Better Pork - October 2001
What you can do to combat rising sow mortality
Giving the problem the attention it deserves, and intensifying your selection and observational skills are necessary first steps in bringing those high levels downby KEN PALEN
These days, sow mortality is becoming more of a problem, with many producers are experiencing mortality rates of more than 10 per cent, and five per cent very common and quite accepted. These high levels should concern us, for they constitute a major financial and managerial problem.A number of factors contribute to these high levels. One is that by the time the problem is recognized, it is often too late to do anything about it. An advantage to having sows in crates is they can be observed every day. But if no real attention is being paid to the sows, or the person working with them has limited observational skills, the benefit is lost.
The person working with the sows needs to be able to evaluate problems, then decide whether the sow should be treated immediately, culled immediately or moved to a pen, or whether a replacement gilt needs to be selected.
Another problem contributing to high sow mortality is poor selection of replacement gilts in the first place. Not all F-1 females produced should become part of the sow herd. There needs to be phenotypic selection based on desirable traits such as leg conformation, similar toe size and muscularity in the hams, as well as teat number, size and placement, and overall femininity. Furthermore, gilts need to be sufficiently developed before they become part of the sow herd. A definite cause of high sow mortality is mating gilts when they are too young and immature, and thus too small at their first farrowing.
Lack of body fat reserves prior to farrowing, depletion of reserves and weight loss are also highly related to sow mortality. Nutrients need to be replenished as soon as possible after weaning, and an ideal body condition score maintained. Hoof integrity and injury also need to be monitored and corrected if problems arise.
Moreover, too much sow mortality is directly related to physical injury, often due to improper handling. Sows are often all moved at once in large groups, physically mistreated by someone in a hurry or moved long distances in narrow alleys. Pens may also not be sized correctly or may have slick floors, which encourage fighting.
Fevers, which result in a loss of appetite, can also be a problem, especially early in farrowing, with problems such as MMA. Sows may also be affected by feed mold toxins interruptions in feed consumption, which can cause ulcers, other diseases such as ileitis and PRRS, and possibly simply a reduced immune function.
In a large sow mortality investigation conducted by PIC, involving eight farms with more than 12 per cent mortality, it was found that the main causes of mortality could be grouped into three categories:
1. Locomotor problems,
2. Gastrointestinal problems.
3. Reproductive complications.Based on necropsy data on all the sows that died, 36 per cent had tenth rib fat depth under 12mm. Also an average of 45 per cent (in a range of 16-79 per cent) had severe ulcers. Mortalities peaked in the summer, with 50 per cent of the deaths (65 per cent in the summer) occurring within three weeks after farrowing and the risk increasing with lower body condition scores. The larger the gilt pool, and the larger the gilt when she first farrowed, the lower the mortality. Sows with fewer stillbirths were less likely to die in the subsequent parity. These findings can be very useful when trying to decrease mortality.
In summary, to reduce sow mortality, select and breed only structurally sound animals with even toe size. Gilts should be carefully selected and adequately developed before and after mating. Cull animals that sit splayed, and sows over six parities. Do not allow sows to lose excessive weight or condition before weaning. Split-wean some pigs in high weight loss sows; also wean them a couple of days early. Skip-breed any thin weaned sows, especially first-parity P1 sows and feed to condition. Maximize feed intake in lactation. Treat sick animals promptly; it may be helpful to receive gilts on medication such as 110 g/t of tylosin phosphate, especially if ileitis is a problem. Remember, decreasing sow mortality starts with the gilt, so make sure you have a large, intensely selected gilt pool. Continue to intensify your selection and observation skills.
Do not breed too young and monitor sows for early signs of problems, such as weight loss and hoof problems. The period to concentrate on is from farrowing to after weaning. The sow mortality problem will only be solved if there is a sense of urgency about it, and it gets the attention it deserves. BP
Ken Palen is a livestock specialist with KenPal Farm Products Inc. Centralia.
© copyright 2001 AgMedia Co-operative Inc..
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Hemorrhagic bowel syndrome - hard to diagnose, hard to treat
Though the root cause of HBS has not been identified, some possible explanations have been suggested and some risk factors proposedby S. ERNEST SANFORD
In a previous article (Better Pork, February 2000), I outlined the differences between "ileitis" (porcine proliferative enteropathy or PPE) and "colitis" (colonic spirochetosis). Hemorrhagic bowel syndrome (HBS) is another, albeit less common, condition that is often mistaken for porcine hemorrhagic enteropathy (PHE), the acute hemorrhagic form of PPE/ "ileitis".As a neophyte pathologist, I am sure I misdiagnosed HBS (see Fig. 1). My misdiagnosis, however, was not in calling it "ileitis" but rather in diagnosing it as an intestinal or mesenteric torsion (Fig. 2). This was aided and abetted by my belief then that the torsion had straightened itself out during the manipulations of lifting and turning the pig during transport and necropsy. By the end of the 1970s, however, I was not only convinced that HBS was a distinct and separate condition from gut twists, but also that complete 360-degree torsions did not unravel themselves spontaneously during transport and necropsy manipulations.
HBS occurs as sudden death in grow-finish pigs. It is usually sporadic, occurring a single pig at a time. However, outbreaks involving death of moderate to large numbers of pigs can and do occur. The cause of HBS is unknown.
Clinical and post-mortem findings include some or all of the following:
1. Previously healthy pig(s) just found dead.
2. Dilated/bloated abdomen with loops of small intestine distended and containing unclotted, darkened blood and gas.
3. The intestinal wall is thin and congested.
4. The stomach is usually filled with feed.
5. No gastric ulcer is present.
6. The rectum contains normal, nondiarrheic feces.
7. My own personal observation is that HBS occurs more commonly in the summer and early fall than at other times of the year.
8. It is rare to observe antemortem clinical signs. The period of clinical disease culminating in death likely lasts from just minutes to less than one hour. Diarrhea is not a feature and case fatality rate is 100 per cent.Using the list above it is relatively easy to differentiate ileitis from HBS. The major differentiating diagnostic features are that: * Pigs go off feed with PHE, which means the stomach is usually empty or nearly empty.
* The intestinal wall is thickened, not thin.
* Blood in the intestinal lumen is often clotted.
* The rectum contains black, tarry, diarrheic feces with PHE.It is also possible to rule out intestinal torsion. The normal position of the cecum is at the back of the abdomen and pointing towards the tail. In the case of a torsion, the cecum moves forward to the front of the abdomen and points towards the head. Ruling out intestinal torsion is even easier if you believe that complete 360-degree torsions do not untwist themselves spontaneously. However, there is still the possibility of a torsion of less than 180 degrees untwisting itself. Does this actually happen? We don't know.
Though, we don't know what actually causes HBS, several causes have been proposed over the last two to three decades. The most convincing and at least partially accepted over the years have been:
* Bacterial overgrowth/"blooms."
* E. coli toxins.
* Clostridial toxins.
* An incomplete torsion or twist of the intestine (already mentioned above).
* Allergic reaction to unknown antigens in the feed.
* Hypersensitivity to feed ingredients.
* Endotoxic shock.The E. coli and clostridial toxins have had the greatest credibility over the years. To date, however, none of the proposed mechanisms has ever been verified.
Risk factors
Several risk factors have also been proposed, based on empirical evidence. Among these are:1. Liquid or whey feeding.
2. Inconsistent feed consumption leading to engorgement.
a. feed system failure
b. out of feed
c. sorting/mixing3. Changes in the pig's environment or social status.
a. Moving a group to a different pen location
b. Social stress
c. Sorting or topping off pens at market
d. Mixing pigs in the same pen e. Other4. Feed or water constituents that may enhance bacterial "blooms."
a. High iron in water
b. Water quality
c. Protein quality
d. Abrupt change of ingredients in ration
e. Abrupt change in proportions of ingredients in ration
f. Mixing errors (mineral, salt, protein, etc)Since we do not know what causes HBS, recommendations for treatment or prevention are sparse and are based more on trial and error than proven scientific methods. Medication with bacitracin methylene disalicylate (BMD) combined with chlortetracycline (CTC) in the feed has been reported to successfully control HBS. In most cases, however, the problem seems to wax and wane or completely resolve itself on its own, irrespective of our efforts. BP
S. Ernest Sanford, DVM, Dip Path, Diplomate ACVP, is a swine specialist with Boehringer Ingelheim Vetmedica (Canada) in Burlington.
© copyright 2001 AgMedia Co-operative Inc..
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Design your concrete to resist those corrosive manure gases
New research shows that you can lengthen the life of your buildings if you tailor the cement used in concrete floors and manure tanks for maximum resistance and durabilityby NADINE FORTIN
Gases originating from a manure storage tank can be irritating to the nose, especially if the storage is located under slatted floor. Steel reinforcement in mortar will also react to gases such as hydrogen sulphide, though in a different way -- by corroding.Reinforced concrete is used in barns for the construction of floors and manure tanks below the floor. These structures are affected by gases forming from anaerobic fermentation in the temporary storage tank. The results? Steel that rusts and concrete that undergoes corrosion, sometimes after only a few years.
A team of scientists from the School of Engineering of the University of Guelph have studied the impact of long-term exposure to hydrogen sulphide on six different types of mortar reinforced with steel. In order to keep the corrosion away from steel as long as possible, it was proven that regular, commonly used cement needed extra components such as silicate fume. Enhanced concrete means extra dollars, but it seems that the investment is worthwhile on the long run.
The mortar used for the experiment is the same as the one used for livestock buildings. Portland cement with a water-cement ratio of 0@45 (CSA recommendation) was used in five of the six treatments. The sixth treatment had a ratio of 0@55 which is also commonly used in the industry. However, the study demonstrated that a higher percentage of water in cement results in inferior durability.
The researchers used three different tests. The first one is called impressed voltage. It measures the corrosion rate of reinforcing steel in concrete under long-term exposure to hydrogen sulphide (H2S) at a concentration of 2000 ppm for a year before testing. This high concentration helps to accelerate the process in order to get results in reasonable time. The reaction of H2S was fast in the first week and declined gradually afterward. The steel bar was also submitted to electrical current. When a longitudinal crack developed in the mortar, time of failure was recorded.
The threshold level that initiates corrosion in the reinforced bar is determined by the electrochemical potential tests. A steel bar embedded in mortar is exposed to H2S for 650 days and submitted to electrical current. The current going through the bar reacted with the pore water of the surrounding mortar, causing the steel to rust and reducing the conductivity in the metal.
The diffusion tests were used to predict the sulphur concentration present in barn concrete. The exposed surface of concrete became saturated with H2S within that first week. Because the surface mortar pores are filled with gas, it acts as a barrier. So, even if the surrounding air has a high concentration of hydrogen sulphide for a very long period, the penetration rate of H2S was no faster. However, the gas saturating the surface of concrete travels through the mortar, reaches the steel bar and acts as a corrosive agent. Scientists measured the sulphur treatment in each sample at 90, 180, 270, 360 days.
When comparing the results of the different tests, mortar containing silica fume cement (SFC) seems to come out as the best material for agricultural structures exposed to manure gases. SFC cracked after 600 hours, while PC55 did it after 165 minutes. SFC also showed the smallest susceptibility to corrosion.
The time required to reach the threshold concentration (3.0 g kg-1) that initiates corrosion is eight times longer for concrete treated with silica fume cement than for cement with a water-cementing ratio of 0?55. Also, SFC has the lowest penetration rate (2 to 3 mm) and offers the longest service life of slats. Compared to regular Portland cement with a W/C of 0?45, the life span of silica fume cement mortar is estimated to be twice as long. BP
Nadine Fortin is technology transfer agent for the Canadian Pork Council and Agriculture and Agri-Food Canada.
Special thanks to study co-author Satish C. Negi, School of Engineering, University of Guelph. Photos : courtesy of Satish C. Negi
© copyright 2001 AgMedia Co-operative Inc..
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