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235 Cards in this Set

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what is the most common toxicosis in sheep?
chronic copper toxicity
what mineral is essential to keep sheep from getting copper toxicosis?
molybdenum
what two species have the most problems with copper toxicosis?
sheep and dogs
what is the mechanism of copper toxicosis?
- copper builds up slowly in liver from diet and is stored in the lysosomes for weeks or months
- when a critical threshold is reached, a stressful event will cause the liver to dump the copper in into the blood
- hemolysis and liver necrosis
what organ systems are targeted by copper toxicosis?
liver, blood, renal
characterize the epidemiologic curve for copper toxicosis. Why is it like this?
- SPORADIC
- because an animal might have too much copper in its liver, but it requires a sufficiently stressful situation in order to cause an acute toxicosis
what are some clinical signs of chronic copper toxicity?
- vomiting (dogs)
- hemolytic anemia
- hemoglobinuria
- anorexia, prostration, weakness
- icterus
- pica (sheep)
what is a pathognomonic lesion of copper toxicity? What are some others?
- GUN-METAL COLORED KIDNEYS
- icterus
- enlarged spleen
how is chronic copper toxicity diagnosed in the sheep?
- serum during hemolytic crisis
- liver in dead animal
- prophylactic checks on liver biopsies or other deaths in the hers
- Cu:Mo ratio on total diet done to correct problem
how is chronic copper toxicity diagnosed in the dog?
- problem breeds checked with liver biopsy around one year of age
- DNA microsatellite marker in Bedlington terriers
- primary cholestatic disease may also cause Cu accumulation
how is chronic copper toxicity treated in the sheep?
- ammonium tetrathiomolybdate
- fluids for kidney problems
- steroids, ascorbic acid
- poor prognosis
how is chronic copper toxicity treated in the dog?
- trientine (chelator), fluids, steroids, ascorbic acid, Vitamin E, S-adenosylmethionine
how is chronic copper toxicity prevented in the dog?
- check on diet Cu, Fe and Zn; prophylactic Zn, penicillamine of trientine (chelators)
- Prophylactic Zn reduces the protein in the intestinal cells that bind Cu and slough into gut
what year of penny did they start putting zinc into them?
1983
what are some sources of zinc?
- pennies minted ≥ 1983
- nuts and bolts
- ointments and skin treatments
- misformulated diets
- galvanized metal (containers, cages)
- game pieces for board games (Monopoly)
- calamine lotion
- dandruff shampoo
what species is zinc toxicosis found?
- dogs
- zoos (seals, ratites, hyenas) - ingesting pennies
- birds and ferrets from galvanized wire cages
- cattle: too much in feed
where in the body is zinc excreted?
bile and pancreatic secretions
what are three mechanisms of action by which zinc is toxic?
1. irritation of the GI tract (zinc salts)
2. hemolysis due to oxidative damage to RBCs
3. chronic: interferes with Cu and Fe uptake from GI tract
acute zinc toxicosis in dogs:
- onset
- clinical signs
- pathologic lesions
- days with hardware; immediate with Zn oxide ointment
- VOMITING (very consistent), diarrhea
- HEMOLYTIC ANEMIA (very consistent), icterus, hemoglobinuria
- depression, lethargy, anorexia
- DIC possible
- Lesions: renal, hepatic, and pancreatic necrosis; hemorrhagic gastritis
what systems are affected by zinc toxicosis in the dog?
GI, RBC, hepatic, renal
what systems are affected by chronic zinc toxicosis in cattle?
GI, RBC, hepatic, renal, bone
chronic zinc toxicosis in cattle:
- onset
- clinical signs
- pathologic lesions
- onset: several weeks
- pica, bloat, anorexia, diarrhea
- PU/PD
- hemolytic anemia
- lameness possible (distal tibia, fetlock)
- lesions: GI ulcers; pale kidneys; necrosis of pancreas, liver, and liver; osteochondrosis
how is zinc toxicosis diagnosed?
- elevated serum (live animal) and liver (dead) Zn concentrations
- depressed Cu concentrations
- radiograph dog's abdomen
- clin path: ↓PCV, nRBC, ↑ALP, ↑ALT, azotemia, ↑amylase and lipase, hemoglobinuria, DIC possible terminally, Coombs' test may be false positive
how is zinc toxicosis treated?
- symptomatic; low-dose phenothiazine or metoclopramide (if no obstruction) for vomiting; fluids to flush kidney; transfusions if necessary
- remove foreign body
- canned pumpkin as bulk cathartic for recent non-symptomatic exposure
- Ca EDTA for serum values > 20ppm, but these values quickly drop after source removal
name 9 liver toxicants
1. Acetaminophen
2. Pine oil, phenol disinfectants.
3. Cu, Zn, Fe
4. Endotoxins (garbage)
5. Halothane
6. Some mycotoxins (i.e. aflatoxin, fumonisin)
7. Some mushrooms (e.g. Amanita phalloides)
8. Rimadyl® NSAID idiosyncratic reaction
9. Some plants (e.g. sago palm, blue-green algae; LA pyrrolizidine)
name 11 toxicants that can cause hemolysis
1. Acetaminophen
2. Cu, Zn
3. Anionic surfactants
4. Onions, garlic
5. Red maple (horses)
6. High dose phenol
7. Vitamin K3 parenteral (menadione)
8. Drug vehicles (e.g. propylene glycol, DMSO)
9. Methylene blue (cats)
10. Snake bites
11. Terminal liver failure
how much lead is absorbed from the GI tract after ingestion?
2-10%
deficiency of which dietary minerals can increase lead uptake by the GI tract?
calcium, zinc, and iron
where is lead stored in the body?
bone
does lead cross the BBB and placenta?
yes
what is the major route of lead excretion?
feces; bile adds to this; urinary route is only important in chelation
comment on the renal excretion of lead
not a major route of excretion unless chelation is involved
what are the systems affected by lead toxicity?
- GIT and CNS (the big ones)
- PNS, hematopoietic, renal
what is the mechanism of action of lead toxicosis?
- binds to SH groups on key metabolic enzymes
- may compete with or replace Zn in enzymes
how does lead cause neurotoxicity? (3)
- capillary damage via endothelial cells
- damage to BBB
- demyelination
how does lead disrupt hematopoiesis?
inhibits enzymes that synthesize heme (Alanine dehydratase and synthetase)
how does lead cause renal toxicity? What is a histopathological indicator of lead toxicosis in the kidney?
- damages renal tubular epithelium
- acid-fast intranuclear inclusion bodies can be found
describe the clinical signs of the GI syndrome of lead toxicosis in dogs
- vomiting, anorexia
- painful, tender abdomen
- constipation followed by diarrhea ± blood
in the dog with lead toxicosis, comment on the timing of neurologic signs versus GI signs.
GI signs may precede neurological signs
describe the clinical signs of the GI syndrome of lead toxicosis in cattle.
- anorexia
- rumen stasis or sluggishness
- constipation followed by diarrhea
what type of seizures are associated with lead toxicosis in dogs?
clonic-tonic
describe the clinical signs of the CNS syndrome associated with lead toxicosis in dogs
- ranges from depression to hysteria
- barking; muscle tremors
- behavioral changes
- clonic-tonic seizures
- they may be intermittent (makes diagnosis difficult)
what is the major clinical sign of lead toxicosis in cattle?
blindness
what are a whole crap-load of clinical signs of lead toxicosis in cattle?
- BLINDNESS; head pressing and/or depression
- bawling or bellowing
- muscle tremors; ears twitch rhythmically
- head bobbing; jaw chomping
- ataxia; incoordination; circling; stumbling
what is a clinical sign of lead toxicosis in horses?
roaring due to effects on recurrent laryngeal nerve
what are some clinical signs of lead toxicosis in water fowl?
- anorexia; diarrhea; weight loss
- weakness; lethargy; coma; death
- may see droopy wings
how is lead toxicosis diagnosed in the lab?
- blood lead (unclotted sample)
- tissue lead from liver and/or kidney
what are two DDx of lead poisoning in dogs with GI syndrome?
1. gastritis (e.g. ate garbage)
2. arsenic
what are six DDx of lead poisoning in dogs with GI syndrome?
1. distemper
2. encephalitis
3. organochlorines
4. strychnine
5. metaldehyde
6. organophosphates
7. carbamates
what are three DDx of lead poisoning in cattle with GI syndrome?
1. simple indigestion
2. polio
3. arsenic
what are nine DDx of lead poisoning in dogs with GI syndrome?
1. hemophilus
2. polio
3. hypomagnesemic tetany
4. nervous Acetonemia
5. brain abscess
6. brain neoplasia
7. organochlorines
8. urea toxicosis
9. salt toxicosis
what is the main way in which lead poisoning is treated?
chelation
EDTA in chelation therapy for lead toxicosis:
- what animals can you use it in?
- which salt of EDTA do you use and why?
- how long is treatment?
- where does it remove the lead from?
- it is potentially toxic to which organ?
- small animal use only
- use the dicalcium salt to prevent hypocalcemia
- treatment is 2-5 days
- it removes EXTRACELLULAR lead, primarily from bone, not from soft tissue. The soft tissue lead will then redistribute to bone, reducing body burden.
- EDTA can be nephrotoxic
what are three chelators for lead toxicosis in small animals?
1. EDTA
2. DMSA (dimercaptosuccinic acid)
3. penicillamine
DMSA in chelation for lead toxicosis:
- what is the brand name?
- where does it remove lead from?
- what species is it formulated for?
- which species it is useful in?
- which other metals will it chelate?
- Succimer™
- removes lead from soft tissue and bone
- it is a human-labeled drug
- especially good for birds; good for dogs and cats
- will chelate As and Zn, as well as lead
Penicillamine for chelation therapy:
- route of administration
- what is the active functional group?
- what metals does it chelate?
- in what types of toxicoses do you give it?
- oral
- has an SH group
- most useful for Copper, but also lead, arsenic, and zinc
- helpful in chronic toxicity cases
what is a very useful chelator for lead toxicosis in cattle?
Thiamin (Vitamin B1)
besides chelators, what supplemental therapies are indicated for lead toxicosis? (5)
1. Saline Cathartic (MgSO4 best - insoluble Pb precipitate formed)
2. Surgery to remove metal object
3. Steroids and Diuretics (Brain Edema)
4. Diazepam or Barbiturates (Seizures)
5. Foods and Fluids (Anorexia)
what are two cattle sources of arsenic and one cat and dog source?
- cattle: old pesticides; ashes from salt-treated lumber
- cat and dog: sweet, syrupy ant baits
what is the most toxic valency of arsenic?
3+
inorganic arsenic toxicosis:
- routes of absorption
- sites of distribution
- excretion
- Well absorbed from GI & through skin
- Well distributed but high in liver and kidney
- Excretion: Fairly rapidly excreted in the urine and also in feces and via bile to intestine.
comment on the crossing of arsenic through BBB and placenta
crosses placenta easily, but not the BBB
what are two mechanisms of action of arsenic toxicosis?
- Combines with SH groups of key metabolic enzymes (Lipoic Acid): Shuts down cellular respiration
- Direct corrosive action on capillaries and is a potent toxicant of the vascular system
what are the target organs of arsenic?
GI and vascular
(per)acute arsenic toxicosis:
- important clinical sign
- GI and other clinical signs
- important post-mortem finding
- INTENSE ABDOMINAL PAIN (remember Napoleon was poisoned with arsenic and had bleeding ulcers)
- vomiting, sever colic
- weakness, staggering, ataxia, recumbency, weak, rapid pulse, signs of shock, severe watery and bloody diarrhea, rumen and GI atony
- PM: severely BRICK RED hyperemic gut
sub-acute arsenic toxicosis:
- clinical signs
- important post-mortem finding
- course
- profuse, watery diarrhea
- PU/PD → oliguria & proteinuria → anuria
- dehydration, acidosis, poor circulation
- PM: BRICK RED HYPEREMIC GUT
- may see death in 4-7 days
how is inorganic arsenic toxicosis diagnosed?
- empirically
- lab findings
- antemortem samples
- PM samples
- onset time and lesions
- lab: ↑PCV and BUN; UA - proteinuria and casts
- antemortem samples: vomitus, feces, urine, hair
- PM samples: liver and kidney
how is inorganic arsenic toxicosis treated (emergency and antidotes)?
Emergency and Supportive Care
- Correct shock & dehydration with fluids & electrolytes
- Lavage and emesis if treated early (1-4 hours)
- Activated Charcoal may help
- Cathartics - not usually recommended

Antidote: BAL, DMSA, sodium thiosulfate, bland diet
what are the targets of organic arsenic toxicosis?
nerves: demyelination and axonal damage; peripheral neuropathy
what is a key clinical sign of organic arsenic toxicosis?
blindness
what genus of fungi are ionophores derived?
Streptomyces
which two species are ionophores most toxic?
horse and sheep (horse > sheep)
rank the following in order of MOST susceptible to least susceptible to ionophores:
- cattle
- chicken
- horse
- sheep
- swine
horse > sheep > swine > cattle > chicken
what other drug type can potentiate ionophore toxicity? Mechanism of action?
macrolides (and some other antibiotics) and inhibit CYP450
which ionophore most commonly causes toxicosis in dogs?
lasalocid
what is the mechanism of ionophore toxicosis?
Toxic action related to influx of ions across mitochondrial membranes of heart & skeletal muscle; calcium accumulation intracellularly -> cell death & necrosis
what are the target organs for ionophores in the horse?
heart and skeletal muscles (both have lots of mitochondria)
what are the three basic ways in which ionophores cause a net influx of Ca2+ into the muscle cells?
1. free radicals
2. lipid peroxidation
3. ionophore binding to sarcolemmal membrane
ionophore toxicosis in the horse:
- onset
- course
- clinical signs
- PM lesions
- onset: 1-5 days
- course of 1 day to several weeks
- immediate anorexia, sweating, ADR, weakness of hind limbs, PU, tachycardia w/ jugular pulse
- PM: pale, flabby heart, hydrothorax, ascites
what would a horse heart look like on PM with ionophore toxicosis?
Pale heart, white streaks: necrosis with secondary dystrophic calcification
how does the "paleness" of the horse heart PM correlate with the chronicity of the toxicosis?
Paleness: the ↑ dose, the faster you die, so ↑ dose → ↓white streaks
what are the target organs for ionophores in ruminants?
cardiac, skeletal muscle, GI
ionophore toxicosis in ruminants:
- onset
- course
- clinical signs
- PM lesions
- onset: 1-5 days
- course: 1 day - several weeks
- anorexia, ADR, diarrhea, myoglobinuria in sheep
- PM: pale heart and skeletal muscles; hydrothorax; ascites
ionophore toxicosis in the dog/cat:
- onset
- course
- clinical signs
- PM lesions
- onset: 1-5 days
- course: 1 day to several weeks
- para/tetra paresis; ataxia/weakness, dyspnea/apnea, ADR
- PM: dog has rear leg skeletal muscle problems; cat has more heart than skeletal muscle problems
what is the usual reason for death in dogs and cats with ionophore toxicosis?
respiratory paralysis
comment on whether the PM lesions in the heart versus skeletal muscle are >, <, or = for the following species:
- cat
- cattle
- dog
- horse
- pigs
- rabbits
- sheep
- cat: heart > SM
- cattle: heart = SM
- dog: SM > heart
- horse: heart > SM
- pigs: SM > heart
- rabbits: heart = SM
- sheep: SM > heart
when in the farm routine is ionophore toxicosis usually seen?
usually occurs following the use of a new concentrate or mineral
how is ionophore toxicosis treated?
- Symptomatic; activated charcoal + saline cathartic; charcoal will bind ionophores and also endotoxins released from death of gm. neg. bacteria
- Fluids
- Steroids may decrease amount of connective tissue
- Vitamin E / selenium for free radical formation
- Stall rest for 6 weeks
what is the name of the toxin in blister beetles?
cantharidin
what type, cutting, and baling type of hay are blister beetles most commonly found?
alfalfa, 3rd cutting (i.e. July hay), when the hay is crimped (rolled)
about how many blister beetles does it take to kill a horse?
about 30
what is the mechanism of action of cantharidin?
- Cantharidin is strong mucosal irritant (i.e. vesicant) that injures oral and GI mucosa going in & renal/bladder structures coming out; previous use as skin blistering agent
- Cantharidin able to produce hypocalcemia by an unknown mechanism
- Heart injury by unknown mechanism
what are the target organs for cantharidin?
GI, renal, cardiac
what are two important clinical signs of cantharidin (blister beetle) toxicosis in the horse?
1. pollakiuria
2. synchronous diaphragmatic flutter (hiccups)
cantharidin toxicosis in the horse:
- onset
- course
- two important clinical signs
- other clinical signs
- PM lesions
- onset: < 2 hours
- course: hours - 3 days
- POLLAKURIA, HICCUPS
- salivation, shock, congested MM, tremors, tachycardia, colic, tenesmus, ADR
- PM: inflamed GI and renal system; myocardial necrosis
how is cantharidin toxicosis diagnosed?
- ID
- clin path
- what are other differentials for synchronous diaphragmatic flutter?
- Blister beetle ID in hay; cantharidin in urine, GI contents or kidney; gone in 3-4 days
- Clin Path: increased PCV, serum protein; hypocalcemia, hypomagnesemia, decreased urine S.G. [1.003-1.008], leukocytosis, increased BUN & creatinine, possible increase CK
- Synchronous diaphragmatic flutter also seen at times in horses consuming pearl millet hay (soluble oxalates) and dusty (endotoxin) hay
how is cantharidin toxicosis treated?
- Symptomatic; activated charcoal followed in several hours by mineral oil
- Fluids with furosemide (after rehydration)
- Bicarbonate for acidosis; Mg sulfate for hypomagnesemia; Ca gluconate for hypocalcemia; flunixin meglumine or butorphanol for pain
what is the toxin found in cotton seeds?
gossypol
rank the following from most toxic to least toxic:
- Whole cotton seed
- cotton seed meal
- cotton seed hulls
- cotton seed oil
- cotton seed meal (most toxic)
- Whole cotton seed (toxic)
- cotton seed oil (no gossypol, but can turn rancid)
- cotton seed hulls (not toxic)
what is the signalment for ruminants that are most susceptible to gossypol toxicosis?
immature (e.g. lambs, calves)
besides ruminants, what two other species can gossypol toxicosis be a problem?
swine (very susceptible) and poultry (intermediate susceptibility)
what are the mechanisms of action of gossypol toxicosis? (3)
- Inhibition of protein synthesis and inhibition of a variety of enzymes in body (e.g. lactic dehydrogenase, GSH-transferase)
- Heart mechanism unknown; possibly ROS (reactive oxygen species) --> oxidative stress; liver secondary to heart
- Able to disrupt male and female reproductive hormone balance; affect sperm motility/morphology.
what are the target organ systems for gossypol toxicosis?
cardiac, hepatic, repro
what is an important clinical sign of gossypol toxicosis?
tachypnea (THUMPS)
gossypol toxicosis:
- onset
- course:
- key clinical sign
- other clinical sign
- PM lesions
- onset: 1-3 mos
- course: several days to weeks (avg. 3-7 days)
- THUMPS (tachycardia)
- ADR, decreased conception, sudden death
- lesions: hydrothorax, hydropericardium, pulmonary edema, dilated and flabby heart with necrosis, icterus, ascites, anemia
how is gossypol toxicosis diagnosed?
- empirically
- lab
- clin path
- other non-gossypol problems with cotton
- Quantitation of free gossypol in diet with characteristic clinical signs & lesions
- Plasma gossypol > 5 ppm
- Clinical pathology increases in CK, LDH; decreased serum Ca, Hb, PCV possible
- Rancidity problems with oil in whole cotton seed also possible (feed refusal, GI disturbances)
how is gossypol toxicosis treated? (3)
- Symptomatic
- Diuretic for pulmonary edema & congestive heart failure
- Remove source
how is gossypol toxicosis prevented? (3)
1. ↑ protein in diet to inactivate free gossypol in gut; pelleting will also help
2. reduce cotton seed meal in diet
3. increase ferrous sulfate content in diet so it is 1:1 with gossypol
what are six cardiac toxicants?
1. Ionophores (CK increased, recent concentrate change)
2. Endotoxins (e.g. garbage problems in dogs)
3. Selenium deficiency/toxicosis (LA problems)
4. Cantharidin (+ renal, hypo Mg & Ca, oral irritation.)
5. Plants (yew, rhododendron, Mt. Laurel)
6. Gossypol (rare, primarily swine & young ruminants, flabby heart)
what are 8 causes of rear leg paresis in the dog?
1. Bromethalin low dose (CNS involvement)
2. 2,4-D (myotonia with rigid muscles, GI)
3. Disc disease or trauma
4. Botulism (flaccid muscles, little/no CNS)
5. Ionophores
6. Tick paralysis
7. Low dose tremorgen mycotoxin (i.e. roquefortine)
8. Macadamia nuts
what is a key clinical sign of salt toxicosis in cattle?
blindness
which systems are affected by salt toxicosis in cattle?
CNS, GI
what are some clinical signs of salt toxicosis in cattle, including one key clinical sign?
- BLINDNESS
- nervous: KNUCKLING, nystagmus, belligerency, seizures, paresis, bruxism
- GI: colic, thirst, diarrhea, mucus covered feces, rumen stasis, nasal discharge
what are three key clinical signs and one key post-mortem sign of salt toxicosis in swine?
1. blind
2. star gazing
3. jaw champing
- eosinophilic cuffing in brain
which species shows perivascular cuffing in the brain with salt toxicosis?
swine
how is salt toxicosis treated in large animals?
access to small amounts of water (0.5% bw) at one-hour intervals until rehydrated
which genus of fungi is the most common source of molds from the STORAGE of feedstuff?
Penicillium
which species of fungus makes aflatoxin?
Aspergillus flavus
which crops are associated with aflatoxin?
CORN, cotton seed, peanuts
which natural conditions favor outbreaks of aflatoxin toxicosis?
years of DROUGHT or insect damage to kernel
what is an easy, but insensitive and non-specific way to detect Aspergillus flavus in ground corn?
black light
comment on the various aflatoxins ingested by cows and how they may be hazardous to humans
Aflatoxin B1 metabolized in body to Afla M1, which comes out in milk; monitored closely by FDA because it is carcinogenic
in which animals is aflatoxin toxicosis most common?
POULTRY AND YOUNG SWINE
what is the main organ system affected by aflatoxin?
liver
what is the mechanism of aflatoxin toxicosis?
- Aflatoxins bind intracellular macromolecules especially in the liver to decrease RNA synthesis; primarily from afla B1 epoxide
- Aflatoxins are immunosuppressive, especially for cell-mediated immunity
- Aflatoxins may decrease synthesis of clotting factors associated with hepatic toxicity
- Aflatoxins are hepatotoxic & carcinogenic
chronic aflatoxicosis:
- onset
- clinical signs
- pathologic lesions
- onset: weeks; high morbidity, low mortality (compare with chronic Cu toxicosis of sheep)
- off-feed, ADR, jaundice, increase in infectious disease
- PM: icterus, bile duct hyperplasia, widespread hemorrhages, ascites, hydrothorax
how is aflatoxicosis diagnosed?
Necessary concentration of aflatoxin in feed along with expected liver changes; clin path changes reflecting liver necrosis, including bilirubin, low BUN, low total protein & albumin
what can be used to bind to aflatoxin and prevent it from being absorbed from the GI tract?
anti-caking clays
what is the main way to treat chronic aflatoxicosis?
dilution is the solution: dilute the food so that aflatoxin levels are low and add anti-caking clays to adsorb
what two species of molds produce trichothecene?
1. Fusarium graminearium
2. Fusarium roseum
what type of mold produces by trichothecenes and what is the main specific toxin that makes animals sick?
- Fusarium molds
- vomitoxin
vomitoxin
- crops
- genus that produces the toxin
- natural conditions favoring growth and production of this toxin
- CORN and SMALL GRAINS
- Fusarium molds
- WET GROWING SEASONS
what goes corn or grain look like when it is contaminated with trichothecenes (e.g. vomitoxin from Fusarium molds)?
pink or rose color; "scabby grain" or "pink ear rot of corn"
in which animals is vomitoxin most toxic?
SWINE and DAIRY CATTLE
what system does vomitoxin affect?
GI
vomitoxin clinical signs:
- onset
- most common clinical sign
- other clinical signs
- pathological lesions
- onset: feed refusal immediate; diarrhea 1-2 days (high morbidity, low mortality)
- most common: feed refusal
- diarrhea, ↓weight gain, ↓milk production, vomiting (small percentage)
- lesions: gastroenteritis
how it trichothecene (vomitoxin) toxicosis diagnosed?
- compatible signs and lesions with concentrations in feed
- onset of syndrome coincides with new batch of feed or silage
how is trichothecene (vomitoxin) toxicosis treated?
only by diluting the feed ± anticaking clays
what three major types of toxins are produced by Fusarium molds?
1. aflatoxins
2. zearalenone
3. ELEM (Fumonisin)
in what crops do you find zearalenone?
CORN and SMALL GRAINS
what toxin might you suspect from corn stored in open-air cribs?
zearalenone
which species is most susceptible to zearalenone toxicosis?
swine
what is the mechanism of action of zearalenone toxicosis?
- Zearalenone acts as an estrogen; similar structure to estradiol with 1/4-1/2 potency of estradiol
- Zearalenone metabolized to zearalenol in the body; may also find zearalenol in feeds; zearalenol further metabolized to zearalenol
what organ system is affected by zearalenone toxicosis?
reproductive system
zearalenone toxicosis:
- onset
- clinical signs
- pathologic lesions
- onset: 4-7 days; high morbidity, low mortality
- prolonged estrus, vulvar swelling, mammary/nipple enlargement, vaginal/rectal prolapse, ↓litter size, anestrus/pseudopregnancy, EED, abortion, problems in boars and barrows
how is zearalenone toxicosis diagnosed?
- Analyze feed for zearalenone content; necropsy results (usually not necessary or available); increased plasma progesterone
- Rule out other estrogenic compounds in diet (e.g. phytoestrogens in clovers or alfalfa, poultry litter sometimes estrogenic); estrogenic syndrome in ruminants more likely associated with these agents
how do you treat zearalenone toxicosis?
- Remove or blend contaminated feed; anti-caking clays will not work; ‘only solution is dilution’; MTB 100 binds in vitro
- Prostaglandin F2-alpha will end anestrus
how is zearalenone toxicosis prevented?
Prevention: shell & dry corn down immediately after picking; don’t store on the cob in a open air bin; check corn before feeding to swine during wet growing seasons
which mold produces slaframine?
Rhizoctonia leguminicola
in which crop is slaframine found?
hay; legumes like clover, alfalfa, etc.
in what species does slaframine cause problems and what is the key clinical sign?
HORSES; it makes them SLOBBER
what is the mechanism of action of slaframine?
- Slaframine is a parasympathomimetic (primarily salivary glands) alkaloid (-ine) that is metabolized in liver within an hour to ketoimine, the active principle
- Ketoimine has a quaternary amine structure similar to acetylcholine that works on cholinergic receptors, especially those associated with exocrine salivary glands; charge prevents crossing blood-brain barrier
slaframine:
- onset
- course
- key clinical sign
- other clinical signs
- onset: 1 hour
- course: 1-3 days
- SALIVATION (continuous or gushers)
- lacrimation, piloerection, anorexia, polyuria, diarrhea, bloat, abortion (rare), death (rare)
what system is affected by slaframine?
GI
how is slaframine toxicosis treated?
- usually nothing
- don't give atropine (ileus); give antihistamines if owners insist
how is slaframine toxicosis prevented?
avoid buying legume hay, especially second cutting clover hay in a wet growing year
ELEM (Fumonisin)
- type of mold
- crop on which it is found
- time of year
- epidemiology
- Fusarium
- grows on corn
- most cases in the coldest months (December, January)
- low morbidity; high mortality; sporadic
which species are susceptible to fumonisin toxicosis?
all equidae and swine (equids > swine)
what organ systems does fumonisin toxicosis affect?
CNS, hepatic (rare)
what are two key clinical signs and a key pathologic lesion of fumonisin toxicosis?
1. BLINDNESS
2. BIZARRE MANIACAL BEHAVIOR (Horse goes bonkers)
- LIQUEFACTIVE NECROSIS OF THE WHITE MATTER OF THE BRAIN
fumonisin:
- onset
- course
- 2 key clinical signs
- other clinical signs
- key pathologic lesion
- onset: 1-4 weeks; abrupt appearance of clinical signs
- course: < 12 hours
- BLINDNESS; HORSE ACTS LIKE A MANIAC
- depression-lethargy, anorexia, facial paralysis, ataxia, head pressing, convulsions, death
- lesions: LIQUEFACTIVE NECROSIS OF THE WHITE MATTER OF TEH BRAIN
what is the key clinical sign of hepatoencephalopathy caused by fumonisin toxicosis?
REPEATED YAWNING
diagnosis of fumonisin toxicosis:
- how
- how to you differentiate from EEE and West Nile?
- what is a major differential for the liver syndrome?
- Brain lesions somewhat pathognomonic; feed analysis of > 10 ppm fumonisins for horses; > 50 ppm for swine
- EEE and West Nile occur during summer months and not winter
- Theiler’s major liver differential; mostly in April-November around this area
how is fumonisin toxicosis treated and prevented?
- Remove corn from the diet; no known effective treatment
- Prevention: only use corn in diet if feed is analyzed by feed mill for fumonisin; otherwise don’t use corn; barley fairly comparable in carbohydrates
what are three genera of fungi that produce tremorgens?
1. Aspergillus
2. Penicillium
3. Neotyphodium lolii
in which plants are Neotyphodium tremorgens found?
perennial ryegrass
what are three types of grass that commonly have tremorgen containing fungi?
1. Perennial ryegrass
2. Bermuda grass
3. Dallis grass
what are Penicillium based tremorgens found?
moldy milk products, English & black walnut hulls, decaying food, garbage, compost piles, road kill, poultry litter, etc.
what are two tremorgens produced by Penicillium molds?
1. Penitrem A
2. Roquefortine
what canine toxicant is in Dr. Blodgett's top 5 toxicoses fo dogs and "gets no respect in the literature?"
tremorgens: Penitrem A and roquefortine
characterize the seizures caused by tremorgens
clonic-tonic
what organ system is affected by tremorgens?
CNS
tremorgens:
- onset
- course
- clinical signs
- onset: minutes - several days
- course: 1 day - 1 week
- muscle tremors, clonic-tonic convulsions, hyperesthesia, paralysis/prostration, nystagmus/anisocoria, salivation, ± vomiting
how is tremorgen toxicosis diagnosed?
- analyze feed, suspect agent, or stomach contents for tremorgens
- check on perennial ryegrass, Bermuda, or Dallis grass availability; toxin analysis
- check on availability of moldy walnuts, milk products, ergot bodies on grass heads, etc.
treatment of tremorgen toxicosis:
- large animals
- dogs
- Large animals often recover from grass problems (perennial ryegrass, Bermuda grass, Dallis grass) unaided; don’t excite more than necessary; change pastures or hay
- Symptomatic treatment in dogs; methocarbamol +/- pentobarbital for muscle tremors & convulsant problems
aflatoxin:
- feed(s) associated
- species susceptible
- target systems
- feed(s) associated: corn (drought)
- species susceptible: poultry, swine, dairy cattle
- target systems: liver, ADR, dairy/residue
vomitoxin:
- feed(s) associated
- species susceptible
- target systems
- feed(s) associated: corn, small grains (wet)
- species susceptible: swine, dairy cattle
- target systems: GI (feed refusal)
zearalenone:
- feed(s) associated
- species susceptible
- target systems
- feed(s) associated: corn (zea)
- species susceptible: swine
- target systems: reproductive
slaframine:
- feed(s) associated
- species susceptible
- target systems
- feed(s) associated: clovers
- species susceptible: horses
- target systems: GI-saliva
fumonisin:
- feed(s) associated
- species susceptible
- target systems
- feed(s) associated: corn
- species susceptible: HORSES, swine
- target systems: CNS, LIVER, pulmonary, heart
penetrem A:
- feed(s) associated
- species susceptible
- target systems
- feed(s) associated: dairy, walnuts
- species susceptible: dogs, cats
- target systems: CNS
Roquefortine:
- feed(s) associated
- species susceptible
- target systems
- feed(s) associated: decaying organic
- species susceptible: dogs
- target systems: CNS
what is the taxonomic Genus of tobacco?
Nicotiana
what is the taxonomic Genus of mistletoe?
Phoradendron
what is the taxonomic Genus of poinsettia?
Poinsettia
what is the taxonomic Genus of holly?
Ilex
what is the taxonomic Genus of purple foxglove?
Digitalis
what is the taxonomic Genus of lily of the valley?
Convallaria
what is the taxonomic Genus of oleander?
Nerium
what is the taxonomic Genus of marijuana?
Cannabis
what is the taxonomic Family of Dieffenbachia - Dumb Cane?
Araceae
what is the taxonomic Family of Split Leaf philodendron?
Araceae
what is the taxonomic Family of Elephant ear plant?
Araceae
what is the taxonomic Family of Caladium?
Araceae
what is the taxonomic Family of Pothos (philodendron)?
Araceae
what is the taxonomic Family of Peace Lily?
Araceae
what is the taxonomic Family of Jack in the Pulpit?
Araceae
what is the taxonomic Family of Skunk Cabbage?
Araceae
what is the taxonomic Genus of Tulip?
Tulipia
what is the taxonomic Genus of Iris?
Iris
what is the taxonomic Genus of Hyacinthus?
Hyacinthus
what is the taxonomic Genus of Amaryllis?
Hippeastrum
what is the taxonomic Genus of Daffodil?
Narcissus
what is the taxonomic Genus of Autumn Crocus?
Colchicum
what is the taxonomic Genus of Jonquil?
Narcissus
what is the taxonomic Genus of Glory lily?
Gloriosa
what is the taxonomic Genus of Christmas trees?
Pinus
what is the taxonomic Genus of Easter Lily?
Lilium
what is the taxonomic Genus of Tiger Lily?
Lilium
what is the taxonomic Genus of Day Lily?
Hemerocallis
what is the taxonomic Genus of Johnson grass?
Sorghum
what is the taxonomic Genus of sudan grass?
Sorghum
what is the taxonomic Genus of corn?
Zea
what is the taxonomic Genus of ergot?
Claviceps
what is the taxonomic Genus of Yew?
Taxus
what is the taxonomic Genus of Buckeye/Horse Chestnut?
Aesculus
what is the taxonomic Genus of Oak?
Quercus spp.
what is the taxonomic Genus of Red Maple?
Acer rubrum
what is the taxonomic Genus of Black Walnut?
Juglans nigra
what is the taxonomic Genus of St. John's Wort?
Hypericum perforatum
what is the taxonomic Genus of Buckwheat?
Fagopyrum sagittatum
what is the taxonomic Genus of Alfalfa?
Medicago sativa
what is the taxonomic Genus of Clover?
Trifolium spp.
what is the taxonomic Genus of Cherry?
Prunus spp
what is the taxonomic Genus of Sudan or Johnson grass?
Sorghum spp.
what is the taxonomic Genus of Flax?
Linum spp.
what is the taxonomic Genus of Sugar Beets (tops)?
Beta spp.
what is the taxonomic Genus of Arrow grass?
Triclochin spp.
what is the taxonomic Genus of Lantana, Red Sage?
Lantana spp.
what is the taxonomic Genus of Horse brush?
Tetradymia spp
what is the taxonomic Genus of Blue Green Algae?
Microcystis or Anabaena
what is the taxonomic Genus of Rhododendron?
Rhododendron maximum
what is the taxonomic Genus of Mountain Laurel?
Kalmia latifolia
what is the taxonomic Genus of Azalea?
Azalea spp.
what is the taxonomic Genus of Water Hemlock?
Cicuta maculata