18 – Toxic Range Plants I Flashcards
1
Q
What are some of the key factors affecting livestock plant poisonings?
A
- *MANAGEMENT ISSUES
o Overgrazed pasture
o Many toxic plants are first to emerge in spring
o Lack of alternative feed - *in general: they will NOT consume toxic plants if there is adequate good quality feed available
- Stress conditions can cause toxic plants to accumulate
- Very few confirmatory diagnostic tests available (rely on clinical signs, plant ID in rumen/stomach contents)
2
Q
What are the plants that cause acute respiratory distress?
A
- Fog fever
- Nitrate
- Cyanide
3
Q
Fog fever
A
- Acute bovine pulmonary emphysema and edema
- *associated with movement of cattle from DRY TO LUSH PASTURES
o Abrupt feed transition OR also in feedlot cattle - Most at risk: >2 years old in good body condition
o Beef more than dairy
o Not in calves - Target organ: LUNGS
- Mechanism: L-tryptophan converted to 3-methylindole by rumen microbes=damage to type I pneumonocytes and Clara cells
4
Q
Fog fever: clinical signs
A
- Onset within 12 hours of consuming lush forage
- **follows 5-10 days after movement to new pasture!
o Multiple animals affected - Mild-moderate dyspnea and coughing=most (self-limiting)
- Severely affected
o Expiratory grunt
o Severe dyspnea, rapid breathing
o Mouth breathing, tongue extension
o Wide-based stance
o Progress to sternal recumbency and death (within 2-3 days)
o Up to 50% morbidity, 25-50% mortality
5
Q
Fog fever: necropsy
A
- Lungs fail to collapse
- Edema and emphysema
- Caudal dorsal aspects (why called atypical)
6
Q
Fog fever management
A
- No effective treatment
- Often unrewarding: NSAIDs, diuretics, bronchodilators
7
Q
Fog fever: DDx for acute dyspnea/respiratory distress
A
- Nitrate
- Cyanide
- Urea
- OP/carbamates
- Larkspur
- *rule out infectious causes: PCR, culture, histo
8
Q
Fog fever: prevention
A
- Limit use of lush pasture
- Feed hay before pasture turnout
- Monensin supplementation
9
Q
Nitrate poisoning
A
- *typically FORAGE RELATED
o Normally accumulates in lower stem > upper stem > leaves - If enough time in rumen: nitrate to nitrite to ammonia for protein synthesis
- Lots of plants that accumulate nitrate (many weeds and forages, get a GOOD HISTORY ON WHAT THEY ARE EATING)
10
Q
What are the factors affecting nitrate accumulation?
A
- Most accumulation in lower stalks and stems
o Highest risk: hay cut during a nitrate accumulation period (**DOUGHT, FREEZE/THAW=conditions of decreased photosynthesis)
o *GREEN FEED OATS, OAT HAY
o *STUBBLE FIELDS: CANOLA, CORN - Young plants>mature plants
- Nitrates do NOT dissipate with cutting
11
Q
Nitrate poisoning: mechanism and toxicity
A
- Target organ: *RBCs
- Mechanism: oxidation of hemoglobin=METHEMOGLOBIN (inability to carry O2)
- *ruminants most SENSITIVE
12
Q
*Why are ruminants most sensitive?
A
- Have a normal pathway that is overwhelmed
- Rate limiting step: NO2 (nitrite) to ammonia
o Nitrite 10x more toxic than nitrate - Cattle > sheep > goats»_space;>monogastric animals
13
Q
Nitrate levels associated with poisoning?
A
- *dry matter basis
- If pregnant=want even less
- <0.15% is safe
- *anything over 1% is potentially fatal (=10,000ppm)
14
Q
Nitrate poisoning: clinical features
A
- *SUDDEN DEATH
o Multiple cattle found dead after introduction of new feed or after grazing stressed forages - Sublethal poisoning in pregnant animals: abortion
- Acute toxicosis (>50% MetHb): RESPIRATORY DISTRESS SECONDARY TO ASHPYXIATION
o *chocolate brown blood
o Weakness
o Polyuria
o Discoloured MM: brown/muddy
15
Q
Nitrate poisoning: management
A
- MEDICAL EMERGENCY
- Antidote: methylene blue: reduces MetHb to Hb
o Often NOT available in sufficient quantities and can be a food residue issue - Remove animals from suspect pasture/suspect feed, minimal handling
o Can consider infusing cold water into rumen (stressful!)
16
Q
Nitrate poisoning: diagnosis
A
- Antemortem: MetHb in WHOLE BLOOD (test not readily available)
o Nitrate/nitrite in blood: short half life - PM: OCULAR FLUID (ex. fetal ocular fluid, or just submit the whole eye)
o More stable than blood=not as likely to miss the conversion - Test suspect feed (>1%, 10000ppm) and water (>450ppm)
- Rumen contents are NOT useful due to PM bacterial conversion
17
Q
Nitrate poisoning: prognosis
A
- Poor livestock with acute respiratory distress
o Mildly affect animals may recover with minimal handling - *encourage producers to test feed
18
Q
Cyanide
A
- FORAGE RELATED
- Cyanogenic glycosides contained within plant vacuoles (highest in leaves, bark, seeds)
- Various cyanide accumulating plants: **SORGHUM SPP.
19
Q
What are some factors affecting cyanide accumulation?
A
- Any damage to the plant that releases the cyanogenic glycosides from the plant vacuoles
- Regrowth following impaired growth and/or poor growth conditions (ex. drought, freezing, cutting)
- Young plants
- Trampled, wilted plants
- Hail damage
- High nitrogen, low phosphorus soil
20
Q
Cyanide: target, mechanism and toxicity
A
- Target: HEME GROUPS
- Mechanism: inhibition of cytochrome oxidase in ETC + inactivation of Hb=ASPHYXIATION (systemic oxygen and ATP deprivation)
- *all species susceptible, but ruminants very susceptible
21
Q
Why are ruminants very susceptible to cyanide?
A
- Ruminant microflora=rapid hydrolysis of cyanogenic glycosides=free cyanide
- *higher rumen pH favors conversion
o Lower pH in monogastrics inactivates beta-glucosides
22
Q
Cyanide clinical features
A
- *sudden death or found dead after grazing stressed forages
- Acute toxicosis: respiratory distress, tachycardia, hypersalivation, tremors
- BRIGHT RED BLOOD
- PM: non specific serosal hemorrhages, congestion hyperemic MM, pulmonary edema (almond smell?)
23
Q
Cyanide: management
A
- MEDICAL EMERGENCY
- ANTIDOTES
- Animals often die before treatment can be given
24
Q
*What are the antidotes for cyanide?
A
- Sodium nitrite +/- sodium thiosulfate
- Hydroxocobalamin
25
Q
Cyanide: diagnosis
A
- Collect and freeze rumen contents in airtight containers
- Antemortem or immediately PM: CHERRY RED BLOOD
- No specific PM lesions
- Test forage or rumen contents
- Plant ID on pasture or in rumen contents
26
Q
Similarities between nitrate and cyanide
A
- Ruminants MOST susceptible
- Forage related
- Cause of acute respiratory distress and asphyxiation
- Levels reduced in forage by proper ensiling
- Lack of specific PM gross lessions
27
Q
What are the differences between nitrate and cyanide?
A
- Nitrate
o Does NOT dissipate in cut forage
o Brown/muddy MM and blood
o Accumulates in corn, wheat, oats
o Livestock can be slowly adapted to higher nitrate rations - Cyanide
o Dissipates in cut forage
o Chery red MM and blood
o Accumulates in johnsongrass, arrowgrass
o NO adaptation is possible
28
Q
What are some neurotoxic range plants?
A
- Water hemlock
- Poison hemlock
- Larkspur
- Lupine
- Death camas
- Locoweed
29
Q
Water hemlock
A
- One of the most acutely toxic plants in the world
- Found near WATER BODIES
- Characteristic features for ID: serrated leaves, ‘vein’ goes to point NOT to the middle, multichambered root
- ALL parts are poisonous (most toxin is in ROOT)
30
Q
Water hemlock: toxicity and mechanism
A
- Toxins: highest in SPRING
o Single root is lethal to adult livestock - Target organ: CNS
- Mechanism: noncompetitive GABA antagonist
o ACUTE NEUROEXCITATION/STIMULATION
31
Q
Water hemlock: clinical features
A
- USALLY FOUND DEAD WITH SIGNS OF VIOLENT STRUGGLE
- Onset: within 15mins
- Initial: salivation, apprehension, facial twitching, colic
- Terminal stages: head and neck jerking, running fits, seizures
- Death from respiratory failure
32
Q
Water hemlock: PM
A
- Myocardial degeneration and necrosis
- Skeletal muscle degeneration and necrosis
- Clin path: high AG metabolic acidosis
33
Q
Water hemlock: management
A
- Intoxication is per acute=often TOO LATE
- Seizure control and other supportive care
34
Q
Water hemlock: diagnosis
A
- *FOUND DEAD WHERE WATER HEMLOCK IS PRESENT
- ID plant in rumen/stomach content
- May have lesions in heart or skeletal muscle
- Detection of cicuotoxins in rumen/stomack contents
- *prognosis: poor to grave
35
Q
Poison hemlock
A
- Looks like a wild carrot
- Grows in moist sites with frequent disturbance
- Species typically affected: LIVESTOCK
o Sprouts early in Spring
o All parts toxic, especially seeds and flowers
o Seeds may accidentally contaminate baled feed or harvested cereals
36
Q
Poison hemlock: target organs and mechanism
A
- Target organs: CNS (acute), fetus (chronic)
- Mechanism: nAChR agonists: initial CNS stimulation followed by depression
37
Q
Poison hemlock: clinical features
A
- Sublethal: weakness, recumbency, CNS depression
- High dose: initial CNS stimulation followed by depression and paralysis
o Rapid onset
o Death from respiratory failure
38
Q
Poison hemlock: management
A
- No specific antidote
- Remove herd to different area
- Seizure/tremor control
- Low stress handling
39
Q
Poison hemlock: diagnosis and prognosis
A
- Plant in rumen/stomach contents
- Pasture with poison hemlock presence
- Detection of piperidien alkaloids in rumen/stomach contents
- *prognosis: poor with high dose, acute poisoning
40
Q
Larkspur
A
- Species affected: CATTLE
- Toxicity: tall > low varieties
- Mechanism: nAChR antagonists=NM blockade and subsequent paralysis
41
Q
Larkspur: clinical features
A
- Animals found dead on pasture
- Onset: within a few hours
o Restless, weak, frequent urination
o Eventually unable to rise: lateral recumbency and bloat
o Death due to paralysis or bloat
42
Q
Larkspur: management
A
- ANTIDOTE: neostigmine or physostigmine
- Position to avoid bloat
43
Q
Larkspur: diagnosis and prognosis and prevention
A
- Evidence of consumption
- ID of plant in stomach contents
- HPLC-MS analysis for alkaloids
- Prognosis: poor to grave
- **Prevention: avoid larkspur containing pastures during toxic window (palatable to cattle)
o EARLY SPRING=HIGHEST (sheep can be used to graze larkspur containing pastures)
