OP poisoning in dog

1. An assignment on
fulfillment of clinical
conference
Prepared by
Rajesh Neupane
B.V.Sc and AH, 8th semester
Roll number 28
1

2. Case information
 Name of the owner :Akash Kunwar
 Name of the dog: Punte
 Address – Siyari rural municipality ,1
 Species – dog
 Breed – local
 Age – 2 months
 Weight – 5 kg
2

3. Case history
 Non vaccinated .
 Bathed with organophosphorus insecticide (dichlorvos )
 Appearance of sign of vomiting and excessive salivation
(ptyalism ) after 30 minutes of ingestion .
 Decreased appetite
 Increased temperature
 Ataxia
 Vomiting
3

4. Physical examination
 Watery eyes
 White visible mucous membrane
 Lachrymation(excessive)
 Excessive salvation
4

5. Case problems
 Muscle tremors
 Ataxia
 Vomiting
 Diarrhea
 Excessive salivation
 Lachrymation
 Difficulty in movements
5

6. pathophysiology
Op compounds are lipid soluble and absorbed from all body surfaces
Body surface including of eyes , GI tract and lungs
After absorption they are rapidly distributed throughout the body
Some OP required the enzymatic activation by liver enzymes
Rapidly distributed through the different part through blood
Show effects in different nicotinic and muscarinic sites

7. Effects of OP compounds
1. Muscarinic effects:
 Profuse sweating
 salivation
 lacrimation, miosis.
 increased tracheobronchial secretions, bronchospasm.
 Vomiting ,abdominal cramps, bradycardia, hypotension.
 involuntary urination and defecation.
2. Nicotinic effects:
 Twitching,
 Fasciculations
 muscle weakness and paralysis is due to prolonged
depolarization.
7

8.  3. Central effects:
Headache
restlessness,
Confusion & convulsions
coma and death occurs usually due to respiratory
failure.
8

9. Differential diagnosis
Disease History Nervous signs Diarrhea and
vomiting
Any othe
Organophosph
ate
Poisoning
Present Present present Bronchosp
Twitching
Excessive
salivation
Canine
distemper
Not evident Present Not evident Hard pad
Biphsic fe
Rabies Not evident Present Not evident Bite mark
Tremorgenic
mycotoxins
No history of
eating of damp
placed foods .
Present Not common
Strychnine
poisoning
No history of
rodenticide.
not found in
legal manner .
present Vomiting is
rare
Death du
paralysis
respirato
m/s

10. Differential diagnosis
Diseases History Nervous signs Diarrhea and
vomiting
Any others
Chocolate
poisoning
No history of
chocolate .
No ingestion of
seeds of coca
plant
Present present polyuria
Polydipsia
Haematuria
Amphetamine No history of
medication
Present only
Scizures and
tremors
Present Myridiasis
Tetanus
Toxins
No history of
wound fracture
surgery
Present
Spasm of
.
Opisthotonus
Not evident Salivation
Dysphagia
Lockjaw

11. Diagnosis
 On the basis of the history and clinical signs . The case was
suspected as organophosphate poisoning .
 Diagnosed by. Clinician Dr. Nandalal Verma
 Prognosis : Excellent
11

12. Treatment
Specific treatment :
1 )Oximes
Parlidine-2-aldoximes:(2-PAM)
dogs and cat :10–15 mg/kg slow IV Or infusion
followed by IM/ SC , 2-3 times daily
Cattle :25-50 mg/kg slow IV or infusion followed
by IM route at 8-12 hrs. interval.
Horses : 10-40 mg/kg slow iv or infusion.
Diacetylmonoximes (DAM)
MOA: pralidoxime prevents ageing and regenerates
AChe by binding it self to anionic sites and
dephosphorylating of AChe. (figure no :4)
12

13. 13

14. 14

15. Treatment contd.
2) Atropine sulphate :
Dogs and cat : 0.2-2mg/kg , ¼ IV and ¾ IM , followed by same
or half dose 3-4hrs interval by IM or SC until clinical signs
subsides.
Cattle,horses,sheep,goats and swine : 0.2-0.5mg/kg ¼ IV and ¾
IM or SC until clinical signs subsides.
Birds : 0.1-0.2 mg, IM or SC as needed.
MOA : atropine reduces the effects of cholinergic at muscarinic
sites only by binding to muscarinic receptors.
3) Diazepam (reduction of seizures and tremors )
(0.05–1 mg/kg IV to effect )
4) Scopolamine : Antimuscarinic agents experimentally used .
Not FDA approved.
15

16. Supportive therapy
1) Emesis
3% hydrogen peroxide :2.2 mL/kg PO to a
maximum of 45 mL
MOA: by irritation of gastrointestional tract .
2) Activated charcoal – sorbitol mixture
(2 g/kg PO)
In case of diarrhea—do not administer sorbitol
containing products .
3 )on dermal exposure ,animal should be washed with
soaps and water and rainsed thoroughly .
16

17. 17

18. 18

19. Case discussion
.
Organophosphorus (OP) compounds are organic esters of
phosphorus which has ability of to inhibit cholinesterase enzyme .
They are used as acaricides ,insecticides . Soil nematicides ,
fungicides ,herbicides &rodenticides.
Classification:
a) Directly acting OP compounds : This insecticides contain P=O
group, so they directly inhibit cholinesterase enzyme and
produce toxicity .e.g. trichlorfon and dichlorvos.
b) Indirectly acting OP compounds : They contain basically
phosphodiesters with P=S bond . Sulphur is not electrophilic so
compounds are inactive as anticholinesterase , this compounds
require activation for conversion from P=S group to P=O
group in the body. Eg malathion , parathion and fenthion .
19

20. classification20

21. Factors affecting toxicity
1)Storage : storage generally enhances the toxicity of most of
OP compounds due to formation of toxic isomers . The
changes are induced by contamination ,heat induced
isomerization and ph. changes .
2)Ambient temperature :High ambient temperature increases
the toxicity. It also increases volatility of certain fumigant
compounds such as dichlorvos .
3)Species : e.g. cattle is more sensitivity than sheep to
dimethoate, ronnel , crufamate and phosmet .Cats are highly
susceptible for acute OP poisoning .
21

22. 4) Age : directly acting OP compounds
(dichlorvos ) that do no require enzymatic
activation are highly toxic to young animals than
indirectly acting OP (parathion ) due to low
development of enzymatic system.
5) Formulations : vehicles that are of organic
solvents or oil increase the OP toxicity due to
better absorption.
6)Other factors : toxicity of OP compounds
decrease due to degradation by sunlight ,water
,microbes , alkali or metal ions such as iron or
copper .
22

23. Neuromuscular junction and
acetylcholinesterase
23

24. Acetylcholinesterase—normally hydrolyzes
the neurotransmitter acetylcholine in nervous
tissue, RBCs, and muscle, resulting in
termination of nervous transmission.

Pseudocholinesterase—found in plasma,
liver, pancreas, and nervous tissue, mainly in
cats.
24

25. Clinical signs
1)Local exposure to vapors ,aerosol or inhalation of OP
results in nasal discharge ,tightness of chest ,wheezing
respiration due to bronchoconstriction and bronchial
secretions .
Exposure to eye results in lachrymation, constriction of
pupil and increased intraocular pressure with conjunctival
hyperemia .
Percutaneous application results in muscular fasciculation
2)Systemic toxicity :
Toxic sign may have quick or delayed onset depending
upon the type of compound and quantity of taken . It lead
for toxicity symptoms as of muscarinic and nicotinic
receptors .
25

26. In delayed acute ,subacute or chronic toxicity cases some of
OP insecticides inhibit an enzyme called neuropathy target
esterase (NTE). This is present in peripheral nerves,
lymphocytes ,brain, placenta and other sides .The NTE
doesn’t have identified function in body but thought to be
axonal transport of nutrients .
The inhibition of NTE results in demylation leading to
paralysis .This delayed toxic axonopathy is called as
organophosphorus induced delayed neuropathy (OPIDN)
large diameter fiber appears to be more affected than smaller
diameter fibers .
The development of OPIDN is not correlated with inhibition
of acetylcholinesterase .
26

27. Post mortem findings
 PM lesions of acute OP poisoning are not specific
,lesions are not manifested in animals .
 In animals that die in several hours :
1. Pulmonary edema and congestion
2. Cyanosis
3. Cerebral edema
4. Patches of necrosis in skeletal muscle
5. Hemorrhages in heart skeletal muscle and others organs
may occurs
6. Intestinal tract may be dilated and filled with fluid
If death is delayed for several days or weeks carcass
is dehydrated and emaciated .
27

28. DIAGNOSTIC PROCEDURES
 History
 Clinical signs
 Estimation of cholinesterase enzyme level in blood and
tissues .The decrease in the activity of cholinesterase
suggests for presence of anticholinesterase in blood or
tissues. Clinical manifestation observed when 50-70% of
AChE level is inhibited in body .
 Atropine response test—administer atropine
at preanesthetic dose 0.02 mg/kg IV. Antimuscarinic
response (dry mouth ,mydriasis, and rapid heart rates )
Detection of insecticides—tissue (e.g.,
brain, liver, kidney, and fat); stomach
contents; gastrointestinal tract; fur or hair.
28

29. Differential diagnosis
 Exposure to other insecticidal products—
1)pyrethrin: natural insecticide products cyasanthumun flower
Pyrethroids: synthetic analogue (flea and tick) :
Moa as follow
A ) non specific CNS stimulants are with primarily with sodium channels ,
abnormal depolarization of action potential
B) Inhibit the binding of GABA with its receptor sites .
Clinical sigs include of the restlessness, incoordination ,tremors ,
hypersalivation etc.
2) fipronil (flea and tick): inhibitory effects on GABA
3) imidacloprid (flea): Bind to irreversibly to nicotinic receptors and
show effects .
29

30. . Chocolate (Methylxanthine) Toxicosis
Excessive intake of methylxanthine alkaloids present in
chocolate. Theobromine and caffeine are most part of
methylxanthine alkaloids.
MOA : Inhibition of phosphodiesterase & increases in
cAMP and increasing cellular calcium levels.
Cause vasoconstriction, increased force of cardiac and skeletal
muscle contraction, CNS stimulation, seizures, bronchodilation,
and tachycardia .
Amphetamine toxicity
Amphetamine is a sympathomimetic that is structurally related
to norepinephrine .
clinical signs :mydriasis, vomiting, diarrhea , tremors, seizures .
30

31. DDx cotd.
 Tremorgenic mycotoxins :
Most commonly associated mycotoxins is penitrem
A, Penicillium species, grow on meat, cereals, nuts,
cheese, eggs, fruits, processed/refrigerated food,
refuse, and compost.
MOA : not exact known but, study in mice suggests
it Inhibit the inhibitory neurotransmitter glycine
which leads for developments of clinical signs as :
Hyperesthesia, tremors and seizures .
31

32. Drugs contraindications
1) Neuromuscular blocking drugs like d-
turbocuraine or suxamethonium. These drugs
generally worsen the paralysis of respiratory
muscle.
2) Phenothiazine tranquilizers may increase the
effect of OP poisoning . It acts by blocking of
action of dopamine in brain .
32

33. References
-Sandu, H.S ,& Brar,R.S (2013).Textbook of veterinary
toxicology. Delhi : Kalyani publication.
-Newmark J (2004): Therapy for nerve agent poisoning. JAMA
Neurology. 61(5): 649-652
-Clarks,C( 2018/10/06)choinestrase inhibitors medical use
.Retrived from: cholinesterase_inhibitors_-
_medical_use_wmd%20[TUSOM%20_%20Pharmwiki].html
33