CHLORINATED HYDROCARBONS

POISONING

Presented by
Aysha Basree (1901003)
Zahid Hasan Rocky (1901002)
Piyal Roy (1901005)
Md Raihan Ahmmed (1901007)
Content
 Introduction
 Source
 Host
 Transmission
 Clinical findings
 Diagnosis
 Treatment
 Introduction
 This group includes DDT, Benzene hexachloride ( and it
pure gamma isomer - lindane ), Aldrin, Dieldrin,
chlordane, Toxophene, Methoxychlor, Isodrin, Endrin and
Heptachlor.
 Methoxychlor is less toxic than DDT, and Isodrin, and
Endrin are more toxic than Aldrin and Dieldrin.
 Benzene hexachloride, aldrin, dieldrin and chlordane are
readily absorbed.
 Source
 Feed
 Accidental ingestion
 Farm materials( if spray is too much)
 Spraying, dipping, or dusting, a thorough and gentle bath
(no brushes)
 Host
Ruminants such as Cattle, Goat, Sheep, Buffalo. Dog and cat
also affected
Predisposing Factor
 Very young animals species are more susceptible
 Lactating and emaciated animals also show increased
susceptibility.
 Transmission
Ingestion, inhalation, aspiration and percutaneous absorption
possible portals of entry and to produce systemic signs these
insecticides must be enter the blood stream.
Mechanism of toxicity:
The chlorinated hydrocarbons are neuro-poisons. By virtue of
their high lipid solubility, these agents can enter the neural
membrane with ease and interfere with normal functioning of the
nerve membrane sodium channels. DDT acts by reducing the
potassium transport through pores; (2) inactivating sodium
channel closure; (3) inhibiting Na'-K and Ca-Mg ATPases and (4)
inhibiting calmodulin-Ca ion binding with release of
neurotransmitter. The cyclodiene compounds act on the chloride
ion ( transport by antagonizing the gamma amino butyric acid
(GABA)receptors in the Cl channels and also inhibit the Ca-Mg
ATPase.
 Clinical signs
Behavioural Changes:
 Initial anxiety
 Aggressiveness
 abnormal posturing.
 jumping over unseen objects,
 wall climbing and madness syndrome.
 Neurological symptoms:
 hypersensitivity to external stimuli,
 fasciculation and twitching of the facial and eyelid muscles,
 spasm and twitching of the fore- and hind quarter muscles
 champing of the jaw and
 Hyperthermia
 If death does not take place at this stage, the animals may go
into coma state,
 Cholinergic manifestations:
 vomiting,
 marked salivation
 Mydriasis
 diarrhoea and
 micturation may also be observed
Accumulate in the fat depots, may be excreted in the milk in
dangerous amounts.
Mobilization of the fat may result in liberation of the compound
into the blood stream and the appearance of signs of toxicity
 Post-mortem lesions :
 There are no specific lesions in the nervous system.
 However acute aldrin poisoning may cause hepatitis and
acute tubular nephrosis.
 Chronic DDT and methoxychlor toxicoses may produce
focal centrilobular necrosis of the liver.
 Diagnosis
 Diagnosis can be made on history of use of insecticides, source
of poisonings and clinical signs.
 Analysis of feed and ruminal content for the presence of
chlorinated hydrocarbon insecticides.
 Chemical analysis of brain, liver, kidney, fat is necessary to
confirm the poisoning of dead animal.
 Blood and urine from live animals may also be analyzed
 Differential diagnosis :
Organochlorines poisoning should be differentiated from following
poisonings:
 Salt poisoning: history and absence of hyperthermia.
 Strychnine poisoning: convulsions are tonic and absence of
behavioural abberations and locomotor disturbances
 Fluoroacetate poisoning: convulsions not elicited by external
stimuli
.
 Cont…..
 Nicotine poisoning: only cholinergic signs are exhibited.
 Anticholinesterase insecticide poisoning: only parasympathetic
signs, no behavioural changes or hyperthermia.
 Lead poisoning: no abnormal posturing.
Treatment :
No specific antidote is available, treatment is only symptomatic and
supportive
 Remove the source of poisoning at once
 Administration of non-oily purgatives.
 Control convulsions by administering barbiturates (pentobarbital
sodium) or benzodiazepines in dogs and cats; and chloral hydrate
or pentobarbital sodium in ruminants. CNS
depressants/anesthetics are contraindicated if the animal is
already depressed.
 Cont…
 A Small dose of atropine sulfate(inj.atrovet) 0.03-0.06 mg/kg bw may
be given to control the parasympathetic signs
 Intravenous administration of calcium borogluconate is recommended
to prevent liver damage and nullify the effect of preconvulsive
increase in K-ion concentrations.
 Activated charcoal(2 kg stat followed by 1 kg daily for 2 weeks) may
adsorb the insecticide that is excreted into the intestine through bile
and suppresses the recycling or enterohepatic circulation of
insecticide and promotes it’s excretion through faeces.
 Phenobarbital (10 mg/kg /day) may be tried to induce hepatic
microsomalenzymes and to promote faster metabolism and excretion.
 Prevention:
 Remove the source
 Take care during dipping
 Do not use overdose of this insecticide during treatment
 Take care during spraying of the farm
Thank
you