EDEMA DISEASE E. COLI (EDEC)
LEVELS: Highly unlikely: No controls necessary; Highly unlikely: No evidence of non-foodborne zoonotic transmission; Highly effective: Routine on-farm biosecurity measures are effective in preventing farm-to-farm transmission; Easy: Distinct clinical signs and/or existing test(s) available at local/regional laboratory(s); Substantial: Unsustainable acute or chronic losses related to severe clinical signs in a high prevalence of animals; Negligible: Little or no market disruption when disease occurs on one or more farms; High risk: Resistance to antibacterial or antiviral treatments is, or can be expected to be a common problem; Minimal risk: Antibacterial or antiviral treatments rarely occur, or are typically limited to short-course individual animal therapy; Available but with uncertain efficacy: Limited treatments available in US or are only effective in some situations; Available but uncertain efficacy: Commercial or autogenous vaccines exist in the US but protection may be inconsistent; Not feasible: Eradication extremely unlikely
OVERVIEW
Edema disease (ED) is caused by Edema Disease E. coli (EDEC), strains that colonize the small intestine via F18 fimbriae and produce Shiga toxin variant Stx2e (verotoxin 2e). First reported in 1938, ED most often occurs in the first few weeks after weaning, though cases may occur through the grower phase. After intestinal colonization, Stx2e is absorbed into the circulation and binds to globotetraosylceramide (Gb4) receptors on vascular endothelium, causing degenerative angiopathy with edema in targeted tissues. Clinical signs include sudden death, subcutaneous and submucosal edema (eyelids, gastric submucosa, mesocolon), neurological signs (ataxia, incoordination, peculiar squealing), and respiratory distress. The case mortality rate ranges from 50% to over 90%, with disease course lasting 4-14 days in affected herds. Diarrhea and fever are NOT common features. Pigs showing neurological signs have a poor prognosis as Stx2e has already bound to receptors. Genetic resistance exists—pigs homozygous for the recessive FUT1 allele lack F18 receptors and are resistant. Commercial injectable Stx2e toxoid vaccines are available and effective at reducing mortality. Treatment with antimicrobials is largely ineffective once clinical signs appear.
FOODBORNE ZOONOTIC TRANSMISSION POTENTIAL
Level: Highly unlikely: No controls necessary
EDEC strains producing Stx2e are not zoonotic through food. While STEC O157:H7 causing human disease may occasionally be found in pigs at low prevalence, porcine EDEC with F18 fimbriae and Stx2e are host-specific and do not cause human illness.
NON-FOODBORNE ZOONOTIC TRANSMISSION POTENTIAL
Level: Highly unlikely: No evidence of non-foodborne zoonotic transmission
Porcine EDEC strains are not zoonotic. The F18 fimbrial type and Stx2e toxin variant causing edema disease are pig-specific pathogens without documented human disease.
EFFECTIVENESS OF ON-FARM BIOSECURITY IN PREVENTING FARM-TO-FARM TRANSMISSION
Level: Highly effective: Routine on-farm biosecurity measures are effective in preventing farm-to-farm transmission
Disease transmission is contained within farms: (1) Oral infection: "The colonization by EDEC, after oral infection, occurs on the tips and sides of villi in the distal jejunum and ileum"; (2) Contagious: "ED most often occurs as sporadic cases or small outbreaks limited to a specific age group with frequent recurrences"; (3) Environmental contamination: Contaminated environment serves as source; (4) Control achievable: Vaccination, dietary management, and husbandry effectively control disease; (5) Genetic selection possible: Breeding for F18 receptor-negative pigs reduces susceptibility.
DIFFICULTY OF DETECTING AND CONFIRMING INFECTION
Level: Easy: Distinct clinical signs and/or existing test(s) available at local/regional laboratory(s)
Diagnosis combines clinical signs, pathology, and laboratory confirmation: (1) Clinical presentation: "subcutaneous and submucosal edema with swelling of the eyelids," "ataxia, staggering gait, incoordination"; sudden death without premonitory signs; (2) Gross lesions: "Gelatinous edema...in the submucosa of the gastric cardia"; "mesocolon is commonly edematous"; (3) Histopathology: "hallmark microscopic lesion of ED is a degenerative angiopathy affecting small arteries and arterioles"; (4) Bacteriology: Culture and virotyping for F18 and Stx2e; (5) Challenge: "bacterial numbers may have declined in more protracted cases...a negative bacteriological result does not necessarily exclude the diagnosis."
FINANCIAL IMPACT ON FARM'S COST OF PRODUCTION
Level: Substantial: Unsustainable acute or chronic losses related to severe clinical signs in a high prevalence of animals
ED causes substantial losses in affected herds: (1) High case fatality: "The case mortality rate ranges from 50 to over 90%"; (2) Sporadic but recurring: "ED most often occurs as sporadic cases or small outbreaks limited to a specific age group with frequent recurrences"; (3) Duration: "the course of the disease in the herd varies from 4 to 14 days"; (4) Subclinical losses: "Subclinical ED may occur. Pigs are clinically normal but develop vascular lesions and may have a decreased growth rate"; (5) Chronic effects: "Chronic ED occurs in a low proportion of pigs recovering from acute cases" with persistent neurological deficits.
EFFECT ON DOMESTIC OR EXPORT MARKETS
Level: Negligible: Little or no market disruption when disease occurs on one or more farms
No trade implications: (1) Not regulated: ED is not a reportable or trade-restricted disease; (2) Endemic worldwide: Occurs in all pig-producing regions; (3) Nursery/grower disease: Resolves before market age; (4) No carcass implications: Affected pigs either die or recover.
PATHOGEN'S ABILITY TO DEVELOP AND SPREAD RESISTANCE
Level: High risk: Resistance to antibacterial or antiviral treatments is, or can be expected to be a common problem
EDEC shares resistance patterns with other E. coli: (1) Multidrug resistance: "Escherichia coli strains isolated from cases of...ED with variable but usually high rates of resistance toward a wide range of antimicrobial drugs"; (2) Plasmid-mediated resistance: Same horizontal gene transfer mechanisms as other E. coli; (3) However: Since treatment is largely ineffective for ED, antimicrobial selection pressure is lower than for diarrheal forms.
AMR DEVELOPMENT DRIVEN BY DISEASE MANAGEMENT
Level: Minimal risk: Antibacterial or antiviral treatments rarely occur, or are typically limited to short-course individual animal therapy
ED management has moderate antimicrobial pressure: (1) Treatment ineffective: "Control of ED using antimicrobials is scarcely effective because Stx2e has already been absorbed into the circulation and been bound to receptors when clinical signs become visible"; (2) Metaphylaxis used: "In-feed or water medication, selected by sensitivity testing of isolated EDEC, administered a few days before the onset of ED, can reduce the severity of the outbreak"; (3) Vaccination preferred: Toxoid vaccines are the primary prevention strategy.
AVAILABILITY OF EFFECTIVE TREATMENT OPTIONS
Level: Available but with uncertain efficacy: Limited treatments available in US or are only effective in some situations
Treatment is largely ineffective once clinical signs appear: (1) Poor prognosis: "pigs showing neurological signs have a poor prognosis"; (2) Antimicrobials ineffective: "Control of ED using antimicrobials is scarcely effective because Stx2e has already been absorbed into the circulation"; (3) Prophylactic medication: May reduce outbreak severity if administered before onset; (4) No antitoxin: Unlike some toxin-mediated diseases, no commercial antitoxin available.
AVAILABILITY OF EFFECTIVE VACCINES OR BACTERINS
Level: Available but uncertain efficacy: Commercial or autogenous vaccines exist in the US but protection may be inconsistent
Stx2e toxoid vaccines are effective: (1) Commercial vaccine: "A commercial injectable vaccine based on genetically modified recombinant Stx2e that showed reduction of mortality due to ED is licensed in several countries"; (2) Early vaccination: "This vaccine, administered in pigs 4 days of age, has been shown to prevent clinical signs, induce detectable levels of neutralizing antibodies 21 days post vaccination"; (3) Duration of immunity: "provide immunity for at least 105 days post vaccination"; (4) Recent developments: "A recent recombinant Stx2e vaccine administered to 2-day-old piglets was effective in reducing clinical signs and preventing mortality from 21 days to at least 112 days"; (5) Passive immunity: "Passive immunization can prevent bacterial colonization and toxemia...demonstrated by injection of piglets with Stx2e-specific antiserum."
FEASIBILITY OF ERADICATING THE DISEASE FROM THE US
Level: Not feasible: Eradication extremely unlikely
Eradication is not feasible: (1) Ubiquitous organism: E. coli is a normal intestinal commensal; (2) STEC prevalence in healthy pigs: "STEC in healthy slaughtered pigs of 25.4%"; "68.3% of pigs were shedding STEC at least once during their finishing period"; (3) Genetic breeding alternative: Breeding for FUT1-resistant genotypes can reduce susceptibility but not eliminate organism; (4) Environmental persistence: E. coli survives in farm environments.