HELP!! Suspect Diazinon Poisoning - Happy Update

[swampducks]

I free ranged my 7 week old guineas and chickens today and now one guinea is dead, another chicken's legs aren't working and the only thing I can think of is the diazinon I poisoned the ants with last week. The birds were on teh deck and shouldn't have been.

Is there anything I can do?

 

[dlhunicorn]

Please do not ever use that product again.

http://extoxnet.orst.edu/pips/diazinon.htm

I am looking into some vetrinary toxicology manuals for you to see what if anything can be done. do not allow your birds access to that area treated until you are sure all traces have been removed from the environment per info in article above. :aww

http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/203902.htm
(MERCK Veterinary Manual)
"Diazinon: Diazinon is an organic phosphate that is commonly used for the control of a variety of insects around poultry houses. It should not be used inside poultry houses. Some producers have used diazinon in poultry houses for the control of fire ants. Chickens will consume the diazinon crystals, which results in lacrimation, diarrhea, dyspnea, and death. Necropsy lesions include lung edema, fatty livers, and severe enteritis. The diazinon crystals can be seen in the crop and gizzard contents."

ETA: This info intended for you to print out and take to vet
http://www.michvma.org/documents/MVC Proceedings/Labonde8.pdf
(AVIAN TOXICOLOGY)-Jerry LaBonde, MS, DVM
"....Insecticides Organophosphates (OP) and carbamates (CBM) are the most common causes of avian insecticide toxicoses. Sources include carbaryl, carbofuran, dieldrin, dursban, diazinon, dichlorvos, malathion, and methyl carbamates. LD-50 concentrations indicate avian species are 10 to 20 times more susceptible than mammals to the toxic effects of these products. In halation is the primary source of exposure, but ingestion from contaminated feeds is also re ported. The mechanism of action of OP and CBM toxins is acetylcholinesterase (AChE) inhibition. OP
bonds to AChE are irreversible, and the CBM bonds are slowly reversible. Death is usually caused by neurological and muscular dysfunction. Initial response to OP toxicity is stimulation leading to nerve impulse inhibition.

Early clinical signs include anorexia, weakness, diarrhea,
crop stasis, ataxia, wing twitching, and prolapsed nictitans. More severe signs are muscular tremors, stiffness, dyspnea with rales, bradycardia, paralysis, and seizures. Death is usually caused by respiratory failure. An organophosphorous ester-induced delayed neuropathy has been observed 2 weeks post exposure to an OP in a White-front Amazon Parrot. This bird exhibited ascending progressive paralysis, and death resulted from respiratory failure. Diagnosis of pesticide toxicoses is based on history, clinical signs, and response to treatment.
If bradycardia is present and does not reverse with administration of 0.02 mg/kg of atropine intravenously (IV), OP toxicity is considered. Cholinesterase assays from whole blood, plasma, serum, or brain tissue are used to determine toxic exposure. These samples are submitted with
paired nonexposed samples to determine whether depressed concentrations of cholinesterase are significant. In acute toxicoses, little or no cholinesterase will be found. Chronic toxicoses show concentrations below 50% of the normal sample. One effect of chronic exposure is decreased egg production and poor hatchability. Depressed AChE concentrations from CBM may not be found owing to rapid regeneration if the samples are not submitted as soon as possible. Submission of
gastric contents and environmental sources aids in diagnostic investigations.
Treatment includes atropine (0.2 mg/kg intramuscularly (IM]) every 3 to 4 hours as needed. One fourth of the initial dose is ad ministered. Pralidoxime (2-PAM, Wyeth-Ayerst, 10 to 20 mg/ kg
IM) is administered every 8 to 12 hours as needed. 2-PAM is only effective if used within the first 24 hours of exposure.. ..."

http://www.ivis.org/advances/Beasley/Cpt2g/ivis.pdf
(from BEASLEY > Veterinary Toxicology)
"....Generally speaking, much of the binding of ACHE by an
OP is regarded as "irreversible". ........
.....Diazinon causes problems, especially in small animals and birds. Commonly used on lawns. It has been recently banned in golf
course use. ........
....Death due to OP or carbamate toxicoses is usually due to one or more of the following effects: Increased respiratory tract secretions and bronchiolar constriction with hypoxia aggravated by bradycardia.
Respiratory depression from nicotinic stimulation to the point of paralysis.
Respiratory paralysis from CNS depression due to central effects of the insecticide (may be the primary cause of
respiratory failure in some species). ...............
..........Treatment (please note that you will need veterinary consult for treatment below re the atropine > here below is a small excerpt )

Activated charcoal (for any recent oral exposure) administered with appropriate precautions to avoid aspiration.

Thoroughly bathe with detergent all animals exposed topically-taking care to avoid exposure of human skin. Use thick rubber gloves,
plastic aprons, etc.

Atropine sulfate (generally avoid use of charged agents, such as atropine methylnitrate or glycopyrrolate, which do not effectively
enter the central nervous system). Atropine sulfate-dosages higher than preanesthetic doses are routinely required for acute toxicoses (OP or carbamate).
Small animal products may contain atropine sulfate at 0.5 or 0.54 mg/ml; large animal products may contain 2 or 15 mg/ml.
May want to avoid atropine sulfate altogether in horses due to gut stasis, (except with life-threatening pulmonary or cardiac
effects). When used in horses, atropine is added to fluids and administered IV while ausculting the abdomen. Administration is
stopped prior to a reduction (to less than normal) in gastrointestinal sounds.
Suggested dose cattle 0.2 - 0.5 mg/kg. One-third of dose administered IV, the remainder given SC or IM.
Atropine is repeated judiciously as needed; but avoid gut and rumen atony. May be required at 4 - 8-hour intervals.
Suggested dose SA and birds 0.2 mg/kg. Some rabbits have atropinase and may require higher dosing, begin at 1.0 mg/kg but
may need to increase to 10 mg/kg.
In all cases, subsequent doses of atropine should depend on the reappearance and severity of clinical signs. Clinical signs to
use for monitoring include degree of respiratory distress, cyanosis, and heart rate. Effects such as miosis and salivation, which
are not of concern in survival, are not used as therapeutic end points for atropine administration......"

http://www.vetsci.org/2007/pdf/249.pdf
(J. Vet. Sci. (2007), 8(3), 249–254 >Metoclopramide protection of diazinon-induced toxicosis in chickens)
small excerpt:
"....The efficacy of metoclopramide for preventing organophosphate
insecticide-induced (diazinon) toxicosis was
evaluated in 7~14 days old chicks. Injection of metoclopramide
at 25 mg/kg, s.c. 15 min before diazinon increased
the oral 24 h median lethal dose of the insecticide in the
chicks by 80%. Metoclopramide alone inhibited the in
vitro and in vivo plasma and whole brain cholinesterase
activities of the chicks. Metoclopramide pretreatment at
100 mg/kg, s.c. reduced the extent of cholinesterase
inhibition that was caused by diazinon (10 mg/kg, p.o.) in
the plasma and whole brain by 24% and 7%, respectively.
Diazinon at 10 mg/kg, p.o. produced signs of cholinergic
toxicosis in the chicks, and these signs included salivation,
lacrimation, gasping and convulsions within 2 h, and the
2-h and 24-h lethalities were 88 and 100%, respectively.
Metoclopramide at the dose rates of 12.5, 25, 50, 100 and
200 mg/kg, s.c. given 15 min before diazinon (10 mg/kg,
p.o.) variably decreased the occurrence of toxic manifestations
in the chicks. The highest dose of metoclopramide (200
mg/kg, s.c.) reduced the 2-h and 24-h lethality of diazinon
to 75% each and it reduced the overall toxicity score of
diazinon by 32%. The data suggest that metoclopramide
pretreatment only partially protected chicks against the
acute toxicity of diazinon..."

http://www.vetserveng.moag.gov.il/N...401C-AA96-DB014EDA7F12/867/Birdtreatment1.pdf
(New treatment regimens in organophosphate (diazinon) and carbamate (methomyl) insecticide - induced toxicoses in fowl )
"Abstract. The objective of this work was to determine optimal treatment regimens for organophosphate (OP) or carbamate insecticide toxicoses in fowl using the antidotes atropine sulfate and pralidoxime chloride (2-PAM). Broiler chicks in treatment groups, each comprising 3 replicates of 6-7 birds / replicate were gavaged on a body weight (BW) basis with the OP and carbamate insecticides, diazinon and methomyl, respectively, at lethal dosages. Treatment groups were injected with either or both of the antidotes at various dosages as soon as clinical signs appeared. Birds appearing healthy 24 hours thereafter were regarded as having been treated successfully. At a dosage of 100 mg/kg BW, atropine was mildly toxic and at 200mg/kg 2-PAM was severely toxic (but not lethal), whereas at dosages of 50 and 100 mg/kg BW, respectively, the antidotes were at their most potent. With diazinon, atropine was only partially effective (12/20 survivors), whereas 2-PAM was extremely efficacious (20/20 survivors); the combination of the 2 antidotes at 2 dosages was slightly less effective (19/20 survivors) than 2-PAM alone. With methomyl, atropine was largely successful (18/20 survivors), whereas 2-PAM was mostly unsuccessful (10/20 survivors); the combination at a high dosage was less effective (15/20 survivors) than atropine alone, but at a low dosage the combination was the most successful (20/20 survivors). These results indicate that anticholinesterase insecticide toxicoses in fowl should not be treated according to textbook recommendations, and antidotal dosage with atropine should be up to 100 times greater than is commonly recommended The specific cause of the toxicoses should be determined before treatment can be given, but as this is often unknown, a combination of antidotes may be the optimal treatment protocol. One of the most important aims of veterinary medicine is to successfully treat sick animals, and treatment is usually specific for an explicit diagnosed cause. With regard to toxicoses, this is not easily performed as the dosage of a substance determines its toxicity and accordingly virtually everything in the environment of animals may be toxic. Of these thousands of substances with potential toxicity to domestic and wild animals, very few in fact have a specific antidotal treatment (1). However, it is fortunate that probably the most potentially hazardous group of compounds, the anticholinesterase organophosphate (OP) and carbamate insecticides, has specific antidotes. Due to the extremely common use of these insecticides for ectoparasite control on pet and farm animals, their use in household and public health, and on field crops and fruit trees, and even maliciously, it is not surprising that toxicoses are often reported in domestic and wild animals (1-4). Signs of poisoning due to OP and carbamate insecticide toxicoses typically develop very rapidly, and treatment should be instigated within minutes of exposure if mortality is to be minimized (1-4). Treatment regimens of such toxicoses in man comprise atropine sulfate administered to counteract muscarinic effects, particularly the life - threatening anoxia, in conjunction with oximes, such as pralidoxime chloride (2-PAM), which speed up the breaking of the insecticide - acetylcholinesterase bond (5-6). Although OP and carbamate insecticides have a similar mode of action, it has been noted that toxicity induced by the least toxic of the carbamate insecticides, carbaryl, should not be treated with oximes, and is even contraindicated, actually enhancing the inhibition of cholinesterases (6-7). .........
......With regard to the dosage for atropine in birds, very few guidelines could be found, but dosages of 0.1-0.2 mg/kg were quoted (2,8),in contrast to higher dosages (0.2-0.5 mg/kg) for other domestic animals (9). .....................
...This present work examined the practical treatment, with atropine sulfate, 2-PAM, or a combination of them both, in toxicoses induced by diazinon (as a very commonly used representative of OP insecticides) or methomyl (as a commonly used representative of the more modern, more toxic, carbamate insecticides) in broiler chicks, as a model for avian species............
...Efficacy of antidotes Diazinon toxicosis. Treatment with atropine at a dosage of 50 mg/kg BW was partially efficacious, with 12 of 20 birds surviving (Table 1). With 2-PAM at 100 mg/kg BW, all 20 treated chicks survived. Combined treatment protocols (atropine at 25 mg/kg + 2-PAM at 50 mg/kg, or atropine at 50 mg/kg + 2-PAM at 100 mg/kg) culminated in slightly reduced efficacy, with 19 of 20 birds recovering............."

 

[swampducks]

Believe me, I won't use it, I've never had poultry before so it's never been a problem, I use it only once in a while when the ants get bad and this year they were bad. Lousy coincidence!

I found all that info you posted too.

But not having access to atropine sulfate I ended up trying that molasses purgative Miss Prissy posted on another poisoning thread.

I am pleased to say the lethargic chicken seems to have recovered. The remaining guineas and chickens (I only have 6 total!) are happily wandering about inside their run eating and drinking.

I spent the last of the daylight hours yesterday and most of this morning raking and watering where I had applied the stuff. The birds aren't free ranging for the next few days till I am SURE the stuff is GONE.

 

[spatcher]

Quote:
Carbaryl is found in Sevin Dust.