Unit 1 - Other Insecticides, Avicides, Herbicides, and Fungicides

Question 1

What are the sources of rotenone?

Answer 1

Restricted use pesticide and old products out of use

Question 2

Rotenone is extremely toxic to what species?

Answer 2

fish

Question 3

Are dogs or cats more sensitive to rotenone?

Answer 3

Cats are more sensitive

Question 4

What is the MOA of rotenone?

Answer 4

It interferes with electron transport synthesis resulting in decreased ATP synthesis

Question 5

What does rotenone interact with?

Answer 5

It is synergistic with pyrethrins/pyrethroids

Question 6

What clinical signs are associated with rotenone toxicosis?

Answer 6

Vomiting, lethargy, tremors, seizures, hypoglycemia

Mass die off in fish populations

Question 7

What samples are used to detect rotenone toxicosis?

Answer 7

Vomitus, blood, and urine

Question 8

How is rotenone toxicosis treated?

Answer 8

Decontamination and supportive care (diazepam, oxygen, and dextrose IV)

Question 9

What type of drug is imidacloprid?

Answer 9

It is a neonicotinoid - very safe

Question 10

What is the MOA of imidacloprid?

Answer 10

It blocks post synaptic receptors in insects

Question 11

Should there be any concern for imidacloprid use?

Answer 11

There is environmental concern because pollinating species are susceptible

Question 12

What are the sources of fipronil?

Answer 12

Frontline, max force bait station, and seed corn products

Question 13

What is the MOA of fipronil?

Answer 13

It inhibits GABA which increases excitation

Question 14

What is the MOA of hydramethylon?

Answer 14

It inhibits metabolism which decreases ATP synthesis

Question 15

What is danger with hydramethylon associated with?

Answer 15

Trauma from eating the containers are more problematic than the drug itself - the drug itself isn’t really a concern

Question 16

T/F: Insect growth regulators like Methoprene and Luferon are very safe products.

Answer 16

True

Question 17

What is 4-Aminopyridine (Avitrol) used for?

Answer 17

It is an avicide that is used to ward off pest birds from certain areas

Question 18

Avitrol has ____ oral absorption and ____ dermal absorption.

Answer 18

rapid, low

Question 19

What is the MOA of Avitrol?

Answer 19

It blocks K channels and increases the release of ACh at synapses

Question 20

When does the onset of clinical signs due to Avitrol toxicosis occur?

Answer 20

15 minutes

Question 21

What clinical effects does Avitrol cause?

Answer 21

Hyperexcitability, tremors, convulsions, salivation, and cardiac and respiratory arrest

Question 22

What may happen in birds when they are exposed to Avitrol?

Answer 22

They become disoriented and emit a distress cry to scare others away

Question 23

What samples can Avitrol be detected in?

Answer 23

Vomitus, stomach content, liver, and bait

Question 24

What does the canine CNS panel at ISU screen for?

Answer 24

Strychnine, nicotine, caffeine, 4-aminopyrindine

Question 25

How is Avitrol toxicosis treated?

Answer 25

Decontamination, fluids, treat acidosis, and supportive care

Question 26

What are the environmental and human health considerations for Avitrol?

Answer 26

All species are susceptible It can cause mass deaths in bird populations Potential for relay toxicosis Food safety impact is unknown

Question 27

What species is the intended use for Starlicide?

Answer 27

Starlings, gulls, and other unwanted birds

Question 28

What is the MOA for Starlicide?

Answer 28

It is unknown - nephrotoxic

Question 29

When is the onset of clinical signs for Starlicide toxicity?

Answer 29

Hours to Days

Question 30

What samples are used for diagnosis of Starlicide?

Answer 30

Stomach/Crop contents, liver, and kidney

Question 31

How is Starlicide treated?

Answer 31

Supportive

Question 32

What is the prognosis for Starlicide toxicity?

Answer 32

Guarded

Question 33

What is an herbicide?

Answer 33

A substance that kills plants

Question 34

What is the difference between a selective and a non-selective herbicide?

Answer 34

A selective herbicide targets specific plants whereas a non-selective herbicide kills everything

Question 35

What type of herbicide is Paraquat?

Answer 35

A non-selective herbicide

Question 36

What degrades paraquat?

Answer 36

Sunlight - 3 days

Question 37

What inactivates paraquat?

Answer 37

Soil and clay

Question 38

Paraquat is ____ soluble, concentrates in the ______, and is excreted in the ______ unmetabolized.

Answer 38

water, lungs, urine

Question 39

What is the MOA of paraquat?

Answer 39

It is taken up by alveolar cells and then is reduced into a free radical when O2 is present

Question 40

What clinical signs due to paraquat toxicosis are early onset?

Answer 40

Vomiting, ataxia, and seizures

Question 41

When do respiratory clinical signs onset due to paraquat toxicosis?

Answer 41

2-7 days

Question 42

What respiratory clinical signs does paraquat toxicosis cause?

Answer 42

Tachypnea, dyspnea, moist rales, hypoxia, cyanosis, and death

Question 43

What gross lesions are associated with paraquat toxicosis?

Answer 43

Congestion, hemorrhage, emphysema

Question 44

What microscopic lesions are associated with Paraquat toxicosis?

Answer 44

Necrosis of alveolar epithelium, emphysema, fibrosis, and renal tubular necrosis

Question 45

What samples are used to detect paraquat?

Answer 45

Lung, urine, stomach contents, and bait

Question 46

What sample is used for histopath in cases of paraquat toxicosis?

Answer 46

lung

Question 47

How is paraquat toxicosis treated?

Answer 47

Early decontamination and supportive care (antioxidants, fluid diuresis, and ventilation

Question 48

What is the preferred decontaminant for paraquat toxicosis?

Answer 48

Bentonite clay

Question 49

What is the prognosis for paraquat toxicosis?

Answer 49

hopeless if signs are present

Question 50

What is the difference between diquat and paraquat?

Answer 50

Diquat does not concentrate in the lung | The affected tissues are the GI tract, liver, and kidney

Question 51

Phenoxy herbicide poisonings are rare unless what happens?

Answer 51

Concentrate or tank mix is ingested

Question 52

Phenoxy herbicides are an indirect cause of what?

Answer 52

nitrate poisoning

Question 53

Phenoxy herbicides have ____ distribution, _____ accumulation, _____ metabolism, and is excreted in ______.

Answer 53

Wide, little, little, and urine

Question 54

What is the MOA of phenoxy herbicides?

Answer 54

Dogs - decreased chloride conductance Decreased ribonuclease synthesis which decreases proteins Uncoupling of oxidative phosphorylation

Question 55

What clinical effects does phenoxy herbicide toxicosis cause in cattle?

Answer 55

Anorexia, diarrhea, rumen stasis and bloat, and oral ulceration

Question 56

What clinical effects does phenoxy herbicide toxicosis cause in dogs?

Answer 56

Vomiting, diarrhea, posterior weakness, and seizures

Question 57

What will you see on chemistry in patients with herbicide toxicosis?

Answer 57

Increased ALP and CPK

Question 58

What samples will you use for diagnosis of phenoxy herbicide toxicosis?

Answer 58

Forage, rumen, and urine

Question 59

How is phenoxy herbicide toxicosis treated?

Answer 59

Decontamination (emesis and AC) and supportive care

Question 60

What clinical signs can roundup (glyphosate) cause?

Answer 60

Ocular irritation, contact dermatitis, and GI irritation

Question 61

What is the MOA of dinitro compounds?

Answer 61

Uncouples oxidative phosphorylation which decreases ATP

Question 62

What concerns do we have with Atrazine toxicosis?

Answer 62

reproductive concerns

Question 63

What are the sources of fungicides?

Answer 63

Seed protectants Fruit, vegetable, crop, and grass applications Wood preservatives

Question 64

Why is toxic chemical is in CCA treated wood?

Answer 64

25% arsenic which presents a hazard to livestock

Question 65

What are the most toxic herbicides overall?

Answer 65

Dipyridyl products