poisonous insects with their effects on health of animals

1. Submitted by : ROLL NO : 07, 20, 43
BVSc &AH,6th sem
Agriculture and Forestry University
Rampur, Chitwan, Nepal

2. • Bees
• Hornets
• Wasps
• Ants

3. Venomous animal vs Poisonous
animal
Venomous
animal
Poisonous
animal
Those which produce
venom in specialized
glands or cells and deliver
it either by biting or
stinging or in some case
by squirting or spiting
Those who possess a
toxin(s) within its tissue
that can have deleterious
effect when ingested.

4. Introduction
Most insects of veterinary and human importance
belong to:
order : Hymenoptera
Under the order hymenoptera the poisonous insect
(have true stingers) fall under THREE important
families:
1. Apidae :honeybees
2. Vespidae : wasps and hornet
3. Formicidae : ants

5. Honeybees, Wasps and Hornets
1. Flying insects
2. Distributed worldwide
3. Found in greater numbers in mild climate
4. Located in secluded places
5. Exposure to them occurs when animal unintentionally
or intentionally disturbs a nest or a swarm.
6. Attacks as a group until they perceive danger has
passed
7. Multiple stinging is dangerous and maybe life
threatening

6. 8. Release of alarm pheromones during stinging which
attracts others bees to the location.
9. Stinging apparatus is modified oviposter connected to
venom sac
10. Grasps the victim’s skin through claws and insert the
sting
Wasps Bees
Able to withdraw
their stingers and
capable of stinging
again
Barbed stinger and
venom sac remain
attached to the skin
when bee fly away
resulting in death

7. Toxic component of venom
1. Histamine
2. Serotonins
3. Kinins
4. Hyaluronidase
5. Phospholipases A and B
6. Formic acid (cytotoxin)
7. Mellitin(specific protein in bee venom)
8. Formaldehyde
Bee venom may also contain toxin from plants like
oleander, rhododendron, azalea,etc

8. TOXICITY
All animals are susceptible to toxic effects and one sting
might release 50ul of venom
TOXICOKINETIC
1. LOCALIZED ACTION: venom remain at the site of
stinging
2. SYSTEMIC TOXICITY: when animal is stung many
times at once, then sufficient venom id absorbed into
sytemic circulation

9. MECHANISM OF ACTION
1. Mild cases : multiple constituents of venom produce
local pain, irritation and swelling.
2. Severe cases: in multiple stings, the systemic
absorption of venom contituents (histamine, kinins,
and proteins) produce:
 Acute allergic response: VASODILATION,
HYPOTENSION, BRONCHOCONSTRICTION and
inflammation and oedema of tissue
 The above is followed by delayed response :
HAEMOLYSIS, RHABDOMYOLYSIS and RENAL
FAILURE

10. MECHANISM OF ACTION
3. ALLERGIC RESPONSE:
Binding of venom components circulating in body with
antibodies associated with mast cell resting in vital
organs
Histamine and other biologically active substance
release
Leakage of fluid out of blood and into body tissues

11. Blood pressure drops dangerously low, fluid build up in
lungs, and laryngospasm and bronchospasm start
If not reversed with in short time, the patient could die
of anaphylatic shock

12. Clinical signs
 Usually begins immediately after sting or up to 30 minutes
later and might last for hours
Localized toxicity Systemic toxicity
• Mild to severe pain
• Heat and swelling
around the sting
• Swollen area may be
itchy and pinkish-red
in color
The above local reaction
normally subside
With in few hours
except in case of large
local reaction also
involving adjacent areas
it may persit up to week
• Redness and swelling on
distant sites from sting like
lips, muzzle, eyelids, tongue,
and vulva
• Pronounced excitement due to
pain
• In horse: diarrhoea,
haemoglobinuria, jaundice,
tachycardia, tachypnoea,
sweating, and prostration
maybe seen
• Attack on head may cause
dyspnoea because of severe
swelling
• Closing of airway and shock
• Rare case of fatal attack

13. POST-MORTEM FINDING
1. LOCALIZED :
I. small puncture sites with possible intercalation of
stinger in the epidermis and dermis
II. Redness, swelling, heat and eosinophilic
accumulation in 0.5 to 2 cm region around the sting

14. POST-MORTEM FINDING
2. SYSTEMIC TOXICITY:
I. Variable lesions like allergic encephalitis, angio-
edema, generalised utricara, and erythema
II. Haemorrhages and edema of all connective tissue
and intestinal wall may be seen

15. Treatment
Specific antedotes for venoms are not available.
a) Removal of stinger by scraping across the site with a
blunt-edged object
b) Wash stinged area with soap and water. Apply ice to
manage swelling, edema and pruritus. Application of
a weak solution of ammonia or sodium bicarbonate
helps
c) Affected area can be rubbed with anti-histaminic
cream

16. d. Analgesic and glucocorticoid (prednisone) can be
administered during large local reaction
e. To decrease the severity of late phase cutaneous
reaction combined H1-H2 receptor antagonist is
suggested
f. Subcutaneous administration of ADRENALINE in
mild to moderate systemic sting reaction and
intravenous administration during severe hypotension

17. ANTS
 Wingless members of the order Hymenoptera
 Some ants have venomous sting while some bite their
pray and then spray venom (carpenter and weaver ant)
 Use their sting as a means of defence
 Fire ants(Solenopsis invicta) use mandible to grasp its
victims and drives and abdominal stinger into the skin
and release venom
 If not removed then it moves around mandible and
inflicts further sting in circular pattern

18.  Ants sting slowly and may inject venom for seconds to
minutes
 0.05ul-0.1ul venom per sting

19. Toxic component
I. Primary constituent: formic acid
II. Various proteins
III. Fire ant venom has DIALKYLPIPERIDINE
ALKALOIDS (hemolytic factor) and very less
protein, allergenic proteins (Soli1-4)

20. MECHANISM OF ACTION
 Toxicity is normally limited to the site of sting
 Dialkylpiperidine alkaloids induce mast cells to release
histamine an other vasoactive amines resulting in
PUSTULE at the sting site.
 The alkaloids are not immunogenic

21. Clinical signs
Local response Systemic allergic reaction
• Initial weal and flare
reaction
• Pain, irritation and
swelling at the site of
sting which develops
over hours into
pruritic, oedematous
and erythematous
lesions that persist for
up to 72 hours
• Characters similar to
those caused by bee
sting
• Anaphylaxis may result
upto 1 percent of stings
• Seizures and
neuropathy with fire
ant sting in some cases
• Bite from aggressive fire
ants may cause focal
necrotic ulcers of the
cornea and conjunctiva
of new born calves

23. Introduction of toad
 Toads belonging to family- Bufonidae
 Distribution- occur natively on every continent
except Antarctica and Australia
 Common toads involved in poisoning-
Bufo marinus (marine toad)
Bufo alvarius (river toad)
Bufo vulgaris (common toad)
 Produce toad venom- thick, creamy-white,highly
irritating substance
 secreted by parotid glands, located dorsal and
posterior to eyes and smaller glands distributed
throughout the skin..

24. How toad venoms are expelled??
 Quickly by the contraction of periglandular
muscles in skin, esp when threatened.
 Highly toxic to
small animals
if ingested.

25. Toxic components
1) Bufodienolids- effects on heart and blood vessels
a) Bufogenins- digitalis like effects
b) bufotoxins- block sodium channels in nerves like
that of local anaesthetics.
2) Catecholamine- contribute to vasoconstriction
3) Tryptamines and their derivatives
 Include serotonin and bufetonine- oxytocic actin
4) Non cardiac sterols- contain cholesterol, provitamin
D, ergosterol, & gamma sitosteral

26. Toxicity
All toads produce toxins but its severity to any animals
depends on-
 Extend of contact
more contact= more toxicity
 Duration of contact
 Types/ species of toad
 Environmental condition ie more warm, the more is the
severity.
 In dogs, severity also depends on
a)Size of dog ie more small breed, the more is the toxicity
because they get more poison per kg body wt
b) Amount of toxin absorbed into blood stream

27. Mechanism of action
 When toad is bitten by an animals, the toxin is released
and is absorbed rapidly across the mucous membrane of
mouth
 Bind to specific receptor site on cardiac cell memb &
inhibit Na/ k ATPase pump
 Cell relies on Na/ Ca pump to maintins its sodium
gradients causing Na pumping out and Ca inward
 Results in excessive cardiac stimulation and ventricular
fibrillation
 Also results in increased extracellular K conc causing
hyperkalaemia
 Death occurs rapidly from heart failure.

28. Clinical signs-
 Encounters with toads are most common in warm or mild
weather
 Signs- variable and range from local effects to convulsions
and death.
 Local effects (profuse, sometimes frothy salivation,
accompanied by vigorous head shaking, pawing at the
mouth, and retching) are immediate, probably because the
toxin is extremely irritating.
 Vomiting is not unusual, especially in severe cases, and
although it may persist for several hours, no further signs
may develop in poisoning by common indigenous toads.
 With more severe intoxication, as from R marina or I
alvarius, cardiac arrhythmias, dyspnoea, cyanosis, and
seizures are characteristic.
 Cardiac and CNS involvement can be life-threatening.

29. Diagnosis
 Seeing a dog or cat mouthing a toad
 Finding toad or toad pieces in vomitus
 Circumstantial evidences and clinical signs
 Haematological and clinical chemistry- increase in
packed cell volume ( PCV), blood glucose, blood urea
nitrogen, K & Ca level.

30. Treatment
 A specific antidote is not available.
 Therapy is directed at minimizing toxin absorption and controlling
associated clinical signs.
1)The mouth should be immediately and thoroughly flushed with copious
amounts of water. ( sticky so gently rub the mucous memb)
2)should be prevented from inhaling aerosols of saliva or water that
contain toad toxin.
 Atropine may reduce the volume of saliva and the risk of aspiration
but should not be used until cardiovascular status is assessed. More
severely affected animals require more extensive therapy.
 If bradyarrhythmias exist, atropine or dopamine should be
considered; tachyarrhythmias should be treated with lidocaine,
phenytoin, propranolol, or procainamide hydrochloride. Digoxin-
specific Fab may be considered in cases of severe arrhythmias
refractory to standard antiarrhythmic therapy.
 CNS excitation, if present, should be controlled by
benzodiazepines, barbiturates, or a combination of the two.
Anesthetics that predispose to ventricular fibrillation (eg, halothane)
should be avoided. Supplemental oxygen and mechanical ventilation
may also be needed if cyanosis and dyspnoea are prominent.

31. Toxicity of spider venom
Introduction
Phylum- Arthropods
Subphylum- Chelicerata
Class- Arachnids
Order- Araneae
Family- Therididiidae
Genus- Lactrodectus mactans
Various toxic spiders
1) The brown recluse spider
2) Black widow spider
3) Armadeiras (armed spiders)
4) Funnel-web spider
5) Hobo spider

32. General properties
proper
ties
The
brown
recluse
spider
Black widow spider Armadeir
as
Funnel-
web spider
Hobo
spider
Propert
ies
violin-
shaped
marking
on its
back
Back and
belly are
brown
F=Shiny, black
hairless body, red
marking on its
abdomen similar to
an hourglass (1-1.5
inch)
M= no hourglass
mark ( 0.5 inch)
Female often eats the
male after they mate,
hence called black
widow
long
arms,
banana
bunch
spiders by
locals
the most
dangerous
spider in
the world, is
aggressive
in the
absence of
provocation
brown-
colored
spider with
gray marks
along its
body

33. Toxic component
Black widow spider Brown recluse spider
alpha-latrotoxin (neurotoxic venom),
also isoleucine,leucine, lipoprotein &
hyaluronidase.
Hyaluronidase, protease,
sphingomyelinase D, esterases &
haemolysin.
Both male & female=toxic but one
female is large enough to envenomate
Venom gland= < 0.2 mg of venom
Median lethal dose = 0.005-1 mg / kg
body wt
Produce a systematic reaction
because its venom is a neurotoxin
Produce a necrotic local lesions at the
site of bite but can cause systematic
reactions like DIC

34. Mechanism of action
Black widow spider Brown recluse spider
Alpha lactrotoxin acts on
neuromuscular junction
Causes the release of Ach from pre-
synaptic nerve fibre until there is
complete depletion of neurotransmitter
Results in severe painful cramping of all
large m/s
Neurotoxic binds to glycoproteins on
neuromuscular synaptic membrane
Allow the opening of cationic channels.
Ca channel binding increases the
membrane” permeability to Ca & cause
depolarization
 Venom is cytotoxic to endothelial
cells.
 triggers the dissseminated
intravascular coagulation &
microthrombi formation within the
capillaries
 Capillary occlusion, haemorrhage &
necrosis
 Bite is slow to heal

35. Clinical signs
Black widow spider Brown recluse spider
 occur almost immediately after the
bite
Dull- numbing pain, that spreads
from the bite region to muscles of
entire body
Pain becomes severe and other
signs like restlessness, vomiting,
anxiety, apprehension, muscle
cramps and rapid, shallow ,irregular
respiration
Later- abdominal rigidity, m/s
fasciculation, tonic clonic convulsion,
sweating, hypersalivation, flaccid
paralysis & shock
death- from respiratory and
cardiovascular failure
Occurs in 2 forms ie cutaneous &
viscerocutaneous forms
Cutaneous- begins as pain, oedema t
biting site and progresses to ulcerated
wound ( resolve in 1-3 weeks) but may
be permanent
Viscerocutaneous- more severe &
produce systematic signs of haemolytic
anaemia, haemoglobinuria, jaundice,
hyperthermia.
 complication associated with
intravascular may include kidney
damage

36. Postmortem findings and diagnosis
 PM finding- no distinctive lesion except for venous
congestion
 Diagnosis-
History of spider bite
Clinical signs
Laboratory analysis is not useful.

37. Treatment and management
 Antivenom of specific black widow spider I/V-
reduces pain and brings reliefs within 15 mins ( human
& small animals)
 Muscle relaxants (methocarbamol), analgesics (
meperidine) & sedatives ( diagepam)- control pain
and muscle relaxant
 Atropine- reduce salivation
 Therapy of shock ( corticosteroids & fluid)-
instituted in severe cases
 BR Spider-haemolytic anaemia should be corrected
with blood transfusion.

39. Types of snakes
Two types
 poisonous/ venomous
 Non- poisonous/ non-venomous

40. Poisonous snakes
 Belongs to several families of snakes such as Elapidae ,
Crotalidae , Viperidae , hydrophiidae and Colubridae
 For toxicological purpose, they have been grouped
into two main classes:
 Elapines
 Viperines

41. Elapines
 Belongs mainly to the family elapidae or cobra family
 Mainly includes cobra ( nag) , mambas, kraits , coral snakes
.
 Have short fangs and tend to hang on and “chew” venom
into their victims.
 Their head is of about the same width as that of the neck
and pupil of their eyes are circular .
 Their third labial touches the eye and nasal shields
 Their venom is mainly neurotoxic and result in paralysis of
of the respiratory centre.
 Animal that survive their bites seldom have any sequelae.

42. Viperines
 Two types of viperines :
 True vipers/ pitless viper belonging to family Viperidae (
e.g. . Russell’s viper)
 Pit vipers belonging to the family Crotalidae ( e.g. .
Rattlesnakes and copperhead)
 Pit vipers have a pit or deep depression on each side of
head between eye and the nostrils
 Pitless vipers are those which have no pit on the head .
 Have broad plates on the belly extending right across and
the pupil is likes
vertically elliptical slits .

43. Difference between Elapines and
Viperines
Characters Viperines Elapines
Lower jaw Can inject venom without
closing the lower jaw
Must close before they can
inject venom
venom Haematotoxic , necrotizing
and anticoagulant
In Some species , have
neurotoxic component also
present
Mainly neurotoxic
Fangs Long and strong Short
Bites through clothes Can cannot

44. Venom gland
 Homologous to the parotid gland
 Situated below and behind the eye , one on each side
 Two grooved or tubular fangs or poison teeth
communicates by mean of duct with the racemose glands
secreting venom ,a secretion meant for digestion .
 Whole mechanism is so arranged that all the venom
secreted by glands is discharged without any leakage when
the fangs penetrates the skin

45. Toxic components
 Snake venom is highly concentrated , clear amber
colored digestive juice of snake.
 Complex mixture of amino acids , proteins , enzymes,
biogenics amines , metals and other inorganic
substances
 In some species , venom may contains up to 20 or more
different components but common components of
venom are:
 Protein
 And non- protein toxins

46. Protein
 Enzymatic and non- enzymatic proteins
 Enzymatic protein
 Snake venom contains about 26 enzymes note: no single
venom contain all these enzymes , they are scattered in
different families and genera. some enzymes are present in
all types of venom :
 Proteolytic enzymes (proteases): digest tissue proteins
;implicated in anticoagulation events.
 Hyaluronidase : solubilizes glycosidic bonds and dissolves
intercellular gel of connective tissue ;help in rapid spread
of venom

47.  Phosphodiesterases : lowering blood pressure in prey
 ATPases: metabolizes ATP to disrupt the prey’s energy
fuel.
 Acetylecholinesterase : hydrolyses acetylecholine ;
interfere with neurotransmission in neuromuscular
junction that make prey lose control of its muscles
 Phospholipases A,B , C : hydrolyse phospholipid and
release saturated and unsaturated fatty acids ;
phospholipase A is strong hemolytic and mycotoxic agent
that contributes to cardiotoxicity
 Lipases : hydrolysis of lipids , thus destroying membranes

48.  Collagenase : digest collegen
 Ribonuclease : acts against RNA
 Deoxyribonuclease : acts against DNA
 Ophio – oxidase : help in autolysis and putrefaction
 Thrombin likes enzymes : cause fibrinogen clot
formation
 L- amino acid oxidase: gives yellow colour to the
venom and catalyses oxidation of L – alpha amino and
alpha – hydroxyl acids ; also triggers some other
enzymes

49. Non – enzymatic protein
 Low molecular weight peptide or polypeptides with no
enzymatic activity
 Mainly includes neurotoxins , haemorrhagins ,
cardiotoxins , myotoxins , cytolisins , and toxalbumins;
neurotoxicity mainly occurs due to presence of certain
peptides ,amides , or polypeptides ; haemorrhagins
present in crotalid venom are vasculotoxic causing
haemorrhage and shock ; mycotoxins cause muscles
necrosis and myoglobinurea and cytolisins cause tissue
necrosis

50. Non – protein toxins
 Non-protein toxins likes lipids , steroids, glycoprotein
, amines , metals( Na, Ca, K , Mg, Zn, Co , Ni , Fe etc )
 They play important roles in the envenomations .

51. Factors affecting toxicity
 Snake venom envenomation is common in animals living in
region inhabited by venomous snakes
 Severity mainly depends on species of snake involved , its age
and size, number and depth of bites , and total quantity of
venom injected
 Fatal snake bites are
 common in dogs due to their relatively small sized and their
their nature of attacking snakes
 Less common in cats as cats avoid snakes
 Horses and cattle seldom die ( except when bitten on head or
neck ) as a direct result of snake bites due to their large sizes
.however , on the basis of per kg body weight , horses are
more susceptible to venom than any other species .

52.  Pigs are less susceptible due to poor absorption og venom
through layers of subcutaneous fat
 Snake bites near the head region (i.e muzzle , lips , neck )
is more toxic than other parts of body . In large animals (
horses and cattle ) , bite near head and neck results in
excessive swelling and dyspnea which may be fatal
 Snake venom injected directly into the blood stream is
more toxic than injected into relatively non- vascular areas
( e.g fat )
 Not all bites by snakes result in envenomation : so called “
dry bites “ may range from 30- 70 % of total bites
depending upon the species and conditions . Amount of
venom injected is regulated by the snakes

53.  If there has been previous bite , the victim develop
humoral immunity and less vulnerable to toxic effect
of venom

54. Toxicity
 Toxicity of viperine venoms can vary substantially e.g
less than 2mg/kg b.wt in rattlesnakes venom and more
than 10mg/kg b.wt in copper head venom
 Toxicity of elapines is less than 1mg/kg b.wt

55. Toxicokinetics
 The venom is deposited with the help of fangs by the
snakes into the victim’s body . Once deposited , rapidly
distributed in body.if venom is deposited directly into
the vein , toxicological effect ensures very rapidly .
Snake venom biotranformed to variable amount and
largely excreted via kidneys

56. Mechanism of action
 MOA is complex and has not been fully understood
 Action varies with types of toxins present in venom
 Effect mainly includes neurotoxicity( primarely elapines )
,haematotoxicity,( viperines ) myotoxicity , nephrotoxicity
and necrotoxicity
 Neurotoxicity : two types neurotoxins :
 Post – synaptic neurotoxin and pre – synaptic neurotoxins
 Post synaptic neurotoxins acts as antagonist of
acetylcholine and mainly binds with cholinergic receptor in
neuromuscular junctions on skeletal muscles , produces
curare likes effects and cause paralysis .it also contain
acetylcholine esterase enzymes which degrades
acetylcholine .

57.  Presynaptic neurotoxins mainly inhibits the release of
acetylcholine at myoneuronal junctions and blocks
neurotransmission
 Pre synaptic toxin – beta – bungarotoxins
 Post – synaptic toxins – alpha and k bungarotoxins
 Hematotoxics – attacks circulatory systems and muscles tissue
causing coagulopathies ( contains both procoagulant and
anticoagulant results in bleeding disorders due to defectives
coagulations ) , cardiotoxicity ( venom induced cardiac changes
as well as release of mediators likes bradykinin, histamine and
serotonins that contributes increase capillary permeability and
intra vascular volume depletion result in cardiovascular shock )
haemolysis ( haemorrhagins present in venom cause hemolysis )

58.  Local toxic effects : venoms enzymes cause local
necrosis and gangrene at site of biting . Similarly , due
to interruption of blood supply because of hemotoxins
result pain , swelling and edema after bite

59. Clinical signs
 Viperines
 Severe local tissue damages and pain that spread rapidly
 Severe pain cause anxiety , restlessness and excitement
followed by incordination of movement and lameness .
 Marked discolouration of tissues occurs within few
minutes
 Dark ,bloody fluid oozes from fang wound
 Epidermis sloughes off
 Finally , unconsciousness and collapse

60.  In small animals
 Vomition
 Hypotension with tachycardia
 Pulmonary edema
 Salivation
 Diarrhoea
 Death occurs mainly as a result of septicemia
 Note: in case of large animals ,death mainly result of
secondary bacterial infection

61.  Elapines
 Pain and swelling is minimal but systemic
neurological predominates
 Muscular weakness lead to paralysis
 Consciousness usually retain till end
 Death due to respiratory paralysis
 Death occur usually within 6 hrs in ellapine and 2-4
days in viperines

62. Treatment
 Should given as soon as possible because irreversible
effect of venom begins immediately after bite
 Specific
 Antivenin therapy
 Choice of antivenin depends on species of snakes
 Antivenin may be monovalent ( against single species )
or polyvalent ( against two or many species .dose
depend on species , pain severity.