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Year 1/2 > FTK 4: LA Feed & Water Toxicosis > Flashcards

FTK 4: LA Feed & Water Toxicosis Flashcards

1
Q

to determine the RISK of feed toxicosis, we should examine WHAT 2 THINGS?

A
  1. CLINICAL SIGNS of animal
  2. what is in feed & if they can CAUSE FEED TOXICOSIS
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2
Q

3 main sources of feed toxins? w/ examples

examples for human-related one

A
  1. NATURAL factors
    –> when plants CONCENTRATE substances to PROTECT FROM INSECTS
    –> ex = nitrate
  2. HUMAN ERROR or MALFEASANCE
    –> = either EXCESS FACTORS IN FEED or FED TO WRONG SPECIES
    –> insecticide/herbicide added
    –> monensin in feed meant for sheep
    –> melamine substitution for protein
  3. INFESTATION PRIOR TO OR AFTER HARVEST
    –> mycotoxins
    –> bacterial toxins
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3
Q

what 2 things should we do if we see clinical signs in animal consistent with FEED TOXICOSIS?

A
  1. sample feed
  2. investigate environment
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4
Q

if we suspect a toxin…
history? (2)
epidemiology? (1)
diagnosis (3)?

A

history?
1. outbreak in MULTIPLE animals in a group
2. usually NOT connected to a known agent

epidemiology?
1. usually SUDDEN course

diagnosis?
1. clinical signs & PE
2. POSTMORTEM exam of lesions, rumen & ingest & SUBMIT TO LAB
3. **SAMPLE FEED FOR TOXINS –> can be hard to get good sample or may be gone by the time we test

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5
Q

4 main MYCOTOXINS found that can cause FEED TOXICOSIS?

A
  1. aspergillus
  2. penicillium
  3. fusarium
  4. claviceps
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6
Q

ASPERGILLUS mycotoxin subsets (3)
limits to food production? (only true for one of them)
target tissue/role?
source?

A
  1. AFLATOXIN
    food production?
    –> must have LESS THAN 20 PPM in FEED
    –> must have LESS THAN 5 PPM in MILK

target tissue/role?
–> liver CIRRHOSIS/CANCER when eaten in high amounts

source?
–> corn, peanuts

  1. OCHRATOXIN A
    target tissue/role?
    –> RENAL TUMORS (nephrotoxic)

source?
–> grain

  1. TREMORGENS
    **technically ASPERGILLUS + PENICILLIUM

target tissue/role?
–> CNS TREMORS

source?
–> MANY

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7
Q

FUSARIUM mycotoxin (5)
for the first one…
appearance?
unique characteristics?
when is risk HIGHEST?

for the rest?
target tissue/role?
source?

A
  1. DON or VOMITOXIN
    appearance?
    REDDISH MOLD on Gibberella ear corn

unique characteristics?
HEAT-STABLE during FOOD PROCESSING/ETHANOL PRODUCTION

when is risk HIGHEST?
IN WET COOL WEATHER DURING SILKING

target tissue/role?
VOMITING & other serious affects

source?
–> corn, barley, wheat, oats

  1. TRICOTHENES (T2 toxin)
    target tissue/role?
    –> MANY ORGANS SUPPRESSED

source?
–> grain

  1. ZEARALENONE
    target tissue/role?
    –> ESTROGENIC, pigs susceptible

source?
–> grain

  1. FUMONISIN
    target tissue/role?
    –> EQUINE LEUKOENCEPHALOMALACIA, causes IMMUNOLOGICAL issues

source?
–> MOLDY CORN, cereal grains

  1. 4-IPOMEANOL
    target tissue/role?
    –> RESPIRATORY BOVINE PULMONARY EDEMA & EMPHYSEMA

source?
–> MOLDY SWEET POTATOES

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8
Q

PENICILLIUM mycotoxins (2)

A
  1. CITRININ
    target tissue/role?
    –> KIDNEYS

source?
–> MANY

  1. TREMORGENS
    **ASPERGILLUS & PENICILLIUM

target tissue/role?
–> CNS TREMORS

source?
–> MANY

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9
Q

CLAVICEPS mycotoxins (2, but same target tissue/role & source)

A
  1. ERGOT (Claviceps purpurea) & ENDOPHYTE FUNGI

target tissue/role?
–> agalactia
–> gangrene
–> ryegrass staggers = neurological, falling over

source?
–> rye/fescue
–> can live in ryegrass SEEDHEADS

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10
Q

how do we control MYCOTOXINS via…

harvest practices? (4)
altering grains? (3)
things we can do to animals themselves? (3)

A

HARVEST PRACTICES

  1. CROP ROTATION
  2. Reduce INSECT infestations via INSECTICIDE
  3. FUNGICIDE application
    –> particularly good for CORN fields
  4. DRYING METHODS at grain harvest

REDUCING TOXIN LOAD IN GRAIN
1. AMMONIATION
2. ALKALI or ACID
3. HEATING

PREVENT ABSORPTION OF MYCOTOXINS in ANIMALS
1. YEASTS
2. ENZYMES
3. CLAY-BINDERS

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11
Q

which 3 mycotoxins are regulated by the FDA? what type of crop are they in?

3 levels & what they mean?

A

3 mycotoxins = aflatoxin, vomitoxin, fumonesin; IN GRAIN

3 levels…
1. ADVISORY = MAXIMAL amount of toxin allowed with NO HEALTH RISKS

  1. ACTION = when toxin has KNOWN HEALTH EFFECTS, so LIMIT sellable grain due to DISEASE
  2. REGULATORY = LIMITS to amount of sellable grain after PUBLIC NOTICE/DISCUSSION
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12
Q

gossypol
= what it is
what 2 species it affects? what’s their tolerance in ppm?
what species it DOESN’T affect/why? how much can they tolerate?
3 common toxic effects?

A

= natural toxin in COTTON SEED to PROTECT PLANT FROM INSECTS that is contained in SMALL RESIN SEEDS

affects SWINE & POULTRY, need LESS THAN 100 PPM IN FEED

DOESN’T affect RUMINANTS because RUMEN PROTEINS CAN BIND IT –> tolerate up to 400 PPM

3 toxic effects?
1. liver toxicity
2. heart failure
3. myocardial degeneration

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13
Q

nitrate toxicity
= what it is
3 sources?
etiology of how nitrate becomes toxic? (5)
clinical signs? (4) + **PATHOGNOMONIC
treatment & at what dosage?
nitrate toxicity from WATER?

A

= when animals consume EXCESSIVE NITRATE from crops/manure

3 sources?
1. TOXIC PLANTS (Pigweed, Lamb’s Quarter, Johnson Grass, Jimson Weed)
2. Excessive animal manure/fertilizer in crops
3. WELL WATER

etiology?
1. nitrate becomes NITRITE (NO2) from BACTERIA & ENZYMES IN MOUTH
2. NITRITE IS 10X MORE TOXIC THAN NITRATE
3. nitrite then GOES INTO RBCs and EXCHANGES ITSELF FOR Cl ions
4. Forms METHEMOGLOBIN + NITRATE
5. INHIBITS O2 BINDING/RELEASE TO TISSUES –> HYPOXIA

clinical signs?
1. difficult/rapid breathing
2. weakness
3. CYANOTIC MEMBRANES
4. CHOCOLATE-COLORED BLOOD***

treatment?
= IV 1% METHYLENE BLUE given at 4 mg/pound of body weight

in WATER…
- likely from SHALLOW WELLS
- LESS THAN 100 PPM IS SAFE, but 100-300 ppm is QUESTIONABLE in cattle

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14
Q

prussic acid toxicity
= overall definition
pathogenesis? (2)
clinical signs? (4)+ pathognomonic
treatment (mixture of 2 things)?
lethality?

A

= occurs when HEAT-TOLERANT PLANTS (sorghm, sudangrass & hybrids) undergo FALL FROST INJURIES/CUTTING/TRAMPLING that initiates chemical dhurrin to be CONVERTED TO PRUSSIC ACID (hydrocyanic acid) that contains a CYANIDE component

pathogenesis?
1. Prussic acid toxicity HALTS CELLULAR RESPIRATION & REDUCTION OF O2 TO H2O
2. O2 doesn’t go into tissues & stays in circulation, so VERY OXYGENATED BLOOD (CHERRY RED BLOOD)

clinical signs?
1. difficult/rapid breathing
2. muscle tremors
3. OXYGENATED MEMBRANES
4. **CHERRY-RED BLOOD

treatment?
= Mixture of SODIUM NITRATE + SODIUM THIOSULFATE

lethality?
usually kills WITHIN A COUPLE HOURS

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15
Q

3 ways to prevent prussic acid toxicity? a rule of thumb?

A
  1. Remove animals from grazing
  2. GIVE (cured) HAY = prussic acid content in sorghum hay decreases ~75% from curing
  3. SILAGE = plants that might have prussic acid have POISON ESCAPE VIA GAS during FERMENTATION

**WAIT 3 WEEKS BEFORE FEEDING HAY/SILAGE

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16
Q

non-protein nitrogen
= definition
4 common sources?
how to ruminants METABOLIZE NPN? (3)
3 syndromes associated with EXCESS NPN?

A

= nitrogen NOT derived from AMINO ACIDS

sources?
1. AMMONIA from FERMENTED SILAGES
2. FERTILIZERS
3. FEED-GRADE UREA
4. LUSH PASTURES (that have been recently fertilized)

ruminants METABOLIZING NPN…
1. UREASE will convert DIETARY NPN into AMMONIA
2. AMMONIA then CAPTURED with carbohydrate-derived keto-acids to form AMINO ACIDS via MICROBES
3. EXCESS ammonia will DIFFUSE THROUGH RUMEN WALL & be converted into non-toxic UREA via LIVER

3 syndromes…
1. SUDDEN DEATH from ammonia toxicity
2. SUBCLINICAL TOXICOSIS that causes IMPAIRED FERTILITY
3. BOVINE BONKERS = CNS disorder from ammoniated FORAGE

17
Q

3 things that influence ABSORPTION of rumen ammonia

A
  1. can utilize up to 40% of crude protein as NPN, but NO MORE THAN THAT
  2. if rumen pH >7, SLOW absorption of UREA & prefers NH4+
  3. if NOT on NPN diet, then must INTRODUCE OVER 5-7 days (ADAPTATION PERIOD) to avoid FATALITY
18
Q

ammonia toxicosis
how does it occur?
3 parameters in blood?
4 clinical signs?
diagnosis? & which one is definitive**? (3)
2 main treatment options?
what treatment should we then do if neither 2 are sufficient?

A

= occurs when amount of EXCESS AMMONIA is TOO GREAT FOR LIVER TO CONVERT TO UREA

3 parameters?
1. SUBCLINICAL TOXICITY = .4 mg/dL
2. CLINICAL SIGNS & TOXICITY = >1 mg/dL
3. CLINICAL SIGNS & DEATH = >2 mg/dL

4 clinical signs?
1. restlessness/excitability
2. colic
3. bellowing
4. hyperthermia

diagnosis?
1. history
2. FEED ANALYSIS for NPN
3. RUMEN ANALYSIS** –> PRESERVE WITH STRONG ACID (mercuric chloride), if rumen ammonia >80 mg/dL and pH >7, MORE DEFINITIVE

treatment?
1. LARGE VOLUMES OF WATER added to RUMEN
–> at 40 F to SLOW UREASE ENZYME conversion of NPN –> AMMONIA
–> 20 L

  1. 5% ACETIC ACID ADMINISTRATION to help drop pH
    –> 2-6 L in cattle
    –> .5-1 L in sheep

IF NEITHER WORKS, THEN DO RUMENOTOMY TO REMOVE NPN MANUALLY

19
Q

PREVENTION of ammonia toxicosis (3)?

A
  1. LIMIT NPN TO 1/3 of CP REQUIREMENT so only 33% max NPN rather than 40% max
  2. Urea?
    –> Can be 3% of grain mix on dry matter basis
    –> Can be 1% total ration
    –> Less than .5 g/kg of body weight
  3. Biuret?
    –> 3% of grain mix
  4. Ammonium salts?
    –> .75 to 1.5 oz/head/day
20
Q

ionophore toxicity
3 reasons why ionophores are added to feed?
what does ionophore toxicity cause?
2 big ionophores?
effects in…
calves?
horses?
sheep?
chickens?

A

3 reasons?
1. INCREASE FEED EFFICIENCY
2. IMPROVED WEIGHT GAIN by changing RUMEN dynamics
3. CONTROL COCCIDIOSIS

ionophore toxicity causes disruption of ION transport

2 big ionophores?
1. monensin
2. lasalocid

effects in…
CALVES = recommended only 1 mg/kg of LASALOCID, otherwise can cause TOXICITY –> SEIZURES

HORSES = MOST sensitive to MONENSIN & LASALOCID, tolerate SMALLEST doses

SHEEP = can tolerate MORE MONENSIN than horses, DO NOT GET LASALOCID

CHICKENS = CAN TOLERATE HIGH MONENSIN & LASALOCID

21
Q

acute bovine pulmonary emphysema & edema
= definition
2 common history findings?
etiology? (2)
what disease can it then cause? what do we see grossly with it?

A

= sudden onset of RESPIRATORY DISTRESS due to ingestion of purple (perilla) mint or MOLDY SWEET POTATOES

2 history findings?
1. 5-10 days on LUSH pasture
2. INGESTION of potatoes/mint

etiology?
1. L-TRYPTOPHAN present in forage gets CONVERTED into 3-METHYLINDOLE, which is TOXIC
2. 3-methylindole GOES TO BLOOD & LUNGS as a PNEUMOTOXIN

disease?
ATYPICAL INTERSTITIAL PNEUMONIA

grossly?
see SUBCUTANEOUS AIR

22
Q

water accounts for ___ to ___ % of a cattle’s body weight & they ___ have access to unlimited water

A

50, 80, should

23
Q

salt toxicosis
DANGER for giving water again after salt toxicosis?
4 clinical signs?
treatment?
2 sequelae?

A

DANGER?
RAPID introduction of water will DECREASE serum Na levels and cause INTRACELLULAR WATER to FLUX INTO NEURONS –> CEREBRAL EDEMA

4 clinical signs?
1. belligerent/aggressive
2. blindness
3. extreme thirst
4. chewing motions

2 sequelae?
1. DRAGGING hindfeet
2. KNUCKLING at FETLOCK joint

24
Q

cyanobacteria toxicosis
when/where are blooms MOST likely?
blooms contain WHAT 2 kinds of toxins that are LIKELY TO CAUSE UBIQUITOUS SUDDEN DEATH?
4 clinical signs in LIVESTOCK?

A

blooms most likely in HOT, DRY, SUNNY WEATHER in LAKES/PONDS

contain NEUROLOGICAL & LIVER toxins

4 clinical signs?
1. lack of coordination
2. labored breathing
3. diarrhea
4. death

Year 1/2 (139 decks)

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