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Toxicology Final > Spiders/Insects > Flashcards

Spiders/Insects Flashcards

1
Q

where is spider venom stored?

A

2 glands located in cephalothorax and delivered via fangs (chelicerae)

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2
Q

are all spiders capable of an envenomating bite?

A

yes except for ones in the family Ulobiridae

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3
Q

spider bite severity

A
  • most only cause local swelling and pain
  • anaphylaxis and other allergic rxns possible
    likely that fewer than 100 species have significant bites
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4
Q

widow spiders (Latrodectus spp) identification

A
  • red, yellow or orange hourglass marking on ventral abdomen
  • fangs of male are too short to cause harm to mammals
  • 5 major species in the US
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5
Q

where are widow spiders found?

A

mostly outside of living spaces, prefer dark secluded spaces: debris piles, densely growing plants
- adults most active during the warm months: due during colder months
- in general are shy and don’t bite unless provoked

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6
Q

widow venom MOA

A
  • mix of 6 neuroactive proteins and enzymes
  • principle toxin is alpha-latrotoxin
  • causes large release and then depletion of ACh and NE at postganglionic sympathetic synapses
  • venom extremely potent! takes tiny amount to kill
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7
Q

what is the widow venom syndrome?

A

lactrodectism

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8
Q

lactrodectism

A
  • widow venom syndrome
  • venom taken up by lymph, enters blood, short lived localized pain at site
  • 30-120 mins then pain spreads to large muscle groups all thru body: peaking at 2-3 hours
  • mild to moderate hypertension and tachycardia
  • signs resolve in 48-72 hrs but weakness, fatigue, insomnia may persist for weeks-months
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9
Q

cats and widow bites

A

cats very sensitive! paralysis occurs early on: severe pain, howling, vocalizations
- hypersalivation, restlessness, V+/D+
- muscle tremors, cramping, may precede an atonic paralysis
- Cheyne-Stokes respiratory pattern may develop prior to death

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10
Q

Cheyne-Stokes respiratory pattern

A

shallow, coarse hard breathing pattern: may develop in cats before death from a widow bite

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11
Q

treatment of widow venom

A
  • antivenin! Lycovac!
  • largely symptomatic
  • opioids for pain, diazepam and methocarb for muscle rigidity, calcium gluconate no longer recommonded
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12
Q

what antivenin is available for widow venom?

A

equine-origin antivenin Lycovac! cheap and effective, long shelf-life
case study shows activity in felines!

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13
Q

Recluse or Violin Spiders: Loxesceles spp

A
  • 50 species, few capable of significance
  • brown recluse (L. reclusa) is only one of medical significance: missouri, arkansas, oklahoma, kansas, etc
  • south american species in LA inflicts serious envenomation
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14
Q

MOA of recluse spider venom

A
  1. necrotizing enzymes: hyaluronidase, esterases, alkaline phosphatases
  2. sphingomyelinase D: phospholipase
  3. inactivates serum hemolytic complement
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15
Q

what are the necrotizing enzymes that recluse spider venom contain?

A
  • hyaluronidase: breaks down collagen
  • esterases: breaks down tissues
  • alkaline phosphatases: breaks down membranes
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16
Q

what does sphingomyelinase D do?

A
  • recluse spider venom
  • phospholipase: binds to cell membranes and induces migration and activation of neutrophils to the site of envenomation
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17
Q

inactivating serum hemolytic complement causes

A
  • intravascular coagulation
  • occlusion of small capillaries
  • tissue necrosis
  • systemic depletion of clotting factors( VII, IX, XI, XII)
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18
Q

clinical signs of brown recluse envenomation in dogs

A

thrombocytopenia, hemolysis, hemorrhage, hypocellular bone marrow
- 3-8 hours after envenomation, site becomes red, swollen and tender = “bulls eye lesion”
- systemic signs rare, but may develop 48-72 hrs after exposure: hemolysis with anemia, tachycardia, pyrexia, rare

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19
Q

treatment of brown recluse induced necrotic lesions

A
  • chemical debridement: Burrows solution (aluminum acetate) or H2O2 and bandage
  • pruritis can be controlled with diphenhydramine
  • antibiotics w infection
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20
Q

pain management of brown recluse venom

A

analgesics: NSAIDs for minor, opioids for severe

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21
Q

what specific medication is for brown recluse venom treatment?

A

Dapsone (4,4 diaminodiphenylsulfone) : inhibits neutrophil migration and may limit the severity of the necrotic lesions
- experimental antivenins developed, effective if given within 4 hrs of envenomation, but none are commercially available

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22
Q

Hobo spiders: Tegenaria Agretis

A
  • native to europe but new to PNW
  • poor climbers; build funnel web at ground level or in basements. males leave webs at night to search for ladies, males are more venomous and more likely to bite
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23
Q

hopbo spider envenomation is called

A

tegenarism

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24
Q

hobo spider envenomation signs

A
  • initial bite relatively painless
  • within 30 mins, expanding area of erythema w lesion reaching 15cm in diameter
  • 15-35 hrs area will rupture with serious d/c
  • wound may require 3 years to heal in fatty tissue
  • in humans signs are headache, nausea, weakness, vision. fatalities are rare
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25
Q

tenegarism is caused by what dangerous spider?

A

Hobo spiders: tegenaria agretis

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26
Q

treatment of hobo spider venom

A
  • supportive and symptomatic
  • local lesion and txt same as brown recluse
  • hasn’t been reported in companion animals
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27
Q

Funnel Web Spiders: Atrax and Hadronyche spp

A

35 species all found in Australia
- A. robustus is most dangerous and human fatalities are reported!
- large, aggressive black spiders

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28
Q

toxic component of funnel web spider venom

A

neurotoxin: rubustotoxin
- 42 amino acid protein
- binds to pre-synaptic neuron and inhibits CNS-mediated NT release while increasing NT release
- affects ANS and skeletal muscles
- other species have similar toxins that are less potent

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29
Q

rubustoxin accompanies what spider bite?

A

funnel web spider: neurotoxin

30
Q

what is more potent: male or female funnel web spiders?

A

males: 6X more potent venom than females

31
Q

dogs and cats and funnel web spiders?

A

relatively resistant: bites only cause mild, transient effects
- humans and primates very sensitive

32
Q

tarantulas :)

A
  • large, ground dwelling spiders
  • males wander in search of females during mating season, may be aggressive then
  • dozen genera that may deliver bad bite
  • species in US are not capable of delivering serious envenomation :))))))
33
Q

clinical signs of tarantula bite

A

muscle spasms, edema, hemoglobinuria, jaundice, circulatory shock may develop

34
Q

toxic tarantulas

A
  • from land down under: south america, africa, australia
  • venom has neurotoxin, potentially a necrotoxin and hemolytic toxin
  • tarantulas of family Therasphosidae (bird eating or whistling) are often kept as pets in Australia: bad for dogs and cats!!
35
Q

dangerous tarantulas

A

selenocosmia, phlogiellus
not native to US but who knows

36
Q

scorpions

A
  • arachnids with large paired claws and 4 pairs of legs
  • caudal portion of abdomen: tail that terminates in the telson: barbed appendage that houses 2 venom glands that exit via a stinger
    1400 species exist everywhere except antarctica. most seen in tropical or temperate regions
37
Q

main genera of scorpions found in US

A

Centruroides
only arizona bark scorpion is considered capable of inflicting a life-threatening sting

38
Q

MOA of scorpion venom

A
  • vary between genera and location
  • venom consists of a mix of low molecular weight polypeptides
  • at least 2 potent neurotoxins have been ID: a-scorpion and B-scorpion
  • these venoms block voltage-sensitive Na and K channels in nerves
39
Q

what do a-scorpion and B-scorpion toxin block?

A

voltage-sensitive K+ and Na+ channels in nerves

40
Q

scorpion venom toxicity. cats and dogs?

A
  • sharp, instant pain at site
  • local edema and pruritis
  • regional L.N may enlarge, potentially an allergic reaction
  • numbness of face, myalgia, tachycardia or bradycardia, seizures
  • lack of evidence that is a big issue in dogs and cats! no fatalities reported
  • potentially 100% fatality of stings in ferrets!
41
Q

treatment of scorpion venom

A
  • analgesics and wound care
  • systemic signs treated symptomatically
  • no FDA approved antivenins
  • no evidence that it’s a huge concern, but good to be prepared!
42
Q

Ixodida

A

ticks! 43 species worldwide, tick paralysis! north america, europe, africa, soviet union

43
Q

tick toxin MOA

A
  • exact MOA unknown
  • suspect that toxin interferes with synthesis and/or release of ACh at the NMJ: results in LMN paresis/paralysis
  • effect similar to botulinum toxin
  • australian tick differs, has effect on CNS centers
44
Q

tick toxin frequency

A
  • tick paralysis seen in basically any animal
  • paralysis has occured following the bite of as few as one tick. heavily infested animals succumb quick
45
Q

clinical signs of tick toxin toxicity

A
  • ascending ataxia that progresses to paresis and flaccid paralysis
  • early animals remain BAR and normal
  • eventually paralysis of respiratory muscles leads to respiratory failure and death
46
Q

treatment of tick toxin

A
  • remove ticks!
  • supportive care + respiratory support
  • topical insecticides
  • prognosis good where ticks are removed before bulbar paralysis
  • australian drug antiserum has been developed but is only effective early
47
Q

Myriapoda

A

centipedes and millipedes
- all centipedes have a pair of modified front legs (forcipules) that serve as fangs and are connected to venomous glands under the head
- legs can also penetrate skin and toxin at attachment point can go in!

48
Q

myriapoda toxicity

A
  • centipede venom not widely studied, but local pain
  • doesn’t lead to systemic toxicosis, causes local irritation and potentially necrosis
  • signs subside within 48 hrs and just need analgesics
48
Q

millipede toxicosis

A

don’t bite, but emit irritating and foul-smelling secretions from repugnatorial glands: irritating to mucosal surfaces, esp the eyes! corticosteroids recommended to decrease inflammation

49
Q

hymenoptera

A

bees, wasps, hornets
venom secreted from special cells in acid gland and transported to venom sace
- honeybees can only sting once due to barbs resulting in the apparatus being pulled from the bee, wasps and hornets can sting multiple times

50
Q

hymenoptera venoms

A
  • honeybees: proteins, peptides, and small organic molecules
  • vespid wasps: peptides, enzymes, amines designed to trigger pain
51
Q

honeybee venoms

A
  • Phospholipases and hyaluronidases present in the venom account for the majority of allergic reactions.
    – Mellitin is a membrane disruptive compound that increases the damage caused by phospholipases and triggers the release of histamine and serotonin.
    – Apamin is a neurotoxin that blocks Ca++-activated K+-channels and is associated with transient peripheral nerve effects.
    – In cats, bee venom can cause contraction of bronchiolar muscles
52
Q

wasp venoms

A

– Primary pain inducing substances are kinins.
– Serotonin, histamine, tyramine, catecholamines and acetycholine can contribute to pain and local vasoactivity
– Several constituents can act as allergens and trigger reactions

53
Q

hymenoptera toxicity

A
  • single sting is a transient, painful prick
  • deaths of livestock from Africanized bees
  • local rxns: swollen, edematous, plaques
  • systemic: convulsions, CNS, shock, V/D, renal and hepatic toxicity
  • classic anaphylactic response to bee and wasp venoms in dogs: IMHA secondary to bees has been reported
54
Q

treatment of hymenoptera venom

A
  • examine to see if stinger remains
  • cold compresses for pain and swelling
  • monitor for anaphylaxis: epinephrine if suspecting it
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Toxicology Final (4 decks)

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