Buying Time for Bison

By Kyle Walker / Originally published August 6, 2015 in The Bigheart Times
Bison at the Tallgrass Prairie Preserve
Photograph by Kyle Walker

It is still unknown how the 2,000 strong Tallgrass Prairie Preserve bison herd contracted a deadly infection in late 2013, but the good news is that preserve managers seem to have beat back the disease in a down-to-the-wire effort to round up and vaccinate the entire herd last spring.

The Nature Conservancy, which owns the Preserve, teamed up with a far-flung network of researchers to test a bleeding-edge vaccine on the Tallgrass herd, which eventually put a stop to the infection.

Back in the fall of 2013, Preserve Director Robert Hamilton and his team noticed signs of ill health among the bison including low body weight and lethargy. These symptoms seemed familiar to Hamilton.

“What’s the famous quote? When you hear hoofbeats, expect horses, not zebras,” Hamilton said. “So we were automatically thinking it was anaplasmosis.”

Anaplasmosis, a red blood cell parasite, periodically crops up in the southern United States and makes trouble for cattle producers. The bison at the Tallgrass Prairie had a run-in with the critters back in the 90s.

But when Hamilton sent blood samples to check for anaplasmosis the tests came back negative. Puzzled Hamilton turned for advice to a veterinarian working for American ranch mogul Ted Turner, who owns over 55,000 bison.

From that meeting was born a new suspect: Mycoplasma bovis.

The perp

M. bovis attacks both cattle and bison. It is in the same genus as the organism that causes pink eye, but Hamilton emphasizes that M. bovis is not contagious to humans and tha the flesh of infected bison is safe for human consumption.

Unlike anaplasmosis, M. bovis does not respond to antibiotics, which work by impairing an organism’s ability to maintain a cell wall, the rigid outer layer of most plant and bacteria cells.

M. bovis is unusual in that it lacks a cell wall entirely.

“It’s kind of like the blob,” Hamilton said. “It has no real sharp, defined boundaries to it.”

In order to verify their theory, Hamilton and company needed lung tissue samples. They selected four animals who seemed to be on their last legs, euthanized them and got to work.

Dr. Cody Golay, a Pawhuska veterinarian, opened the animals up to get at that lung tissue…

“And those lungs were the size of a football,” Hamilton said. “They should be two to three feet long.”

An infection of M. Bovis produces a number of symptoms. Affected animals grow lethargic and arthritic, but the killer is what the infection does to a bison’s lungs. An infected bison’s lungs fill with mucus, harden and shrivel, which eventually kills the animal.

According to Dr. Karen Register, a researcher at the National Animal Disease Center, this may be the result of an “overly zealous immune response” on the part of the bison’s immune system, which seems to be the case in cattle.

But she cautions against assuming that cattle and bison respond in the same way to M. bovis.

“It’s possible that this is also what happens in bison,” Register said in an email, “but we simply don’t know. We also have to consider that M. bovis almost always causes respiratory disease in cattle only when other co-infecting … pathogens are present. This is very different that what seems to be happening in bison.”

The Nature Conservancy sent tissue samples from these four animals to OSU, where the theory was confirmed. M. bovis was the culprit.

The next question was what to do about it.

Ted Turner’s herds had already encountered M. bovis, and Turner Enterprises had been working on a vaccine based on the two strains of the bacteria that had wrought the most havoc.

There was no guarantee, however, that the strain infecting the Tallgrass Prairie bison would respond to the vaccine manufactured for the Turner herds. The next step was to use genetic sequencing to compare the strains, a process which took place at the USDA’s National Animal Disease Center in Ames, Iowa, and at Newport Laboratories in Minnesota.


“The results of that was a good news, bad news thing,” Hamilton said. “The bad news was that the strain in our herd was different.”

But the sequencing also gave Hamilton some reason to hope: The Tallgrass strain closely matched the Turner strain in two genes that are associated with M. bovis vaccine effectiveness in cattle.

The running assumption has been that these two genes are also relevant in bison. But this “may or may not be correct,” Register said.

These genes encode proteins that the immune systems of infected cattle recognize as foreign, and these proteins prompt an immune response.

“We say these proteins are highly immunogenic, meaning that they stimulate a vigorous antibody response,” register said.

But just because a protein is immunogenic doesn’t mean it is protective, meaning that the antibody response will eliminate the disease.

“We know nothing at all about which proteins of M. bovis are the most immunogenic in bison,” Register said. “They may or may not be the same proteins that are most immunogenic in cattle. On top of that limitation, because we know almost nothing about which M. bovis proteins are protective in cattle, it’s very difficult to predict which might be protective in bison.”

“So this is like the blind man and the elephant … We’re trying to understand the big picture based on only a few genetic characteristics.”

To make matters worse, these proteins tend to vary across different strains of M. bovis, hence the concern for a close match between the Tallgrass strain and the strains on which the Turner vaccine was based.

“This left Bob (Hamilton) with a difficult decision, considering the time constraints that he had for vaccinating the herd,” Register said. “Should he use the immediately available, but somewhat mismatched Turner vaccine or wait until Newport labs could produce one that would perfectly match the problematic M. bovis in the Preserve bison?”


This was not a fun choice for Hamilton. Ideally, Newport Labs could have produced a tailored vaccine, but that alternative had a high cost.

“The downside is, that takes 8 to 12 weeks,” Hamilton said. “That would have put us into the heat of the summer … And how many would we have lost in that 8 to 12 weeks?”

But there were three other options.

The first was to do nothing.

“That would have been an interesting, kind of cold-blooded evolutionary biology exercise,” he said. “The one’s that survived obviously would have been resistant, but at what cost?”

They could have waited to administer the vaccine until the normal fall roundup, then several months away.

Instead of these routes, they chose to conduct an emergency spring roundup and vaccinate the animals as soon as possible. To do so was to risk exacerbating the illness by putting more stress on the animals, but Hamilton felt that the risk was worth taking.

And to all appearances it seems to have worked. Though the Preserve lost around 5 percent of the herd, not on animal has succumbed since the vaccine was administered in May. But how M. bovis got into the Tallgrass herd in the first place is still an open question. The infection is though to be spread by nose-to-nose contact and through water or feed; it’s not airborne and there’s no evidence that the strain which infect cattle also infect bison.

“We have no idea how we got it in our herd,” Hamilton said. “We have not brought in any outside animals since 2002.”

Hamilton is cautiously optimistic about the future; he knows that M. bovis could always seize the upper hand again.

“Don’t give yourself too much of a hug yet. You’re dealing with a living organism,” He said. “This is evolutionary biology in front of us … [M. bovis’] lifespans are so short, their world is changing as we speak.”