CASE NOTES


Beef measles, should we bother about looking for it in Australian abattoirs?

David J Jenkins, School of Animal and Veterinary Sciences, Charles Sturt University, Wagga Wagga, NSW 2678

Posted Flock & Herd August 2015

INTRODUCTION 

Bovine cysticercosis is caused by infection with the intermediate stage of the human tapeworm Taenia saginata. Bovine cysticercosis is also colloquially referred to as Cysticercus bovis or beef measles. Infection in the bovine intermediate host manifests as small, blister-like cystic lesions about 5-10mm in length occurring most commonly in cardiac, tongue, diaphragm and/or masseter musculature, but muscles throughout the body may be infected. Each cyst contains a single parasite scolex which, if consumed by a human in raw or inadequately cooked beef, results in infection with a tapeworm, commonly around 4 metres in length. This parasite occurs worldwide. In developing countries, cattle usually become infected through accidental ingestion of T. saginata eggs whilst grazing pasture contaminated with human faeces through indiscriminate defecation. In sporadic outbreaks in more developed countries, pasture contamination commonly occurs through raw sewage passing onto pasture as a result of a sewage treatment facility malfunction, particularly on-farm domestic septic tanks (Jenkins, unpublished data) or feed lot workers defecating in feed silos, irrigation ditches and hay paddocks. Eggs of T. saginata can withstand the impacts of sewage treatment, passing out of sewage treatment plants still infective to cattle. Eggs may remain viable on pasture under Australian conditions for 8 to more than 14 weeks.

A recent publication on T. saginata infection in Australian cattle1 concluded that bovine cysticercus in Australian cattle is “extremely rare”. However, a characteristic feature of bovine cysticercosis in countries where the parasite occurs uncommonly in cattle, such as Australia, are “cysticercosis storms”2. These occur as a result of sudden exposure of immunologically naïve cattle to the eggs of T. saginata.  The result is large numbers of animals, often in a restricted geographic area, becoming infected at the same time, commonly with heavy infections. The longevity of the cysts in cattle is variable (weeks to years) but it is common to find both dead and viable cysts in an infected beast. Dead cysts may occur as small caseous lesions with associated fibrosis and/or hard calcified nodules. The longevity of cysts is influenced by intensity of infection (cysts die more quickly in the most heavily infected animals) and age of the animals at the time of infection. 

Transmission of T. saginata relies on humans (definitive hosts) eating cattle (intermediate hosts). The human health impacts of infection with the tapeworm stage of T. saginata are usually minimal. Treatment consists of administration of a single dose of a cestocidal drug such as niclosamide or praziquantel. Infection in cattle is usually without veterinary consequences. 

This paper reports on an outbreak of bovine cysticercosis in a feedlot in NSW. The impact of this outbreak was major for the producer resulting in serious direct financial loss from condemnation and downgrading of carcasses, loss of a lucrative contract to supply meat to a national supermarket chain, and loss of reputation as a producer of high quality beef.

This outbreak of bovine cysticercosis was confined to animals fed on feedlot rations, infection never being detected in animals exclusively pasture-fed in paddocks adjacent to the feedlot enclosures. Therefore the source of the infection, in our opinion, had to be from a component of the feedlot rations. Following our investigations, it seems most likely that the source of the infection arose from human faeces-contaminated copra meal imported from Papua New Guinea (PNG), since all available evidence indicates the Australia-sourced ingredients could not have been contaminated. 

The use of traditional meat inspection methods, namely, gross examination of the sites of predilection, heart, diaphragm, tongue and masseters, are reliable in detecting infection in cattle with heavy infections. However, light infections mainly occur in naturally infected, pasture-grazed, animals. In cattle with light infections only about 30% of infected animals were identified. Therefore, it is not unreasonable to assume that additional infected cattle in this outbreak of bovine cysticercosis went undetected. 

The likely scenario for how this outbreak arose was that a person defecated in a copra meal hopper in PNG, after oil extraction and subsequent milling but prior to bagging for sale in Australia.  The faeces, coated in ground desiccated coconut, probably passed as a single mass into the bag subsequently dispatched to the feedlot. A curious aspect of this incident is that it appears to be an isolated outbreak, possibly because copra meal is most commonly used in rations fed to horses and sheep, neither of which can act as intermediate hosts for T. saginata.

Measures to preclude an event such as this happening again would include either heat treatment or freezing of bags of copra meal, however, realistically, it is unlikely these measures would ever be implemented.

ACKNOWLEDGEMENTS

The author acknowledges with grateful thanks the contribution of Dr Bob McKinnon (DV Tamworth) in this study.

REFERENCES 

  1. Pearce BHG, Traub RJ, Davis A, Cobbold R, Vandelinde PB. Prevalence of Cysticercus bovis in Australian cattle. Aust Vet J 2010;88:260-262
  2. Jenkins DJ, Brown GK, Traub RJ. “Cysticercosis storm” in feedlot cattle in North West New South Wales. Aust Vet J 2013;91:89-93

 


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