CASE NOTES


A case of botulism in a dairy herd

Helen Schaefer, South East Local Land Services, Bega

Posted Flock & Herd March 2015

INTRODUCTION

The first recorded case of botulism goes back to 1735 when German sausages were blamed for an episode of food poisoning. The term botulism was not employed until 1870 when a German doctor named the disease "botulism" after the Latin word for sausage, botulus. The bacteria was isolated in 1895. The first of the neurotoxins it produces was identified in 1944.

Botulism is caused by the Gram-positive, spore forming anaerobe, Clostridium botulinum, and affects animals, birds and humans. Cl. botulinum spores are present around the world in soil, water and marine sediments, and are resistant to destruction with the potential to survive in the environment for over 30 years. The bacteria can also be found as a normal inhabitant of the intestinal tracts of cattle, horses and poultry.

This case demonstrates the challenge it can be to diagnose a disease which has limited diagnostic aids, particularly when it does not present as classically recognised. It also raises a challenge to the veterinary profession in some areas, to be proactive in disease prevention in livestock industries as the practices of those industries change.

CASE REPORT

History

Timeline:

Chart 1: Deaths and recoveries during the outbreak

Working on 3 "rule out" fronts:

  1. Botulism - via silage pH (too high >4.6) + attempt isolation of the toxin from silage + syrup
  2. Seed toxicity - confirm the ID. + potentially the levels of toxin
  3. Metabolic disease - the mid-lactation hypoCa theory that the farmer was quite keen on was highly unlikely given the blood results so far, however it would be good to get some more "on the spot" samples of a few to be sure...if any more go down.

Farmer now also considering the possibility of botulism from the silage or the syrup.

To further progress the "rule outs"

  1. Botulism:
  2. Toxicity:
  3. Metabolic:

Test Type: Botulism Type C Antibody - ELISA


Test Type: Botulism Type D Antibody - ELISA

Table 1: Animal Health Laboratories Report from 21st July 2014

Update:

19/1/2015 :- Spoke to farmer: no issues with botulism since 17/6/14. Full rate of silage feeding since 3/9/14. Cows averaging 30L per cow per day. Are having some issues with high somatic cell counts. Have not re-introduced the DCS syrup as yet - were about to when the cell count went up; don't want to change anything until that is resolved.

Will continue to vaccinate with 7-in-1, for salmonella and botulism (at different sites/sides) and drench, the entire herd, annually.

DISCUSSION

Bovine botulism is endemic in Australia and has most often been associated with extensive enterprises in Queensland, Northern Territory and Western Australia where cattle develop pica associated with phosphorous and/or protein deficiency. This induces them to chew on bones or eat carrion to satisfy their cravings. Over the last decade or so botulism has become more common in intensive systems, with the increase of feedlots involved with beef production and the use of conserved fodder via total or partial mixed rations in dairy herds.

During its vegetative growth state, which is encouraged by warm anaerobic conditions, C.perfringens produces neurotoxins, seven types of which have been identified (A-G). Ideal situations for neurotoxin production include rotting carcasses and decaying vegetation. Disease in cattle most commonly occurs when individuals ingest the preformed toxin. Toxin types C and D are responsible for almost all cases of botulism in cattle in the southern hemisphere. Type B toxin is more common in Europe and Northern America. The toxin is absorbed from the intestinal tract, enters the bloodstream and is transported to peripheral cholinergic nerve terminals. Inhibition of the release of acetylcholine ensues and leads to flaccid paralysis, with death being caused by respiratory paralysis.

Botulism is recognised as being a difficult diagnosis to make, particularly in geographical areas not recognised as having experienced botulism outbreaks previously. The difficulty is increased in the absence of the classical signs associated with botulinum toxicity such as sudden death, tongue paralysis, tongue protrusion, dysphagia, drooling. Diagnosis has generally relied on clinical signs, ruling out other possibilities and the demonstration of toxin, the latter of which can be very challenging.

What can be learned from this case?

Does the case involve -

A botulism outbreak in an intensive system generally involves the majority of deaths occurring within the first week, followed by a number of clinically affected animals who recover over the next couple of weeks, with intermittent deaths occurring for up to 3 weeks.11,15 ?

The clinical signs of botulism do depend on the dose of the toxin ingested and the immune status of the animal. Sub-lethal botulism in cattle is now recognised as a syndrome, though perhaps it is not as widely recognised as it ought to be, particularly with respect to intensive systems. There have been a number of cases where the only sign observed of botulism is muscle weakness, and many cases where animals have been observed to recover from botulism, especially later in an outbreak.,

The absence of any other clinical signs can be useful to rule out other diseases eg.hypomagnesaemia, listeriosis.

Given that botulism, particularly as the sub-lethal syndrome, can be confused with a number of other diseases, eg. milk fever, pathology can be very useful to rule out differential diagnoses.

There are no pathognomonic lesions for botulism discernible on post mortem or laboratory examination of tissues

Silage can provide an ideal environment for the botulism bacteria to grow, particularly if a dead animal ends up in the pit, such as a rodent, bird, snake or cat., Hay can also be contaminated by such carcasses. The risk of significant numbers of animals being affected with botulism, if such contamination exists, increases when the silage or hay is put through a mix-all type process and is evenly distributed through the ration. While this process can lead to a lower dose being consumed by individuals, it does promote the ingestion of the toxin by more of the herd.

...THINK BOTULISM:

Botulism antibody-ELISA

The cut-off at 11EU and 7EU for types C and D respectively is statistically calculated to exclude "false-positives" at a level of 99% or better. There is therefore, a reasonable chance of "false negatives" occurring.

ACKNOWLEDGEMENTS

For being vital members of the team effort:

REFERENCES

  1. www.botulism-symptoms.com
  2. Wilkinson JM (1999) Silage and animal health. Nat.Toxins, 7:224
  3. George Weston Technologies, Analytical Reports June 2014
  4. George Weston Technologies, Analytical Reports June 2014
  5. McKenzie, RA (2012) Australia's Poisonous Plants, Fungi and Cyanobacteria.CSIRO Publishing
  6. McKenzie, RA (2012) Australia's Poisonous Plants, Fungi and Cyanobacteria.CSIRO Publishing
  7. Virbac Animal Health July 2011
  8. De Witte K, Taylor L. Managing the risk of botulism in beef and dairy herds. The Australian Cattle Veterinarian
  9. Parkinson TJ, Vermunt JJ, Malmo J. Diseases of Cattle in Australasia. A comprehensive textbook. Vetlearn 2010 p320
  10. Western Australian Agriculture Authority Botulism in cattle 2013
  11. Radostits OM, Gay CC, Hinchcliff KW, Constable PD. Veterinary Medicine. A textbook of the diseases of cattle, horses, sheep, pigs and goats. 10th Edition. Elsevier Ltd 2007 p824-826
  12. Jubb TF, Ellis TM, Gregory AR (1993) Diagnosis of botulism in cattle using ELISA to detect antibody to botulinum toxins. Aust.Vet. Journal, 70: 226-227
  13. Main D, Gregory A (1996) Serological diagnosis of botulism in dairy cattle. Aust. Vet. Journal, 73: 77-78.
  14. De Witte K, Taylor L. Managing the risk of botulism in beef and dairy herds. The Australian Cattle Veterinarian.
  15. McKenzie, Ross pers comm. 18th June 2014
  16. Poe, Ian pers comm 23rd June 2014
  17. Wilkinson JM (1999) Silage and animal health. Nat.Toxins, 7:224
  18. De Witte K, Taylor L. Managing the risk of botulism in beef and dairy herds. The Australian Cattle Veterinarian.
  19. Parkinson TJ, Vermunt JJ, Malmo J. Diseases of Cattle in Australasia. A comprehensive textbook. Vetlearn 2010 pp320,321
  20. Sharpe AE, Brady CP, Byrne W, Moriarty J ,O'Neill P, McLaughlin JG. Major outbreak of suspected botulism in a dairy herd in the republic of Ireland. The Veterinary Record, March 29,2008
  21. Palmer D. Department of Agriculture and Food, Western Australia pers comm
  22. Jubb TF, Ellis TM, Gregory AR (1993) Diagnosis of botulism in cattle using ELISA to detect antibody to botulinum toxins. Aust.Vet. Journal, 70: 226-227
  23. Gregory a, Ellis T, Jubb T, Nickels R, Cousins D (1996) Use of enzyme-linked immunoassays for antibody to types C and D botulinum toxins for investigation of botulism in cattle. Australian Veterinary Journal, 73:55-61
  24. Radostits OM, Gay CC, Hinchcliff KW, Constable PD. Veterinary Medicine. A textbook of the diseases of cattle, horses, sheep, pigs and goats. 10th Edition. Elsevier Ltd 2007 p826

 


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