But what if the signs of this fungal disease are much more subtle?
Ergot is caused by Claviceps spp., fungi that grow in cereal crops and release substances that are toxic to both humans and animals. In most cases, livestock are exposed to the fungus through feed that contains contaminated grain.
Veterinarians and cattle producers usually associate ergot toxicity with obvious clinical signs such as neurological issues, hoof sloughing (when dead tissue separates from live tissue), and necrosis of the ears and tails of beef cattle.
However, researchers such as Drs. Jaswant Singh and Barry Blakley of the Western College of Veterinary Medicine (WCVM), believe even low levels of ergot toxicity cause other harmful, subclinical effects on cattle such as delayed reproductive cycles and decreased milk production.
Scientists know that ergot causes vasoconstriction (narrowing of blood vessels), especially in peripheral tissues such as cows' ears, tail and hoofs. However, no one has yet studied the possible vasoconstrictive effects in the bovine ovary.
In 2015, the focus of my summer research project was to take ultrasound images of beef cows' ovaries and track any changes during the period of time that the cattle ate ergot-contaminated feed.
Specifically, I was interested in whether the cows ingesting ergot-contaminated feed began their reproductive cycles later than cows eating ergot-free feed. Delayed reproductive cyclicity would have serious consequences for the beef industry, compromising the cows' reproductive efficiency.
Until a cow resumes normal cycling after calving, she's unable to become pregnant, leading to the disappointing "open" status of a non-pregnant cow later in the season.
The Canadian Food Inspection Agency (CFIA) has set the acceptable, maximum level of ergot in cattle feed at 2,000 parts per billion (ppb). However WCVM researchers believe that this level exceeds what is considered safe for animals to eat.
To test this theory, we fed three different concentrations of ergot to three groups of cows every day for three months. All test concentrations were below the CFIA's acceptable standard because we wanted to try to find a level at which subclinical effects dissipated.
Through ovarian ultrasound exams, we tracked the ovulation times and follicle growth in the research study's cows. By comparing the average time it took normal cows to ovulate post calving, we could determine if ergot had an effect on the time it took for our research cows to resume normal cycling behaviour.
Previous research in dairy cows has shown that another subclinical effect of ergot is decreased prolactin, a hormone that stimulates milk production after calving. Less prolactin leads to less milk production and decreased nutrition available for the suckling calf. That means the calf can't grow to normal standards, which is costly for the cattle producer.
"Our hypothesis is that if prolactin production is affected in beef cows, as it is in dairy cows, then the calves will not grow very well," says Singh.
To test this earlier finding, we analyzed the cows' prolactin levels from blood samples taken once a week. In an indirect way to measure milk production, we also weighed the suckling calves weekly to determine if prolactin levels and calf weights are correlated, and if these factors are related to ergot levels in the cows' feed.
Since decreased calf growth is a possible consequence of ergot toxicity, we wanted to determine the threshold of ergot concentration at which calf growth is no longer affected.
The question facing producers is whether it makes more economic sense to clean ergot-contaminated grain (lowering ergot concentrations) or to simply pay more for grain with low-level ergot contamination to minimize the disease's toxic side effects? As well, are the toxic effects of this disease problematic enough to consider lowering the CFIA's accepted level of ergot in cattle feed?
We hope our research findings will help to answer some of these questions. Our ultimate goal is to find the concentration of ergot at which clinical and subclinical effects are no longer seen in cattle — ensuring healthier herds and more efficient cattle production.
Saskatchewan's Agriculture Development Fund and the WCVM's Interprovincial Undergraduate Student Summer Research program provided financial support for this study.
Jill Keogan of Brooks, Alta., is a second-year veterinary student who was part of the WCVM's Undergraduate Summer Research and Leadership program in 2015. Jill's story is part of a series of stories written by WCVM summer research students.
Ergot is caused by Claviceps spp., fungi that grow in cereal crops and release substances that are toxic to both humans and animals. In most cases, livestock are exposed to the fungus through feed that contains contaminated grain.
Veterinarians and cattle producers usually associate ergot toxicity with obvious clinical signs such as neurological issues, hoof sloughing (when dead tissue separates from live tissue), and necrosis of the ears and tails of beef cattle.
However, researchers such as Drs. Jaswant Singh and Barry Blakley of the Western College of Veterinary Medicine (WCVM), believe even low levels of ergot toxicity cause other harmful, subclinical effects on cattle such as delayed reproductive cycles and decreased milk production.
Scientists know that ergot causes vasoconstriction (narrowing of blood vessels), especially in peripheral tissues such as cows' ears, tail and hoofs. However, no one has yet studied the possible vasoconstrictive effects in the bovine ovary.
In 2015, the focus of my summer research project was to take ultrasound images of beef cows' ovaries and track any changes during the period of time that the cattle ate ergot-contaminated feed.
Specifically, I was interested in whether the cows ingesting ergot-contaminated feed began their reproductive cycles later than cows eating ergot-free feed. Delayed reproductive cyclicity would have serious consequences for the beef industry, compromising the cows' reproductive efficiency.
Until a cow resumes normal cycling after calving, she's unable to become pregnant, leading to the disappointing "open" status of a non-pregnant cow later in the season.
The Canadian Food Inspection Agency (CFIA) has set the acceptable, maximum level of ergot in cattle feed at 2,000 parts per billion (ppb). However WCVM researchers believe that this level exceeds what is considered safe for animals to eat.
To test this theory, we fed three different concentrations of ergot to three groups of cows every day for three months. All test concentrations were below the CFIA's acceptable standard because we wanted to try to find a level at which subclinical effects dissipated.
Through ovarian ultrasound exams, we tracked the ovulation times and follicle growth in the research study's cows. By comparing the average time it took normal cows to ovulate post calving, we could determine if ergot had an effect on the time it took for our research cows to resume normal cycling behaviour.
Previous research in dairy cows has shown that another subclinical effect of ergot is decreased prolactin, a hormone that stimulates milk production after calving. Less prolactin leads to less milk production and decreased nutrition available for the suckling calf. That means the calf can't grow to normal standards, which is costly for the cattle producer.
"Our hypothesis is that if prolactin production is affected in beef cows, as it is in dairy cows, then the calves will not grow very well," says Singh.
To test this earlier finding, we analyzed the cows' prolactin levels from blood samples taken once a week. In an indirect way to measure milk production, we also weighed the suckling calves weekly to determine if prolactin levels and calf weights are correlated, and if these factors are related to ergot levels in the cows' feed.
Since decreased calf growth is a possible consequence of ergot toxicity, we wanted to determine the threshold of ergot concentration at which calf growth is no longer affected.
The question facing producers is whether it makes more economic sense to clean ergot-contaminated grain (lowering ergot concentrations) or to simply pay more for grain with low-level ergot contamination to minimize the disease's toxic side effects? As well, are the toxic effects of this disease problematic enough to consider lowering the CFIA's accepted level of ergot in cattle feed?
We hope our research findings will help to answer some of these questions. Our ultimate goal is to find the concentration of ergot at which clinical and subclinical effects are no longer seen in cattle — ensuring healthier herds and more efficient cattle production.
Saskatchewan's Agriculture Development Fund and the WCVM's Interprovincial Undergraduate Student Summer Research program provided financial support for this study.
Jill Keogan of Brooks, Alta., is a second-year veterinary student who was part of the WCVM's Undergraduate Summer Research and Leadership program in 2015. Jill's story is part of a series of stories written by WCVM summer research students.
Share this story