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Animal hygiene > must know > Flashcards

must know Flashcards

1
Q

Sterilization =

A

• No aerobic or microaerophilic bacteria can grow on culturing media used in medical bacteriology,

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2
Q

Disinfection =

A
  • Eliminating/destroying infective and facultative pathogenic microorganisms by substances known to have disinfective capacity.
  • Freeing from pathogenic organism, or rendering them inactive
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3
Q

Factors affecting efficiency of disinfection:

A

Biological factors • Survival of germs • Resistance to disinfection o Technological factors • All in all out • Value of service period of cleaning disinfectant

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4
Q

gama rays function:

A

causing irreversible destruction in structure of proteins and DNA

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5
Q

W-rays (lamps) function:

A
  • Changes DNA = wear protective glasses and clothes

* Only for disinfection of dust free surface (limited value) = Photooxidation - Two compounds

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6
Q

Disinfection of stables steps:

A
  1. Removal of equipment and dry cleaning
  2. Pre-cleaning → wet wash with appropriate detergents
  3. Sanitizing and disinfecting the water system → Header tanks, drinkers, pipelines
  4. Movable equipment
  5. disinfection
  6. Fogging and aerial disinfection
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7
Q

Disinfection of vehicles

A 
• Dry cleaning
• Cleansing and rinsing
• Disinfection
• Cab disinfection
Finally → park on a slope to drain and dry, remove vehicle, wash concrete surface with appropriate disinfectant, then disinfect overalls and boots.
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8
Q

Disinfection of wells

A
  • 30 g/m3 chlorine powder

* 100 ml/m3 sodium hypochlorite Monitoring the

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9
Q

efficiency of disinfection, how to check:

A
  • Direct swabbing technique
  • Agar cylinder techniques
  • Agar sausage method
  • Agar-carrying linen
  • Ready to use test
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10
Q

Physical methods of sterilization/disinfection:

A
  1. Heat
  2. irradiation
  3. UV light
  4. Other Physical Methods
    • Ultrasonography (Gr -)
    • High pressure (Gr-/+)
    • Microwaves - only vegetative form
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11
Q

Biological Methods of sterilization/disinfection:

A

Feedstuff/Manure fermentation
• Competition
• Antimicrobial metabolites
• Changing environment (E.g. silage)

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12
Q

Chlorine based compounds:

  • general properties
  • example of compounds
A

▪ Room temperature → toxic gas
▪ Water soluble
▪ Penetrates cell membrane, destroys cellular enzyme with SH- radicals.
▪ increased temperature reduces capacity
▪ Organic materials decrease capacity
▪ Corrosive!

  1. NaOCl
    against → vegetative bacteria + all viruses, but no acid fast bacteria or spores
  2. Chlorinate lime – bleach
    Disinfectant of wells, other water resources and surfaces (roads)
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13
Q

Iodine based compounds

  • basic function
  • colour
  • example of compound
A

▪ Iodophores → iodine + organic substrate (surface active materials)
● + phosphoric acid → solubilising the iodine (detergent)
● + buffers → ↓ pH
● + polyvinyl-pyrolidine → bind up to 30% of iodine

→ oxidizes function groups of germs
▪ Colour → dark brown to light yellow
▪ Surface friendly and powerful cleaning effect due to detergent content

  1. Betadine (pavidone-iodine)
    - Advantage → Bactericidal, viricidal, fungicidal
    - Disadvantage → skin sensitive, partially inactivated by organic debris
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14
Q

Aldehydes

  • spectrum
  • genral properties
  • not mixed with….
  • forms:
A

• Efficient, broad spectrum
• -CHO- radicals → destroy cell wall
• Formaldehyde
1. Formalin: = Used in solution and gas form for surface disinfection
2. Irritant, odorous, suffocating, cough evoking, colourless gas
3. Attacks all mucous membranes
4. No hindering by organic materials
5. Formaldehyde gas or water solution
• May be neutralized with NH3
• Safety → not to mix with NH4 solution, H2O2, Heavy metal solutions
6. Paraformaldehyde
• White, crystallized, smelly powder, Gas disinfection of smaller stables
7. Glyoxal
8. Lysofom

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15
Q

Peroxide based compounds

  • main properties
  • compounds ant their characterisitcs
A

• Deliberates mono atomic oxygen → destroys membranes and organic molecules of bacteria

  1. Hydrogenperoxide
    = Colourless, odourless, aggressive, mildly acidic liquid → decomposes quickly.
    - Strong corrosive → pure form is not used.
    Disinfection of utensils in 3-10% concentration
  2. Peroxy acids
    = Formic and acetic acid.
    Also may contain phosphoric acids and stabilizers
  3. Peracetic acids
    = Aggressive fluid with vinegar like odour.
    Food industry and production of SPF animals → wide antimicrobial effect, quick decomposition after use. Not to be used with alkalis
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16
Q

Surfactants (tensides)

  • general properties
  • groups
A

• Water and alcohol solution → reduces surface activity surfaces, helps remove dirt, enhances efficiency of
other disinfectants

  1. Anion active tensides (alkali sulphates, soaps) = Strong lipid solvent. No disinfective capacity
  2. Cation active tensides (sterogenol, Bradophen-H)
    = Disinfectant capacity.
    Decreases surface activity of cell membrane and increases its permeability.
    - Efficiency decreased by hard water
  3. Non ionic tensides (TWEEN 80) = Do no dissociate in solutions. Mild disinfection capacity, often in
    combination
  4. Ampho-tensides (acidic and alkali groups)
    = Acidic surrounding → as cationic active tensides. Basic surrounding → as anionic tensides
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17
Q

Acids and alkalis

- groups, examples and properties

A
  1. Inorganic acids → nitric-, hydrochloric-, sulphuric-, phosphoric acids: Strong corrosives, not used
  2. Organic acids → formic-, lactic-, malonic-, glutamic-, propionic acids: Used in combination with other
    disinfectants, especially with anionic tensides. Increases virucidic and sporocidic action
  3. Alkalis → NaOH, KOH : Were used by dairy industry. Hot solution in 2-4% concentration → bacteria and
    viruses. Hot solution in 6% concentration → sporocide. Strong corrosive effect
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18
Q

Miscellaneous

- groups, examples and properties

A
  1. Phenols and cresols → virucides and sporocides, extremely toxic, pollute environment
  2. Alcohols → based on water extraction, Gr+ and vegetative bacteria, used in combination (skin)
  3. Others → glycols, guadinins
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19
Q

Gaseous disinfectants:

  • examples
  • general properties and uses
A

(=gas state at room temperature)

  1. Etyhlene oxide
    = Sweet ether like smell.
    - Good penetration → paper, cellophane, plastic containers.
    - Attack –SH, -amino, -carboxyl and hydryl radicals of proteins.
    - Strong bactericide, virucide and sporocide. - Inflammable / explosive.
    Inhalation → headache, nausea, mucosal irritation.
    Uses → textile, containers, feed
  2. Beta propionlactone → gas sterilisation
  3. Methyl bromide → insecticide
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20
Q

Effects of animal production on the nature and society

A
  1. Harmful emissions → greenhouse effect, damage ozone layer, damage life quality, transmission of
    diseases, acid rain (soil acidification)
  2. Pests → rodents, birds, insect
  3. Animal wastes → soil and water pollution, infections
  4. Food safety and quality → direct effects, indirect effects
  5. Effects on animal health → reproductive failures, management related diseases
  6. Labour health
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21
Q

Definition = Animal wastes/byproducts →

A

entire bodies or parts of animals or products of animal origin not intended for human consumption, including ova, embryos and semen.

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22
Q

SRM I =

A
  • Head without the tongue, thymus, spleen, spinal cord of bovine animals over 6 months, and the intestines (duodenum → rectum) of bovine animals of all ages
  • Skull including brain, eyes, tonsils, spinal cord of bovine animals over 12 months.
  • Vertebral column including dorsal root ganglia of bovine animals over 30 months.
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23
Q

• SRM II =

A

• Skull and brain, eyes, tonsils and spinal cord of ovine and caprine animals over 12 months or which have a permanent incisor erupted through the gum, and the spleen of ovine and caprine animals of all ages

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24
Q

Catergory I materials:

A

a. All body parts including hides, skins of:
• Animals suspected of being infected by TSE or the presence of TSE has been confirmed
• Animals other than farm animals and wild animals
• Pet animals, zoo animals, circus animals
• Experimental animals
• Wild animals when suspected of being infected with transmissible diseases
b. SRM (specified risk material)
c. Products of animal origin containing residues of environmental contaminants
d. All animal material collected when treating waste water from category 1 processing plants
e. Catering waste from means of transport operating internationally
f. Mixtures of category 1 material with either category 2 or category 3 material or both, including any material destined for processing in a category 1 processing plant

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25
Q

Category II matrial

A

a. Animals and parts of animals that died and not listed in category 1 by products, including
animals killed to eradicate an epizootic disease
b. Manure and digestive tract content
c. Materials collected from water from slaughterhouses d. Products of animal origin containing residues of drugs and other contaminants.
e. Mixture of Category 2 material with category 3 material
f. Animal byproducts other than category 1 material or category 3 material

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26
Q

Category III material:

A

a. Parts of slaughtered animals, fit for human consumption, but are not intended for human
consumption for commercial reasons.
b. Parts of slaughtered animals, which are rejected as unfit for human consumption but are not affected by any signs of disease communicable to humans or animals and derive from carcasses that are fit for human consumption.
c. Hides and skins, hooves and horns, pig bristles and feathers originating from animals that are slaughtered in a slaughterhouse, after undergoing ante-mortem inspection, and were fit, as a result of such inspection, for slaughter for human consumption.
d. Blood from slaughtered animals, except ruminants, that had Ante mortem inspection (fit for
human consumption)
e. By products from producing products for human consumption (including degraded bones and
greaves)
f. Former foodstuffs of animal origin or former foodstuffs containing products of animal origin,
other than catering waste, which are no longer intended for human consumption for commercial reasons or due to problems of manufacturing or packaging defects or other defects which do not present any risk to humans or animals.
g. Raw milk originating from animals that do not show clinical signs of any disease communicable through that product to humans or animals
h. Fish or other sea animals (except for mammals), caught in the open sea for the purpose of
fishmeal production
i. Fresh by products from fish from plants manufacturing fish products for human consumption
j. Shells, hatchery by products and cracked egg by products originating from animals which did
not show clinical signs of any disease communicable through that product to humans or animals
k. Blood, hides and skins, hooves, feathers, wool, horns, hair and fur originating from animals that did not show clinical signs of any disease communicable through that product to humans or
animals
l. Catering waste other than as referred to in category II wastes.

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27
Q

Principles of disposal and treatment of Category 1

A

Category 1
• Direct incineration in incineration plant or in co-incineration plant
▪ The gas products at the end of the burning process: ● Should be Homogenous
● Should Have 850oC temperature for at least 2 sec.
● The oxygen content of the gas should be at least 6%
• Processed in a processing plant into meat bone meals (MBM)
▪ Disposed as waste by incineration or
▪ Disposed as waste by burial in landfill

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28
Q

Principles of disposal and treatment of Category 2

A

Category 2
• Processed in a processing plant into meat bone meals which then will be:
▪ Disposed as waste by incineration or
▪ Disposed as waste by burial in landfill or
▪ Disposed as waste by composting or
▪ Disposed as waste by bio gas production
❖ MBM from categories 1 & 2 is forbidden to use in animal feeds.

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29
Q

Principles of disposal and treatment of Category 3 waste materials

A

Category 3
• Direct incineration in incineration plant or in co-incineration plant
• Processed in a processing plant
▪ Disposed as waste by incineration or
▪ Disposed as waste by composting
• Category 3 materials (a) to (j) can be processed into pet food dog chews and technical materials other than
fertilizers etc

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30
Q

Methods of ventiation:

A
  1. Natural: Windows, doors, gates, chimney trunk
  2. Mechanical
    • Pressurised
    • Extraction
    • Even
    • Recirculation
    • Ventilation units
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31
Q

Evaluation of ventilation (one negative score for each)

A
  • False ingoing air
  • False outgoing air
  • Recirculation from dung channel
  • Whirl zones
  • Exposure of drought/cold
  • Air velocity >0.4m/sec close to animals
  • Change of air velocity close to animals
  • NH3 concentration of air velocity >10ppm
  • Precipitation on construction elements
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32
Q

Characteristics of aerosols

A

• Non homogenous distribution
• Size: 10-4 – 102 μm
>20 μm → sedimentation within minutes
~10 μm → sedimentation: less than 25 minutes
<5 μm → slow sedimentation, over 1.5 hours
• Increasing humidity → agglomeration → increased sedimentation

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33
Q

Tolerable levels of aerial contaminant in animal confinements

A
  • Total dust → 3mg/m3 (empirical)
  • CO2 → 3000 ppm (limit value set by EU)
  • NH4+ → 20 ppm (limit value set by EU)
  • H2S → 0.5 ppm (limit value set by EU)
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34
Q

Methods of measuring aerosol particles

A
  1. Particle counting → Konimeter 10 particle counter
  2. Gravimetric methods
    ▪ Sedimentation: circular aluminiumfoil covered with film of Vaseline
    ▪ Persometer
3.  Measurement of aerial germ count
▪ Microbial contamination of air → contamination infection → rate of survival depends on: 
● Humidity of the air
● Frequent change of air temperature 
● Bactericide irradiation
● Aerial oxygen content
● Open air factor
  1. Sedimentation
    ● Determines the number of Colony forming units that sediment onto the surface of culturing media in petri dish within given time of exposition
  2. Slot sampler
    ● 20-33 mm long, hair thin slot beneath turntable petri dish with media
3. Andersen air sampler
● Utilizes the principle of the slot sampler by applying 6-8 stages
● Tiny holes of different diameters 
4. Centrifugal air sampler
● Sampling drug and test strip
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35
Q

Gaseous contaminants:

A
  1. Ammonium
  2. CO2
  3. Hydrogen sulfide
  4. Carbon Monoxide
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36
Q

Measuring gaseous contaminants:

A

Instruments:
- Pump: manual or mechanical
- sampling device: impingers (capillary, cyclone)
or test tubes (with absorbants + indicators)

  1. Dräger sampler: CO2
    - hydrazine absorbent and crystal violet redox indicator
  2. Automatic air sampler: CO2
  3. Measures to measure ammonium:
    - ▪ Indophenol colorimetric method
    ▪ Nessler reagent (Potassium tetraiodomercurate)
    ▪ Ammonium ion selective electrodes
    ▪ Dräger sampler: test tube contains bromphenol blue that binds the ammonium quantitatively
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37
Q

The degree to which ammonia forms the ammonium ion depends on…

A

the pH of the solution.
If the pH is low, the equilibrium shifts to the right: more ammonia molecules are converted into ammonium ions. If the pH is high (the concentration of hydronium ions is low), the equilibrium shifts to the left: the hydroxide ion abstracts a proton from the ammonium ion, generating ammonia.

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38
Q

Components of microclimate:

A
  1. Air quality → gas components, aerosols, air born germs
  2. Physical factors → dry/wet bulb temperatures, cooling power, mean radiant temperature, air velocity, thermal properties of floor
    - Determine the heat sensation of animals
  3. Others → light regime, noise, barometric pressure, etc.
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39
Q

Temperature:

- ways to easure it

A 
● Mercury or ethanol thermometers
● Thermo elements
● Resistant thermometers
● Thermistors
● Simplest way of assessing the critical temperature → Six-type max-min thermometer
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40
Q

Instruments for short term measurements of microclimate:

A

▪ Temperature
▪ Relative humidity
▪ Estimation of the convective and radiant heat loss from animals
▪Estimation of the convective and radiant heat loss from animals
▪ Air velocity

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41
Q

Relative humidity is measured by:

A

● Hygrometers

● Psychrometer

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42
Q

Cooling power is measured by

A

the Hill-katathermometer

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43
Q

Instruments for long term measurements of microclimate:

A

▪ Thermographs
▪ Hygrographs
▪ Thermo-hygrographs
▪ Barographs

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44
Q

Data processing with regards to the microclimate:

A
  • With regard to heat sensation and production

* With regard to the thermal properties of the stable

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45
Q

13.

- Name the most important energy therms regarding animals:

A
  1. Gross energy (GE) = faecal energy
  2. Digestible energy (DE) = urinary energy
  3. Metabolizable energy (ME)
  4. Non productive energy requirement → maintenance, locomotion, thermoregulation
  5. Productive energy (NE) → req. for fat deposition (50 kJ/g), req. for protein deposition
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46
Q

Factors that modify the gross energy intake

A
  • Available feeding space
  • Population density
  • Defected feed
  • Environmental temperature
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47
Q
  1. Factors that modify the digestibility of the feed
A

• Anti-nutritive substances
• Particle size of the feed
• Dry versus wet feed
• Cold environment enhances the intestinal motility → reduction of available time for digestion
▪ In sheep every OC ↓ below the lower critical temperature → ↓ digestibility by 0.1-0.2%

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48
Q
  1. Factors that modify the non productive energy requirement
A
  1. Factors that increase the genetically coded maintenance requirement
    ▪ Acclimatisation to cold
    ▪ Genetic selection (e.g. dwarf lines)
  2. Factors that increase the locomotor activity
    ▪ High population density
    ▪ Oestrus
  3. Factors that increase the thermoregulatory heat production
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49
Q
  1. Critical temperature of animals are affected by number of factors:
A
  1. Species, Breed, Age
  2. Single or group keeping, and size of the group
    ▪ Increased group size → lowered critical temperature
  3. Plane of nutrition → Insulation of the skin
  4. Thermal properties of the floor → Concrete > Asphalt > dry straw bedding
  5. Air velocity
  6. Mean radiant temperature
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50
Q
  1. Define heat equilibrium:
A

Heat produced in the system vs. heat loss of the system

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51
Q
  1. Heat balance equation:
A

Heat balance: QA = LB+LV
• QA - animal heat production
• LB - Heat loss through construction
• LV - heat loss through ventilation

Optimal innside temp. should be reach heat balance

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52
Q
  1. Steps in developing heat equilibrium:
A
  1. Assess animal heat production
  2. Assess heat loss through stable construction
    Depends on: Thermal transmittance, surface of a building element, difference inside/outside temp.
  3. Assess heat loss through ventilation
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53
Q
  1. Methods of heating
A
  1. Room heating = Hot air blown inside through ducts.
    Central heating. Floor heating. Heat exchanges
  2. Local heating = Infrared bulbs. Infra gas heaters. Heating mats. Floor heating
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54
Q
  1. Heat balance of the animal organism

- Equation:

A

Q + (Rg+Cg) = (R + C1 + C2 + E)±S

• Left side of the equation → heat gain
▪ Q → heat production of the animal
▪ Rg → Heat gain by irradiation from the surrounding
▪ Cg → conductive heat gain

• Right side of the equation → heat loss ▪ R → heat loss by radiation
▪ C1 → conductive heat loss
▪ C2 → convective heat loss
▪ E → evaporative heat loss
▪ ±S → heat stored in, or lost from the animal in any given period

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55
Q
  1. Heat exchange between the organism and the environment
A
  1. Net radiant heat exchange
    - heat gain by irradiation inn/outdoors
  2. Heat exchange by convection
  3. Heat exchange by conduction
  4. Evaporative heat loss
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56
Q
  1. Heat gain by irradiation outdoor
A

● Solar energy reflected by the soil and vegetation
● Direct solar irradiation
● Diffuse irradiation (Electromagnetic waves are diffused by the aerial contaminants) X
● Long wave irradiation emitted by the soil and vegetation
● Atmospheric irradiation = energy absorbed by the vapour, CO2 and ozone content of the air
from the solar energy reflected back by long wave electromagnetic waves XX

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57
Q
  1. Heat gain by irradiation indoor
A

● Radiation reflected by walls and floors
● Long wave irradiation emitted by the walls and floor
● Diffuse irradiation (Electromagnetic waves are diffused by the aerial contaminants) X
● Atmospheric irradiation = energy absorbed by the vapour, CO2 and ozone content of the air

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58
Q
  1. Heat exchange by convection =
A

exchange of heat energy between the body surface and the energy content of the air molecules that form layer on the body surface

—> natural or forced heat exchange

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59
Q
  1. Heat exchange by conduction

- the temp. is affected by:

A

▪ Food or water that has lower temperature than the core temperature of the body
▪ Floor

60
Q
  1. Forms of evaporative heat loss
A

● Percutan water diffusion
● Active sweating
● Vapour loss via the respiratory tract

61
Q
  1. Regulation of heat balance is a balance of:
A

• Afferentation → Centre → Efferentation

62
Q
  1. Efferentation of the heat loosing mechanisms
A

▪ Behavioural changes (locomotor innervation)
▪ Change in the buffer air layer (mm. arectores pilorum)
▪ Decrease of heat resistance of the fur (vasodilatation)
▪ Increased respiratory rate

63
Q
  1. Efferentation of the heat conservation and production mechanisms
A

▪ Behavioural change (locomotor innervation)
▪ Change in the buffer air layer (mm. arectores pilorum)
▪ Increase of heat resistance of the fur (vasoconstriction)
▪ Non shivering thermogenesis (sympatyco adrenerg activity)
▪ Shivering thermogenesis (excitation of motor nerves)

64
Q
  1. Decompositions of feed mixtures, types of decomposition:
A

→ Chemical decomposition and microbiological decomposition

65
Q
  1. Why are lipids sensitive to oxidation:

Process of peroxidation of feed lipids:

A

Lipids are sensitive to oxidation due to double bonds between carbon atoms in the chain of unsaturated
fatty acids

▪ Oxygen reacts with double bonds of unsaturated fatty acids → formation of peroxide
● Peroxides are labile structures and easily give down a proton
o Formation of peroxide radix (ROO+)
▪ Formation of hydroperoxide radix = highly reactive molecule that might contribute to formation of oxidative stress

66
Q
  1. substances that might lead to lipid peroxidation:
A

Mono atomic oxygen, super oxides, H2O2, Hydroxyl radicals, hypochlorite acids

67
Q
  1. Oxidative stress effect:
A
  • May damage cell membranes and membranes of IC organelles
  • May hinder enzyme activity in the cell membranes
  • May prevent destroying of molecules that form in metabolic processes but represent danger to the organism → e.g. Lipofuchsin
68
Q
  1. Protective mechanisms against oxidative stress
A
  1. Non enzymatic anti oxidants → tocopherol (mainly alpha), Vitamin C, ubiquinons, flavonoids,
    carotenes, Vit. E, ferriting, metallothionein, glutathione
  2. Enzymatic antioxidants
    ● Superoxide-dismutase (Cu, Zn, Fe atoms)
    Highly reactive molecules that might contribute to the formation of oxidative stress
    ● Glutathion peroxidase (Se, Vit. E, riboflavin)
    ● Haemoxygenase 1 and 2
    ● Cytochrome oxidase
69
Q
  1. Oxidative stress

▪ May arise due to:

A

● Excessive presence of free radicals in the feed
● Failure of protective mechanisms due to deficiencies in Se, Vit. E, Carotenes, Vit. A, etc…
● Or both!

70
Q
  1. Oxidative stress and related diseases:
A
  1. muscle dystrophy
  2. placental retention
  3. retarded growth
  4. Hepatosis dietetica
  5. mullberry heart disease
  6. decreased egg production and hatchability
71
Q
  1. Preventiontitive measures oxidative stress:
A
  1. Prevention of rancidity of feeds
    - Saturation of fatty acids by hydrogen treatment of hot fats in presence of catalysators
    - Use of antioxidants
    - Appropriate storage conditions → protection from excessive heat, humidity and light
  2. Promoting anti oxidative mechanisms of the organisms
    - prevent Zn deficiency
    - Supplementation of feeds with surplus riboflavin or with vitamin E.
72
Q
  1. Biogen amines:
    - effect:
    - greater and smaller
    - depends on
A
  1. Decomposition of feed proteins
  2. Toxicity of biogen amines
    - Greater → neurine, histamine, spermine
    - Smaller → putrescine, cadaverine
    ▪ Depends on concentration, synergism, population sensitivity, feeding length
73
Q
  1. Biogen amines:

▪ May cause:

A

● Edema and inflammation of stomach and intestines
● Damage of the liver
● Dystrophy of renal epithelium (putrescin)
● Epithelial erosions and ulcers in gizzard of broilers

74
Q
  1. Classification of feed flora:
A
  1. According to origin
    - Plough land flora (pre harvest species) → epyphyta, endophyta
    - Store house flora
  2. According to multiplication on the feed
    - Non proliferating flora: passive (from air, other sources) or active (biological substances)
    ▪ Proliferating flora: decomposition of nutrients → toxic agents, and dysbiosis
  3. According to pathogenicity
    ▪ Facultative pathogen germs
    - Exotoxin producing → Cl. Botulinum, S. aureus
    - Endotoxin producing → Salmonella, coliforms, Clostridium, Bacillus, Proteus, Pseudomonas
    ▪ Obligate germs (feed infection) → B. anthracis, M. tuberculosis, Brucella, TGE, BSE
75
Q
  1. Conditions of microbial gradation:
A
  1. Initial number of germs: the greater the germ count the speediest of gradation
  2. Water content of the feed and gradation of germs
    - Correlation with water activity (aw) of feeds
    = is characterized by the equilibrium relative humidity
    - Minimum water activity of germs of feed hygiene importance
  3. Temperature = Thermophyl → >40C, Mesophyl → >25-24C, Psychrophyl → <25C
  4. Presence of oxygen → aerobic, microaerophyl, anaerobic
    - Aerobic cond. + high aw → yeasts and Bacillus spp.
    - Aerobic conditions + low aw → moulds
  5. Presence of nutrients = Mono-, di and polysaccharides: organic acids. Lipids and proteins: free radicals and biogen amines
76
Q
  1. consequneces of feed spoilage:
A
  1. Deterioration of organoleptic characteristics → feed refusal
  2. Decreased nutritive value → 10-30% of all, 30-40% beta carotene, 50-70% vitamin E
  3. Generation of toxic substances by secondary metabolism (mycotoxins, bacterium toxins)
  4. Consumption of masses of feed microbes → enteral dysbiosis
77
Q
  1. what are mycotoxins?
A
  • Mycotoxins are a product of secondary metabolism of microscopic fungi
  • They are extremely resistant to external influences
  • They cause extreme human and animal health hazards all over the world
78
Q
  1. General outcomes of mycotoxins
A
  1. Depressed immunity, Decreased feed consumption, Feed refusal
  2. Retarded growth and phenotypic development, Rough hair, Decreased production
  3. Embryo mortality – abortion
  4. Silent/irregular oestrus, sham oestrus during pregnancy, decreased rate of conception
  5. Increased disease incidence → Abomasal displacement, foetal membrane retention, ketosis, fatty liver syndrome, metritis, mastitis
79
Q
  1. Prerequisites of mycotoxin intoxication
A
  • Presence of one or more mycotoxins in the feed/food
  • Appropriate concentration of the mycotoxin, Sufficient length of consumption
  • Individual/herd level sensitivity
80
Q
  1. Development of mycotoxicosis
A

• Input of mycotoxin → metabolism of mycotoxins
▪ Excretion of mycotoxin metabolites → food safety, pollution of the environment
▪ Mycotoxin/metabolite binds to receptors
● Animal health consequences
● Food safety consequences

81
Q

Classification of mycotoxins in livestock and poultry production

  • store house moulds
  • field moulds:
A
  1. Store-house moulds
    ▪ Aspergillus and penicillum species → aflatoxins, ochratoxins
    ▪ Water content of the grain → 14-24%
    ▪ Equilibrium relative humidity: ≥ 70%
    ▪ Prior to harvest intact seeds are resistant for multiplication of fungi
    ▪ Multiplication needs seed damage ← mechanical (harvest), insects
    ▪ Temperature → varies according to the needs of fungi
  2. Field moulds
    ▪ Fusarium species → zearalenone (F-2), trichothecenes (T-2), fumonisns (B1, B2, B3, B6, etc…)
    ▪ Stachibotrys atra (alternans) → satratoxins (Macrocyclic trichothecenes)
82
Q
  1. Metabolism of mycotoxins:
A

• Digestive tract → faeces
• Portal circulation
• Liver → bile
▪ Part of the mycotoxins will be metabolized by neutralization, oxidation, reduction, synthesis…
▪ The more toxic substances (zearalenon – alfa zearalenon) will cause on of the following:
● Acute toxicosis
● Chronic form with characteristic symptoms
● No clinical signs, but decreased production, and impaired immune response

  • Blood circulation
  • Urinary excretion
83
Q
  1. The role of rumen in the metabolism of mycotoxins
A

▪ Under normal circumstances of pH 6-7:
● Aflatoxin B1 → 40% is metabolised
● Zearalenone → alfa zearalenol, beta zearalenol
● T-2 toxin → HT-2 toxin
● Diacetoxyscirpenol → monoacetoxiscirpenol
● Deoxynivalenol → epoxynivalenol
● Ochratoxin A → ochratoxin-alfa and fenilalanin
▪ During rumen acidosis (pH 4-5) →Decreased capacity for detoxification

84
Q

19, 20. Zeralenone general characteristics:

A 
Chemically Zearalenone (F-2 toxins) is the lactone of the resorcilic acid, mainly produced at 6-12C by:
• Fusarium avenaceum, F. roseum, F. equisetti, F. graminearum, F. clumorum, F. lateritium
 • There are about 13 analogues, alfa zearalenone is the most active form
85
Q
  1. Zeralenone, Way of action:
A
  • ZEA Penetrates cell membrane and binds to the cytosolic 17 beta-estradiol receptors (E2)
  • The ZEA-E2 complex penetrates the nucleus
  • As a consequence the activity of mRNA is modified which results in production of proteins that are normally produced by the estradiol-E2 complex
  • Zearalenon: oestrogen like effects
86
Q
  1. Effects of zearalenone
A

• Considered as one of the phyto-estrogens (eg. Coumetrol, genistein, etc…)
• Target organs → endometrium and ovaries, anterior pituitary (lactotrophic cells), mammary gland
• Receptors
▪ There are alpha and beta receptors which differ in respect to C terminal ligand binding and N-terminal trans-activating domains.
▪ Binding of ZEA to oestrogen receptors is about 100 times less efficient than that of the natural estradiol
▪ Breed differences may be explained by the binding capacity of ZEA to receptors
• In oestrogen dependent tissues ZEA had a carcinogenic effect in humans
▪ In cases of endometrial hyperplasia and adenocarcinoma the concentration of zearalenone in
samples of endometrium was many times higher than in healthy women

87
Q
  1. ZEA in ruminants:
A

• Zearalenone is transformed in the rumen → alpha zearalenol → alpha zearalanol
▪ Alpha zearalanol has an anabolic effect → used earlier as active substance of growth promoter
• Food safety considerations
▪ Target organs → endometrium, ovaries, hypophysis front lobe lactotroph cells, mammary gland
▪ ZEA and derivatives are excreted by the udder
● Dangerous milk concentrations need extremely high dietary contamination!
● It might menace the health of infants but protection of consumers need no food safety interventions for the time being.
▪ Threshold dietary concentration of reproductive disorders in cows and heifers → 0.4 mg/ feed kg

88
Q
  1. ZEA in pigs
A

• Effects in pigs
▪ Folliculus theca cysts → 4-5 times more estradiol + estrogenic ZEA → expressed estrus, no eggs in ovaries
▪ Hypertrophy, hyperplasia and metaplasia of endometrium, metaplasia in epithelium of cervix
▪ Enlarged uterus, edematic endometrium, hemorrhages in the propria, enlarged and increased
number of uterine glands, fluid accumulation in the womb
▪ Infertility
● Inadequate ovarian function
● Disturbed implantation, early embryonic death
● Disturbed spermiogenesis

89
Q
  1. ZEA in poultry
A

• Ducks, geese, turkey and guinea fowl are sensitive, but egg production is hardly affected
• Males are sensitive
▪ Fatty degeneration of the upper cell layers of the germinal epithelium in the seminiferous tubules.
▪ Under long lasting effects → decreasing size of the testicles
▪ Fatty infiltration, local necrosis and calcification:
● In the sperms, Spermatids, Praespermids. Spermatocysts

90
Q
  1. Trychothecenes in ru:
A

In ruminants → due to speedy metabolism no practical relevancies.

91
Q
  1. Trychothecenes in pigs affect:
A
  1. Reproduction
  2. Metabolism
  3. immune system
92
Q
  1. Trychothecenes effect on reproduction in pigs:
A

• Reproduction
▪ Stoppage of the ovarian cycle
▪ Degeneration of the tertiary follicles
▪ Due to lack of estrogenic hormones and because no CL are formed → no progesterone produced
▪ As a result:
● Size of the uterus is smaller than normal
● Uterinal glands are atrophic
● There is no ovulation and the ovarian cycle stops, there is no return to cycle
● Gilts and sows loose appetite
● Sows frequently vomit and come hypo and/or agalactic
● Decreased rate of conception
● Increased culling rate of sows and gilts

▪ Joint effect of ZEA and TRI
● Return to heat beyond 21 days of service
● Increased rate of silent sows and gilts
● Decreased litter size
● Occasionally estrogenisms
● Sporadic abortions and early farrowings.

93
Q
  1. Trychothecenes effect on metabolism in pigs:
A 
• Metabolism
▪ Inhibition of protein synthesis 
▪ Thyroid → decreased size and decreased serum T4
▪ Increased adrenocortical activity:
● Feed refusal 
● Decreased weight gain
94
Q
  1. trychothecenes effect on immune system in pigs:
A

▪ Mechanism of effect:
● Direct toxic effect on immune cells → damage of the ribosomes
● Decreased production of cytokines, enhanced adrenocortical activity
● Increased production of glucocorticoids

▪ Effects on the immune system:
● Humoral immune response to both T- and B- dependent antigens decreases
● Decreased blastogenic response induced by specific antigens and by nonspecific mitogens
● Hindered delayed hypersensitive skin reaction
● Enhanced IgA production → immunocomplex formation → glomerulonephritis
● Decreased IgG and IgM production
● Lymphoid depletion in the primary and secondary immune organs
● Decreased macrophage activity

95
Q
  1. Consequences of Trychothecenes’s effects on the immune system (generally, not just pigs):
A

● Enhanced sensitivity of murines (rodents) to S. enteritidis infection
● Decreased resistance to S. typhimurium infection
● Increased sensitivity to A. fumigatus infection in rabbits
● Swine dysentery
● Increased sensitivity to CRD (Chronic respiratory disease – Avian Mycoplasmosis) in poultry.

96
Q
  1. trychothecenes effect in Domestic hens:
A

• Effects
1. Decreased egg production
2. Altered egg composition → vitamins, protein, lysosyme, Ca, Mn, Cu, Fe
3. Small decrease of eggs’ weight
4. Decreased pigmentation of eggs → “turkey eggs”
5. Effects on hatchability (decreases from about 85-90% to around 50% and sometimes even
5-10%):
● Strong contamination → early embryonic death
● Smaller contamination (decreasing amount – decreasing effect):
o Embryonic mortality around day 6 → “blood stained eggs”
o Embryo survives but too weak to break through the egg shell
o Chicken breaks through, but is weak, high mortality in the first week
6. Transient feed refusal, cannibalism may appear
7. Plumage becomes dry and fragile, cobs and wattles become pale
8. Libido of males is decreased

• Pathology = Follicle degeneration in the ovaries, Atresia of the follicles, Involution of the oviduct,
Amyloidosis of liver and spleen

97
Q
  1. trychothecenes effect in Broilers:
A
  • Clinical signs
    ▪ Decreased feed intake, decreased weight gain
    ▪ Watery faeces
    ▪ Delayed/incomplete feathering
    ▪ Dermatonecrosis → commissures of the mouth, tongue, palate, pharynx
    ▪ Sometimes neural symptoms, locomotor disturbances
  • Pathology = Degeneration of parenchymatic organs, Acute haemorrhagic liver dystrophy
  • Pathophysiology
    ▪ Lymphocyte depletion (thymus, spleen, peyer’s patches)
    ▪ Lymphocyte damages: caryorrhexis, pycnosis
    ▪ Bone marrow: damage of myeloid and erythroid cells
98
Q
  1. Fumonisins:
    - occurence
    - caused by
A

• Occurance → south Africa, but today everywhere in the corn belt (Midwestern US)

• Caused by Fusarium moniliforme, F. proliferatum, Alternaria alternate - Produces fumonisin B1, B2 and
almost 100 others

99
Q
  1. Effects of fumonisin toxins
A

• Fumonisin molecules are structurally similar to sphyngolipids
• Sphyngolipids are structural molecules in the cell membranes having a role in cell growth and
differentiation, and in the intracellular signal transmission
• Fumonisins therefore:
▪ Block the biosynthesis of sphyngolipids
▪ Lead to formation and accumulation of cytotoxic sphinganin

• General effects: neuro toxic, immune, carcinogenic, pulmonary edema (pigs)
• Effect on humans: Primer liver carcinoma, esophageal carcinoma
• Effect on horse: Equine leuko encephalomalacia (minimum 10 mg/feed kg)
• Effect on ruminants: <200 ppm → anorexia and mild weight lost
•Effect on pigs:
- Pulmonary edema
- fetopathogenic effect:
→ Expressed pulmonary edema, hydrothorax and hepato dystrophy
→ partial feed refusal, death within 5 days

100
Q
  1. Legal control of fumonisins:

- max. tolerable conc.

A

• Maximum tolerable concentration of Fumonisin B1 and B2 in daily rations of calves, lambs and kids younger than 4 months of age → 20 mg/feed kg

101
Q
  1. Aflatoxins:
    - produced by:
    - found in which products:
    - types and structures
A

• Produced by → Aspergillus flavus, A. parasiticus, A. niger
▪ In protein rich seeds, soybean, rice, coffee, maize and other cereals
• Aflatoxin B1 and B2 → coumarin ring condensed with bifuran and pentanon ring
• Aflatoxin G1 and G2 → coumarin ring condensed with lactone ring
• Aflatogin M1 and M2 → hydroxilated form in dairy cows (due to liver metabolism)

102
Q
  1. Aflatoxins:

• Effects

A

▪ Every species is susceptible to aflatoxins, but the degree is very different depending on the species

▪ Acute aflatoxicosis
● Clinical signs: anorexia, weariness, lilac red skin, ataxia, opisthotonus, hind leg stretching
● Histology: hepatic dystrophy, vacuolar degeneration and necrosis of hepatocytes, caryorrheis, pycnosis, haemorrhages
● Pathology:
o Abdominal hyperemia and edema
o Swelling and yellow colouration of liver with haemorrhage on the surface
o Swollen kidneys
o Pericardial serous fluid accumulation
o Catarrhal enteritis

▪ Subacute toxicosis
● Clinical signs: anorexia, weariness, decreased production
● Histology: proliferation of bile vessels, vacuolar degeneration of hepatocytes
● Pathology
o Liver → ↓size, fibrosis, cancer, definite yellow colouraion
o Fluid accumulation → SC, pectoral-abdominal cavity, pericardium

103
Q
  1. Ochratoxins
    - produced by:
    - most known:
A
  • Produced by → Penicillium verrucosu, Aspergillus ochraceus, A. carbonarius
  • They are dihydro-iso-cumarin derivatives bound to phenylalanine
  • Group of 7 compounds, the most known of which is Ochratoxin-A
104
Q
  1. Ochratoxins

• Effects

A

▪ Target organ → kidney
● Degeneration of the renal tubules and later → interstitial fibrosis
● As a result → insufficient tubular resorption → PUPD
● In addition makes susceptible for renal uricosis and precipitation of uric acid in the urethra
▪ Lymphocyte depletion in the lymphoid organs → hindered immune response?
▪ Calves are sensitive until full development of rumen

105
Q
  1. Ochratoxins

Species specific effects

A

● Pigs = OH-A is bound to albumin in blood, Nephropathy, Accumulation in lungs, liver, muscle, spleen, kidneys.

● Ruminants = Calves are sensitive until the rumen is fully developed, Metabolized by the rumen flora

● Broilers = Swollen, pale kidneys, Accumulation in kidneys

● Laying hens = Decreased egg production, Decreased hatchability

▪ Public health aspects → Balkan endemic nephropathy (mortality, kidneys reduced in size)

106
Q
  1. Ochratoxins

• Legal aspects

A

▪ Recommendation by the task force of the Hungarian academy of science → 0.20 mg/kg
▪ Human cannot be infected by consuming meat and milk, but through contamination of (for example) coffee.
▪ Ochratoxicosis poses a real danger in animal agriculture → calves, pigs, and poultry.

107
Q
  1. Main mycotoxin contaminants of cereals
A
  • Wheat → deoxnivalenol (DON)
  • Corn → T2 (Trichothecene)
  • Sunflower → Ochratoxin (OTA)
  • Bran → Deoxynivalenol, residue just under secondary epidermis layer → under bran layer
108
Q
  1. Regulations concerning mycotixin contamination of cereals:
    - classification:
A

Through analyzing concentration and composition → classified into A, B, C:
• A → either free from the 8 mycotoxins tested or peak concentrations were harmless ▪ Direct feeding, processing
• B → One or more mycotoxins at different concentrations → used with care ▪ Dilution with non-contaminated cereals ▪ Incorporated into feed of animals not sensitive to the mycotoxin
• C → extreme contamination → cannot be diluted below the critical level ▪ Excluded from all feeds

109
Q
  1. Effects of mycotoxins depend on:
A
  • Individual/herd sensitivity
  • Duration of exposure
  • Composition of contaminants
  • Dietary concentration
110
Q
  1. mycotoxins:
    - acts:
    - codex standards
    - recommendations by hungarian feed codex:
A
  • Acts: ochratoxin B1, Ochratoxin-A → legal consequences
  • Codex standards: fusarium toxins, ochratoxins → recommendation and orientation

Recommendations by the Hungarian feed codex
• Toxic concentration: brings about characteristic clinical and pathological symptoms
• Depressive concentration: depressed production with no characteristic clinical or pathological symptoms
• Tolerable concentration: lower than the depressive level

111
Q
  1. Prevention of mycotoxic infection in the period of vegetation
A
  • Use of fusarium resistant grains
  • Appropriate agro technology
  • Optimising of storing
112
Q
  1. Disinfection/decontamination from mycotoxins at harvest
A 
o Physical methods
▪ Air flow selection
▪ Washing
▪ De-hulling
▪ Heat treatment 
▪ Baking
▪ Autoclaving
▪ Microwave treatment

o Chemical methods
▪ Fungicide treatment → propionic acid + fumaric acid, sorbinic acid
▪ Destruction of toxins → Ca(OH)2, mono methylamine, ozone, chlorine gas, NH4+, H2O2, formaldehyde

• Best → combination of the physical and chemical methods

113
Q
  1. ways to decrease of the effects of mycotoxins:
A
  • Feeding with tolerant species
  • Dilution with non-contaminated feeds
  • Excess supplementation with vitamins, minerals and trace elements.

• Use of absorbents
▪ Zeolites, bentonites, charcoal, Na-K-Al-silicate, silicates + formic acid + Ca-propionate + antioxidants
▪ These do not bind a-polar mycotoxins
▪ Need big quantitiy

• Biological additives
▪ Primarily adsorption → Saccharomyces cerevisiae culture
▪ Adsorption + enzymatic effect
● Saccharomyces telluris
● Mycofix plus
● DETOXA 2000
• A mycotoxin neutralizing feed additive containing biologically active enzymes and adsorbents
• Suitable for disintegration of zearalenone, thrichothecene and fumonisine toxins in the digestive system

114
Q
  1. Examination of the microbiological-hygienic status of feed:
    - Indicator microorganisms
A

• Certain groups of saprophytes that characterize the general microbiological status of feeds and feed
mixtures and may refer to hazards of feeding.
• They are examined in routine control of feed mixtures, as follows:
▪ E. coli: indicates faecal contamination of the feed, which in turn may refer to contamination with
obligate pathogenic micro-organisms

▪ Coliforms, enterobacteria and enterococci: refer to the general hygienic status of the feed, they
may indicate earlier contamination with faeces, however they also may reflect the bad hygienic conditions of production, store, transport of the feeds.

▪ Total germ count (count of total mesophylic bacteria)
● May indicate general contamination of the feed with saprophyte aerobe microorganisms.
● Further analysis (morphology of colonies, microscopic examination) may reveal the source of contamination.

▪ Spore forming anaerobe putrefactive germs: refer to decomposition of nutrients by Clostridia in
aerobic circumstances

▪ Proteolytic bacteria: refer, besides the general contamination, to proteolytic activity of the mesophyll microflora

115
Q
  1. Indication of spoilage of feeds (spoilage indicators)
A
  • Store house moulds → Aspergillus, Wallenia, Scopulariopsis, Mucor
  • Mesophyl bacteria → Coagulase negative Staphylococci, micrococci, Bacillus spp.
  • Indicators of soil contamination → streptomycetas
116
Q
  1. Pathogens in feeds =
A 
→ all kinds 
• Frequent 
▪ Salmonella spp.
▪ Clostridium perfringens 
▪ Listeria 
▪ Campylobacter spp.
117
Q
  1. Water requirements of farm animals depends on:
A
  • Age, sex, lactation, form of feed (ex. Roughage, slop or dry feeding)
  • Dry matter intake (4-6 l/kg DM)
  • Temperature • Antibiotic content of the ration
118
Q
  1. Characteristics of good drinking water
A

Good drinking water is odour- and colourless, transparent, has pleasant temperature and is free from strange materials.

119
Q
  1. Physical characteristics of drinking water:
A

A. Taste and odour of the water is determined by soluble materials:
● Salt
● MgSO4 and NaSO4 makes the water bitter, NaNO3 lends a sweetish taste
● Iron content makes the water ink taste
● Humins (water from marsh lands) forms marsh taste ● Rotten materials in the water makes musty smell
● Water may have tar-, phenol or chlorine (over 0.3 mg chlorine content) odour
● In case of protein degradation the water may get a rotten egg smell due to H2S content.

B. Colour of the water
● Fe(OH)2 makes the water yellowish
● CaCO3 makes the water turbid
● Algae lends greenish colour

C. pH of the water
● Farm animals may refuse to drink waters that have pH ≤ 5 and ≥ 9.
● Alkali pH may refer to protein degradation and provides better condition for survival of
salmonellas and leptospiras
● Fish are extremely sensitive to pH

D. Solid content of the water → Sand and soil content may deposit in the rumen and intestines

120
Q
  1. Hygienic aspects of soluble materials in the water
A

A. Hardness of the water
● Changing hardness is caused by the calcium bicarbonate and Magnesium bicarbonate content and may be distracted from water by boiling.
● Stable hardness is caused by calcium carbonate and magnesium carbonate
● Total hardness = changing hardness + stable hardness
o German hardness: there are 4 categories: I. soft, II. Slightly hard, III. Medium hard, IV. Hard depending on the calcium oxide conc.
● Hard water may be responsible for urolithiasis, digestive disorders and forming
insoluble hard layers in water ducks.

B. NaCl causes no problems.
Chickens are the most sensitive among farm animals.

C. Iron and Manganese content
● Iron salts over 0.5 mg/l may decrease the production (fish are extremely sensitive)
● High Iron and manganese content helps the multiplication of iron-manganese bacteria in
fish ponds → suffocating of fish through covering of brachiae.

Poisonous materials
● Lead may cause chronic poisoning even at small concentration (≤0.1 mg/l!)
● Fluorine may be present in waters in industrial areas o At 1-5 concentration → fluorosis (spots on dental enamel)
● Copper may poison sheep → contamination with manmade fertilisers.
● Arsenic causes poisoning in farm animals
● Saponines.

121
Q
  1. Hygienic aspects of water contaminants
A

A. Ammonium results from degradation of organic materials, and indicates faecal or other organic pollution. Origin should be traced by on the spot examination.

B. Nitrites also indicate fresh contamination with organic materials

C. Nitrates are the final oxidation product of decomposing nitrogen containing organic materials.
● Nitrite + Nitrate → Methaemoglobinaemia of cattle and pigs at ≥ 250 mg/l

D. Oxygen consumption of water
● Chemical oxygen consumption indicates the amount of oxygen (mg) requested for complete oxidisation of all organic materials present in 1 l of water
● Biological oxygen consumption is the amount of oxygen (mg) requested for oxidisation
of organic material in 1 l of water within 3-5 days
● Measured by potassium permanganate oxidation

122
Q
  1. Water as vector for infectious diseases
A

A. B. anthracis → in mud spores live over 40 years
B. Human diseases → typhus, paratyphus, cholera
C. Salmonellas in surface waters of overcrowded duck farms
D. Leptospiras → prefer alkali pH
E. Pseudomonas spp. → disease in animal with decreased resistance (Pneuomnia, pleurisy, G.I
inflam.)
F. Mycobacterium, Brucella spp. and Pasteurella spp.
G. Viruses → FMD, swine fever, etc…
H. Parasite eggs
❖ Presence of E. coli indicates faecal contamination
● Coli count → number of colonies cultured from 100 ml of water
● Coli index → the least amount of water (ml) that contained 1 colony forming unit of E. coli

123
Q
  1. Cleaning and disinfecting of water
A

• Solids → by sedimentation and/or filtration
• Microorganisms → By adding compounds of active chlorine content
▪ Cl2 + H2O = 2HCL + “O”
▪ 50-60 g chloride of lime/m3

124
Q
  1. collection of water samples:

- how to do it

A 
A. Field inspection of all relevant factors that may be connected to water quality
▪ Water sources
▪ Equipment
▪ Probable sources of contamination
▪ Vocal questionnaire

B. Collection of the sample
▪ Spot sample → taken from one place at a given time
▪ Average sample in time → mixture of samples taken from a given spot in successive time

C. Sample collection for chemical examination
▪ Into glass or plastic bottles that had been carefully cleaned and rinsed with distilled water.
▪ Bottles are closed by glass, rubber or cork stoppers that had been cleaned, sterilised and rinsed
with distilled water.
▪ In case of examination for the presence of heavy metals, stoppers should be made of the material of the bottle!
▪ When the compounds to be determined are influenced by aerial oxygen, the sampling bottle should be filled up with the water several times, then finally filled up and closed by a stopper with the minimum air between the surface of the water and the bottom of the stopper.

D. Sample collection for bacteriological examination
▪ Glass utensils should be sterilised by hot air (160oC for hours)
▪ Rubber stoppers should be sterilised by boiling water for 20 minutes.

125
Q
  1. Physiology of stress
A

Organism exposed to constant environmental effects
Maintenance of internal environment
- Organisms avoid stimuli that would shift equilibrium
- Defence mechanisms is put into force if stimuli (endogenous, exogenous) is very strong and may disturb internal equilibrium (Noxious stimuli)
o Specific response: Specific AB against special viruses.
o Non-specific: when specific response is not available. Same to every stimulus.
= “Stress reaction,” or “GAS: General adaptation syndrome”

126
Q
  1. Mention different stressor groups and examples
A
  1. Physiological stressors: Mechanical stimuli, Electricity, Radiation, Temperature(heat/cold stress), Weather, Limitation of movements
  2. Pathogenic stressors: virus, bacteria, parasites
  3. Feeding stressors: irregular feeding, deficiencies (vit, min, trace elements), intoxifications
    - Deficiencies (vit, min, trace elements): required for proliferation of protecting cells and immune cells (APP, antibodies, cytokines, antioxidants) = Important defence mechanisms against infections, oxidative stress etc.
  4. Emotional stressors: Pain, lack of stimuli
  5. Management: excessive noise or light, bad microclimate, high population density (dominant animals, movement restrictions etc), transportation, iatrogenic ACTH, surgical interventions
    (castration etc)
127
Q
  1. Phases of stress
A
  1. Initial stage: Release of ACTH immediately. Often, but not always, accompanied by Cannons alarm reaction. Effect of cathecholamines declines within a few minutes, but ACTH level remains high.
  2. Resistance: able to resist the stressors. Glucocorticoids in high amounts (Cortisole, corticosterone – interspecies differences)
    = long lasting mobilization of energy reserves of body.
    A. Immune system inhibited: inhibition of inflammatory agents (Eicosanoids, bradykinin, histamine, collagenase) and immune mediators (IL-1, IL6, interferon, TNF) Predispose to germ related multifactorial disease
    B. Mobilization of glucose + anti-insulin effect —> steroid induced diabetes mellitus
    C. Proteins catabolized for GNG (muscles decomposed)
    D. Lipid: redistribution of fat to liver (fatty liver), lipolysis E. Energy need: covered by burning of fat
    F. Hormonal:
    - Production of glucocorticoids —> Negative feedback on CRH, ACTH
    - Production of sex steroids (E2, Testosterone, P4) –> Negative feedback to FSH and LH
    - Decrease TSH, GH

If stressor persist, it is two possibilities:
3. Exhaustion: E reserves are used up à collapseà Death 4. Adaptive disorders: ulcers, chronic hypertension, hepatic failure etc due to long term
glucocorticoid

128
Q
  1. Factors influencing how an animal perceive a stimulus:
A

experience, genetics, age, physiological state.

These factors modify the animals organization of its biological defefences

129
Q
  1. There are 4 biological defence mechanisms available, but not all four are necessarily utilized by the animal.
A
  1. Behavioral response: most economical response. Comes at a lower cost to the animal than activation of the other stress defence systems. Not approproate for all stressors.
  2. Autonomic nervous system response: fight or flight (cannon stress response), short acting response
    o Cardiovascular: changes in heart rate, blood pressure
    o GI: decreased GI activity
    o Adrenal gland: Catecholamines
  3. Neuroendocrine response: Long acting response. HPA – hypothalamic-pituitaryadrenal axis
  4. Immune response: Immune system suppressed by HPA axis, but also that immune system in its own right is one of the major defenses responding to a stressor.
130
Q
  1. Animal welfare ↔ Food safety
A 
• Rights: stand up, lay down, stretch, turn around, groom 
• Webster’s 5 freedoms: 
▪ From thirst, hunger, malnutrition
▪ From discomfort 
▪ From pain, injury, disease 
▪ To express normal behaviour
▪ From fear and distress •

Animal welfare is an attribute of the animal and not of external circumstances:
▪ Adaptive capacity towards environmental challenges
▪ Good ➔ Mental and physical stability
▪ Bad ➔ ↓production, reproduction failure, diseases, mortality

131
Q
  1. Measurement of factors of welfare:
A

• We can measure welfare with objective methods, without moral or ethical consideration
• Needs
▪ Basic – biological demands
▪ Provision of means to meet biological demands
● All resources of the organism to destroy infectious agents and to prevent tissue damages and pathogenic events are available resources and depend to a large extend on animal welfare

132
Q
  1. Diagnosis of stress:
A

Challenges in how to measure stress and distress.
- Diff btw non-threatening stresses (good stress) and threatening stress response (Bad stress, «distress»)
Key to differentiate is the biological cost of stress

  • We have relied on a variety of endocrine, behavioral, autonomic nervous and more recently immunological ways to measure stress. Unfortunately, none of these measures have proved to be a litmus test for stress:
    o Individual variability of stress response
    o Term stress are loosely applied to many situations. It is unreasonable to expect that a single indicator of stress will be appropriate for all type of stressors
    o Cannot be used to diff btw non-threatening stress and distress
    o Even more problematic when we attempt to evaluate stress outside laboratory settings
    o No specific tests that applies to all stressors.
    o There are 4 biological defence mechanisms available, but not all four are necessarily utilized by the animal.
    o Identify factors influencing how an animal perceive a stimulus (experience, genetics, age, physiological state)
    o No way to account for each animal prior experiences, its social relationship with its or its genetic predisposition
  1. Behaviour: may provide potential clues to distress. Unfortunately, our current lack of
    undertanding of behaviour of animals during stress limits value of using behavior as a means for predicting distress
  2. Autonomic response: automonic responses affect very specific biological systems and the biological effects are of relatively short duration. Very difficult to measure the system response.
  3. Neuroendocrine response: technical challenges of measuring these systems who stresses the animals.
133
Q
  1. Management of stress
A

Stress is unavoidable, we can never expect to develop conditions that will always keep out animals stress free.
But we can try to maintain a more or less constant environment, with set feeding time, no overcrowding, constant normal temp. good quality food, etc.

134
Q
  1. The concept of germ load
A

▪ Saprophytes
● Gram positive obligate anaerobes (lactobacilli, bifido bacteria)
● Gram negatives (fusobacteria)
● Obligate and symbiota yeasts
▪ Facultative pathogen germs: E. coli, haemophylus spp., mycoplasma spp., salmonella spp.
▪ Under normal conditions:
● The internal microbiological environment keeps balance with the germ load (external environment)
● The rate of multiplication and rate of mortality of germs within the organism is controlled by the defense mechanisms and keeps balance.
▪ However this balance might be overruled, which gives way to excessive multiplication of certain
germs leading to germ related multifactorial disease

135
Q
  1. Factors contributing to germ load
A

▪ Number of germs in the environment
● Cleaning and disinfection of stables and operation of stables (all in-all out)
● Tenacity (persistence) of germs
▪ Composition of the micro-flora
▪ Virulence of germs in the environment (virulence markers → pylus antigens, villi)

136
Q
  1. Germ load depends on the characteristics of the germ
A

▪ Resistance of the germ
▪ Quantity requested for infection
▪ Immune inductive capacity
▪ Spreading features of the germ → ventilation, feeding system, population density
▪ Therefore all housing, feeding, management and handling factors contribute to the establishment of germ related multifactorial disease:
● Increasing the number of germs in the environment ● Help increasing virulence of population
● Facilitate the change of the composition of the microflora

137
Q
  1. Reducing the germ load can be done by:
A

▪ Regular cleaning, all in – all out
▪ Rational control of population density and air volume per animal
▪ Reduced number of animals per compartments
▪ Improvement of ventilation
▪ Use of wet feeding versus dry feeding
▪ Controlled air temperature

138
Q
  1. Definitions of unifactoral and multifactoral diseases:
A
  1. Unifactoral disease: one definite reason (infectious disease, poisoning, injuries, deficiency)
  2. Multifactoral disease (and polyfactorial disease, technopathies, management related diseases, production diseases): more than one, interacting reasons. Causative agents and factors of disposition (environment)
139
Q
  1. Non-infectious multifactorial disease
A

Most of reproductive disorders

  • Poultry —> Breast blister, twisted leg syndrome, tyrkey syndrome 65, tibial dyschondroplasia, curled toes disease, pododermatitis
  • Farm animals —> Fat mobilization syndrome, Acid-base disturbances
140
Q
  1. Infectious multifactorial disease (germ related)

- consequences:

A
  • Huge economic loss
  • Endemic
  • Special prevention methods needed. Heard health programmes
141
Q
  1. Infectious multifactorial disease examples in different species:
A
  • Bo: E-coli diarrhea, BRDC, Mastitis
  • Su: E-coli diarrhea, peri-weaning intestinal disorders, MMA syndrome, Salmonellosis, Chronic respiratory disorders, mycoplasma pneumoniae, arthropic rhinitis, pasteurellosis, streptococcus
  • Poultry_ Necrotic enteritis, CRD, rheovirus infection
142
Q
  1. Interaction btw housing - management factors and the germ load
A

Housing condition (ventilation and temperature, feeding, population density, cleaning and disinfection) may contribute to the establishment of germ related multifactorial disease due to:

  • Increase concentration of germs
  • Increasing virulence of germ - Facilitate change of composition of microflora

Reduction of germ load

  • Regular cleaning and disinfection. All in-all out
  • Proper ventilation and controlled air temp - Control of population density
  • Feeding: Wet feeding vs dry feeding (aerogen germs?)
143
Q
  1. Interaction btw housing- management and defence mechanisms
A
  • Skin: dense and stable residential flora forming barrier against invading microorganisms
  • –> Composition is regulated by desquamation, desiccation, low pH of sebum.
  • In wet and humid conditions the structure of the skin breaks down, flora changes à predispose to infections
  • GI tract: o Eubiosis:
    § Produce essential vit
    § Decompose: non-absorbed nutrients
    § Challenge: immune system
    § Prevent: adhesion of pathogenic germs
    • Physical properties: flushing activity (saliva, bile), intestinal motility
    • pH: low gastric pH (bacteriocida, virucidal effect)
    • Macrophages and other phagocytic cells + lysosome (antibacterial, antiviral enzymes)
    o Dysbiosis: stress (decreased intestinal motility), increased gastric pH, mass intake of feed microbes (spoiled feed etc) —> proportional of escort and residual flora increases (E-coli, Salmonella, clostridium, pseudomonas etc)
    —> Decrease production + digestive disorders
  • Urinary system
    o Flushing of low pH urine
    o Vagina: desquamation, high glycogen content (substrate for lactobacilli, increased lactic acid production, decreased pH)
    o —> Urinary stasis (stress, low physical activity, over condition)> Ascending infection
  • Respiratory tract
    o Non-specific
    § Control of nasal cavity: air turbulence, control of temp and humidity, adsorption of harmful gases
    § Mucociliar escalator system: ciliary movements, glands and goblet cells. § Alveolar macrophages: phagocytosis, PG, IF and LT production § Antibacterial substances: lysosomes, lacroferrin, transferrin, complement
    § K-cells: produce vasoactive lung peptides —> vasomotor control of lung, histamine and serotonin production
    § Clara cells: non-ciliated cells in epithel of bronchioles à degradation
    of inhaled toxins, pesticides, carcinogenic material
    § à Environmental effects influencing coordination of cilium, quantity and quality of mucus, activity and number of macrophages and other cellular components affecting the non-specific defence mechanisms of respiratory tract
    • Low temp —> increased heat loss –> Thermoregulation important
    • Air quality —> Proper ventilation required
    o Low humidity: Decreased humidity of air —> decreased motility of cili, increased dust
    o High dust content
    o High NH3 –> damage, paralyse the mucociliar escalator system
  • Mammary gland
    o Flushing effect
    o Phagocytic cells
    o Bacterial inhibitors: lysosomes, lactoferring, lactoperoxidase etc
144
Q
  1. Nonspecific defense mechanisms include…
A

the skin, mucous membranes, secretions, excretions, enzymes, inflammatory responses, genetic factors, hormonal responses, nutritional status, behavior patterns, and the presence of other diseases.

145
Q
  1. Challenges of large scale farming
A
  1. Increasing consumer demands in both quality and quantity
  2. Decreasing land space for farming
  3. Increasing pressure for reducing emission - Limited availability of labor (workers)
  4. Increasing cost of production
  5. Climate change
  6. Appearance of new animal and zoonotic diseases as well as more stricter regulation for use of antibiotic
  7. Increase pressure for animal welfare
    With these challenges, detailed monitoring is needed to ensure welfare and health of animals and high-quality product to consumers to reach desired profitability
146
Q
  1. Moniotoring of environment and animals in large scale farm:
A

Environment

  • Micro-climate: Temp, solar and thermal radiation, ventilation (air velocity, air quality, RH sensor) and light
  • Feed: quality and quantity
  • Water: quality and quantity

Animal
- Productivity: yields, costs, return of investments
- Reproduction: reproduction rates, costs, signs of heat
- Health:
o Prevalence of diseases
o Body condition, temp, RR, HR, Rumination, cough
o Feces and urine
o Behavior and activity
o Locomotion

Animal hygiene (2 decks)

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