From birth, the piglet’s digestive system is geared towards processing milk-based fat, protein and carbohydrate. These are relatively simple molecules that the primitive gut can cope with. As the piglet grows, colonisation of the gut occurs with a wide range of microbes, most of which will originate from the sow. In the healthy piglet, there is a stable balance between helpful and harmful organisms in an environment that is influenced by the fact that the piglet eats a liquid diet of simple composition (milk) little and often.
When weaned, under conventional “crash” weaning systems, massive changes occur to the gut of the pig. The diet changes from liquid “on tap” to solid based, containing fat, protein and carbohydrate that will be vegetable based. Cooking of cereals and other processing will assist the digestibility and the inclusion of whey proteins and other milk products will offset the changes that the pig meets. The patterns of feeding may also change in that engorgement is more likely to occur “over-loading” the gut.
The stomach is acidic normally and acts not only to kill off potential harmful microbes entering with the food but to control the pH of the intestine, thus limiting microbial over-growth. There is a tendency for this effect to be lost or reduced post weaning, potentially allowing a gut environment more favourable to microbial growth.
Furthermore, the lining of the intestine consists of villi – microscopic finger like projections which vastly increase the surface area, allowing improved digestion and absorption of nutrients. In response to the stress of weaning and as a result of meeting foreign proteins, these villi shrink, reducing surface area and, hence, digestive and absorptive capacity. This will allow undigested food to pass further down the gut where microbial proliferation will occur causing scour.
Control of weaning diarrhoea
Weaning is a complex step involving dietary, environmental, social and psychological stresses which interfere deeply with feed intake, gastro intestinal tract development and adaptation to the weaning diet. The first organ suffering from nutrient shortage immediately after the weaning is the gastro intestinal tract and this has dramatic consequences on its anatomy and functions, including barrier function against harmful antigens and pathogens. Therefore, addition of organic acids to the drinking water appears as critical for solving post weaning disorders.
The morphology of the piglet's gastrointestinal epithelia drastically changes at weaning. Villous height decreases and crypt depth increases; these changes appear to be induced by weaning and not by the creep feed offered at weaning. In the same time, there is a transient decrease in intestinal Lactobacilli and increase in coliforms.
A lot of just weaned piglets usually show a malabsorption syndrome known as non-infectious diarrhoea, which is characterised by increased excretion of fatty acids and carbohydrates in the faeces, watery stools and degenerative changes in the villi of the small intestine. In the majority of these cases, opportunistic pathogens take advantage of the presence of non-infectious diarrhoea and cause the post-weaning diarrhea syndrome (PWDS). The most important pathogens are:
1) TGE (Transmissible Gastroenteritis):
a) Caused by virus that belongs to a group called coronaviruses, and destroys digestive cells (villi) in pig’s intestines, thus no digestion/absorption, which can lead to diarrhoea.
b) The most deadly, and the most feared by producers.
2) Rotaviral diarrohea:
a) Caused by groups of rotavirus (groups A, B and C), and destroys the lining of the small intestine.
b) Rotaviruses are resistant to lipid solvents & many disinfectants, and they can survive for a long time.
3) Colibacillosis (E. coli):
a) Caused by certain E. coli strains that are classified as enteropathogenic, which can propagate rapidly, and produce toxins (enterotoxin).
b) Toxins can cause massive fluid and electrolytes losses from the body, and the result being a large amount of pale yellow, watery feces.
c) Its effects might be a secondary to the damage caused by TGE or rotavirus.
This major cause of these post-weaning disorders is that the weaned piglet lacks sufficient capacity to acidify its own stomach content by hydrochloric acid. Thus, the pH value in the stomach may stay at 4-5 for at least two hours after feeding, leading to suboptimal protein digestion and insufficient killing of microbes by low pH value. During this period, more than half of the dry matter already has been transferred from the gastric lumen to the duodenum; the resulting poor digestion and high bacterial count can easily lead to weaning diarrhoea.
Organic acids can simply be added to the drinking water with a dosing pump (see figure 3). The addition of organic acids to the drinking water increases the speed at which stomach contents reaches the optimal pH value of around 3, where the proteolytic enzyme pepsin has its optimum efficacy. Acidification also leads to lower gastric emptying which further contributes to an optimal digestion process. These mechanisms support the piglets in the stressful post weaning period and reduce the risk of having the post weaning diarrhoea syndrome.
The morphology of the piglet's gastrointestinal epithelia drastically changes at weaning. Villous height decreases and crypt depth increases; these changes appear to be induced by weaning and not by the creep feed offered at weaning. In the same time, there is a transient decrease in intestinal Lactobacilli and increase in coliforms.
A lot of just weaned piglets usually show a malabsorption syndrome known as non-infectious diarrhoea, which is characterised by increased excretion of fatty acids and carbohydrates in the faeces, watery stools and degenerative changes in the villi of the small intestine. In the majority of these cases, opportunistic pathogens take advantage of the presence of non-infectious diarrhoea and cause the post-weaning diarrhea syndrome (PWDS). The most important pathogens are:
1) TGE (Transmissible Gastroenteritis):
a) Caused by virus that belongs to a group called coronaviruses, and destroys digestive cells (villi) in pig’s intestines, thus no digestion/absorption, which can lead to diarrhoea.
b) The most deadly, and the most feared by producers.
2) Rotaviral diarrohea:
a) Caused by groups of rotavirus (groups A, B and C), and destroys the lining of the small intestine.
b) Rotaviruses are resistant to lipid solvents & many disinfectants, and they can survive for a long time.
3) Colibacillosis (E. coli):
a) Caused by certain E. coli strains that are classified as enteropathogenic, which can propagate rapidly, and produce toxins (enterotoxin).
b) Toxins can cause massive fluid and electrolytes losses from the body, and the result being a large amount of pale yellow, watery feces.
c) Its effects might be a secondary to the damage caused by TGE or rotavirus.
This major cause of these post-weaning disorders is that the weaned piglet lacks sufficient capacity to acidify its own stomach content by hydrochloric acid. Thus, the pH value in the stomach may stay at 4-5 for at least two hours after feeding, leading to suboptimal protein digestion and insufficient killing of microbes by low pH value. During this period, more than half of the dry matter already has been transferred from the gastric lumen to the duodenum; the resulting poor digestion and high bacterial count can easily lead to weaning diarrhoea.
Organic acids can simply be added to the drinking water with a dosing pump (see figure 3). The addition of organic acids to the drinking water increases the speed at which stomach contents reaches the optimal pH value of around 3, where the proteolytic enzyme pepsin has its optimum efficacy. Acidification also leads to lower gastric emptying which further contributes to an optimal digestion process. These mechanisms support the piglets in the stressful post weaning period and reduce the risk of having the post weaning diarrhoea syndrome.
Drinking water acidification with organic acids
Health and performance of the pigs is what drives profits in pig production. Therefore farmers want to build the most modern animal houses, to have a quality feed and to select pigs with the best genetics. It is easy to forget that drinking water is the most important nutrient for farm animals and that the animals drink at least twice as much as they eat solid feed.
Acidifying the drinking water can help to improve the quality of the ‘forgotten nutrient’. Increasing the quality of the drinking water can result in improved performance of the animals, with lower bacterial load in the water and in less chance of the formation of ‘biofilm’ (an organic layer of ‘slime’ in the pipes, in which bacteria and fungi grow).
This article describes the benefits of acidification of drinking water with organic acids and the special importance that it can have for piglets in the post weaning period.
Lowering the pH
Compared to feed, which usually has a high buffering capacity (due to protein sources and minerals), water has a very small buffering effect. The only parameter which can have an effect is the hardness of water. When applying a product which has one single acid ingredient in drinking water, the pH decreases very quickly and if the dosage is too high, the pH can lower too much, leading to a negative result (lower water intake with decreased performance). Therefore choosing a product which has a synergistic formulation of organic acids is more favourable to these single acid products.
These organic acids have a buffering effect which makes the pH decrease slowly. A synergistic mix of organic acids also has a greater antibacterial effect, is more palateable, and is less corrosive compared with a single acid.
How do organic acids work?
The general chemical formula of an organic acid is R-COOH (undissociated form). In this form they have the ability to split off a proton (H+), which lowers the pH of the environment. The pKa value is the pH at which 50% of the organic acids have split off their proton, and is different for each organic acid. Due to the lower pH the growth of pathogenic bacteria (e.g. E. coli, Salmonella and Campylobacter) is inhibited and the growth of beneficial bacteria (e.g. lactic acid bacteria) is stimulated. This pH effect is the only effect that single acids have, on the other hand organic acids also have an antibacterial activity.
The antibacterial activity of organic acids is related to the reduction of pH, as well as their ability to dissociate, which is determined by the pKa-value of the respective acid, and the pH of the surrounding environment. The antibacterial activity increases with decreasing pH-value. Organic acids are lipid soluble in the undissociated form, in which they are able to enter the microbial cell (see figure 1). Once in the cell, the acid releases the proton in the more alkaline environment, resulting in a decrease of the pH in the cell. This influences microbial metabolism inhibiting the action of important microbial enzymes and forces the bacterial cell to use energy to release protons, leading to an intracellular accumulation of acid anions. This accumulation depends on the pH difference across the membrane. Generally the antimicrobial effect of organic acids increases with increasing concentrations.
Organic acids exert their antimicrobial action both in the water and in the gastro intestinal tract of the animal. If the water is acidified, the pH in the digestive tract of the pigs will be lowered. This has a positive effect on the digestion especially in the stomach and the small intestines.
Acidifying the drinking water can help to improve the quality of the ‘forgotten nutrient’. Increasing the quality of the drinking water can result in improved performance of the animals, with lower bacterial load in the water and in less chance of the formation of ‘biofilm’ (an organic layer of ‘slime’ in the pipes, in which bacteria and fungi grow).
This article describes the benefits of acidification of drinking water with organic acids and the special importance that it can have for piglets in the post weaning period.
Lowering the pH
Compared to feed, which usually has a high buffering capacity (due to protein sources and minerals), water has a very small buffering effect. The only parameter which can have an effect is the hardness of water. When applying a product which has one single acid ingredient in drinking water, the pH decreases very quickly and if the dosage is too high, the pH can lower too much, leading to a negative result (lower water intake with decreased performance). Therefore choosing a product which has a synergistic formulation of organic acids is more favourable to these single acid products.
These organic acids have a buffering effect which makes the pH decrease slowly. A synergistic mix of organic acids also has a greater antibacterial effect, is more palateable, and is less corrosive compared with a single acid.
How do organic acids work?
The general chemical formula of an organic acid is R-COOH (undissociated form). In this form they have the ability to split off a proton (H+), which lowers the pH of the environment. The pKa value is the pH at which 50% of the organic acids have split off their proton, and is different for each organic acid. Due to the lower pH the growth of pathogenic bacteria (e.g. E. coli, Salmonella and Campylobacter) is inhibited and the growth of beneficial bacteria (e.g. lactic acid bacteria) is stimulated. This pH effect is the only effect that single acids have, on the other hand organic acids also have an antibacterial activity.
The antibacterial activity of organic acids is related to the reduction of pH, as well as their ability to dissociate, which is determined by the pKa-value of the respective acid, and the pH of the surrounding environment. The antibacterial activity increases with decreasing pH-value. Organic acids are lipid soluble in the undissociated form, in which they are able to enter the microbial cell (see figure 1). Once in the cell, the acid releases the proton in the more alkaline environment, resulting in a decrease of the pH in the cell. This influences microbial metabolism inhibiting the action of important microbial enzymes and forces the bacterial cell to use energy to release protons, leading to an intracellular accumulation of acid anions. This accumulation depends on the pH difference across the membrane. Generally the antimicrobial effect of organic acids increases with increasing concentrations.
Figure 1: Antibacterial activity of organic acids
Organic acids exert their antimicrobial action both in the water and in the gastro intestinal tract of the animal. If the water is acidified, the pH in the digestive tract of the pigs will be lowered. This has a positive effect on the digestion especially in the stomach and the small intestines.
Porcine Reproductive & Respiratory Syndrome (PRRS)
PRRS is caused by a virus which was first isolated and classified as an arterivirus as recently as 1991. The disease syndrome had been first recognised in the USA in the mid 1980's and was called "mystery swine disease". It has also been called blue ear disease. The name porcine arterivirus has been proposed recently.
The virus of PRRS has a particular affinity for the macrophages particularly those found in the lung. Macrophages are part of the body defences. Those present in the lung are called alveolar macrophages. They ingest and remove invading bacteria and viruses but not in the case of the PRRS virus. Instead, the virus multiplies inside them producing more virus and kills the macrophages. Once it has entered a herd it tends to remain present and active indefinitely.
Up to 40% of the macrophages are destroyed which removes a major part of the bodies defence mechanism and allows bacteria and other viruses to proliferate and do damage.
A common example of this is the noticeable increase in severity of enzootic pneumonia in grower/finisher units when they become infected with PRRS virus.
It may take up to a year for all breeding stock, particularly in large herds, to become infected for the first time and although the virus appears to spread rapidly in a herd it may be some 4 -5 months before at least 90% of the sows have become sero-positive. Some sows remain naive. Furthermore, it is not uncommon for sow herds 1-2 years after infection to contain less than 20% of serological positive animals. This does not however necessarily mean they are not still immune nor does it mean that they have stopped passing on immunity to their offspring. Adult animals shed virus for much shorter periods of time (14 days) compared to growing pigs which can excrete for 1-2 months.
The clinical picture can vary tremendously from one herd to another. As a guide, for every three herds that are exposed to PRRS for the first time one will show no recognisable disease, the second would show mild disease and the third moderate to severe disease. The reasons for this are not clearly understood. However the higher the health status of the herd, the less severe are the disease effects. It may be that the virus is mutating as it multiplies, throwing up some strains that are highly virulent and some that are not.
PRRS infects all types of herd including high or ordinary health status and both indoor and outdoor units, irrespective of size.
The virus of PRRS has a particular affinity for the macrophages particularly those found in the lung. Macrophages are part of the body defences. Those present in the lung are called alveolar macrophages. They ingest and remove invading bacteria and viruses but not in the case of the PRRS virus. Instead, the virus multiplies inside them producing more virus and kills the macrophages. Once it has entered a herd it tends to remain present and active indefinitely.
Up to 40% of the macrophages are destroyed which removes a major part of the bodies defence mechanism and allows bacteria and other viruses to proliferate and do damage.
A common example of this is the noticeable increase in severity of enzootic pneumonia in grower/finisher units when they become infected with PRRS virus.
It may take up to a year for all breeding stock, particularly in large herds, to become infected for the first time and although the virus appears to spread rapidly in a herd it may be some 4 -5 months before at least 90% of the sows have become sero-positive. Some sows remain naive. Furthermore, it is not uncommon for sow herds 1-2 years after infection to contain less than 20% of serological positive animals. This does not however necessarily mean they are not still immune nor does it mean that they have stopped passing on immunity to their offspring. Adult animals shed virus for much shorter periods of time (14 days) compared to growing pigs which can excrete for 1-2 months.
The clinical picture can vary tremendously from one herd to another. As a guide, for every three herds that are exposed to PRRS for the first time one will show no recognisable disease, the second would show mild disease and the third moderate to severe disease. The reasons for this are not clearly understood. However the higher the health status of the herd, the less severe are the disease effects. It may be that the virus is mutating as it multiplies, throwing up some strains that are highly virulent and some that are not.
PRRS infects all types of herd including high or ordinary health status and both indoor and outdoor units, irrespective of size.
Dysenterie
De ziekte dysenterie Dysenterie, ook wel bekend als ‘Vibrio’, is een infectie in de dikke darm die diarree veroorzaakt.
Verschijnselen Dysenterie komt vooral voor bij vleesvarkens en opfokvarkens, maar ook bij gespeende biggen en zeugen kan de ziekte zich voordoen. Kenmerkend is een betonkleurige diarree, meestal gemengd met slijm (glimmend) en soms met bloed (stolsels, donkere slierten). Meestal is dit enkele weken na opleg te zien. Het duurt namelijk enkele weken voordat de ziekteverschijnselen na het moment van infectie merkbaar worden. Vaak treden verschijnselen pas op na een voerverandering of verhoging van het rantsoen.
Oorzaak Dysenterie, ook wel bekend als ‘Vibrio’, wordt veroorzaakt door de kiem Brachyspira hyodysenteriae. Binnen de familie van de Brachyspira worden meerdere soorten onderscheiden, zoals B. innocens, B. murdochii, B. intermedia en B. pilosicoli. Alleen B. hyodysenteriae en B. pilosicoli zijn de pathogene (ziekteverwekkende) kiemen binnen deze familie.
Besmettingsroute Brachyspira wordt in grote aantallen uitgescheiden met de mest en daarom is mest het belangrijkste materiaal waarmee deze infectie verspreid wordt. Varkens, mensen, huisdieren, ongedierte en vliegen kunnen Brachyspira verspreiden. Dieren die worden aangevoerd kunnen ook met Brachyspira besmet zijn en zijn daarmee een belangrijke bron van besmetting voor bedrijven.
Schade Dysenterie zorgt voor schade in de vorm van een verminderde groei. Vaak ontwikkelen zich ‘slijters’. Een enkele keer treedt door een uitbraak sterfte op, soms zelfs bij zeugen.
Diagnose dysenterie
Vanoudsher wordt voor de diagnostiek van Brachyspira gebruik gemaakt van een immuun fluorescentie test (IFT). Een ongunstig testresultaat in de IFT toont alleen aan dat een lid van de familie Brachyspira in de mest aanwezig was. Deze IFT maakt echter geen onderscheid tussen de verschillende Brachyspira-soorten. Een ongunstige uitslag kan dus net zo goed veroorzaakt worden door een niet ziekmakende Brachyspira. Een behandeling instellen op basis van een ongunstige IFT kan dus onterecht zijn. Het is daarom beter de gebruik te maken van zogenaamde PCR testen. Met deze testen zijn B. hyodysenteriae en B. pilosicoli van elkaar en van de andere soorten te onderscheiden, zodat een juiste diagnose mogelijk is. Het onderscheid tussen B. hyodysenteriae en B. pilosicoli is belangrijk omdat B. pilosicoli een mildere ontsteking van de dikke darm veroorzaakt en dus ook een milder ziekteverloop, maar wel met afwijkende mest.
Risicofactoren dysenterie Mest is de belangrijkste verspreidingsbron van Brachyspira. Via varkens, mensen, huisdieren, ongedierte en vliegen kan Brachyspira worden verspreid. Ook de aanvoer van dieren op het bedrijf is een belangrijke bron van besmetting.
Aanpak van dysenterie Therapie Ter bestrijding van dysenterie zijn verschillende antibiotica beschikbaar. Overleg hierover met uw dierenarts. De basis is een zogenaamde curatieve behandeling van één tot twee weken van alle aanwezige varkens in een afdeling of soms zelfs van het hele bedrijf, gevolgd door een nabehandeling van enkele weken met een lagere dosering. De curatieve behandeling wordt via het drinkwater of met injecties (zieke dieren) uitgevoerd.
Preventie De belangrijkste maatregelen zijn het verbeteren van hygiëne: niet dezelfde laarzen gebruiken voor besmette en niet-besmette afdelingen, vliegenbestrijding, professionele muizenbestrijding en strikt all-in/all-out hanteren. De
voeding speelt eveneens een rol. Streef naar geleidelijke voerovergangen, makkelijk verteerbare eiwitbestanddelen in het voer en voldoende ruwe celstof.
De belangrijkste preventieve maatregelen zijn:
• all-in/all-out hanteren
• lege afdelingen zorgvuldig reinigen, ontsmetten en laten drogen
• per afdeling vleesvarkens van één herkomst opleggen
• zorgen voor geleidelijke voerovergangen
• zorgen voor lichtverteerbaar voer, liefst met voldoende ruwe celstof
• goede vliegenbestrijding hanteren
• goede ongediertebestrijding hanteren
• zorgen voor goede erfverharding (erf en gangen opruimen en schoonhouden)
• zorgvuldig gebruik maken van een toevoegstal voor de aanvoer van gelten en beren
Verschijnselen Dysenterie komt vooral voor bij vleesvarkens en opfokvarkens, maar ook bij gespeende biggen en zeugen kan de ziekte zich voordoen. Kenmerkend is een betonkleurige diarree, meestal gemengd met slijm (glimmend) en soms met bloed (stolsels, donkere slierten). Meestal is dit enkele weken na opleg te zien. Het duurt namelijk enkele weken voordat de ziekteverschijnselen na het moment van infectie merkbaar worden. Vaak treden verschijnselen pas op na een voerverandering of verhoging van het rantsoen.
Oorzaak Dysenterie, ook wel bekend als ‘Vibrio’, wordt veroorzaakt door de kiem Brachyspira hyodysenteriae. Binnen de familie van de Brachyspira worden meerdere soorten onderscheiden, zoals B. innocens, B. murdochii, B. intermedia en B. pilosicoli. Alleen B. hyodysenteriae en B. pilosicoli zijn de pathogene (ziekteverwekkende) kiemen binnen deze familie.
Besmettingsroute Brachyspira wordt in grote aantallen uitgescheiden met de mest en daarom is mest het belangrijkste materiaal waarmee deze infectie verspreid wordt. Varkens, mensen, huisdieren, ongedierte en vliegen kunnen Brachyspira verspreiden. Dieren die worden aangevoerd kunnen ook met Brachyspira besmet zijn en zijn daarmee een belangrijke bron van besmetting voor bedrijven.
Schade Dysenterie zorgt voor schade in de vorm van een verminderde groei. Vaak ontwikkelen zich ‘slijters’. Een enkele keer treedt door een uitbraak sterfte op, soms zelfs bij zeugen.
Diagnose dysenterie
Vanoudsher wordt voor de diagnostiek van Brachyspira gebruik gemaakt van een immuun fluorescentie test (IFT). Een ongunstig testresultaat in de IFT toont alleen aan dat een lid van de familie Brachyspira in de mest aanwezig was. Deze IFT maakt echter geen onderscheid tussen de verschillende Brachyspira-soorten. Een ongunstige uitslag kan dus net zo goed veroorzaakt worden door een niet ziekmakende Brachyspira. Een behandeling instellen op basis van een ongunstige IFT kan dus onterecht zijn. Het is daarom beter de gebruik te maken van zogenaamde PCR testen. Met deze testen zijn B. hyodysenteriae en B. pilosicoli van elkaar en van de andere soorten te onderscheiden, zodat een juiste diagnose mogelijk is. Het onderscheid tussen B. hyodysenteriae en B. pilosicoli is belangrijk omdat B. pilosicoli een mildere ontsteking van de dikke darm veroorzaakt en dus ook een milder ziekteverloop, maar wel met afwijkende mest.
Risicofactoren dysenterie Mest is de belangrijkste verspreidingsbron van Brachyspira. Via varkens, mensen, huisdieren, ongedierte en vliegen kan Brachyspira worden verspreid. Ook de aanvoer van dieren op het bedrijf is een belangrijke bron van besmetting.
Aanpak van dysenterie Therapie Ter bestrijding van dysenterie zijn verschillende antibiotica beschikbaar. Overleg hierover met uw dierenarts. De basis is een zogenaamde curatieve behandeling van één tot twee weken van alle aanwezige varkens in een afdeling of soms zelfs van het hele bedrijf, gevolgd door een nabehandeling van enkele weken met een lagere dosering. De curatieve behandeling wordt via het drinkwater of met injecties (zieke dieren) uitgevoerd.
Preventie De belangrijkste maatregelen zijn het verbeteren van hygiëne: niet dezelfde laarzen gebruiken voor besmette en niet-besmette afdelingen, vliegenbestrijding, professionele muizenbestrijding en strikt all-in/all-out hanteren. De
voeding speelt eveneens een rol. Streef naar geleidelijke voerovergangen, makkelijk verteerbare eiwitbestanddelen in het voer en voldoende ruwe celstof.
De belangrijkste preventieve maatregelen zijn:
• all-in/all-out hanteren
• lege afdelingen zorgvuldig reinigen, ontsmetten en laten drogen
• per afdeling vleesvarkens van één herkomst opleggen
• zorgen voor geleidelijke voerovergangen
• zorgen voor lichtverteerbaar voer, liefst met voldoende ruwe celstof
• goede vliegenbestrijding hanteren
• goede ongediertebestrijding hanteren
• zorgen voor goede erfverharding (erf en gangen opruimen en schoonhouden)
• zorgvuldig gebruik maken van een toevoegstal voor de aanvoer van gelten en beren
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