plant has some carcinogens which cause urinary bladder hemangiosarcoma. The
lesions in bladder lead to hematuria.
The main sign of disease is large quantities of blood being discharged through urine. This leads
to severe anemia, characterized by pale mucous membranes and pounding heart beat. The animals
are likely to be recumbent because of weakness and they die in a week or so.
There is no recommended treatment. Animals can be salvaged for slaughter. Animals must be
removed from affected pasture. The main handicap in control is that the fern grows very fast and
it’ s difficult to prevent animals from gaining access to it.
SENECIO POISONING
Seneciosis in farm animals represents the severe poisoning by pyrrolizidine alkaloids from plants
of the genus Senecio. There are two forms of the disease. Acute poisoning is due to ingestion of
large quantities of the plant over a short period of time. This causes death within a few days. Prior
to death, acutely affected animals (cattle) show anorexia, may display abdominal pain and
sometimes diarrhea. Chronic poisoning is due to ingestion multiple lower doses over a longer
period of time. The most constant clinical signs of chronic poisoning include depression, anorexia,
weight loss, ascites (under jaw and brisket), and jaundice. Other signs are tenesmus, often followed
by rectal prolapse, and animals also have a rough hair coat.
There is no effective treatment once clinical signs appear. It’ s advisable to remove and destroy
the contaminated feed. Sheep are less susceptible than cattle and horses are more susceptible than
cattle.
CROTALARIA POISONING – Signs are similar to Senecio poisoning. The toxic principle is
an alkaloid monocrotaline. Chicken, horses, cattle and swine are mostly affected. Poisoning
occurs from consuming the green plant; hay contaminated with crotalaria, or dried seed in
harvested grain.
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Both Senecio and Crotalaria produce liver cirrhosis and the above signs are related to liver
insufficiency (i.e. weight loss, emaciation and icterus)
LANTANA CAMARA POISONING

Lantana camara is a weed that often threatens livestock due to its toxicity. Red varieties are thought
to be the most toxic. Livestock are often forced to eat them due to inadequate feed. Significant
lantana toxins are the triterpene acids, lantadene A, Lantadene B and their reduced forms. A toxic
dose for a 500 kg cow varies from 5 to 20 kg of fresh leaf.
Symptoms of poisoning include the following:

a. Excessive skin sensitivity to sunlight (photosensitization)
b. Liver damage
c. Yellow discoloration (jaundice) of the whites of eye and gums, and skin of nose and mouth.
d. Reddening and inflammation of unpigmented white skin.
e. Painful and ulcerated muzzle.
f. Reddening and discharge from the eyes (conjunctivitis)
Activated charcoal is a very effective treatment of poisoning in cattle and sheep. Give 2.5 kg in
20 liters of electrolyte replacement solution for cattle and 500 g in 4 liters of electrolyte
replacement fluid for sheep/goats.
SNAKES AND SNAKE VENOMS

In domestic animals snake bites are most frequent in dogs. Bites are usually around the head, neck
and lower limbs.
Snake bites can occur under the following conditions:
i) Accidental when animals step on the snake
ii) Animal itself may attack a snake iii) Snake
may attack animal while grazing
Snake venom is a mixture of proteins secreted by special glands found in or near upper jaw. The
mixture is pressed out of the gland by the biting process. It comes out through a groove in the
fung. Most venoms have enzymes that seem to enhance the virulence and rate of spread of venom.
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The enzymes include cholinesterase, hyaluronidase, ribonulease, oxyribonuclease and proteolytic
enzymes.
Venom Classification
It is based on clinical picture after the snake bite.
Neurotoxins affect CNS. They are found in cobras and mambas. Animals bitten exhibit nervous
signs including restlessness and incoordination. Death is due to respiratory failure.
Haemotoxins interfere with blood clotting. Some are coagulants while others are anticoagulants.
There is capillary damage, leading to hemorrhage. The bitten area becomes swollen because of
hemorrhage. Examples of snakes here are vipers
Diagnosis of Snake Bites

It is difficult because the offending snake is usually not around. You may be able to identify two
fung marks.
Treatment
It requires speed. The animal must be restrained and a tourniquet applied where applicable.
Sometimes its necessary to excise the area of bite. Glucocorticoids and antibiotics are helpful.
You can inject polyvalent antivenin or specific antivenin if you know the snake.
BEES
Their venom contains histamine and two polypeptides – apamin and mellitin. Venom also has
hyaluronidase. Serious cases of bee stings are due to allergic reactions. Apply anti-histamines
topically and remove stings
SCORPIONS
They have their venom apparatus at the tail. Venom has complex mixture of pharmacologically
active compounds. Compounds isolated include phospholipase, acetycholinesterase,
hyaluronidase, toxic proteins, free amino acids and serotonin.
Antihistamnies and sedatives can be given.
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Reproductive Disorders
Introduction to reproduction and reproductive disorders
Reproduction is the process by which animals produce offspring for the purpose of continuing the
species. The process of reproduction begins with copulation, which is the mating of a male and
female of the species.
Sperm cells from the male are deposited in the female reproductive tract and try to unite with an
egg cell. When fertilization (a sperm cell and egg cell unite) occurs, an embryo begins to develop.
The embryo attaches to the wall of the uterus where it is protected, receives nourishment, and
develops. When the new offspring reaches the end of the gestation period, it is delivered from the
female reproductive tract in a process called parturition.
To completely understand the process of reproduction, a basic knowledge of the reproductive tract
structures and functions is required. This will have been covered in your anatomy lectures.
Additional resources on the anatomy and physiology of the reproductive tract can be found at
https://cals.arizona.edu/classes/ans215/lectures/MaleReproductiveSystemXVII.pdf (male) and
https://cals.arizona.edu/classes/ans215/lectures/FemaleReproductiveSystemXVI.pdf (female).
Reproductive disorders are conditions that lead to the inability or loss of normal functioning of the
process of reproduction. In the following lectures we will look at infertility and abortion. We are
then going to discuss neonatology which is how to take care of newborns and finally look at some
reproductive diseases.
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Physiology of parturition in Domestic Animals
Parturition is the physiological process by which the pregnant uterus delivers the fetus and
placenta from the maternal organism. It is important to be familiar with normal parturition as it
occurs so that there may be immediate recognition of any problems in order to assist at the proper
time. It is a very critical management phase in the production cycle of livestock. Ensuring that
parturition goes smoothly is the key to avoiding serious economic losses as well as maintaining
the well-being of one’s herd.
A majority of births occur without any incidents or problems; however, things can go wrong during
parturition that vets and livestock producers must be prepared to deal with when they occur.
Significance
Preterm labour occurs in 7% pregnancies (<37 weeks) and accounts for >75% mortality and long
term disability.
Post term labour occurs in approximately 5-10% pregnancies (>42 weeks) and leads to increased
obstetrical complications
Signs of approaching parturition
Generally similar but vary in certain respects vary from species to species. However it is important
to know the Breeding date: important in estimating parturition time.
a. Prior to parturition most animals tend to segregate themselves from the rest.
b. Nest building in multiparous species.
c. Pelvic ligaments, become progressively more relaxed, causing sinking of croup ligaments
& muscles. This is due to edema and changes in collagen fibers in connective tissue:
Estrogen and relaxin effects.
d. Relaxation of pelvic ligaments: elevation of tail head.
e. The vulva becomes progressively edematous and more flaccid until it is 2 to 6 times its
normal size.
f. Udder enlarged and edematous. Begins about fourth month in heifers; noticed in last 2 to
4 weeks in pluriparous animals. Edema may be extensive in young animals & interfere
with walking. May extend from the udder to the xiphoid region i.e. physiological edema.
Looks like a hernia in the umbilical region.
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g. Just prior to parturition udder secretion changes from a honey-like dry secretion to a
yellow, turbid, opaque cellular secretion, i.e. colostrum.
h. Tenacious, whitish, stringy type of mucus may be seen from vulva from 7 months and
becomes more profuse as parturition approaches.
i. Anorexia & restlessness during last few hours before parturition.
j. Signs of abdominal pain: kicking abdomen, raising & switching the tail, lying down &
rising.
Initiation of parturition
Hormonal factors are of prime importance. The process starts in hypothalamus of fetal brain:
placental ageing, nutritional & uterine restrictions to growth, accumulation of waste leads to stress
in the fetus. The fetus starts producing the stress hormone cortisol.
Fetal hypothalamus and the pituitary gland needed for accumulation of cortisol in the fetal and
then maternal blood.
Stress of the fetus from aging (reduced uterine space and nutrition, accumalated waste) triggers
plasma adrenocorticotrophin (ACTH) and cortisol production from fetal adrenals
Plasma adrenocorticotrophin (ACTH) and cortisol concentrations rise progressively in the last 15–
20 days of gestation
This sustained release of glucocorticoids is essential for organ maturation and also provides the
trigger for the initiation of parturition
The prepartum surge of fetal cortisol leads to an increase in the estrogen-progesterone ratio (a rise
in the 17-estradiol-progesterone (E2/P4) ratio).
Elevated cortisol causes conversion of placental P4 (progesterone) to E2 (estrogen).
Blood levels of P4 drop, E2 rises.
The rise in placental E2 causes synthesis of prostaglangin F2 α (PGF2α).
Estrogen, in turn, stimulates intrauterine PG production ( a rise in PGE2and PGF2  production)
and also triggers the expression of contraction-associated proteins within the myometrium, leading
to initiation of labor and delivery of the fetus
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Mechanical stimulation of the cervix and anterior vagina increases the firing rate of oxytocic
neurones in the hypothalamus; the resulting increase of circulating oxytocin levels is associated
with the rather explosive nature of expulsion of fetuses (Ferguson Reflex: Positive feedback)
Hormones of parturition
PGF2α
Major site of production is endometrium in response to declining P4 & rising E2 levels. It causes:
• Luteolysis.
• Stimulates myometrial contractility.
• cervical dilation.
Relaxin
Levels rise rapidly in late gestation & decline rapidly after parturition. Prostaglandin stimulates
the release of relaxin which dilates cervix, increases pelvic area (softening & relaxation of
iliosacral junction, symphysis, & pelvic ligaments) & facilitates fetal expulsion.
Oxytocin
Released as fetus engages in the birth canal. Augments parturition by stimulating release of large
amounts of PGF2α. Together with PGF2α causes myometrial contractions: peristaltic uterine
contractions to propel fetus.
Mechanics of parturition
Successful parturition depends on 2 mechanical factors:
i. The ability of the uterus to contract (myometrial contractions).
ii. The capacity of the cervix to dilate sufficiently to allow fetal passage
Myometrial contractions
Myometrial activity is under P4 influence during pregnancy which ensures a conducive
environment for fetal development.
Dilation of the cervix
Cervix retains conceptus during pregnancy. Cervix is firmer & more rigid than uterine wall due to
a higher content of connective tissue (collagen).
Cervical dilation is due to changes in physical characteristics of cervical collagen (‘ripening’)
A few hours prior to parturition cervix softens and gradually dilates: due to hormonal influence at
onset of parturition.
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Labour
Factors Affecting Labor
The 3 Ps:
i. The Passages: size and shape of soft and bony birth canal
ii. The Passenger: size and disposition of fetus
iii. The Powers: uterine contractions and maternal expulsive forces
Labour usually occurs in three stages:
Stage I: Cervical Dilation
This is the beginning of uterine contractions till cervix is dilated & continuous with vagina. Fetal
position & posture must be optimal.
Contractions start at apex of cornua in montocous species; cranial to presenting fetus in polytocous
This causes the fetus to be propagated towards cervix
Uterine contractions are painful and thus the animal will show:
• Restlessness
• Pawing
• Getting up and down
• Sweating
• Urinating frequently
As fetus progresses through cervix:
Allantochorion ruptures and urine like fluid released. This usually marks end of first stage
Stage II: Fetal Expulsion

Distension of cervix & vagina causes initiation of the Ferguson’s reflex. This produces expulsive
force of abdominal muscular contractions (straining) due to the effect of oxytocin. Oxytocin
accentuates myometrial contractions. This is seen as Straining characterized by few contractions
and a few minutes of rest.
Fetus enclosed in amnion appears at vulva. As straining continues amnion ruptures and feet appear
(one slightly ahead), followed by nose and head lying between the knees. The greatest effort
associated with expulsion of head and chest. The dam may rest at this time before final bout.
The dam may be on lateral recumbency with limbs extended and the umbilical cord breaks as the
neonate or dam moves.
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Stage 2 ends when the umbilical cord is broken.
Stage III: Expulsion of Placenta

Rhythmic uterine contractions originating at apex continue after birth. These cause inversion of
allantochorion. Presence of detached placenta within birth canal initiates further straining &
expulsion of placenta. Neonates’s nursing helps stimulate uterine contractions aiding in placental
release.
Expulsion is rapid in mare than ruminants. Of adjacent piglets fused: expelled as one or more
masses interspersed with piglets, bulk 3 to 4 h after last piglet
Methods of induction of parturition

In inducing parturition, use is made of the known hormonal mechanisms of regulation of gestation
and parturition in different animal species
For the clinician responsible for the delivery of a viable fetus, the more urgent concern is not the
proper method for induction of parturition, but the proper time for induction
Critical period of inductions
• Cow: 273-279 days (Term 282 days)
• Ewe/Doe: 145 days (T 150)
• Sow: 110 days (T 114)
• Mare: 330 days (T 350)
Inducing parturition before these periods could jepadise fetal viability and compromise on milk let
down as prolactin will not have built up to sufficient levels.
Indications of Induction
a. Managerial
-allow delivery when assistance is available
-allow bulk management of neonates
-allow foster mothering in some spp (sows)
b. Prolonged gestation
c. Severe joint problems (athritis)
d. Injury/ obstructions of birth canal
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e. Fetal death/muminification
f. Dropsy (edema) of fetal membranes
g. Diseased dams to salvage neonates
Hormonal Protocol
Cows:
Corticosteroids: 16-30mg of dexamesone after 265th day of gestation. Parturition occurs in 80%
of cows in 30-60hrs post tretment
Rationale: stimulate placental synthesis of estrogens to shift the P4/E2 ratio that triggers
production of PGE and PGF2, lysis of CL and uterine contractios
Consequence: a number of animals retain placenta and give antibiotics and detachment occurs 10
days later
PGF2: 20-40mg or 500iu Cloprostenol after 265th day. Parturition in 90-100%. Time for delivery
is longer, dystocia cases are higher, neonatal survival poorer and retained placenta
Estrogens can be used but residue problems (not used)

Sows:
PGF2: 10-12mg or 175iu Cloprostenol on days 112 or 113 of gestation. Delivery in 80% of sows
in 33hrs. If done before day 111, neonatal loses are very high
Dexamesone use: Okey but high variability and longer delivery time
Ewes: 10-20 mg of dexamesone on day 140-
Doe: 15mg PGF2 at day 140-142
Topic summary
In this topic we have learnt about the normal birthing process in animals. This knowledge is critical
in case we are to identify abnormal birthing processes (dystochia). We have looked at the signs of
approaching parturitions, the physiological basis of parturition and finally the stages of labour.
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Neonatology
Introduction
This refers to the care of the neonate. A neonate is a new born animal. Life during the periparturient
period is fraught with hazards. These include:
• Dystocia
• Failure to ingest colostrum
• Hypoglycemia
• Hypothermia
• Trauma
• Predators
• Infectious diseases
Proper care of the neonate helps reduce mortalities that occur during this period.
Care of the neonate
The attitude and activity of the young should be noted prior to their being handled.
Normal neonates usually hurdle together, especially during periods of inactivity. Abnormal litters
may be spread about, not seeking one another or the dam.
Hungry neonates may be restless and may cry, but should quiet down and sleep when they are full.
Those that are constantly restless or vocal, remain from the group, or seem to lack vigor should be
examined carefully.
RESPIRATION - 1
At the time of parturition an attendant should be present to remove the placenta that may be
wrapped around the muzzle and nose and cause
The onset of fetal respiration may begin before the fetus is completely expelled in some
parturitions, especially those that are delayed.
The heart rate, mucous membrane color and respiratory efforts should then be evaluated for
possible asphyxiation.
If respiration in the newborn is delayed, it should be stimulated:-
a. Mucus should be removed from the mouth and nose
b. The newborn should be laid on its side on straw, not loose chaff or shavings that might be
inhaled, with the head and forequarters slightly lower than the hindquarters.
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c. The newborn can be held head down, while carefully supported, be swung through a small arc
to promote drainage. CARE: Cerebral haemorrhage
d. Vigorous rubbing of the newborn with straw, hay, towels or shaking its head, or tickling its
nostrils, will help bring about respiratory activity.
e. A resuscitator may be useful in saving weak newborns. The first step in ventilatory support is
to place an endotracheal tube into the trachea.
Calf resuscitation equipment

Attempts to inflate the lungs by blowing through the neonate’s nose or by using a mask will result
in air filling the stomach, since the resistance to stomach inflation is less than the resistance to
displacement of the lung liquid.
Disinfection of the umbilicus

This may not be a problem if births occur in a clean area.
If birth was normal and the umbilical cord was not ruptured in the process, leave the cord intact
for about 5 minutes. Contraction of the uterus will force placental blood into the neonate, thus
increasing its chances of survival.
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If parturition takes place in an unclean environment or if navel infections are prevalent on the farm,
the navel should be disinfected.
Tincture of iodine or weak iodine can be applied soon after the umbilical cord has been cut as a
preventive measure against omphalitis caused by environmental contamination or overzealous
licking from the dam.
COLOSTRUM - 1
Placental transfer of immunity does not occur in domestic animals except to a small degree in the
dog and cat. Neonates are thus born essentially without antibodies.
In addition Immunologic competence is present at birth, but endogenous antibody production does
not reach protective levels in the newborn until a few weeks of age.
Thus initial protection against disease is provided by passive transfer of immunoglobulins from
the dam via colostrum. Passive immunity through colostral absorption by the newborn during the
first hours of life is therefore very important.
Colostrum intake is so critical that it is likely to determine how well or how poorly an individual
will perform during its life.
Colostrum consists of the accumulated secretions of the mammary gland over the last few weeks
of pregnancy together with proteins transferred from the maternal blood stream under the influence
of estrogens and progesterone. Immunoglobulins are absorbed intact through the wall of the small
intestine.
The ability of the intestines to absorb the immunoglobulins is time dependent, decreasing from
100% at birth to closure approximately 24 hours later.
Pre-milking in cows, sometimes practiced to avoid severe edema of the udder may reduce the
immunoglobulins available to the newborn calf because of their dilution in large quantities of milk
stimulated by this practice.
The principle transfer of globulins from blood to milk occurs the last 3 days of the gestation period.
Besides the important immune bodies obtained from colostrum, the colostrum:
a. Has laxative properties,
b. Is about 5 times as high in protein as in milk (cow),
c. Two times as high in fat and minerals as in milk (cow),
d. Ten times as high in iron as in milk (cow),
e. Is high in vitamins A, D and E, which are present in very low levels in the newborn.
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If for some reason colostrum from the dam is not available, another source may be indicated.
Colostrum may be frozen and stored for such emergencies.
If colostrum is not available a transfusion of plasma, or of the dam’s blood or blood from an animal
of the same species is indicated to provide the necessary antibodies. In large animals 500 to 800
ml of blood or serum is usually administered subcutaneously. In smaller animals 20 to 100 ml.
Three egg yolks per 100-500 ml of cow milk given every three hours for a day has been tried with
good results
HANDLING AND FEEDING OF ORPHAN ANIMALS

This is necessary when the dam dies at parturition or fails to give sufficient milk. The young of a
species thrives best on the milk of its own kind. Therefore having the orphan adopted by another
post parturient female of the same species is indicated. This is fairly easy and can often be done
in all domestic animals when such an animal is available.
Occasionally it is necessary in the sow to make the young smell like the foster dam’s offspring by
rubbing her fetal membranes or genital discharges over the orphan, or sprinkling the entire litter
of orphans and sow with a material having a similar strong odor such as weak cresol solution or
an aerosol deodorant.
In the absence of a foster mother, the newborn can be raised with proper care and attention by
artificial feeding.
In calves the problem is simple, since cow’s milk in nearly universally available. In the other
animals the composition of the milk from the various species should be taken into consideration.
Milk of the ewe, doe, and cow are almost similar in composition. The milk of the sow is richer in
fat.
Several homemade milk formulas have been suggested: they usually consist of evaporated milk
diluted with an equal part of water and mixed with one tablespoon of corn syrup, one egg yolk,
liquid vitamins or liquid proteins.
The milk substitute should be given at the dam’s body temperature. All equipment should be
washed promptly after each use, thoroughly rinsed and sterilized.
The same equipment should be used each time, as familiar odors and shapes will stimulate the
newborn to feed.
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The newborn should be fed every 1 to 3 hours for the first week and then every 4 to 12 hours
thereafter. The amount fed to the young of large animals should be 10% of the body weight,
divided into the aforementioned number of feedings.
The newborn can be bottle-fed.
If symptoms of diarrhea develop, the amount of milk should be reduced markedly for 24 to 48
hours and oral and parenteral antibiotic, electrolyte and supportive therapy instituted.
The orphan should be encouraged to eat solid food as early as possible so that the amount and
frequency of milk feeding can be reduced. Semi-solid food can be added to the milk formula after
2 weeks of age.
Additional activities of postpartum care include:-
a. Protection against cold extremes. Heat loss can rapidly occur in newborns because of
evaporation and convection. Care should be taken to keep them warm and dry.
Hypothermic newborns will not suckle or breathe adequately.
b. Dextrose-containing fluids can be given intravenously to provide a readily available energy
source.
c. Forced feeding of newborns that lack strong reflex responses may result in pulmonary
aspiration of the colostrum. Furthermore, if the newborn is hypothermic, its ability to digest
and absorb milk-based nutrients will be markedly slowed.
d. The possibility should be recognized, especially with primiparous animals, of the dam
injuring the neonate.
e. Examine for abnormalities soon after birth. Early recognition of a congenital abnormality
and disposal of a hopelessly deformed neonate often will save the owner the expense of
prolonged care and treatment
f. Vaccines. Administer as the disease problems of the premises and area dictate.
NEONATAL DISEASES
Neonatal diseases are often fatal even when diagnosis and intensive therapy are quickly instituted.
The following neonatal conditions typically affect newborns:
Starvation and maternal neglect.
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Maternal neglect or agalactia resulting in starvation may account for 10 to 20% of neonatal
mortality during the first week of life. Finding such early deaths should always indicate necropsy
and examination of the dam. The starved or neglected neonate will usually have an empty stomach
and a full bladder, suggesting that it had not eaten and that urination had not been stimulated (small
animals). The remaining neonates must be hand raised.
Cannibalism.
Rarely occurs. An overzealous dam may accidentally injure or kill the neonate while eating the
placental membranes, but other cases of cannibalism should be suspect, since the consumed
neonate may have been malformed and dying if not already dead. Repeated disturbances of the
dam and her litter or other stress such as loud noise have been associated with cases of cannibalism.
Bacterial infections.
Sudden death of the newborn within the first week of life is typical septicemia or bacterial
pneumonia. E. coli, Staphylococci spp., and Streptococci spp. are commonly associated with
bacteraemia in newborns. Infections may originate in utero, while traversing the vagina, or through
contaminated milk from infected mammary glands.
Omphalitis/ navel ill.
Bacterial infections via the umbilicus (navel) are much higher when calves are born in a dirty
calving environment. These infections can be prevented by adequate navel treatment in calves and
adequate passive antibody transfer (three litres of good quality colostrum during the first 6 hours
of life but preferably within the first two hours). Navel infection may remain localised to the navel
but can also lead to peritonitis and in more severe cases to septicaemia and focal infections such
as joint ill and meningitis. In most cases of joint ill and septicaemia, bacteria gain entry through
the gut within the first few hours of life before colostrum ingestion rather than from umbilical
infection.
Clinical signs of navel ill
The umbilicus is typically hot, painful, and moist. The calf is dull and reluctant to suck and may
stand with an arched back. It is essential to determine whether the bacterial infection has spread
further into the peritoneal cavity, liver and bloodstream with possible localisation in joints and the
brain. In older calves the umbilical infection may be limited to an abscess at the navel.
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Umbilical infection is limited to a large abscess at the navel in this bull calf.
Spread of infection from the umbilicus into the peritoneal cavity leading to septic peritonitis causes
rapid deterioration in the calf's condition, abdominal distension caused by gut stasis, and death
within 2-3 days.
Spread of infection from the umbilicus into the peritoneal cavity. Note the widespread
peritonitis and distended loops of intestine.
o The umbilicus is typically hot, painful, and moist.
o Potential for spread further into the peritoneal cavity, liver and bloodstream with possible
localisation in joints and the brain
Differential diagnoses
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Differential diagnoses your veterinary surgeon will consider include:
o Localised peritonitis
o Urachal infection
o Umbilical hernia
Diagnosis
Diagnosis is based upon a thorough clinical examination taking care to check for other focal
bacterial infections. Ultrasonography is useful to investigate involvement of the umbilical vessels
and urachus, and to differentiate a hernia from an umbilical abscess.
Treatment
Penicillin for 5-7 days remains the antibiotic of choice for umbilical infections. Other antibiotics
may be prescribed by a veterinary surgeon for calves with meningitis and polyarthritis following
septicaemia. Umbilical abscesses can be lanced after needle aspirate or ultrasonography, then
flushed daily for three to five days.
The prognosis is hopeless for those calves with significant peritoneal infection.
Umbilical abscesses can be lanced after needle aspirate or ultrasonography, then flushed
daily for three to five days.
Prevention/control measures
o Maintain strict hygiene in the calving environment.
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o Treat the umbilical remnant at birth, and 2-4 hours later with iodine where possible.
o Ensure adequate and timely colostrum ingestion (three litres of good quality colostrum
during the first 6 hours of life but preferably within the first two hours).
A persistent, patent or pervious urachus.

This is invariably seen with infection of the navel either as a cause or a result of an open urachus.
Seen most commonly in the newborn foal and rarely in cattle. It is often followed by pyemia,
septicemia, and navel or joint ill. Antibiotics administered over a period of 10 to 14 days is
indicated together with local treatment of the navel with antibiotics or disinfectants. If after several
days the urine continues to flow through the urachus keeping the navel and surrounding skin moist,
the lower 4 to 5 inches of the urachus should be cauterized with a small swab containing Lugol’s
solution or the instillation of 2 to 5 ml of 5 to 10% formalin solution.
Retained meconium.
In the foal the meconium in the rectum may be found in hard pellets and become impacted within
24 or 36 hours after birth. The diameter of the bony pelvis is very small in the newborn foal. The
affected foal usually nurses normally but within 24 to 48 hours after birth exhibits symptoms of
colic and persistent or intermittent straining. Impaction may be confirmed by inserting a lubricated
finger into the rectum and palpating the mass of hard pellets of meconium. This condition is not
uncommon in foals, and for that reason it is recommended that all newborn foals be given an
enema soon after birth. The enema may be of physiological saline, mineral oil, olive oil, castor oil,
mild soap and water etc.
Rupture of the bladder or urachus.

May occur in rare instances in the foal. It probably occurs due to a full bladder at parturition or
when the navel is ruptured. The foal appears normal for 12 to 24 hours; but by the second to fourth
day the foal is depressed, pulse and respirations are increased, and the abdomen is slightly to
markedly distended. Tapping the abdominal cavity with a sterile needle will release the urine and
confirm the diagnosis. Blood tests show a rise in blood urea nitrogen. Laparotomy on the midline,
and repair of the ruptured bladder is indicated. Supportive and antibiotic therapy with good nursing
often results in a successful termination.
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Neonatal isoerythrolysis, or hemolytic icterus of the newborn.
A hemolytic disease of foals. It is due to an incompatible blood group reaction between serum
antibodies of the dam (concentrated in colostrum) and erythrocytes of the neonate.
Hemolytic crisis occurs when a mare that is negative for the antigen inherited by the fetus from
the stallion is isoimmunized. Mares become isoimmunized to certain types of erythrocytes either
through
Placental breakdown and absorption of the antigens from the placental tissue or fetal blood at
previous gestation periods,
or 2.) By transfusions of blood,
or 3.) Injection of fetal tissue vaccines.
When these mares are bred to stallions which transmit to the fetus the type of erythrocyte to which
the mare was previously immunized the disease develops.
The icteric condition develops when the apparently normal foal suckles and receives in the dam’s
colostrum large amounts of antibodies composed of hemagglutinnins and hemolysins.
It is very rarely observed in foals from primiparous mares. It is usually not observed in foals until
the mare’s third or fourth parturition.
The condition is not due to an Rh-like factor as in humans but is caused by an isoimmunization of
pregnancy due to intraspecies blood group factors (red cell antigens).
The symptoms usually develop rapidly after the foal begins nursing, with mild to severe clinical
symptoms occurring from 12 to 96 hrs after birth.
These include: anorexia due to weakness, usually no rise in body temperature, increased pulse and
respiration rate, slight to marked jaundice and anemia, and in severe cases prostration and
hemoglobinuria.
Treatment consists of removing the foal from the mare. In severe cases several blood donors should
be obtained and the blood of the dam and the foal tested against various donors’ blood. If they are
compatible, a large blood transfusion of 1500 to 2000 ml should be given. Inject the blood in one
jugular vein while removing an equal amount from the other. Administration of antibiotics and
exercise restriction are advisable.
Topic summary
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In this topic we have learnt how to take care of the newborn. We have looked at important aspects
of neonatology as well as how to handle orphaned neonates. Finally we have looked at diseases
likely to occur during this period.
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INFERTILITY IN DOMESTIC ANIMALS
Definition of terms
Fertility – This denotes:
• The desire and ability to mate
• Capacity to conceive and nourish the embryo
• The power to expel a normal offspring and membrane
Sterility – The absolute inability to reproduce
Infertility – A degree of reduced fertility which can result in failure to produce or delay in
producing the annual live calf (in the cow)
Causes of infertility
Infertility in cattle has many diverse causes. These can be grouped into four general groups:
1. Anatomical factors
2. Functional forms
3. Management problems
4. Infectious causes
Anatomical causes of infertility
These refer to abnormalities in the structure of the reproductive organs. You can have congenital
abnormalities (occurring before birth) or acquired abnormalities (occurring during the life of the
animal).
Several important congenital abnormalities are described below:
1. Ovarian agenesis – This is a condition where one or both ovaries are absent
2. Ovarian hypoplasia – A condition in which one or both ovaries are small, narrow and
functionless
3. Abnormalities of the fallopian tubes – These can include unilateral aplasia, segmental
aplasia and duplication of the fallopian tubes
4. Freemartinism – Occurs in female calves born co-twin to male ones. The placental
membranes connect the fetus to the dam are shared, and the placental fluids are exchanged
between the two fetuses. The exchange of fluid and blood between the two calves mixes
the antigens responsible for carrying the unique sex characteristics of each calf. The twins
develop with some sex characteristics of both the male and female.
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This transfer of hormones and antigens causes the female's reproductive tract to be severely
underdeveloped, and in some cases they express characteristics of a male reproductive
system. Often the ovaries are underdeveloped and are not capable of producing eggs. The
uterus is also underdeveloped, and the reproductive tract does not supply sufficient
hormones necessary to maintain a pregnancy.
5. Segmental Aplasia of the mullerian ducts – Developmental anomalies in the mullerian
ducts leads to abnormal development of vagina, cervix and uterus. The ovaries develop
normally. Thus the animal will cycle normally but the tubular organs will be blocked.
6. Atresia of the vulva – An abnormally small vulva. Commonly found in Friesian and jersey
heifers.
Acquired abnormalities
These include conditions acquired during the life of animal that affect the fertility of the animal.
They include:
1. Adhesions of the uterus – the uterus becomes adhesed to the omentum, intestines or
abdominal wall. Most common following caeserian section operations
2. Parturient trauma of the genital tract – Damage to uterus, cervix, vagina or vulva during
giving birth. May be caused by the fetus being too big with or without forced traction of
the fetus.
3. Tumours of the female genital organs – these can affect any organ of the reproductive tract.
Functional causes of infertility
These are abnormalities in the normal functioning of the reproductive tract. These include:
1. Hormonal imbalances - imbalance of oestrogen and progesterone during crucial stages of
the cycle may affect embryo survival, conception rate among others.
2. Fatty liver syndrome – Incidence of fatty Liver syndrome has been shown to depress
fertility.
3. Lameness - Lameness has been shown to reduce conception rates.
4. No observed estrus – A normal animal comes on heat regularly after a specific time period.
In cows this is after every 21 days. This is known as an estrus cycle. These cycles begin
at puberty and should be maintained throughout the animal’s life. Several factors may
cause this no observed estrus. These include:
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i. The ovaries may be quiet and inactive – true anestrus – can be caused by defective
production of hypothalamic hormones or failure of ovaries to respond to produced
hormones.
ii. There is normal cyclic ovarian activity but the cow is not showing normal behavior
signs – silent heat/ sub estrus. Can be caused by genetic predisposition or nutrition
(Vitamin A, phosphorus, copper or cobalt deficiencies)
5. Ovulatory defects – These include problems with the normal ovulatory processes. This can
be divided into Delayed ovulation and anovulation.
Management Causes of Infertility

Nutrition
Nutrition can have an effect on various fertility indices. The various nutrients have both direct and
indirect effect on the structure and function of reproductive organs or on hormone production.
Various effects of nutrition on fertility are described below.
Effect on time of puberty – Achievement of puberty in domestic animals is a function of body
weight rather than the age of the animal. Inadequate growth rates among heifers due to inadequate
energy and protein intake may lead to delayed age at puberty. As the feeding level increases the
age at puberty decreases
Effect on conception – Too high levels of nutrition (leading to obesity) or malnutrition may lead
to failure of conception. Obesity leads to fat deposition around the ovaries leading to suboptimal
ovulation. Inadequate nutrition leads to cessation of cyclical activity with other effects being silent
heat, ovulatory defects, conception failure, fetal and embryonic death.
Specific minerals affecting fertility include energy, proteins and the minerals phosphorus, copper,
cobalt, manganese, iodine, selenium and vitamin A.
Poor estrus detection
This is a very important management cause of perceived infertility. This is when, in the absence
of a bull, the herdsman does not notice an animal on heat. The reasons for this are numerous and
include:
1. Ignorance of the true signs of estrus
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2. Large herd sizes where the herdsman is not able to effectively monitor all animals in a
herd.
3. The relatively short time that an animal is in estrus. An animal is usually in estrus for about
6 hours meaning that herdsman have a small window in which to detect an animal on heat
4. The nature of housing. Crowded, confined or extremely muddy cow sheds may mean that
the mock mounting associated with estrus does not happen.
Incorrect timing of artificial insemination
Ovulation in a cow occurs an average of 10-12 hours after the cow starts showing signs of heat.
This is usually the best time to inseminate. The correct timing of AI is dependent on the true and
accurate identification of estrus and accurate identification of the animal in estrus.
Infectious infertility in cattle

Infections of the genital tract can affect fertility by altering its environment so that there may be
impaired sperm transport, sperm death, development and survival of the conceptus (leading to
abortions, still births, fetal mummification, fetal maceration) or birth of weak calves.
Specific infections occur without any predisposing factors and tend to affect groups of animals
whereas non-specific infections require a predisposing factor and tend to infect individual cows
with the organisms involved being opportunistic pathogens normally present in the genital tract.
Non Specific infections of the reproductive tract
These include:
Puerperal metritis – This is infection of the uterus occurring a few days after parturition. It usually
follows abnormal labour or difficult calving. Bacteria involved include Actinomyces, streptococci,
staphylococci and coliforms. These infect the non-involuted uterus sometimes releasing toxins that
are absorbed into the body.
Endometritis – This is inflammation of the endometrium. It has a profound effect on fertility.
Microorganisms reach he uterus at coitus, parturition or insemination. It causes infertility by
extending the calving to conception interval, increase in the number of services per conception
and it can result in sterility due to irreversible changes in the genital tract.
Pyometra – This is the progressive accumulation of pus in the uterus. It can occur as a sequel to
endometritis. There are two forms of pyometra. This include closed cervix and open cervix
pyometra. These have differing clinical presentation.
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Salpingitis, cervicitis and vaginitis. – These are the infection of the oviducts, cervix and vagina
respectively.
Specific Causes of infectious infertility

Trichomoniasis
This is a classical venereal disease transmitted from asymptomatic carrier bulls, which become
infected by serving an infected cow. Bulls remain carriers for life remaining asymptomatic
throughout. Younger bulls are less liable to become persistent carriers than older bulls. The
organism lives within the crypts and folds of the penile integument and preputial mucosa.
Control is through AI. T fetus survives cryopreservation quite well
The number of trichomonads needed to establish an infection in the cow is large and cows can be
infected via insemination with contaminated semen. T fetus colonise the uterus, cervix and vagina.
In the uterus it produces a catarrhal endometritis and vaginitis with edema of vulva, perivaginal
tissue and uterine wall. Affected animals show intermittent vulva discharge, uterine manipulation
provokes a discharge from vulva in which motile trichomonads can be demonstrated.
The disease doesn’t prevent fertilization but causes embryonic death; typically after maternal
recognition (day 16) hence irregular extended return. Some animals exhibit normal or short
returns. Many pregnancies fail at between 30-50 days, this is the time of establishment of
placentomes. EED may be accompanied by pyometra. cows experience a series of embryonic
deaths before they become pregnant and carry a calf to term, return to fertility depends upon
development of immunity to the parasite. Infected cows will conceive and carry to term once
immunity has developed. Nevertheless although cows are free of parasite after normal gestation
immunity has been lost by the end of gestation so that cows again become susceptible to infection.
Outcome of infection:
• Successful pregnancies with out clinical signs of infection
• Return to multible services with no obvious signs of disease
• Failure to conceive and development of edema of endometrium with mucoflocullent
discharge
• Become pregnant but abort in 2-4 months
• Develop pyomtra and become acyclic
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Diagnosis is based on demonstration of presence of trichomonads in uterine pus, vaginal discharge,
cervical mucus or aborted material. Preputial samples (scrapes and washes) are also used. Control
is based on Treatment, vaccination and elimination of bulls.
Campylobacteriosis (Vibriosis)
This is a venereal disease causing infertility and, occasionally, abortion. It is caused by the
bacterium Campylobacter fetus, which lives in the crevices of a bulls prepuce, but usually does
not become established in the bull until it is about 4 years or older.
It is spread from an infected bull to a cow during the breeding act. Bulls also may be infected by
breeding infected cows. Although semen from reputable bull studs is usually clean because of
proper health examinations of the bulls and treatment of semen, this disease can be transmitted
through artificial insemination if these precautions are not taken.
Untreated, infected bulls can remain carriers for a long time. They also can be clean yet transmit
the germ from an infected cow to a clean cow.
It causes endometritis in cattle, resulting in failure to conceive or death of the embryo. Affected
cows may conceive and not return to heat 21 days later. However, the newly formed embryo may
then die, become absorbed by the cow and then she may exhibit estrus from 27 to 53 days after
breeding.
Diagnosis is difficult and depends on identifying cultures of the organism from the genitalia of the
infected cow or bull, or from the abomasum of an aborted fetus. Prevent vibriosis by vaccinating
cattle, using artificial insemination, treating infected animals, or combining all three.
Campylobacteriosis and trichomoniasis comparison

Both cause early abortions and infertility.
Campylobacteriosis is caused by the bacteria Campylobacter fetus subspecies venerealis.
Trichomoniasis is caused by protozoan infection with Tritrichomonas foetus.
Both diseases are transmitted and carried by bulls that have no obvious signs of infection.
Infected cows generally abort early in pregnancy and while the abortion may not be seen, the
farmer may notice cows returning to service.
An infertility problem, rather than obvious abortions, is a sign of both campylobacteriosis and
trichomoniasis.
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After infection and early abortion, cows usually recover, but carrier animals may still be in the
herd. These cows may pass the disease back to a bull. Bulls are immune if vaccinated against
campylobacteriosis.
Organisms of both diseases are usually spread during mating. However, bulls mounting each other
at stud or at artificial insemination centers, and the use of contaminated grooming equipment or
veterinary instruments, have all been incriminated in the spread of the infection.
Clinical signs and diagnosis
Both cause inflammation of the vagina, cervix, uterus and fallopian tubes in the cow. This
inflammation usually prevents successful implantation of the embryo in the uterus and leads to
early abortion.
This results in cows returning to heat and poor pregnancy test results. Young cows are usually
worst-affected, because they have no previous exposure and immunity. However, animals of any
age can be infected if not previously exposed to the diseases.
Diagnosis of trichomoniasis usually requires samples from the prepuce of an affected bull send to
the laboratory. Similar techniques are required to diagnose camplylobacteriosis.
Prevention and treatment
Commercial vaccines for campylobacteriosis will not only prevent the disease, but will also cure
infected bulls. Cows can be vaccinated against campylobacteriosis, but it is cheaper to vaccinate
bulls and maintain freedom from disease in this way.
Preventative measures include culling obviously-infected cows, enforced sexual rest (a minimum
of three months) and treatment of bulls with specific anti-trichomoniasis drugs.
Brucellosis
This is Zoonosis caused by Brucella abortus, B. melitensis, B. suis, B. ovis and B. canis, it causes
widespread economic losses due to abortion and extended calving intervals.
Transmission Brucellosis is normally acquired by ingesting the bacteria, Infection may also occur
through the mucosa of the eye, nose and teat, and through the endometrium if the cow is artificially
inseminated with infected semen. The multi-layered mucosa of the vagina seems to protect against
infection following natural service.
The bacteria show a preference for the pregnant uterus, foetus and the lymph glands of the udder.
Both the membranes and foetus respond to Brucella infection by increasing their production of
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erythritol, a simple carbohydrate, which increases the growth rate of the bacteria. This usually
results in abortion at about 6 to 8 months of gestation. In some cases the dead foetus is not aborted,
but is retained in a mummified or macerated form. If a calf is born alive it is likely to be weak and
to contract calf scours easily.
Aborting infected cows or heifers are a major source of infection for other cattle and people
handling them. Aborted material and vaginal discharges from infected females are heavily infected
with Brucella, and these contaminate pastures, pens and buildings. Organisms are also present in
the milk of infected cows.
Foetal membranes are commonly retained because of uterine inertia, placentitis or both. Puerperal
metritis may develop and cows may remain infertile for some time.
After abortion, uterine infection normally declines within a month. The animal may not abort on
the next conception, but she will continue to discharge the Brucella. Some calves are born infected.
Many lose the infection quickly but a few do not. The latter do not show any signs of the disease
and represent "latent infection". The organism remains dormant until the animal becomes
pregnant. Calves born to serologically positive dams are, therefore, at risk of developing the
disease in the future and ought to be carefully screened when pregnant. Udder and milk infection
lasts several months or years and may be the source of uterine infection during subsequent
pregnancies.
Diagnosis Brucellosis should be suspected whenever a cow aborts unexpectedly, except in a
Brucella-free herd. Confirmation requires bacteriological examination, culture of the organism or
serodiagnosis.
• In the milk ring test (MRT), a drop of haematoxylin-stained antigen is added to 1 ml of
milk. This is incubated at 37°C for half to 1 hour. This test is widely used, fairly efficient,
economical and easy to perform. A positive result is shown by the development of a clump
of stained organisms deposited in a ring on the surface of the preparation. The negative
result is bluish milk covered by an uncoloured layer of cream. It is used for surveillance of
milk samples. Milk should be tested monthly.
• More sensitive and specific tests include the complement fixation test (CFT), which detects
IgG1 and IgM antibodies this is the most accurate and sensitive test for brucellosis and
distinguishes between antibodies of infection and vaccination. However, it must be
performed by a trained technician.
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Control
• Brucellosis can be controlled through strict hygiene in the handling of potentially infected
material and by vaccinating all animals. To eradicate the disease, all infected animals must
be slaughtered.
• Cows, especially those that react positively to serological tests for brucellosis, should be
isolated from the herd before calving and their calves monitored for latent infection.
Pregnant animals should be observed for imminent abortion and all aborted material must
be disposed of properly.
• Cattle should be bought only from Brucella-free herds
• Where the incidence of brucellosis is high, calves should be vaccinated with the attenuated
Strain 19 vaccine at 3 to 6 months old.
• Bulls should not be vaccinated. Strain 19 organisms have been isolated from the genitalia
of vaccinated bulls
• Once the incidence of the disease is substantially reduced by vaccination, a test and
slaughter programme can be attempted to eliminate infected animals.
Leptospirosis
Importance and transmission :Bovine leptospirosis is a systemic disease caused by spirochaetes.
It is characterized by fever and, sometimes, mastitis and abortion. It should be suspected when
abortion occurs in cows showing other symptoms such as icterus and haemoglobinuria.
The Leptospira serotypes associated with bovine abortion are L. pomona, L. canicola,, L.
icterohaemorrhagica and L. grippotyphosa. They are all sensitive to antiseptics and desiccation
and their virulence and pathogenicity are highly variable. L. pomona is the serotype most
commonly implicated in bovine abortion.
Animals infected with Leptospira excrete the bacteria in their urine. Direct or indirect contact with
the urine of infected animals is the major route of infection in both animals and man. The usual
route of infection is via the digestive tract, but the disease may be contracted via the respiratory
and reproductive tracts, eyes or skin. In cows, infection is often followed by pyrexia and reduced
milk production.
When an animal launches an immune response the organism localizes in tissues inaccessible to
antibodies, thus kidney tubules, cotyledons and fetus. In the pregnant cow the organisms show an
attraction for the uterus and attack the foetus or endometrial capillaries. This may result in abortion
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during the last trimester or the birth of a weak or dead calf. Aborted foetuses show no characteristic
lesions other than subcutaneous oedema and fluid-filled cavities. Foetal membranes may be
retained, sometimes causing metritis and infertility. If the bacteria invade the udder they may cause
mastitis or agalactia. The udder is flaccid and milk becomes thick, yellow and clotted.
Diagnosis: Leptospirosis should be suspected following abortion associated with acute illness and
the presence of blood in the milk for some days. However, leptospirosis can cause abortion without
giving any other obvious symptoms.
Leptospirosis is usually diagnosed from blood serology. The bacteria can be cultured but they are
usually difficult to isolate from the foetus or membranes, because autolysis of the foetus between
infection and abortion quickly results in the death of the bacteria.
Treatment and control: Leptospirosis can be self-limiting. Therefore, all newly-purchased animals
should be kept in quarantine and tested for the disease. Rodents on the farm should be controlled
and contamination of drinking places should be avoided by isolating infected animals.
Treatment with streptomycin readily eliminates kidney infection. Each aborting cow should be
treated with streptomycin at 25 mg/kg bodyweight. Cows usually abort once and may not have to
be culled. However, cows that recover can be re-infected.
Neospora caninum
First discovered as a protozoal cause of encephalomyelitis in dogs. Infected dams can produce
calves which are apparently normal but are congenitally infected or born alive with neurologic
limb defects. Abortions can be sporadic but storms also are common, cows can abort in successive
pregnancies. The dog is the definitive and also intermediate host. Tachzoites are found in bovine
placenta and nervous tissues, bradyzoites are found in bovine neural tissues
Horizontal infection can occur through colostrum, fetal membranes, fluids and oocyte
contaminated feeds there is a poor understanding of mode of infection, but prevention of access
by dogs to fetal membranes and abortuses and avoiding soiling of feeds by dog feaces may help
reduce horizontal spread.
Abortion
Abortion is the termination of pregnancy after organogenesis is complete but before the expelled
fetus can survive. If pregnancy ends before organogenesis, it is called early embryonic death. A
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dead, full-term fetus is a stillbirth (its lungs are not inflated). Many etiologies of abortion also
cause stillbirths, mummification, and weak or deformed neonates.
Noninfectious Causes
The actual incidence of abortions in cows due to genetic factors is unknown. Some genetically
caused abortions may not have phenotypically recognizable lesions. Most lethal genes cause early
abortion or early embryonic death.
Vitamins A and E, selenium, and iron have been implicated in bovine abortions, but documentation
based on experiments is available only for vitamin A.
Heat stress causes fetal hypotension, hypoxia, and acidosis. High maternal temperature due to
pyrexia may be more important than environmentally induced heat stress.
Although severe trauma may rarely result in abortion (the bovine fetus is well protected by the
amniotic fluid), farmers undoubtedly blame too many abortions on the cow “getting bumped.”
A number of toxins can cause abortion in cows. Ponderosa pine needles can cause abortion if
ingested in the last trimester; the cows may become moribund after delivery and hemorrhage
excessively. The main abortifacient compounds in Ponderosa pine needles are isocupressic acid
and labdane resin. Locoweed (Oxytropis or Astragalus sp) contains an indolizidine alkaloid that
can affect the corpus luteum, chorioallantois, and neurons, resulting in abortion or deformities.
Broomweed (Guttierrezia microcephala) ingestion can also cause abortion, as can coumarins from
rat poison, many grasses, or moldy sweet clover. Sodium iodide, IV, has been contraindicated in
pregnant cows, but no abortions or adverse effects occurred in pregnant cows treated with a single
high dose in some studies. Mycotoxins, especially those with estrogenic activity, have been
implicated in bovine abortions. Nitrates or nitrites have also been incriminated, but experimental
evidence is controversial.
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CAUSES OF INFECTIOUS ABORTION IN CATTLE
Disease Clinical features Abortion Abortion Placenta Foetus Diagnostic
rate time confirmation
Brucellosis (B. abortus) Abortion. Oral High, in 6-9 Leathery & opaque Pneumonia. S/c Culture of
Contagious abortion infection. 90% cows susceptible months + placenta with oedema. foetal organs.
are carriers. herds neonatal oedema. Necrosis of Pleuritis. Large Elisa, Rose
Zoonosis death cotyledons. % no lesions Bengal,
Milkring,
Complement
fixation
serology tests.
Stamps
cytology.
Histopath.
Campylobac- Infertility. Irregular Low < 5%, 3-5 Semi-opaque, little Flakes of pus on Culture of
teriosis (Campylobacter moderately may be up to months thickening. peritoneum. foetal stomach,
foetus ) prolonged dioestrus. 20% Petechiae, localized Usually no placenta and
Rare abortions avascularity and lesions uterine
oedema exudates. Bull
sheath wash /
scrapings.
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Leptospirosis (L.interrogans Abortion may occur 0 - 30% Late, 6 Avascular placenta Foetal death Isolation
pomona and L. hardjo etc.) at acute febrile months + yellowbrown common - difficult. Direct
stage, or without & cotyledons, oedema. autolytic foetus. examination of
illness neonatal Placentitis Icterus may urine of cow.
occur Positive serum
agglutinatin
test 14-21 days
after fever.
Histopath
Trichomoniosis Tritrichomonas Infertility - return to Moderate, 5 2-4 Flocculent material Foetal Culture of
foetus heat at 4-5 months, – 30% months and clear, serous maceration & foetal stomach
abortion and fluid in uterine mummification. and uterine
pyometra exudates. Pyometra exudates
common within 24 hours
of abortion.
Culture bull
sheath wash /
scrapings
Neosporosis (Neospora spp.) Sporadic or abortion High in dairy 4 - 6 No macro lesions Autolyzed and Histopathology
storms. Repeated cows months rarely white and
abortions foci in muscle histochemistry
and heart on formalin
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fixed foetal
brain tissue.
Serology.
Infectious infertility in small sheep and goats
Disease Transmission Clinical signs Control
Bacterial Passive venereal, male to male Epididymitis in males, 3rd Mixed strain S19 and killed B.
Brucellosis (B.ovis, B. homosexual transmission trimester abortions in females ovis adjuvant vaccination, rev.
melitensis) with RAB, stillbirths, neonatal 1 B. melitensis vaccine,
mortality hygiene, slaughter
Genital actinibacillosis (A. Ram to ram homosexual Epididymitis and orchitis in Slaughter of affected males.
seminis) transmission rams, no signs in females
Campylobacteriosis (C. Ingestion 3rd trimester abortions, Adjuvant vaccine, doubtful

fetus/C. jejuni) stillbirths, neonatal mortality efficacy
Salmonellosis (S. arbotus ingestion 3rd trimester abortions with Vaccines of poor efficacy,
ovis, dublin, typhimurium…. metritis, neonatal mortality hygiene
Listeriosis (L. ingestion Abortion after 3 months, Killed vaccine/Live

monocytogenes) RAB, metritis, septicaemia attenuated vaccine
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Enzootic abortion ingestion Late 3rd trimester abortions, Killed vaccine/Live attenuated
(Chlamydia psittaci) stillbirths, weak lambs, vaccine
neonatal deaths, no other signs
of infection in ewes.
Protozoa Ingestion Late 3rd trimester abortions, S48 tachyzoite vaccine in

Toxoplasmosis (T. gondii) stillbirths, neonatal mortality, some countries.
no other signs of infection in
ewes.
Viruses insects Abortions across trimesters, Vaccination

Rift valley fever neonatal deaths, neonatal
achondroplasia
Border disease Ingestion Abortions in all trimesters, None known

stillbirths, neonates with long
hair, female infertility
Nairobi sheep disease Ticks (Rhipicephalus Abortions across trimesters, Inactivated vaccine, vector
appendiculatus) acute onset, high mortality control
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Infertility Disorders in pigs
MASTITIS, METRITIS, AGALACTIA SYNDROME
Synonym Farrowing fever, Puerperal fever, Post parturient fever
This is a condition involving an agalactia associated with temperature and mastitis, failure of milk
let down, upset of piglets and the sow resulting in neonatal death, baby piglet scour and death due
to hypoglycemia.
Etiology: Mastitis-metritis-agalactia syndrome (MMA) or post-partum dysgalactia syndrome

(PPDS) is a disease of multiple etiology and has close links with coliform mastitis and cystitis in
sows. The actual cause of this condition is an infectious mastitis, metritis, endocrine dysfunction,
overfeeding during pregnancy, constipation and nutritional deficiency. Multiple pathogens can be
involved in the mastitis such as E.coli, Klebsiella spp., Enterobacter spp., Mycoplasma spp. as
well as Streptococci and Staphylococci.
Agalactia may be as a result of deficiency of prolactin. Factors interfering with release of
prostanglandin from the uterus hinder prolactin production necessary for lactogenesis immediately
prior to farrowing. Mycotoxin in the feed and vitamin E/Selenium deficiency has been suggested
as a cause. Other aetiological factors are related to endotoxins produced by E. coli, subclinical
endometritis, retarded lactogenesis, hormonal imbalance, teat malformation and stress.
Predisposing causes include; Psychic problems in the sow. The suckers stimulate the sow by
nosing the udder vigorously. Lack of milk ejection in the first 24 hours after farrowing may be a
powerful predisposing cause of MMA. Other factors like disturbance, heat wave, unsuitable
farrowing crates that enrage the sow, lack of husbandry by the attendant would jeopardize milk let
down. Low fibre diet, fatness at farrowing and confinement has been found to be risk factors for
sows. Sudden change of the feed could result in gastrointestinal disturbances and predispose the
syndrome.
MMA occurs mainly in the first and 2nd litter sows due to lack of experience. The mode of infection
of the udder is via the teat canal. MMA Syndrome requires rapid intervention to save the life and
the future productivity of the sow as well as the lives of the piglets.
Clinical signs
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The time of occurrence is between 12 and 48 hours after farrowing. There is agalactia, swelling
of the mammary glands, lethargy, fever, anorexia, disinterest in piglets, depression, refusal to lie
over or suck the piglets, hot udder, swollen and firm, subcutaneous edema, redden regions for the
white pigs, a few drops of abnormal fluid extracted from affected quarters.
The sow may be normal for 18 hours then lies on the sternum and refuses to suckle the piglets who
make noise as they look for food.
Other signs include, restlessness, standing up or lying down, killing piglets by trampling and
crushing them, fever of 41o C, no milk on the teats, increased pulse rate, constipation and metritis.
Differential diagnosis
1. Eclampsia- this is a metabolic disease which responds to Calcium and magnesium therapy.
2. Failure of milk ejection reflex in first litter gilts. This responds to oxytocin.
3. Mammary hyperplasia in gilts.
4. Primary agalactia-there is reduced milk supply and responds to oxytocin and careful
management
5. Other septicaemias
6. Non infectious swelling of mammary glands- there is failure of milk letdown with swelling
7. Parturient psychosis-the sow is antagonistic and savage and kills piglets while glands are full of
milk. Treatment- Stressnil
8. Erysipelas and ergotism due to high temperature.
Treatment
1. Antibiotic- Penicillin-streptomycin (Penstrep)
Others- Neomycin, tetracycline, trimethoprim-sulphadimidine
2. Oxytocin- 30-40units IM or 20-30 units IV.-induce milk letdown.
3. Corticosteroids-dexamethasone
4. Furosemide-for udder edema
5. Supportive treatment- water fomentation of mammary glands and hand milking for 10-15
minutes every few hours
NB- Sows treated with antibiotic, oxytocin and corticosteroids recover after 1-2 days. If there is
no treatment, recovery is after 5 days but the piglets will be dead by that time.
Piglets should be removed from the sow immediately the syndrome is diagnosed and fostered or
fed separately. Keep them warm and observe for hypoglycemia.
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Control
1. Hygiene
2. Clean and disinfect farrowing crates/quarters
3. Wash pregnant sows before placing them in farrowing crates
4. Check diet and comfort of the sow
5. Add bran to the ration to improve gut motility
Infertility in Male animals

Reproductive abnormalities causing subfertility and infertility in male animals have classically
been divided into two main classes: conditions causing partial or complete failure of normal
service (impotentia coeundi) and conditions causing partial or complete inability to impregnate
normal cycling females (impotentia generandi). The first group can be further divided into
conditions causing unwillingness or inability to mount and conditions that prevent normal
copulation from occurring despite normal libido.
Superimposed upon both groups are considerations of whether the subfertility/infertility is due to
a primary pathological abnormality or suboptimal husbandry or breeding management.
Abnormalities of Coitus (Impotentia coeundi)

Disorders associated with partial or complete failure of coitus can be considered under the
following:
• Immaturity or inexperience of breeding male; - Young breeding males may be presented for
failure to mate simply because they are peripubertal and/or sexually inexperienced. When
immaturity is suspected as the cause of poor libido, little can be achieved other than to ensure good
husbandry management and exposure to cycling females. Lack of sexual experience and/or
suboptimal rearing conditions can adversely affect the expression of sexual behaviour in young
males. For example, when bull calves are reared in groups, they regularly exhibit mounting
behaviour as puberty approaches and usually learn to copulate quite quickly. However, when
reared
in isolation, such mounting behaviour does not occur and can take some time to be learnt,
especially in those AI stations where steers are used as mount animals. Similarly, young colts in
racing yards may be violently dissuaded from exhibiting male behavior by their grooms. As a
Page 78 of 89
consequence, such negative behavioural reinforcements have to be reversed before these young
horses can be used for mating.
Unwillingness to copulate can also result from poor mating management. Slippery floors, roofs
that are too low, females that are too big, and stockmen that are insensitive in their handling of
their charges can all contribute to unwillingness to copulate.
• Inability or unwillingness of the breeding male to mount; - Most lesions affecting locomotion
impair ability and willingness to copulate. Lesions of the back and hindlimbs are the most
important of such incapacities, but, for example, in the boar, in which the forelegs are used to clasp
the female, painful lesions of the carpus can also impair mating.
In production animals and horses, foot lesions are probably of greatest significance. Gross
pathology of the foot, such as sole abscess, laminitis, white line disease, infectious interdigital
dermatitis, and interdigital fibroma, cause significant pain, and, as a consequence, the affected
male will either be unwilling to mate or its frequency of mating will be markedly reduced. Poor
conformation of the foot is less obvious but equally important as a cause of low libido. Animals
with overgrown hooves, in which the distribution of weight has been adversely affected, are
frequently unwilling to mount or, if they do mount, are unwilling to remain mounted for long
enough for successful copulation to occur.
• Inability of the breeding male to achieve intromission; - Inability to achieve intromission is a
relatively frequent cause of infertility in domestic animals. Conditions that cause failure of
copulation include failure to achieve an erection, abnormalities of erection that prevent
intromission, and lesions of the penis and prepuce that prevent protrusion of the penis.
• Failure of the breeding male to ejaculate. - There are a few conditions in which ejaculation
does not occur,
despite normal mounting. Such conditions can be broadly divided into those in which the
ejaculation reflex is impaired and those in which localised pain makes the animal unwilling to
ejaculate. The former conditions generally occur when some damage has occurred to the neural
pathways between the glans penis and the
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spinal cord. Strangulation of the penis, with ensuing damage to the sensory dorsal nerve of the
penis, causes ejaculation failure, whereas, in older bulls, compression of the spinal nerve roots by
age-related exostoses can also preclude ejaculation.
Localised pain is similarly effective in preventing ejaculation. Localised peritonitis in the caudal
abdomen of ruminants causes pain during the ejaculatory thrust, so affected animals are often
willing to mount but unwilling to complete an ejaculatory thrust.
Animals with back pain behave similarly, although they may be less willing to mount. Finally,
some painful conditions of the penis, such as orf in rams, make the animal unwilling to achieve
intromission and ejaculate, despite their willingness to mount.
Conditions Causing Failure of Fertilisation (Impotentia Generandi)

Fertilisation failure, despite normal copulation, generally characterizes diseases of the testis
(including abnormalities of spermatogenesis), epididymis, and accessory glands. Many of the
conditions causing failure of fertilisation can be diagnosed by an examination of the external
genitalia of the male, but others can only be diagnosed by semen evaluation.
Moreover, diagnosis of failure of fertilisation on the part of the male animal requires elimination
of female factors through examination either of records or of the females themselves. Likewise,
causes of fertilisation failure that represent pathologies of the reproductive tract must be
differentiated from management factors (e.g., overuse) that adversely affect fertility.
Examples include:
Conditions affecting the testis – orchitis, hypoplasia, cryptorchidism, testicular neoplasia,
testicular degeneration
Sperm abnormalities – cytoplasmic droplets, problems with the head etc
Conditions affecting the epididymis – epididimytis, sperm granulomas
Conditions affecting the accessory sex glands -
Page 80 of 89
MASTITIS
It refers to the inflammation of mammary glands regardless of cause. It is a major endemic disease
especially of dairy cattle. It is characterized by physical, chemical and usually bacteriological
changes in milk and by pathological changes in the glandular tissue. The most important changes
in milk include discoloration, the presence of clots and the presence of large numbers of
leucocytes. There is swelling, heat and pain on palpation of the glands
Causes
Causes of mastitis can be physical or infectious. Infectious mastitis usually occurs as an immune
response to bacterial invasion of the teat canal by variety of bacterial sources present on the farm,
while physical can occur as a result of chemical, mechanical, or thermal injury to the animal’ s
udder.
Many infective agents have been implicated as causes of mastitis. In cattle the most common
causative bacteria include Streptococcus agalactiae and Staphylococcus aureus with Escherichia
coli becoming a significant cause in housed or confined cattle. Leptospirae, including Leptospira
interrogans cause damage to blood vessels in the mammary glands and gross abnormality of the
milk. They are more correctly classified as systemic diseases with mammary gland manifestations.
Fungal infections include Trichosporon spp., Aspergillus fumigates, A.
nidulans, Candida albicans and Cryptococcus neoformans.
In sheep Pasteurella hemolytica, Staph aureus, Actinobacillus lignieresi, E. coli, Strep uberis and
Strep agalactiae are recorded. Goats are much less affected by mastitis, but causative organisms
include Staph aureus, Mycoplasma agalactiae, M mycoides var. myciodes, Strep agalactiae and
Strep pyogenes.
In pigs, causative organisms include Aerobacter aerogenes, E. coli, Klebsiella spp., Pseudomonas
aeruginosa, Strep agalactiae, Strep uberis and Strep dysgalactiae. In mares mastitis is rare but
Corynebacterium pseudotuberculosis, Pseudomonas aeruginosa, Strep zooepidemicus and strep
equi have been recorded.
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Spread of infection
Infection for each mammary gland occurs via the teat canal, the infection originating from two
main sources, the infected udder and the environment. The contamination of milkers’ hands, wash
cloths and machine cups by milk from infected quarters may quickly lead to the spread of infection
to the teats of other animals.
Prevalence
In most countries, surveys of incidence of the disease show comparable figures of about 40%
morbidity amongst dairy cows. In sheep prevalence varies between countries and this prevalence
may also affect the lamb survival rate.
Economic losses
Mastitis assumes major economic importance only in dairy cattle. It is the most important disease
with which the dairy industry has to contend. This loss is occasioned much less from fatalities,
although fatal cases do occur, than from the reduction in milk production from the affected
quarters. The clinical syndrome may vary from a peracute inflammation with toxemia to a fibrosis
which develops so gradually that it may escape observation until most of the secretory tissue has
been destroyed. There is the additional danger that the bacterial contamination of the milk from
affected quarters may render it unsuitable for human consumption, or interfere with the
manufacturing process, or provide a mechanism of spread of infection to humans.
The major losses therefore arise from:
• Milk thrown away due to contamination by medication or being unfit to drink.

• A reduction in yields due to illness and any permanent damage to udder tissue.
• The extra labor required to tend to mastitic cows.
• The costs of veterinary care and medicines.
• The cost of reduced longevity due to premature culling.
Diagnosis
The clinical findings in mastitis include abnormalities of secretion, abnormalities of the size,
consistency and temperature of the mammary glands and frequently a systemic reaction. All these
can be used to make a diagnosis. Severe inflammation of the quarter, with a marked systemic
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reaction is classified as peracute; severe inflammation of the quarter without a marked systemic
reaction is classified as acute; mild inflammation with persistent abnormality of milk is classifies
as subacute; while recurrent attacks of inflammation with little change in milk is classifies as
chronic. Mastitis is said to be subclinical when there is evidence of inflammation, e.g. high somatic
cell count in the milk without any visible abnormality of the milk or udder.
Culturing of milk samples is a standard method of examination of mastitis. It may be carried out
on individual quarter samples or on composite samples from all quarters. Sampling must be carried
out with due attention to cleanliness since samples contaminated during collection are worthless.
Teats must be cleaned and properly dried after washing.
Treatment and Prevention

Parentral treatment is advisable in all cases of mastitis in which there is marked systemic reaction,
in order to control or prevent the development of a septicemia. The systemic reaction is usually
brought under control by standard doses of antibiotics or sulphonamides but complete sterilization
of affected quarters is not usually achieved because of the relatively poor diffusion of the drug
from the bloodstream into the milk. It is therefore necessary to use higher-thannormal rates in
order to produce therapeutic levels of the drug when doing parentral treatment.
Because of convenience and efficiency, udder infusions are the preferred method of treatment.
Disposable tubes containing suitable drugs in a water-soluble ointment base are best suited for the
treatment of individual cows. For chronic cases of mastitis, particularly those caused by Staph
aureus, are often treated most satisfactorily when the cow is not lactating. Treatment at this time
is also a good prophylaxis.
The major control measures include the following;

• Keep all details of cell count figures on a monthly basis and use these to monitor mastitis
in a herd
• Ensure milking machinery is tested regularly and thoroughly at least once a year. Faulty
machines can lead to a mastitis build-up.
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• Use an affective iodophor-plus-lanolin teat dip on each quarter as the cluster is removed.
Wash udders with clean running water and preferably use clean paper towels to dry the
udders
• Dry-cow therapy: The farmer's veterinary surgeon will not only advise generally on
mastitis control, but will also recommend the appropriate treatment at the end of lactation.
This will include the infusion of a specially formulated, long-lasting antibiotic into each
quarter, to destroy residues of infection and to counter new infections in the dry period.
Page 84 of 89
Farm and Breeding Records
Introduction
What is it to 'keep records'?
To keep records is simply to collect relevant information that can help you to take good decisions
and to keep track of activities, production and important events on a farm. Records can be about
any performance of the animals, economic development, or any activity of the farmer or
veterinarian. It is important to keep record keeping simple, and to keep records systematic. If
records should be of use for the farmer, than they must be complete (none missing), they should
be true (collected carefully). When record can't be trusted because they are not complete or true,
time should not be spent on it at all.
The records can:
a. Be used in determining profitability of various techniques used at the farm

b. Be used to keep your memory on what you did and/or what happened
c. Be used in decision making, especially on a strategic level
d. Be used to compare the efficiency of use of inputs, such as land, labour and capital, for
example when implementing a new / alternative systems
e. Help the farmer / investor in improving the efficiency of farm's operations
The real value is to support the farmer and the advisors to keep track and take decisions. Too often,
records are only kept for the purpose of official reporting, e.g. to the Ministry headquarters for the
parasitical and not used as a tool on the farm/ranch for making the decision in time.
The records should be simple, easy and quick to interpret, and then they can be supplemented with
remarks which can explain some unusual events or findings.
What can records be used for?
If a farmer wants to build a financially successful livestock enterprise, record keeping is a must.
The records can be used to further develop the farm and the herd, and thereby the sector in the
country. For many farmers, it helps to think of their farm as a business, and to see that good care
and good management actually also influences the production and profitability of the farm.
Records are important in (animal) farming because:
a. To keep track of all animals (Identification records)

b. Evaluation of livestock for selection (breeding records; financial records; production
records)
c. Control of inbreeding and aid in breeding planning (breeding records)
d. Aid in selecting animals with the right characteristics for breeding (production, health, feed
efficiency) to improve the herd or flock
e. To rationalize labour
f. Aids in feed planning and management
g. Aids in disease management; keeping track about treatment (disease records)
h. Aids in finding the effective treatments
Page 85 of 89
i. To assess profitability/losses (financial records)
j. Improves bargaining power on products, because you can see the investment and the price
of the production (financial records)
k. Credit/loan access (financial records)
Types of Records
The major types of records which are all described below:

1. Identification
2. Breeding
3. Production
4. Feeding
5. Disease and treatment records
6. Financial records
1. Identification Records
An identification method should be cheap, not harming the animal, reliable to read at a distance
of at least 2-3 metres and by preference be permanent.
Identification of the animals is of course not necessary if a farm has only one animal of a certain
species, sex and age group.
Identification of animals is usually through use of numbering, by marking of the animal and by
description of certain characteristics of the animal. The latter is the most animal friendly, and can
be done in practice by drawing e.g. the different color spots of the animals, or certain cowlicks, or
taking photos. Giving the animals names and keeping a table with the characteristics of the animal
and link it to the name can work in many cases.
Intrusive methods of identification can be subdivided into 2 categories: permanent at the animal
itself (which affect the animals most when doing it) and non-permanent.
a) Permanent Identification
Tattooing (ear or under)

Brand (Hot iron, freeze and chemicals)
Ear-notching, Punching
Tags (Ear-tags, Flank-tags, tail-tags and Brisket-tags; permanent if they do not fall off)
b) Non-Permanent identification
Collars or neck or leg straps (chains)
Paint and dyes (can be very animal friendly, but if the paint is full of chemicals it is not healthy
and is not recommended, please check)
2. Breeding Records
The importance of breeding records is to measure the productive efficiency of the herd and to
enable selection. For example, many farmers would like a cow or a goat which gives birth yearly,
Page 86 of 89
or a sow 2 litters per year. Therefore, an accurate up-to-date breeding record of each individual
female is necessary. An indicator for fertility/efficiency of mating or inseminations is e. g the
number of matings or inseminations needed to get an animal pregnant.
If many matings or inseminations are needed, it can indicate that there is a problem with the female
or the male, or it can indicate that the observation of the heats is not efficient, or the semen, the
technique of insemination is insufficient, or the feeding is imbalanced. If the cow is taken to a bull,
it can be the cow or the bull which has a problem. Data for insemination or service with a male
also is needed to be reminded when the female should be prepared before giving birth, e.g. like in
the cow's case, to be dried off in time.
The most important data in breeding records include:
Pedigree/parentage (name or other identification of parents and grand parents)

Fertility (dates of all services (this also allows calculating the number of services per
conception), dates of giving birth (allows to calculate the age of first calving/giving birth and the
period between successive birth) (Age at first service, age at first calving, date of calving, number
of services per conception)
Birth details (number and weight of newborns, was assistance necessary? Stillborn / perinatal
deaths / vitality score)
Example of a cow card for planned fertility management
Last Examination remarks
Date of vet Service Expected
calving e.g. pregnancy
examination date calving date
date diagnosis
. . . . .
. . . . .
. . . . .
. . . . .
. . . . .
. . . . .
. . . . .
. . . . .
3. Production Records
These records are useful in measuring the performance of the animals and the herd. It contributes
greatly to the economic appraisal of the enterprise. It can help farmers take decisions on
investments, based on how many animals produce how much on the farm, so how much surplus
can the family expect?
Page 87 of 89
The records can also be used by the whole sector to improve the genetics of the animals in the
country, with specific focus on the production.
Production records are kept of:
Animal products like eggs per hen per week and milk per cow per day in combination with milk
quality data, and of
Animals which are slaughtered, in terms of for example weight, weaning age and weight, daily
gain, production period, and how many animals e.g. per litter reached slaughtering.
Production records are also necessary when farmers start selling products together, to know how
much is available every day or every week or in a certain period.
4. Feeding Records
Feeding records give information about the amount, type and quality of the feed.
Feeding records can be used both for day to day management and adjustment of the feed ration.
Together with the production data, it can for example be used to adjust if a milking cow needs
more concentrate, or help in decisions about examining animals which seem to not grow, but still
eat very much. It can also be used for planning of activities related to feed conservation and
establishment of grazing areas in the following season.
The important feeding records are:
Produced and available fodder on farm; quantity and if possible quality of the different feeds.
Including content of energy, protein and minerals
A feeding plan which tells how much feed is required per day per animal in different age groups
(grown-ups, newborn, pregnant the first time etc.) or per group of animals (hens):
Left-over feed if any (per head and per feed, if possible)
Spoilage (per batch)
5. Disease and treatment records
Disease and treatment records are necessary to keep track of the disease events in which each
animal is involved during its lifetime. This can guide to better management practices by leading
the attention to repeated events or certain vulnerable groups of animals over time (e.g. it can show
how animals almost always need disease treatments during weaning). It provides information about
the health status of each individual animal and the whole heard, and it can help ensuring important
vaccinations given at the right time.
On basis of the disease and treatment records, success of interventions both for prevention and
treatment can also be evaluated.
Page 88 of 89
After treatment with dewormers, acaricides and antibiotics and other medicines, milk, eggs and
meat cannot be eaten by humans for some time. The records are essential for keeping track of this,
e.g. when this withdrawal time is over. In organic animal husbandry, the withdrawal time is
normally longer than the ordinary withdrawal time (double, or three times)
Disease and treatment records can for example involve:
Disease occurrence and date

All handlings to cure diseases (also non chemical treatment)
Vaccination
Dipping/spraying
Treatment
De-worming
Postmortem
6. Financial Records
The records of the costs and earnings related to the animal farming be kept for cash analysis and
enterprise appraisal.
In most households, the most necessary records are simple overview over the family cash flow,
that is, the total economy in the household: what comes in? and what do we buy?
In addition to this, keeping records of the animal enterprises is and important part, because it can
show whether it gives an income to the family or not. If records are kept particularly for the animal
herd as an income generating commodities, it will help the family to see what they invest in it, and
what it costs to produce it. Also in relation to the animal farm, an investment is more than an
expenditure, an investment hopefully enables and improves the production in the future. It is also
important to count approximately how many hours of work it has taken in the animal herd, because
it can help price setting.
Economic records are of paramount interest in providing the farmer with information concerning
the profitability of his farm. Moreover they are of great help in decision making at the right time.
For example, is it profitable to feed concentrates, is it advisable to apply for a loan or credit to
invest in a machinery or technology?
Answering these questions is only possible if adequate records are available. Moreover, for tax
purposes and for the purpose of getting loans or credit, economic records are required.
Page 89 of 89

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BARATON COLLEGE IN

COLLABORATION WITH UNISA

DEPARTMENT OF ANIMAL HEALTH AND PRODUCTION

METABOLIC, NUTRITIONAL AND REPRODUCTIVE DISODERS

00223 ANHP / 00223ANPR (Certificate)

ANHP 0315/00223: Metabolic, Nutritional and Reproductive

Is this course for you?

Introduction to the course

Diagnosis: finding out the cause of disease.

C. Disease control and treatment

Aetiology and Pathogenesis

Aetiology and Pathogenesis

LACTATION TETANY (GRASS TETANY, HYPOMAGNESEMIC TETANY, WHEAT

SELENUIM AND VITAMIN E

In acute poisoning, ingestion of excessive amounts of salt results in gastroenteritis due to

Confirmation depends on detection of elevated levels of sodium chloride in blood or in tissues

Poisonous Principles Found in Plants

LANTANA CAMARA POISONING

Symptoms of poisoning include the following:

SNAKES AND SNAKE VENOMS

Diagnosis of Snake Bites

Stage II: Fetal Expulsion

Stage III: Expulsion of Placenta

Methods of induction of parturition

Estrogens can be used but residue problems (not used)

Calf resuscitation equipment

Disinfection of the umbilicus

HANDLING AND FEEDING OF ORPHAN ANIMALS

Starvation and maternal neglect.

Omphalitis/ navel ill.

A persistent, patent or pervious urachus.

Rupture of the bladder or urachus.

Management Causes of Infertility

Infectious infertility in cattle

Specific Causes of infectious infertility

Campylobacteriosis and trichomoniasis comparison

Infectious infertility in small sheep and goats

Disease Transmission Clinical signs Control

Campylobacteriosis (C. Ingestion 3rd trimester abortions, Adjuvant vaccine, doubtful

Listeriosis (L. ingestion Abortion after 3 months, Killed vaccine/Live

Protozoa Ingestion Late 3rd trimester abortions, S48 tachyzoite vaccine in

Viruses insects Abortions across trimesters, Vaccination

Border disease Ingestion Abortions in all trimesters, None known

Synonym Farrowing fever, Puerperal fever, Post parturient fever

Etiology: Mastitis-metritis-agalactia syndrome (MMA) or post-partum dysgalactia syndrome

Infertility in Male animals

Abnormalities of Coitus (Impotentia coeundi)

Conditions Causing Failure of Fertilisation (Impotentia Generandi)

The major losses therefore arise from:

• Milk thrown away due to contamination by medication or being unfit to drink.

Treatment and Prevention

The major control measures include the following;

a. Be used in determining profitability of various techniques used at the farm

Records are important in (animal) farming because:

a. To keep track of all animals (Identification records)

The major types of records which are all described below:

Tattooing (ear or under)

The most important data in breeding records include:

Pedigree/parentage (name or other identification of parents and grand parents)

The important feeding records are:

5. Disease and treatment records

Disease and treatment records can for example involve:

Disease occurrence and date