Lesson 9 Copyright © Zuzana Široká
Rape toxicosis
It is not toxicosis to all intents and purposes but occurs due to growing rape hybrids, mainly
one called “OO”, which has a good taste to animals, especially to roe deer (OO hybrid means,
that it doesn’t contain erucin, which is a substance causing unpleasant taste). Thanks to
exceeding intake of rape, which contains mainly proteins and only little pulp, roe deer suffers
from severe GIT problems, e.g. tympanias, foaming fermentation of paunch content, changes
of bacterial microflora, which in a great amount of affected animals leads to death. This is
called acute form of poisoning. During this also innervation, senses and reflexes are slowed
down.
If rape intake lasts for a long period, animals suffer from chronic toxicosis caused by Smethylcysteinsulfoxide that is present in rape. In gut (due to bacterial microflora) it is
changed to dimethyldisulfide which is toxic. It interacts with sulfhydryl (-SH) groups of body
proteins. Main is interaction with glutathione (which protects red blood cells). Due to
decreased levels of glutathione, blood cells´ membranes are instable, haemolytic anaemia
comes up and sensitive animals (young, old, ill, pregnant) die.
Protection is not to grow rape on large areas, to prefer smaller fields with bigger variety of
crops to offer wild animals wider spectrum of different food.
Treatment is only symptomatic, and since it is poisoning of wild animals, there is usually
none, we only find dead animals.
Botulism
Clostridium botulinum is a producer of one of the most potent poisons in the world – of
botulotoxin. Intoxications are quite rare and attack usually animals bred at home due to
incorrect storage of their food, esp. meat, meat cans and other preserved food.
Botulism is typically alimentary poisoning. Toxin is swallowed with contaminated food.
Botulotoxin is released from food in stomach by hydrochloric acid and is absorbed by
stomach mucosa right to the blood. Its final destination is nervous system. There inhibits
acetylcholine release and causes immediate blockage of neurotransmission.
Among first signs of intoxication belong apathy, fatigue, later lost of stability and paralysis. In
birds we can easily distinguish paralysis of muscles of neck. Pupila is mydriatic and lately
comes up lost of palpebral reflex. The eye stays open and cornea dries up. Typical sign is
paralysis of mimic muscles, animal cannot swallow spits and death comes due to collapse of
respiration muscles.
Pathological examination doesn’t show any specific finding.
Treatment is only symptomatic, we start with gastrolavage or application of emetics, if there
is no sign of paralysis of swallowing and respiration muscles. Then we administer Carbo
activatus and physostigmin. This agent inhibits ACHE, and acetylcholine stays for longer
time on synapsis. Other steps of care are to put animal into safe place, covered with cloth and
to give it food by parenteral application to avoid aspiration of it.
Zootoxins
Snake toxins:
More than 80 % of snakes possess glands with venoms. These glands derived from saliva
glands during evolution. We distinguish two types of venomous tooth through which the
poison is delivered to the body of beast.
Native toxin is a fluid of white to orange colour. While staying fluid on air, quickly loses its
strength thanks to proteolytic enzymes contained in poison too. For medicinal purposes is
kept exsiccated. Main and active part of snake toxins are proteins and enzymes
(cholinesterase, proteases, ATP-ase, hyaluronidase etc.).
They can have many effects on many body systems: they are neurotoxins, haemotoxins,
cardiotoxins etc.
In middle Europe, the most common poisonous snake is viper. Its venom consists of
haemorhagins –directly affect endothelium of veins (these are mainly enzymes). Then there
are circulatory toxins – they have vasodilating effect and cause rapid decrease of blood
pressure and circulatory collapse. Also release from tissues histamine and bradykinine, which
also dilate veins and cause paralysis of muscles of veins. Other parts of the poison are
coagulative agents, which in different conditions cause or inhibit coagulation of blood
(phospholipase A, glycoproteins). And the last part of poison is formed by neurotoxins which
destroy lipids in CNS and cause lack of ATP in mitochondria. That leads to circulatory
collapse due to blockage of circulatory and vasoregulatory centres in brain.
Clinical signs after a snake bite: pain of affected place, oedema, petechias, necrosis or
gangrene. Other, complex signs are epistaxis, cough due do bronchospasmus, decrease of
blood pressure, colic, vomiting, paralysis and coma. In some people or animal can appear
anaphylactic shock.
Treatment: immobilization of affected leg, rather no ligature, no incision of wound.
Application of antiserum, corticoids, central analeptics, blood transfusion etc. Beware of
allergic potential of antiserums, sometimes can cause anaphylactic reaction worse than
primary snake bite. All the patients must be carefully monitored all the time they are treated.
Wasp and bee toxins:
Only females have the poison which forms 30 % of their body weight.
It consists of three parts:
F1 mellitin
F2 enzymatic fraction
F0 protein fraction
Mellitin is a protein mixture which doesn’t contain amino acids with sulphur. Acts as an
haemolytic agent, damages blood and lymphatic veins, irritates mucosas, causes rapid
decrease of blood pressure and respiration collapse
Enzymatic fraction contains lipase, phospholipase, lyase.
Protein fraction is less toxic.
Instead of proteins, bee and wasp poison contains also histamine, acetylcholine, serotonine
and apamine. Apamine increase permeability of veins and have cytotoxic effects.
Wasp and bee toxins are potent allergens and in many affected ones cause anaphylactic shock.
Other zootoxins:
Scorpios – mainly neurotoxins and enzymes
Spiders – again neurotoxins and enzymes