Animal Health and Disease
LO:

Understand and be able to demonstrate how disease often reflects the balance between host
immunity and pathogen dose and virulence with the environmental conditions impacting both
host immunity and pathogen dose and virulence.
Current issues in AUS sheep industry
 Flock/sheep no. declining
 Good lamb and wool prices
 Pasture availability; drought now in most parts
 Peri-natal mortalities
 Internal parasites; worms & anthelmintic resistance
 External parasites; lice & acaricide resistance/residues
 OJD, Footrot
 Clostridial/anthrax diseases
 Droughts/floods; grain poisoning, pregnancy toxaemia
 Welfare issues; mulesing, live sheep trade problems
 Exotic diseases preparedness e.g. bluetongue, fmd, tse
Diseases may be caused by:
1. Infectious agents; bacteria, virus, fungi, prions
2. Parasitic agents; external, internal
3. Nutritional causes; deficiencies, excesses or imbalances, starvation et
4. Metabolic disorders; physiological
5. Physical agents; trauma, injury, hypothermia etc’
Impact of diseases
1. Reduced growth
2. Reduced reproductive rates
3. Reduced milk production
4. Reduced fleece quantity and quality
5. Damaging hides and fleeces
6. Causing carcass/meat condemnation
7. Zoonotic impact
Step for disease investigation
 Owner’s complaint
 History of the incident
 Knowledge of the farm, client and environment
 Animals affected, number, age and sex
 Inspection of affected animals
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Clinical exam
Post mortem exam
Specimen collection
Lab examination
Diagnosis-prognosis-treatment-control-prevention
Peri-natal mortality
 Peri-natal mortality is the loss of lambs pre and post lambing
o Prevalence of peri-natal mortality can be very high, of the order of 25-80%
o Well managed flocks can have less than 5% perinatal mortality
o In general, 71% of cases are related to pre-natal events, 13% w post-natal events and
16% are undiagnosed
 Peri-natal mortality in lambs is mostly flock issue
o Most an be corrected by identifying them and adjusting at the flock management level
To improve peri-natal mortality
Main focus should be on:
 Pre breeding health of ewes and rams
 Improving conception rate
 Nutrition and management of pregnant ewes
 Lambing management
 Management of ewes w suckling lambs
 Management of health of lambs
 Good management should aim at keeping lambing% = weaning %
Parasites
Drench resistance
 Mainly due to excessive frequency of treatment and under-dosing
o Haemonhus and ostertagia are 2 most common spcs. w resistance problems
 Faecal Egg Count Reduction Test (FECRT) can help determine drench resistance
Control program objectives
 Maintain optimal productivity (not 100%)
 Encourage host immunity
 Minimize treatments; cost & seasonal variation
 Avoid or slow the development of resistance
 Epidemiology of parasite to time treatments and prepare pastures of low infectivity for most
susceptible stock
 Winter v uniform v summer rainfall
Considerations in worm control programs
 When contamination of pastures occur; differs between regions for different parasites
 Creating safe v clean pastures
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Lambing paddocks highly contaminated from 12 weeks post-lambing onwards
Susceptibility of young sheep; treating lambs at weaning usually necessary
Wean and move by 12-13 weeks from start of lambing
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Flock management; compact lambing, wean early, flock structure
Right drench at right time & strategic treatments- e.g. pre lambing, pre weaing
Grazing management; young sheep and ewes to clean pastures, after drench move to clean
pastures, sheep <-> cattle grazing
Nutrition & immunity – supplementary feeding
Monitoring for worms & resistance; FEC monitoring + FECRT, quarantine drenching
Breed resistant sheep- long term goals
IPM
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Control programs
 Winter rainfall zones; DRENCHPLAN
o 2 summer broad spectrum treatments
 Strategic, usually no immediate benefit
o Further broad spectrum strategic treatments
 Lambs at weaning usually the only one
o Tactical treatments if required
 Young sheep in winter
 Ewes at marking time
 Others- depending on seasonal changes
 Summer rainfall zones; WORMKILL
o Concentrate treatments in oct-feb period
o Closantel treatments in Oct, Dec, Feb prevent the important spring-summer deposition
o Broad spectrum treatments in dec-feb for young sheep
o Subsequent tactical treatments as required
 Rangelands WESTWORM- single summer treatment
Control management- preparation:
 Ungrazed entirely for a season- cropping
 Grazed by catte- 6m interchange
 Grazed by treated sheep
 Grazed by dry adult sheep- less likely to be infected
Winter rainfall- feb-july (6m)
Summer rainfall- sept to dec & nov to feb (4m)
Tactical treatments
 Maybe necessary in higher rainfall areas
 Often young sheep and ewes require 1 or more tactical treatments during the year
 FEC’s to determine need for treatment e.g. drought break
Why sick animals don’t grow
1. Understand the mechanisms that generate general symptoms of ill-thrift in sick animals.
o HPEI: agent of disease, environment, host defense/response  disease
2. To apply HPEI to decipher pathogen induced growth inhibition.
o Pathogen induced G inhibition on the host
3. Describe the physiology behind the lack of performance in sick animals.
o Microbial invasion inflammation/local tissue damage (local response to address
immediate incursion); and systemic to protect whole body
o Mediated by 3 macrophages derived cytokines
 Interleukin-1
 Interleukin-6
 Tumor necrosis factor (TNF)
 Cytokines: soluble mediators of the immune system
o Low molecular weight proteins
o Regulate all important biological processes e.g. cell growth, cell activation,
inflammation, immunity, tissue repair
o Secreted by range of cells e.g. T cells, B cells, macrophages, neutrophils etc
o E.g. interleukins (1-19)
 Transforming growth factors
 TNF
 interferons
4. Provide several management mechanisms for minimizing the incidence and or severity of
illness in animals.
 Cytokines: soluble mediators of the immune system
o Low molecular weight proteins
o Regulate all important biological processes e.g. cell growth, cell activation,
inflammation, immunity, tissue repair
o Secreted by range of cells e.g. T cells, B cells, macrophages, neutrophils etc
o E.g. interleukins (1-19)
 Transforming growth factors
 TNF
 Interferons
 Features of cytokines
o Immune cells usually make more than one cytokine when activated
o Effects wide variety of cells and tissues
o Each cytokine can have several different functions, depending on which cell it binds to
o Different cytokines may act on a single target ell
o Many cytokines work best in association w other cytokines e.g. synergy
o Cells can only respond to cytokines if they express the appropriate receptor
o Effective at low conc.
o
o
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Tend to act (paracrine) or control the activity of cells that produced them (autocrine)
but they can also act systemically (endocrine)
Short half life
Cytokines can be inhibited by receptor antagonists
Systemic response to inflammation; proinflammatory cytokines: IL-1, IL-6, TNF

Fever: act on brain
o Increases body temp (to kill pathogen, and help immune system work better)
o Induce sleep and suppress appetite
o Metabolic changes:
 Increase protein catabolism and mobilizing pool of amino acids
 Leads to muscle wasting, but amino acids are available for protein synthesis
o Acute phase proteins are induced:
 Induce liver cells to increase protein synthesis and secretion; in very earlyu
period of injury
 Function is host defensive e.g. C-reactive protein (CRP)
 CRP binds to invading organism and damaged tissue promoting their
phagocytosis
 Inhibits neutrophil release of damaging radical, reducing tissue damage
and enhancing tissue repair
Why sick animals don’t grow:
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Microbial invasion macrophage stimulation cytokine production IL-1, IL-6, TNF loss of a
appetite, depression, neutrophilia, fever ; acute phase protein response
Growth gap in pigs in clean vs dirty environments
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12% difference in growth
Dirty: high levels of proinflammatory cytokines, acute phase APP
o Treated IL-1 ra (receptor antagonists); improved growth, reduced C-reactive proteins
o Blocked aspects of host-pathogen interaction axis which allowed them to perform
better
Reduce pathogen load by:
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Keeping clean environment
Good nutrition
Avoid stress; avoid overpopulation
Quarantine, biosecurity procedures
Vaccinations of the young
Vaccinations of mothers in specific timing
A healthy start in life
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Explain the challenges of providing protective immunity in the young
o Lagtime getting antibodies produced; much lower compared to after 2nd Ag exposure
 Bc of primary response gets limited response
Justify recommendations for optimising the protection of the young from pathogens.
Describe the acquisition of maternal immunity in various species e.g. bovine and avian.
 Vaccinate mother late in gestation to provide antibodies to the young
 In utero:
o Transfer of antibody (maternal imunity) depends on structure of plaventa e.g.
 Humans and primates: maternal blood direct contact w trophoblast; so
maternal IgG transferred to feturs ; newborn has circulating igG leflect that of
mother
o Dogs and cats; chorionic epithelium in contact w endothelium of maternal capillaries; on
5-10% IgG transferred mother to fetus
o Ruminants; no transplacental transfer of IgG
Ruminants:
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Colostrum; suckling – IgG, followed by IgA&IgM
High % of Ig absorption when suckled in first 6 hrs after birth  % declines after
Failure of passive transfer of matrnal immunity in colostrum
1. Production failure (premature births, premature lactation)
2. Ingestion failure; e.g. multiple births- not enough colostrum, poor mothering, poor suckling
drive, damaged teats, jaw defects
3. Absorption failure; fail to absorb sufficient Ig at risk of infection
Transfer of maternal immunity- Hen
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IgG from blood; IgM and IgA from oviduct in hen
IgA ad IgM in albumin ingested by chick protects intestine
IgG in yolk absorbed into blood
Immunity in the young
Optimise immunity and protection in the young by:
1. Nutrition for mother and young
2. Colostrum; Ensure good mother and young drinking early on and vaccinate mother within
month of parturition for good colostrum
3. Vaccination of young when maternal antibody declining
4. Biosecurity, clean environment
Sheep Health
LO: Understand and be able to demonstrate how disease often reflects the balance between host
immunity and pathogen dose and virulence with the environmental conditions impacting both host
immunity and pathogen dose and virulence
Pathogen- bacterial disease
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Mycobacterium avium subsp. Paratuberculosis
o Obligate parasite (needs host for reproduction) and pathogen of animals; infecting
intestine
o Distinct S(sheep) and C(cattle) strains w different host infection patterns
Clinical signs; chronic wasting- eat but don’t put on weight
OJD transmission
 Usual route of infection is faecal-oral; through contaminated pastures
 In-utero infection; issue only if ewes clinically affected
Post mortem diagnosis: gross pathology
 Thickened ileum
 Lymphangitis
 Enlarged mesenteric lymph nodes
Lab diagnosis of OJD
 Collect faeces – smear and ZN stain, culture, PCR
o Pooled faecal culture
 Collect blood
o Plain tube for serum
 ELISA test for antibodies
 Total protein, albumin, calcium (all low)
 Delayed type hypersensitivity test
 Biopsy/necropsy
OJD control
1. Cull cases
2. Pasture management:
o Reduce stocking rate
o Increase pasture spelling
o Rotational cropping
o Graze adult cattle
OJD vaccine- Gudair (CSL)
 Registered for sheep nd goats
 Single dose of killed M. ptb in oil adjuvant
 Inject sub-cutaneously behind ear
 In lambs at 4-12 weeks of age
 Efficacy 95%
o Reduces mortalities of OJD
o Delays shedding of M. ptb
o But doe not prevent infection or shedding
 Causes injection site and regional lymph node lesions
 Severe reactions likely after self-administration in humans
Control of OJD
 Prevention of entry
o Fences and other biosecurity measures
o Maintain a close flock
o Purchase “clean stock” w sheep health statement
 Reduction of impact (reduce prevalence)
o Management (sheep, beef and dairy cattle differ)
o Vaccination
 Eradication
Public health
 Farmers
o Johne’s disease has animal welfare impacts
o Disease control programs can have sig psychological impacts, direct and indirect
o Vaccine self-administration
 The community
o M. ptb has been associated w Crohn’s disease?
o Milk pasteruisation temps for M. ptb needs to be higher than those required to kill M.
bovis
o Milk, meat, environmental and drinking water contamination w M ptb may become a
major issue
Anthrax
 Sudden death (acute disease)- mainly young and healthy animals
Control/prevention
 Vaccination may be required in endemic areas
 Anthrax spores survive for a long time; leading to endemic contaminations
 Don’t conduct post mortem if you suspect anthrax
 Safe disposal of dead animals/ lime treatment of the site
Wildlife Disease
West Nile Virus
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Some birds poor reservoir (don’t carry a lot of the virus in their blood)
Good reservoirs are temperate species common in disturbed hckabitats of low diversity
Higher densities of good reservoirs > higher probability of a mosquito getting infected
W climate change mosquitos will migrate away from topics to less diverse temperate regions w
are favoured by good reservoirs
Squirrels and Lyme disease
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Transmitted via tick that feeds on many species
White footed mice are most competent reservoirs and transmit it to 90% of ticks that bite them
Squirrels and others carry it but don’t transmit it
Habitat fragmentations favours mice because of loss of predators and competitors
More infected ticks means more infected people
Yellow-necked mice and tick borne encephalitis
 Virus transmitted tick to tick via simultaneous feeding on mice
 Very few mice ticks die off
 Many mice few ticks per mouse so probability of transmission decreases
 In between  optimal transmission
 No deer  no ticks
 Many deer  many ticks feed on deer instead of mice so ticks survive but don’t transmit
microbe to each other
Disease has a role in ecosystem health
Many potential pathogens:
 Are beneficial to host immune system maturation and digestive/metabolic function
 Allow predators and scavengers to access prey
 Maintain selective pressure for host viability and general resistance to disease
 Maintain pop numbers at sustainable level
o High host densities result in increased transmission and reduced resources, expression
of disease and reduction in host density
o Can either increase or decrease boom-bust oscillations
Vaccines and vaccinations
1.
What is immunization and how does it generate an immune response
Immunisation: the administration of an antigen to confer immunity
Vaccines/vaccination: the generation of an acquired immune response
2.
Forms of immunisatione.g. passive and active, including examples.
Passive immunity: administration of preformed antibody from an immunized;
o
Provides immediate but temporary resistance; e.g. colostrum, yolk sac
Active immunity: protection due to development of an immune response following stimulation w
antigen in vaccine or during infection
3.
Features of an ideal vaccine
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Prolonged strong immunity; i.e. antigenicity
Immunity conferred to immunized animal and newborn
No adverse side-effects
Cheap, stable, suitable for mass administration
Additional features:
o Stimulation of antigen presenting cells (APC)
o Stimulation of T and B cells & their memory cells
o Antigen persists – provide longer period of protection
 High antigenicity and no side-effects often incompatable
o E.g. Live vaccine; high antigenicity but also high risk
o Popular viruses; act as enfogenous antigen and will trigger cytotoxic T cells
o Hazard: vaccine viruses may themselves cause the disease
o Attenuation of live vaccines reduces the hazards
4.
Characteristics of liveand inactivated vaccines–including techniques for attenuating live
vaccines.
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Live vaccine: e.g. scabby mouth
o Vaccinate lambs; rub dried, infected scab material onto scratches on inner thigh
develops solid immunity and complete recovery
o Vaccinated animals may spread disease so must be separated from unvaccinated stock
for a few weeks
o Attenuation: reduces the virulence of the living pathogen so they cant cause disease
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Often involves adaption of organism to new environment, becoming avirulent in
usual host
1. Loose adaption for usual host or conditions e.g. anthrax grown environment (w
enzyme) where looses ability to form capsule
2. Genetic manipulation of requirements for growth e.g. streptomycin dependency in
Salmonella species
3. Repeated culture in “foreign host cell” e.g. canine distemper virus: lymphoid vs
kidney cells
4. Growth in different host e.g. mammalian viruses grown in eggs
Killed vaccine
o Fewer risks but lower antigenicity (includes adjuvant)
o Safer; tend to act as exogenous antigens- not suitable for protection against intracellular
pathogens
o Main side effect is tissue damage at site of injection
 Influenced by the adjuvant used
- Antigen must remain antigenically similar to living organism; avoid protein denaturation or
lipid oxidation
- Use chemicals e.g. formaldehyde which form cross-links between proteins and nucleic acids;
provides structural rigidity
- Bacterins; vaccines that kill bacteria
1) Contain inactivated toxins- toxoids
Advantages of live vaccines
 Few inoculating doses
 No adjuvant required
 Induction of IFN
 Relatively cheap
5.
Advantages of inactivated vaccines
 Stable on storage
 Unlikely to cause disease through
residual virulence
 Unlikely to contaminating organisms
Adjuvants, including examples, and how they work.

Adjuvant: substance that accelerates, prolongs, or enhances antigen-specific immune responses
when used w vaccine antigen
 Increases the affectivity of vaccines containing inactivated organisms via:
o Acting as slow release antigen depot
o Promote antigenicity by trapping antigens at sites where they are accessible to
lymphocytes
o Stimulate antigen-processing
o Stimulate macrophages
o Generally an adjuvant is administered w the antigen
 Types of adjuvants
1) Aluminium salts: aluminium phosphate and aluminium hydroxide- on injection form a depot so
slows rate of antigen elimination
2) Water in oil emulsion; also depot forming adjuvant
o Mineral oil stimulates local chronic inflammatory response granuloma at site of
injection (too much)
3) Bacterial productions
o E.g. killed Mycobacterium
4) Surface active agents: e.g. saponin derived from bark of tree- must isolate non-toxic component
o Saponin used directly or incorporated in other complexes
o Stimulate antigen processing and presentation
o Irritant and proinflammatory
5) Cytokines: regulatory role fine-tuning immune responses
 Adjuvants: widely used in farm animals; insoluble salts, stable in storage, produce small granuloma
on injection
6.
Examples of new generation antigens/vaccines
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7.
Recombinant antigen protein
o Isolate DNA encoding for antigen of interest
o Insert DNA into bacterium so recombinant antigen is expressed
o Harvest recombinant antigen and incorporate into vaccine
Live recombinant organisms:
o Vaccines contain recombinant organisms expressing genes for immunizing antigen
o E.g. Vaccinia; rabies
Genetically attenuated organisms
o Genetic engineering enables modification of genes of an organism so they become
irreversibly attenuated e.g. herpesvirus in pigs
Naked DNA
o Injection of piece of DNA coding for antigen of interest
Synthetic peptides:
o When structure of a protective epitope is known, may be chemically synthesized and
used alone in vaccines
Delivery options for vaccines –pros and cons
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Nanopatch; patch w thousands of microscopic points
Advantages
Disadvantages
 Efficient
 Not effectively kept cold in third
world countries
 Pain-free
 Cheaper; does not require
refrigeration
 Self administration
1)
2)
3)
4)
5)
6)
8.
Injection
Spray
Drinking water
Eyedrop
In-ovo (IM)
Dermal
Rules for vaccination programmes/reasons for vaccine failure
1. Newborns are passible protected by maternal antibodies- difficult to successfully immunize
animals early in life
2. Once born, active immunization is only successful after passive immunity has waned
3. Prevalence of the disease
4. Class and age of stock
5. Need for booster?
6. Seasonal occurance
Vaccine failure
1. Vaccine is ineffective;
- contains wrong organism
- method of vaccine production destroyed
- insufficient antigen in vaccine
2. No protective response due to incorrect administration
- Live vaccine may have died
- Mass administration; not all animals drank water
- Incorrect route of administration
- Animal passively protected
3. Correct administration and animal responds, but not protected
- Animal already has disease
- Wrong strain or organism used
- Wrong antigens included in the vaccine
- Animal non-responder
4. Natural immune response may be suppressed: i.e. immunocompromised
- Heavily parasitized animal
- Malnourished animal
- Stressed animals
- Maternal immunity present
Wildlife disease
What is wildlife disease surveillance
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Necropsies
o Ad hoc basis
o Culling operations
Veterinary supervision
o Of protected systems
o Zoos
o Research
Sentinel animals
Trapping of vectors
o Rodent serology & necropsy
o Arthropods for PCR/culture
Active investigation of reported disease
Dedicated trapping and sero-surveys
Types of surveillance
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Passive: monitoring of ind or mass mortality/morbidity
Active: (structured) investigation of mortality/morbidity events
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Dynamics of disease
Reservoir
Surveillance
Wildlife Disease 3
Sheep Health Lecture 3
External parasites of sheep
AUS:
 Flystrike- blow fly; Lucilia cuprina
 Lice infestation- sheep lice; Bovicola ovis
5 main types of flystrike
1. Body strike
2. Breech or crutch strike
3. Poll strike
4. Foot strike
5. Pizzle strike
Flystrike prevention
 Select for
o Lower breech wrinkle
o Lower breech cover
o Lower dags
o Cull for high urine stain
Sheep lice- Bovicola ovis
 Economic loss due to
o Wool quality and quantity
o Treatment costs chemicals & labour
o Environmental impact; use of pesticides
 Animal welfare
Environmental factors for lice build-up
 Season; temperature and humidity
o Sheep lice prefer 37 degrees and 70-90% humidity
 Rainfall; humidity/moisture
 Wool length; shearing helps
Diagnosis
 Clinical inspection; wool partings
 Lab test- lice detection kit
Lice infested sheep
 Lice feed on dead skin, skin secretions and bacteria normally found at surface of skin
 Lice do not suck blood or eat wool fibres but cause thickening of skin
 Presence irritates sheep sheep bites, scratch & rub on trees and fences
Prevention
 Biosecurity
o Fencing- sheep proof- stray sheep
o Quarantine introduced sheep
o Good neighbor
o Buffer zones; creeks, bush, railway lines, roads
o Non sheep vectors; sheep handlers, trucks, shearers etc
General lice and fly strike control principles
 Treating with an effective chemical/pesticide soon after shearing
 Minimising or avoid use of pesticides in the 6 months before shearing
 Using the most effective and safest method of pesticide application; avoid development of
resistance
 Prevention and quarantine
 Good management practices
Good management and husbandry practices
 Mulesing wrinkly sheep?
 Timing of shearing and dipping
 Timing of crutching
 Tail docking
 Quarantine of introduced sheep
 Complete mustering
 Regularly inspecting the flock
 Recording all pesticide treatments
Pizzle rot
 Caused by interaction of Cornyebacterium renale and urea from high protein diet
 Common in Wethers, seen in Rams also
 High protein diets – Increased urea- alkaline urine
o Break down to ammonia
o Cause irritation and ulceration
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o Infection C. renale and other bacteria
o Can cause severe damage and blockage
Prevention/treatment
o Prevent/reduce high protein diets
o Cleaning the area to prevent fly strike
o Treatment w antiseptic and antibiotics
Reproductive diseases
 Brucellosis in Rams
o Brucella ovis- epididymitis in rams
 Abortions in ewes
o Viral (Akabane disease)
o Brucellosis, Campylobacter, Chlamydia, Coxiella (Q-fever), Toxoplasma
Ovine brucellosis causes
 Mainly infertility and sterility in rams
o Occasionally
 Abortion in ewes
 Arthritis in lambs
 Prevention
o Cull any infected rams
o Check/test before you buy rams
Rye grass toxicity- staggers/tetany
 Annual rye grass toxicity
o Caused by toxin produced by bacteria in ryegrass carried by nematode
 Perennial rye toxicity
o Caused by fungus in rye grass
Clinical symptoms of staggers/tetany
 Neurological symptoms
o Changes in behavior
o Tremors, twitching of muscles
o Swaying and staggering movements
o Jerky movements of legs
o Collapse w extended head, arched back, rigid legs
Management
 Grazing management
 Pasture management
 Rotational grazing
 Extra feed supply during lean pasture seasons
Poultry Health and Diseases
LO:
1.
To understand the role of biosecurity in maintaining healthy and productive poultry flocks.
2.
To appreciate the key components of an overall management programme to reduce the
incidence of disease of farm.
3.
To be aware of the main disease problems facing Australian Poultry producers and current
control/prevention strategies
Basics of Disease Control
1. Biosecurity
2. Vaccination
o Breeder Immunity
 Breeder health status can be responsible for up to 80% of broiler health
problems
 Diseases which are egg transmissible (e.g. Mycoplasma, IBD, FAV, CAV,
Salmonella)
o Broiler Vaccinations
 Marek’s Disease
 Infectious Bronchitis (spray)
3. Health monitoring
4. Medication
Variety of disease types/scenarios
1. Lethal and highly contagious diseases:
o Newcastle disease virus (NDV)
 100% mortality
 Where did virulent NDV come from?
 NA sequence of virus indicates home grown (AUS); almost identical
molecular characteristics to low pathogenic virus
o Avian Influenza virus
 Birds become depressed, die suddenly
2. Pathogens of concern for public health
o On-farm contamination
 Salmonella
 Contaminated feed
 Environmental sources; litter, insects, personne
 Vertical transmission
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Campylobacter
 Horizontal transmission
 Influence of bird age
3. Immunosuppressive diseases
o Marek’s disease virus (MDV)
 Lymphoma, immunosuppressive
 Classical form: paralysis of legs & wings; between 8-20wks
 Acute form:
 Lymphomas develop in skin around feather follicle
 Produces tumors in visceral organs
 Virus tranmissed by dander released from feather follicle of infected birds,
inhaled by susceptible birds
 Control:
 Preventative vaccination, genetically resistant stock and management
 Live vaccines administered to day old chicks; 90% protection
4. Ubiquitous organisms, reduce productivity;
o Coccidiosis
 Diseases of poultry raised on ground; resulting in slow growth
 Ubiquitous protozoa, control expensive; continual medication and development
of resistance
 Seven species of protozoa cause coccidiosis
o Infectious Bronchitis virus (IB)
 Targets respiratory tract; cough, sneexing, watery nasal discharge
 Direct bird-bird airborne faecal transmission
 Broilers
 Affects feed conversion and weight gain
 Pale, swollen & blotchy kidneys
 Mortality up to 30%
 Control:
 Biosecurity
 Vaccination
o Live attenuated; at hatch to prevent infection in young
o Prime breeders and layers w inactivated vaccination prior &
throughout lay
Fish Health and Immunology

To demonstrate an understanding of the important aspects of teleost immunology and
compare it to mammals
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Fish are the most primitive vertebrates, and those in schools and warm environments
require a highly developed response.
All fish pathogens contain antigens; viral particles, bacteria, fungi, toxins and animal
parasites
Has 2 lines of defence
1) First line of defense: EXTERNAL
 Consist of skin, scales, and mucous membranes also secretions produced by
fish
2) Second line of defense: INTERNAL
 Triggered by chemicals, employs antimicrobial proteins and phagocytic cells
and inflammatory response
Mucus
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Skin
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Lymph
Skin, gills & gut of fish are covered in mucus
Continual trapping of micro-organisms and sloughing; inhibits colonization by opportunistic
pathogens
Mucus is a glycoprotein layer containing;
 Immunoglobulins; antibodies
 Lysozymes; can kill bacteria
 Complement: mediates the inflammatory response
Protective barrier
Covered in mucus
o Specific immunoglobulins
o Lysozyme
Rapid healing
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4 times volume of blood
Important for movement of immune cells, chemicals and enzymes around the body
No secondary lymph nodes in fish
Major lymphoid tissues
 Kidney
o Head kidney; making white and red blood cells
o Blood flows through kidney antigens are trapped/exposed to macrophages and
endothelial cells; captures ~70% of blood borne bacteria
o Head kidney; major producer of antibody (memory)
 Spleen
o Secondary to kidney
o Made of red and white pulp
 Red pulp; contains macrophages and lymphocytes
 White pulp; important in plasma filitration & capturing blood borne substances
 Liver
o Involved in production of complement cascade components
 Thymus
o Production of T cells
o Not always seen across different fish species
Complement
 Cascade of >20 serum proteins and gylcoproteins act as enzymes
 Activated by antibodies/bacterial antigens
 Can work at low temps 0-4 degrees in fish
o Leads to direct killing/opsonization and phagocytosis
o Works on gram negative bacteria
Lysozyme
 More active in fish than higher vertebrates
 Targets bacterial cell wall peptidoglycans  lysis
 Activates complement pathway and phagocytosis
C reactive proteins
 Pattern recognition proteins that are important components of acute phase of infection/injury
 Higher levels in fish
 Binds to phosporyl choline on surface of bacterial cell walls
 Activates the complement pathway
Natural antibodies
 Produced without an apparent specific antigen stimulation; high production in fish
 Low specificity; binds to bacterial, parasitic and viral proteins
Lymphocytes
 Mammals & fish both
o T cells; responsible for CMI
o B cells; responsible for antibody production
Antibodies
 Human:
o IgM, IgE, IgG, IgA, IgD
 Fish
o IgM, IgT, IgD
Factors that affect immune response of fish
Different between fish and human:
 Mammals are endothermic while fish are ectothermic

Low temperature slows the acquired immune response
o Slower cellular response
o Slower production of antibody
o Slower intracellular killing of micro-organisms
 Other factors that may directly alter the immune response of fish
o Drug treatments
o Photo period/season
o Life transitions- larval-juvenile-adult
 Stress
o Fish produce cortisol alters immune system decreased leucocyte migration &
antibody production
To discuss the production factors that impact on the immune system of fish and make them more
susceptible to infection
Farmed fish get sick because:
1) Increased stocking densities (lower profit margins)
2) Infected carriers (largely broodstock)
3) Infected facilities
4) Poor nutrition (we are way behind)
5) Substandard water quality
6) Biggest problem: greater susceptibility via weakening of resistance under intensive
culture conditions

To demonstrate an understanding of vaccinology to improve fish health and welfare
IP injection is the preferred method for juvenile to adult fish
o
o
Delivery
 Best protection achieved by injection by most expensive
Low cost
 Low value animal
 Large number of animals need to be treated
The antigens used in vaccine are critical to its success bigger, more complex is better, and must
be structurally stable. Fish vaccines require more antigen than mammals. Temperature, season
and photoperiod may affect the immune response to vaccination in fish.
Sheep Health Lecture 4
Footrot is a contagious bacterial disease of ruminants worldwide
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
Causes major economic losses; wool and meat production reduced by 8-10%
Breed (esp Merino) + Moisture/temp + virulence of strains present = disease expression

Pathogen: Dichelobacter nodosus
o Essential causative agent
 Gram negative bacteria
 Strict anaerobe, requires specialized media – e.g. hoof agar
o Parasite of skin of foot
 Sheep, goat, cattle
 Survives only 5-10 days on pastures
Diagnosis of footrot
1. Infection of sheep
o Assess clinical severity – benign or virulent?
2. Confirmatory tests
a. Smear and stain
b. Culture of Dichelobacter nodosus
c. Virulence tests – elastase, gelatin gel, zymogram, PCR
d. Serogroup (if vaccinating)
Treatment/control
 Hoof trimming and pairing
 Footbath – zinc sulphate
 Antibiotic injections
o Broad spectrum w higher dose; cost and antibiotic resistance issues as a flock level
treatment option
 Vaccinations
o Multivalent vaccines (whole cell or recombinant)
o Specific vaccines (whole cell or recombinant – mono or bivalent vaccines)
Advantages and disadvantages of footrot vaccines
Advantages
- Protective
- Curative
Disadvantages
- “Antigenic competition” in
multivalent vaccines
- Protection is serogroup specific;
presence of multiple serogroups in
flocks make it difficult
Alternative:
o
Sequential targeting if more than 2 serogroups
CLA: Caseous Lymphadenitis
Cause: Conyebacterium pseudotuberculosis
 Sub-clinical disease
 Abscessation in lymph nodes  CHEESY GLANDS

Major cause of condemnation of carcasses
o Damages export reputation
o Wool production losses
Pathogenesis
 Organisms deposited in wounds  cutaneous infection  migration to regional lymph nodes 
lymphadenitis
 Lymph node abscess can spread to lungs, liver, kidney etc
 Lung abscess can extend to bronchial and mediastinal lymph nodes
 Sheep w lung lesions communicating to exterior are main source of infection:
o Skin lesions (cuts) are infected
CLA Vaccination
 6in1
o Course= primary, secondary, annual booster
o Annual booster 2 weeks pre-shearing
o Reduces challenge and prevalence of lesions
 Benefits?: vaccination less than 100% protective of
o Skin lesions; production loss or lymph node and lung infection
 But vaccinates have lower prevalence, fewer lesions
o Continued use reduces CLA in a flock per sheep
Control
 Vaccinate
 Changing vaccination and bleeding needles frequently
 Shearing: young from old, reduce holding time
o Antiseptics to disinfect shearing combs
 Dip less and use bacteriostats/antiseptics in dips
Enterotoxaemia: sheep (cattle)

Clostridium perfringens
o Proliferates in small intestine on change to “starch” diet
o Epsilon toxin: severe, sudden toxaemia, endothelial damage: extravasation, edocardial
haemorrhage
o “mayonnaise” intestinal contents, rapid autolysis (esp. renal)
Diagnosis (Fresh)
 Glycosuria: glucose in urine
 Presence of Cl perfringens in gut smears
 Demonstrate toxin (mice protection) AG electrophoresis
Control
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
Diet, roughage, weaning, exercise, marking
Immunization: ewes 2 weeks prior to lambing
o Marking; primary then 6wks later booster (weaning)
Clostridial vaccines: ruminants
Fleece Rot
Pseudomonas aeruginosa
 Opportunistic pathogen
o Skin infection, wool discolouration, lead to secondary fly strikes, attracts pregnant
female blowflies & encourages egg laying, provides moisture for eggs to hatch and
protein for larvae to feed
 Shearing helps prevent – seasonal problem in hot and humid conditions
Dermatophilosis (dermo, lumpy wool)
Dermatophilus congolensis
 Affects mostly young sheep after episode of wetting and delayed drying
 Formation of hard scab in wool
 Economic loss:
o Lowered production
o Lowered wool values
o
o
o
Treatment costs
Deaths
Restriction of management options
Control of fleece rot and lumpy wool
 Breeding:
o Selection of strains and bloodlines performing best in particular env
 Selection of shearing time
o Minimize long wool during wet season
 Minimizing yarding of wet sheep
o Prevents contamination and contact w infected animals
Health management
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Good nutrition
o Conditions scoring, mouthing for teeth wear, diets for different classes of stock, pasture
management
Timely and effective treatment
o Vaccination, appropriate drenching if and when required
Health programs
o Minimize disease risks (market assurance programs)
Good biosecurity/quarantine measures
o Access of outside people and vehicles on famrs
Good fences
o Keep stock in and strays out
Investigate anything unusual
Sheep Health 5
Understand how different vaccines are made and used for disease control programs with example of
footrot vaccines
Need for recombinant footrot vaccine
 D. nodosus – slow growing
 Whole cell antigen production is an expensive process
 Fimbrial antigen is enough for vaccine
 Pseudomonas is easier to grow
 Very good host to produce fimbrial antigen of D. nodosus
 Cost of vaccine production
Cloning and making of recombinant antigen
 PCR to isolate fimbrial gene
 Recombinant Pseudonomas cells w D.nodosus fimbrial gene
 Pure D. nodosus fimbrial protein (antigen for vaccine production)
Formulation of vaccine
 Pure recombinant antigen + adjuvant (oil) + buffer  homogenization vaccine bottling->
transport
Process involved in sequential specific vaccination
1. Identify serogroups present
2. Identify virulent serogroups among
3. Whole flock vaccination (include up to 2 serogroups in a vaccine)
4. Repeat if other serogroups present every 3 months
5. Whole flock inspection in non-spread period – cull non-responders
“Reverse Vaccinology” approach to footrot vaccine development
 Traditionally vaccine candidate antigens are identified/selected by biochemical, immunological
or microbiological approach
 “reverse vaccinology” is identification of vaccine candidate antigens from genome sequence
Process of new vaccine testing
 Antigen screening and identification of antigen/s
 Antigenicity testing
 Safety and immunogenicity
 Efficacy testing in pen trials
 Field trial testing
 Registration for commercial use***
Biosecurity in production farm animals

The more animals are kept in closer proximity to each other and in contact w their faeces, the
more rapidly disease can spread and outbreaks become more severe and can be explosive
Main ways diseases can spread
 Animals
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o Movement of animals (target species)
o Disposal of dead animals
o Wild birds, feral animals, rodents, insects
o Semen
o Eggs
People
o Farm staff, visitors, vets, contractors, vaccination crews, shearers
o Boots, clothing, hair
Airborne
Fomites
o Vehicles, transport, machinery
o Veterinary equipment
o Saddles, harnesses etc
Feed and water
o Faecal contamination
o Raw materials
o Post-production contamination
o Mould growth
Benefits of biosecurity
 Greater productivity of stock – better health
 Reduced risks to the farm – disease entry
 Early detection and management
 Reduced costs is there is an outbreak – faster eradication before it gets to your farm
Effectiveness of biosecurity (disease exclusion)
 Works well against diseases where the causative organism:
o Doesn’t survive well outside the host
o Requires relatively close contract for transmission
o Diseases where we don’t have any other alternative control
 Not effective alone when causative organism:
o Has a long survival time in the environment
o Is ubiquitous
o Has an airborne route of transmission
o Has an effective and robust vector
o Is not very susceptible to disinfectants
o Where the consequences of an outbreak are severe
 The latter diseases need extra control mechanisms such as vaccination or medication
Biosecurity in farm animals – basic components
1. Distance from other premises w same species or species which share diseases
o Most effective control method
o Most expensive and difficult to maintain
o Only really used w elite breeding stock esp poultry
2. Single age (all in all out)
o Breaks disease cycle
o Especially important w disease w long carrier state (asymptomatic carriers)
3. Closed herd/flock
o No introductions to the farm
o Must have a self-contained breeding/replacement program or all-in, all-out
management
4. Isolation of introductions
o Allow time to see if disease is present
o Must maintain adequate separation of farm or of no value
o Staff involvement caredul
o Only possible w a limited no. of introductions
 E.g. poultry introductions are usually thousands; where to isolate and how to
move multiple times?
o Choosing a site within a facility to isolate animals w contagious diseases – designated
and separated
o Must be able to prevent direct contact between animals
o Sentinels are ideal
o Must be able to prevent exposure of other animals to body fluids from contagious
animal
o Must be able to prevent exposure via common water sources or run-off from isolated
areas
o Minimization human and vehicle traffic
5. Herd/flock immunity (vaccination)
o Vaccination will restrict ability for disease to establish or spread
6. Exclusion of contract – Quarantine/Hygiene
o Contact time
o Youngest to older
o Shower in/out
o Change of clothing
o Foot baths and hand washes
o Disinfection of fomites
o Dedication of staff (no species at home)
o Staff and fomites
 Control who enters; limit entry points
 Visitor register
 PPE
 Signage; visible, simple; visitors must report to staff
 Clean and disinfect tools and vehicles
o Restrict unwanted animals and people
 Fencing
 Hygiene
 Livestock treatment program
 Paddock rotation/spelling
7. Control of nosocomial infections (hospitals)
o General infection control practices; vets should wash hands before and after each
patient
Each industry treats biosecurity differently
 Horses: mainly concerned w nosociomial infections and individual animals
 Ruminants: relatively minimal
o Mainly introduction of new stock
 Intensive industries (pigs and poultry)
o Restricting entry of pathogens to farm; herd or flock concern, not ind animal
o Always run at a high risk level
General biosecurity considerations at farm level – simple procedures – grazing systems (ruminants)
 New livestock introductions (including working stock – horses, dogs)
o Trusted source (National Vendor Declaration)
o Animal health statements
o Inspect stock on arrival – and daily
o Isolate for 10 (?) days
National Livestock Identification System (NLIS)
 Traceability for cattle, sheep and goats and pigs now
 Animal identification (visual or electronic ear tag)
 Property identification (PIC)
 Web based database – records movement data
 A life history for each animal and determine contacts
National Vendor declaration (NVD)
 Each time livestock bought/sold/moved, livestock consignment must be accompanied by form
of movement documentation usually combined LPA NDV
 Separate forms for each species
 Requires info on PIC of source property, type of animal, number and destination
 Declaration on use of hormonal growth promotants, feed containing animal fat, how long
owned and history of issues or had treatments in withholding period
General biosecurity
 Feed water and bedding materials
o Commodity/by-product vendor declaration
o Fit for purpose; free from contaminants
o Store properly; clean and dry
o Inspect water sources, prevent feral animal access
o Treat water (chlorine)
 Restricted animal material as feed and no swill feeding
 Moving animals off property
o Must be fit to travel

o Supply an NVD and health statement
Animals at shows or sales
o Clean pens
o Feed and water
o Don’t share equipment
o Isolate on return
Biosecurity on horse industries
1. General infection control practices and protocols whose goal is to prevent the spread of
contagious infectious agents from animal to animal to human within a facility
2. Surveillance of the facility and animals for particular infectious agents, w aim of identifying
environmental contamination and potentially averting outbreaks of disease
3. Identification, investigation and management of disease outbreaks
Biosecurity in the pig industry
 99% of new disease will come from introduced pigs
 Important to purchase from 1 supplier w equal or better health status
 Keep pigs in quarantine for 6 weeks off-site. Use sentinel pigs too
 Quarantine buys time in case supplier crashes with a disease
 Fencing to keep feral pigs and people out
 Supply visitors w boots and overalls
 Have a ‘down time’ before visitors can visit your farm
 Record people movement and have controlled entrance for vistors
 Position farm away from abattoirs, livestock auctions, livestock transport routes
 have stock loading ramps and perimeter fence. Don't let dirty trucks or people onto the farm.
 keep rodent populations and wild birds down
 make sure pigs are identified according to state legislation and you have a PIC
 dispose of dead pigs by burial or compost
 make sure visitors and staff know what swill is and don't feed it to pigs
Biosecurity measures in poultry
Salmonella Enteritidis
 new to AUS poultry
 Notifiable
 Can spread inside egg
 Spreading on egg trays and packaging through network of egg trading practices
 Extreme importance of fomite transmission
Epidemiology 1
Temporal patterns of disease
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Sporadic:
o Disease occurs infrequently and without discernible pattern
Endemic
o The disease is virtually always present, often at low occurrence
Epidemic
o No. of cases in a pop clearly exceeds what is normal
Pandemic
o
Widespread epidemic spanning countries and/or continents
How disease occurs
(HAE not HPE): Agent
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
Agent(s) of disease needs to be present for disease to occur but its presence alone is not always
sufficient to cuase disease
Infectious and non-infectious agents
Types of agents
 Microorganisms; virus, bacteria, fungi..
 Genetic; e.g. canine hip dysplasia
 Chemical; monesin poisoning in horses
 Toxic; e.g. crofton weed
 Physical; e.g. metatarsal fatigue fracture
Properties of agents
 Infectivitiy; proportion of exposed animals that become infected
 Pathogenicity; proportion of infected animals that develop clinical disease
 Virulence; severity of disease in a host, proportion of clinically diseased animals that become
very sick or die
 Transmission
o Mode, direct (aerosol, contact) or indirect (fomites, vectors, airborne), direction;
horizontal (or lateral) or vertical
 Natural history of disease
o Evolution of disease over time in a natural situation without medical intervention
Agent factors
 Dose (infectiousness, contact time, amount)
 Infectivity, virulence
 Toxicity
 Environmental persistence
Host factors
 Species, age, breed/strain, genetic make-up/ pedigree, body condition, previous exposure,
innate resistance immune status, reproductive and production status; intrinsic (fixed) or
extrinsic (changeable)
Types of hosts
 Reservoir
 Definitive
 Dead end/accidental
Environment
 Geology, climate
 Vector density
 Stocking density, animal movement
 Feed quality
 Housing, fencing
 Mixing, moving and reproductive cycle
Goal: optimize health, welfare and production by reducing disease by:
1. Understanding HAET relationships of the disease
2. Decide which disease/s to reduce
3. Identify what is causing the problem
4. Design, implement & evaluate control measures
Prevalence= no. of cases / total pop at risk
 Proportion of animals in a pop experiencing an event at a givent point in time
Incidence = no. of new cases in time period / animal years at risk in time period
Cattle reproduction
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Be familiar with the primary determinants of herd health, production and welfare
Understand the relationship between herd reproductive performance and herd productivity.
Be familiar with the life cycle of dairy cattle and the primary determinants of reproductive
performance for heifer replacements and adult cows.
Be familiar with the normal reproductive cycle of cattle and ways in which it can be manipulated
Be familiar with common methods of heat detection
Be familiar with monitors utilised to assess herd reproductive performance
Determinants of Dairy Health, production and welfare
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

Nutrition
o Feeding the correct ration to the right cow at right time and right length of time
Comfort
o Social, environmental, physical
Reproduction
o Lactation
Relationship between reproduction and herd performance
 Milking cows => income
 Dry cows and replacement heifers cost money but do not generate income
 Milk production changes across lactation
 Efficient reproductive management minimizes no. of stock on feed that are not producing milk
 Reproductive efficiency keeps herd at a productive stage of lactation
Calving interval
 Gestation – 9 months
 Calving to conception interval variable
o For a calving interval of 12 months
 Calving to conception interval = 3 months
o For calving interval of 13 months
 Calving to conception interval = 4 months
Days in milk
 If average days in milk for herd increases, milk production is likely to decrease