December, 1996 . Volume 19, Number 11
December, 1996 . Volume 19, Number 11
During the past winter transmissible gastroenteritis (TGE) has again reared its ugly face in North Carolina. TGE is a highly infectious enteric disease that affects all ages of swine, but causes high levels of mortality mainly in pigs less than two weeks of age. It is a highly contagious infection characterized by diarrhea, vomiting and fever. Epidemics often occur as many herds are serologically negative and thus have no defense against the disease. Farmers find the disease particularly disruptive as it is unpredictable and unresponsive to treatment. However, inasmuch as these large acute outbreaks are devastating, chronic TGE is the greatest problem.
Chronic TGE sticks around as a continual low-level problem. It can cause mortality or slow growth in piglets both in the farrowing crate and the nursery. It can predispose pigs to secondary disease outbreaks in the grow/finish barn. Chronic TGE is difficult to eliminate and control. Chronic TGE often begins as an improperly handled acute TGE outbreak in a herd. It has often been noted that smaller herds that are "less intensive" and allow the disease to spread quite quickly with little interference seems to have no signs of TGE after the initial outbreak. Alternatively, larger herds that use all-in all-out facilities, and also purchasing gilts from outside sources, often along with a TGE vaccination program, tended to see more chronic TGE problems.
Consequently, we treat an outbreak of TGE differently from most diseases. We actually try to spread the disease as quickly as possible and as thoroughly as possible. Our purpose is to expose each animal to the disease so that it either dies or survives with immunity to further outbreaks. It goes against our innate desires to control and reduce disease, but it has been correct.
We can explain the reasons epidemiologically. TGE outbreaks are quite easy to graph and explain. This is because it is a single factor disease caused by the TGE virus, it spreads relatively quickly throughout the herd and the immunity once gained to the actual disease is essentially for the life time of the animal. Thus a disease outbreak is affected by a) the ability of the disease to pass from one animal to the other, b) the time it takes for an animal, once infected, to pass the disease on to the next animal, c) the introduction of non-infected animals to infected animals before the outbreak is over.
With these factors we can graph a disease outbreak as shown in Figure 1. In a herd where contact is made among all animals the disease quickly spread throughout the herd, virtually no animals are left that have not been infected. In a herd where the virus has difficulty traveling from pig to pig the disease is slow. The disease survives in a herd approximately three months after the last clinical signs are seen. If there are no further animals to be infected as they are all immune ythe disease dies out in the herd. Thus the aim would be to spread the live virus as quickly as possible throughout the herd by taking guts and manure from infected litters and pigs and introducing it to the various components of the farm unit.
How do we keep the virus alive in the herd? It is simply by introducing new non-immune pigs to the disease before it dies out of the herd, i.e., within 90 days after the outbreak. This can be done probably by the following processes:
This prolongation of the TGE outbreak brings into focus a third population of animals, the progeny of the infected sows that receive colostral immunity. These piglets that were not diseased but were protected by the colostrum of their dam become open to the disease at some period after birth. These piglets then become infected and become another source for the virus. As can be imagined, the outbreak can become chronic as various sources of naive animals continue to enter the herd to allow the prolonged survival of the TGE virus in the herd.
It is for these reasons that the best time to avoid chronic TGE is at the point of identifying an acute TGE outbreak. Vaccines and isolation should be avoided. Instead, we should potentiate the rapid spread of the virus throughout the herd. With chronic TGE already occurring in the herd, the main suggestion is to provide an active infection in as much of the breeding stock and gilts during early gestation as possible. This would involve identifying litters with actual TGE and feeding back the material to the sows and gilts, and then using vaccines as a preventive. Creating a herd of sows and gilts that have active immunity should result in a decrease and gradual elimination of the disease in the herd.
Though these are the basic rules of control of TGE, there is a large question how the disease functions in herds infected with PRCV. PRCV is a closely related virus that resides in the lungs and creates only a mild pneumonia, if there are any effects at all. It has spread rapidly through NC without any major reports of problems. It appears that immunity to PRCV provides partial protection to a herd infected with TGE. It appears that the disease spreads more slowly and is less severe. Are we getting chronically infected herds as the disease spreads more slowly? The answer might be "no" on the most part. It appears that PRCV mast slow down the spread to the point that herd does not become chronically infected usually. The acid test will occur this winter as we watch herds that were infected last winter.
Take Home Message
TGE is a disease to avoid through good biosecurity. If you do get it, however, the aim is to spread the disease as thoroughly as possible. It appears that a PRCV will actually help us in controlling this devastating disease.
John Deen
1996 Healthy Hogs Seminar
One of the difficult parts of managing respiratory disease is evaluating its full effect upon productivity in the grow/finish herd. Often, some of the costs of the disease, as well as its control, are not measured when evaluating the effects of respiratory disease. This paper will give a list of possible areas to look at when examining respiratory disease. Some of these factors are difficult to measure, and therefore, have been ignored in many cases.
Sometimes we cannot measure the full effect of a disease, but nonetheless, we should keep these factors in mind. Though not exhaustive, such a list of possible effects should include productivity measures such as average daily gain and feed conversion but also include other factors such as labor, facility design, and throughout.
Feed Conversion
On the most part, respiratory diseases have been thought to have relatively small effects upon feed conversion. This is especially true when only low levels of respiratory disease are seen in diseases such as mycoplasmal pneumonia. However, a small part of the population can be affected quite seriously. These can be called the "lungers" of the herd. In these cases, feed conversions ratios can be as poor as six to ten. When we look at lean meat deposition, the numbers can quite often be negative. Most of the effect upon feed conversion is through decreases in feed intake, and therefore, longer periods of time for the pig to grow with higher maintenance requirements. It is only in stock with a very low level of disease that the FCR is affected severely.
Average Daily Gain
One of the major effects of respiratory disease is upon the growth rate of pigs. This can be seen through decreases in growth rates as much as 10, 15, or 20% on average. What the average does not show is that the effect of respiratory disease can be uneven across the herd where some pigs are affected much more severely than others. Twenty-five percent of a group may be affected up to 40% in their average daily gain and some pigs may not be affected at all. This is a substantial cost in all-in-all-out farms as the throughout is determined by the slowest growing pig.
Secondary Conditions
Respiratory disease can increase the susceptibility to a number of secondary conditions. This includes gastroesophageal ulcers, rectal prolapses and even enteric diseases.
Carcass Quality
Carcass quality can also be affected by respiratory diseases. Some of the effects can be direct. For instance, the lungs may adhere to the rib cage thus causing trimming problems. Another problem may be that some of the pigs are growing very slowly and therefore are marketed at light weights out of the grow/finish barn. Finally, the carcass composition of the pig may be reduced in quality as respiratory disease may reduce the rate of lean meat deposition.
Labor
Labor may be increased greatly in a herd that is affected by respiratory disease. Straightforward effects such as increased treatment time may be usually identified. Added to treatment time should be the cost of constantly monitoring the pigs for signs of respiratory disease. It should also be recognized that there is some labor, and it is particularly onerous labor, that is involved in removing pigs that have died or euthanizing pigs that are in very poor condition. The presence of respiratory pathogens also demands that more time should be spend in monitoring and controlling the ventilation system as these pigs are more susceptible to rapid increases and decreases in temperature.
Preventive Measures
Of course, the cost of vaccines and the cost of medications should be included in any measurement of the effect of respiratory disease. It should also be recognized that many of these interventions may have a negative effect on their own. For instance, respiratory disease vaccines may, in themselves, decrease growth rates and feed intakes by demanding energy for an immune response or decreasing the appetite of pigs. Some antibiotics may negatively affect water intake due to their flavor.
Feed Costs
It has been shown that the nutrient density of diets may need to be higher for pigs suffering from respiratory disease. This can be due to a wide number of reasons but the most logical reason is that extra nutrients are required to mount a good immune response.
Building Design
It should be obvious that much of our building design, site definition, and method of production is defined by the control of disease. In many cases, it is respiratory disease that has created some of the definition of number of barns per site and flow of animals. It is often surprising that we can take many "short-cuts" when respiratory pathogens are not present on a site.
Aesthetics
It should be noted that in many cases, pigs that are affected by respiratory disease provide a poor appearance and may, in the end, provide a lees pleasant environment to work in. It is more comfortable to work among a group of healthy pigs than those that cough, show signs of disease, etc. In the long run, there may be greater employee satisfaction with a healthier group of pigs.
Ability to use new technologies
It appears that many respiratory conditions are exacerbated by advances in technology. As we produce leaner, more efficient pigs they increase in their susceptibility to infectious and non-infectious diseases. Respiratory diseases will increase as a constraint in efficient pork production.
Take-Home Message
All these costs together show that a great deal of investment can be used for prevention. The saying "well begun, is half done" is as true now as 30 years ago. Steps in providing a healthy, pathogen-free population of pigs out of the nursery into the grow/finish barn should be always our goal.
John Deen
1996 Healthy Hogs Seminar
Research conducted at the University of Kentucky may help swine producers cut down on the amount of nitrogen in hog waste. Gary Cromwell, animal scientist, says research trials have shown that the amount of nitrogen excreted by hogs can be reduced by feeding a lower level of protein, supplemented with amino acids, without sacrificing growth and performance.
In one experiment, Cromwell fed finishing pigs a diet containing 12% protein, supplemented with .15% lysine, instead of the usual 14% protein. Pig growth was equal to that achieved with the higher protein diet. The amount of nitrogen present in the urine and feces was reduced by 19% in the lower diet.
In another study, Cromwell fed a diet with 10% protein and supplemented the diet with lysine, threonine, tryptophan and methionine. Rate of gain for the pigs fed the reduced-protein diet was comparable to those fed a high-protein diet, but the amount of nitrogen excreted was reduced by 34%. In addition, the ammonia emission from the manure was cut in half.
"Lysine is an amino acid that is one of the building blocks of protein. Threonine, tryptophan and methionine also are amino acids found in protein. By balancing the feedstuffs for amino acids, we were able to significantly reduce the mount of nitrogen excreted," says Cromwell.
Cromwell notes that using the threonine and tryptophan-fortified diet is more expensive than simply feeding more soybean meal, the usual source of protein. Before long, he expects tryptophan and threonine will be available at prices that make these types of diets cost effective.
HogHealth
Vol. 6, No. 5
Survival in the pork industry requires sows that consistently produce large litters. To achieve this goal, one scientist recommends renewing an emphasis on lifetime feeding programs for all gilts and sows.
Richard Simms, swine specialist at the University of Tennessee, advises that meaty and lean gilts self-feed on a 16% protein (0.8% lysine) ration during the growing-finishing stage until they weigh about 250 lbs. As producers select the gilt pool, he recommends giving the animals a mineral-fortified sow ration containing 1% calcium and 0.8% phosphorus.
After mating, limit both replacement gilts and sows to only 4-5 lbs of a fortified, 16% protein sow ration, Simms advises. Research indicates that excessive energy consumption in early pregnancy may disrupt litter development.
HogHealth
Vol. 6, No. 5