Preventing Dairy Cow Ketosis: Transition Cow Management

- Well, it's a little bit after 11, so we will start today's webinar, and today we are gonna actually talk again about preventing cow ketosis.

This time, we are gonna focus more on the transition cow management, not so much on the nutrition.

Before we start and I introduce our speaker, just general things, you know that this webinar is recorded, and will be posted on Penn State website, and I'll be sending the links with recordings to the participants.

Attendees are encouraged to ask questions, and please tie them into the Q&A box, and the questions would be answered either during, you know, the talk, depends on Dr. Van Saun, or after.

And after the webinar, again, you will see a survey will pop up on your screen, so if you can take a little bit time, maybe five minutes, and complete it, we would definitely appreciate it.

So now to our speaker, I would like to introduce Dr. Van Saun, who is a Professor and Extension Veterinarian at the Department of Veterinary and Biomedical Sciences at Penn State University.

He has been in that position actually for last, what?

24 years or so.

He earned his DVM degree at Michigan State, and PhD at Cornell University.

His interest includes transition cow metabolism, metabolic diseases, and their prevention.

And Dr. Van Saun actually was a speaker during our webinar last week, and he will be speaker for additional two webinars on February 13, when we are gonna talk about hypocalcemia control, and February 20 about subacute ruminal acidosis.

So Dr. Van Saun, I will stop sharing, and please go ahead.

- All right, thank you, Michael, and welcome everyone.

I would say good morning, or good afternoon, or good day, or good evening, last time we had people from eight different countries, spanning all time zones, so welcome.

We're gonna get into the second part of our topic on "Preventing Dairy Cow Ketosis", and as Michael said, focus on the transition management side of things.

Michael gave you a little bit of background, I was in private veterinary practice in a large dairy practice in northern New York state, and then also in Michigan for a bit, and then I served as a ambulatory clinician or rural vet service clinician at Michigan State University, and at Oregon State University, and through my clinical activities, especially when I first got out into practice, I recognized how critical two disciplines were to the success or failure of my clientele, and that was obviously reproduction and nutrition.

Now they do teach us a fair amount of reproduction in veterinary school, but not near the intensity of nutrition that we would need to be out in the field, and helping manage and evaluate nutritional programs, and so that's where I picked up my graduate education, working at Cornell University, at the Department of Animal Science, and then took that out back to the field, and with all of that, have, you know, done some international consulting in many areas in Europe, and speak around the country and internationally on these kind of topics to try and share perspective, and as an extension veterinarian, what we do is basically take the research, and translate it into practical application.

And so that's what I wanna try and do today.

What I wanna get across in this seminar is focus on these non-nutritional factors of ketosis, and at least highlight other issues besides just blaming the nutritionist for problems.

I'm gonna then narrow down into the newest research that seems to be coming to the forefront in the role of inflammation, this inflammatory process in the disease ketosis.

And then we'll back up a little bit, and see how feeding management practices, cow facility management can maybe increase the inflammatory process, or augment this issue, and bring about the problems that we see.

And then we'll finish up with some summary recommendations.

So, you know, the question here is, can the cow's environment be responsible for ketosis?

And hopefully at the end of this, you'll be able to answer yes and explain why.

Let me take a moment, and just for those of you who weren't on the seminar last Thursday, just give you a quick summary.

We talked about and defined the disease ketosis, and you can see here, I got it, it's a metabolic disease, essentially glucose deficiency, the glucose is a key player, but the glucose deficiency has to be coupled with excess fat mobilization.

And we showed that not all elevated ketones alone are problematic.

And you know, that's one of the challenges in many communications with a number of my colleagues at various universities, we've all recognized that some cows can have elevated ketones, and not be missing a beat, right?

So we do though characterize this disease ketosis by basically elevated ketones, whether we're measuring them in urine, or in milk, or in blood, but I think one thing that we don't always, you know, we have access to this, unless we use lab is looking at the nonesterified fatty acid concentrations, or the parameter that we use to measure fat mobilization.

Now what we tried to focus on in the last webinar is factors that reduce intake by the cow around the time of calving, both prepartum and postpartum, in combination with some other risk factors, one being heavier body condition score.

This leads to greater risk of ketosis.

And so that was the main nutritional nuances here.

And so we focused on the amount of dietary fiber in the prepartum diet, how that can either positively or negatively impact intake, we talked about energy content of the diet, and the far off dry cow, if you feed excess energy in the far-off period, that's the first month after dry off, that had a much greater negative effect according to the research on cow performance than by feeding a steam up ration, or heavy starch close-up ration.

And then we also looked at some of my work on protein side, and recognized that cows do mobilize protein to help support their glucose needs, and if those cows that mobilize too much protein, that sets them up for some metabolic challenges that can contribute to the ketosis.

And in other things, other disease conditions, and we highlighted, especially hypocalcemia, which will be the topic of our next webinar, all contribute to the potential for reducing this intake.

And then nutritional management, as I kind of finished up in that webinar is not, you know, it is basically only one aspect of ketosis prevention.

We need to think about how nutrition goes in the full package here.

So let's come back and look at non-nutritional factors, and where we're coming from.

This was an interesting diagram that was actually published in Washington State University Extension Bulletin, and it was adapted from two published papers of path -- Or three published papers on path analysis that came out of the Cornell group, you can see in the 1980s, mid-80s and 90s.

And what they showed was the factors or cows, and they focused on the close-up pen, these different factors, and how all these arrows here sort of talk or are associations that, you know, mastitis can be associated with, age and vaccination status and so on.

And you can see, you know, this, the postpartum disease problems that we see in our dairy cows are not isolated diseases, but they're really a collection, you know, I'd almost call it a postpartum syndrome.

Now what's intriguing here is if I highlight some of these factors, you can see age, so cow factors are important, we know that older animals, younger animals have different issues relative to difficulty of birth and risk of mastitis, and certainly, risk for milk fever, then look at the management factors, how we manage the calving or maternity pen, how we manage body condition score, stocking density of our pens, use of vaccines, and use of dry cow treatments, these are all under management's control.

And you can see these account for the majority of the pen, the close-up pen factors that contribute to risk of all of these diseases.

And then we have an environmental one here too, just the season that the cow is dry can influence some of these, and you can see the last two things are the things that we focused on last time, the ration itself, and dry matter intake, but the point here is, these are only a small portion of all the different things that could lead to the problems of transition cows.

So if we only focus on nutrition, we're gonna miss a lot of potential problems.

Now, the other thing I wanna focus on is this role of the immune response.

Now, we often get confused, we know what the immune response is, we know that's a protective system, but we also know that the immune response is sensitive to inflammatory signaling, and that's where this role of inflammation has become a centralized focus.

And there's good reason for that relative to ketosis, because as we're gonna discuss, the cells responsible for the immune response, the white blood cells, the various types of white blood cells that do the signaling or the effector cells, they all preferentially metabolize glucose.

And so glucose becomes the central theme.

We need glucose to make milk, and we know if we lose too much glucose through milk, through high milk production, and the ability to replace that missing glucose gets compromised, then we get into this ketotic period.

So what I've done is, those of you who've had some, you know, disease-associated education, you may have heard of the epidemiologic triad of infectious disease, or just called the disease triad, and I think those same principles can be applied to what I call the triad of transition.

And what this means is we need to think about how the environment, how cow management, and the nutrition all interplay, and how the cow sees these three things relative to her success, or failure through the transition period.

And so last time we focused on the nutritional factors, like dry matter intake, and calcium homeostasis, and energy density, and metabolizable protein adequacy, and then just nutrient balance in general, micronutrient status, antioxidant, and availability of water.

Now we're gonna kind of talk about some of these other factors, you know, we highlighted that body condition is certainly an important risk factor, heavy body condition, but the hygiene of the cow, grouping strategies, pen moves, feeding management, feed bunk management there, and how we evaluate the animals in the postpartum period to try and recognize those in need, and then the environmental factors.

How much feed bunk space are we providing, are the cows in a clean, comfortable stall?

How much social disruption is occurring?

Heat abatement issues for heat stress, overcrowding, and then just pathogen exposure from, you know, not managing our bedding.

And so these are the things that also can contribute to the challenges that the cow faces, and end up causing some of these milk or ketosis problems.

So this graphic that I'm showing you here is, again, a graphic that we generated from two different feeding trials, I see my line shifted on you, and what it's looking at is dry matter intake during the prepartum period, and then dry matter intake in the first five weeks postpartum, and what we did, these were two controlled feeding trials we performed at Penn State University in the early 2000s, these were studies looking at monensin feeding, and starch level and so on in the prepartum diet, on postpartum performance, but we retrospectively went back and looked at cow performance, and did some measurements, and so the blue line here were cows that we wanna have on our farm, they went through the transition period totally unscathed, though they just, you know, ate their way through, calved, didn't have any postpartum problems, and went on, and made good amounts of milk.

The red line represents those cows that had one disease event.

Now this could have been lameness, this could have been retained fetal membranes, it could have been ketosis, it could have been mastitis, you know, we didn't characterize all of this could have been displaced abomasum or milk fever, and then the black line is two or more events.

And what we see here is what we highlighted last time is cows that go on to have disease, 'cause the disease occurs in the postpartum period here, but something is going on prepartum that sets those animals up for their postpartum disease.

And then we see the very significant negative effect on dry matter intake for animals that have disease.

And that's what a lot of the immunologists are focusing on is the things that we measure, like beta hydroxybutyrate, and non-esterified fatty acids.

The research tells us those things really don't have this kind of negative effect on dry matter intake.

But pro-inflammatory mediators, when the immune cells respond to some process, things like interleukin-1, tumor necrosis factor alpha, they have very negative effects on dry matter intake.

That seems counterintuitive, you would think, with a disease process, because we know animals go into a state of hypermetabolism, but this seems to be a key linchpin to this whole process.

What I'm showing you here is just the number of papers, just a smattering of papers, this is out of the Guelph Group down here, what they found was cows that go on to have subclinical ketosis have longer lying bouts in the prepartum period, and they suggest that standing lying behavior might be a useful monitoring tool, this is a summary paper from the University of British Columbia Group, Dan Weary and Nina Von Keyserlingk, where they looked at feeding behavior, they identified feeding behavior, this kind of drop in dry matter intake being associated with cows that go on to have metritis, and cows that go on to have ketosis.

This paper here again out of Guelph is looking at rumination time or chewing, chewing behaviors, changes in feeding patterns, and then this one again suggests that prepartal standing behavior, more standing around, not eating and so on, is also another key player, and liver function biomarkers here with inflammation.

So this is really starting to tie these things together for us.

Here's another paper, where you can see, they have healthy cows in the white bars, and then metritis, subclinical ketosis, metritis plus subclinical ketosis, and multiple diseases, and so they recognized here that when cows feel sick, they're less able to compete successfully for access to the feed bunk, so that's an important aspect, and then they use higher feeding rates when they have access.

So depending on your starch content, your fiber content, that could end up maybe causing some, you know, leaky gut syndrome from inflammation, and so on, because of high starch, and some acidosis, right?

So, you know, we have these coping mechanisms that try to allow these animals to maintain their dry matter intake, but it may have other effects there.

All right, so transition cow problems.

Speaking to the group at the University of Wisconsin Veterinary School that go out and do quite a bit of farm investigations, Dr. Ken Nordlund, who's now retired, he was kind of head of this, Gary Etzel and others were involved, what they presented was they felt that nutrition was only about 15, maybe 20% of the problem situations, and what they focused on, and what they found in their experience, the major causes of transition cow problems were things that impeded normal cow behaviors, excessive stocking density, and too many pen moves.

All of these are stressors that are gonna stimulate an inflammatory response, and then that starts us down this pathway.

So what do we see in transition cows experiencing these stressors?

This is, you know, just normal mechanisms that we can identify, we see decreased dry manner intake, and decreased milk production, we see increased body fat mobilization, and wasting of muscle tissue, so that's the protein mobilization, and what happens is the body through processes of what we call homeorhesis, direct nutrients to important functions.

So they divert nutrients away from milk production to this stress response into the immune system to try and maintain normality, or fight off the challenge.

And so a number of studies, and body, or there's groups of researchers at various universities that have started to really look at these pro-inflammatory cytokines, as I mentioned, Tumor Necrosis Factor Alpha, interleukin-1, beta-interleukin-6, and the stress hormones such as glucocorticoids, epinephrine, cortisol, as potential markers and indicators of this role of inflammation.

So I see a question here, what tests and things should we measure pre-calving, such that we can preempt these problems?

That's a great question, a number of us have looked at these things, we do know elevation of nonesterified fatty acids in the prepartum period seems to be one of the more important ones, but many of the other parameters that we've looked at, I've looked at albumin, we've looked at cholesterol, there are other parameters that people -- Bilirubin, total proteins, things like that, but nothing has really jumped out, especially relative to when we would really need it, which is in the far-off dry period, so we had enough time to intervene and head off the problem.

I'm more excited about the possibility of looking at and developing commercially available pro-inflammatory cytokine measures, I mean, right now, we can do these in the labs, but these are not things that are readily available out on the market that we could do either on the farm, like we can do BHB, or glucose, or something like that.

So unfortunately the answer to your question is we really don't have a parameter, things that I've been looking at on top of this as more a collective, what I'll call metabolic profile, and it takes us back to the 1970s, and Jack Paine from the Compton, England, I think there is some value to looking at a combination of metabolites too, because the issue is not one thing goes wrong, but it's a collection of things that go wrong.

So if we come back to this issue here of decreasing dry matter intake around the time of calving, this leads to the negative energy balance, negative protein balance, increasing nonesterified fatty acids, this can lead to immune alteration, we're focusing on the potential for ketosis here, and we can see the diseases like displaced abomasum, hypocalcemia, ketosis itself, lameness, all contribute to lower dry matter intake.

But these diseases happen in the postpartum period for the most part, and not in the prepartum period, so they don't explain this well-established decline in dry matter intake prior to calving.

And that's where environmental, pathologic stressors stimulate pro-inflammatory mediators, and these then are the key players to decreasing dry matter intake around this time of calving.

We also know based on work in humans, if you are diabetic, one of the challenges with diabetes is there are pro-inflammatory mediators made or synthesized in fat tissue, there's macrophages within fat tissue, and mobilization of the body fat, as well as just a low level signaling seems to have some effects on dry matter intake.

So I think the work that's coming out of Dr. Baumgart's lab at Iowa State University, where they said it's this pro-inflammatory process that initiates some of the issues that bring us into this, I'm not ready to jump full two feet in to say this is the only way it happens, but this is certainly makes a strong statement relative to recognizing this drop in dry matter intake.

So let's now focus on this role of inflammation, and you know, what is inflammation, and how does it potentially contribute to ketosis?

So this is some work by one of my colleagues, where it's following up on some work that was done or initiated, initially described around 2008 from Italy, Dr. Bertone, Giuseppe Bertone's group, where they gave injections of an aspirin-like compound, a nonsteroidal anti-inflammatory compound, and they saw greater milk production in those cows that received the anti-inflammatory compound.

And this is looking at a similar study, like I said, my colleague here, Dr. Barragan, where they looked at cows that received aspirin boluses versus controlled cows, and they looked at beta hydroxybutyrate concentration as a marker of deranged metabolism, and you can see that overall, there was a reduction in BHB, and then we could see even at seven and 14 days, there was a decline in the aspirin-treated cows versus the non-treated control cows.

And so, you know, why is this, why would it just taking an aspirin, and we see there, there's many environmental social management factors that can contribute to this inflammatory response.

Some of these that I see commonly is overcrowding of transition pens.

We can't or we don't build our transition systems to accommodate the big flux, you know, ideally, cows in a farm, in a perfect world, you would have the same number of cows calving per week or per month throughout the year.

But we all know that never happens, or we don't even come close, and we have slugs of cows, and that's usually when we get into the problem is we decrease the social space per cow, decrease the feed bunk space for the cow, accessibility to the feed bunk, even though we're delivering all the appropriate amounts of feed and so on, these things take a social stress toll, right?

Social upheaval, right?

We see this where we mix younger cows with older cows, or if we have pen changes, you know, we kind of shot ourself in the foot, so to speak, trying to overthink this whole process, where, you know, we wanted to better feed to the nutrient requirements of the cows, and so we had far off dry cow groups, and close-up dry cow groups, and a maternity group, and then an immediate colostrum group, and in a post-colostrum group, and then a fresh cow group, and high group, and so on and so forth, and every time we move these cows, cows are social creatures, they have to reestablish their hierarchy, who's the boss cow, and who's the, you know, the lower level cows.

Then of course, with climate change, and all these other things, we're seeing much more heat stress issues, and then feed availability bunk space.

So these are all things that I wanna try and focus on here to try and indicate other than nutrition, we can have this.

Now this is from one of the labs that's doing quite a bit of work in this inflammatory process, Dr. Barry Bradford, started a lot of this work when it was at Kansas State University, he is now at Michigan State University, this is a great paper if you have access, well, Journal Dairy Science is an open access journal now, so I would strongly encourage any of you to get a hold of this paper, and you can see what's going on is, you know, the flame here is indicating this inflammatory process that's taking place, and you can see social stressors, releasing catecholamines can contribute to this, heat stress, through heat stress, or heat stress proteins, uterine involution, metritis, these are all gonna have inflammatory mediators, these cytokines, eicosanoids, mastitis, any real infectious disease is gonna contribute to this, the leaky gut that the Iowa State Group is talking about, if we get a drop in pH in the colon, the colon isn't as protected as the rumen from acidosis, and so we can have bacteria die off, release of endotoxin, which is this LPS, and then that can contribute and be absorbed and contribute.

And then just normal oxidative stress, the ongoing metabolism of cells of the cow's body, the cow, remember, she's constantly perceived as the race car, the Formula 1 race car compared to a beef cow, and so that race car mentality requires high levels of metabolism, and during metabolism, we generate, everybody generates reactive oxygen species, and these can also contribute to inflammation.

And so what Dr. Bradford and his group have proposed in this concept here is measures of systemic inflammation, and again, this will depend on factors that we can measure, and that's what I'm thinking might be our next opportunity for investigation, but all cows will go through some inflammatory process in the calving period, and if those cows have the right antioxidants, which is another area of interest, so this would be our trace minerals, our fat-soluble vitamins like vitamin A, D, and E, we have this big surge right after parturition, but if the systems are in place, we can rapidly resolve that inflammatory response, keep it under control, and this results in normal metabolic adaptation to high milk production, reproduction, and that's exactly what we want out of our cows.

However, if there's a slowed resolution to this, the inflammatory signaling goes on for a longer period of time, then the consequences of having prolonged inflammation take up some of these essential nutrients, leading to negative energy balance, the risk, the greater risk of metabolic disease, like ketosis that's so dependent on the glucose, infertility problems, because the reproductive system is signaling or reading the signals from the body, and if you don't have enough nutrients, you don't wanna get pregnant, because that fetus becomes, I hate to say, a parasite within the animal, because it's taking nutrients away from that animal.

And so what they suggest is, you know, things that we might see is, you have a single acute insole, all right?

So let's say you had an immediate, severe heat stress, heat change, you're gonna have this cytokine storm, and we've heard about cytokine storms and the negative consequences of those, as we endured the pandemic, this COVID-19, they talked a lot about some of the real negative highly associated with death scenarios were due to cytokine storms.

But if our system is intact, we can resolve these cytokine signals with anti-inflammatory cytokines, anti-inflammatory eicosanoids, so part of this is coming from some of the nutrition, and then we can maintain, and recover homeostasis of the system.

Another thing is more a chronic subacute signaling.

And, you know, if we just get, you know, a single kind of process, the anti-inflammatory process can sort of keep this to a dull roar, and ultimately, maintain this, so it can outlast this signaling.

Where we get into problems is this kind of thing is where you get repeated insults, and these could even be very mild insults, but one after the other, after another, after another, and it starts to get this buildup, and buildup, and ultimately, the body just can't keep this under control.

And so this is really, you know, the take home point here in this inflammatory process is one, know that inflammation has a negative, can have a negative effect, but the more we add stress factors, the overcrowding, poor environment, think about the pathogen load that's going on, and how much potential mastitis, or metritis, you know, when you have cows in this kind of situation, this collectively then becomes the ketotic or the sick cow.

Now why is this immune response such a challenge?

Well, the immune response, you know, what we see is if we compromise this immune response through lack of nutrient availability, we see a decline in the respiratory burst in the phagocytes, so they're not able to kill off the bacteria, killing, you know, decreased killing activity, decreased phagocytosis by the neutrophils, we see a decrease in the signaling to bring more support, reinforcements in, we see a decrease in the ability of the cells to replicate, and maintain the immune response, and we see a decline in the the antibody production.

So these are all things that we start to see this initially with the upregulation and loss of nutrient ballots.

And so again, the Bauman lab, or Baumgart lab, excuse me, at Iowa State University, they looked into this, and asked the question, "How much glucose does it take to support the immune response", right?

So, we again, if we think about this, glucose is the predominant or preferred nutrient to support the developing fetus, mom is dependent upon dietary factors to maintain her glucose, 'cause she has to have some starch in her diet, or other factors that can, or other sources that can provide propionate, through the fermentation system for gluconeogenesis, otherwise, she has to go to amino acids, and we don't want that to happen very long.

But as I mentioned, the immune cells, all the immune cells, the lymphocytes, the neutrophils, all the phagocytic cells, the macrophages, predominantly use glucose, or exclusively use glucose to support their activities.

And so they did a study where they artificially elevated the immune response through a pro-inflammatory injection of a lipopolysaccharide and they then delivered glucose intravenously, and monitored glucose balance, and then calculated how much glucose it took to maintain a normal blood glucose concentration.

And they basically used 1,092 grams of glucose in 12 hours.

That's equivalent to, if this inflammatory process went on, for a full day, that's 2,184 grams of glucose in 24 hours.

That's essentially burning through a five-pound-bag of sugar.

Think about that.

One day, eating a five-pound-bag of sugar.

On an energy basis, this is equivalent to 8.7 Megacals per day.

So that's adding, you know, if you think about the energy requirement, just the maintenance energy requirement, this is getting close to 60% increase, and then this would be equivalent to 30 kilograms of milk being lost, because it takes about 72 grams of glucose to generate one kilogram of milk.

You really have to sit and think about this a little bit and take that in, and if you are following and understanding what I'm saying just by activating that immune response, and that's a survival mechanism, we're diverting all this glucose to keep that going.

Now it doesn't always happen in a black and white kind of way, and what we see is in some cases, depending on the level of inflammatory process, you know, we're not gonna burn through all that sugar, and that some will be available, but this is the bottom line.

If we don't have that glucose, we can't make it, then that leads us into the fat mobilization, and then that sets us up for the ketosis disease process that we described.

Now here's some other research that basically reinforces this concept.

Here are these three graphics, the more solid line here, it doesn't look like it up here, this is the healthy cows, and then this dashed line is from cows that were ketotic, and we're looking at LPS, lipopolysaccharide, a pro-inflammatory compound, and then the binding protein, days relative to calving, this would be in the prepartum period, and then right around the time of calving.

And what we see is an increase in circulating inflammatory markers in pre- and postpartum ketotic cows.

So something is going on to upregulate or increase this.

Now in this case, the source of the inflammation that started this wasn't identified, they hypothesized that it could be part of the leaky gut based on the type of diet that they were feeding, and again, as I said earlier, they showed that pro-inflammatory mediators are very potent suppressors of intake, and the activation of the inflammatory response is nutritionally costly, consuming both glucose and amino acids.

Okay.

So now let's get into some of these other aspects, so how, you know, beyond diet composition, how could feeding management affect or contribute to ketosis.

Well, I think the first thing we need to do, one, let's recognize we really don't have a lot of research that has monitored cows, and manipulated diets through the calving period.

This is one of the few studies, this was presented at the Cornell Nutrition Conference a number of years ago, and there was a similar study done at Guelph University when I did my -- Or not Guelph, excuse me, that was Minor Institute, I did my work and followed cows like this for my PhD work at Cornell.

But this is an interesting study, here again, we're using dry matter intake, this is the prepartum period, we see that drop, that physiologic drop in dry matter intake, and then this is the different dietary treatments in the postpartum period.

Now the red line that I highlighted here is a high starch, high fiber diet, all right?

And so that gives us a good response, you know, a preferred response, essentially, of maintaining higher intakes postpartum.

This line here, the triangles is a high starch, low fiber diet, so we see a very negative effect, most likely due to the high starch, low fiber, where we're gonna have more potential acidosis, maybe hind gut acidosis, and leaky gut syndrome, or just increase in inflammatory mediators.

But then you can see low starch, high fiber, these gray circles, or low starch, low fiber, a similar kind of intermediate response.

So if we are gonna feed a higher starch diet, we really have to maintain the adequate effect of fiber, and so that's our newest area of interest is, you know, how much fiber and what kind of starch levels should we be talking about in this transition going from our close-up pens, maternity pens, into the fresh cow pen, or the high production pen.

Now this study here kind of reinforced just what I described there, here, this is looking at Rumen pH, and the time below a pH Rumen pH of 5.8, so this would be our classic SARA, and this is for diets where they were fed a lower starch, which is a 21% starch with a 37% neutral detergent fiber, and then a high-starch-diet, which was 27% starch, and 32% neutral detergent fiber.

So that neutral detergent fiber really is within what typical would be seen typically would be seen for our high-producing animals.

And you can see right away, days in milk over the first, you know, 21 days, a much lower Rumen pH, and the time here, this is in minutes per 24 hours, much greater time where we see the pH below 5.8.

So essentially setting these cows up with SARA, and this certainly could be a contributor to part of this inflammatory process.

Now another thing and work by Nigel Cook at Wisconsin, and Rick Grant, when he was at Minor Institute, basically said, "Cows are no different than us." How many of us out there would want more than 24 hours in a day to try and get everything done?

I know I got a number of classes I'm teaching, and exams that I gotta grade on top of writing some papers, and giving these talks and things like that, I could use a lot more hours in the day, but that just isn't in the cards.

And the same thing with the cows.

And if we expect a cow to eat 25, 30 kilograms of dry matter, she's gotta spend some time doing that.

But what we do know is cows ideally should spend about half of their day resting, taking the weight off their feet, and ruminating, ruminating to generate the saliva, and the bicarb, and so on, and so this is sort of for the generic cow, about 13 hours or 54% of her time should be resting her feet ruminating, sleeping, five hours of her time, which seems kind of short for the amount that they eat, eating, and then about three hours, depending on your system, whether you're 2X, 3X, and how you do it associated with milking time, social time, you know, cows do, our social critters then they, they're gonna work or interact, and then drinking is a small amount, even though they're consuming many gallons of water.

And so what we need to think about is in our facilities, can these cows achieve, can all the cows in a pen achieve these opportunities for expressing their behaviors.

And so we need to think about bunk design relative to space per cow, you know, this is where the six row barns are challenged on bunk space, feed availability, where we leave the bunk empty for too long, feed accessibility, here's an example, a post and rail system, which seems to be a fairly popular system in our transition diets, thinking that things are wide open, but in this particular farm, if you notice, the cows sort of have to come in sideways, 'cause this bar is too low, and you also notice that a lot of food gets pushed up, so if they don't do a good job at pushing up, we got a situation, where the cows really don't have good access to their feed.

And then down here, this is looking at the percent of cows feeding, using a headlock system, and a post and rail system, you generally see a post and rail system if they got enough space, it's gonna be a little bit better, but really there's not, other than this point right here, there's not a huge difference between headlocks and post and rails.

And some of the work out of the University of British Columbia would suggest some kind of barriers here to prevent antagonistic interactions between cows at the feed bunk in transition pens might be preferred.

So in terms of feed bunk space and feed bunk design, ideally for our larger-framed animals, our Holsteins, the sementales, for those of you over in Europe, we want it to be 48 inches or 129 centimeters from the platform that the cow stands on to the bottom of the rail, and then we want the retention barrier here to prevent cows from stepping over and putting their feet into the feed to be about 21 inches, or about 53 to 54 centimeters, and then ideally, the feed platform should be about three to six inches or seven and a half to 15 centimeters above where the cow's feed are, and that places them in what we consider the ideal grazing position.

Here's a couple of examples of bad situations, these are from some Czech farms I visited, again, we can you, you look at this post and rail, you look at the indentations on the withers area here on many of these cows, some of these cows have calluses here from rubbing, if you feel this bar, the back part and underside of this bar is polished smooth, in this particular farm you can see, it doesn't have high walls, ventilation is somewhat compromised, but when I measured this, and explained to the owner of the farm the situation, they came in right away, increased the bar height, and I've revisited this farm the following year, and they said "The milk production in this fresh cow pen just was another 10 kilos more in milk production in this pen." They were just flabbergasted at the response of the cows.

Another example here, similar kind of scenario, where we see these lesions on the nuchal ligament just in front of the withers here, and this bar's gonna be really polished, this bar was, I think, below 100 centimeters or so.

All right, what about the other facilities?

That's sort of the feeding, getting the feed, and having feed available, how does animal management and the associated facilities impact ketosis?

So some of the stressors that we might have with management facility is, can't emphasize enough, the overcrowding, or increased what we call stocking density, co-mingling of cows and heifers, depending on when that occurs, excessive pen moves, or group changes, heat stress, so if we don't have heat abatement, overall cow comfort, and cow hygiene, and then the dietary changes of starch and fiber that the cows are exposed to, and we kind of highlighted that a little bit already.

This is from the paper in Vet Clinics in North America, from Cook and Norlund from the University of Wisconsin, when they first came out with, you know, sort of this idea of these pen moves, and the number of pen moves that occur, you know, if you look at this traditional one, you have one, two, three, four, five different pen moves, in a fairly, you know, one-month-period or so, month and a half at most, and so they had some recommendations of at least dropping the number of pen moves, and then this also will be tied in with putting heifers and cows together in terms of deciding that.

We did some work on a local commercial farm here, just south of the university, and put leg bands, pedometers on the cows, and in this particular farm, they had a far-off and close-up pen, and then essentially a maternity early lactation pen, and what we saw was when cows move from the close-up, or the far-off to the close-up, they had social disruption for about three days, there was a drop in resting behavior, lying time, and so on for some of these cows, and then what was interesting in this farm is the heifers were kept in a single pen, and we saw no change until they went into the early lactation pen, where they were intermixed with mature cows for the first time, and they got hammered in that pen, they lost about three hours of resting time, and really had some challenges in getting up and running.

So again, this is some of that data here, you know, I took the ideal cow behavior, here's the heifers, you can see they maintained their lying times, but then they dropped quite a bit, and then cows, you know, not as big change, but they also dropped moving into this mixed pen, so this fresh cow pen.

Some other work, this was some data that, again, Nigel Cook presented in this paper, primiparous or heifers with multiparous grouped together, this was a large cow facility, two-row type facility, they saw a decline in milk production in the first 83 days, when the stocking density went from 80% to 120% of the stalls, all right?

And then they looked at stocking density in the closeup pen versus milk production, and you can see for every 10% increase in stocking density over 80% there was basically just under our 750 mils or .7 kilograms per day in milk loss.

Some environmental factors, we wanna minimize the cow's stress response by ensuring adequate cow comfort, this means proper stall resting area, sufficient feed bunk, and watering space, multiple waterers, heat abatement with good ventilation, and then clean, dry bedding of sufficient cushion.

So just some pictures of some challenges, this cow obviously doesn't have much lunch space, say with this cow here, you notice how they're starting to move the dividers to make 'em more comfortable, this was a farm in Turkey, where the cows were bending the bars to try and make their stall fit them better.

So transition grouping approaches here, many of us have sort of followed the Goldilocks dietary approach to transition cows to try and control not only milk fever, but some of the postpartum disease, these are those controlled energy diets, we can get away with a single group with them, however, you probably wanna shorten up the dry period to 45, 50 days, there still is some work that suggests a two-group-system, a far off close-up is a very good system, especially for animals that may have a heavier body condition to better manage those, we could also try and separate the heifers out if we have enough facility space and animal numbers, but this becomes problematic with our smaller herds, and then the bigger question is, do we wanna even separate out another group of what we call special needs, and these would be animals that we've identified as having twins, or cows that are too thin, or too fat, having entered into the dry period.

There is some interest now in an all in-all out kind of approach in managing maternity pens or transition pens, in general, and obviously the main advantage of this is the social disruption is minimized, because the cows stay with exactly the same animals, there are same herd mates throughout this whole challenging period.

The bigger problem for adopting this kind of approach is the facility, the amount of facilities that's necessary for the farm, and it greatly increases capital costs in that, but there are some farms that have done this, and been successful.

I think all the work coming out of the University of Florida, the University of Arizona, Dr. Dahl's work down at University of Florida really emphasizes the effects of heat stress on transition cows.

We see a reduction in dry matter intake, we see reductions in milk yield, we see decreased fat and protein content, growth rate reduction in our heifers, decreased reproductive performance, this is embryo loss and so on, and of course, we see the increased incidence of health disorders, especially things, some of the infectious diseases, like ...

Or immune-associated diseases like retained fetal membranes, metritis and lameness.

And so there's been a number of studies that have been published in the last 10, 15 years that have really highlighted this issue of the heat stress, especially in the transition, the dry cow.

So this is some work summarized by Dr. Dahl and colleague down at the University of Florida, where they looked at cooling during the dry period, and the effect on milk production, and you can see across all these different studies, there was a positive effect, you know, highly variable, but a positive effect on milk production by, these are kilograms per day increases from cows that were cooled during the dry period versus those that were not.

All right, so some summary points here, some final thoughts on how we prevent ketosis, so the key points on ketosis, remember, that ketone body production is an essential and normal metabolic adaptation to the initiation of lactation.

And this is conserved through many, many, many different species, from the bacteria, all the way on up.

And so it's to address this period of negative energy balance.

The problem with ketosis is it's not just a loss of glucose homeostasis, and elevated BHB, but there's other contributors that disturb the homeostasis, homeorhesis that's necessary to keep this stabilized through, and the cows come through, and we know cows can do it.

The effects of elevated BHB do not account for the observed clinical signs of ketosis, but they do have a negative effect on immune function.

And then finally, this active inflammation can account for the reduced feed intake, loss of glucose and amino acids to support the immune response, and then this then exacerbates these necessary metabolic adaptations during this transition period that can lead us down this pathway of ketosis.

So some of the things we need to consider from a prevention standpoint, we gotta start with body condition scoring in the lactation period, especially late lactation, and obviously, prevent overconditioning, we wanna minimize the number of fat, the percent of fat animals in a group, and also the thin animals.

Now I have 3.0 body condition score less than that, I know there is some groups out there that suggest a body condition of 2.75 is adequate with dry cows at this point, because they do have higher intake, I'd like to see some more data on that, and be able to support the high levels of milk production that our cows genetically can do before I start suggesting that.

Management should factor, or should focus, excuse me, on minimizing potential stressors through the dry and early lactation period to try and keep this inflammatory process down to a dull roar.

We know it's gonna happen, it's just a natural process, but we don't want it to get augmented over and over again with things like heat stress, so heat abatement, overcrowding, making sure we got adequate feed space, increasing the social interactions that are negative, you know, these might be the number of waters, I recommend at least two watering stations within each group, and the number of regrouping and how much cow space, and then cow comfort, I mean a number of farms that we've been dealing with that have, you know, looked at their transition cow problems and recognized that the challenges that they have have invested in new transition cow facilities with larger stalls and addressing this, this cow comfort, and been pleased with that investment.

So some of the facility recommendations from the work that I've cited, we're generally now recommending about 30 inches or more of feed bunk space in the prefresh and fresh pens, we wanna limit those pen moves, reduce the time in maternity, we wanna stock those prefresh, postfresh pens at about 80 to 85% capacity, especially if you're using a post and rail feeding system.

Maintain good cow comfort in the stalls, this is suggesting that stalls should be wider instead of 48 inches, they should be 51 inches, plan for managing those calving surges, and again, provide that heat abatement strategies, and be ready for those.

So some of the best transition management practices are those farms that set a high priority on feeding and facilities for those transition cows, provide a consistent, properly balanced diet that addresses issues of intake and variability amongst the individuals within a pen, we wanna minimize those excess energy intake, especially in that far-off dry period, ensure adequate or better metabolizable protein intake, and although we recognize that nutrition is an important factor here, the effect of facilities can play a more important factor in the role of postpartum disease risk, we wanna ensure cows are comfortable, can express their normal behaviors, and are free from these induced stressors.

So with that, Mike, I'm ready to answer, I see a few questions coming in.

Appreciate -- - You have two questions -- - The time ... - We have two questions coming in, and the first one ask "If a cow is dried or high body condition score, what can be done?" - Yeah, that's a great question, we get that all the time.

Some of the work that I cited and talked about last time, there is some evidence supplementing high levels of rumen-protected niacin, one of the B vitamins, and rumen-protected choline can help with these cows that are high body condition score, niacin seems to suppress the fat mobilization, and choline helps deliver export fat, so those are two options, another thing I've seen is, I've had good luck providing additional bypass protein sources or metabolizable protein in general on some of these heavier cows, and I think it's probably the role that these amino acids may play in the availability of amino acids for gluconeogenesis to keep that blood glucose level up, also, we know when this inflammatory state starts that I described today, many of these pro-inflammatory cytokines that I've cited are proteins or peptides, and so where do those amino acids come from?

Well, if we look at the blood, we see things like albumin decreases, we see declines in retinal binding protein and transferrin, a lot of what we call constitutive type proteins, and so those then can have some challenges, and I showed last time cows that had high BHBs with high nonesterified fatty acids, the ones that typically showed disease had lower albumin concentrations, and so I think there's an interactive role between energy, lipid mobilization, and protein status, and so I would probably wanna feed a little higher protein to those fat girls there.

- And the last question is, "If you already do good management and practices, would you suggest giving aspirin after every calving to combat inflammation response?" - And the answer to that my colleague has answered recently, and the answer is no.

This is not a practice that should be blanket, matter of fact, I believe in his paper that's either just been published, or about to be published, they saw some very negative effects of giving aspirin to heifers in not having a problem or anything, and also animals that seemingly didn't have some issues, where they recognized metritis or anything like that didn't have as good a response.

So I think we need to target this, similar to the recent work that's come out with calcium boluses, blanket giving calcium boluses has been shown not to be very good.

So we do need to identify these animals, and this comes back to the original question that was asked of me, what tests and things should we do to measure pre-calving, that we can measure pre-calving, that we can preempt these problems, and again, as I answered, we really don't have a good answer at this point, we got some ideas, but it does show that we need to identify these animals that are at-risk, so that we can target them to be appropriately intervened with, but not blanket treat, because it seems to have negative effects.

- Well, thank you.

Very good information.

Thank you, Dr. Van Saun.

- You're welcome. - And we don't have any more questions, so that would conclude our webinar.

Just would like to remind attendees if they can fill the survey that they're gonna see on the screen after the webinar, and I will be sending the notes, present those notes to all participants. - Yeah.

- Thank you very much, and hopefully I will see you in February.

- All right, thanks, Michael. - Thank you.