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Ketosis syndrome in sows

4 comments
It’s true that we have rarely considered the sow as a dairy animal. A sow can produce up to 10 liters of milk at its production peak. If we consider that the effort the sow makes per hour in order to produce milk is almost equal to that of a cow, why do we continue to apply a collective treatment when it comes to feeding the sow?

Dairy sows and their individual treatment


It’s true that we have rarely considered the sow as a dairy animal. A sow can produce up to 10 liters of milk at its production peak. If we consider that the effort the sow makes per hour in order to produce milk is almost equal to that of a cow, why do we continue to apply a collective treatment when it comes to feeding the sow?



The current type of production brings us to treat a group of sows collectively, but in the future we will have to rethink this treatment, especially in maternity. Some intents to do this exist already, above all when working with liquid feed and when the feed curve is adjusted during maternity based on need.

Faced with this situation, three key questions arise: Is it possible for sows to have ketosis syndrome? And if it is, when does it appear? And of course, what is ketosis syndrome?

Is it possible for sows to have ketosis syndrome?
The answer to this question is yes. However, we come upon very few references in scientific literature with respect to this situation. This is basically due to the fact that on the one hand, very little research has been done on the subject, and on the other hand, clinics do not have the resources for diagnoses. Actually, one of the articles that speaks to the appearance of ketosis syndrome was accidental; It was about one of the sows in Atlantic Veterinary College veterinary hospital waiting for a cesarean section to obtain SPF pigs. (Janet E. Alsop, 1994)

If it is possible, when does it appear?
If we follow the logic used with cows or with humans, we would assume that ketosis syndrome appears post-partum. But this is not the case: ketosis syndrome in sows appears pre-partum. It is worth mentioning that we aren’t talking about a certain physiological pre-partum ketosis, but rather a ketosis syndrome that induces anorexia (ketone levels of 4 to 8 mmol/L).

What is ketosis syndrome?


Biochemically it is characterized by ketonemia, ketonuria, hypoglycemia, and a decrease in liver glycogen levels. In cattle this occurs when we have well fed cows with high milk production levels confined to stables and, in situations with specific nutritional deficiencies, in free range cattle.

It is due to an insufficient metabolizable energy (ME) ingestion, caused by poor diet (primary ketosis deficiency) or to an insufficient ME ingestion due to lack of appetite associated with another illness (secondary ketosis deficiency).

When a nutrition deficit exists (low ingestion), the production of milk is reduced basically due to a lack of glycogenic precursors, while later on there is decrease in the glucose levels available for the mammary gland because there is less hepatic glucose synthesis. We cannot forget that the mammary gland requires high quantities of glucose which, at the same time is the precursor to lactose.

However, given that Mother Nature is “wise”, the mammary gland continues to produce milk due to hormonal stimulation and therefore, the use of glucose, which then causes a state of hypoglycemia.

This hypoglycemia tries to compensate by lowering insulin levels, increasing somatropin (ACTH) and glucagon. These changes cause the mobilization of fats and proteins in the organism, in an intent to maintain energy balance and glycemia in normal conditions.
The fats mobilized pass to the plasma in the blood in the form of non-esterified fatty acids (NEFA). The NEFA are trapped by the liver and pass to the β-oxidation instead of being esterified to glycerol to form triacylglycerol (triglycerides).

This high proportion of β–oxidations produces a high quantity of acetyl-CoA that penetrates part of the tricarboxylic acids cycle (Krebs cycle) and the rest is converted into ketones. As a consequence, an increase in ketogenesis appears.

The peripheral tissues have a limited capacity to use those ketones. Therefore their production is more than their consumption, resulting in an elevated concentration of ketones.
These ketones aren’t just toxic for the liver but they are also highly anorexic, which leaves us with a sow stuck in a vicious cycle, one we have to try and get her out of.

Article Comments

This area is not intended to be a place to consult authors about their articles, but rather a place for open discussion among pig333.com users.
26-Jul-2011Wouter van HertenWouter van HertenHello Miquel,
First of all thanks for the interesting article.
During the last few years I think that the incidence is higher especially in pregnant gilts with a high bodyscore. Most of the treatments we use are based on gluconeogenesis. What are your treatments for individual sows and for the whole group?
Kind Regards,
Drs. Wouter van Herten
Veterinary Practise Deurne
15-Jan-2013PaoloPaoloI had occasion to check post-partum sows with milk production drop (generally by day 2-4 pp)and lack of appetite, for ketonic bodies in sows urine (with commercial strips) and found around 50% positive. Feeding mistakes in last two weeks of pregnancy was the main cause. Use of inectable propylen-glicole (something as 15 cc of same preparation for cows) was able to bring sows back to feed and milk production.
26-Apr-2013Gonzalo CarmonaGonzalo CarmonaExcelente artículo
14-Nov-2020 samluck143a sow farrowed but she is still not putting weight on fore feet and her forefeets are curled. what can be the cause
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