Welcome. We're going to continue talking about mastitis, and today we're going to talk about swine - so mastitis and swine, and we have an expert with us today. And this is Dr. Corinne Bromfield, who is our University of Illinois AACUP vet. And Corinne, can you briefly explain what that means? I would love to. So, the AACUP here at the University is the Agricultural Animal Care and Use Program. And basically, we are the veterinarians that cover our animals on agricultural research and teaching. OK. So, any animal here on campus that's an ag-animal, that is used in research or teaching, in any way, I'm gonna provide their vet care. OK. Excellent. Thank you. And we're glad to have you here talking about swine, and she is a swine expert, and that's one of the many reasons we have her here, to share some time with us. First thing we want to do, though, is to remind you a little bit about kind of some of the anatomical differences. Remember, in most of our mastitis module, we talked about dairy cows. And so here we're shifting to another species, I just want to kind of set things up by reminding you a few things. So let's go to the first slide, and just to remind you that - in the sow, this is the underline of a sow - and just again, with each one of these glands, there are actually two glands: anterior, posterior. And each one of those has its own opening, its own lactiferous sinus, its own streak canal coming out, and that can, to some degree, play into mastitis as we talk about that a little bit. Let's go to the next slide and again remind you some of the other anatomical differences and really important differences between the species. In the cow, the cow mammary gland is a cross-section of cow mammary gland, and I've colored in yellow down here the cisterns, the teat cistern here, the gland cistern, and then the cisternal ducts, the very large ducts that go up into the gland, and those are areas of collecting milk. They're not secreting milk, they're not synthesizing milk, that's up here in the alveolar part. As opposed to the pig which does not have that kind of collecting system, they have a lactiferous sinus, but it really doesn't hold very much milk. So most of the milk in that animal is here, and this is again going to play into the difference in terms of how we think about mastitis in dairy cows versus swine. So Corrine, can you kind of talk very briefly about what difference that makes. Well, so very briefly, it plays into our treatment because in a cow, we can do some intramammary treatment and actually put the treatment directly into those cisterns. Intramammary infusion directly up into the gland. In a sow, we don't really have that option, because not only do we have two different teat orifices, but we really have no place where the intramammary treatment would sit and would stay. But additionally it also changes the course of disease. So with our cows, we're collecting milk and we're holding milk within the utter. With the sow, it's pretty much as soon as she makes it, she's going to be releasing it, and the piglets are going to take it away. They nurse every 50 minutes roughly on average. Yeah give or take. So as the milk is being produced, it is being withdrawn. So it changes a little bit how the disease actually affects the sow. Let's go to our next slide. So again, this just kind of leads us into, falling off on that, how do we think about this in these different animals. For example, how do we detect in the cow, strip cup, California mastitis test, somatic cell count. Again, we talked about this in some of the other videos, in terms of how we do that. In the case of the pig- how do you know? Well, so in the case of the cow I'm sure you've talked about, you're looking at abnormal milk in a lot of cases. So that's why you're using your strip cups. For flakes or clots? Correct. In the sow, we don't really look at the milk ourselves, because we're not collecting the milk for anything. The milk is being produced for the piglets. And so what we see, classically when we have a problem, is we see thin and hungry piglets. So piglets that are constantly after mom, constantly trying to get her to lay down, and they just look like they have no milk, they aren't growing off of anything, because mom isn't producing milk. And then how does that feed into again with the types of animals the types of sows that we have in this country, in the United States and in Europe. There are the European based breeds. And they have a very strong teat order, in other words, this piglet going to nurse off of a particular teat and that's it. It's not going to be moving around. So that gets back to kind of, how do you identify, could you say, identify what the problem is and so on. Absolutely so like you said, piglets are very territorial. And once they've decided that this one is their teat, that's going to be their teat the whole time. So if mom, if the dam has enough teats that each of the piglets can get their own teat, then it's going to be reasonably easy to see if she has an issue in one or two of the ducts, because those one or two piglets are probably going to have problems. If she doesn't have enough teats that each pig can have their own teat, then there's going to be a little more fighting. But additionally, when the piglets have a teat that they've chosen, when this is their teat perhaps, and it's not producing milk, they're going to start fighting with the other piglets, and they're going to start looking for ways to get milk. Because a hungry piglet isn't going to sit down and say, oh well, I have no milk. He's going to go looking for it. Right. So Corrine, I'm an old guy, in the old days we used to think about something call MMA, mastitis-metritis-agalactia. And, I know that's kind of changed a little bit. Can you talk a little about how people have changed the way they think about that set of diseases? Oh sure. So MMA, classically was like you said mastitis-metritis-agalactia syndrome. And it was a group of combined syndromes that we typically see in sows, post farrowing. So when we see these combined syndromes we see mastitis-so an inflammation of the mammary gland. We see, we can sometimes see metritis, following farrowing, metritis being an inflammation of the lining of the uterus. And then agalactia, and agalactia would be a lack of milk production. So classically, we called these this one syndrome, this MMA syndrome. We talked about it all together because we thought we were seeing all these cases all together. But lately we're finding that that's not really the case. So before we were seeing mastitis, metritis, and agalactia. And when we see these three together that's MMA. Right. But right now, mastitis and agalactia, we can see why those go together. So mastitis is our inflammation, if we've got a bacteria or a pathogen that's causing a problem that's giving us inflammation, it very easily shows us that she's going to stop producing milk. Now the metritis, we're really not seeing necessarily in conjunction with these two. And so we're starting to refer to this syndrome as postpartum dysgalactia syndrome, so that's dysgalactia, and that's an incorrect way of producing milk perhaps. So it's not gone, like we see in agalactia, but it's not correct. It's not right. And so by not right, typically we're talking about, she's not producing enough. Right. OK. So this postpartum dysgalactia syndrome, there's some different information out there. We're not certain whether it's that the sow's body doesn't quite kick into producing milk the way that she's expected to for her piglets, or if it's, she's starting to produce milk, but she's got maybe a subclinical infection, and with a subclinical infection we see a down regulation perhaps, of producing milk. And again when we see a down regulation or we see less milk, we're going to see thin and hungry piglets. It's interesting that part of this goes back, there's some some old studies done, old study done actually here at University of Illinois, where they recognized that, and they were using coliform toxin, endotoxin and LPS, very very early in lactation, like day two, there was a very fairly narrow window of time in which that actually suppressed prolactin secretion. There seem to be fairly specific at that particular point, and that doesn't necessarily translate to other species apparently. So, something fairly particular about pig. And remember that peripartum prolactin surge is what's driving lactogenesis. And so if you inhibit that at exactly the right time, you may be ending up with, again, a little bit less milk production than you might expect if the animal had not had it. And so, whether that endotoxin is coming from coliform mastitis or from an infection in the uterus, again, this all feeds back into this idea of how this used to be the way people thought about things. But as Corrine says, it's starting to kind of come apart a little bit in thinking about things in a different way. Thank you. That was there was very good. You're welcome.
