Toxicology Final Exam

Front 1

what is the most common toxicosis in sheep?

Back 1

chronic copper toxicity

Front 2

what mineral is essential to keep sheep from getting copper toxicosis?

Back 2

molybdenum

Front 3

what two species have the most problems with copper toxicosis?

Back 3

sheep and dogs

Front 4

what is the mechanism of copper toxicosis?

Back 4

- 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

Front 5

what organ systems are targeted by copper toxicosis?

Back 5

liver, blood, renal

Front 6

characterize the epidemiologic curve for copper toxicosis. Why is it like this?

Back 6

- 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

Front 7

what are some clinical signs of chronic copper toxicity?

Back 7

- vomiting (dogs)
- hemolytic anemia
- hemoglobinuria
- anorexia, prostration, weakness
- icterus
- pica (sheep)

Front 8

what is a pathognomonic lesion of copper toxicity? What are some others?

Back 8

- GUN-METAL COLORED KIDNEYS
- icterus
- enlarged spleen

Front 9

how is chronic copper toxicity diagnosed in the sheep?

Back 9

- 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

Front 10

how is chronic copper toxicity diagnosed in the dog?

Back 10

- 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

Front 11

how is chronic copper toxicity treated in the sheep?

Back 11

- ammonium tetrathiomolybdate
- fluids for kidney problems
- steroids, ascorbic acid
- poor prognosis

Front 12

how is chronic copper toxicity treated in the dog?

Back 12

- trientine (chelator), fluids, steroids, ascorbic acid, Vitamin E, S-adenosylmethionine

Front 13

how is chronic copper toxicity prevented in the dog?

Back 13

- 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

Front 14

what year of penny did they start putting zinc into them?

Back 14

1983

Front 15

what are some sources of zinc?

Back 15

- 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

Front 16

what species is zinc toxicosis found?

Back 16

- dogs
- zoos (seals, ratites, hyenas) - ingesting pennies
- birds and ferrets from galvanized wire cages
- cattle: too much in feed

Front 17

where in the body is zinc excreted?

Back 17

bile and pancreatic secretions

Front 18

what are three mechanisms of action by which zinc is toxic?

Back 18

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

Front 19

acute zinc toxicosis in dogs:
- onset
- clinical signs
- pathologic lesions

Back 19

- 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

Front 20

what systems are affected by zinc toxicosis in the dog?

Back 20

GI, RBC, hepatic, renal

Front 21

what systems are affected by chronic zinc toxicosis in cattle?

Back 21

GI, RBC, hepatic, renal, bone

Front 22

chronic zinc toxicosis in cattle:
- onset
- clinical signs
- pathologic lesions

Back 22

- 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

Front 23

how is zinc toxicosis diagnosed?

Back 23

- 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

Front 24

how is zinc toxicosis treated?

Back 24

- 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

Front 25

name 9 liver toxicants

Back 25

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)

Front 26

name 11 toxicants that can cause hemolysis

Back 26

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

Front 27

how much lead is absorbed from the GI tract after ingestion?

Back 27

2-10%

Front 28

deficiency of which dietary minerals can increase lead uptake by the GI tract?

Back 28

calcium, zinc, and iron

Front 29

where is lead stored in the body?

Back 29

bone

Front 30

does lead cross the BBB and placenta?

Back 30

yes

Front 31

what is the major route of lead excretion?

Back 31

feces; bile adds to this; urinary route is only important in chelation

Front 32

comment on the renal excretion of lead

Back 32

not a major route of excretion unless chelation is involved

Front 33

what are the systems affected by lead toxicity?

Back 33

- GIT and CNS (the big ones)
- PNS, hematopoietic, renal

Front 34

what is the mechanism of action of lead toxicosis?

Back 34

- binds to SH groups on key metabolic enzymes
- may compete with or replace Zn in enzymes

Front 35

how does lead cause neurotoxicity? (3)

Back 35

- capillary damage via endothelial cells
- damage to BBB
- demyelination

Front 36

how does lead disrupt hematopoiesis?

Back 36

inhibits enzymes that synthesize heme (Alanine dehydratase and synthetase)

Front 37

how does lead cause renal toxicity? What is a histopathological indicator of lead toxicosis in the kidney?

Back 37

- damages renal tubular epithelium
- acid-fast intranuclear inclusion bodies can be found

Front 38

describe the clinical signs of the GI syndrome of lead toxicosis in dogs

Back 38

- vomiting, anorexia
- painful, tender abdomen
- constipation followed by diarrhea ± blood

Front 39

in the dog with lead toxicosis, comment on the timing of neurologic signs versus GI signs.

Back 39

GI signs may precede neurological signs

Front 40

describe the clinical signs of the GI syndrome of lead toxicosis in cattle.

Back 40

- anorexia
- rumen stasis or sluggishness
- constipation followed by diarrhea

Front 41

what type of seizures are associated with lead toxicosis in dogs?

Back 41

clonic-tonic

Front 42

describe the clinical signs of the CNS syndrome associated with lead toxicosis in dogs

Back 42

- ranges from depression to hysteria
- barking; muscle tremors
- behavioral changes
- clonic-tonic seizures
- they may be intermittent (makes diagnosis difficult)

Front 43

what is the major clinical sign of lead toxicosis in cattle?

Back 43

blindness

Front 44

what are a whole crap-load of clinical signs of lead toxicosis in cattle?

Back 44

- BLINDNESS; head pressing and/or depression
- bawling or bellowing
- muscle tremors; ears twitch rhythmically
- head bobbing; jaw chomping
- ataxia; incoordination; circling; stumbling

Front 45

what is a clinical sign of lead toxicosis in horses?

Back 45

roaring due to effects on recurrent laryngeal nerve

Front 46

what are some clinical signs of lead toxicosis in water fowl?

Back 46

- anorexia; diarrhea; weight loss
- weakness; lethargy; coma; death
- may see droopy wings

Front 47

how is lead toxicosis diagnosed in the lab?

Back 47

- blood lead (unclotted sample)
- tissue lead from liver and/or kidney

Front 48

what are two DDx of lead poisoning in dogs with GI syndrome?

Back 48

1. gastritis (e.g. ate garbage)
2. arsenic

Front 49

what are six DDx of lead poisoning in dogs with GI syndrome?

Back 49

1. distemper
2. encephalitis
3. organochlorines
4. strychnine
5. metaldehyde
6. organophosphates
7. carbamates

Front 50

what are three DDx of lead poisoning in cattle with GI syndrome?

Back 50

1. simple indigestion
2. polio
3. arsenic

Front 51

what are nine DDx of lead poisoning in dogs with GI syndrome?

Back 51

1. hemophilus
2. polio
3. hypomagnesemic tetany
4. nervous Acetonemia
5. brain abscess
6. brain neoplasia
7. organochlorines
8. urea toxicosis
9. salt toxicosis

Front 52

what is the main way in which lead poisoning is treated?

Back 52

chelation

Front 53

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?

Back 53

- 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

Front 54

what are three chelators for lead toxicosis in small animals?

Back 54

1. EDTA
2. DMSA (dimercaptosuccinic acid)
3. penicillamine

Front 55

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?

Back 55

- 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

Front 56

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?

Back 56

- oral
- has an SH group
- most useful for Copper, but also lead, arsenic, and zinc
- helpful in chronic toxicity cases

Front 57

what is a very useful chelator for lead toxicosis in cattle?

Back 57

Thiamin (Vitamin B1)

Front 58

besides chelators, what supplemental therapies are indicated for lead toxicosis? (5)

Back 58

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)

Front 59

what are two cattle sources of arsenic and one cat and dog source?

Back 59

- cattle: old pesticides; ashes from salt-treated lumber
- cat and dog: sweet, syrupy ant baits

Front 60

what is the most toxic valency of arsenic?

Back 60

3+

Front 61

inorganic arsenic toxicosis:
- routes of absorption
- sites of distribution
- excretion

Back 61

- 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.

Front 62

comment on the crossing of arsenic through BBB and placenta

Back 62

crosses placenta easily, but not the BBB

Front 63

what are two mechanisms of action of arsenic toxicosis?

Back 63

- 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

Front 64

what are the target organs of arsenic?

Back 64

GI and vascular

Front 65

(per)acute arsenic toxicosis:
- important clinical sign
- GI and other clinical signs
- important post-mortem finding

Back 65

- 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

Front 66

sub-acute arsenic toxicosis:
- clinical signs
- important post-mortem finding
- course

Back 66

- profuse, watery diarrhea
- PU/PD → oliguria & proteinuria → anuria
- dehydration, acidosis, poor circulation
- PM: BRICK RED HYPEREMIC GUT
- may see death in 4-7 days

Front 67

how is inorganic arsenic toxicosis diagnosed?
- empirically
- lab findings
- antemortem samples
- PM samples

Back 67

- onset time and lesions
- lab: ↑PCV and BUN; UA - proteinuria and casts
- antemortem samples: vomitus, feces, urine, hair
- PM samples: liver and kidney

Front 68

how is inorganic arsenic toxicosis treated (emergency and antidotes)?

Back 68

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

Front 69

what are the targets of organic arsenic toxicosis?

Back 69

nerves: demyelination and axonal damage; peripheral neuropathy

Front 70

what is a key clinical sign of organic arsenic toxicosis?

Back 70

blindness

Front 71

what genus of fungi are ionophores derived?

Back 71

Streptomyces

Front 72

which two species are ionophores most toxic?

Back 72

horse and sheep (horse > sheep)

Front 73

rank the following in order of MOST susceptible to least susceptible to ionophores:
- cattle
- chicken
- horse
- sheep
- swine

Back 73

horse > sheep > swine > cattle > chicken

Front 74

what other drug type can potentiate ionophore toxicity? Mechanism of action?

Back 74

macrolides (and some other antibiotics) and inhibit CYP450

Front 75

which ionophore most commonly causes toxicosis in dogs?

Back 75

lasalocid

Front 76

what is the mechanism of ionophore toxicosis?

Back 76

Toxic action related to influx of ions across mitochondrial membranes of heart & skeletal muscle; calcium accumulation intracellularly -> cell death & necrosis

Front 77

what are the target organs for ionophores in the horse?

Back 77

heart and skeletal muscles (both have lots of mitochondria)

Front 78

what are the three basic ways in which ionophores cause a net influx of Ca2+ into the muscle cells?

Back 78

1. free radicals
2. lipid peroxidation
3. ionophore binding to sarcolemmal membrane

Front 79

ionophore toxicosis in the horse:
- onset
- course
- clinical signs
- PM lesions

Back 79

- 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

Front 80

what would a horse heart look like on PM with ionophore toxicosis?

Back 80

Pale heart, white streaks: necrosis with secondary dystrophic calcification

Front 81

how does the "paleness" of the horse heart PM correlate with the chronicity of the toxicosis?

Back 81

Paleness: the ↑ dose, the faster you die, so ↑ dose → ↓white streaks

Front 82

what are the target organs for ionophores in ruminants?

Back 82

cardiac, skeletal muscle, GI

Front 83

ionophore toxicosis in ruminants:
- onset
- course
- clinical signs
- PM lesions

Back 83

- onset: 1-5 days
- course: 1 day - several weeks
- anorexia, ADR, diarrhea, myoglobinuria in sheep
- PM: pale heart and skeletal muscles; hydrothorax; ascites

Front 84

ionophore toxicosis in the dog/cat:
- onset
- course
- clinical signs
- PM lesions

Back 84

- 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

Front 85

what is the usual reason for death in dogs and cats with ionophore toxicosis?

Back 85

respiratory paralysis

Front 86

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

Back 86

- cat: heart > SM
- cattle: heart = SM
- dog: SM > heart
- horse: heart > SM
- pigs: SM > heart
- rabbits: heart = SM
- sheep: SM > heart

Front 87

when in the farm routine is ionophore toxicosis usually seen?

Back 87

usually occurs following the use of a new concentrate or mineral

Front 88

how is ionophore toxicosis treated?

Back 88

- 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

Front 89

what is the name of the toxin in blister beetles?

Back 89

cantharidin

Front 90

what type, cutting, and baling type of hay are blister beetles most commonly found?

Back 90

alfalfa, 3rd cutting (i.e. July hay), when the hay is crimped (rolled)

Front 91

about how many blister beetles does it take to kill a horse?

Back 91

about 30

Front 92

what is the mechanism of action of cantharidin?

Back 92

- 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

Front 93

what are the target organs for cantharidin?

Back 93

GI, renal, cardiac

Front 94

what are two important clinical signs of cantharidin (blister beetle) toxicosis in the horse?

Back 94

1. pollakiuria
2. synchronous diaphragmatic flutter (hiccups)

Front 95

cantharidin toxicosis in the horse:
- onset
- course
- two important clinical signs
- other clinical signs
- PM lesions

Back 95

- 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

Front 96

how is cantharidin toxicosis diagnosed?
- ID
- clin path
- what are other differentials for synchronous diaphragmatic flutter?

Back 96

- 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

Front 97

how is cantharidin toxicosis treated?

Back 97

- 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

Front 98

what is the toxin found in cotton seeds?

Back 98

gossypol

Front 99

rank the following from most toxic to least toxic:
- Whole cotton seed
- cotton seed meal
- cotton seed hulls
- cotton seed oil

Back 99

- cotton seed meal (most toxic)
- Whole cotton seed (toxic)
- cotton seed oil (no gossypol, but can turn rancid)
- cotton seed hulls (not toxic)

Front 100

what is the signalment for ruminants that are most susceptible to gossypol toxicosis?

Back 100

immature (e.g. lambs, calves)

Front 101

besides ruminants, what two other species can gossypol toxicosis be a problem?

Back 101

swine (very susceptible) and poultry (intermediate susceptibility)

Front 102

what are the mechanisms of action of gossypol toxicosis? (3)

Back 102

- 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.

Front 103

what are the target organ systems for gossypol toxicosis?

Back 103

cardiac, hepatic, repro

Front 104

what is an important clinical sign of gossypol toxicosis?

Back 104

tachypnea (THUMPS)

Front 105

gossypol toxicosis:
- onset
- course:
- key clinical sign
- other clinical sign
- PM lesions

Back 105

- 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

Front 106

how is gossypol toxicosis diagnosed?
- empirically
- lab
- clin path
- other non-gossypol problems with cotton

Back 106

- 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)

Front 107

how is gossypol toxicosis treated? (3)

Back 107

- Symptomatic
- Diuretic for pulmonary edema & congestive heart failure
- Remove source

Front 108

how is gossypol toxicosis prevented? (3)

Back 108

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

Front 109

what are six cardiac toxicants?

Back 109

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)

Front 110

what are 8 causes of rear leg paresis in the dog?

Back 110

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

Front 111

what is a key clinical sign of salt toxicosis in cattle?

Back 111

blindness

Front 112

which systems are affected by salt toxicosis in cattle?

Back 112

CNS, GI

Front 113

what are some clinical signs of salt toxicosis in cattle, including one key clinical sign?

Back 113

- BLINDNESS
- nervous: KNUCKLING, nystagmus, belligerency, seizures, paresis, bruxism
- GI: colic, thirst, diarrhea, mucus covered feces, rumen stasis, nasal discharge

Front 114

what are three key clinical signs and one key post-mortem sign of salt toxicosis in swine?

Back 114

1. blind
2. star gazing
3. jaw champing
- eosinophilic cuffing in brain

Front 115

which species shows perivascular cuffing in the brain with salt toxicosis?

Back 115

swine

Front 116

how is salt toxicosis treated in large animals?

Back 116

access to small amounts of water (0.5% bw) at one-hour intervals until rehydrated

Front 117

which genus of fungi is the most common source of molds from the STORAGE of feedstuff?

Back 117

Penicillium

Front 118

which species of fungus makes aflatoxin?

Back 118

Aspergillus flavus

Front 119

which crops are associated with aflatoxin?

Back 119

CORN, cotton seed, peanuts

Front 120

which natural conditions favor outbreaks of aflatoxin toxicosis?

Back 120

years of DROUGHT or insect damage to kernel

Front 121

what is an easy, but insensitive and non-specific way to detect Aspergillus flavus in ground corn?

Back 121

black light

Front 122

comment on the various aflatoxins ingested by cows and how they may be hazardous to humans

Back 122

Aflatoxin B1 metabolized in body to Afla M1, which comes out in milk; monitored closely by FDA because it is carcinogenic

Front 123

in which animals is aflatoxin toxicosis most common?

Back 123

POULTRY AND YOUNG SWINE

Front 124

what is the main organ system affected by aflatoxin?

Back 124

liver

Front 125

what is the mechanism of aflatoxin toxicosis?

Back 125

- 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

Front 126

chronic aflatoxicosis:
- onset
- clinical signs
- pathologic lesions

Back 126

- 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

Front 127

how is aflatoxicosis diagnosed?

Back 127

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

Front 128

what can be used to bind to aflatoxin and prevent it from being absorbed from the GI tract?

Back 128

anti-caking clays

Front 129

what is the main way to treat chronic aflatoxicosis?

Back 129

dilution is the solution: dilute the food so that aflatoxin levels are low and add anti-caking clays to adsorb

Front 130

what two species of molds produce trichothecene?

Back 130

1. Fusarium graminearium
2. Fusarium roseum

Front 131

what type of mold produces by trichothecenes and what is the main specific toxin that makes animals sick?

Back 131

- Fusarium molds
- vomitoxin

Front 132

vomitoxin
- crops
- genus that produces the toxin
- natural conditions favoring growth and production of this toxin

Back 132

- CORN and SMALL GRAINS
- Fusarium molds
- WET GROWING SEASONS

Front 133

what goes corn or grain look like when it is contaminated with trichothecenes (e.g. vomitoxin from Fusarium molds)?

Back 133

pink or rose color; "scabby grain" or "pink ear rot of corn"

Front 134

in which animals is vomitoxin most toxic?

Back 134

SWINE and DAIRY CATTLE

Front 135

what system does vomitoxin affect?

Back 135

GI

Front 136

vomitoxin clinical signs:
- onset
- most common clinical sign
- other clinical signs
- pathological lesions

Back 136

- 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

Front 137

how it trichothecene (vomitoxin) toxicosis diagnosed?

Back 137

- compatible signs and lesions with concentrations in feed
- onset of syndrome coincides with new batch of feed or silage

Front 138

how is trichothecene (vomitoxin) toxicosis treated?

Back 138

only by diluting the feed ± anticaking clays

Front 139

what three major types of toxins are produced by Fusarium molds?

Back 139

1. aflatoxins
2. zearalenone
3. ELEM (Fumonisin)

Front 140

in what crops do you find zearalenone?

Back 140

CORN and SMALL GRAINS

Front 141

what toxin might you suspect from corn stored in open-air cribs?

Back 141

zearalenone

Front 142

which species is most susceptible to zearalenone toxicosis?

Back 142

swine

Front 143

what is the mechanism of action of zearalenone toxicosis?

Back 143

- 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

Front 144

what organ system is affected by zearalenone toxicosis?

Back 144

reproductive system

Front 145

zearalenone toxicosis:
- onset
- clinical signs
- pathologic lesions

Back 145

- 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

Front 146

how is zearalenone toxicosis diagnosed?

Back 146

- 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

Front 147

how do you treat zearalenone toxicosis?

Back 147

- 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

Front 148

how is zearalenone toxicosis prevented?

Back 148

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

Front 149

which mold produces slaframine?

Back 149

Rhizoctonia leguminicola

Front 150

in which crop is slaframine found?

Back 150

hay; legumes like clover, alfalfa, etc.

Front 151

in what species does slaframine cause problems and what is the key clinical sign?

Back 151

HORSES; it makes them SLOBBER

Front 152

what is the mechanism of action of slaframine?

Back 152

- 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

Front 153

slaframine:
- onset
- course
- key clinical sign
- other clinical signs

Back 153

- onset: 1 hour
- course: 1-3 days
- SALIVATION (continuous or gushers)
- lacrimation, piloerection, anorexia, polyuria, diarrhea, bloat, abortion (rare), death (rare)

Front 154

what system is affected by slaframine?

Back 154

GI

Front 155

how is slaframine toxicosis treated?

Back 155

- usually nothing
- don't give atropine (ileus); give antihistamines if owners insist

Front 156

how is slaframine toxicosis prevented?

Back 156

avoid buying legume hay, especially second cutting clover hay in a wet growing year

Front 157

ELEM (Fumonisin)
- type of mold
- crop on which it is found
- time of year
- epidemiology

Back 157

- Fusarium
- grows on corn
- most cases in the coldest months (December, January)
- low morbidity; high mortality; sporadic

Front 158

which species are susceptible to fumonisin toxicosis?

Back 158

all equidae and swine (equids > swine)

Front 159

what organ systems does fumonisin toxicosis affect?

Back 159

CNS, hepatic (rare)

Front 160

what are two key clinical signs and a key pathologic lesion of fumonisin toxicosis?

Back 160

1. BLINDNESS
2. BIZARRE MANIACAL BEHAVIOR (Horse goes bonkers)
- LIQUEFACTIVE NECROSIS OF THE WHITE MATTER OF THE BRAIN

Front 161

fumonisin:
- onset
- course
- 2 key clinical signs
- other clinical signs
- key pathologic lesion

Back 161

- 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

Front 162

what is the key clinical sign of hepatoencephalopathy caused by fumonisin toxicosis?

Back 162

REPEATED YAWNING

Front 163

diagnosis of fumonisin toxicosis:
- how
- how to you differentiate from EEE and West Nile?
- what is a major differential for the liver syndrome?

Back 163

- 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

Front 164

how is fumonisin toxicosis treated and prevented?

Back 164

- 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

Front 165

what are three genera of fungi that produce tremorgens?

Back 165

1. Aspergillus
2. Penicillium
3. Neotyphodium lolii

Front 166

in which plants are Neotyphodium tremorgens found?

Back 166

perennial ryegrass

Front 167

what are three types of grass that commonly have tremorgen containing fungi?

Back 167

1. Perennial ryegrass
2. Bermuda grass
3. Dallis grass

Front 168

what are Penicillium based tremorgens found?

Back 168

moldy milk products, English & black walnut hulls, decaying food, garbage, compost piles, road kill, poultry litter, etc.

Front 169

what are two tremorgens produced by Penicillium molds?

Back 169

1. Penitrem A
2. Roquefortine

Front 170

what canine toxicant is in Dr. Blodgett's top 5 toxicoses fo dogs and "gets no respect in the literature?"

Back 170

tremorgens: Penitrem A and roquefortine

Front 171

characterize the seizures caused by tremorgens

Back 171

clonic-tonic

Front 172

what organ system is affected by tremorgens?

Back 172

CNS

Front 173

tremorgens:
- onset
- course
- clinical signs

Back 173

- onset: minutes - several days
- course: 1 day - 1 week
- muscle tremors, clonic-tonic convulsions, hyperesthesia, paralysis/prostration, nystagmus/anisocoria, salivation, ± vomiting

Front 174

how is tremorgen toxicosis diagnosed?

Back 174

- 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.

Front 175

treatment of tremorgen toxicosis:
- large animals
- dogs

Back 175

- 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

Front 176

aflatoxin:
- feed(s) associated
- species susceptible
- target systems

Back 176

- feed(s) associated: corn (drought)
- species susceptible: poultry, swine, dairy cattle
- target systems: liver, ADR, dairy/residue

Front 177

vomitoxin:
- feed(s) associated
- species susceptible
- target systems

Back 177

- feed(s) associated: corn, small grains (wet)
- species susceptible: swine, dairy cattle
- target systems: GI (feed refusal)

Front 178

zearalenone:
- feed(s) associated
- species susceptible
- target systems

Back 178

- feed(s) associated: corn (zea)
- species susceptible: swine
- target systems: reproductive

Front 179

slaframine:
- feed(s) associated
- species susceptible
- target systems

Back 179

- feed(s) associated: clovers
- species susceptible: horses
- target systems: GI-saliva

Front 180

fumonisin:
- feed(s) associated
- species susceptible
- target systems

Back 180

- feed(s) associated: corn
- species susceptible: HORSES, swine
- target systems: CNS, LIVER, pulmonary, heart

Front 181

penetrem A:
- feed(s) associated
- species susceptible
- target systems

Back 181

- feed(s) associated: dairy, walnuts
- species susceptible: dogs, cats
- target systems: CNS

Front 182

Roquefortine:
- feed(s) associated
- species susceptible
- target systems

Back 182

- feed(s) associated: decaying organic
- species susceptible: dogs
- target systems: CNS

Front 183

what is the taxonomic Genus of tobacco?

Back 183

Nicotiana

Front 184

what is the taxonomic Genus of mistletoe?

Back 184

Phoradendron

Front 185

what is the taxonomic Genus of poinsettia?

Back 185

Poinsettia

Front 186

what is the taxonomic Genus of holly?

Back 186

Ilex

Front 187

what is the taxonomic Genus of purple foxglove?

Back 187

Digitalis

Front 188

what is the taxonomic Genus of lily of the valley?

Back 188

Convallaria

Front 189

what is the taxonomic Genus of oleander?

Back 189

Nerium

Front 190

what is the taxonomic Genus of marijuana?

Back 190

Cannabis

Front 191

what is the taxonomic Family of Dieffenbachia - Dumb Cane?

Back 191

Araceae

Front 192

what is the taxonomic Family of Split Leaf philodendron?

Back 192

Araceae

Front 193

what is the taxonomic Family of Elephant ear plant?

Back 193

Araceae

Front 194

what is the taxonomic Family of Caladium?

Back 194

Araceae

Front 195

what is the taxonomic Family of Pothos (philodendron)?

Back 195

Araceae

Front 196

what is the taxonomic Family of Peace Lily?

Back 196

Araceae

Front 197

what is the taxonomic Family of Jack in the Pulpit?

Back 197

Araceae

Front 198

what is the taxonomic Family of Skunk Cabbage?

Back 198

Araceae

Front 199

what is the taxonomic Genus of Tulip?

Back 199

Tulipia

Front 200

what is the taxonomic Genus of Iris?

Back 200

Iris

Front 201

what is the taxonomic Genus of Hyacinthus?

Back 201

Hyacinthus

Front 202

what is the taxonomic Genus of Amaryllis?

Back 202

Hippeastrum

Front 203

what is the taxonomic Genus of Daffodil?

Back 203

Narcissus

Front 204

what is the taxonomic Genus of Autumn Crocus?

Back 204

Colchicum

Front 205

what is the taxonomic Genus of Jonquil?

Back 205

Narcissus

Front 206

what is the taxonomic Genus of Glory lily?

Back 206

Gloriosa

Front 207

what is the taxonomic Genus of Christmas trees?

Back 207

Pinus

Front 208

what is the taxonomic Genus of Easter Lily?

Back 208

Lilium

Front 209

what is the taxonomic Genus of Tiger Lily?

Back 209

Lilium

Front 210

what is the taxonomic Genus of Day Lily?

Back 210

Hemerocallis

Front 211

what is the taxonomic Genus of Johnson grass?

Back 211

Sorghum

Front 212

what is the taxonomic Genus of sudan grass?

Back 212

Sorghum

Front 213

what is the taxonomic Genus of corn?

Back 213

Zea

Front 214

what is the taxonomic Genus of ergot?

Back 214

Claviceps

Front 215

what is the taxonomic Genus of Yew?

Back 215

Taxus

Front 216

what is the taxonomic Genus of Buckeye/Horse Chestnut?

Back 216

Aesculus

Front 217

what is the taxonomic Genus of Oak?

Back 217

Quercus spp.

Front 218

what is the taxonomic Genus of Red Maple?

Back 218

Acer rubrum

Front 219

what is the taxonomic Genus of Black Walnut?

Back 219

Juglans nigra

Front 220

what is the taxonomic Genus of St. John's Wort?

Back 220

Hypericum perforatum

Front 221

what is the taxonomic Genus of Buckwheat?

Back 221

Fagopyrum sagittatum

Front 222

what is the taxonomic Genus of Alfalfa?

Back 222

Medicago sativa

Front 223

what is the taxonomic Genus of Clover?

Back 223

Trifolium spp.

Front 224

what is the taxonomic Genus of Cherry?

Back 224

Prunus spp

Front 225

what is the taxonomic Genus of Sudan or Johnson grass?

Back 225

Sorghum spp.

Front 226

what is the taxonomic Genus of Flax?

Back 226

Linum spp.

Front 227

what is the taxonomic Genus of Sugar Beets (tops)?

Back 227

Beta spp.

Front 228

what is the taxonomic Genus of Arrow grass?

Back 228

Triclochin spp.

Front 229

what is the taxonomic Genus of Lantana, Red Sage?

Back 229

Lantana spp.

Front 230

what is the taxonomic Genus of Horse brush?

Back 230

Tetradymia spp

Front 231

what is the taxonomic Genus of Blue Green Algae?

Back 231

Microcystis or Anabaena

Front 232

what is the taxonomic Genus of Rhododendron?

Back 232

Rhododendron maximum

Front 233

what is the taxonomic Genus of Mountain Laurel?

Back 233

Kalmia latifolia

Front 234

what is the taxonomic Genus of Azalea?

Back 234

Azalea spp.

Front 235

what is the taxonomic Genus of Water Hemlock?

Back 235

Cicuta maculata