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AVBS3005 > Management Strategies > Flashcards

Management Strategies Flashcards

1
Q

What are the 5 basics of disease control?

A

Biosecurity
Disease control programs
vaccination
medication
health monitoring

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2
Q

Biosecrurity emphasis increases with_____

A

Intensification (more intensive farming)

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3
Q

Biosecrurity emphasis increases with_____

A

Intensification (more intensive farming)

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4
Q

What are the main ways disease is spread?

A

Animals:
Movement of animals
Disposal of dead animals
Wild birds, feral animals, rodents, insects
semen
eggs
People:
Farm staff, family, visitors, vets
Contractors, vaccination crews, shearers
Boots, clothing, hair
Airborne
Fomites
Vechiles, transport, machinery
Veterniary equipment
Saddles, harnesses, etc.
Feed and water
Faecal contamination
Raw materials
post-production contamination
Mould growth

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5
Q

What are the benefits of biosecurity?

A
  • Greater productivity of stock – better health
  • Reduced risks to the farm – disease entry
  • Early detection and management
  • Reduced costs if there is an outbreak – faster eradication
    before it gets to your farm
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6
Q

When is biosecurity not effective?

A
  • Has a long survival time in the environment
  • Is ubiquitous
  • Has an airborne route of transmission
  • Has an effective and robust vector
  • Is not very susceptible to disinfectants
  • Where the consequences of an outbreak are severe
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7
Q

What are the basic components of biosecurity in farm animals?

A
  1. Distance from other premises with same species or species
    which share diseases
  2. Single age ( all in, all out)
  3. Closed herd/ flock
  4. Isolation of introductions
  5. Early detection of incursion
  6. Herd/ Flock immunity (vaccination)
  7. Exclusion of contact – Quarantine/ Hygiene
  8. Control of nosocomial infections (hospitals)
    ❖ Approach from each livestock industry varies
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8
Q

What are the basic components of biosecurity in farm animals?

A
  1. Distance from other premises with same species or species
    which share diseases
  2. Single age ( all in, all out)
  3. Closed herd/ flock
  4. Isolation of introductions
  5. Early detection of incursion
  6. Herd/ Flock immunity (vaccination)
  7. Exclusion of contact – Quarantine/ Hygiene
  8. Control of nosocomial infections (hospitals)
    ❖ Approach from each livestock industry varies
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9
Q

HPE of disease

A

Physical and toxic damage
Manipulate &/or avoid host defense mechanisms
Uses changed environment to enhance capacity to cause disease.
Environmental factors provide opportunity for pathogen to proliferate
Environmental factors in/directly cause disease. e.g. flood.
Environmental factors diminish the effectiveness of host defence mechanisms.
Host resist pathogen through defense, innate and adaptive
Host behavioural patterns alter environmental effects, increasing opportunities for pathogen

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10
Q

How do antibiotics improve sick animals growth?

A

Increase growth in conventional environments
Minimised number and severity of interactions with disease

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11
Q

Why does microbial invasion cause animals to slow growth?

A

Loss of appetite
Fever
Depression/sleepy
neutrophilia
Acute-phase protein response

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12
Q

What is the bodies response to microbial invasion?

A

Microbs cause inflammation/ local tissue damage
–> local response (address immediate invasion)
–> systematic response to protect body

Systematic respone (pro-inflammatory cytokines):
IL-1
IL-6
TNF

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13
Q

What do cytokines do?

A

regulate biological processes (cell growth, cell activation, inflammation, immunity and tissue repair)

Secreted by T cells, B cells, macrophages, neutrophils etc.

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14
Q

Features of cytokines:

A

diff cytokines may act on a single target cell
immune cells usually make more than one cytokine when activated
cytokines are effective at low concentration
* tend to act locally (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

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15
Q

Symptoms (systematic response) for inflammation

A

Fever:
- act on brain
- increase body temp
- induce sleep and supress appetite
Metabolic changes:
- increased protein catabolism and mobilising a pool of amino acids
- eventually leads to muscle wasting, but the amino acids are avalible for protein synthesis
Acute phase proteins:
- induce liver cells to increase protein synthesis and secretion
- produced within hours of injury, rapid rise concentration which then subsides within 24-48hours
- C-reactive protein (CRP).
- CRP binds to invading organism & damaged tissue
promoting their phagocytosis.
-inhibits neutrophil release of damaging radical, reducing
tissue damage and enhancing tissue repair.

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16
Q

The shorter the gestation length

A

The more developed the immune system is

17
Q

Transfer of maternal immunity in-utero

A

Transfer of antibody (maternal immunity) depends on structure of placenta:
e.g.
Humans and primates (hemochorial placenta) – maternal blood direct
contact with trophoblast – so maternal IgG transferred to fetus – and
newborn have circulating IgG levels reflect that of mother.
Dogs and cats (endotheliochorial placenta) chorionic epithelium in contact
with endothelium of maternal capillaries – only 5-10% IgG transferred
mother to fetus.
Ruminants – syndesmochorial,
Horses and pigs epitheliochorial placenta – no transplacental transfer of Ig.

18
Q

Transfer of maternal immunity

A

Colostrum (growth factors, immune factors and nutritional factors)
- mostly IgG
- rest split evenly between IgA and IgM

  • non ruminants mostly IgA
  • levels of immunoglobliuns in milk change between species depending on their needs
19
Q

Failure of passive transfer of
maternal immunity in colostrum

A
  1. production faliure (premature births, premature lactation and dripping of mammary secretions before birth)
  2. Ingestion failure (multiple births, if ammoutn of colostrum prod not increased proportional with number born)
    Poor mothering, newborn weakness, poor suckling drive or physical proble,s such as damaged teats or jaw defects
  3. Absorption failure (fail to absorb sufficient Ig –> risk of infection)
20
Q

Optimise immunity and protection in the young
by:

A
  1. immunise mother during pregnancy
  2. good mothering
  3. good nutrition
  4. clean (low path load) enviro
  5. careful scheduling of vaccination of young
21
Q

What is immunisation?

A

the administration of an antigen to confer immunity

22
Q

What are the differnt types of immunity?

A

ACTIVE PASSIVE
Natural Artificial Natural Artificial
Exposing vaccination from mother antitoxins
to disease - colostrum
causing
agent

23
Q

What are the features of an ideal vaccine:

A
  1. provide prolonged strong immunity - i.e. high antigenicity
  2. immunity conferred to immunised animal and newborn
  3. no adverse side-effects
  4. Cheap
  5. Stable (cold chain requirements?)
  6. Suitable for mass administration
24
Q

What are additional features of an ideal vaccine:

A
  1. Stimulation of APC (antigen presenting cells)
  2. Stimulation of T and B cells and their memory cells
  3. Antigen persists - provide long period of protection
25
Q

What is often incompatible with vaccines

A

High antigenicity and no side-effects

26
Q

Pros and cons of Live vaccine

A

High antigenicity
High risk

  • vaccine virus may cause disease

(reduce risk by attenuating)

27
Q

Why should you attenuate a virus?

A

reduces the virulence of the living
pathogen – so they can’t cause disease
i.e. avirulent.
Often involves adapation of organism to new
environment, becoming avirulent in usual host
1. Loose adaption for usual host or conditions e.g. anthrax grown
environment (with enzyme) where looses ability to form capsule
2.Genetic manipulation of requirements for growth e.g. stretomycin
dependency in Salmonella species
3. Repeated tissue 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.

28
Q

Pros and cons of Inactivated (killed) vaccine

A

Fewer risks
Lower antigenicity
Safer - act as exogenous antigens
Main side effect is tissue damage at site of injection (adjuvant use)
-antigen must remain antigenically similar to the living
organism – avoid protein denaturation or lipid oxidation.
- use chemicals such as formaldehyde which form cross-links
between proteins and nucleic acids – provides structural
rigidity.
-Vaccines that contain killed bacteria called bacterins
- Contain inactivated toxins- toxoids

29
Q

What is an Adjuvant

A

A substance that accelerates, prolongs, or enhances antigen specific immune responses when used concurrently with a vaccine antigen.

(adjuvants increase the affectivity of vaccines containing inactivated organisms via (mechanisms))

30
Q

How do adjuvants work?

A

Increase affectivity of vaccines containing inactivated organisms via:
- acting as a slow release antigen depot
- Promote antigenicity by trapping antigens at sites where they are accessible to lymphocytes
-Stimulate antigen-processing
-Stimulate macrophages.

31
Q

What are the different types of adjuvants?

A

Aluminium salts
Water-in-oil emulsion
Bacterial products
Surface active agents
Cytokines: regulatory role fine-tuning immune responses

32
Q

What are other types of vaccine production?

A

Recombinant antigen protein
Live recombinent organisms
Genetically attenuated organisms
Naked DNA
Synthetic peptides
mRNA vaccines

33
Q

What are methods of vaccine delivery?

A

oral
intramuscular
intranasal
suncutaneous
intraperitineal
(nanopatch)

34
Q

Six rules of thumb apply to active vaccination

A
  1. Newborns are passively protected by maternal antibodies –
    difficult to successfully immunise animals early in life.
  2. Once born, active immunisation is only successful after
    passive immunity has waned.
    3.prevelance of disease
  3. Class and age of stock
    5.Need for booster
  4. seasonal occurance

AVBS3005 (8 decks)

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