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Animal Health and Welfare Module 1
Animal Health and Welfare Module 1
Animal Health and Welfare Module 1
i. Welfare is the state of the animal, and how it is coping with the conditions in which it lives.
An animal’s welfare can range from negative to positive. A complete assessment of welfare
requires consideration of multiple facets of the animal’s state.
An unbiased and thorough assessment of an animal’s state should be encouraged regardless
of its species, role or utility. While the goal may be to classify welfare as good/bad or
acceptable/unacceptable, it will always involve considering different information often with
ethical components.
ii. Animal welfare means how an animal is coping with the conditions in which it lives. While
practical considerations may sometimes limit steps that can be taken to improve an animal’s
welfare, these considerations should not impact the assessment of the animal’s welfare state.
The maximum satisfaction of these freedoms engenders improved animal welfare. It is presumed to
be vitally important to comprehend “how animals fee” scientifically.
1. Freedom from hunger and thirst
• Inputs: ready access to fresh water, and a diet that maintains full health and vigour,
e.g. how often stockperson delivers feed
• Outputs: body weight; body condition score; evidence of dehydration on the skin-
pinch test
Each of the Five Freedoms can overlap with the others. For example, if an animal is hungry, he or
she will seek food and eat it – this is normal behaviour. If the animal cannot find food, or if the
environment does not allow him/her to show normal food-seeking behaviour, s/he may become
distressed. Therefore, if animals are not free from hunger and are not free to express normal
behaviour, they may also not be free from distress.
All life ends in death; therefore, freedom from death is not something that we can provide to any
organism. However, we kill most of the animals that we keep. The issue of whether or not we should
kill animals is an ethical one. The avoidance of death in animals has an ethical value for many
cultures. Moreover, from the animal’s point of view, animals have an interest in life and, generally,
will try to avoid death.
Even though we cannot guarantee freedom from death to any animal, the manner of an animal’s
death does concern animal welfare. For example, if someone keeps a dog as a pet and does not feed
the animal properly, the animal will die of malnutrition and associated diseases. In that case, the
animal’s death comes about because several of the Five Freedoms have been compromised (freedom
from hunger, freedom from disease, freedom from distress and, possibly, freedom to express normal
behaviour
A popular approach to animal welfare based on three overlapping needs was developed. They
suggested that full consideration of welfare must include an assessment of:
1. Functioning: The physical fitness of the animal. Animals should have good health, normal
bodily functions, and normal growth and development.
2. Natural Living: The ability of animals to lead reasonably natural lives. They should be able
to perform important types of normal behavior. Animals should also have some natural
elements in their environment, such as fresh air or the ability to socialize with other animals
in normal ways.
3. Affective States: The emotional state of the animal. Animals should feel well mentally and
should not be subjected to excessive amounts of negative emotion and unpleasant affective
states (e.g., pain, hunger, distress). Animals should also experience some positive emotions in
the form of pleasure or contentment.
Ideally, the three areas of need should fully overlap, indicating that an improvement in one need
would concurrently improve the other needs. In reality, this is often not the case and an improvement
of one need may be accompanied by no change or a negative change in one or more other needs.
Animal Welfare & Health - 2015 13
Difference in the views between Animal Welfare and Animal Rights
Animal welfare is distinct from rights. Animal rights addresses the legal and moral standing of
animals in society and, in its most extreme, seeks to end the use of animals by humans. While a
person with animal rights orientation may seek improvements on the immediate step
Animal welfare
It is accepted that human beings may sacrifice nonhuman animals, the five freedoms
Animal rights
If the right to life is guaranteed for a human being, the right must be given
The complete elimination of animal experiments and the complete elimination of eating meat
Concepts in Animal Welfare
Welfare concerns the quality of an animal’s life, not how long the life lasts (quantity)
Three approaches when considering animal welfare
For example, if a single hen is housed in a wire cage on her own and has food, water, a perch, a
nesting box, and an area for dust-bathing, her physical functioning is likely to be good. Her mental
state is likely to be good too, although she may feel frustration because of social isolation which may
occur even if other birds are close by, in other cages. She will also be able to perform important
behaviours like nesting before she lays. However, some people would still have concerns for her
welfare because keeping a chicken in a cage is not ‘natural’. The cages actually impact on other areas
of welfare including the health of the animal, e.g. wired floors are likely to cause injuries; if an
animal is frustrated then he or she may self-mutilate or perform stereotypical behaviours, which can
cause physical damage. So in this example, the chicken’s welfare is affected in terms of all three of
the ‘naturalness’, ‘physical’ and ‘mental’ areas of welfare.
These three areas of welfare should never be looked at in isolation and we should focus on the centre
of the diagram where they all overlap. It requires a holistic approach to welfare, incorporating all
three and understanding the relationships between the areas.
Physical area (functioning: slower movement, weight loss because the animal is unable to access
enough good grass or extra feed), andmental area (feelings: pain, hunger, perhaps fear, if separated
Animal Welfare & Health - 2015 14
from the flock, and therefore is more vulnerable to predators).
Stockman – A person who looks after the livestock or a property. He or she is responsible for the care
for livestock and treatment for their injuries and illnesses.
It is proposed that the following attributes should be considered as the “Three Essentials of
Stockmanship”, analogous to the “Five Freedoms”.
Knowledge of animal husbandry. Sound knowledge of the biology and husbandry of farm
animals, including how their needs may be best provided for in all circumstances.
Skills in animal husbandry. Demonstrable skills in observation, handling, care and treatment
A good stockman will stay quiet when working with livestock. If the herd is not doing what you
want, it is not because they can’t hear or see you. It is because you are in the wrong place doing the
wrong thing. Move calmly, purposefully and in a straight lines. Why, the herd will be able to predict
your movements and respond appropriately to them.
If you move like a predator [hesitating, followed by sudden movements and in curves around them],
the herd will treat you like a predator.
A good stockman is patient, keeps doing the right things until the animals responds correctly. You
need to realize that if you make animals do something before they are ready them it is no longer low
stress handling. Train cattle how to behave every time you are with them.
Every animal, and even more so every group of animals, has a range within which it can give
optimal performance. The range one would like to keep all animals in is the ‘thermocomfort’ zone.
Within this range animals are not merely capable of giving an optimal performance, but also feel
such comfort that they have no preference for any particular location--- neither huddling nor
separating --- to keep warm, respectively. They are in complete harmony with their environment.
Outside this zone, both higher and lower, is the temperature zone known as the ‘thermoneutral’
zone, and it is vital to try and maintain stock within this all the time if they are housed, and at least
most of the time if they are outdoors. It is the zone where there are no metabolic demands on the
animals. They maintain homeothermy by quite extensive fluctuations in their behavior, by changes in
their hair disposition or blood circulation at the surface, and by perspiration and panting.
If the temperature falls below the lower critical temperature, the animal will need to use more
food to keep warm, so that either the animal produces less if it is on a fixed feeding scale or eats
more to keep warm and still produce at an optimal level.
If temperatures continue to go upwards or downwards, above or below the upper or lower critical
temperatures, respectively, the animal continues to try and maintain its homeothermy by various
metabolic means, but in due course the deep body temperature is altered and it will at extemes
eventually collapse and die.
Upper critical
temperature
Thermcomfort
Thermoneutral zone
zone
Lower critical
temperature
Table.1.1
Species Thermoneutral
zone
Dairy cattle 10~18℃
Adult pig 15~20℃
Layer 21~23℃
Broiler 18~21℃
In order to maintain their body temperature while subject to a wide range of environmental
conditions, domestic livestock must preserve a thermal balance between their heat production and/or
gain from the environment and their heat loss to the environment. This thermal balance can be
expressed by the equation.
M=E±F±Cd±Cv±R±F±W
M : heat production
E : the heat loss from skin and respiratory passages by evaporation
Cd : heat lost or gained by direct contacts between the body and surrounding surfaces by conduction
Cv : heat lost or gained by convection due to contact between the air and skin and/or linings of the
respiratory passages
R : Radiation
F : the heat loss or gained bringing ingested food and/or water to body temperature
W : Work
Grazing behavior
- The length of daytime grazing of cattle apparently varies according to the degree of climatic
stress, the breed and type of cattle utilized and the quantity and quality of the pasture available.
- When high-grade Bos Taurus-type cattle are grazed in a humid tropical climate the length of
daylight grazing is radicallycurtailed and confined almost entirely to early morning and late
afternoon periods
- The length of the night grazing period fluctuates according to the degree of climatic stress.
Intake and utilization of feed and water
a) Feed intake
- As would be expected from the effect of temperature on grazing behavior the available climatic
chamber date suggest that high ambient temperatures depress the feed intake of domestic
livestock, but that in the case of cattle the feed intake of Bos taurus is depressed at lower
ambient temperatures than is that of B. indicus breeds.
- The effect of very high temperatures is very pronounced, food consumption and rumination
practically ceasing in B. tauras -type cattle as ambient temperatures rise above 40℃.
- Increasing humidity at ambient temperatures above 23.9℃ also depresses the feed intake of all
The major indirect effect of climate on livestock is on the quantity and quality of the feed available
for them. Other indirect effects are on the incidence of disease and parasites and the storage and
handling of animal products.
DIAGNOSIS
Coming up with a diagnosis is an art that is perfected through practice and experience. It involves
four main facets namely history taking, clinical examination, post mortem and laboratory sample
analysis.
History taking – History of a case is composed of information obtained from the animal owner
or keeper. This information is very important and should be carefully gathered as the animal
cannot speak for itself. Many animal owners or keepers may conceal or give incorrect
information to avoid being blamed for negligence leading to occurrence of disease. History
include information such as duration of illness, number of others affected in the flock/herd or
surrounding farms, whether onset was sudden or gradual. Similar past cases, vaccination record,
past treatment etc.
However, the information gathered in the history should be relevant to the case at hand. Lengthy
history full of irrelevant information may be confusing and misleading. Although history taking
is usually the first step in diagnosis, more information may be obtained during or after clinical
examination or indeed after post mortem and laboratory analysis.
At the end of history taking a list of suspected problems or diseases is drawn up.
Clinical examination – During this stage the animal is examined by mere visual assessment or
observation, palpation, percussion and by use of equipment such as thermometer, stethoscope
etc.
Abnormalities and lesions observed are what are known as clinical signs (preferred in animals)
or symptoms (preferred in humans). At the end of clinical examination a tentative diagnosis may
be reached.
Laboratory analysis – Samples from the sick animal are collected and submitted to the
laboratory for analysis. The samples may include whole blood, blood smear, serum, tissue
biopsy, urine, faeces, parasites etc.
After analysis of laboratory results it is possible to arrive at a definitive diagnosis.
Post mortem – This is performed after the sick animal has died or sacrificed. It is systematic
dissection and examination of a carcass to find the cause of death or illness. Tissue/organ
samples may be collected and submitted to the laboratory for further analysis.
After integration of the history and results from clinical examination, laboratory analysis and
Animal Welfare & Health - 2015 32
post mortem a definitive diagnosis is reached.
Always remember that “not all the signs will appear all the time”
Mycoplasma
These are also classified into bacteria but these have no cell wall on their cells and these are
smaller than general bacteria. They range 0.3-0.8µm. They multiply in either situation; within
cells and outside cells.
e.g. Contagious Bovine Pleuro-Pneumonia(CBPP) etc.
Rickettsia
These are also classified into bacteria but these multiply only within cells. These have cell wall
and these are smaller than general bacteria. They range 0.3-2.0µm
e.g. Anaplasmosis, Cowdriosis etc.
Fungi
These vary greatly in size, the largest being visible to the naked eye. They are often resistant to
environment influences and are sensitive to a narrow range of therapeutics.
e.g. Dermatophytosis etc
Viruses
These are the smallest pathogenic factor in size from 10 to 300nm
Parasites
Protozoa - Unicellular eukaryotic (true nucleus) organisms most are free living.
e.g. Babesiosis, Theileriosis, trypanosomiasis etc.
Helminths(internalparasite) - Round worm (nematode), flukes (trematode) and tapeworm
(cestode).
Ectoparasites – Common ectoparasites on farm animals include fleas, lice, mites and ticks.
2.3 Epidemiology
2) Environmental factor
It is described as anything except for causal agent factor and host factor.
[environmental factorsⅠ]
❑ Biological factors: all living thing in the environment…
❑ Weather factors: temperature, humidity, atmospheric pressure, day-light length…
❑ Geographical factor: water quality, air pollution…
3) Host factor
It is mainly classified into three factors.
❑ Genetic factors: hereditary disease, predisposition, constitution, family history…
❑ Physical factors: age, sex, race, physique, physical activity…
❑ Mental factors: character, disposition, behavior, sexual behavior……
Source
of
infection
Infection Susceptible
route host
3) Susceptible host
Infection does not always occur even if pathogens invade inside animal’s body. Normally
immunity inside host animal protects the body from pathogens’ proliferation so that
pathogens can be eliminated from the body. It can be progressed by vaccination.
In the population, if the number of immunized animal against certain pathogen is much
more than the number of susceptible (non-immunized) animal, the pathogen cannot make
itself epidemic.
In addition, host’s susceptibility is influenced by stress, nutritional condition, age, breed and
genetic factor. Transport in a long distance, high density in the house or exposure to the
heat/cold can be stress to animals and predispose them to respiratory disease or
gastrointestinal disease.
TYPES OF IMMUNITY – This may be divided into two categories; innate and acquired.
Innate immunity is something that is inherent in an animal and is not due to the presence of
antibodies. This may be absolute or partial, for example horses are absolutely resistant to foot-
and-mouth disease (resistance manifested by a species or by races, families, and individuals in a
species).
Various physical barriers by skin, mucous membrane or various secretions may also be
included in innate immunity.
Phagocytosis may also play significant role as innate immunity.
Inflammation is biophylactic reaction against tissue injuries caused by various bacterial
infections. It may mobilize also against mechanical and thermal injury, injury caused by
chemicals or as the result of allergic reaction.
Fever is also one of the measures in innate immunity for protection the body from invaders’
multiplication.
Acquired immunity may either be active or passive. Active acquired immunity is attached by
stimulation of production of antibodies either by an infection (recognized or not) or by
immunization i.e. by introduction of an antigen of some kind into the body.
Passive acquired immunity is achieved by transferring antibodies from another animal that has
been actively immunized. Newly born animals are able to passively acquire immunity in a
unique and peculiar manner. Colostrum contains a rich store of antibodies against infections that
the dam was exposed to. A newly born animal is able to absorb these antibodies from its
alimentary canal once ingested, hence acquires the immunity against those particular infections.
However, this absorption is only possible during the first 12-24 hours of the neonate’s life.
COMPONENTS OF THE IMMUNE SYSTEM – The defence lines of the body may be divided
into three major components. The first component includes mechanisms that prevent entry of
disease-causing agents into body as physical barrier such as tough, thick skin or the ability to
cough and sneeze. The second component includes mechanism that deal with disease-causing
agents that manage to enter body as parts of innate immunity such as phagocytosis of invaders by
phagocytes, fever, acute inflammation. The third component includes mechanism that generates
highly specific resistance to a diversity of microorganisms as the function of acquired immunity.
When the body is exposed to antigenic substances, the antibody response follows a characteristic
pattern. From the first antigenic encounter, it takes 10-14 days before antibodies are detected in
blood. This initial antibody response, the so-called primary immune response (1º), does not
reach a very high level and does not persist for a long time.
2º
1º
6mon
1 2 3 4 5wk
th
Primary Secondary
expose/immunization expose/immunization
When a second challenge is encountered there is a brief decrease in the detectable levels of
antibodies in blood, for a day or two, then a dramatic rise, reaching a peak of 10-50 times that of
initial immune response within a short period of time. The second immune response (2º) is
maintained at a high level for a long time, declining slowly over a period of many months.
Further antigen challenges (booster) can each increase the antibody levels until such a point that
no more increase can be achieved by further challenges.
The body is able to retain the memory of the antigen encountered for many months or years such
as that subsequent antigen encounters (infections) result into an antibody response similar to the
secondary immune response. The interval between the primary and secondary antigen challenges
is very important for maximum antibody response. If the interval is less than 10 days, the
secondary response is usually very low; also when the interval is too long. The intervals for
subsequent boosters may be in weeks and later months or years.
Feed and water – provision of adequate quality feed and water is very important for an animal to
stay alive, to maintain an energetic body and a sound immune system. This enables the animal to
fight infection before it turns into clinical disease.
Shelter – provision of appropriate shelter ensures the animal is protected from adverse weather
conditions thus minimizing stress on it.
Biosecurity – these are measures aimed at preventing the introduction of disease-causing agents in
the animal’s environment. They include:
Restriction of unnecessary visitors, especially those from other farms
Provision of disinfection facilities at the farm and individual animal pen entrances
Disinfection of pens and equipment e.g. after every batch of chickens in all-in-all-out
programmes
Acquisition of replacement animals from disease-free sources
Isolation of new arrivals for observation of disease before mixing with existing stocks
Safe disposal of litter and other contaminated materials
Practicing general hygiene on the farm
Quarantine literally implies government regulation for prevention of spread of infectious disease
by which an animal(s), which have come from infected countries or areas, are detained at the
frontiers or ports of entrance, or at other official centers for a period of isolation, before being
allowed to mix with stock of the country.
Sterilization is the killing and elimination of all micro-organisms that include bacteria, fungi and
viruses. Sterilization is mainly classified into physical methods.
Disinfection is the elimination of disease-causing micro-organisms that include bacteria, fungi and
viruses. Disinfectants are the agents that achieve disinfection and usually chemicals. The
effectiveness of disinfection is heavily dependent on thorough preliminary cleansing of surfaces to
be disinfected. The cleansing is intended to remove organic materials that considerably reduce the
power of disinfectants.
- Burning
Way to reduce micro-organisms to ashes by flame.
- Boiling
Tools are placed in the boiling water for 15-30min.
- Steam
Way to kill micro-organisms by using steam(100℃) for 30-60min.
※Fermentation
It’s a characteristic way in agriculture. When we produce compost from animals’ excrement we
can kill pathogen organisms or eggs of parasites in the excrement by fermentation heat made by
thermoduric bacteria. The fermentation heat reach 60-80℃.
-[iodization]
Iodoform
• Application: Viruses, Bacteria, Fungi, Protozoa
• These are less sensitive under organic materials than chloric disinfectants.
• These are less corrosive than chloric.
• These don’t irritate animal’s organs.
• Objects: mainly, skin, mucus membrane
② Aldehydes
Formaldehyde [HCHO]
• Application: Viruses, Bacteria, Fungi, Protozoa
• These are potent disinfectant.
• These irritate and poisonous to eyes and nasal mucous membrane.
• Objects: fixative[ 37% saturated solution as Formalin],
equipment [1-3%],
airtight room [as gas]
Glutaraldehyde [CHO(CH2)3CHO]
• Application: Viruses, Bacteria, Fungi, Protozoa
• These are potent disinfectant.
• These are less irritating than Formaldehyde.
• These are little corrosive against metals.
• Objects: mainly, sheds, equipment, excrement
Animal Welfare & Health - 2015 44
③ Surface active agents
Cationic surfactant
• Application: some bacteria(excluding Mycobacterium, Spore of Bacillus and
Clostridium), some viruses
• These effects decrease under organic materials.
• These don’t irritate animal’s skin or mucous membrane.
• Example; Benzalkonium chloride, Benzethonium chloride
• Objects: Mainly, equipment, skin, mucous membrane
•
Ampholytic surfactant
• Application: some bacteria (including Mycobacterium), some viruses
• These effects decrease under organic materials.
• These don’t irritate animal’s skin or mucous membrane.
• Objects: Mainly, equipment, skin, mucous membrane
④ Phenols
Phenol [C6H6O]
• Application: some bacteria (excluding Spore of Bacillus and Clostridium), some
viruses, Fungi
• These can work even under organic matter comparatively.
• These are bad-smelling and poisonous so we can’t use them for skin or mucous
membrane.
• Objects: mainly, sheds, wall, excrement
Cresol [C7H8O]
• These are stronger than phenol.
• Usually we use these as cresol soap.
⑤ Alcohol
Ethanol [C2H5OH]
• Application: some bacteria(excluding Spore of Bacillus and Clostridium), some
viruses, some fungi
• These are less poisonous.
• These are effective as 70-80% concentration.
• Objects: mainly, hands [70% solution]
Isopropanol [C3H7OH]
• Application : some bacteria (excluding Spore of Bacillus and Clostridium), some
Animal Welfare & Health - 2015 45
viruses, some fungi
• These are less effective against virus than Ethanol.
• These are used as 50-70% concentration solution.
• Objects: mainly, hands
⑥ Oxydol
Oxydol [H2O2]
• Application: some bacteria(excluding Spore of Bacillus and Clostridium, some
Mycobacterium), Viruses, Fungi
• Objects: mainly, wound[3%]
⑦ Biguanide
Chlorohexidine gluconate
• Application: some bacteria(excluding Spore of Bacillus and Clostridium,
Mycobacterium)
• These effects decrease under organic materials.
• Using with alcohol or cationic soap, these are more effective.
• Objects: mainly, skin, equipment
In all-in-all-out system, cleaned up houses should be kept empty for a while until next
introduction.
Surroundings of shed should be kept clean with weed-killer and be prevented from the
appearance of harmful insects. Soil of surrounding sheds should be disinfected by slaked lime
or bleaching powder (chlorinated lime).
2.6 Vaccination
Vaccination is the production of active immunity in an animal against a specific infection by
using a vaccine. The vaccine contains antigens that stimulate production of specific antibodies in
the body.
2.6.1 Types of vaccines – there are three types of vaccines namely live vaccine, killed (dead or
inactivated) vaccine and toxoid, usually toxoid is classified into killed vaccine.
(a) Live vaccines contain actual living organisms, in most cases modified (attenuated) in
a way that they do not produce the disease. Such kind of vaccines is referred to as a
live attenuated vaccines. Occasionally a related non-attenuated live but non-
pathogenic organism is used. Live vaccines produce a more lasting immunity.
(b) Dead vaccines may contain either killed organisms, part of the organism or genetic
material. Dead vaccines produce a more solid immunity after a booster.
Toxoid is defined a modified or inactivated toxin that has lost toxicity but retains the
ability to stimulate the production of antitoxin (antibody against a toxin).
2.6.2 Vaccine handling, storage and usage – it is absolutely essential that vaccines are handled,
transported, stored and used as recommended because they are very sensitive to certain
environmental factors. The “cold-chain” must be maintained from the time of
manufacturing to the time of usage. General recommendations are outlined below,
however, it is always important to read the manufacturer’s instructions carefully and
abide by them.
Recommendations;
❑ Vaccines must be stored and transported at 2-8℃. Most vaccines must not to be
frozen.
❑ Vaccine must be protected from direct sunlight.
❑ Reconstitute only enough for immediate use and do not use leftovers.
❑ Remains of vaccines must be disposed of burning or burying
❑ Vaccines must be shaken thoroughly when reconstituting
❑ Use new sterile syringes and needles, particularly for live vaccines
Disease prevalence – in endemic areas a disease may show seasonal variations and
vaccination should be undertaken prior to the expected season of most prevalence. It may
not be necessary to vaccinate against diseases that do not occur in the area. There is a risk
of introducing a disease through vaccination if live vaccines are used.
Age of animals – many vaccines have age limitations e.g. generally calves less than 3
months should not be vaccinated and S19 (brucellosis) vaccination is only recommended
in heifers before their first service. The vaccination status of the dam may dictate when
young animal are first vaccinated because material antibodies acquired by the young
animal may interfere with response to vaccination for a certain period after birth. Young
animals often require a booster earlier than the adults.
There are several methods of controlling external parasites infection on farm animals. These
methods include plunge dipping, race spraying, hand spraying, pour-on, spot-on, greasing, use of
impregnated ear tags and hand dressing.
2.8.4 Pour-on
Pour-on involves pouring special “pour-on”acaricide on the dorsal aspect of the animal, from the
head to the tail. The amount of acaricide applied is calculated according to the weight of the
animal. It is poured evenly using devices such as squeeze bottle or syringe. The acaricide the
permeates downwards to the rest of the body.
2.8.5 Spot-on
Spot-on involves application of special “spot-on”acaricide onto specific spots or areas where
ectoparasites are located. Grease containing acaricide, “tick grease”, is also applied to specific
areas habited by ectoparasites.
2.8.6 Hand-dressing
Hand-dressing involves removal of ectoparasites from the animal by hand.
2 )Implementing biosecurity measures as standard practice helps ensure that all those working
with farm animals or coming into contact with them do not spread disease when they enter
or leave a premises. This is important whether or not any disease outbreaks have been
reported. Some diseases are zoonotic - they can be transmitted between humans and
animals - therefore there are good public and occupational health reasons for having
biosecurity measures. Proper biosecurity which effectively reduces the incursion and spread
of disease reduces disease control costs and helps prevent the spread of plant diseases too.
3 ) Definitions
a) 'Biosecurity' is the prevention of disease causing agents entering or leaving any place
4 ) Disease is not always apparent, especially in its early stages. Any person visiting a premises
with farm animals and not carrying out effective biosecurity measures on entry and on
leaving a premises runs the risk of spreading diseases to or from that premises. It is
important to apply bio-security measures even when animals have been removed from
the premises, as disease causing agents and their vectors can persist after the animals
have left. The biosecurity
measures taken should reflect the risk involved.
8 ) The appropriate bio-security measures depend on the risk associated with the visit.
The risk of spreading disease varies with the degree of exposure to the animals and their
products (e.g. manure, used bedding, milk, etc) and the likelihood of passing infection
on to others. Factors that determine the risks associated with visits include:
a) Type of premises – e.g. arable, livestock, mixed, horticultural;
b) Restrictions applied to the premises – e.g. animal disease control;
c) Restrictions applied on all premises in a defined area – e.g. Restricted Infected Area /
Infected Area;
d) Extent and reason for the visit – e.g. farm house, animal handling or
inspection, land inspection.
Unnecessary contact with animals is best avoided.
Visits to more than one premises with farm animals where there is direct contact with farm
animals
The risk of spreading diseases is minimised when appropriate bio-security measures are observed.
Non-essential visits to premises with farm animals should be suspended.
1) Where appropriate the visit should be made with the agreement of the owner or
premises manager and any reasonable requests for additional bio-security measures
should be observed, especially if you have visited another premises with farm animals
in the previous 3 days.
3) If other vehicles are taken on to the premises they should, wherever possible, be parked
on hard standing away from farm animals and must be visibly free of animal excreta,
slurry etc. Vehicles or trailers should not normally be taken into areas where farm
animals have access – these arrangements should be confirmed, where appropriate, with
the owner or premises manager in advance of the visit. Before leaving the premises all
visible contamination with manure, slurry or similar material must be removed
(including where appropriate, cleaning of the inside of vehicles, especially foot wells
and pedals). If this is not possible, vehicles and trailers must be cleaned before they are
taken onto another premises with farm animals, either at the end of the day or before the
next visit.
4) Owners or farm managers are recommended to have facilities available for disinfecting
vehicles, footwear and clothing. If facilities are NOT available on farm cleansing and
disinfection should be arranged as soon as possible and before the next visit to a
premises with farm animals.
5) Suitable protective clothing and footwear must be worn on all premises where visits
include entering areas where farm animals are present or to which they normally have
access. The type of protective clothing and footwear required depends on the nature of
the visit, e.g. the protection required for a visit to a dairy herd would differ from that
required for a visit to an extensive premises on moorland. Contractors such as shearers
should ensure clothing is changed and washed between visits to different premises.
6) The purpose of the protective clothing and footwear is to prevent any contamination
being carried from premises to premises. Protective clothing and footwear may be
disposable or re-usable. The following are examples of types of protective clothing:
a) Disposable boiler type suits. These can be used once and should be discarded
Animal Welfare & Health - 2015 58
at the end of the visit to the premises. They can be left on the premises with the
owner's agreement or bagged and suitably disposed of later, as can disposable
overshoes for footwear.
7) All equipment used must be clean on arrival and on departure. Great care must be taken
when cleaning electrical apparatus or tools. Where possible equipment should be
protected from contamination e.g. using plastic bags. Health and Safety rules mustbe
observed. Where equipment can be cleansed and disinfected this must be done before
entry to the premises and again on departure.
2.11.1 ANTHRAX
(Splenic fever)
Anthrax is a peracute or acute disease of all warm-blooded animals including man. It is characterized
by septicaemia, sudden death, high mortality and oozing of dark, thick blood from natural
orifices.
The causative agent is spore-forming bacteria called Bacillus anthracis. The spores can withstand
100℃boiling for 30min and can remain infective for over 20years on pastures.
TRANSMISSION
Infection gains entry into the body by ingestion, inhalation and through the skin. Incubation period is
1-5 days.
CLINICAL SIGNS
Peracute form (An affected animal may die in 1-2 hrs after onset)
Sudden death without any previous observed signs
High fever, muscle tremors and mucosal congestion
Acute form (course 2 days)
Sudden fever (42℃), respiratory distress, staggering, excitement followed by depression and
congested mucosae
Pregnant animals may abort, milk may be blood-stained and production is reduced
POSTMORTEM FINDINGS
Dark, thick, non-clotting blood, may ooze from natural orifices
Absence of rigor mortis
Carcass rapidly undergoes decomposition.
Spleen is very large sometimes
TREATMENT
TRANSMISSION
Blackleg is a soil-borne infection and may gain entry through deep wounds. In cattle the infection is
endogenous and common in beef breeds, in animals that are in excellent health, gaining weight and
usually the best of the group. This may be particularly serious in feedlots.
CLINICAL SIGNS
Sudden onset with others dead without any previous observed signs
Severe lameness usually with severe swelling of upper part of affected leg
Hot and painful crepitus swelling which later becomes cold and painless
Fever (40-42℃), depression and anorexia
POSTMORTEM FINDINGS
Blood-stained froth from nostrils and anus
Rapid clotting blood
Affected muscle is dark red to black, dry and spongy and has a sweetish (clover) smell
TREATMENT
Not very effective
TRANSMISSION
A small percentage of cattle are carries and become clinically ill under different stresses. The
organisms are then shed through saliva and nasal discharge. Other animals get infected through direct
and indirect contact.
CLINICAL SIGNS
Sudden death without previous observed signs.
Dullness, lagging behind, fever, salivation and nasal discharge
Edematous swelling of ventral neck and brisket
Respiratory distress
POSTMORTEM FINDINGS
Edema of head, neck and brisket region
Straw-coloured fluid in edematous region
TREATMENT
A variety of antibiotics (sulfonamides, tetracyclines, and penicillins) are effective, if
administered early
CONTROL
Reduce stress i.e. transportation, handling etc
Vaccination (inactivated)
2.11.4 BLOAT
(Ruminal tympany)
CLINICAL SIGNS
Sudden death, or found dead
In primary pasture bloat, obvious distention of the rumen is sudden especially on the left side.
Difficulty breathing and increased rate of respiration, mouth breathing and protrusion of the
tongue
Grunting and kicking at the belly
Death 3-4 hours after onset of signs
In secondary bloat, the abdomen is distended and there is a ‘ping’ sound on percussion
TREATMENT
In life-threatening cases, an emergency rumenotomy may be necessary; it is accompanied by an
explosive release of ruminal contents and, thus, marked relief for the cow.
A trocar and cannula may be used for emergency relief, although the standard-sized instrument
is not large enough to allow the viscous, stable foam in peracute cases to escape quickly enough.
NB trocar or cannula should be stabbed at left paralumbar fossa (usually, it is observed as
inverted-triangular dent encircled by last rib, tips of transverse processes of lumbar vertebrae
and cord of the flank). If trocar or cannula is mistakenly stabbed at thoracic cavity through
between the ribs, it causes a more fatal condition to the cow.
After relief use antifoaming agents such as oils (vegetable oils and mineral oils at doses of 250-
500ml). Dioctyl sodium sulfosuccinate (docusate) is commonly incorporated into the oil.
Large bore stomach tube in secondary bloat
NB it is passed through nostril up to rumen and it can find large pockets of rumen gas that can
be released. After slight passing the tube, if you cannot breathe though you can blow through the
tube, it indicates the tube is correctly placed in the esophagus. If you can blow and breathe
through the tube, it indicates the tube is incorrectly placed in the trachea.
Animal Welfare & Health - 2015 64
2. Diseases which are accompanied by mainly abortion or genital abnormalities
- Brucellosis ◆
- Bovine venereal epididymits vaginitis (Epivag) ◇?
- Akabane disease ◇
- Coxiellosis (Q fever) ■
2.11.5 BRUCELLOSIS
(Contagious abortion, Bangs’ disease)
It’s a contagious disease characterized by abortion in late pregnancy and a subsequent high rate of
infertility in the female and to a lesser extent, orchitis and infection of accessory sex glands in male.
It is caused by bacteria Brucella abortus. This organism is readily destroyed by common
disinfectants.
TRANSMISSION
Transmission is mainly through consuming infected pastures, other feedstuff and water supplies.
Aborted fetuses, foetal membranes, vaginal discharges, milk and faeces from infected animals are
most probable sources of contamination. Venereal transmission is considered unimportant. Other less
important modes of transmission include penetration through intact skin and conjunctiva.
CLINICAL SIGNS
Abortion after 5 months of pregnancy in susceptible, unvaccinated cows is the cardinal feature
of the disease
Stillborn calves, retained placentas, metritis and reduced milk yield
In the bull, orchitis and epididimytis occur occasionally
TRANSMISSION
Transmission is venereally or through close contact. AI with semen from clinically or sub-clinically
infected bulls is also a possible mode of transmission.
CLINICAL SIGNS
Acute onset of signs i.e. 24-48 hours after mating
The vulval lips become swollen and tender
Red vesicles develop on the vaginal mucosa, rupture and give rise to haemorraghic ulcers.
Unruptured vesicles develop into pustules
Similar lesions will appear on the penile shaft of the bull which will become reluctant to serve
Abortion is a common result of the infection. Abortion occurs after the 5th month of pregnancy
Reduced volume and quality of semen in bulls
Permanent sterility may result in both bulls and cows
TRANSMISSION
Infection is by inhalation of infective droplets coughed out by carriers or active cases. This bacteria
can survive only a few hours outside the body thus close contact is necessary for transmission to
occur e.g. at watering points, in kraals etc.
CLINICAL SIGNS
Acute fever (41℃), anorexia and respiratory distress
Animal stands in shade, its head and neck extended, slightly arched back and elbows turned out
Pain on percussion of the chest
Death after 1-3 weeks
POSTMORTEM FINDINGS
On section, the lung shows characteristic variation in colour of the lobules from red to gray, each
lobule is separated by a partition containing straw-coloured fluid which later becomes thickened,
firm and yellowish giving it a marbled appearance
Chest contains large amounts (up to 10 litres) of clear fluid containing shreds of fibrin
TREATMENT
Only in endemic areas (under government supervision)
Antibiotics e.g. sulphadimidine, streptomycin, tetracycline and tylosin may be used
Elimination is most recommended in new areas
CONTROL
Report to relevant authorities immediately
Restrict animal movements (under government supervision)
Blood testing and slaughter of reactors
Vaccination (inactivated)
2.11.8 TUBERCULOSIS
(TB)
Tuberculosis is an infectious disease affecting virtually all vertebrates. It is commonly described as a
chronic wasting disease, but may be acute. The TB- causing agent has a waxy covering that renders it
much more resistant to external influence including disinfectants.
The three most important forms of TB are the, human, bovine and avian forms. These forms are
caused by Mycobacterium tuberculosis, M. bovis and M. avium respectively.
TRANSMISSION
POSTMORTEM FINDINGS
TB granulomas (swellings) may be found in any of the lymph nodes or any organ
The granulomas may be capsulated with a caseous core
Miliary abscesses in the lungs (pus is yellow to orange, thick cream to crumbly cheese). These
lesions may coalesce (merge) to an extent of replacing an entire lobe
TREATMENT AND CONTROL
Treatment is not recommended in animals
Test-and-slaughter (tuberculin)
Test-and-segregation
2.11.9 THEILERIOSIS
(Corridor disease, East coast fever-ECF)
An acute tick-borne disease of cattle characterized by high fever, lymph node enlargement,
respiratory distress, weakness and high mortality.
It is caused by a protozoan parasite called Theileria parva.
TRANSMISSION
The parasites are transmitted to cattle by infected vector ticks, Rhipicephalus appendiculatus and R.
zambeziensis.
CLINICAL SIGNS
Vary according to level of infection
Fever (42℃), enlarged lymph nodes
Depression, anorexia, loss of condition, reduced milk yield
Respiratory distress, lacrimation and nasal discharge/froth
High mortality (may be more than 90%)
CONTROL
Tick control is very important
Restrict animal movement to avoid tick infestation
Vaccination is now possible
TRANSMISSION
Spread of the disease is mainly through feed and direct contact. FMD may be transmitted from one
country to another by birds or wind. Transmission through meat products has made FMD one of the
most serious diseases in the world.
CLINICAL SIGNS
Fever (in early stages only), dullness, inappetence and shivering
Smacking of lips, difficulty in chewing and swallowing, indicating pain in the mouth
TREATMENT
No treatment
Give antibiotics for secondary bacterial infection
CONTROL
Vaccination
Quarantine of affected farms (under government supervision).
2.11.11 BABESIOSIS
(Redwater)
It is a tick-borne disease of domestic and wild animals. It is characterized by fever, anemia,
haemoglobinaemia and haemoglobinuria.
In cattle the disease is caused by Babesia bovis and B. bigemina.
TRASMISSION
The natural and main vectors of redwater are ticks of Boophilus spp. may also transmit this disease.
CLINICAL SIGNS
Fever (42℃), loss of appetite, reduced milk yield
Haemoglobinura (red water), anemia, abortion and jaundice sometimes
POSTMORTEM SIGNS
Jaundice, pallor of tissues and edema in most parts of the body
Thin watery blood, enlarged and deep orange liver
Red- brown urine in the bladder
TREATMENT
Imidocarb (Imizol®) is very effective
Diminazine aceturate (Berenil®)
2.11.12 ANAPLASMOSIS
(Gall sickness)
An infectious disease of ruminants, characterized by anemia, jaundice and fever. It is caused by
rickettsia of the genus Anaplasma. A. marginale and A. centrale are responsible for the disease in
cattle and wild ruminants while A.ovis causes anaplasmosis in sheep. A. marginale is the most
pathogenic of the three.
TRANSMISSION
Spread from animal to animal occurs chiefly by vectors ticks. Anaplasma may alsobe transmitted via
unsterilized surgical instruments and needles.
CLINICAL SIGNS
Anaplasmosis is most severe in adults
Depression, sometimes aggression, anorexia and fever (40-41℃)
Marked anemia, jaundice, weight loss and dehydration
Reduced milk yield and abortion
POSTMORTEM FINDINGS
Jaundice, pallor of tissues, this watery blood and emaciation
Enlarged and deep orange liver with a distended gall bladder
Spleen is enlarged and dark
DIAGNOSIS
Blood smears and serum should be submitted to the lab for confirmation
TREATMENT
Imidocarb (Imizol®) is very effective
Early tetracycline treatment may be useful
CONTROL
Tick and fly control is cardinal
Restricted animal movement to avoid tick infestation
2.11.13 COWDRIOSIS
(Heartwater)
An infectious, non-contagious, disease of ruminants characterized by fever, nervous signs, edema of
body cavities and diarrhea.
It is caused by Ehrlichia (Cowdria) ruminatium.
TRANSMISSION
Ticks belonging to genus Amblyomma (Bont ticks) are the major transmitter of cowdriosis.
CLINICAL SIGNS
Fever, loss of appetite, rapid breathing, listlessness
Nervous signs such as circling, high-stepping gate, exaggerated blinking and chewing
movements with terminal convulsions
NB: Indigenous cattle show high level resistance
POSTMORTEM FINDINGS
Hydropericardium, hydrothorax and hydroperitoneum
TRANSMISION
Tsetse flies, Glossina spp, are the most important vectors of trypanosomiasis. The trypanosomes are
ingested by the tsetse fly from an infected animal. The trypanosomes multiply in the fly and are
injected into a susceptible animal as the fly feeds. Transmission is also possible by mechanical
transfer through other biting flies, surgical instruments and needles.
CLINICAL SIGNS
Very variable
Intermittent fever, anemia and loss of appetite
Chronic weight loss
Enlarged lymph nodes, ocular discharge
Abortions are common
Mortality is high without medical intervention
Stress such as lack of food and water worsen the disease
POSTMORTEM FINDINGS
Very variable too
Anemia, emaciation and depleted fat stores
Enlarged lymph nodes, spleen and liver
TREATMENT
A number of trypanocides are available
Diminazene aceturate (Berenil®)
Isometamidium (Samorin® or Trypamidium®)
Pyrithidium bromide (Prothridium®)
Quinapyramine sulfate (Antrycide®)
CONTROL
Aim of control:
To interrupt the life cycle of the parasite either in the host or vector
Control methods:
Use of trypanocides in animals
Animal Welfare & Health - 2015 73
Control of tsetse flies can be achieved by regular dipping of animals, spraying of insecticides on
fly-breeding areas, use of insecticide-impregnated screens, bush cleaning and so on.
Also animals can be treated prophylactically
2.11.15 DERMATOPHILOSIS
(Senkobo, Cutaneous streptotrichosis)
An infectious disease of the epidermis, frequently affecting cattle, sheep and goats. It characterized
by formation of scabs on the affected skin.
It’s caused by Dermatophilus congolensis.
TRANSMISSION
D.congolensis can survive in a quiescent form, in scab material, for several months providing
conditions are dry. The infective form is activated by humidity (rain), high temperature and various
factors that reduce the natural barrier of skin such as ticks, biting flies or thorny bushes.
CLINICAL SIGNS
Sites commonly affected are head, neck, chest, root of the tail and back of udder
Papules appear from which serum comes out and hair get matted together into
“paintbrush”fashion.
Scab formation follows later
The skin thickens to form “wart-like”lesions
Severely affected animals are anorexic, lose condition and may die
TREATMENT
Infected animals usually heal spontaneously after 2-3 weeks
CONTROL
Slaughter or isolation of affected animals
Control ticks, biting flies and thorny bushes to avoid injury to the skin
TRANSMISSION
Transmission is through biting flies and contact. Pure-breed exotic cattle are most susceptible.
CLINICAL SIGNS
Fever, lacrimation, nasal discharge and hyper-salivation
Round, slightly raised, firm and painful nodules on the skin
Nodules may slough-off leaving sores
TREATMENT
No treatment
Use antibiotics to prevent secondary bacterial infection
Vaccination
Quarantine is not very helpful
2.11.17 DERMATOPHYTOSIS
(Dermatomycosis, Ringworm)
An infection of the skin, hair and nails caused by one or several genera of fungi collectively called
dermatophytes.
In cattle Trichophyton spp are the usual cause of ringworm, however, Microsporum spp may also
cause infection.
TRANSMISSION
Dermatophytosis is most common in the season when the skin remains wet for a long time with high
temperatures. Direct contact with infected animals is the common method of spread of ringworm,
however, indirect contact through any inanimate objects, particularly bedding, harness, ropes and
CLINICAL SIGNS
The disease is most common in calves.
Alopecia with thick round, raised, sharply circumscribed gray-white crust
Lesions are most commonly found on the neck, head and perineum
Secondary bacterial infection results in pruritus otherwise ringworm itself is not itchy
TREATMENT
Topical washes or sprays of 4% sulphur
0.5% chlorhexidine, 1% povidine-iodine
Griseofulvin, miconazole and clotrimazole
2.11.18 MANGE
A contagious skin disease characterized by alopecia (hair loss), pruritus and hypersensitivity. It is
caused by a number of species of mites.
TRANSMISSION
Chiefly through direct contact, although beddings and grooming tools may be additional methods of
spread.
CLINICAL SIGNS
Appearance of small nodules and pustules in particular areas
Pruritis, hair loss, skin thickening and scab formation may soon follow
Lesions usually first appear in particular areas such as around the muzzle, face, neck, brisket,
root of the tail and udder before spreading to other parts of the body.
TREATMENT
Subcutaneous or pour-on ivermectin (Ivomec®)
Flumethrin (BAYTICOL®) can be applied even to dairy animal.
Suitable dips such as coumaphos, phosmet, amitraz etc.
2.11.19 PINK-EYE
(Infectious keratitis, Blight, Infectious kerato-conjunctivitis)
It is an infectious disease of cattle, sheep and goats characterized by conjunctivitis, lacrimation and
varying degrees of corneal opacity and ulceration. It is most severe in exotic breeds of cattle.
In cattle, the common cause is Moraxella bovis, in sheep Branhamella ovis (Neisseria ovis).
CLINICAL SIGNS
In cattle and goats young ones are most affected, in sheep only adults
Photophobia, rapid blinking, and lacrimation
Pussy ocular discharge, conjunctivitis (reddening of eye)
Extensive corneal opacity which may lead to blindness if not treated
TREATMENT
Ophthalmic treatment with preparations such as zinc sulphate, tetracycline & doxycycline
Subconjunctival injection of antibiotics e.g. penicillin, nitrofurazone, tetracycline or penicillin-
streptomycin mixture (Pen-strep®)
CONTROL
Hygiene and fly control, especially in the dairy and calf pens
Preparation of shelter wood
CLINICAL SIGNS
Excitement, hypersensitivity and unsteady walk
Sternal recumbency, depression, head turned to one side
Anorexia is complete, dry muzzle and cool skin (36-38℃)
Lateral recumbency, coma, flaccid lims and bloat due to position
CLINICAL SIGNS
Bright and alert, eats and ruminants well, but with slight-reduced appetite
No abnormalities except will not stand up
50% of downer cows will get well within 4 days if properly nursed
Recovery is unlikely if recumbency is over 7 dats
TREATMENT
Usually responds well to calcium treatment
Good nursing is the best treatment. Provide the most comfortable bedding possible and turn the
animal from side to side several times (at least 3-4 times).
Hind limbs should be flexed and extended and massaged several times daily.
Prevention and prompt treatment of milk fever essential
TRANSMISSION
Infection gains entrance through broken skin on the lower part of the foot. The disease occurs during
all seasons, but tends to be more prevalent during the wet season.
TREATMENT
Clean the foot and soak in 5% copper sulphate or apply aerosol spray e.g. chloramphenicol in
genitian violet preparation
In addition to this topical treatment give antibiotic injection (e.g. sulphonamide, oxytetracycline)
CONTROL
Screen new arrivals
Animals should avoid wet grounds
Footbathing with 5-10% copper sulphate or 5% formalin at places such as entrance to the dip
tank or milking parlour. In severe cases it best to let the animals stand in the bath for about 1 min
once every week.
CLINICAL SIGNS
Diarrhoea, dehydration, weakness and death within one to several days of onset
Generally, diarrhea due to bacteria occurs in calves less than 14 days while the virus cause
diarrhoea in calves 5-15 days old calves. Diarrhoea due to Cryptosporidium spp occurs in calves
5-35 days old.
TREATMENT
Oral fluid therapy
Absorbents such as kaolin or charcoal
Antibiotics
Only withhold milk if diarrhoea is due to inappropriate feeding
2.11.24 MASTITIS
Mastitis is inflammation of the mammary gland. Inflammation has five properties; swelling, pain,
reddening, hotness and loss of function. Although these properties are ever present in a mastitic
udder, it is not always easy to detect one with mastitis by palpation or visual examination alone.
Mastitis is probably the most common disease in dairy cows with great economic importance. It
occurs wherever cattle are kept for commercial milk production. There are many factors that cause
mastitis but the most common and important one is bacterial infection.
PREDISPOSING FACTORS
The major predisposing factor is injury to the teat and canal. This may be caused by poor
milking techniques such as:
Strip milking and two finger milking
Faulty milking machine e.g. misshapen teat-cup liners, high vacuum, incorrect pulsation rate
and failure for teat-cups to drop after all the milk has been removed
Incomplete milking in presence of germs (pathogenic bacteria)
Failure to adequately induce milk let-down
Delay in milking when milk let-down reflex operates
Rough handling of milking cows
Wet and dirty bedding
Contagious mastitis
Contagious Mastitis is caused by bacteria live on the skin of the teat and inside the udder.
Contagious mastitis can be transmitted from one cow to another during milking. The causative
bacteria included contaminated milk are transferred to the skin of the udder and teats by milker’s
hands, udder cloth, milker etc.
DIAGNOSIS
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Observing clinical signs of the disease
Field test – These tests detect physical and/or chemical changes of milk. They include salty taste
detected by use of the tip of the tongue, strip cup with black surface plate to detect wateriness or
clots of the foremilk and in California Mastitis Test (CMT) the milk forms a gel when mixed
with some types of detergent like TEEPOL®.
Laboratory test, which include check of physical and/or chemical changes of milk, cell count
culture and isolation of bacteria, sensitivity of bacteria to antibiotics.
TREATMENT
Early recognition of mastitis and treatment is essential for a cure
Before local medication is applied the infected udder is thoroughly milked, and the teat
disinfected.
Treatment may be applied locally or systemically
In severe cases milk the mastitic udder several times daily.
Local treatment
Lactating cow
Intramammary infusions/injections containing antibiotics such as penicillin are highly effective.
However, the withdrawal period as recommended by the manufactures must be observed strictly
to avoid exposing consumers to milk with high levels of antibiotics that may cause allergic
reactions.
It is recommended that all quarters be treated even when mastitis has been detected in only one
quarter. However, due to economic reasons only the affected quarter may be treated. Treatment
of all quarters is then left to situations when mastitis is persistent, recurrent or in outbreaks.
From time to time a small number of cases will be incurable. Seek professional advice for a
decision whether to continue treating or to dispose of the case. However, continuous culling is
very wasteful and is not encouraged.
Dry cow
Dry cow therapy is given after the last milking before drying off. During this period maximum
benefit of treatment is achieved because the antibiotics stay a longer period in the udder and it
helps in reducing the incidence of mastitis.
Systemic
Systemic treatment is usually given when intramammary treatment alone is less effective. It is
often intramuscular, or less often, intravenous. It is highly recommended that the same type of
antibiotics used in the udder be used systemically.
Animal Welfare & Health - 2015 83
PREVENTION AND CONTROL
For a mastitis control programme to succeed, mastitis history of the herd must be available and
the full co-operation of the herdsman must be sort. The herdsman must fully understand ways in
which mastitis may be introduced into the herd and how it spreads.
Medical treatment alone is of limited value if not accompanied by efforts towards prevention of
transfer of bacteria.
Routine monthly testing (e.g. with CMT) of all quarters of every cow helps to detect early cases
and subclinical infection.
TICKS
Ticks are of great veterinary concern and economic importance in livestock production in Zambia.
Ticks have the ability to transmit a large variety of infectious agents some of whom cause disease
that are able to cause very high mortality eg corridor disease. The cost of treatment of these diseases
and that of tick control are usually very high. Ticks act as disease reservoirs as some disease-causing
agents have to pass through them to complete their life cycle.
Heavy tick infestation can lead to anemia and hides from such animals are down-graded and fetch
low prices on the market. Animals may also react to their salivary fluids and toxins, a condition
called tick toxicosis (sweating sickness, tick paralysis). They also cause skin wounds that can get
bacterial infection.
LIFE CYCLE
The life cycle of the ticks various widely. Generally eggs are laid in the soil and hatch into larvae,
which attach themselves to a passing host on which they may develop through one or more nymphal
stages before becoming adults. The nymphs and adults have four pairs of legs while the larvae have
TYPES OF TICKS
Depending on the number of hosts they pass through to complete the life cycle, ticks can be
categorized into four main groups; one-host ticks, two-host ticks, three-host ticks and multiple host
ticks.
One-host ticks – all the three stages (larva, nymph and adult) are spent on one animal e.g. Boophilus
spp.
Two-host ticks - larva attaches to an animal, feeds, engorges and moults into nymph then drops off,
moults into an adult which re-attaches to another host. The adult feeds and drops as an engorged tick
e.g. some species of Rhipicephalus spp. and Hyalomma spp.
Three- host ticks - each stage (larva, nymph and adult) feeds, engorges and drops off before re-
attaching to the next host e.g. Amblyomma spp, some species of Rhipicephalus and Hyalomma spp.
Multi- host ticks - larvae feed on one host and drop to the substrate to moult; the several nymphal
instars each feed separately, drop, and molt; adults feed several times (but don’t moult) e.g. Most of
Ornithodorus spp. (except for O. lahorensis)
TYPES OF TICKS
Generic Name DISEASES TRANSMITTED in Afirca
ONE-HOST TICKS
Boophilus spp. Babesiosis, Anaplasmosis
Dermacentor albipitus
Otobius megnini
TWO-HOST TICKS
Hyalomma spp.
Rhipicephalus bursa
Rhipicephalus evertsi
Ornithodorus lahorensis
THREE-HOST TICKS
Amblyomma spp. Cowdriosis
Dermacentor spp.
Haemaphysalis spp.
Ixodes spp.
Rhipicephalus spp. (except R.evertsi and Theileriosis(East Coast Fever)
Generally, one-host ticks are easier to control than two-host or three-host ticks. For strategic dipping,
the following may be used; longer interval (2-5 weeks) between dipping with higher acaricide
concentration for one-host ticks or short interval (5-7 days) with a lower acaricide concentration for
two- and three-host ticks. However, this requires accurate identification of the ticks to be controlled.
Other factors that form part of a network of interrelated variables leading to helminth parasitism
include the microclimate and macroclimate of the environment, grazing habits, immunological and
nutritional status of the host, the presence of intermediate hosts and vectors and the number of
infective larvae and eggs in the environment.
Nematodes(Round Worms)
The common stomach worms of cattle are Haemonchus placei, Ostertagia ostertagi and
Trichostrongylus axei.
TRANSMISSION
Ingestion of infective larvae in faeces and contaminated feed and water. Development to infective
stage is delayed in cold weather.
CLINICAL SIGNS
Young animals are more susceptible
Diarrhoae and sometimes constipation
Anemia, hypoproteinaemia leading to edema of the jaw (bottle jaw)
Anorexia, weight loss, weakness rough coat and potbelly
POSTMORTEM FINDINGS
Presence of worms in abomasum
Pin-point haemorrhagic areas and small nodules in the Gastro-intestinal Tract(GIT)
Gastric congestion and superficial ulcers
TREATMENT
Drug treatment alone cannot effectively control worms, it must be used together with other
measures such as:
Animal Welfare & Health - 2015 87
Treatment of all animals at once to avoid contamination
Movement of animals to uncontaminated pasture to avoid reinfestation
Provision of adequate nutrition
Anthemintics include the following:
Thiabendazole, mebendazole, albendazole, fenbendazole, oxfendazole and cambedazole
Also levamisole and ivermectin
CONTROL
Aims of control:
Prevention of heavy worm exposure to animals
Minimaised pasture contamination
Minimized effects of parasite burden on the animal
Encourage the development of immunity or resistance of animals to helminthes
Methods of control:
Alternate grazing of different host species
Alternation of grazing and cropping
Timing of dosing based on knowledge of the seasonal changes of infestation
Integrated rational grazing of different age groups within the one species
Trematodes(Flukes)
Liver fluke disease is caused by members of the genera Fasciola, Fascioloides and Dicrocoelium.
Fasciola hepatica is the most important trematode of domestic ruminants. Paramphistomum spp.
cause stomach fluke disease.
TRANSMISSION
Snails, Lymnaea spp, act as intermediate hosts for flukes. The snails prefer low-lying swampy areas
with slow moving water, also in constantly moist areas. Eggs are passed out in faeces of the host,
hatch in water and picked up by the snail. In the snail the fluke develop infective stage and leaves the
snail to attach to herbage. Infective stages of flukes are gested with herbage as the animal feeds.
CLINICAL SIGNS
Infestation is usually asymptomatic in cattle
In heavy chronic infestation anaemia, unthriftiness, weight loss and reduced milk yield may be
observed
POSTMORTEM FINDINGS
Presence of large number of flukes in bile ducts
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Calcification of bile duct walls is common in cattle
Bottle jaw and distended abdomen in very severe cases
Anemia, ascites, edema and emaciation may be observed too
TREATMENT
Triclabendazole, mebendazole and albendazole
Rafoxanide(Ranide®, Flukanide®), nitroxynil(Trodax®) and closantel
CONTROL
Aims of control:
Reducing the number of flukes in the host animals
Reduce the snail population in the environment
Minimize the exposure of livestock to snail-infested ground
Methods of control:
Use of fasciolicide
Drainage of land (where possible)
Use of molluscicides such as copper sulphate, copper pentachlorphenate and sodium
pentachlorphenate
Avoid grazing animals in swampy areas
Cestodes(Tapeworms)
Tapeworm infestation have little apparent effect on the health of farm livestock, however, heavy
infestation in young animals may cause failure to thrive. Common tapeworms include Moniezia
expansa, M. benedini and Cysticercus bovis.
TRANSMISSION
Eggs are passed in faeces of host, which are taken up by intermediate host (oribatid mites) and
finally the final host.
CLINICAL SIGNS
Most infestations do not cause clinical signs but on occasions heavy infestation may result in
unthriftiness, pot-belly and poor coat
Vague digestive disturbances including constipation and mild diarrhoea
Sometimes anemia and edema may be present
POSTMORTEM FINDINGS
Most commonly, tapemorms are present small intestines
Site of attachment may be indicated by presence of an ulcer.
Emaciation and anemia
Animal Welfare & Health - 2015 89
TREATMENT
Niclosamide
Cambendazole, oxfendazole, fenbendazole and albendazole
CONTROL
Dosing with above cesticides
Alternation of grazing and cropping is less helpful
Control of nematodes
Aims of control:
Prevention of heavy helminth exposure to animals
Minimized pasture contamination
Minimized effects of parasite burden on the animal
Encourage the development of immunity or resistance of animals to helminthes
Methods of control:
Alternate grazing of different host species
Alternation of grazing and cropping
Timing of dosing based on knowledge of the seasonal changes of infection
Integrated rational grazing of different age groups within the one species
Control of trematodes
Aims of control:
Reducing the number of flukes in the host animals
Reducing the snail population in the environment
Minimize the exposure of livestock to snail-infested ground
Animal Welfare & Health - 2015 90
Methods of control:
Use of fasciolicide
Drainage of land (Where possible)
Use of molluscicides such as copper sulfate, copper and sodium pentachlorphenate
Avoid grazing animals in swampy areas
Trematodes Bithionol(po)
Bromophenophos(po)
Doramectin(sc,im) Dectamax
Diazinon(spray,etc) Neocidal,Spectracide
Fenthion(spray,etc) Tiguvon
Chlorfenvinphos Supona,Steladon
Malathion Cynthion
Famphur Warbex
Phosmet Prolate
Flumethrin Bayticol
Cyhalothrin Grenade
d-Allethrin Aeroblast
permethrin
Benzyl benzoate
2.11.27 POISONING
General practical measures for management of poisoning or intoxication are usually directed towards
removal of unabsorbed poison from the animal and its environment. a few poisons and toxicants
have specific antidotes. However, identity of the poisonous substance involved is often unknown and
identification by analytical laboratories or manufacturers usually takes long. Despite this, the clinical
condition of the patient require immediate therapeutic intervention.
If the case history fails to pin-point the identity of the toxicant, the animal health attendant should
proceed along the lines exemplified below and in a sequence determined by severity of the clinical
sighs.
UREA POISONING
(ammonium poisoning)
Urea poisoning is usually an acute, rapidly progressing, highly fatal condition. It is caused by
After ingestion, urea and NPN undergo hydrolysis and release excess ammonia. The ammonia is
rapidly absorbed from the GIT resulting in onset of signs in 10-30 min after feeding. The toxicity
may be accelerated if these are fed together with soyabean meal.
CLINICAL SIGNS
Severe abdominal pain resulting in violent struggling and bellowing
Bloat and frothing at the mouth and nose
Muscle tremors, incoordination, weakness, respiratory distress and bloat
Hypersensitivity to sound and movement
TREATMENT
Only successful in very early stages of the condition
Prompt & efficient emptying of rumen through a large bore stomach tube or rumenotomy
Oral administration of a weak acid e.g. 4 liters of vinegar or 5% acetic acid
Oral administration of magnesium sulfate with a large quantity of water
Sodium thiosulfate solution
CLINICAL SIGNS
Usually sudden deaths in the best-conditioned lambs are first signs of enterotoxaemia
Neck-twisting, circling and pushing the head against fixed objects
Occasionally adult sheep are affected; they show weakness, incoordination and die within 24
hours
POSTMORTEM FINDINGS
Hyperemic areas in the intestines and fluid-filled pericardial sac. This is particularly the case in
young lambs
In adults hemorrhagic areas on the myocardium, abdominal muscles and serosa of the intestines
may be found
Bilateral pulmonary edema and congestion frequently occur, but usually not in lambs
Rapid postmortem autolysis of the kidney has led to the popular name “pulpy kidney disease”
CONTROL
Ewe immunization probably is the most satisfactory method of control of pulpy kidney in lambs
In feedlots it can be controlled by reducing the amount of concentrate in the diet (this is may not
be economical)
Immunization of all animals with a toxoid when they first enter the feedlot probably will reduce
losses to an acceptable level. Two injections 2 weeks apart will protect them throughout the
feedlot period
TRANSMISSION
Discharges from ruptured lymph nodes contaminate the environment with the organism, which can
survive for long periods outside the host. Infection can then gain entry by contamination of skin
abrasions and wounds that arise for a variety of reasons, e.g. shearing of sheep, castration and
fighting among goats. The organism can survive for about a day in commercial dips and dipping of
sheep, particularly those that had recently been sheared, can lead to infection.
CLINICAL SIGNS
Enlargement of one or more lymph nodes.
Superficial lymph nodes may rupture, discharging thick, green pus
Pneumonia, drop in milk yield and paralysis may be experienced due to involvement of internal
organs
External abscesses around the head and neck occur more commonly in goats, while the visceral
form is more common in sheep. Internal abscesses should be considered as a potential diagnosis
for “thin ewe” syndrome
POSTMORTEM FINDINGS
Abscesses in one or more palpable lymph nodes and in almost all internal organs
Abscesses are encapsulated by fibrous tissue
Abscess contents are light green or cream to yellow in sheep while in goats they are commonly
creamy
At first pus is semi-fluid but thick and later become firm and dry
TREATMENT
Not satisfactory although the organism is sensitive to antibiotics because antibiotics cannot reach
inside of abscess.
CONTROL
General hygiene in sheep and goats yards and pens
High standard of hygiene during shearing and castrating i.e. drop instruments in an antiseptic
before each use
Elimination of all animals with enlarged lymph nodes
Acquire replacements from clean flocks
Burn or bury the pus from the abscess
TRANSMISSION
D.congolensis does not normally penetrate the natural barriers of healthy skin. Factors th
at influence the development and transmission of dermatophilosis include those that weaken
this barrier like prolonged wetting by rain, high humidity, high temperature and various
ectoparasites. Also thorny bushes, shearing tools and grooming tools.
CLINICAL SIGNS
Lesions in goats first appear on the lips and muzzle then spread while in sheep they first appear
on the dorsal parts of the body
The crust are often pyramidal in a sheep wool
Crusts are thick, up to 3 cm in diameter and roughly circular
Heavy mortalities may occur in very young animals but generally the health of the animal is
unaffected unless lesions are widespread
``
TREATMENT
Shear the sheep and dip or spray with 0.2-0.5% zinc sulphate or 0.2% copper sulphate (this may
stain wool)
Topical antibacterial shampoo therapy
Soaking with chlorhexidine, benzoyl peroxide
Topical treatment with povidone-iodine
IM injection may also be given e.g. penicillin or Pen-strep®
CONTROL
Isolation the affected animals
Use separate grooming and shearing tools
Cull affected animals
Control ectoparasites
Delay dipping with acaricide for about 10 days after shearing
Avoid dipping sheep with long wool
TRANSMISSION
Transmission of foot rot to healthy animals requires a warm, moist environment. Injuries to the feet
enhance the transmission.
CLINICAL SIGNS
Most obvious is lameness, which may be very severe
Swelling and moistening of the skin in the interdigital space
The horny layer of the hoof is separated from underlying tissues
Discharge from affected foot has a foul smell
Loss of body condition
Rams affected in hind feet may be unable to serve and similarly ewe with affected hind feet may
be unable to bear the weight of a ram at service
TREATMENT
Treatment may be local or systemic
Local treatment
This requires removal of all detached hoof tissue
Then treatment with either aerosol spray, foot bathing or foot soaking
Solutions common for foot bathing include 10% zinc sulphate, 10% copper sulphate or 5%
formaldehyde, for aerosol spray in addition to these include 20% cetrimide, and 1.3%
tetracycline. Let the animal stand in foot bath for at least one minute.
※ traditionally, treatment consisted of foot bathing utilizing antibacterial solutions after careful
hoof trimming to remove all dead forn and expose infected tissue and bacteria air. However, foot
soaking for 30 min to 1 hr has shown to be more effective even when trimming is not done. The
most effective solution is 10% zinc sulphate with 0.2% of laundry detergent containing nonionic
surfactants such as sodium lauryl sulphate.
Systemic treatment
Injection of Pen-strep®, tetracycline or erythromycin
VIRAL DISEASE
2.12.5 RIFT VALLEY FEVER
(Infectious enzootic hepatitis)
It is an acute, mosquito-borne, viral disease of cattle, sheep and human beings. It is characterized, in
lambs, by hepatitis, high mortality and fever while in adult sheep by abortion. It is caused by a
phlebovirus.
TRANSMISSION
Infection is transmitted by biting insects, chiefly mosquitoes.
CLINICAL SIGNS
Rapid onset in kids and lambs with fever, listlessness, anorexia, weakness and death
In lambs less than one week old mortality may be more than 90%
In adult sheep there may be fever, anorexia, unsteady gait, vomiting diarrhea and abortion.
Abortion may be the only sign
POSTMORTEM FINDINGS
Focal liver necrosis
Enlarged, soft, friable, yellow brown to dark red liver
CONTROL
Moving stock to high-altitude areas with less mosquitoes
Stabling plus spraying against mosquitoes
Vaccination
TRANSMISSION
In a flock transmission is by contact with either affected animals or inanimate objects. It is believed
that damage to the skin is necessary for the virus to gain entry into the body. The scab remains
NON-INFECTIOUS
CAUSE
Underfeeding in late pregnancy is the primary predisposing factor. Overfeeding ewes particularly
those carrying twins or triplets in early pregnancy predisposes them to ketosis more than ewes in
poor condition and carrying single lambs. Anything that interrupts feed intake (e.g. storms, transport,
other disease conditions) may induce the disease. Under-fed ewes use up all the sugar reserves in the
body and naturally turn to body fat. During metabolism of the body fat, poisonous substances called
ketones are produced and accumulate in the bloodstream causing the condition called ketosis
CLINICAL SIGNS
Separation from the flock, aimless walk, and apparent blindness
Inappetence, walking into objects, muscle twitching especially around the face, grinding of teeth
and head turned to one side
Abnormal postures, incoordination, recumbency and coma death after 3-4 days
TREATMENT
Treatment is not very satisfactory unless the ewe is close to lambing
Glycerol or propylene glycol administered early reduces mortality
The above plus an anabolic steroid, vitamin B and fluid therapy
Caesarean section or induced abortion may lead to recovery (in early stages of the disease)
NB: Once signs are advanced, no treatment is highly effective. Fluid therapy is aimed at correcting
the acid base disturbance in blood. In absence of biochemical analysis, give glucose with IV isotonic
sodium bicarbonate or lactated ringer’s solution.
CONTROL
Avoid obesity in early pregnancy
Raising plan of nutrition in the last 6 weeks of pregnancy
If adequate and suitable feed is not available for the entire flock during late pregnancy, early
cases can be identified by gentle driving, then should be separated from the flock and given
special care and nourishment
Any interruption of food intake should be avoided.
PREDISPOSING FACTORS
Some of the predisposing factors of post weaning diarrhoea caused by E.coli include stress due to
separation from the sow, new environment, change of diet, mixing with piglets from other litters and
uncomfortable unsanitary weaning pens.
CLINICAL SIGNS
Yellow to grayish brown muddy or watery diarrhoea
Reduced feed consumption but normal water intake
Reduced growth rate, gaunt abdomens and lusterless hair coats
One or two pigs, in good condition, found dead
Staggering and incoordination in terminal stages
POSTMORTEM FINDINGS
Dehydration and loss of condition
Small intestines have yellow contents that may be blood-stained
Congestion of small intestine mucosa
TREATMENT
Treatment of in-contacts at first sign of this disease is recommended
Oral (especially through water) antibacterial drugs such as ampicillin, neomycin, sulphonamides
and tetracycline
Agemates in same piggery should be considered for treatment as well
CONTROL
Minimized stress associated with weaning
Avoid sudden change of diet; probably continue the pre-weaning diet for about 14days after
weaning
Preferably wean by removing the sow and keep the litter as one for some time
Where weaners from different litters are mixed, group them in equivalent sizes
TRANSMISSION
Soil and surface water contamination represent routs of exposure. Asymptomatic carriers are the
usual source of infectious organisms but bacteria may also be introduced to animal production unites
by surface water runoff, wild mammals, wild birds, pets, and biting insects. E.rhusiopathiae
commonly resides in the tonsillar tissue. Sometimes infection occurs through wounds.
CLINICAL SIGNS
Acute form
Sudden onset of high fever(42℃) followed by prostraction, complete anorexia and thirst
One or two dead pigs or severely affected ones show red or purple discoloration of some parts of
the skin. The skin lesions may take the form of the classical diamond-shaped plagues
Affected pig squeal excessively when handled
Require assistance to stand, and prefer to lie down soon after being forced to stand
Chronic form
Obvious enlargement of joints(arthritis) with mild lameness and stiffness
There may also be alopecia and sloughing of the tail and tip of the ears.
POSTMORTEM FINDINGS
Acute form
Skin lesions may be present
Hemorrhages throughout the body, congestion of lungs and liver.
Chronic form
Inflammation of limb and intervertebral joints
No pus in the enlarged joints
Synovial fluid is thicker with fibrinous material which is amber colored
Erosion of the articular surface may be present
Inflammation of the heart may occur with or without arthritis
CONTROL
Vaccination (live) is available although it does not give complete protection
Elimination of carriers, good sanitation, and a regular vaccination program is effective in
controlling the disease
2.13.3 SALMONELLOSIS
It commonly affects weaned and growing-finishing pigs, however, other group may also be affected.
Salmonellosis in pig is usually opportunistic infection. Asymptomatic carriers are cause of infection
with human through their products (meat).
It is caused by Salmonella Choleraesuis, S. Typhimurium and S. Enteritidis.
CLINICAL SIGNS
Fever and watery diarrhoea which may be yellow and contain shreds of necrotic debris
Septicemia characterized by hepatitis, pneumonia, and cerebral vasculitis
POSTMORTEM FINDINGS
Slightly thickened ileum and colon with necrotic debris on the mucosal surface
Mesenteric lymph nodes are enlarged, edematous and sometimes reddened
VIRAL
CLINICAL SIGNS
Fever(40-42℃), for about 4 days and death in 7-10 days
Anorexia, listlessness, incoordination and cyanosis
Diarrhoea and vomiting
Pregnant sows may abortion
Mortality may reach 100% in clean herds
Survivors are usually carriers for life
POSTMORTEM FINDINGS
Hemorrhages of lymph nodes, renal cortex and enlarged congested spleen
Hairless portions are edematous and cyanotic
Excess fluids in body cavities
TRANSMISSION
CLINICAL SIGNS
Reduced appetite, reduced growth rate general unthriftness
If left untreated, piglets remain permanently stunted
Helminthes may be excreted in feces
In severe infection in piglets, sometimes coughing and respiratory signs are found due to larvae’s
transfer to lungs
POSTMORTEM FINDINGS
Leukoderma on liver (milk spots) due to inflammation against larvae’s invading into liver
Spreading of infection is chiefly by contact and adult mites do not usually survive for more than a
few days away from the host. Adult sows are often the source of infestation for young pigs at
CLINICAL SIGNS
Presence of small red papules and general reddening of the skin
Affected areas are intensely itchy and wounds develop because of scratching or biting
Thickening and roughening of dry skin which is covered by grayish crusts and is thrown into
large folds later
AGALACTIA SYNDROME
(Mastitis-metritis agalactis complex-MMA, Periparurient hypogalactis)
The agalactia syndrome occurs between 12 and 48 hours after farrowing and is characterized by
anorexia, lethargy, disinterest in the piglets, fever, swelling of the mammary glands and agalactia.
The cause is believed to be multifactorial but has not been determined adequately.
CLINICAL SIGNS
Sows are usually with a normal milk flow for the first 12-18 hours after farrowing
After 24 hours the sow show signs of decreased milk production, milk ejection is absent or only
for a brief period, piglets nurse for an extended time leading to injury of teats
Sow is disinterested in her piglets, generally lies in sternal recumbency and is unresponsive to
squealing and sucking demands
The litter is noisy, may drink surface water or urine and may develop diarrhoea
Many piglets are emaciated, weak and may die from starvation
Crushed piglets are common
IRON DEFICIENCY
Iron deficiency is most common in young sucking piglets that have diets lacking in iron, particularly
those kept indoors. Iron deficiency causes anemia and unthriftiness.
It sometimes occur in cattle, however, it is less frequent than piglets.
CAUSE
The cause is basically inadequate intake of dietary iron, milk being a poor source of it. Body iron
deposits are not adequate to maintain haemopoiesis for more than 2-3 weeks, particularly in pigrets.
CLINICAL SIGNS
Highest incidence is at about 3 weeks of age
Reduced food intake, and consequently growth rate
Diarrhoea, dyspnea and lethargy
Skin is pale and sometimes yellowish in white pigs
Death is usually sudden
Edema of the head and forequarters
POSTMORTEM FINDINGS
Pallor and edema of tissues, thin and watery blood
Enlarged heart and liver
TREATMENT
Intramuscular
A dose of 100-200mg of iron in the first 7 days of life
An additional dose at 2-3 weeks of age is said to increase the growth rate
Oral
Daily dosing of iron-pyrophosphate solution at a rate of 300mg per day for 7 days
Painting of a ferrous sulphate solution on the sow’s udder. The disadvantage is that this solution
is sticky
Pigs may also be raised on iron grating or soils rich in iron
NB excessive oral dosing may cause diarrhoea in which case treat intramuscularly
Dietary supplementation
Animal Welfare & Health - 2015 107
Sows are fed diets with 200mg iron per Kg. the piglets will ingest about 20g of sows faeces that
has enough iron to prevent the anemia.
SALT POISONING
Salt (NaCl) may be toxic when excessive quantities are ingested and intake of water is limited.
Optimally, with fresh water fully available, pig feeds should contain 0.5-1% salt.
Especially, pigs have low resistance to salt poisoning.
CLINICAL SIGNS
Increased thirst, pruritus and constipation
Affected animals may become blind, deaf and unaware of their surrounds
May wander aimlessly, push against objects and circle around one point
Seizures, if water deprivation is prolonged, followed by recumbency, coma and death
POSTMORTEM FINDINGS
Blood-filled pinpoint ulcers on congested and inflamed gastric (stomach) mucosa
TREATMENT
Immediate removal of the salt source
Fresh water provide, initially in small quantities at frequent intervals to avoid exacerbation of
clinical signs
For all affected animals, the treatment should slowly return the animal to normal water and
electrolyte balance over 2-3 days.
2.14.1 SALMONELLOSIS
TRANSMISSION
Pullorum disease is transmitted mainly through the egg (transovarian), from infected or carrier
breeder chickens. Infection may also spread through direct contact or from contaminated objects
such as incubators, chick boxes, breeders’ and attendants’ hands, feet and clothing.
CLINICAL SIGNS
Young birds (1-3wks of age)
Pullorum in chicks causes typical white bacillary diarrhoea (chalky white) that paste the cloaca
High mortality within 3 weeks of age
Birds huddle near heat source, do not eat and appear sleepy
Ruffled feathers and drooping wings
Adult
Adult carriers are mostly asymptomatic
Poor feather development, inappetence, depression and retarded growth
Occasionally reduced egg-laying rate
POSTMORTEM FINDINGS
Unabsorbed yolk sac with blood-tinged or cintants
The heart, liver, spleen and lungs etc. may have nodules
Firm cheesy material in the caeca
In adults ovules are misshapen, angular and attached to body of the ovary by stalks
Egg material may be attached to the wall of the peritoneal cavity
TRANSMISSION
Transmission is mainly through infected droppings, bird carcasses and infected clothing, shoes,
utensils and other fomites. Infection occurs through the eggs (transovarian transmission).
CLINICAL SIGNS
Sudden death without any sign of illness
Listlessness, loss of appetite and increased thirst
Ruffled feathers, drooping wings, tail and head
Yellow-green watery droppings with a foul smell
Mortality may be as high as 50%
PSTMORTEM FINDINGS
Yellow-green droppings on the vent
Swollen and friable liver, enlarged kidney and spleen
Liver turns greenish bronze on exposure to air and lungs are yellow-brown
Whole carcass may be congested or jaundiced
Intestinal contents may be blood-tinged and gelatinous
TREATMENT
Treatment and control are basically as for pullorum disease.
Sulphonamides, tetracyclines, furazolidone
Carriers remain after treatment
CONTROL
Test-and eradicate is the best method of control
Vaccination is possible but is not desired if an eradication programme is in place
Thorough disinfection of pens
2.14.2 COLIBACILLOSIS
(Colisepticaemia)
It is a common systemic disease of economic importance in poultry. It is caused by Escherichia coli.
CLINICAL SINGNS
Sudden death without any sign of illness
Respiratory disease with gurgling noises (rales)
Listlessness, reduced appetite, poor feed conversion
Uneven and retarded growth
POSTMORTEM FINDINGS
Cheesy material in airsac is thick and cloudy
Airsac is thick and cloudy
Fibrinopurulent airsacculitis, pericarditis and perihepatitis
2.14.3 MYCOPLASMA
(Chronic respiratory disease- CRD, Infectious sinusitis)
It plays a significant role in the respiratory disease complex resulting in poor performance and
reduced egg production, suboptimal hatchability and livability of chicks and poults. It also results in
downgrading of carcasses of broilers and turkeys. It’s caused by Mycoplasma gallisepticum.
TRANSMISSION
The spread is through both the egg and directly from chicken to chicken.
CLINICAL SIGNS
Varying degrees of respiratory distreaa
Rales, difficulty in breathing, coughing and sneezing
Mortality and morbidity are low in cases where there is no secondary infection
POSTMORTEM FINDINGS
Air sacs are thickened and opaque
Gelatinous accumulations in air sacs
2.14.4 OMPHALITIS
(Navel ill, “Mushy chick” disease, Yolk sac infection)
A condition characterized by infected, unhealed navel in chicks, poults and other young fowls. It is
caused by a large variety of bacteria.
PREDISPOSING FACTORS
Conditions that lead to disease outbreak include the following:
Shell contamination on the breeder farm
Failure to control humidity in the hatcher
Other factors which lead to delayed hatches
CLINICAL SIGNS
High number of chicks dead in the boxes
Chicks are often wet and “mushy” with foul smell
The yolk sac is unabsorbed and fluid may be seen oozing resulting in discoloured and matted
underside of many chicks
POSTMORTEM FINDINGS
Yolk has an abnormal appearance, sometimes thick and curdled or sometimes watery and
reddish brown
Yolk sac may rupture causing peritonitis that makes examination of other abdominal organs
difficult
TRANSMISSION
Transmission is by direct contact, airborne droplets and contaminated drinking water. The
chronically ill and carrier birds act as reservoir of the infection.
CLINICAL SIGNS
Depression, reduced appetite, nasal discharge and rales
Swelling of face and wattles
Egg production is delayed in pullets and severely reduced in producing flock
VIRAL DISEASES
TRANSMISSION
CLINICAL SIGNS
High mortality and depression
Respiratory signs which include gasping, wheezing and gurgling
Nervous signs which include twisted neck (torticollis), drooping wings, dragging legs and
circling
Watery-greenish diarrhea
Egg production drops by 30 to 50%
POSTMORTEM FINDINGS
Very variable
Inflamed trachea and/or froth in air sacs
Haemorrhages in the proventriculus and intestines
2.14.7GUMBORO DISEASE
(Infectious Bursal Disease-IBD, Infectious Bursitis)
It is an acute, highly contagious viral disease of young chickens. The gumboro disease virus causes
disease by destroying antibody-forming cells (lymphocytes) located in the brusa of Fabricius (cloacal
bursa), spleen and thymus resulting in immunodeficiency. This virus is highly resistant to
disinfectants and once it infects a poultry house or farm, it is extremely difficult to eradicate.
Gumboro disease is caused a birna virus (infectious bursal disease virus; IBDV).
TRANSMISSION
Infection is easily spread from bird to bird by way of droppings. Other means of transmission include
infected clothing, utensils and other objects.
CLINICAL SIGNS
Usually birds between 3 and 6 weeks of age are most affected
Incoordination, watery diarrhoea, soiled vents
Depression, hunddling and paleness
POSTMORTEM FINDINGS
Enlarged bursa which may have cheesy material or haemorrhages
After day 3 of the disease, the bursa may become smaller than usual (atrophied)
Haemorrhages in the caecal tonsils, pectoral, thigh and muscles
TREATMENT
No treatment
Control secondary bacterial infection with antibiotics
Vaccination is the most successful method of control
Good management practices
Disinfection of pens after every batch(all-in-all-out programmes are benefic
TRANSMISSION
It is transmitted by infected air droplets and also ingestion of contaminated feed and water.
Transmission is also possible by cintact with infected chickens and contaminated objects.
CLINICAL SIGNS
Infectious bronchitis most severe in young chickens
Coughing, sneezing and tracheal rales
Severe respiratory distress
In chickens, mortality may be high (up to 60%) if the urogenital system is affected
In adult chickens, respiratory sighs include wet rales, gurgling and wheezing
Egg production will drop dramatically (5-50%), and eggs are often deformed, thin/wrinkle
shelled and have watery albumen
POSTMORTEM FINDINGS
Cheesy exudate in the trachea and bronchi
Air sac are thickened and cloudy
Airsacculitis, perihepatitis and pericarditis
Kidneys may be swollen and pale, with distended tubules and ureters
TRANSMISSION
Transmission to penmates is through contact with affected skin. Mosquitoes and other biting flies
may accelerate the spread.
CLINICAL SIGNS
Only a few birds develop lesions at a time
Thick scabs on unfeathered skin (chicken) and upper neck (turkey)
Sometimes scabs appear on feet and legs only
Lesions on the membranes of the mouth, esophagus, pharynx, larynx and trachea
Mortality is 1-2% if only the skin is affected may be high in the other form 40%
DIAGNOSIS
Characteristic lesions
Submit lesion for lab examination
TRANSMISSION
It is highly contagious and easily spread among chickens. The main source of infection is dander
from feather follicles which remain infective in the premises. Young chickens pick the infection by
oral and respiratory routs.
CLINICAL SIGNS
Weight loss, depression, some form of paralysis (one leg in front the other behind and sometimes
wing drooping)
Mortality is variable 5-10%
The condition is very rare in immunized birds
POSTMORTEM FINDINGS
Enlarged nerves particularly the sciatic and/or wing nerves
Tumors in various organs such as liver, spleen, heart, lung, kidney and proventriculus
PARASITIC
2.14.11 COCCIDIOSIS
Coccidiosis is a parasitic disease caused by protozoa of the Eimerridae family. In poultry, the species
belong to the genus Eimeria and occur in the intestines.
In chickens the seven most important species are Eimeria acervulina, E. necatrix, E. tenella, E.
maxima, E. brunette, E.mitis and E.praecox. In geese E. truncate affects the kidneys and not the
intestines.
TRANSMISSION
Transmission is by ingestion of droppings, water or feed containing coccidian oocysts.
POSTMORTEM FINDINGS
Haemorrhagic lesions in different portions of the intestines
Inside the intestines may be a blood clot, cheese-like materials or thick mucus
Cloaca and intestinal walls are thickened
TREATMENT
Amprolium
Sulfamethazine, sulfadimethoxine
Chlortetracycline, Oxytetracycline
CONTROL
Aim of control
To prevent the build-up of coccidian to a stage where clinical disease occurs, but retain low level
infection to continuously induce immunity
Methods of control
Use of coccidiostats in feed or water
Frequent raking of litter in order to keep it dry and disturb the development of oocyst into
infective stages especially in moist places such as around drinkers and feeders
Maintaining chickens on wire floor at all times, if possible is the best option
Use anti-coccidial drugs once in a while even without disease outbreak
2.14.12 HELMINTHS
(Worms)
In poultry nematodes are the most significant helminthes in terms of number of species and
economic impact, however, cestodes are also found. The most common genera are Ascaridia,
Heterkis and Capillaria.
TRANSMISSION
The helminth problem is most significant in range birds than in donfined ones, however, severe
CLINICAL SIGNS
Inactivity, reduced appetite and retarded growth
In large numbers, intestinal blockage may occuer
Some worms may migrate via cloaca to the oviduct and become en-shelled
POSTMORTEM FINDINGS
Worms in the intestines
Harmorrhages may be present in intestines
NON-INFECTIOUS
CAUSE
Increase in intravascular hydrostatic pressure due to right ventricular failure is the main cause of
ascites in broiler chickens. Due to increased pressure, the fluids perfuse out of the blood vessels and
accumulate in the abdominal cavity resulting in ascites.
Modern broiler chickens have been selected for rapid growth rate, high feed utilization efficiency and
a large pectoral muscle mass. These factors have a high oxygen demand and can easily lead to heart
failure and respiratory acidosis.
CLINICAL SIGNS
POSTMORTEM FINDINGS
Variable amounts of clear yellow fluid clots of fibrin in the abdomen
The liver may be swollen and congested or firm and irregular or shrunken
Lungs are extremely congested and edematous
CONTROL
Reduced growth or reduce feed intake in order to reduce the bird’s oxygen requirements
Environmental temperature, humidity and air movement should be controlled to prevent
excessive body heat loss; avoid chilling
If, upon any such inspection as aforesaid, the inspector is of opinion that any livestock on the
premises on which milk is produced or cooled or cream is separated is so diseased as to be likely to
affect injuriously dairy produce, he shall, if he is not a Veterinary Officer, report the disease to a
Veterinary Officer, and shall, in the meantime, place a temporary brand on all the suspected or
affected animals, and may prohibit the sale or use of milk from any such animal until a Veterinary
Officer has declared the animal free from disease likely to affect dairy produce.
(4) If, in the opinion of a Veterinary Officer, there are grounds for believing that any livestock on
the premises is suffering from tuberculosis, he shall, at the earliest moment, subject the animal or
animals to a test. Such test shall be one of the variations of the tuberculin test, and the manner in
which it shall be carried out shall be laid down by the Director of Veterinary Services from time to
time. Should any animal react to the test, any Veterinary Officer shall order its immediate destruction
and shall also give instructions as to the manner in which the carcass shall be disposed of.
(As amended by G.N. Nos. 158 and 364 of 1964) Tuberculosis
4. If, upon any inspection as aforesaid, the inspector is of opinion that any person is affected with a
disease of an infectious or contagious nature which is likely to contaminate dairy produce, he shall
report the fact to a Medical Officer, and, if the Medical Officer certifies that such person is affected
with such a disease, the inspector may, by written order, order the isolation or the removal of such
person for such time as the Medical Officer thinks necessary. Human disease
5. Forthwith, upon the request of an inspector, every owner of dairy produce premises shall allow
the inspector to make a list of the persons supplying dairy produce to such owner. Every such owner
or his agent shall give to the inspector any personal assistance and information which he is capable
of giving to aid the inspector in discovering the cause of any defect or deterioration in dairy
produce. List of suppliers
8 of 1961
An Act to provide for the prevention and control of stock diseases; to Act No.
regulate the importation and movement of stock and specified articles; to 13 of 1994
provide for the quarantine of stock in certain circumstances; and to Government
provide for matters incidental to the foregoing. Notices
[27th December, 1963] 319 of 1964
497 of 1964
1. This Act may be cited as the Stock Diseases Act. Short title
"carcass" means the carcass of any stock and includes part of a carcass, and the
meat, bones, hide, skin, feathers, hooves, horns, offal or other part of any stock;
"Director" means the Director of Veterinary Services and includes the Deputy
Director of Veterinary Services;
"disease" means foot and mouth disease, rabies, rinder-pest, lumpy skin
disease, contagious epididymitis and vaginitis, sheep pox, swine fever,
Newcastle disease, epidemic tremor, contagious bovine pleuro-pneumonia,
anthrax, contagious abortion, quarter evil, tuberculosis, bovine vibriosis, swine
erysipelas, glanders, streptothricosis, anaplasmosis, redwater, heartwater, East
Coast fever, trypanosomiasis, epizootic lymphangitis, ulcerative lymphangitis,
sarcoptic mange, psoroptic mange (scab) and any other disease of stock which
the *Minister may, by statutory notice, specify;
"owner", in relation to any stock, includes the person for the time being having
the management, custody or control of such stock;
"railway company" means Zambia Railways and any other railway operating in
Zambia;
"stock" includes cattle, horses, sheep, goats, mules, donkeys, pigs, animals of
the antelope species in captivity, domestic fowls, turkeys, geese, ducks and any
other domesticated or captive animal or bird which the Minister may, by
statutory notice, declare;
2.3 Epidemiology...................................................................................................................................................33
2.4 IMMUNOLOGY.............................................................................................................................................37
2.5.2 STERILIZATION/DISINFECTION.........................................................................................................42
2.8.4 Pour-on......................................................................................................................................................51
2.8.5 Spot-on......................................................................................................................................................51
2.8.6 Hand-dressing...........................................................................................................................................51
2.10.2 GENERAL BIO-SECURITY MEASURES WHEN IN DIRECT CONTACT WITH FARM ANIMALS
........................................................................................................................................................................... 56
2.10.4 MEASURES WHICH MUST BE OBSERVED FOR VISITS TO PREMISES UNDER SPECIFIC
RESTRICTIONS...............................................................................................................................................58
2.11.1 ANTHRAX.............................................................................................................................................60
2.11.4 BLOAT................................................................................................................................................... 62
2.11.5 BRUCELLOSIS......................................................................................................................................64
2.11.8 TUBERCULOSIS...................................................................................................................................66
2.11.9 THEILERIOSIS......................................................................................................................................67
2.11.11 BABESIOSIS........................................................................................................................................69
2.11.12 ANAPLASMOSIS................................................................................................................................70
2.11.13 COWDRIOSIS......................................................................................................................................71
2.11.14 TRYPANOSOMIASIS..........................................................................................................................71
2.11.15 DERMATOPHILOSIS..........................................................................................................................73
2.11.17 DERMATOPHYTOSIS........................................................................................................................74
2.11.18 MANGE................................................................................................................................................75
2.11.19 PINK-EYE............................................................................................................................................75
2.11.24 MASTITIS............................................................................................................................................80
2.11.27 POISONING.........................................................................................................................................84
2.13.3 SALMONELLOSIS...............................................................................................................................84
2.14.1 SALMONELLOSIS...............................................................................................................................84
2.14.2 COLIBACILLOSIS................................................................................................................................84
2.14.3 MYCOPLASMA....................................................................................................................................84
2.14.4 OMPHALITIS........................................................................................................................................84
2.14.11 COCCIDIOSIS.....................................................................................................................................84
2.14.12 HELMINTHS.......................................................................................................................................84