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Acquired Specific Immunity

(63) This is the immunity that the pig acquires as it goes through life. It may be obtained actively or passively.

Actively produced specific antibodies
When a foreign protein or part of a protein (called an antigen) enters the body, the body responds by producing antibodies in the lymphocytes of its lymphatic tissues. This is known as antigenic stimulation.

Antigens stimulate the production of antibodies which circulate in the blood and body fluids. They are secreted onto epithelial surfaces and specifically adhere to the antigen. The surface of the antibody fits snugly on to the complex corrugated surface of the antigen. The adherent antibodies may then have one of several effects. They may:

  • neutralise the antigen (common with some viruses), or
  • enable white blood cells to phagocytose it (such antibodies are called opsonins), or
  • in conjunction with complement, disable and possibly destroy it.
In some infections they may have little or no effect.

Active antibody production in pigs is mostly brought about by natural exposure of the lymphocytes to the surface proteins on viruses, bacteria and parasites or by exposure to toxins.

It can also be induced artificially by the inoculation of vaccines or toxoids (denatured toxins which have lost their potency but retain their ability to stimulate antibodies).

Or it can be stimulated by the deliberate feeding of substances such as faeces (i.e. so-called 'feed back').

Delayed production
When a new pathogen invades a pig the antibody response takes about 10 to 14 days to reach maximum levels. This delay is important in relation to natural infection and also to vaccination, since protection is not immediate. Pigs keep meeting new infections throughout their lives, particularly when they are young. If a new infection is pathogenic it may be 5 to 7 days before specific antibodies against the pathogen start to appear, during which time the pig could succumb to disease.

Furthermore if it occurs at a time when the pig is disadvantaged, e.g. having just been moved and mixed in a different pen or during a change of feed, the antibody response may be partly suppressed.

When a pathogen which has infected the pig previously invades the pig again the antibody response is much quicker because the lymphocytes which were primed by the first infection are still present. This is also true in a pig which has not been previously infected but has been vaccinated.

Antibodies are large proteins called immunoglobulins (Ig) of which there are three main types, IgG, IgM and IgA. They can be humoral (i.e. circulating in the blood and body fluids) and thus getting into all the body organs and tissues, or they can be local on the surface of mucous membranes such as those lining the respiratory and alimentary tract. These are called mucosal associated antibodies.

Humoral antibodies
Over 80% of the humoral immunoglobulin circulating in the blood of the mature pig is IgG, about 10% is IgM and most of the rest is IgA.

If a pig is vaccinated by intramuscular or subcutaneous injection against an infectious pathogen that invades the body (e.g. against diseases such as erysipelas or swine fever) the humoral antibodies produced are effective in blocking the invasion.

Mucosal associated antibodies
If a pig is vaccinated (e.g. into the muscle or under the skin) against an intestinal infection such as TGE virus or enterotoxigenic E. coli which multiply and do their damage in the gut, the humoral antibody response induced is unlikely to prevent the organism multiplying in the gut or to greatly reduce the diarrhoea that results.

To be fully effective in the gut, the immunising antigen must stimulate a local immunity mainly by acting on the lymphatic tissues of the intestines ("Peyer's patches"). This results in the production of IgA just below the surface layer of the gut. The IgA passes through the cells of the mucous membrane and attaches to another molecule called the secretory component. It is then called secretory IgA and consists of two IgA antibody molecules joined together by the secretory component. This combination increases their potency, makes them resistant to digestion by gut enzymes, and more readily absorbed by mucus. Since the mucus coats the whole lining of the intestines and the respiratory tract, the secretory IgA acts as a shield against potentially pathogenic infections.

In contrast to humoral antibodies, therefore, mucosal associated antibodies in the pig are principally IgA, in the form of secretory IgA.

Cell-mediated immunity
There are two broad categories of immune reaction to infection:

  1. Humoral immunity in which a major component is antibodies in the blood.
  2. Cell-mediated immunity which need not involve antibodies.

Although they can occur independently, they usually both occur at the same time with greatly enhanced benefit. Cell-mediated immunity is initiated by lymphocytes originating from the thymus gland (T lymphocytes), whereas humoral immunity involves lymphocytes that are derived originally from the bone marrow (B lymphocytes). Cell-mediated immunity also involves other types of cell such as macrophages and natural killer cells.

Whereas its important for you as a pig farmer to have some understanding of humoral immunity because of its association with blood testing, maternal immunity (colostrum and milk) and vaccination, it is much less important for you to understand cell-mediated immunity except to be aware that it exists.

Passively acquired immunity
So far we have been considering active immune reactions that result from stimulation of the pig's immune system by invading antigens but immunity can be passive without the pig's immune system being stimulated. Passively acquired immunity, usually termed "passive immunity", is acquired naturally by the newborn piglet through the ingestion of colostrum and milk or artificially by the injection of antiserum or oral dosing of colostrum substitutes.

Unlike human babies and puppies, no antibodies are transferred through the placenta from the sow to her piglets before birth. Normally, piglets are born in a vulnerable state without any humoral or mucosal associated antibodies and no acquired cell-mediated immunity. Fortunately, towards the end of gestation when the sow's mammary glands develop, the first secretion they produce, colostrum, is rich in antibodies representing the whole spectrum of the sow's own circulating antibodies. A first instinct of the newborn piglet is to find and suck a teat. Normally, a sow has voluntary control over milk let down, but during farrowing this control is weak. The piglets nuzzle the teat and surrounding gland and then suck the teat. This results in a rapid let-down of colostrum. In the first twelve to twenty four hours of life the piglet's intestines are able to absorb whole antibodies before the enzymes in the intestines digest them. Consequently, within a short period after a good first suck, the piglet's blood contains the full spectrum of its dam's antibodies often at about the same level as that of the sow.

Four points must be emphasised.

  1. Without maternal antibodies the piglet is highly susceptible to infection. It is essential for the piglet's survival that it drinks colostrum soon after birth before pathogenic micro-organisms have had time to multiply and invade. It is also essential that it ingest enough colostrum to provide adequate protection until it has actively produced its own humoral antibodies.
  2. The ability of the piglet's intestine to absorb colostral antibody is short-lived, but is shortened still further when the piglet has drunk. Thus, if a piglet that has had no colostrum, is to be cross-fostered onto another sow, or given substitute colostrum orally, it should be done in the first few hours of life and no other nutrients should be given in advance. The fostering sow must also still have colostrum available.
  3. Being passively acquired the amount of antibody in the blood stream is finite and can be exhausted by exposure to excessive antigen. Put another way, there is a maximum amount of colostral antibody that a pig can absorb into its blood stream. Overwhelming doses of bacteria will use it all up.
  4. The passively acquired colostral antibodies in the blood gradually waste away to about half the initial level by about ten to fourteen days, although they may persist at a reasonably protective level against most pathogenic antigens for six to twelve weeks. (See Fig.3-4). The time taken to decline to ineffective levels varies depending upon the amount of colostral antibody taken in by the piglet and on the type of infection or toxin against which the antibody acts. In some exceptional cases (e.g. against Mycoplasma hyopneumoniae, parvovirus and Leptospira bratislava they may persist much longer, sometimes up to four and a half months.

Mucosally-associated antibodies are present as IgA and secretory IgA in colostrum but at low levels relative to the other types of antibody (IgG and IgM). However, the normal milk which follows colostrum contains sufficient secretory IgA to get absorbed in the surface mucus and protect the piglets intestines provided the piglet sucks the sow every one to two hours. This is sometimes called lactogenic immunity.

It is not surprising that mature sows provide a better maternal protection to their piglets than first litter gilts. They are older and have had greater exposure to infections. The protection provided by gilts is frequently inadequate, for example, to cope with the challenge of virulent E. coli. Thus gilt litters tend to suffer from diarrhoea more often than sow litters. To boost the protection of their piglets it is good practice to expose gilts to farrowing or weaner house faeces for about four weeks prior to their anticipated farrowing. High dose levels however are required to be effective in the case of E. coli.

In severe intractable outbreaks of E. coli diarrhoea, TGE or PED, diarrhoeic piglet faeces may be mopped up from the floor with paper towels and put through a grinder along with the intestines of dead piglets. These should be untreated piglets in the case of E. coli diarrhoea because the antibiotics will neutralise the effect. The resultant emulsion is suspended in an equal quantity of water and a cupful poured on to the feed of sows and gilts which are in late pregnancy. This is done twice or three times per week from about four weeks until one week before farrowing. Some people grind up bits of afterbirth with the faeces because they think that it makes the feed-back more effective. This procedure is not recommended because organisms such as Eperythrozoon suis, leptospira, toxoplasma and PRRS virus may be spread. Furthermore it may predispose gilts to cannibalism and savaging.

Feedback is usually an effective method of stopping an outbreak of neonatal scour in piglets caused by viruses. There is of course a delay before the effect comes about because the pregnant sows and gilts need at lest ten days to respond fully. There is much less effect on scouring which occurs at 10-14 days of age compared to that which occurs within 5 days of birth.

There are other dangers in using feed-back. It is not effective against piglet dysentery caused by Clostridium perfringens type C and may make the situation worse. Also it should not be used in herds with endemic swine dysentery, or if it is used, it should be done on a modest scale with care (e.g. anti-dysentery medicines may have to be included in the soup). Nor should it be used when there are clinical cases of other diseases (e.g. erysipelas) occurring in the herd because it will spread them. An additional problem is that many people find feed-back aesthetically displeasing and are reluctant to do it. On balance it is not recommend except for TGE.

An effective alternative for E. coli diarrhoea originally used in the USA was to grow the E. coli from the diarrhoeic piglets in milk and feed the milk to pregnant females. This method has been largely superseded by the introduction of commercial vaccines which are very efficient to stimulating an immunity.

It is common practice to expose gilts to faeces from the floors of service pens 4 to 5 weeks before mating. This is done to ensure that the maiden gilts have been exposed to both parvovirus and other potentially damaging organisms well before they become pregnant. There are now however, efficient vaccines against parvovirus.

Antibodies can also be acquired passively by injecting antisera. They will protect the pig for 7 to 10 days against the specific infection that the antiserum was prepared against. This used to be a common practice in pig medicine before antibacterial medicines and effective vaccines were widely available. This is rarely done now.

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