Territory Stories

Botulism Poisoning in Cattle in the Northern Territory

Details:

Title

Botulism Poisoning in Cattle in the Northern Territory

Other title

Agnote

Creator

Fitzpatrick, S.

Issued by

Northern Territory. Department of Regional Development, Primary Industry, Fisheries and Resources

Collection

Serial No. 651; Agdex No. 420/654; Agnote; E-Journals; PublicationNT; Agnote

Date

2006-12

Notes

This publication contains may contain links to external sites. These external sites may no longer be active.; Made available via the Publications (Legal Deposit) Act 2004 (NT).

Language

English

Subject

Agriculture; Weeds; Biological control; Animals; Farm animals; Periodicals

Publisher name

Northern Territory Government

Place of publication

Berrimah

Series

Agnote

Volume

No: K29, September 2006

File type

application/pdf

ISSN

0157-8243

Use

Attribution International 4.0 (CC BY 4.0)

Copyright owner

Northern Territory Government

License

https://creativecommons.org/licenses/by/4.0/

Parent handle

https://hdl.handle.net/10070/252490

Citation address

https://hdl.handle.net/10070/543817

Page content

Northern Territory Government Page 3 of 6 survey, 93% of producers indicated that they fed supplement at some stage throughout the year1F1Fii. However, cost and practical problems mean that supplementation programs are not totally effective in satisfying need. 2. Carcass and bone chewing. This is commonly seen in the NT. It is habit forming and even when dietary phosphorus and protein are adequate, animals continue to chew bones and will be exposed to the risk of botulism poisoning. Adequate supplementation programs will not cure the problem in deficient areas. 3. Bacteria distribution. Bacteria producing type C and type D toxin are present in all pastoral regions of the NT. 4. Toxin. Cattle are very susceptible to botulism toxin. Toxin production occurs in an anaerobic environment, with moisture and an optimum temperature of around 23C (15-35C). All these conditions can be found in a rotting carcass. Toxin can last for a year at 30C and is rapidly inactivated at 37C, so the amount of toxin present is not constant. Not all carcasses are necessarily toxic but the proportion of toxic carcasses in tropical environments can be very high. 5. Any carcass. All decaying carcasses are potentially infective, including those of cattle, horses, donkeys, pigs, birds, wallabies and rodents. 6. Susceptible cattle. Unvaccinated and improperly vaccinated cattle can be assumed to be fully susceptible. Even properly vaccinated cattle can succumb if the amount of toxin is high enough to over power the body's immune system. Natural immunity can develop in cattle which have been exposed to the natural toxin and have recovered. CLINICAL SYMPTOMS Visual symptoms of botulism poisoning can vary dramatically depending on the amount of toxin ingested, pre-existing immunity and the stage of poisoning. The period of time for the ingested toxin to show effect on the animal usually varies between three to seven days, depending on the quantity of toxin ingested. In very severe cases the animal can die in less than 24 hours without signs of illness. Animals may ingest low doses of toxin and not be affected, especially if they have antibodies to the toxin. The toxin binds to nerve endings and prevents nerve impulses to muscles. This leads to a floppy or flaccid paralysis, which usually progresses throughout the body... Early symptoms result from the paralysis of the tongue, throat and the stomach. Often the earliest sign of botulism poisoning is refusal to drink and a lack of appetite, related to the paralysis of the throat. This leads to dehydration that is evident by sunken eyes, hollow paunch, unpliable skin and strange behaviour. The tongue may protrude and the animal may drop cud and drool saliva. The animals voice may alter or fail. The first observed signs may be depression, muscular weakness and incoordination which makes the animal appear lame. Muscle weakness and paralysis usually begins with the hind legs, and progresses forward to the forequarters, head and neck. The beast may be drowsy and stagger, stumble, knuckle over and possibly arch its back. The animal may become aggressive and often attempt to charge anyone who comes close. On falling down, the beast may appear very weak and have great difficulty in rising. It may not even be able to lift its head (limber neck). Initially the beast lies in a normal resting position with its head on the ground or turned towards the flank (sternal recumbency). As the paralysis worsens, the animal may go into a semiconscious state and when it goes onto its side (lateral recumbency) it is unlikely to get up again. Semicircular marks in the ground may be the only evident sign when a carcass is found, resulting from the uncontrolled paddling movement of the legs. Death usually results from respiratory failure or exposure between one to four days following the onset of clinical