Edema disease

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Please read chapter on Colibacillosis first


An acute, often-fatal enterotoxemia of recently weaned pigs caused by a few serotypes ofEscherichia coli. It often is characterized by edema at certain sites, sudden deaths, and occasionally by neurologic signs related to lesions in the -brain.


Edema disease (ED) occurs primarily in recently weaned pigs. It occurs rather frequently in countries that practice intensive swine production. In the US, edema disease is considered sporadic in occurrence, has not been eliminated by modern technologies, and in fact can cause considerable loss in modern production systems.

Historical information

Edema disease is a unique form of colibacillosis first reported in 1938. It was reported only occasionally during each of the next two decades. Following World War II, swine production was intensified and highly nutritious rations were introduced. The frequency of ED then increased. Much of the present information on ED is the result of research completed during the last 25 years.


Edema disease is caused by toxins produced in the small intestine by pathogenic serogroups of Escherichia coli (E. coli). Most have pilus type F18 or F4 (K88), and elaborate shiga-like toxin (variably referred to as SLT-IIe, Stx2e, verotoxin, edema disease principal, neurotoxin, or vasotoxin). Enterocyte receptors for pili are genetically determined and variably present, depending on genotype of the pig. Purified Stx2e given intravenously to experimental pigs results in typical edema disease. Other forms of colibacillosis (diarrhea) can be caused by some of the same pilus types that cause ED but have a different pathogenesis because of the variety of enterotoxins that may be elaborated.


Because outbreaks of ED in nurseries sometimes occur repeatedly, pathogenic serogroups probably persist in the environment of the farrowing rooms and/or nursery or are reintroduced by carrier dams.

Several factors appear to influence the bacteria that cause ED. Specific enterocyte receptors are a function of pig genotype. Some receptors are not present until postweaning. Maternal antibody in colostrum and milk may be a factor. Nutrition also plays a role since ED occurrence can be influenced by ration type and frequency of feeding. High protein diets, certain dietary constituents, and rotavirus may make the intestine more favorable for colonization of enteropathogenic E. coli.


Pathogenic E. coli colonize and proliferate in the small intestine by pilus-mediated attachment to the epithelial cells. Enterotoxins produced by pathogen strains induce the disease, with Stx2e causing damage to small arteries and arterioles. Degenerative angiopathy leads to increased vascular permeability and accumulation of edema at various sites, most notably colon, stomach, small intestine, eyelids, and brain. Damage to vessels in brain can cause malacia in the brain stem and basal ganglia, a feature in subacute stages of the disease having central nervous system (CNS) disturbance. High doses of Stx2e may cause acute hemorrhagic gastroenteritis or sudden death.

Clinical signs

Onset of the disease usually is around two weeks postweaning. Onset often is signaled by finding a few thrifty pigs dead. Morbidity usually is low but mortality is high in pigs that show signs. Signs include anorexia, ataxia, stupor and recumbency often accompanied by paddling and running movements. When caught, affected pigs may respond with an abnormal squeal, a consequence of laryngeal edema. Diarrhea usually is not present in pigs with typical ED but may be present in other pigs in the same group. Swelling of the face and eyelids may or may not be present. Sick pigs die within a few hours or days. The few that survive often have neurologic deficits. The course of ED in a herd usually is around two weeks. However, the disease may reappear as other batches of pigs reach the age group at risk.


Several affected pigs should be necropsied since not all will show typical lesions. In some pigs found dead, congestion of viscera may be the only appreciable gross change. Usually, some will have evidence of edema of subcutis of the face or eyelids, gastric submucosa, or in the mesentery of the spiral colon. Fluid may be increased in the peritoneal cavity, chest or pericardial sac. Occasionally there are hemorrhages under the epicardium or endocardium. The brain may have unique hemorrhagic and malacia lesions in brain stem or basal ganglia in less acutely affected pigs. These lesions are very suggestive of ED.

In subacutely or chronically affected pigs, microscopic degenerative changes can be found in small arteries and arterioles at many sites. The changes sometimes are apparent in vessels supplying the brain. Histologic sections of brain stem and basal ganglia may confirm suspected areas of hemorrhage and malacia.


The history, signs and lesions often are adequate for a tentative diagnosis. Bacterial culture of the small intestine from a nonmedicated typical pig will yield high populations of hemolytic colonies of E. coli. It is useful to genotype the isolate for confirmation of virulence factors and perhaps for epidemiologic reference. Typical microscopic vascular lesions help confirm diagnosis.

Edema disease must be differentiated from other causes of neurologic signs (pseudorabies, water deprivation or organic arsenical poisoning) or septicemia and meningoencephalitis caused by Streptococcus suis, Salmonella serotype Choleraesuis, erysipelas, or Haemophilus parasuis.


Treatment of pigs affected with ED can be frustrating since toxin production in the gut is quite advanced by the time clinical signs become visible. Affected pigs must be treated parenterally. Antimicrobials may be of some value in less severely-affected pigs. Supportive therapy to counteract acidosis and dehydration is valuable in early cases. During an outbreak, efforts are directed toward reducing the incidence of infection in the remainder of the population at risk. Administration of antimicrobials and acidifiers in the water may be helpful. In severe outbreaks, removing feed and replacement with a ration containing less protein, a lower percentage of soybean meal, or higher proportion of rolled oats is required.

No prevention method is universally accepted or successful because the erratic occurrence of ED makes intervention strategies hard to assess. Seven general strategies should be considered when formatting control strategies for affected farms.

  1. Management factors include minimizing environmental stresses (e.g. temperature variation, drafts, damp conditions), limited commingling, and using all in/all out (AIAO) system with scrupulous sanitation.
  2. Nutritional considerations include creep feeding, restricted feeding, multiple feedings (small quantities 3-6 times/day) after weaning, adding oats (high in fiber) to the rations, acidifiers (organic or inorganic acids) added to feed or water, decreased protein in the ration, addition of zinc oxide (2500 ppm) to the ration, and addition of plasma protein.
  3. Antimicrobial intervention is often practiced. Various antibiotics have been added to rations or water but the efficacy is difficult to evaluate because outbreaks do not occur regularly; some affect only a few pigs, some pigs are naturally immune, and outbreaks end spontaneously. Antimicrobial resistance eventually dooms this strategy over the long term.
  4. Immunoprophylaxis can be successful by passive or active protection. Oral ingestion products (milk, plasma protein, egg powder) containing antibody can help to prevent colonization and disease. Disadvantages of passive protection are cost, lack of cross-protection between pilus or toxin types, and possibility of susceptibility remaining following cessation of feeding. Active immunity can be induced against specific adhesins or toxins. Oral vaccination with live or killed cultures that contain F18 or F4 (K88) pili but lacking genes for toxin production have been successful. Toxoids prepared from Stx2e have also been demonstrated effective against ED but are not commercially available. Whole-cell bacterins have been much less effective.
  5. Competitive exclusion, a process whereby receptors for E. coli are occupied by nonvirulent agents, is being investigated and may offer opportunity for control in the future.
  6. In herds negative for ED, it is prudent to prevent introduction by careful scrutiny of disease history of breeding stock. Eradication may be possible by using depopulation and disinfection.
  7. Natural resistance to ED is possible in pigs genetically lacking receptors for F18 and/or F4 (K88) pili. Genetically resistant pigs have been developed.