Department of Animal Protection and Welfare and Public Veterinary Medicine

Faculty of veterinary hygiene and ecology

University of Veterinary Sciences Brno

Sample case studies with solution

The poisoning in dog

In July 2004, an owner brought to the clinic golden retriever (weight 35 kg) and in anamnesis he gave us this information: 2 hours ago the dog ate 500 grams of a strange bait made of granules of green-blue colour. Later, the dog started to have clonuses of legs, hypersalivation, vomiting, haematemesis, diarrhoea, tachycardia and hyperthermia. During the clinical examination also dilatation of pupils and nystagmus were found.

The veterinarian started immediately an intravenous infuse therapy containing diazepam and pentobarbital and also administered calcium to the dog. But the status of the dog despite the therapy deteriorated more and more, tremor was very strong, continual convulsions occurred and the dog must have been euthanised.

During the section, hyperaemia of liver and kidneys was observed. Also the degeneration of hepatocytes and cells in ganglia in brain. Moreover petechial to ekchymatose haemorrhages on GIT mucosa, hyperaemia and intersticial haemorrhages in lungs, massive subendocardial and subepicardial haemorrhages. 

1. Make differencial diagnosis of poisonings which might cause the clinical signs and PA findings described above.
2. Which intravital and postmortal samples would you withdraw and what would you like to assess in them?
3. Was the therapy given to the dog adequate and sufficient? Were there also other possibilities of therapy?

SOLUTION:

Among the agents that are used to kill animals (dogs especially) and could cause the signs described above belong metaldehyde, organophosphates and carbamates or strychnine.

Despite the fact that most of the signs could match organophosphates and carbamates, there is one sign that excludes them as a source of poisoning. It is mydriasis observed during the intoxication. OP and carbamates cause severe miosis, which is an absolute opposite.

Strychnine on the other hand causes severe convulsions of striated muscles but especially after the smallest stimuli - visual or acoustic, which wasn’t observed in our case. Moreover, mydriasis occurs in this poisoning only during the contraction of muscles, it is a transient feature. Also PA examination in strychnine poisoning is absolutely non-specific, while in our case we found severe damage of many organs and structures.

So we identified metaldehyde as the most probable cause of poisoning. The first clue could be the colour of the bait - Vanish slug pellets containing metaldehyde, which is available in the Czech Republic, is of bluish colour.

Metaldehyde works absolutely non-specifically, in the body is decomposed to acetaldehyde. But acetaldehyde is rarely detected in the tissues and so the mechanism of action of metaldehyde is still unknown. We predict that it influences GABA receptor system, causes its inhibition and thus tremor and seizures.

Typical clinical signs of metaldehyde poisoning are hyperthermia and mydriasis, which were present in our case. Also PA findings – haemorrhages on heart – are characteristic for metaldehyde poisoning.

For laboratory examination, we should take samples of blood, liver and gastric content. It is necessary to determine the activity of butyrylcholinesterase – dif. diagnosis of OP + carbamates; in stomach content we could assess eg. carbofuran, strychnine or metaldehyde. It is possible to detect strychnine also in liver and other organ samples and we can detect it even many months after the death. In blood samples we could ask for the measurement of acid-base balance too (to prove metabolic acidosis, which is often present in metaldehyde poisoning). 

In principle, the therapy was lead well. But because the animal was taken to the vet very early after the ingestion of poison, he should have tried to eliminate the rest of it form GIT, administered emetics, carbo activatus, laxatives. Anticonvulsive therapy was excellent, only we should be careful with barbiturates which might decrease respiration and eventually influence the metabolism of metaldehyde. We should monitor heart action and respiration, decrease the body temperature as soon as possible and rectify the acid-base balance.

The poisoning of water birds on the Štefan pond

Anamnesis:

The Štefan pond is a pond where carps and ducks are bred. During the very hot days of late August 2006, a massive death of water birds living on and round it was detected. Both domestic and wild animals (ducks, swans, baldicoots, herons) had died.

Clinical signs:

Difficult breathing, opened beak during aspiration, diarrhoea, difficulties with moving, often using wings while moving - all these signs were described during the intoxication. Birds were sitting and leaning on the beak, head was laid on the back or on the ground in front of the animals.

Pathological examination:

No specific pathological findings, only congestion of organs and in several birds catarrhal enteritis was found. All the birds were in very good nutritional condition.

Water examination:

Temperature : 24°C

pH: 8,2

Whole ammonia: 1 mg/l

Oxygen concentration early in the morning: 1 mg/l

COD: 40 mg/l

BOD: 20 mg/l

Strong turbidity, low transparency of water

Decrease of water level - 25 cm from normal status

Questions: 

1. Evaluate the results of physiochemical examination of water
2. According to data available identify the cause of poisoning of water birds
3. Withdraw proper samples and propose laboratory examination
4. Propose further procedure to save affected but still living animals
5. What should be the preventive measures to protect water birds from similar poisonings in the future

 SOLUTION:

1. The examined water is not of acceptable quality, there are many parameters that exceeded the tolerable level   

- Whole ammonia is high, for both cyprinids and salmonids exceeds the values recommended for fish breeding (optimum is up to 0,05 and up to 0,0125 mg/l of NH₃ for cyprinids and salmonids respectively). After the conversion according to pH and temperature there was found level of 8 % (0,08 mg/l) of toxic non-ionized form of ammonia.

- There s also a very low concentration of oxygen in the water, levels are lower than that considered as lethal for both cyprinids and salmonids - LC 50 for cyprinids is 1-2 mg/l.

- On the other hand, COD and BOD are very high, optimum is up to 30 and up to 15 for COD and BOD respectively (in cyprinids).

- The decrease of water level relates to the warm period of year with a very low level of rainfall. Organic substances in water concentrate, there is a lot of zooplankton in the water, decreased concentration of oxygen and anaerobic environment is formed in the water. These are very good conditions for Clostridium botulinum.  

2. According to data recorded, we may say that the most probable source of poisoning was botulotoxin produced by Clostridium botulinum in the sediments of the pond. Its occurrence is typical in two waves during the year - first wave occurs during late spring. The second and bigger wave is typical for August when in the CR there usually is a drought and high temperatures, which is exactly what was seen in our case. Clostridium botulinum, a producer of botulotoxin, prefers anaerobic environment and this condition was also fulfilled (low water level, lack of oxygen). Clinical signs and pathological findings – difficult breathing, so called limber neck, paralysis of muscles - were the same as described in botulotoxin poisoning in the literature, which again proves our diagnosis of botulism.

3. In botulotoxin poisoning we should withdraw blood samples and make a biological test with blood plasma – mice neutralisation test. It is also possible to detect clostridium from sediments and cadavers by cultivation.

4. We have to do these measures – aeration of water, decrease the number of fish and ducks bred on the pond. As a therapy we could administer repeatedly carbo adsorbens and administer physostigmine.

5. Among preventive measures that are usually possible to do during whole year belong gathering, removal and disposal of cadavers, aeration of water, adjustment of water flow according to climatic conditions. Also it is possible to make the vaccination of wild animals, do the decontamination of outlets of animals, the bottom of the pond and sediments. Feed should be given to the animals on the ground far from water to avoid contamination of water with organic material (organic stuff increases the eutrophisation of water and the consumption of oxygen from water).

Cattle poisoning

In the livestock breed, a disease with these signs was observed:

Anamnesis: 

A common feed was used – hayage, silage, straw and a mixture of grain feeds for cattle fattening. The night before the clinical signs were first observed, several animals had unfastened from their boxes and moved to the room where the feed was stored. Except the feed, also dietary salt, calcium nitrate and calcium hydrate were stored there. Sacks with these chemicals were disturbed.

Clinical signs: 

In the vast majority of the animals in stable increased salivation, thirst and hyperventilation was found out. In several animals also the paralysis of hind legs was diagnosed and 7 pieces of cattle died in seizures. Conjunctivas and non-pigmented mucosas were cyanotic. 

Pathological examination:

One dead animal was sent for the section. Pathologist found hyperaemia of mucosa of rumen and small intestine, gastritis and enteritis, dilatation of big vessels of splanchnic area, haemorrhages in small intestine and brain. Mucosas and serosas were hyperaemic and dark coloured. Liver was swollen and hyperaemic, in kidney cortex severe haemorrhages were found. Blood was not coagulated and it was of brownish colour. 

Laboratory examination:

Liver without any finding, NaCl: 1550 mg/kg

Kidneys without any finding

Rumen content – nitrates +++

Small intestine – nitrates +++, nitrites +++, NaCl ++

Feed mixture – 9g NaCl/kg

Drinking water without any finding

Blood – 28 % of methaemoglobin

According to data available, try to analyse the case, tell whether the amount and type of samples were withdrawn and laboratory analyses performed correctly. Propose adequate therapy and prophylactic measures.

SOLUTION:

The first thing which was wrong and which could avert the intoxication was bad locking of the storage place and insufficient securing of animals` movement from boxes. And also inappropriate storage of fertilizers in the same room with feed!

According to the data given, we can say that this case was a nitrate poisoning (calcium nitrate). Clinical signs may indicate also salt poisoning, but laboratory examination didn’t prove it (salt in liver was of physiological value, chlorides in blood plasma unfortunately weren’t assessed, which was a fault).

Increased salivation, thirst and paralysis of hind legs may be the result of nitrate poisoning too, nitrates in overdose have the similar osmotic effect on the organism as salt. Moreover, nitrates were in guts converted to nitrites (their high concentration was determined in guts) which damaged haemoglobin (they oxidized it to methaemoglobin) and caused hypoxia, cyanosis and dark colour of blood. The concentration of methaemoglobin assessed in the blood matches severe tissue hypoxia with all its manifestations – asphyxia, tachycardia, seizures.

Drinking water was all right according to the information available, feed too (0,9 % of NaCl in it, limit is up to 1 % of NaCl in the feed).  

The proposed therapy should include the evacuation of stomach and application of activated charcoal to absorb the rest of toxic agent from GIT. We must administer methylene blue as an antidote in the concentration of 1-4 mg/kg body weight dissolved in physiological solution (beware, administer it only to those animals which are not going immediately to slaughter because of their status, otherwise methylene blue would degrade the meat quality).

During the examination of the poisoning it would be very useful to send more samples from more animals to laboratory examination and more pieces of dead animals to section. Samples from only one animal doesn’t have to be representative, other cows should have died of something else – NaCl, or combined poisoning by both salt and nitrates. The procedure and therapy might have been different then.

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