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Articles from 2003 In April


First COOL Hearing Set

The first congressional field hearing on the potential impact of the country-of-origin labeling (COOL) law will be 10 a.m., April 22 in the Mills Anderson Justice Center Auditorium at Missouri Southern State College, Joplin, MO.

Sen. Jim Talent (R-MO), chairman of the Senate Agriculture Committee's Subcommittee on Marketing, Inspection and Promotion, is holding the hearing.

Supporters and opponents will be given an opportunity to testify at the hearing, says Talent. "Our farmers and ranchers need more information on COOL and they need it as quickly as possible," he stresses.

The Agriculture Department has agreed to hold a dozen public meetings on this issue.

Monitoring Immunity Through Diagnostics

Diagnostic assays or tests are tools used by producers and veterinarians to assess the disease and immune status of pigs.

Depending on the specific diagnostic assay, laboratory tests detect antibodies or proteins that are produced in large quantities by the pig in an immune response to an infection or the presence of an infectious agent.

Immunity is essentially the pig's resistance to infection. Diagnostic assays do not measure immunity. Rather, they look for evidence of disease exposure in response to vaccination, antibodies or infectious agents.

In terms of immunity, the underlying assumption is that prior infection or vaccination has stimulated an immune response that will provide some level of protection from disease symptoms in the future.

For these reasons, diagnostic tests are direct measures of exposure or vaccination, and indirect measures of immunity.

Population Measures of Immunity

Population testing provides a direct measure of the disease exposure pattern (or vaccination coverage) in a herd and an indirect measure of the herd's level of immunity. Population sampling over time provides a picture of the dynamics of infection in a herd and the basis for making sound management decisions regarding prevention and control of disease.

Sampling the same pigs over time, or taking samples from pigs of different ages within a production system, can provide useful information on the dynamic interaction between infection and immunity within the herd.

Understanding the rate at which a disease changes in a herd can help strategically plan the timing of therapeutic interventions, such as vaccination or medication.

For example, repeated samples can be used to determine when the levels of maternal antibodies in young pigs have declined to the point that they will no longer interfere with the pigs' immune response to vaccination.

Tests Not Perfect

While the use of diagnostic assays is helpful in understanding and identifying the disease exposure or vaccination success in a herd, the interpretation of test results can sometimes be perplexing.

The major source of confusion in test interpretation is the false belief that a diagnostic test is perfect. In fact, every test has some inherent level of error.

This just means that, like every other tool in your toolbox, you need to be aware of the limitations and appropriate applications of diagnostic tests. Even if the level of test error is low, it will inevitably occur, and some day an animal you expect to be negative will test positive, or vice versa. Understanding how the tests work can eliminate some of this confusion.

Understanding the Tests

Diagnostic assays either measure the immune response induced by infection or detect the pathogen itself. Most common diagnostic assays are based on detection of antibodies specific to the pathogen. Typically, serum is used as the sample, although thoracic fluid and colostrum are also used.

Antibody detection assays have distinct advantages in detection of a pathogen. The sample (usually blood) is easy to collect, handle, and store; antibodies are abundant in blood and can usually be detected for a long time after infection. With most diseases, antibodies are detectable long after the pathogen is not.

The pathogen may be detected by isolation (growing it in the laboratory), staining and visualization by microscopy. Recently, highly sensitive polymerase chain reaction- (PCR) based assays have become available. The assays differ from earlier tests in that they detect the genetic material of the pathogen, are generally able to detect low numbers of the pathogen, and are not limited by the requirement to grow the agent.

Regardless of the approach — antibody detection or pathogen detection — it is important to know the limitations of each assay and care must be taken to not over-interpret results.

Antibody Detection (Serology)

Serological assays are the most common diagnostic tool used in swine population medicine. When a pig is infected with a pathogen, the immune system responds to the invasion by activating specific immune cells and producing antibodies. Serology is based on antibodies detected in the bloodstream.

Many different antibodies are produced during an infection. Some are highly effective against the infectious organism; others are not. Therefore, the presence of antibodies indicates exposure to an organism, not necessarily protection against disease.

At best, diagnostic assays provide indirect evidence of prior exposure to an organism. Time between exposure to a pathogen and detectable levels of antibodies depends on the pathogen, the assay, and the ability of the immune system to respond.

For example, an organism like Mycoplasmal pneumonia, which is in the airway of the pig and not in close contact with the immune system, may take weeks to months to produce a measurable antibody response.

In contrast, swine influenza virus can induce the production of antibodies as quickly as five days after exposure.

Antibodies induced by vaccination are usually measurable within 10-14 days.

Single serum samples are a poor measure of herd health status. Sequential sampling, including samples collected several weeks apart, provides information on time of exposure to a pathogen and the level of disease within a herd. With a few exceptions, serological assays can't differentiate vaccination from infection.

An example of “differentiable” vaccine is the pseudorabies (PRV) vaccines developed in the 1980s and 1990s. The fact that antibodies against these vaccines could be differentiated from infection with wild-type virus greatly facilitated PRV eradication.

Assays Detect Pathogens

Antibodies often linger after the disease is gone. Antibody detection isn't solid proof that the pathogen producing the antibodies is linked to the latest disease problem.

In contrast, detection of a pathogen along with clinical disease is strong proof of its involvement.

Several different approaches for pathogen detection are available:

  • Fluorescent antibody and immunohistochemistry (IHC) combine immunology and pathology to detect pathogenic microoganisms in tissues. Most disease changes in tissues aren't unique to specific infectious agents.

    However, pathologists can combine microscopic examination with the use of antibodies to confirm the presence of specific pathogens. In these procedures, the antibody is attached to the infectious agent, then the antibody is detected by reacting it with a fluorescent dye or other color-coded tag.

    These assays are extremely useful because they are able to confirm the association of the pathogen within the diseased tissues — strong evidence that the pathogen caused the disease.

  • Polymerase chain reaction (PCR) has revolutionized our ability to directly detect pathogens. PCR assays detect the genetic material (DNA or RNA) of a pathogen. Unlike isolation/identification tests, PCR can detect an organism whether it is infectious or dead. By itself, PCR is merely a procedure to replicate nucleic acid. The entire process of extracting the genetic material, replicating the nucleic acid, and detecting the PCR product makes it a diagnostic assay.

    PCR-based assays have been rapidly adapted to the detection of animal health pathogens. This is an area of very active research and refinement.

    Currently, PCR can be used as a qualitative (Yes/No) assay for the presence of an organism, or as a quantitative assay for measuring the number of organisms present. Two of the more common assay formats are “nested” PCR and real-time PCR.

    Discuss strengths and weakness of PCR assays with your veterinarian or laboratory diagnostician.

    As with all tests, PCR-based assays aren't perfect. Both false negative and false positive results occur. In addition, unlike serology, PCR-based assays are highly “sample-dependent.” Different samples from the same animal can give very different results.

    For example, a serum sample from a porcine reproductive and respiratory syndrome (PRRS) virus-infected boar may be PCR negative, while a semen sample from the same animal is positive. This occurs because the infectious agent targeted by a PCR-based assay isn't uniformly distributed throughout the body. For that reason, understanding the biology of the infectious agent is extremely important.

  • Restriction fragment length polymorphism (RFLP) is an assay sometimes used to compare the genetic makeup of a pathogen. Its most common use in swine health has been to compare PRRS viruses in epidemiological (presence of disease in a population) studies. The assay is based on the use of several enzymes that cut the viral genome at very specific genetic sequences.

    In PRRS virus, the pattern of fragments gives a three-numbered result, 2-5-2, for example. Interpretation of RFLP results assumes that viruses with similar fragment patterns are genetically similar. However, no association has been shown between specific PRRS virus RFLP patterns and the severity of clinical disease. To a large degree, the use of RFLP is being replaced by genetic sequencing.

  • Genetic sequencing produces the genetic code of a pathogen for a specific segment of its genetic material. At present, sequencing is used primarily with viruses and is available through most diagnostic laboratories. When used with computer “free-ware” on the Internet, the genetic makeup of different virus isolates can be compared and/or genetic changes in isolates from a herd can be tracked over time.

    But, sequencing has limitations, too. For most viruses, the exact genetic sequence responsible for virulence is unknown. Also, only a small portion of the virus' genetic material is sequenced and potentially important differences are not identified.

    Sequencing can be helpful in tracking viral changes on an individual farm over time. But until the clinical significance of the genetic code is better understood, interpretation of sequences and application sequence results to intervention strategies will be problematic.



Five Steps to Monitoring Herd Immunity

Designing a plan to monitor herd immunity has never been easy. But it has become more complex as herds get larger and more highly stratified.

Designing a monitoring plan involves working through specific steps:

  1. Have a specific purpose for monitoring

    The purpose may be to test for porcine reproductive and respiratory syndrome- (PRRS) induced disease by monitoring sow herd immunity, or to determine when to vaccinate young pigs by monitoring interfering maternal antibody levels. Whatever the purpose, you should be able to state it clearly, in a single, short sentence.

  2. Tailor the sampling plan to your purpose

    In general, this involves determining how many animals will be tested, how frequently samples will be collected, and which test (s) will be run. The issues of sample number and sampling frequency are complex. A discussion of these issues in the 2003 PRRS Compendium (to be released by the National Pork Board in June 2003) may be helpful.

  3. Be prepared to interpret the results

    Understand how the test works and what it measures. Some degree of variation in test results is expected, regardless of the laboratory. Establish a relationship with laboratory personnel and use their insights.

  4. Be prepared to respond to the results

    Because bad things can happen to good people, you should have an action plan in place before you submit the samples.

  5. Put a pencil to it

    Can the expense of monitoring be justified? Specifically, are the losses that will be avoided greater than the expense of monitoring? If the answer is “no”, then re-think your approach.


In Search of Disease-Resistant Pigs

Raising pigs that are healthy and disease free is a goal of every pork producer. Biosecure facilities help meet this goal, yet enteric and respiratory diseases persist.

Porcine reproductive and respiratory syndrome (PRRS), the associated porcine respiratory disease complex (PRDC), and enteric diseases continue to cause major economic losses worldwide. Can the genetic components of immunity and disease resistance help pork producers prevent these diseases and cut their losses?

Mapping Pig Genes

Pig genetic maps have been developed internationally (see www.genome.iastate.edu/maps/pigbase.html). The major mapping goal over the last decade has been to identify pigs with genetic alleles (alternative forms of a gene) that result in better pork meat quality, growth and improved reproductive traits.

Molecular genetic tests have been developed, and are now used routinely, for selecting pigs with improved traits. The estrogen receptor (ESR) alleles and the porcine stress syndrome (RYR1) are examples. Yet, for disease work, there has been limited progress.

Mapping Bacterial Diarrhea Resistance

Historical precedence says identification of disease-resistant pigs should be possible. Pigs that are fully resistant to bacteria-induced diarrhea (Escherichia coli) were identified as early as 1978; their resistance was due to a total lack of expression of the intestinal E. coli K88 receptor. Pigs without this receptor do not bind the bacteria as it passes through their intestine; thus, they are completely resistant to E. coli K88 infection.

However, the genetic test for identifying these resistant pigs was very difficult. They could be identified either by their ability to live through an infectious episode or by a bacterial binding test with pieces of their intestines after death. Lack of adherence to intestinal tissues resulted in the identification of the K88 adhesin or the genetic locus, K88.

Despite mapping studies and use of modern genomic tools, scientists have only localized this K88 gene to a general area on swine chromosome 13 (SSC13). To date, there is no publicly available, quick molecular test for blood cell DNA to identify K88 resistant pigs.

Resistance to another bacterial infection, also associated with presence or absence of an intestinal receptor, was the E. coli F18 receptor. Molecular research showed that this receptor was associated with alleles of the FUT1 gene on chromosome 6 (SSC6).

In 1999, Polish researchers developed a molecular test for FUT1 alleles and demonstrated that allele inheritance was associated with resistance to postweaning diarrhea due to E. coli F18 infections. Because there is a molecular test, breeding companies do offer E. coli F18-resistant breeding stock.

Genetic Mapping of Disease Immunity

Direct mapping approaches have been used to define genetic markers associated with immunity and disease resistance. Iowa State University researchers proved that different vaccine responses could be attributed to pig genetics.

Work at our Immunology and Disease Resistance Lab showed preliminary data for the genetic basis of resistance to foodborne parasite infections, Trichinella spiralis and Toxoplasma gondii.

German researchers are attempting to map genes associated with pseudorabies virus resistance. They have also targeted differences in susceptibility/resistance against the parasite, Sarcocystis miescheriana, in the European Pietrain and the Chinese Meishan pig breeds.

Case Study: Salmonella Resistance

Recent studies in England, on mapping resistance and susceptibility genes for salmonellosis, illustrate the difficulty of most infectious disease mapping studies. The team began by identifying salmonella-resistant and salmonella-susceptible breeding stock, then bred them to develop a reference family. All progeny were challenged with a defined dose of salmonella bacteria.

A large amount of data (phenotypes) on pig immunity to infection, including serum and blood cell activity and tissue bacterial burden, was collected. Additionally, genomic mapping information (genotypes) on each pig still has to be generated.

These studies suggested a role for several phenotypic markers in resistance to salmonellosis, including blood neutrophil function and cell proliferation. Much more data is needed to identify the exact genetic alleles encoding resistance.

Indeed, when some pigs bred to be resistant turned out to be relatively susceptible, the potential complexity of genetic inheritance of resistance was revealed. Salmonellosis, like most infectious diseases, will likely require favorable alleles at several genes to generate substantial disease resistance.

Key Questions Remain

Still very much in its early stages, research to date has raised serious questions that must be answered as targets for genetic resistance to infectious disease are established. For example:

  • Should research focus on a single or multiple disease agents?

  • Is there data indicating that disease resistance is heritable?

  • What disease responses (phenotypes) need to be targeted for best resistance — mortality? morbidity? carrier status? shedding capacity? sow transmission? boar transmission?

  • How much genotypic data is needed?

  • Would identifying highly susceptible animals be useful for targeted drug or vaccination treatments?

  • Would selection for faster recovery from disease be an advantage?

  • How will production traits be affected by selection for disease resistance?



Alternate Approaches

Can pigs with improved immunity be identified? The above questions outline several issues that need to be addressed for genetic studies of infectious disease to advance.

Is there an alternate approach? For PRDC, several infectious agents contribute to this disease complex — PRRS virus and viral and/or bacterial infections. With so many infectious organisms there must be numerous receptors and genes that would encode resistance. Thus, different approaches are required. The genetic questions then become:

  • Can pigs that resist respiratory infections be identified?

  • Could pigs with improved immune responses to infections be identified and shown to be genetically more resistant to respiratory infections?

  • Is it possible that pigs that make higher levels of the anti-viral cytokine, interferon-gamma (IFNg), would be genetically more resistant to PRDC?


Canadian researchers have developed lines of pigs selected for high/low levels of a suite of immune traits: antibody production and cell-mediated immune responses. Their high-responder pigs did develop higher vaccine responses, grew faster, and had lower disease scores following infection with mycoplasma. The exception, however, was their arthritis scores were greater in the high line and likely due to differences in cytokine production between the selected lines. These pigs have not been directly tested for resistance to a wide range of diseases; this is important information to know.

Innate vs. Specific Immunity

The mammalian immune system is complex, as has been noted in the other articles in this issue. It is important to understand the difference between immediate, innate immune response and the slower, cell-mediated, specific immune response when a disease challenge occurs.

The innate immune system acts immediately in response to infectious insults (see Figure 1). It is dependent on immune factors, termed cytokines, and immune cells, including macrophages, neutrophils and natural killer (NK) cells. While innate immunity may be quick, it is not specific and may not be potent enough to control most infectious organisms.

To effectively battle viral and bacterial infections, animals require cell-mediated immune responses. Animals need “B” cells to make antibodies to bind up viruses or bacteria. “T” cells are needed to kill infected cells or to produce the immune cytokines to activate and enhance immune responses. “T” cells are also essential for long-term memory, such as the memory response to infection after vaccination.

Molecular Gene Expression Data

How can an animal's immune system be quantitated? Like your personal physician, scientists can now test swine blood cell numbers and subsets. As was found for salmonella resistance, some immune cell activities can be associated with resistance.

Indeed, molecular tests can be used to compare how active immune cells are. Molecular “gene expression patterns” can be generated and quantities of different immune factors compared for pigs at different ages or times after infections.

The Immunology and Disease Resistance Lab has worked with researchers at the Beltsville Human Nutrition Center to develop molecular gene expression patterns to help identify genes controlling numerous immune, disease and vaccine responses. In the future, even broader gene expression systems, referred to as microarrays, will enable scientists to test thousands of genes for simultaneous analyses.

Finding the Pigs

We must ask ourselves — can pigs with enhanced innate immunity be identified? Will they be healthier?

Previously, our lab and others had shown that newborn pigs have poorly developed immune systems. It takes several months for pigs to have an adult level of immune cytokines and cells. Using molecular assays, it is now possible to compare pigs at the same age and potentially identify those with higher levels of innate immune factors.

We might find pigs whose genetically determined level of innate immune response helps them to jump-start their infectious disease responses and/or quickly shift their responses to anti-viral, cell-mediated immune responses.

However, immunity needs to be controlled so that it does not overreact and cause pathology to take over. The “best” pigs, therefore, might be those that respond quickly to an infectious agent, prevent it from replicating, and then stop their immune reaction.

Alternatives to Antibiotics

Continued consumer demands for decreased antibiotic usage in food animals increases the need for alternative genetic disease resistance approaches to be developed. Identifying pigs with desirable immune responses should enable producers to decrease dependence on drugs.

A major issue for scientists now is to identify exactly which genetic alleles result in “better immunity.” As new, serious disease organisms are identified, aggressive efforts to identify pig genes that control resistance, and stimulate protective immunity will be required.

Alternately, genomic research efforts can be targeted at the infectious organisms (microbes). Thus, microbial genomic efforts should lead to disease-specific diagnostics, and high throughput screening assays for cost-effective, targeted drug testing.

Vaccine-Ready Pigs

Vaccinations help pigs respond more quickly to known infectious agents, thus preventing disease-related losses. Although it may be impossible to select pigs with resistance to a wide range of diseases, it may be possible to identify pigs that have better innate immune system or better anti-viral cell-mediated immune response levels. In other words, we may find pigs that are genetically more responsive to anti-viral vaccines — that is, “vaccine ready.”

Disease-Resistant Stock

Will we select/produce disease-resistant stock for specific tasks? The high expense of disease resistance studies means that producers and regulators have to determine which are the highest priority diseases to address with their limited resources.

Should we select for respiratory disease resistance, or is food safety, and salmonella resistance, more important?

As national bio-safety and bio-defense issues are defined, our priorities may be substantially altered. Limited research funds and facilities necessitate that we choose our priorities wisely. Tough questions remain.

If foot and mouth disease- (FMD) resistant pigs were available, would we use them to stock areas close to active infection or to restock previously infected farms after depopulation and decontamination?

The Potential is Great

Studies targeting the genetics of disease resistance are essential for improved pig health and pork quality. As scientists identify breeding stock that is healthier, by virtue of its innate disease-resistant properties, they will also help decrease our dependence on antibiotics.

Studies which incorporate specific production parameters and nutritional concerns in their design will help producers select the breeding stock which possesses the necessary resistance characteristics: higher respiratory disease resistance for confined pigs, higher parasite resistance for pasture pigs. There is an enormous benefit that will come from such studies.

There is great potential for genetic studies of disease resistance to reveal novel host effector mechanisms that will lead to new biotherapeutics and cost-effective approaches for disease control and growth optimization.

Figure 1. Cells Regulating Immune Responses

All immune cells in the blood, the hematopoietic cells, are derived from bone marrow stem cells. These hematopoietic stem cells give rise to two main lineages: one for lymphoid cells (lymphoid progenitor) and one for myeloid cells (myeloid progenitor). The common lymphoid progenitor will differentiate into either T cells or B cells depending on the tissue to which it travels (homes). In mammals, T cells develop in the thymus while B cells develop in the fetal liver and bone marrow. Pigs use special areas of their intestines, termed the Peyer's patches, for B cell maturation. B cells produce the antibodies so crucial to immune and vaccine responses. To produce antibodies, B cells must become antibody-forming cells (AFC), or plasma cells. Innate immune responses are carried out by natural killer (NK) cells that also derive from the common lymphoid progenitor cell. The myeloid cells differentiate into the committed cells on the left. The platelets help blood to clot and thus heal injured tissue. Three other myeloid-derived cell types, the monocyte, macrophage and dendritic cells are critical in helping the immune system recognize what is foreign, and thus stimulating specific immune system responses. Finally, the “granulocytes,” a term used for eosinophils, neutrophils and basophils, have specialized functions, e.g., neutrophils will use antibodies to trap and kill invading bacteria.

Adapted from http://www.ed.sc.edu:85/book/immunol-sta.htm. Courtesy of Department of Pathology & Microbiology, University of South Carolina School of Medicine, Columbia, SC

Fig 2. Making Road Maps of Genes

Scientists worldwide are learning more about the genetic makeup of pigs. The eventual payoff could mean less expensive meat products, lower levels of fat, higher milk production and improved health and resistance to disease. Genome mapping could take the guesswork out of breeding the most productive animals.

The genome maps, comprised of “genetic markers,” are 95% covered for the pig. These markers, equivalent to route markers on a road map, give scientists an idea of where they are in the pig genome and what they are near when attempting to find genes that are linked to important traits.

The goal is to eventually enable scientists to pinpoint the exact location of every gene in an animal. The genome maps will someday allow the livestock industry to produce animals that are genetically resistant to certain diseases or parasites.

  1. Within each cell nucleus are chromosomes grouped in pairs (one inherited from the father, one from the mother). Pigs have 19 pairs of chromosomes.

  2. Chromosomes consist of tightly coiled strands of DNA.

  3. Within the DNA are nucleotide bases commonly abbreviated by the letters A, T, C and G, which stand for adenine, thymine, cystosine, and guanine. Adenine always pairs with thymine, while cystosine always attaches to guanine. There are approximately 3 billion base pairs of nucleotines in a single cell of a pig.

  4. The small section of the chromosome in the box shown here, for example, could contribute some information toward determining an animal's blood groups or interferon genes. It is this unique sequence of nucleotide bases and their lengths that spell out genetic instructions.

  5. For more complex traits, such as milk production, disease resistance, antibody production, or reproductive capacity, the information would be contained in several genes on many different chromosomes.

  6. Scientists use different methods to break up the long strands of DNA and the nucleotide sequences on them. They then designate “markers” or reference points located on or near genes.

  7. This is the map of swine chromosome 6 from the USDA funded swine genome mapping site: http//www.genome.iastate.edu/pig.html. The RYR1 gene locus on chromosome 6 in the pig, for example, encodes the “stress” gene syndrome. The RYR1 position is also known as the Ryanodine receptor, the calcium release channel, or the Halothane (HAL) locus. Next is TGFB1 (transforming growth factor beta 1), which is an immune system regulatory factor. Further down chromosome 6 is the EAH (erythrocyte antigen H) gene for the blood group H antigen.



Adapted from U.S. Department of Agriculture Agricultural Research Service display.

Report Brings Cautious Optimism

The USDA Hogs and Pigs report for March 1, 2003, came in very close to the average of the trade estimates.

The market herd was a little smaller than our estimate. However, the breeding herd estimate by USDA was very consistent with gilt and sow slaughter indications.

Slaughter for the first quarter of 2003 was over 2% above our expectations based on the December report. USDA revised the market inventories up for both the September and December reports.

The report's 4% decline in the breeding herd and the 2% decline in the market inventories are progress in the right direction. Still, the decline is not enough to push hog prices above breakeven for the average producer for many months during 2003.

Demand at the consumer level did show a little growth last year. Hopefully this growth will continue through 2003.

Farrow, Slaughter Projections

The number of sows farrowing in the December-to-February period was down nearly 2.5% rather than the 1% indicated in the December report. This is more consistent with the breeding herd being down 3% on Dec. 1.

Farrowing intentions for both periods March-May and June-August, 2003 are down nearly 3.5%. Even though the breeding herd on March 1 was down nearly 4.5%, a farrowing number down nearly 1% less than the reduction in the breeding herd is not only possible, it is likely due to productivity growth.

Table 1. Market Hogs on Farms March 1, U.S.
Weight Category 2003 as % of 2002
Under 60 lb. 98
60 - 119 lb. 98
120 - 179 lb. 98
180 lb. and over 101


Farrowing intentions for both the second and third quarter this year show the potential for about a 3.5% decline from 2002. At this time, because of anticipated productivity growth, we doubt slaughter for the fourth quarter of 2003 and the first quarter of 2004 will be down this much due to productivity growth.

Slaughter during March, up about 1.7%, is consistent with the 180 lb. and heavier market inventories which were up 1.2% from last year. The heavier weight market inventories indicate slaughter for April-June will be down about 2.5% from 2002. The probabilities are extremely high that the April-June slaughter in 2003 will be the smallest quarterly slaughter for this year. The lighter weight market inventories suggest July-September slaughter will be down about 2% from last year.

Other Meat Supplies

USDA is estimating beef supplies will be down nearly 3% in 2003 compared to 2002.

USDA is forecasting broiler production to be down in the first three quarters of 2003, but up sharply in the fourth quarter, compared to last year.

Cold storage stocks remain high and will continue to put negative pressure on prices.

Hopefully, 2003 will be the 13th consecutive year of pork export growth. Pork exports in 2002 were 6.6 times larger than in 1990. Any growth in exports will be positive to cash hog prices.

Ongoing Structural Change

The March 1 report continues to reflect the change in the structure of the hog industry with the quite modest drop in market inventories and pig crops following 17 consecutive months of losses to the average hog producer based on the Iowa data.

Our estimates of prices and slaughter by quarter for the next year are in Table 2. We believe the $5-8 increase in the second quarter price is not only possible, but also likely. Hopefully, all of the negative price factors in the second quarter of 2002 will not occur again this year.

Table 2. Estimated Commercial Hog Slaughter by Quarter and Live Hog Prices 1998-2003
Year Period Commercial Slaughter, Million Head Terminal Market Barrows and Gilts/Cwt. 51-52% Lean Hogs/Cwt.
1998 1 24.776 $34.74
2 23.628 39.42
3 25.039 33.62
4 27.586 19.49
Year 101.029 31.82
1999 1 25.579 $26.55 $28.83
2 24.288 33.06 35.18
3 24.953 32.78 35.70
4 26.724 33.88 36.29
Year 101.544 31.57 34.01
2000 1 25.039 $39.11 $41.14
2 23.125 47.99 50.43
3 24.097 44.19 46.44
4 25.715 38.33 40.78
Year 97.976 42.41 44.70
2001 1 24.578 $40.77 $42.83
2 23.280 50.21 52.05
3 23.635 48.04 51.05
4 26.469 34.97 37.30
Year 97.962 43.50 45.81
2002 1 24.148 $37.23 $39.43
2 24.280 32.77 34.99
3 25.120 31.09 33.86
4 26.715 28.52 31.34
Year 100.263 32.40 34.91
2003 1 (part. est.) 24.600 $33.85+/- $36.35+/-
2 (projected) 23.675 38 - 41 40 - 43
3 (projected) 24.615 36 - 39 38 - 41
4 (projected) 25.915 34 - 37 36 - 39
Year (projected) 98.805 35 - 38 37 - 40
2004 1 (projected) 24.000 $36 - 39 $38 - 41

Prevention vs. Treatment of Disease

Our mothers and grandmothers knew the value of disease prevention after years of respiratory disease and diarrhea in children.

Likewise, the sharpest pork producers challenge their veterinarians to provide appropriate disease prevention plans and monitor their results.

Disease prevention or control begins with understanding what diseases and risks are present and extends to implementation and monitoring. Careful review of sources and health status lays the groundwork for the future.

Following a complete review of health status, control measures are necessary to limit the negative impact of known pathogens. Change must be deliberate and controlled to adequately monitor results. Performance of the growing pig is the ultimate indicator.

Source Screening is Critical

Whether selecting a gilt supplier for a breeding herd, or weaned pigs for the grow-finish system, understanding your source is critical. The simple “standard” disease-free checklist is not sufficient to make plans.

Questions for the gilt supplier need to include health status for diseases like pseudorabies, porcine reproductive and respiratory syndrome (PRRS), atrophic rhinitis, Actinobacillus pleuropneumonia, Transmissible gastroenteritis, mange and swine dysentery.

Review with your veterinarian how the source manages Streptococcus suis, Haemophilus parasuis, swine influenza virus (SIV), Mycoplasmal pneumonia and others.

PRRS has taught us that sourcing questions begin at the conception of the source animal. Development of the gilt prior to birth may impact her entire life in terms of disease status and immune development. History tells us we want fetal development of PRRS-negative gilts.

A PRRS-positive commercial sow herd needs to expose breeding gilts to their own strain of PRRS virus; however, they need a PRRS-negative source and they need to expose the replacement gilt to PRRS virus prior to 2 months of age.

The supplier of weaned pigs to the grow-finish population also must openly provide herd vaccination history, weaning age history, current health monitoring protocols and contact information for health changes.

First-time pig buyers should ask the source herd questions regarding farrowing crate number in relation to herd population, their gilt entry protocols, short-term and long-term health goals, and even plans in the event of a health break at either location (Table 1).

Successful long-term relationships depend on shared goals for the health of the entire system. Biosecurity is only part of this plan. Sow herd disease management and grow-finish health plans complement each other.

Breeding Herd

Incoming gilts and young-parity females entering the breeding herd are being recognized as major sources of diseased piglets. These animals pose an immediate challenge to sow herd stability and a greater challenge to the grow-finish population.

Few systems are large enough to segregate gilts and first-parity females onto separate sow sites. Systems with this edge believe grow-finish has the most to gain from segregation of piglets reared on those young females.

All sow herds must keep a consistent flow of replacements. Usually, weekly gilt entry leads to a modified, continuous-flow gilt development where multiple-aged gilts are raised near or even in the same finisher barn.

Maternal colostrum protection, weaning age, early vaccinations, and disease exposure help to create immunity in gilts less than 50 days old.

PRRS-positive commercial herds may take gilts from a known naïve PRRS source and expose them to PRRS to prepare them for entry. Immunologists tell us that cell-mediated protection requires four months without re-infection for complete PRRS virus control. An early exposed gilt could still have a changed PRRS virus with her sisters and bring new PRRS strains into the breeding herd.

Table 1. Questions for the New Weaned Pig Source
1. Current disease status of sow herd and sow herd source
2. Current monitoring program
3. Number of farrowing crates and sow herd inventory
4. Genetics of both male and female
5. Grow-finish closeout history
6. Weekly piglet production for last 26 weeks
7. Current sow herd vaccination program
8. Current piglet medication program
9. Source information for health break
10. Short-term and long-term health goals


Controlling PRRS

PRRS control measures deserve attention. Herds in the acute stages of a break have seen some benefit from killed virus vaccination to reduce shedding and shorten the activity period. This is likely valuable only if PRRS virus does not continue to evolve and mutate in the herd.

Other herds have stabilized using positive nursery pigs or even serum from actively positive groups to expose entire populations. The same rules must apply to be successful — exposure prior to 2 months of age, followed by four months of inactivity.

Immunologists also caution, don't create large numbers of PRRS virus populations through uncontrolled activity. At our clinic, we have attempted to sequence virus and serologically monitor every gilt group monthly to gain confidence regarding early exposure.

Eliminating PRRS

The elimination of the PRRS virus is a common topic of discussion now that many gilt suppliers have established PRRS-free herds. The risk of naïve entry poses another problem for the commercial producer.

Our clinic has helped many producers evaluate the cost benefit of off-site breeding with entry of PRRS-naïve gilts in late gestation (Table 2). Failures still occur as herds don't fully stabilize for PRRS and virus breaks back. Even so, the benefits of improved productivity and grow-finish performance make this alternative very attractive, even if the sow herd is only PRRS free for 12-16 months.

Other Gilt Programs

As bad as PRRS is, it's not the only preventable disease we manage in swine production. Gilt development programs must also include the more easily controlled organisms such as mycoplasma, SIV and ileitis. In later development, pre-breeding gilts also require parvovirus, leptospira (five strains), and erysipelas boosters with herd maintenance vaccination protocols for disease prevention.

Pre-breeding vaccines are often better if they follow a controlled feedback program in herds where segregated production may lead to naïve breeding stock. Feedback must be controlled due to the risk of creating uncontrolled PRRS viremia (presence of virus in the blood).

Table 2. PRRS Elimination Project (Herd Roll)
Current Production Post Elimination
Sow Herd Impact Analysis
Sow Herd Size 2,400 2,400
Litters/Sow/Yr 2.38 2.45
Pigs Born Alive/Sow 10.21 11
Preweaning Mortality 12% 9%
Pigs Weaned/Sow 8.98 10.01
Weaning Weight 10.5 10.5
Number Weaned 51,321 58,859
Weaned Pig Cost $33.82 $29.49
Annual Sow Farm Costs $1,735,682.23 $1,809,382.23 (production plus herd roll cost)
Herd Roll Cost
Breeding Project Cost (10 months)
Gilt Housing cost/gilt $30.00
Additional Breeding Costs/gilt $28.00
Additional Testing Costs/gilt $3.00
Additional Transport and Labor Costs/gilt $6.00
Total Herd Roll Cost $73,700.00*
Grow-Finish Impact Analysis
Nursery Medication Cost (all) $2.65 $1.65
Nursery Mortality 3% 2%
Finisher Medication Cost (all) $3.50 $2.50
Finisher Mortality 5% 3%
ADG (wean-to-finish) 1.45 1.55
Feed Effic (wean-to-finish) 3.00 2.75
Feed Cost/lb Gain (no meds) $0.185 $0.185
Slaughter Weight 265 265
Grow-Finish Space Cost $17.50 $17.50
Transport $2.00 $2.00
Number Sold 47,215 55,916
Cost of Production $106.55 $100.22
Cost of Production (cwt) $40.21 $37.82
Difference in Production from Disease Elimination $354,007.99
*The total of $67/gilt for 10 months of gilts on a 2,400-sow farm with a selection rate built in = $73,700.


PRRS-naive herds can collect small amounts of mummified fetuses, sow manure, placenta and piglet manure every week and provide this material to gilts in late development. Feedback must be discussed in a whole herd health program context and must be done for a specific reason (Table 3).

We have stopped using cull sow exposure due to inability to verify or quantify PRRS shedding in those females.

Likewise, we have not attempted tonsil scrapings to create an exposure material. Whatever exposure method is used for PRRS, stick to the rules of immunology — exposure prior to 2 months of age and four-month recovery without reexposure.

In sum, disease prevention begins with the sow herd. Quarterly monitoring may be sufficient for commercial production. Continual evaluation of efficacy of prevention measures lies with the quality of the weaned pigs.

Sow herds require, as a minimum, routine vaccination for parvovirus, leptospira and erysipelas prior to breeding, and most need E. coli and clostridium vaccinations prior to farrowing. Many herds are weighing bi-annual SIV vaccination vs. pre-farrow flu vaccination. Again, weaned pig quality is the guide.

Autogenous vaccine products are being debated as organisms like SIV have changed. Commercial products will be the first choice for most for organisms like mycoplasma, SIV and erysipelas.

However, autogenously derived vaccines will likely be the choice for system-specific or herd-specific organisms like Haemophilus parasuis, Actinobacillus suis and possibly even E. coli and clostridium. Results should be measured and cost analysis instituted.

Growing Pig Population

Vaccination and herd health must be attended to regularly in both the sow herd and the growing pig population. Producers who have segregated themselves from the sow herd need to begin each new group with current information. The previous four group closeouts and the last four weeks of weaning are a good place to start.

Piglet receiving is the best chance to make plans for health and disease prevention. Systems with multiple sources have an even greater challenge to achieve this knowledge level.

Maternal Immunity Decline

Sow herd maternal immunity will decline at different rates for different disease organisms. It may also differ dramatically for organisms given as part of a pre-farrow vaccination program (i.e. SIV). Maternal immunity may be several weeks for SIV, but only days for Strep suis or Haemophilus parasuis.

Pulse dosing of feed or water-soluble antibiotics may be an effective method of preventing the over-growth of opportunistic bacterial organisms. Pulse dosing will help bridge the period from maternal protection to the piglets' immunity development.

Strategic placement of antibiotics also provides protection (from bacterial overgrowth) during periods of known exposure to viral organisms such as PRRS or SIV.

Monitoring of intervention strategies requires attention to details. Historical mortality and treatments are best broken down by week of entry (Figure 1). This allows production plans to anticipate problem areas. Seasonal variation is also necessary data.

Disease Intervention

A disease intervention strategy requires evaluation of multiple factors. The ileitis example (Table 4) illustrates how weekly mortality charts helped identify the problem graphically, and then cost-benefit analysis evaluated the solution economically.

Ileitis is an interesting disease model in that we have both a vaccine and feed-grade antibiotics for strategic placement. Economics and pig performance must both weigh in to monitor the results of this decision.

Oral vaccine technology has certainly made the grow-finish management of disease easier. Salmonella, ileitis and erysipelas can all be prevented today with appropriate use of these products.

Seasonal use of erysipelas vaccine in late winter will provide summer protection, although an injectable booster of erysipelas in the finisher is often necessary in severe cases. Ileitis and salmonella protection both appear to be quite strong when properly administered.

Value of Weaning Age

Often overlooked is exact piglet weaning age and its contribution to quality and growth. Recently published research from Kansas State University (KSU) evaluates long-term growth performance in relation to age at weaning.

The KSU research cites two age group sets for weaning: 12 to 21 days and 15.5 to 21.5 days. Death loss dropped from 9.4% to 3.6% as weaning age increased in the first age group and went from 3.9% to 2.5% in the second study. Piglet grow-finish throughput improved nearly 4 lb. for each day weaning age increased.

Furthermore, the grow-finish system achieved an increase in profitability of nearly 90¢ for each day added to weaning age.

Sow herds commonly resist increasing weaning age due to the illusion that weaning younger improves throughput. Weekly breeding variation further impacts the age variation among weaning groups.

In actuality, weaning later adds value to the sow unit two-fold: sow fertility is improved and subsequent total born number increases. There is also a dramatic reduction in wean-to-service interval in young-parity females. The cost to the sow unit may be the addition of farrowing crate space, about $2,000/crate for controlled environment, high-quality construction.

Don't Underestimate Management

Finally, management is still a major factor in disease prevention of the growing pig. Sow herd systems are producing PRRS-postive and mycoplasma-positive pigs into growing pig groups with nearly identical weaned pig quality and totally opposite grow-finish performance.

Receiving protocols must cover ventilation, feed budgets, antibiotics and vaccination plans. Numerous protocols have been established for “starting” weaned pigs. Producers must use proper management plans and then monitor pig quality. Daily stockmanship requires multiple feedings at delivery. Failure to do so can widen inequality among penmates.

Table 4. Ileitis Intervention Cost
Current Program Intervention Program
Population size, head 1,000 head 1,000 head
Mortality, % 12.83% 5.07%
Cost/dead pig, by age $70.00 $60.00
Mortality cost $8,981.00 $3,042.00
Med cost/pig (all) $2.50 $3.50
Total med cost $2,500.00 $3,500.00
Intervention savings (no credit for growth rate): $4,939.00*
*The savings reflect the difference in mortality costs and subtracting $1,000 for the higher medication costs during intervention.


Early feed management can prevent starvation and weakness in the first weeks after weaning. Feed budget allocation can also prevent cost over-runs in this growth segment.

Some producers maintain excellent air quality, feed quality, feed budgets and treatment protocols, while others fall terribly behind in some or all of these management areas.

Disciplined, planned prevention programs, followed by continual performance monitoring, allow producers to repeatedly achieve high quality, healthy production.

Table 3. Feedback Protocol

To control TGE, enteroviruses, parvovirus, rotavirus and E. coli, collect pig feces. For control of parvovirus, piglet tissues from mummies should be harvested.

Collection Procedures
Retain viscera from one stillborn and one newly born weak pig per 10 head of gilts.
Collect all the mummies that are available that day.
Collect ½ cup of manure per gilt to be fed back.
Mix this material with equal parts of cold water.
Feed two cups per gilt.
Feed at least twice per week for two weeks.
Begin the feedback when the gilts are in the isolation/gilt developer.
Include all females 2-3 weeks pre-farrowing to boost colostrum protection.

PRRS Research Awards

Boehringer Ingelheim Vetmedica, Inc. awarded three, $25,000 research grants to develop practical methods for control of the virus that causes porcine reproductive and respiratory syndrome (PRRS). Winners are:

  • Darwin Reicks, DVM, Swine Vet Center, St. Peter, MN, “Timeline for Detection of PRRS in Semen by Polymerase Chain Reaction Testing and Sensitivity of Pooling Samples;”

  • Scott Dee, DVM, and Satoshi Otkake, DVM, both of the University of Minnesota, “Assessing the Risk of PRRS Virus Transmission by Transport Vehicles,” and

  • Jeff Zimmerman, DVM, Iowa State University, “Determination of the Infectious Dose for Transmission of PRRS Virus by Oral Exposure.”



An added $12,500 research award was presented to Robert Morrison, DVM, University of Minnesota, “Controlling PRRS: The Use of Geographic Information Systems to Determine Area-Based Prevalence and the Association between Proximity of Non-Linked Herds and Percent Homology in Pig Farms.”

National Officers Elected

The National Pork Producers Council (NPPC) installed a new officer lineup at Pork Industry Forum, March 6-8 in Dallas, TX.

New NPPC President is Jon Caspers, co-owner of Pleasant Valley Pork Corp., Swaledale, IA, a farrow-to-finish operation marketing 20,000 hogs annually.

Keith Berry of Greencastle, IN, is president-elect. Berry owns and operates a 125-sow, farrow-to-finish operation with his son. He also farms 1,500 acres of corn and soybeans.

Tyler, MN, pork producer Don Buhl is the new vice president. He owns Buhl's Ridge View Farm, Inc.

New members of the NPPC board of directors are: Charlie Arnot, Kansas City, MO; Bryan Black, Canal Winchester, OH, and Terry Holton, Shawnee Mission, KS.

Veterinarian Officers Named

The American Association of Swine Veterinarians unveiled a new slate of officers for 2003-2004 at their annual meeting in Orlando, FL, in early March.

New president is Rick Sibbel, DVM, Ankeny, IA, technical services manager at Schering-Plough Animal Health.

President-elect is John Waddell, DVM, who owns a private swine consulting business at Sutton, NE. Vice president is Tom Gillespie, DVM, owner of a swine veterinary practice in Rensselaer, IN.

Building Immunity is a Balancing Act

The ability of the pig to resist disease requires a well-developed immune system. Even with a “perfect” immune system, disease resistance will fluctuate in the herd depending on animal age, nutrition, stress and the level of pathogens.

When this resistance dips and/or the level of pathogens increases, a disease outbreak will occur in the herd.

There are three components to the pig's immune system: natural, innate and acquired immunity (see Figure 1 on page 7). This system is like a three-legged stool. All three have to be present and functioning to maintain disease resistance.

Natural Immunity

Natural immunity is the barrier comprised of skin, normal secretions (mucous, stomach acid, saliva, tears, urine, skin secretions); also, the presence of commensal or helpful microorganisms that compete against pathogens and a working respiratory tract (including turbinates in the nose).

There are also genetic and nutritional components to natural immunity. For example, some breeds of hogs lack a receptor in their digestive tract for Escherichia coli to stick to, making them resistant to this diarrheal disease.

Stress and dehydration can have a large effect on natural immunity by decreasing natural secretions and making the skin and the mucosal linings of the respiratory, digestive and reproductive tracts more prone to infection.

Innate and acquired immunity have a hand and glove relationship. Dependent on each other, they form a complex network of cells and tissues that interact to constantly conduct disease surveillance throughout the hog's digestive, respiratory and reproductive systems.

Innate Immunity

The innate immune system is the inbuilt or preexisting system that first responds to pathogen infection. It consists of:

  • White blood cells (neutrophils, eosinophils, monocytes, natural killer cells and macrophages),

  • Complement (a protein that can stick to a number of organisms), and

  • Special immune system hormones called cytokines (interferon, inflammatory mediators).



All play a key role in attracting immune cells to the site of infection and making all immune cells grow and mature.

The innate system looks for different kinds of pathogens using receptors that recognize shared parts of bacteria, fungi and viruses. This system is not specific to any one type of organism (a system called antigen specific) and doesn't “remember” previous exposures to an organism (no memory) (Figure 2).

The neutrophils and macrophages attack and kill many bacteria and fungi often with the help of complement.

The major innate defense against viruses is interferon, which are glycoproteins released by virus-infected cells. Interferon causes the infected cell to die and surrounding cells to be virus-resistant.

Macrophages and natural killer cells also destroy virally infected cells. A special kind of macrophage called an antigen-presenting cell (APC) ingests the pathogens and breaks them into small pieces called antigens. These cells also produce cytokines that activate cells from the acquired immune system.

Adjuvants in vaccines help the APC ingest the vaccine organisms and also help to produce more cytokines. Adjuvants are chemical and/or biological substances added to vaccines to make them work better. These APC “loaded up” with these specific antigens move to the lymph nodes where they interact with the acquired immune cells.

Acquired Immunity

The acquired immune system is activated during vaccination. Specific for each swine pathogen, it is enhanced by vaccines and will be “remembered” (memory) so the animal's resistance to disease will be increased (Figure 3). Depending on the pathogen, the animal is protected for months or years following disease exposure or vaccination (Figure 4).

There are two types of acquired immunity:

  • Cell-mediated immunity involves immune cells acting directly against pathogen-infected cells.

  • Humoral immunity involves specific immune proteins (antibodies) that are directed against pathogens. This system uses “T” cells, “B” cells, cytokines and antibody to provide this long-term protection (Figure 1). The T and B cells are specialized white blood cells responsible for acquired immunity. The T cells provide cell-mediated immunity. They get their name because they develop in the thymus, a specialized immune organ needed for T cell growth.



The T cells are divided into two groups — T helper and T cytotoxic cells. The T helper cells' major job when they “recognize” or see their specific antigen is:

  • To produce cytokines to help the other T and B cells grow and divide, and

  • To grow and divide themselves to produce more cells to fight future infections. The T cytotoxic cell (cytotoxic means “cell killer”) is a specialized T cell that is helped to grow and divide by the T helper, but whose job is to destroy pathogen- infected cells.



These antigen-specific cells find and destroy infected cells without hurting the cytotoxic T cells, leaving the cytotoxic T cells to kill more infected cells.

The B cells grow and divide with the aid of the T helper. Their job is to become antibody-producing factories. They produce specific antibodies against pathogens; some of these antibodies are produced and secreted into respiratory, reproductive and digestive tracts and some are secreted in milk.

Prior to farrowing, many antibodies are concentrated in the first milk as colostrum to be transferred to the piglet. Immune cells (mainly macrophages and some T cells) are also transferred in colostrum.

The antibody on the surface of the respiratory, reproductive and digestive tracts help protect the pig by sticking to the pathogens even before their cells get infected. The antibody in the bloodstream also provides specific protection, even if the animal gets infected.

The pig is born with billions of T and B cells. Each cell has an antigen that it specifically “recognizes.” However, the number of cells specific for any antigen is small (1 out of 10,000 cells).

To get a good acquired immune response, these T and B cells must recognize the antigen, and then be stimulated to grow multitudes of pathogen-specific cells.

The APC cells initially interact with the T cells. There is a dose effect. The more APC to interact with the T cells the better the response and “memory” of the response. The T helper cell is vital to activating this acquired response, interacting with the APC and then dividing and producing cytokines to make other T and B cells grow and mature.

Passive, Active Immunity

Acquired immunity can be further divided into passive and active immunity. Passive or maternal immunity comes from the sow and is transferred to the newborn pig through the colostrum (sow's first milk containing high levels of antibodies). Because the young piglet has an immature immune system, the immunity of 14- to 21-day-old piglets hinges on the passive immunity provided by colostrum.

Passive immunity provides short-term protection for piglets. Length of protection depends on the level of sow antibodies absorbed by the piglet, and how fast the antibodies are broken down over time. Half of the antibodies will be gone at 8-16 days of age; all antibodies are gone by 30-60 days.

Because this rate of disappearance varies by type of antibody and piglet, the length of disease protection from passive antibodies can also vary greatly.

For protection, the piglet's own immune system has to become “active” at a young age to produce cell-mediated immunity and antibodies in response to vaccines and pathogens.

Window of Susceptibility

There is a “window” of disease susceptibility when passive immunity wanes and before protective immunity is reached. Passive antibodies can actually interfere with this process, such as a young pig given a live virus vaccine for porcine reproductive and respiratory syndrome (PRRS). Passive antibodies prevent the virus from growing and inducing active piglet immunity.

Most vaccines administered to young piglets are killed bacterial vaccines that have adjuvants. These killed products have two advantages in stimulating active immunity, even in the presence of passive immunity. First, they don't have to grow to induce active immunity. Second, the adjuvants aid in the development of active immunity by stimulating the APC, and also by protecting the bacterial antigens from passive antibody.

Gilt Development

Developing the gilt and providing a good activation of the immune system is key for introduction into the sow herd. The gilt's immune system develops quickly, responds well to pathogen exposure and vaccination at 3-4 months of age.

Gilts need to be vaccinated against known herd pathogens. Since most vaccines are killed, bacterial vaccines, gilts need to receive the proper vaccination regime — a primary vaccination, then a few weeks later, a booster dose for a good, active immune response.

Exposure to cull sows before breeding also provides an opportunity for gilt exposure and development of an active immune response against herd pathogens. Sows, because of their prior vaccination and exposure history, can be given boosters semiannually to maintain active immune protection.

Immune Energy Function

A key point to understand is that activating the innate and acquired immune systems is an energy-dependent process. Just as there is a minimum amount of energy needed for normal maintenance of the pig's bodily functions, energy is used to mount an immune response.

A major reason for the development of high-health pig systems is to redirect this energy to growth and lean deposition. The goal of early weaning is to remove the piglet from the sow before passive immunity disappears, and the pigs become infected with pathogens from the sow that will activate the immune system and cause disease.

All-in, all-out management lessens pathogen spread between groups. Confinement housing reduces exposure to environmental pathogens (Figure 5).

Conventionally reared pigs weaned at 21-28 days and raised in continuous-flow, outside lots are exposed to pathogens from the sow, environment and other pigs. These pigs respond to pathogens, diverting energy from growth and lean and decreasing rate of gain and feed efficiency (Figure 6).

The major goal for immune system activation is to prevent disease, which greatly affects economic return caused by death loss, decreased feed efficiency and average daily gain (Figure 7).

Balancing Act

This is the balancing act that pork producers deal with. High-health pigs lack exposure and active immunity against common pathogens. This makes organisms like Streptococcus suis, Haemophilus parasuis and Mycoplasmal pneumonia troublesome in many herds, requiring animal vaccination for disease protection.

Vaccination activates the immune system to confer disease protection, but also causes energy loss that could be used for gain and lean deposition (Figure 8). Each time a pig is vaccinated, there is a net loss of energy for gain and lean deposition. The development of one-shot vaccines has been an excellent tool to minimize this loss.

But this overall loss from vaccination is very small compared to loss from disease. Sometimes vaccines are used for diseases that cause few problems. In these cases, the economics of vaccination need to be evaluated.

Swine Immunity Review

The amount of knowledge on swine immunology seems to double every year. Unfortunately, many of the “principles” of immunology are based on studies done in mice and people, which haven't all held true for hogs.

An issue with swine immunity is the idea that vaccines can be a “cure all” for disease problems. Vaccines are not a substitute for management, proper nutrition, adequate facilities or biosecurity. Maintaining a healthy pig means having a healthy immune system. Overcrowding animals and inducing stress will disable the immune system. The immune system is highly susceptible to poor nutrition, particularly to vitamin and mineral deficiencies. Increasing pathogen loads by continuous-flow systems and poor cleaning and maintenance will overwhelm the ability of the immune system to protect against pathogens.

Conclusion

The swine immune system provides surveillance and the forces to win the battle against disease. However, like any army, the immune system needs to be prepared and “trained” properly through proper nutrition, management and vaccination.

But it is not perfect and can be overwhelmed by high levels of pathogens, stress and the lack of exposure to common pathogens. Our ability to fine-tune and enhance the pig's immune system and increase animal productivity will only improve over time.

Figure 1. Basic Immune Responses

Skin and mucous membranes

skin/mucosal secretions, stomach acid, commensal organisms, GI passage, respiratory tract (turbinates and trachea), flow of urine/tears, coughing

Cellular and humoral defenses

complement, interferon, phagocytosis, cytokines, natural killer cells

Cellular and humoral defenses

T helper cells, cytotoxic T cells, B cells, antibodies, cytokines

Figure 2. Innate Immune Response

Inbuilt immunity to resist infection

  • Not antigen-specific
  • Not enhanced by second exposure
  • Has no memory
  • Uses cellular and humoral components
  • Is poorly effective without acquired immunity
  • Necessary for turning on the acquired immune response


Figure 3. Acquired immunity

Immunity specific for the infection

  • Is antigen-specific
  • Learned by experience
  • Enhanced by vaccination
  • Has memory
  • Uses cellular and humoral components
  • Is poorly effective without innate immunity

Vaccines How They Work, Why They Fail

Vaccination is an important tool for disease control in swine herds. The goal of herd vaccination is to decrease the number of susceptible animals, reducing clinical disease and pathogen spread.

Passive and active immunity are the two methods used for disease protection.

Passive immunization produces immediate and temporary resistance to disease through transfer of antibodies from resistant animals to susceptible animals. Maternal antibodies are the primary source of passive immunity.

Active immunity involves exposure of the animal to an organism by either vaccination or natural exposure, resulting in a protective immune response.

Active Immunization

Active immunization by vaccination is the most common type of immunity used to protect pigs from disease. Sow vaccination results in both active immunity and disease protection for the sow and passive immunity through antibodies in the colostrum for the pigs.

In contrast to passive immunity, active immunization has a number of advantages, including prolonged protection against disease.

An active immune response occurs when cells present an antigen from either infection or vaccination to lymphocytes, resulting in a primary immune response. It takes about a week for the primary immune response to develop, and longer for the stronger, secondary immune response (Figure 1).

The vaccine and the adjuvant administered determine the nature, length and effectiveness of the immune response. The advantage of vaccination over “controlled” infection with the organism is the identity and amount of each pathogen has been established. Therefore, vaccination is a safer, more reproducible method for exposure to pathogens.

Ideally, the protective immune response induced by a vaccine will be identical to the response from infection, with none of the adverse side effects associated with disease.

Types of Vaccines

Vaccines consist of either live or killed pathogens. Each type of vaccine has advantages and disadvantages summarized in Table 1.

The goal of live vaccines is to closely mimic natural infection with minimal disease. In contrast, killed vaccines consist of inactivated organisms similar to the living organisms.

Site of administration is based on vaccine type, the adjuvant and what works best to produce immunity. Most vaccines are given systemically, either in the subcutaneous tissues under the skin or in the muscle.

Several vaccines are effectively administered orally. Animals must be healthy enough to eat or drink so all animals ingest an adequate amount of the vaccine.

Needleless injection systems are also increasing in popularity and can be very effective. They can enhance the uptake of vaccine antigens by antigen-presenting cells, improve immune response and safety.

Killed Vaccines

Killed vaccines are made of inactivated bacteria or viruses. They can consist of the whole organisms, or select proteins from the organism, such as the cell membranes or smaller pieces called subunit vaccines. The organisms are chemically inactivated, leaving them as similar as possible to the live organisms.

Inactivated, purified antigens alone usually don't induce an adequate immune response. Therefore, adjuvants are used to increase the immune response by trapping the antigen at sites that enhance their uptake by antigen-presenting cells and increase exposure to lymphocytes.

Adjuvants also induce inflammation, further activating the various cells of the immune system of the pig.

Compounds used as adjuvants include aluminum salts, water-in-oil or oil-in-water emulsions, natural bacterial fractions, surface-active agents and their combinations.

Two doses of an inactivated vaccine are normally needed for a strong immune response. Occasionally, one vaccination is enough to induce protection, as with some mycoplasma vaccines. With one-dose vaccines, infection serves as the booster.

Table 1. Pros, Cons of Live vs. Killed Vaccines
Live Vaccines
Advantages Disadvantages
More rapid protection Potential to revert to virulence
Longer lasting immunity May be immunosuppressive
One dose usually sufficient May cause abortion
No adjuvant needed May be contaminated with other viruses
Improved cell-mediated immunity Must be handled carefully to keep alive
Costs less
Killed Vaccines
Advantages Disadvantages
Safety Not as immunogenic (likely to cause disease)
No reversion to virulence Requires adjuvants
Less likely to suppress immunity Usually requires two vaccinations
Increased vaccine stability Immunity of shorter duration


One-dose vaccines may not be effective, however, when factors that decrease vaccine efficacy are present. Examples include infections occurring too quickly following vaccination or when the infection overwhelms the initial immune response, when infection occurs too quickly following vaccination or the infection overwhelms the initial immune response.

Inactivated vaccines tend to produce strong antibody responses; however, cell-mediated immune responses can also be generated.

Live Vaccines

Live vaccines, too, can consist of either viruses or bacteria. Virulent live organisms can't be used safely in vaccines, however.

A number of methods are used to attenuate or reduce the ability of the organism to cause disease.

One of the most common is to grow an organism a long time in a laboratory. Continuous culturing often causes the organism to lose the mechanism to cause disease.

While this technique has effectively produced live vaccines, there remains a danger that when the pathogen is put back into the host, reversion to virulence will cause disease.

Another technique to decrease organism virulence is to alter or remove specific genes associated with disease. This technique only works if the deleted gene is not required to produce a protective immune response.

Genetic alteration of the organism can also differentiate vaccine from wild-type responses. Pseudorabies vaccines are an example where genetic modification produced a virus incapable of causing disease and allowed differentiation of vaccine from natural infection.

Similar gene deletion technology has been used in other vaccines. Other genetic alterations of pathogens are being developed to produce safer and more efficacious vaccines.

Live vaccine use in animals with a suppressed immune system increases disease risks, so their use is not recommended.

Typically, a single dose of live vaccine is enough to induce a strong immune response, therefore, adjuvants are not required.

DNA Vaccines

In recent years, vaccines have been studied that contain specific genes known to induce protection against either viruses or bacteria. This technology is based on the DNA or genetic material from the organism being injected into the animal. The cells in the animal produce the specific proteins coded by the DNA, which then induce an immune response. An advantage is DNA vaccines use specific genes, rather than the whole organism, preventing any possibility of disease.

In addition, genes from multiple pathogens can be combined and specific cytokine genes added to provide the immune response needed for disease protection. The primary drawbacks of DNA vaccines are their costs and the lack of knowledge of the genes needed for protection against many pathogens.

Herd Immunity, Vaccine Failures

In a perfect world, all vaccines would always protect all animals. However, there are many reasons why vaccines fail. In some cases, the vaccine may be ineffective. Always use vaccines from reputable manufacturers.

Of greater significance is the failure of known, effective vaccines to induce protective immunity. This type of failure may be due to improper vaccine administration, improper syringe use, or inactivation of a live vaccine through poor storage or handling. A syringe used for antibiotic therapy or chemical sterilization of a syringe will destroy a vaccine.

Carefully following manufacturer's directions for vaccine storage, handling and administration with new syringes and needles will prevent these problems.

Some animals in a herd will always fail to mount an effective immune response. Genetic or environmental factors, improper vaccination technique, or vaccine handling may cause this failure. The range of immune responses within a herd tends to follow a normal distribution pattern (Figure 2).

Response to vaccination will vary between vaccines, the herd conditions and other factors that may impact vaccine efficacy. Any factor that decreases the number of animals protected by vaccination increases the economic loss to the producer.

Since the development of an immune response is a biological activity, any factor that affects the normal function of the pig also potentially impacts its ability to induce immunity. Inadequate environment or improper nutrition will have a profound impact on this ability.

The presence of maternal antibodies or the circulation of immunosuppressive pathogens, such as porcine reproductive and respiratory syndrome (PRRS) virus, can increase the number of animals that fail to develop adequate protective immunity following vaccination.

Maternal antibodies can be an important factor affecting vaccine efficacy. Their importance varies with the vaccine and disease. For example, low levels of maternal antibodies against swine influenza virus (SIV) have been shown to block vaccine efficacy.

In contrast, very high levels of maternal antibody levels are required to block mycoplasma vaccines.

The presence of PRRS virus circulating in pigs at the time of vaccination appears to diminish the protective capabilities of mycoplasma and SIV vaccines. How this mechanism works remains unknown. PRRS virus infection is an important factor to consider in any vaccine program.

Organisms use a number of different techniques to survive in the pig. Some affect vaccine efficacy.

One evasive mechanism is the location of the organism. For example, Mycoplasmal pneumonia, which colonizes the cilia in the respiratory tract, is physically separated from the immune system. This makes a good immune response by vaccination or infection challenging.

Other organisms regularly change the proteins on their surfaces or their genetic makeup. Some do this intentionally to escape the immune system, while other changes are unintentional mistakes.

For example, as PRRS virus replicates within cells, mistakes are made. This results in a constant changing of the genetics of the virus. If there are enough changes over time, a new strain of the virus is formed. Then, the immune system must begin the process of developing a new immune response again.

Another evasive technique used by viruses is to combine genetic materials from different strains to produce a genetically different virus, as occurs with SIV. The new H1N2 subtype appears to have developed from the H1N1 subtype combining with the H3N2 subtype. The ability of the earlier immune response to each subtype to protect against the new subtype will depend on how closely the new subtype matches the old.

By constant and frequent change, pathogens are able to evade the immune system and survive. Vaccines developed against one strain or subtype of bacteria or virus may not be effective against new organisms.

The amount of change differs between pathogens. The toughest pathogens exhibit the most variation. The success of the pathogen is reflected in a vaccine's failure. Addressing this problem may require changes in vaccine development and licensing procedures.

Summary

Vaccines are important tools for herd immunity. Limited knowledge has sometimes led to production of less than optimal vaccines for some of our more problematic swine pathogens.

Vaccine failure can have many genetic, environmental or management causes.

Overall animal health, the presence or absence of maternal antibodies and immunosuppressive pathogens must also be considered for herd vaccination programs.

As our knowledge of the swine immune system and the pathogens increases, technology will provide vaccines with increased efficacy and ease of use for pork producers. rActive immunization by vaccination is the most common type of immunity used to protect pigs from disease.

Table 2. Glossary or Terms of Immunity

Adjuvant: Any substance that enhances the immune system when administered with an antigen.

Antigen: Any foreign substance that can induce an immune response.

Antigen-presenting cell: Cells that can ingest, process and present antigen on their cell surface for T cell activation. The main antigen-presenting cells are macrophages, dendritic cells and B lymphocytes.

Cell-mediated immunity: An immune response mediated by T lymphocytes and macrophages.

Cytokines: Proteins made by cells that affect the behavior of other cells. Used by cells to communicate with each other.

Humoral Immune Response: Antibody-mediated immunity. Lymphocytes active in producing antibodies are B lymphocytes.

Lymphocytes: A small white blood cell that comprises the primary effector cells of the immune system. B lymphocytes produce antibodies and T lymphocytes are responsible for mediating cell-mediated immunity.

Macrophages: Large cells in the tissues that engulf and process foreign substances.

Pathogen: An organism that causes disease.

Virulence: The ability of an organism to cause disease.