CASE NOTES


BOTULISM CAUSING HIGH MORTALITY IN A SMALL BEEF HERD

Nigel Gillan, District Veterinarian, Mudgee

Posted Flock & Herd December 2016

INTRODUCTION

Botulism is a disease caused by toxins produced by the anaerobic bacterium Clostridium botulinum, and is characterised by progressive, flaccid paralysis. In cattle the disease most often results from the ingestion of preformed botulinum toxin, and in some situations morbidity and mortality may be high. The case described here, diagnosed on clinical findings and confirmed by laboratory testing, resulted in the deaths of 11/19 adult cattle in a small beef herd in the Central Tablelands of NSW.

CASE REPORT

History

The owners of a small beef herd reported that eight of 19 cows had been found dead over a one week period. The owners did not live on the property, and the losses had been reported by a neighbour. When the owners arrived at the property, a further three animals were recumbent and unable to rise.

The herd consisted predominantly of non-lactating adult cows over 6 years of age. Steers and a bull were also present.  The entire mob had been grazing the paddock in which deaths occurred for approximately two months. No other illness or deaths had been seen in this time.

In the paddock in which deaths occurred, animals had access to a machinery shed, a storage shed, and a large pile of discarded car batteries. There were no agricultural chemicals stored in either shed. Some sheep were also run on the property, and a sheep carcass was found near a dam in the paddock. The carcass was decomposed, with predominantly only bone and wool remaining.

Feed availability in the paddock was moderate, and all animals were in good body condition. No supplementary feed had been provided. The cattle had not received any vaccinations.

Figure 1: Part of a sheep carcass near a dam in the paddock in which deaths occurred.
Figure 2: Part of a sheep carcass near a dam in the paddock in which deaths occurred.

Clinical Examination

The three recumbent animals (one bull and two cows) were examined briefly (prior to euthanasia on the grounds of poor prognosis and welfare considerations). Two were in sternal recumbency with hind limbs abducted. The third was laterally recumbent and moribund. Menace response was decreased in one animal and absent in one. No tongue protrusion was noted. In all three animals, mild to moderate protrusion of the eyes was noted, giving a ‘startled’ appearance.

Necropsy Findings

The eight carcasses of animals which had died over the past week were briefly examined, but were unsuitable for necropsy. No obvious external pathology was noted, and in all cases there were minimal or no signs of struggle. Several animals had blood from the nose, mouth, or vulva. An Anthrax ICT was performed with a negative result.

Two of the euthanased animals (a bull and a cow) were subjected to a full necropsy. Gross findings were minimal. In each case, rumen contents were fibrous with very little fluid. Contents of the large intestine were also dry, and contained small amounts of mucus and both fresh and digested blood.

At this point, the differential diagnoses being considered were botulism, lead toxicity, urea toxicity, or a plant toxicity (unknown plant). Other possible causes of recumbency and rapid death, such as nitrate/nitrite toxicity, ruminal acidosis, or bloat, were ruled out based on history and paddock inspection findings.

A range of tissue samples were collected for laboratory testing. Samples (bone, remnant (autolysed) spinal cord, and several maggots) were also collected from the sheep carcass found near the dam.

Figure 3: The carcass of an affected animal, with no evidence of struggling prior to death.
Figure 4: The carcass of an affected animal, with some evidence of struggling prior to death.

Laboratory Testing

Ammonia concentrations in aqueous humour from two animals were within the normal range (116µmol/L and 68µmol/L; normal range 0-200µmol/L). Lead concentrations in fresh kidney samples from two animals were within the normal range (0.7µmol/kg and 0.6 µmol/kg wet weight; normal range <2.0µmol/kg wet weight).

Sections of kidney, liver, jejunum, and colon were submitted for histopathology. Histopathological changes in these organs were generally mild and were deemed to be incidental. Specific findings were enterocolitis, eosinophilic, minimal to moderate, multifocal (likely caused by exposure to internal parasites); and interstitial nephritis, lymphoplasmacytic, minimal, multifocal (indicating previous immunological response).

Samples of liver from one necropsied animal, bone from the sheep carcass, and maggots associated with the sheep carcass were submitted for Clostridium botulinum toxin antigen ELISA. All three samples were positive for botulinum toxin.

DISCUSSION

Botulism is a disease characterised by progressive, flaccid paralysis, caused by toxins produced by the anaerobic bacterium Clostridium botulinum. The bacterium is ubiquitous in the environment and proliferates in decaying organic matter, such as animal carcasses (Galey et al, 2000; Kennedy and Ball, 2011). Of the eight types of toxin known to be produced by C botulinum, only types B, C, and D have been shown to produce disease in cattle (Kelch et al, 2000). These toxins inhibit the release of acetylcholine in presynaptic cholinergic neurons, preventing transmission at neuromuscular junctions, parasympathetic end plates, and cholinergic ganglia of the sympathetic nervous system and in adrenal glands (Galey et al, 2000).

There are several ways in which clinical botulism develops (Galey et al, 2000; Kelch et al, 2000; Radostits et al, 2000):

Of these, ingestion of preformed toxin is the most common cause of disease in livestock (Galey et al, 2000; Kelch et al, 2000).  A review of cases of botulism in England and Wales found that “proximity to broiler chicken litter” was a “key epidemiological factor” in all sheep incidents and 95% of cattle incidents (Kennedy and Ball, 2011).  Other reported sources include rations contaminated with animal carcasses (Galey et al, 2000), or improperly fermented silage or haylage (Kelch et al, 2000). In extensively grazed herds in northern Australia, pica (depraved appetite, leading to licking, chewing, or ingestion of foreign material such as bones) is the primary cause of botulism (Petherick, 2005).  Pica is thought to be related to dietary deficiencies of phosphorus, protein, or energy (Radostits et al, 2000).

In this case, it is likely that the sheep carcass found near the dam was the source of botulinum toxin, and that cattle were affected after chewing or eating bones. It is possible that an underlying phosphorus deficiency was a factor contributing to the development of pica.  Alternatively, the source may have been dam water contaminated by botulinum toxin from the sheep carcass, as decaying material was found close to the water’s edge. Occasional outbreaks linked to dead animals in drinking water have been reported (Radostits et al, 2000).

The primary clinical sign of generalised muscular paralysis in this case was consistent with the typical presentation of botulism. Of particular note on physical examination was mild to moderate eye protrusion (giving a ‘startled’ appearance), which has been reported elsewhere as resembling a bilateral corneal nerve block (Laven et al, 2010). The commonly reported clinical sign of tongue protrusion was not noted in this case.

Often, botulism is a presumptive diagnosis or diagnosis of exclusion, because confirmatory laboratory tests with high sensitivity are lacking (Radostits et al, 2000; Laven et al, 2010).  In this case, toxin was detected in a bone fragment from the sheep carcass, in maggots associated with the sheep carcass, and in liver tissue from an affected animal. Thus a definitive diagnosis was possible.  Maggots on carcasses suspected to be a source of botulinum toxin may be a useful sample to collect for botulinum antigen ELISA testing. Necrophagous flies and their maggots feeding on intoxicated carcasses are known to be a source of toxin in cases of avian botulism (Vidal et al, 2013; Hubalek and Halouzka, 1991).

The producer was advised to vaccinate the remaining animals with a botulinum vaccine. The possibility of an underlying phosphorus deficiency was not confirmed by further testing, but it was suggested that providing high phosphorus lick blocks may be warranted.  The producer was also directed to remove any remaining carcasses from the paddock, and to dispose of any carcasses found in future.  This case demonstrates the dangers of allowing livestock access to animal carcasses.  Besides botulism, other serious disease risks include Foot and Mouth Disease, Anthrax, and BSE. For this reason, clear advice should be provided whenever livestock are found to have access to restricted animal material (RAM). In NSW, it is an offence under the Stock Diseases Act 1923 (NSW) to feed a prohibited substance to stock. In addition, an owner or person in charge of stock must “take all steps that are reasonably practicable to prevent stock from having access to a prohibited substance” (Stock Diseases Act 1923 (NSW) s.20FB). In the Stock Diseases Regulation 2009 (NSW) Reg 70, restricted animal material is defined as “tissue, blood or feathers derived from the carcass of an animal, including any substance produced from or containing any such tissue, blood or feathers (but does not include tallow or gelatin)”. In this case, all animals were vaccinated and no further losses were reported.

ACKNOWLEDGEMENTS

The author wishes to thank Effie Lee (Pathologist, EMAI) for the histopathology report and Lydia Tong and Rod Reece (Pathologists, EMAI) for additional comments on laboratory findings.

REFERENCES

  1. Galey FD, Terra R, Walker R, Adaska J, Etchebarne MA, Puschner B, Fisher E, Whitlock RH, Rocke T, Willoughby D, Tor E (2000) ‘Type C botulism in dairy cattle from feed contaminated with a dead cat’, Journal of Veterinary Diagnostic Investigation, 12:204-209
  2. Hubálek Z, Halouzka J (1991) ‘Persistence of Clostridium botulinum type C toxin in blow fly (Calliphoridae) larvae as a possible cause of avian botulism in spring’, Journal of Wildlife Diseases, 27(1):81-85
  3. Kelch WJ, Kerr LA, Pringle JK, Rohrbach BW, Whitlock RH (2000) ‘Fatal Clostridium botulinum toxicoses in eleven Holstein cattle fed round bale barley haylage’, Journal of Veterinary Diagnostic Investigation, 12:453-455
  4. Kennedy S, Ball H (2011) ‘Botulism in cattle associated with poultry litter’, Veterinary Record, 168:638-639
  5. Laven RA, Malmo J, Vermunt JJ, Parkinson TJ, ‘Neurological Disease’, in Parkinson TJ, Vermunt JJ, Malmo (2010) Diseases of Cattle in Australasia, VetLearn, Wellington
  6. Petherick JC (2005) ‘Animal welfare issues associated with extensive livestock production: The northern Australian beef cattle industry’, Applied Animal Behaviour Science, 92:211-234
  7. Radostits OM, Gay CC, Blood DC, Hinchcliff KW (2000) Veterinary Medicine: A Textbook of the Diseases of Cattle, Sheep, Pigs, Goats and Horses. 9th Edition, WB Saunders, London
  8. Stock Diseases Act 1923 (NSW)
  9. Stock Diseases Regulation 2009 (NSW)
  10. Vidal D, Anza I, Taggart MA, Pérez-Ramírez E, Crespo E, Hofle U, Mateo R (2013) ‘Environmental factors influencing the prevalence of a Clostridium botulinum Type C/D Mosaic strain in nonpermanent Mediterranean wetlands’, Applied and Environmental Microbiology, 79(14):4264-4271

 


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