On a July afternoon under the blistering Okanagan sun, a microscopic force delivered sudden death to an apparently healthy bighorn ewe.
Her radio-collar told us she died at 7 pm July 18. When we reached her location, the air still sticky at 3 am, we found her intact, bedded with neck outstretched and head resting on her left cheek. A scavenging bird got there before we did, perching on her shoulder to pull tissue from her neck. With no pooled blood on the ground, the bird was feeding on the carcass post-mortem. Her teeth, horns, hooves, and hair were in great condition. Her limbs were not broken.
Finding a sheep dead, fully intact, is rare. Especially in summer.
The collar’s GPS data showed she spent July 1 – 15 in an open grassland area she had not previously used since being radio-collared in February. She moved progressively south 1.7 km during July 15 – 18, a normal movement rate, to where she died in a forested gulley. The location is within her usual range but not typical habitat for this sheep, suggesting that she was seeking shelter from the intense heat or died suddenly while passing through the area.
It had been unbearably hot for several weeks already, but wild sheep are one of those species that can manage comfortably in dry deserts and chilly mountain tops. Heat stress seemed unlikely.
But what would cause sudden death?
Clostridial bacteria, to be precise. They are widespread in soil and in the intestinal tracts of vertebrates. In small numbers they can exist in the intestines without producing disease. These bacteria can be very dangerous though, causing problems by producing toxins. When bacteria multiply rapidly, large amounts of toxin can damage the intestines, be absorbed into the bloodstream, and ultimately cause fatal poisoning. The collective term for this disease is enterotoxemia – blood poisoning caused by a toxin produced in the intestines.
Clostridium perfringens, common in the digestive tract of many domestic farm animals, has the shortest reported generation time of any organism: just 6.3 minutes in lab cultures. This explosive bacterial growth means infections can progress very quickly from fever to loss of mobility (ataxia), difficulty breathing (dyspnea), coma and death, often within hours.
Six types of Clostridium perfringens have been identified by the toxins they produce (A, B, C, D, E and F). Type D (Alpha and Epsilon toxins) is associated primarily with sheep, causing damage recognized as “Pulpy kidney disease” or “Overeating disease”.
We suspected that this bighorn’s death was heart-related with possible enterotoxemia before sending tissues to the lab. Why?
Field necropsy gave up 3 big clues.
- Kidney fat. Lots of it. In many animals, the amount of fat stored around the kidneys is correlated with nutritional status. Her kidney fat was a thing of beauty, leaving no reason to think she was struggling nutritionally. And at 162 lbs, she was a heavy ewe. With no obvious sign of injury or illness, sudden death had probable cause.
- Rapid degeneration of the kidneys. Once plucked from their beds of fat, the kidneys quickly lost their plump healthy appearance and became shriveled and blistered with gas bubbles. Field necropsy in the heat of summer is not ideal, and all tissues will degrade quickly in those conditions. But the overgrowth of Clostridial bacteria after an animal dies puts tissue degeneration into overdrive. The clostridial toxicity that is associated primarily with sheep is often referred to as “Pulpy kidney disease” because the kidneys can have a visibly soft and pulpy consistency as the tissue deteriorates.
- A soft heart. The sponginess we felt in the heart was because the muscle tissue was filled with air and fluid — otherwise known as being emphysematous and edemic, if you like technical lingo. Lab results confirmed that Clostridial bacteria had proliferated in the muscle, causing inflammation (myocarditis) and heart failure.
But this story has a twist.
While we were right to suspect heart failure, we were wrong about enterotoxemia.
The rapidly degenerating kidneys we saw were actually natural decay, accelerated by the typical proliferation of C. perfringens after death. Evidence pointed instead to perfringens’ cousin, Clostridium novyi, as the culprit.
Unlike perfringens, which is commonly ingested as an active bacteria, novyi is ingested, circulated, and deposited in tissues as spores that remain inactive until low oxygen conditions allow them to germinate and multiply. The presence of C. novyi is usually associated with ‘black disease’ in domestic sheep and cattle, where rapid bacterial growth can be triggered by parasites that damage the liver.
Clostridium novyi infection is common in domestic animals, including sheep, cattle, dogs, and pigs, but there is only one other reported case in wildlife: black disease in the liver of a captive forest reindeer in Scotland.
Even more rare are C. novyi infections in the heart.
We are not aware of any reports in wild or domestic animals, and only 1 report of C. novyi infection in a human heart.
In this case we don’t know why C. novyi spores in the heart suddenly germinated (or how they got there in the first place), but we do know there was no prior sign of heart disease. It leaves the possibility that heat stress created the right conditions for Clostridium novyi growth in this bighorn ewe.
[su_box title=”Publication” box_color=”#DFF0D8″ title_color=”#333333″]
A detailed report of these findings has been accepted for publication as:
Tony Redford, J. Clint Cubberley, Pamela Hengeveld, Erin Zabek, Ann P. Britton. Myocardial necrosis associated with Clostridium novyi infection in a bighorn sheep (Ovis canadensis). Journal of Wildlife Diseases. 2017. DOI 10.7589/2016-09-221
Having trouble accessing the paper? Request a copy from one of the authors.[/su_box]
Footnote: Enterotoxemia occurs in wild and domestic sheep more often than in any other animal.
It’s a sad irony really. As the nickname “Overeating disease” implies, it’s too much of a good thing. Death by chocolate, so to speak.
When sheep suddenly carbo-load, gorging themselves on mom’s milk (lambs), lush pastures or farm feed supplements, gut bacteria can multiply rapidly. Occasionally, an injury can also give bacteria the opportunity to cause widespread infection. Because of how quickly the bacterial toxins proliferate, treatment is not usually possible.
In farm settings, prevention includes vaccination to protect against the toxins, as well as gradual feed changes and other practices that reduce the risk that domestic sheep will overeat when turned out to green pastures.
Protecting wild sheep from the risk of “Overeating disease” is more difficult, although this example provides yet another compelling reason why wild sheep should not be fed indiscriminately or harboured on farm pastures.
Is it contagious? No. Is it an epidemic? Also no. Repeated exposure to low levels of bacteria can produce immunity. Although sometimes an outbreak may result in death of several individuals, acquired immunity means that most will recover after suffering a bout of ugly “food poisoning” illness.
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Doing a field post-mortem investigation at 3 am got me thinking about how much technology has changed field biology in the last 10 years. Subscribe below to get it delivered to your inbox.
About the author —
Pamela Hengeveld has worked on wild sheep and goat projects throughout British Columbia since 1997, beginning with census of bighorn sheep in Kootenay National Park. Since 2002, she has been working as project leader and liaison in multi-stakeholder collaborations focused on ecology and management strategies for Stone’s sheep, bighorn sheep, and mountain goats. Her academic background includes graduate research on ecology and harvest management of bighorn sheep populations in BC, evaluating population recovery after a pneumonia die-off in South Okanagan herds, and investigating the effects of bighorn sheep harvest regulations as an artificial selection on horn growth in rams. You can reach her at synergyecology.ca