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Identifying Edema Disease Takes Careful Diagnosis

Edema disease (gut edema) has been recognized for over 70 years. Despite having a good understanding of the toxin-producing Escherichia coli (E. coli) that causes this disease, it remains a risk for all pork production systems and remains a major frustration when it occurs.

Edema disease (gut edema) has been recognized for over 70 years. Despite having a good understanding of the toxin-producing Escherichia coli (E. coli) that causes this disease, it remains a risk for all pork production systems and remains a major frustration when it occurs.

Sudden deaths in the nursery may signal an outbreak of edema disease, albeit there are many other possible causes. Clinical signs of common causes of sudden death and/or nervous signs in nursery pigs is depicted in Table 1.

Very careful examination of individual pigs usually reveals the early clinical signs that may be useful for diagnosis. With edema disease, others in the group may have eyelid edema (Figure 1), unsteady gait, or be found down with central nervous system (CNS) signs. Normally, they do not have a fever.

Necropsy may reveal no lesions or perhaps mild edema in the stomach wall or mesentery. Often, intestines will be reddened. However, these observations alone do not establish a diagnosis. Submission of a complete set of fresh, refrigerated and formalin-fixed tissues can confirm a cause and rule out other possibilities (Table 2).

E. coli is always present in the gut of normal mammals. The isolation of E. coli from intestine is not sufficient for diagnosis, but must be coupled with lesions and/or evidence of colonization (histopathology). Most diagnostic laboratories can also genotype the E. coli isolated to determine if it has the ability to produce the toxins that cause disease (Table 3).

Edema disease occurs most frequently in pigs about two weeks after weaning (5 weeks of age), but outbreaks have been documented from 2 weeks to 4 months of age (grow-finish). Often, flows of pigs or individual nursery facilities will suffer repeated outbreaks. No seasonal effect is suspected. Figure 2 documents total cases per month for the period 2005-09.

Treatment or prevention of edema with antimicrobials is not predictably or consistently effective in the long term. Indeed, neither has a bevy of other nostrums been demonstrated to be consistently effective. Animals showing clinical signs usually do not respond to treatment. Prevention is always the goal for control of this disease.

Edema disease in swine is caused by a shiga-like toxin produced by hemolytic colony types of E. coli. The circumstance by which this occurs involves three major factors. First, the E. coli must also be able to attach the intestine by fimbria (colonize), usually fimbria type 18 (F18) or with type K88 (F4). Second, the pig’s intestine must have a genetically determined receptor to which the fimbria can attach; genetically resistant pigs do exist for both F18 and F4 attachment. Third, once E. coli is attached, it must be genetically capable of producing the shiga-like toxin, which in swine is referred to as Stx2e. E.coli also can produce toxins (e.g. Sta, Stb, LT) that cause hypersecretory diarrhea.

Disease Control
Knowing these three factors offers three avenues for specific disease control. First, it is possible to prevent attachment by breeding genetically resistant pigs that lack the receptor for the particular fimbria types. Second, oral administration of F18- or F4-positive E. coli lacking the genes for Stx2e toxin production can either prevent colonization (competitive exclusion) or generate gut immunity to the offending strain. This type of vaccination procedure has been quite effective on some farms, but there is variation in cross-protection between subtypes of F18 fimbria. Third, it is possible to vaccinate pigs against the effects of the shiga-like toxin Stx2e by preparing a vaccine-toxoid. Unfortunately, this product is not commercially available. Of these three preventative methods, the use of a modified-live, avirulent vaccine has been the most useful.

A multitude of interventions have been suggested to address alleged risk factors, but none are “magic bullets.” Consistent execution of nutrition, husbandry, pig comfort, hygiene and management practices, pig flow and environmental control are always important. The environment can harbor organisms between groups, therefore it is very important to clean and disinfect the entire facility, top-to-bottom, between groups, including water lines, utensils, walks, office areas and equipment.

Other preventative interventions include: oral vaccination of the pigs (not sows) with avirulent live vaccine, management of protein source and quantity in the diet, acidification of water or feed, altered mineral levels (e.g. zinc) in the diet, increased fiber in the diet, control of other pathogens (e.g. rotavirus) and preventative antibiotics or nutraceuticals. The list of “cures” is long because there is not a single consistently efficacious intervention. A “holistic approach” will usually offer improvement.

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Kent Schwartz, DVM
Iowa State Veterinary Diagnostic Laboratory