Selenium Flashcards
What is the most common source of selenium toxicosis?
selenium accumulating plants
**seleniferous plants
T/F: All selenium deficiency diseases are necrotizing
true
What are the geographic locations of selenium deficient soil?
Northwest
Northeast
Southeast
Great lakes
What are the geographic locations of selenium rich soil (2-10ppm) ?
South Dakota North Dakota Wyoming Montana Nebraska Kansas Utah Colorado New Mexico
What is the basic selenium requirements for animals?
0.1 mg/kg (depends on vitamin E)
What animals have selenium in their feed supplements?
Used in supps for cattle, sheep, swine, and poultry
What animals are most susceptible to grazing upon seleniferous plants?
cattle, sheep, and horses
*swine and poultry may eat grain grown in selenium rich soil
Up to how many ppm Se do obligate accumulators hold?
15,000 ppm Se
these plants require Se for growth
What plants are Se obligate accumulators?
Astragalus - locoweed/ milk vetch
Stanleya - prince’s plum
Oonopsis- golden wood
Xylorrhiza - woody aster
T/F: Obligate Se accumulating plants are very palatable to herbivores
FALSE
Up to how many ppm do faculatative Se accumulating plants hold?
25-100 ppm Se
These plants DO NOT require Se for growth, they just accumulate it
What are some examples of facultative Se accumulating plants?
Aster
Atriplex - saltbush
Castilleja - paintbrush
Up to how many ppm do passive Se accumulating plants hold?
1-25 ppm Se
accumulate Se passively when in Se rich soil
What are some examples of passive Se accumulating plants?
crop plants such as: Corn wheat oats barley grass hay
What category of Se accumulating plants are the most common to cause toxicosis?
Passive accumulators
these are the most edible plants
When may you see selenium toxicosis in small animals?
Improper use of selenium medicated shampoos
T/F: Waterfowl are resistant to selenium contaminated water
FALSE
Causes teratogenic effects
What are the three oxidative states of selenium?
selenate (+6)
selenite (+4)
Selenide (-2)
**selenate and selenite can be toxic
Selenide is not absorbed and will go straight through and out the GI tract
T/F: Selenium is an irritant to mucus membranes
TRUE
In therapeutic doses Selenium and vitamin E do what?
Prevent cellular degeneration and cell membrane damage
Se also:
- Plays a role in conversion of T4 - T3
- is a component of glutathione peroxidaes - acts as an antioxidant
- binds with the -SH group of glutathione
What is the acute toxic oral dose of selenium (selenite) in horses, cattle, and swine?
Horse - 3.3 mg/kg
cattle - 10 mg/kg
swine - 17 mg/kg
Highly toxic
Toxicity:
organic selenium > selenate/selenite > selenide > synthetic organoselenium compounds
The selenium oral subacute toxic level for swine is ____ ppm for 3 days or more
20 - 50 ppm
The chronic toxic level for horses, cattle, and swine is ____ ppm for several weeks or months
5-10 ppm
What kind of soil will promote formation of selenate?
Arid alkaline soil of the great plains
T/F: Elemental Se is highly toxic
False
relatively non toxic
What kind of diet can reduce Se toxicity?
high protein diet and ingestion of other elements that bind Se (such as copper)
T/F: The soluble organic selenium in plants is more rapidly absorbed than selenite, selenate, and selenide
TRUE
- readily absorbed in the small intestine
- elemental Se is NOT absorbed - insoluble in water
Where is Se distributed in the body?
throughout - more so to the liver, kidney, and spleen
In chronic toxicity - high levels will be in the hair and hooves
How is Se excreted?
Mostly in the urine but it also crosses the placental (teratogenic) and can be excreted in the milk
What heavy metal will increase biliary excretion of selenium?
Organic arsenic
What is the MOA of selenium toxicosis?
- Irritation of the GI mucosa (acute and subacute)
- Dramatic depletion of tissue glutathione (GSH)
- Selenium replaced sulfur in amino acids causing abnormal proteins (hoof/hair damage)
- decrease ATP
- decrease tissue ascorbic acid
What is the main cause of death in acute and subacute Se toxicosis?
Respiratory insufficiency from pulmonary edema and hemorrhage
due to decreased energy –> capillary damage
What is death in chronic Se toxicosis most commonly associated with?
Starvation and thirst resulting from weakness, lameness, blindness
What is the time frame and clinical signs associated with acute Se toxicosis?
Onset in a few hours to a few days
GI signs: colic, bloat, watery dhr
Resp. signs: labored respiration with fluid sounds in the lung, bloody froth from the nares, cyanosis
Fever, polyuria, mydriasis, uncertain gait
death in hours
What is the layman’s term for Subacute Se toxicosis in cattle?
Blind staggers
*dude to locomotor signs (patients are not blind)
What are the clinical signs associated with subacute Se toxicosis?
Stage 1: poor appetite, aimless walking, circling, normal resp/temp
Stage 2: added - depression, incoordination, foreleg weakness/walking on the knees, anorexia
Stage 3: colic, hypothermia, emaciation, clouded corneas - near blindness, paresis, coma, death in hours
*sheep are similar but stages are less well defined
What clinical signs are associated with Se toxicosis in swine?
“porcine focal symmetrical poliomyelomalacia”
Neuro signs - incoordination, lameness, paralysis
alopecia, hoof abnormalities, separation of the hoof
What clinical signs are associated with chronic Se toxicosis?
Rough hair coat, loss of hair from mane/tail
Hoof deformities and sloughing, stiffness of joints, and lameness
Partial blindness, anemia, lethargy, emaciation, infertility, and birth defects
aka Alkali dz
What lesions are associated with Acute Se toxicosis?
HGE, congestion of organs, hemorrhages, pulmonary edema, hydrothorax, - gut contents have foul rotten garlic smell
What lesions are associated with subacute Se toxicosis in swine?
Focal symmetrical poliomyelomalacia
Abnormal hooves, cardiac damage, and hepatic necrosis are all lesions associated with which stage of Se toxicosis?
Chronic
T/F: When sending the hoof for chemical analysis (Se) you should wash it first
TRUE
this is an exception to the rule - but you want to make sure selenium from the soil on the exterior of the hoof is not contaminating the actual tissue
What specimens should be collected for chemical analysis in acute Se toxicosis?
blood, kidney, liver
specimens in chronic toxicosis = hair and hoof
Blood or plasma glutathione peroxidase activity correlates well with blood Se concentration in which species?
Cattle, sheep, and swine
NOT horses
What are DDX for acute Se toxicosis?
Pneumonia, infectious hepatitis, enterotoxemia, and pasteurellosis
What are DDX for acute Se toxicosis?
Molybdenum tox, fluoride tox, freezing, ergotism, laminitis
What treatments are available for Se. toxicosis?
No specific antidote
Saline cathartics
Symptomatic therapy - O2, IVF, tx for HGE
Acetylcysteine
What should be done to prevent Se toxicosis?
- Test soil/forage regularly, *remove animals from seleniferous areas, *addition of copper to the diet, *high protein diet, *increasing sulfur containing proteins may prevent toxicosis
- addition of organic arsenicals to the diet to increase biliary excretion of Se
What is the prognosis of acute Se toxicosis?
POOR - animals die quickly
