Organophosphate Poisoning In Cats And Dogs Biology Essay

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Many common substances in our world contain organophosphate compounds which have the potential to cause an acute cholinergic crisis if ingested, inhaled or absorbed through the skin. Some of these substances include pesticides, lubricating oils, hydraulic fluids and coolant fluid. In dogs, it is more common to see poisoning via ingestion. Cats can present with signs for OP poisoning commonly when certain brands of spot-on dog flea treatment (such as excelpet) are used on them, from these, the OP are absorbed through their skin as well as being ingested when the cats clean themselves. Cats are more sensitive to OP than dogs.

Organophosphates (OP) can lead to an acute cholinergic crisis by their mechanisms of action. OP target and inhibit acetylcholinesterase (AchE) by irreversibly binding to it. This then causes a flood of acetylcholine (Ach) in the synapses. AchE is important in breaking down Ach and this mechanism is essential to avoid a buildup of Ach in the synapses and thus avoiding overstimulation of receptors. The constant stimulation of the receptors leads to an over-depolarizing state of the cholinergic synapses resulting in the cholinergic crisis.

Basis for selective effects of the disease

Acetylcholine is an important neurotransmitter in the peripheral nervous system and the central nervous system. In the Peripheral nervous system, it acts on several different sites including the muscarinic receptors of the parasympathetic system and skeletal muscle innervation. In the central nervous system Acetylcholine is involved in excitatory actions.

When organophosphates are introduced into the body, and attacks Acetylcholinesterase, the excess Acetylcholine can result in numerous effects related with the function of Acetylcholine. In the Peripheral nervous system the effects of the parasympathetic system are evident. An acronym called SLUGDE is useful in describing the major clinical signs. SLUDGE stands for salivation, lacrimation, urination, gastrointestinal movements, defecation, and emesis. Excess acetylcholine will also continue to depolarize skeletal muscles leading to constant twitching, weakness, eventually paralysis and death from respiratory paralysis. The excitatory nature of acetylcholine coupled with the accumulation of acetylcholine in the Central nervous system causes anxiety, restlessness, hyperactivity and generalised seizures.

How can it be diagnosed?

There are a couple of approaches to diagnosing organophosphate poisoning. One is to take blood samples specifically looking at cholinesterase activity, upon presentation, then several other blood samples at regular intervals and see if there is a decrease in activity. This method generally is only used in human cases due to the specialized equipment required.

The other approach, used most commonly in the veterinary profession, is to put the clinical signs together (SLUDGE, muscle twitches and CNS signs) and give a dose recommended to the animal, of atropine. Atropine reverses the effects of the Parasympathetic nervous system, and thus, if there is a reduction of the SLUDGE signs, a diagnosis is usually drawn from this. Treatment for the central nervous system signs and the muscle twitching will need to be administered as well, but usually not before the atropine test is performed. The use of atropine as a diagnostic tool for this disease is very significant. It is a quick, inexpensive and relatively safe diagnostic tool.

Copper deficiency â€" White matter disease

Aetiology and Pathophysiology

Copper deficiency is a disease seen more commonly in sheep and goats than cattle. In the majority of cases, it is seen in lambs born to copper deficient mothers. There are two main causes of this disease, those being a general deficiency in copper through diet and/or soils which pasture is growing, and the other is when the animal has a diet high in molybdenum. Molybdenum is another trace element required for normal bodily function, however an excess of this interferes with copper availability in the rumen. It causes an insoluble copper-molybdenum-sulphur compound which is eliminated by the body.

The two types of copper deficiency seen in lambs from copper deficient mothers are congenital (defects present at birth), and delayed (can take up to 6 months to show signs).

Copper deficiency affects the axons ability to maintain their myelin sheaths. Myelin lipids, in particular cerebroside are thought to be depleted, causing the damaged myelin. Impaired myelin integrity increases the chance an electrical signal from the neuron will be lost and not transferred to the muscles.

The precise mechanisms behind these actions are not fully understood, and the mechanism behind the myelin lipid depletion is not known.

Basis for selective effects of the disease

Copper deficiency affects the myelin proteins and myelin sheath integrity. The clinical signs associated with this disease reflect this defect by showing inability to stand, blindness, and hind limb ataxia (in delayed form). These signs are connected to the pathogenesis of the disease because the signals from the axons are not being received at the muscles and the muscles therefore have very limited ability for movement and/or paralysis.

Upon post mortem, gross lesions, such as multifocal cysts in the white matter of the cerebellum can be observed, as well as histological changes like chromatolysis of motor neurones in the spinal cord and Walliarian degeneration in the distal regions of white matter tracts.

How can it be diagnosed?

It is suggested that liver samples can be taken to analyze the copper concentrations. This method of diagnosis has flaws though, if multiple samples are taken from multiple animals it may not be possible to accurately identify if there is a copper deficiency problem, as different sheep can have different levels of copper in their liver with/without showing symptoms. Also this diagnostic tool is logistically difficult. Blood samples can also be taken, however, they can be unreliable is molybdenum is the culprit behind the deficiency. Pasture analysis can be performed, but it will only give a very rough guide for copper status of the herd. Post mortem of diseased animals is a great diagnostic tool as lesions in the white matter of the cerebellum and histological changes such as Walliarian degeneration and chromatolysis will be present.

A valuable diagnostic tool for this disease is knowledge of clinical signs and being able to link them to copper deficiency.

Transmissible Spongiform Encephalopathies â€" Grey matter disease

Aetiology and Pathophysiology

Transmissible spongiform Encephalopathies (TSE) are prion diseases caused by mis-folded proteins. These can occur through genetic mutations where animals carry a rare mutant prion allele which causes proteins to fold abnormally, they can occur sporadically, or they can also be infectious through ingestion. TSE are infectious to different species, ie a sheep TSE can infect cows by feeding infected sheep meat to cows, and a cow TSE can infect humans by humans eating infected beef.

Prion proteins promote the mis-folding of proteins from their normal alpha-helical shape to a beta plated sheet. This change then disables the proteins ability to undergo digestion. The protein is then transmitted to the nervous tissues and finds its way up to the brain. It is believed that the prions replicate in a process not fully understood, and from there, spread throughout the nervous, but seen most often in the spinal cord. Lesions such as vaccuolation of grey matter, neuronal loss, astrocytosis and amyeloid plaque formation occur and can be seen under the microscope.

Basis for selective effects of the disease

Animals infected with TSE can show an array of signs including â€" ataxia, mental confusion, apprehension and hesitation, changes in temperament, aggressiveness, fear, hypersensitivity to touch and light, hyperesthesia, apparent blindness, poor coordination, paralysis and muscle tremors.

These signs are all apparent because of the progressive death of the brains neurons. The signs associated with coordination (ataxia etc) and emotion (fear, aggression etc) are usually seen as the first signs in TSE disease as they are all controlled by the cerebellum, which is where a significant proportion of abnormal prion protein accumulates. The other signs are usually seen later when there is wide spread disease to the rest of the brain.

How can it be diagnosed?

There is no available method for diagnosis in live animals. Before a herd is culled, there should be a reasonable amount of evidence available to suspect a TSE disease including: signalment, disease history, suggestive history, management history, clinical signs, evidence of opportunity for BSE and neurohistological changes for one or more animals post mortem. The suggested method of diagnosing TSE in a herd is to cull one animal showing signs of TSE infection and perform diagnostic tests.

In order for diagnostic tests to be performed, appropriate specimens of tissue are required. These include sections of the obex (where the fourth ventricle narrows to become the central canal of the spinal cord), the eyes can be collected too if the animals was showing signs of blindness and sections of the cerebellum.

The diagnostic tests available are ELISA, immunohistochemistry and the Western blot test. The ELISA is usually the test carried out first. If there is no positive result, then the other two tests are performed.