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 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.
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.
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.
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).
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.
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