Occurrence: Worldwide, especially high health status herds.
Age affected: Weaners, growers/finishers.
Causes: Bacterium – Lawsonia intracellularis; poor hygiene.
Effects: Diarrhoea, wasting, pallor, black dung, sudden death.
Necrotic Enteritis (NE) / Necrotic Ileitis
Occurrence: Worldwide, especially high health status herds.
Necrotic enteritis (NE) is the end stage of several intestinal diseases. Most cases are a stage in Proliferative Enteropathy (PE, ileitis), which can also cause regional ileitis (RI), porcine intestinal adenopathy (PIA) and proliferative haemorrhagic enteropathy (PHE).
Proliferative Enteropathy is caused by a bacterium, Lawsonia intracellularis, which reproduces in cells. It is a Gram negative, curved, rod-shaped organism with tapered ends and can be grown artificially in cell cultures by a few specialised laboratories worldwide. The organism can produce microcolonies after 7-14 days and can survive outside cells for up to 2 weeks at 5°C but not multiply. Pure cultures of the organism cause all forms of the disease. The bacteria enter cells lining the intestine, usually those of the end of the small intestine (ileum) and sometimes those in the large intestine, and multiply, causing the cells to become immature in appearance, eliminating the absorptive villi and encouraging the crypts between them to lengthen, thus making the intestinal lining non-absorptive, thick and lumpy in infected areas. Inflammation occurs with loss of red (and some white) blood cells and infected intestinal epithelial cells. As the intestine recovers, the thick mucosa may break down and become necrotic as in Necrotic Ileitis, eventually giving rise to thickening of the muscular coats in Regional Ileitis or ‘hosepipe gut’. Faster breakdown can cause massive blood loss into the ileum to cause Proliferative Haemorrhagic Enteropathy. Recovered pigs are immune to re-infection.
The commonest underlying condition is Lawsonia intracellularis infection which is spread from pig to pig via infected faeces, usually between pigs at mixing. As the organism can survive for short periods outside the pig, transmission can occur indirectly following the consumption of contaminated feed and water or by moving susceptible animals into contaminated pens or vehicles. The organism can persist in mice, and these and other species may represent a source of infection.
Clinical disease is most commonly seen in recently-weaned pigs and lasts for about 6 weeks. In has an incubation period of 3-6 weeks and can occur in animals for any age from 3-4 weeks to adults. The first signs are failure to gain weight or loss of weight and varying degrees of inappetence. Affected pigs appear pale, may vomit, are anaemic and may have blackened faeces due to the presence of black, altered blood.
Some animals pass loose granular faeces which spread on concrete like portions of wet cement especially where infections with organisms such as spirochaetes are present. After 4-6 weeks affected pigs may recover completely. Some die suddenly at this stage with proliferative haemorrhagic enteropathy. These usually appear pale with a low body temperature (37.8°C, 100°F) 1-2 hours prior to death and may be of any age from 6-10 weeks upwards.
Breeding stock may die suddenly from proliferative haemorrhagic enteropathy when the disease first enters a herd. Twelve percent of a newly infected herd may be affected and 6% may die. Some recovered animals remain stunted. They may appear thin, pale and may have mild diarrhoea.
These are the animals most likely to have developed necrotic enteritis.
Proliferative enteropathy and its related syndromes (NE, PIA, PHE and RI) should be considered if growing pigs become pale with loss of condition and blackened faeces is present. In older pigs, these signs and the sudden deaths from proliferative haemorrhagic enteropathy could also be due to gastric ulceration. Diarrhoea or loose faeces is not a reliable indicator of the disease. L. intracellularis can be identified in faeces by the Polymerase Chain Reaction (PCR) and antibody to it may be detected in the blood of infected herds.
Proliferative enteropathy, the underlying disease, can be confirmed at post-mortem examination of affected pigs. They are usually pale and may be in poor condition. The terminal ileum is thickened, pale and its lining is contorted into folds which resist stretching. Parts of the large intestine may also be affected. There may be clots of blood in the affected bowel and this blood appears black once it reaches the large intestine. Gastric ulceration is absent.
The affected gut lining can be covered with dead tissue in the stage of the disease known as Necrotic Enteritis. Laboratory tests confirm the presence of the disease or infection. Characteristic changes in the arrangement of the cells of the intestinal lining can be seen by microscopy. The organisms can be demonstrated in, or isolated from, these cells and confirmed as Lawsonia intracellularis.
Individual clinically-affected pigs may be treated with injectable long-acting tetracycline or antimicrobials such as tylosin, tiamulin and lincomycin. Water medication of affected groups with tetracycline, tylosin, tiamulin or lincomycin usually results in a clinical cure of cases of the underlying condition. Treatment may be less effective in pigs which actually developed necrotic enteritis.
Chlortetracycline treatment in feed for two weeks will have the same effect and valnemulin, tiamulin, aivlosin or tylosin are also effective. As disease can recur 3 weeks after the end of treatment in infected groups, a second course of treatment is often given 18 days after the end of the first course.
When spirochaetosis, salmonellosis or other bacterial disease is present, the treatment should be modified accordingly. Control is based on treatment. This may be given continuously at low level, but disease will recur after the treatment is discontinued. Most commonly, two courses of treatment are given, beginning 18 days after entry to a house or earlier if the disease occurs before this.
Disinfection with quaternary ammonium, iodine and oxidising disinfectants at the end of periods of treatment and rodent control reduce the chances of re-infection. Herds founded by hysterectomy and maintained in isolation are usually free from the disease, but may become infected. Breeding stock should come from clean herds. Vaccination with a live attenuated strain of L. intracellularis can be given to recently weaned pigs and prevents clinical disease and reduces or prevents infection with pathogenic L. intracellularis.