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Flett & Carmichael
Veterinary Surgeons
Garrison Rd, Hatston,
Kirkwall
Orkney
KW15 1GN
Telephone: 01856 872859 Fax: 01856 878832
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Botulism in farm animals
Here is the info I have on Botulism. There’s no economically viable way of diagnosing it. Toxin tests exist but are prohibitively expensive. I’ve included the differential diagnoses in case any of them are relevant – I wondered about H.somni infection although it’s probably a long shot and not something I’ve seen in practice? If I think of anything else I’ll let you know.
CLINICAL SIGNS
Cattle – Intoxication produces a progressive, symmetrical, flaccid, cranial and peripheral nerve paralysis beginning with the hind legs and progressing anteriorally. The speed of progression is variable (probably dose related) resulting in peracute, acute and chronic forms of the disease. Some cases may present as sudden deaths. Otherwise clinical signs may be first observed from around 24 hours up to 17 days after exposure to the toxin. Some or all of the following clinical signs may be observed: -
• Anorexia and adipsia.
• Afebrile and no loss of sensibility.
• Lack of muscle tone resulting in progressive weakness starting with shifting of weight on hind limbs at rest, knuckling of fetlocks and unsteady gait.
• Dilated pupils with poor response to light.
• Flaccidity of the tail, eyelids, jaw and/or tongue which in some cases may be easily withdrawn, or may protrude from the mouth at rest due to lack of muscle tone in the tongue.
• Difficulty chewing and swallowing with drooling of saliva.
• Sternal recumbency often with the head swept round to one side, followed (terminally) by lateral recumbency.
• Respiratory depression with abdominal breathing.
• Dry mucous membranes.
• Occasionally initial diarrhoea but usually sluggish rumen and intestinal movements and later constipation.
Nervousness, apprehension and unilateral neurological signs are not typical features of botulism.
Morbidity is very variable. Mortality is very high (90%) with many animals requiring euthanasia on welfare grounds.
Sheep and Goats – the clinical signs are similar to those in cattle, except that the muscles of mastication and swallowing are not as obviously affected. Characteristically sheep and goats develop an arched back with a drooping tail, head and neck. Sheep in the early stages of clinical disease have an unusual, stilted gait.
DIFFERENTIAL DIAGNOSES
Cattle and sheep
Metabolic Disease: -
Hypocalcaemia, Hypophosphataemia, Downer cow syndrome, Post parturient paresis, Ketosis, Hypokalaemia.
Infections: - H. somni (thromboembolic meningoencephalitis), Listeriosis, BSE, Paralytic rabies, other viral and chlamydial encephalitides, Brain abscess.
Intoxications: - Hepatoencephalopathies (terminal changes), Lead (subacute/chronic), OP poisoning.
Miscellaneous conditions: - Peripheral neuropathies, Myopathies, Acidosis.
RISK FACTORS
a) Access to poultry litter, in particular that from broiler units. Disease has been seen in animals grazing several hundred metres away from fields where poultry litter has been stacked or spread. Movement of hazardous material eg carcases containing preformed toxin, by scavenging foxes, birds etc. is thought to be the likely explanation for these cases. Wind borne transmission of spore infected dust is also possible, though whether this would be capable of causing disease (by toxicoinfection) is less certain.
Disease has also been seen in housed animals fed conserved forages e.g. silage, made from crops in fields where poultry litter was spread as a fertiliser prior to cropping
b) Access to any other decaying carcase material especially where incorporated into feeds
c) Access to water contaminated by decaying carcase material.
d) Access to spoiled decaying plant crops/vegetable material.
DIAGNOSIS
It is generally accepted that there are no pathognomonic gross pathological, or histopathological features in cases of botulism. Indeed in most cases there are no observable primary lesions.
There are no characteristic biochemical or haematological findings in cases of botulism. Affected animals frequently show evidence of neutrophilia and hyperglycaemia, but these are non-specific and may be stress related.
Nevertheless in the process of arriving at a diagnosis of botulism (based largely on clinical signs and history) it is important to use laboratory tests to exclude possible differential diagnoses which cannot be eliminated by clinical examination and/or enquiry.
The following examinations should be considered where material is available:-
• Full haematology
• Biochemistry - calcium, magnesium, phosphorus, potassium, BHB, and tests for liver/kidney/muscle damage/function on blood.
• Toxicology - test for lead (heparin blood or kidney).
• Gross post mortem examination. In particular, stomach contents should be examined for evidence of suspicious material e.g. bones, decaying carcase material.
Histopathological examination of the brain, liver, kidney, heart and lung. Examination of the brain is particularly important as cases of polioencephalomyelitis have been confused with botulism.
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Hatston Veterinary Centre Ltd, trading asFlett & Carmichael
Registered Office: Unit 1, Garrison Road, Hatston Industrial Estate, Kirkwall KW15 1GN
Registered in Scotland No. : 340215 Vat : 790 1000 70