Escherichia coli (edema disease)
LEVELS: Highly unlikely; No human illness; Already in the herd; Laboratory-dependent; Minor; Negligible; Some; Available, or not needed
| Register id | ecoli_edema_disease |
| Type | bacteria |
| Scientific name | Escherichia coli |
| NCBI taxid | 562 |
| Evidence | 2 document(s) |
| Assigned | 2026-09-04, against criteria version 093366e352a2 |
Overview
Edema disease is caused by strains of Escherichia coli that carry the F18 fimbria and produce Shiga toxin 2e. It strikes in the first few weeks after weaning and can be sporadic or sweep a whole batch. The toxin damages small blood vessels, and the result is fluid accumulation — swollen eyelids, a characteristic hoarse squeal from a swollen larynx — followed by staggering, incoordination and often death; the first sign in a group is frequently a well-grown pig found dead. Pigs that survive the acute phase may be left with permanent nervous signs, and once neurological signs appear the outlook is poor. Some infected pigs never look ill but still develop the vascular lesions and grow more slowly. Susceptibility is partly genetic: pigs of one FUT1 genotype lack the gut receptor the bacterium needs and are simply resistant, which is why some herds never see it. The strains are common in normal pigs — 68% of US finishing pigs shed Shiga-toxin-producing E. coli at some point — so this is a disease of circumstance rather than of introduction.
C1 Zoonotic potential
Likelihood of transmission from pigs to humans
Highly unlikely: Human infection with the agent has never been reported, or has been reported but is not attributed to pig or pork exposure
CONFIRMED by Eric. The assignment reached this level from the evidence, and he has reviewed and ratified it.
Confirmed by Eric. CONFIRMED. "c1l1, agree with assessment"
Basis. ch49 49.3, the whole public health section for the chapter, and it is about ONE pathotype: "A STEC subgroup known as EHEC, particularly EHEC O157:H7, O26, and other non-O157 serogroups, may be sporadically present in the intestines and feces of pigs and are known to cause bloody diarrhea, hemorrhagic colitis, and hemolytic uremic syndrome in humans infected through food or water contaminated by animal feces. PIGS ARE NOT CONSIDERED A MAJOR SOURCE OF O157 EHEC, AS THE PREVALENCE RATE IS TYPICALLY VERY LOW." Surveys of healthy slaughter pigs: Alberta 1.4%, Japan 1.4%, Ireland 0.21-0.63%, UK 0.3%, Sweden 0.08%, Norway 0.1%, United States 2%.
How this level was decided
Level 1, and the chapter draws the distinction this entry needs in its own etiology section: "In pigs, the most important STEC are those that cause ED, and these are known as EDEC. These strains produce the Shiga toxin variant Stx2e... Another subgroup of STEC, known as EHEC, is highly pathogenic in humans (e.g. O157:H7)." So both are Shiga toxin producers, and the chapter separates them by toxin variant and by host. Stx2e is the edema disease toxin; the human disease is caused by other Stx variants. FLAGGED as the one entry in this batch where the level deserves a second look, because "Shiga toxin-producing E. coli" is the phrase that describes both, and 68.3% of US finishing pigs shed STEC at some point. NOTE, A FRAMEWORK GAP RATHER THAN AN ENTRY ONE: half of 49.3 is antimicrobial resistance -- the mcr-1 colistin resistance plasmid, third and fourth generation cephalosporins, fluoroquinolones, and pigs carrying a greater diversity of mcr variants than other hosts. That is the largest public health story attached to E. coli in pigs and the 8-criterion framework scores it nowhere, C1 measuring transmission of the agent rather than horizontal transfer of a resistance gene. Recorded on all four E. coli entries so the absence is visible.
C2 Zoonotic impact
Severity of human illness caused by the agent
No human illness: Agent does not cause illness in people
Basis. ch49 49.3, the whole public health section for the chapter, and it is about ONE pathotype: "A STEC subgroup known as EHEC, particularly EHEC O157:H7, O26, and other non-O157 serogroups, may be sporadically present in the intestines and feces of pigs and are known to cause bloody diarrhea, hemorrhagic colitis, and hemolytic uremic syndrome in humans infected through food or water contaminated by animal feces. PIGS ARE NOT CONSIDERED A MAJOR SOURCE OF O157 EHEC, AS THE PREVALENCE RATE IS TYPICALLY VERY LOW." Surveys of healthy slaughter pigs: Alberta 1.4%, Japan 1.4%, Ireland 0.21-0.63%, UK 0.3%, Sweden 0.08%, Norway 0.1%, United States 2%.
How this level was decided
Level 1, following C1. No human illness is attributed to Stx2e-producing edema disease strains. THE LABEL MUST NOT BE READ AS A STATEMENT ABOUT SHIGA TOXINS -- the chapter describes haemolytic uraemic syndrome from EHEC two paragraphs away. It records that the pig disease and the human disease are caused by different members of the same group.
C3 Herd introduction risk
Effort required to keep the agent out of the herd
Already in the herd: Present in most herds, or carried by pigs themselves, so there is no introduction event to prevent
Basis. ch49 49.4.2: "Cha et al. (2018) demonstrated a high prevalence of STEC in commercial pigs in the United States, reporting that 68.3% of pigs were shedding STEC at least once during their finishing period." "Meng et al. (2014) reported a prevalence of STEC in healthy slaughtered pigs of 25.4%. The Stx2e gene was detected in 7.3% of fecal samples collected at Italian abattoirs." 49.5.1.7: susceptibility is controlled by the pig's own FUT1 genotype -- "pigs with the FUT1AA genotype are resistant to ED, while pigs with FUT1AG and FUT1GG genotypes are susceptible".
How this level was decided
Level 1. Two thirds of US finishing pigs shed a Shiga toxin-producing E. coli at some point in the finishing period, and a quarter of healthy slaughter pigs carry one. The organism is part of what pigs already have, and what determines whether an individual gets edema disease is its own inherited receptor genotype rather than whether the agent arrived. There is no introduction event to prevent. Scored with the other three E. coli entries.
C4 Detection difficulty
Difficulty of recognizing and confirming infection
Laboratory-dependent: The presentation does not point to this disease specifically, but local or regional laboratories can confirm it with a validated assay once it is suspected
CONFIRMED by Eric. The assignment reached this level from the evidence, and he has reviewed and ratified it.
Confirmed by Eric. CONFIRMED. "c4l2, agree with assessment. In some cases the lesions are virtually pathognomonic but any reasonable lab should be able to confirm - L2 is correct"
Basis. ch49 49.5.2.3: "The disease may be sporadic or may affect an entire herd and may be first recognized as sudden death without signs of disease. Some affected pigs become inappetent, show subcutaneous and submucosal edema with swelling of the eyelids, emit a peculiar squeal, and show ataxia, staggering gait, incoordination." 49.5.4.1: "Edema disease must be differentiated from other common causes of nervous signs in weaned pigs, including pseudorabies, teschoviral encephalitis, Streptococcus suis or Glaesserella parasuis induced meningitis, and water deprivation/salt intoxication." 49.5.4.2: "Because bacterial numbers may have declined in more protracted cases, such as subacute or chronic ED, a negative bacteriological result does not necessarily exclude the diagnosis of ED." "Subacute or chronic ED is diagnosed by histopathology, especially by the demonstration of subacute to chronic arteriopathy."
How this level was decided
Level 2, and a deliberate step up from the two diarrhoeal entries at level 1. The presentation does not point here: sudden death and neurological signs in a recently weaned pig is shared with four other named causes, and the characteristic gastric and mesenteric oedema "may be absent in a significant number of cases". Confirmation is regional laboratory work -- haemolytic culture plus Stx2e PCR plus histopathology -- but it is a three-method workup rather than an overnight plate, and the chapter warns that a negative culture does not exclude the diagnosis because the organism has often gone by the time the pig is moribund. FLAGGED as a level 1 or 2 judgment: eyelid oedema with a peculiar squeal in a recently weaned pig is close to pathognomonic when it is present.
C5 Production cost
Financial impact on the infected farm's cost of production
Minor: Small and generally short-lived losses with little effect on overall cost of production
CONFIRMED by Eric. The assignment reached this level from the evidence, and he has reviewed and ratified it.
Confirmed by Eric. CONFIRMED. "c5l2, agree with assessment, very low prevalence disease which shows up sporadically in individual pigs and rarely in clusters often in litters on new startup breeding herds"
Basis. ch49 49.5.2.3: "Edema disease mostly occurs during the first few weeks after weaning, although cases may be observed through the grower phase. The disease may be sporadic or may affect an entire herd." "Subclinical ED may occur. Pigs are clinically normal but develop vascular lesions and may have a decreased growth rate." "Chronic ED occurs in a low proportion of pigs recovering from acute cases... growth stops, and sick pigs often show unilateral nervous disturbances." 49.5.6.1: pigs showing neurological signs "have a poor prognosis". The chapter gives cost figures for neonatal diarrhoea and PWD but none for ED.
How this level was decided
Level 2, scored with the other enteric entries. Individual outcomes are bad -- once neurological signs appear the pig usually dies, and survivors are often permanently damaged -- but the disease is sporadic, hits a narrow window after weaning, and burns out. The subclinical form adds a quiet cost in reduced growth. Small and generally short-lived losses. FLAGGED as the least evidenced C5 in the batch: the chapter costs neonatal diarrhoea at $53 per sow and PWD at $179, and gives no figure at all for edema disease.
C6 Market impact
Duration of material disruption to pork and pig markets
Negligible: Little or no material disruption to supply or demand when disease occurs on one or more farms
CONFIRMED by Eric. The assignment reached this level from the evidence, and he has reviewed and ratified it.
Confirmed by Eric. CONFIRMED. "c6l1, old disease, never occurs at scale large enough to have market impact"
Basis. No trade measure, movement control or consumer response is recorded. Edema disease occurs "in pigs in all countries where pigs are raised commercially" and 68.3% of US finishing pigs shed STEC at some point.
How this level was decided
INFERRED. Under the standing note SCORING/market_impact, an agent carried by most US finishing pigs and diagnosed for decades, with no market move on record, is level 1.
C7 Treatment potential
Potential for treatment to improve outcomes
Some: Treatment exists but is inconsistent, requires extralabel use, or works only in some circumstances
Basis. ch49 49.5.6.1, and the chapter states the mechanism rather than just the outcome: "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. This is why pigs showing neurological signs have a poor prognosis. 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."
How this level was decided
Level 2, and a deliberate split from the two diarrhoeal entries at level 1. The label reads "treatment exists but works only in some circumstances", and the chapter defines the circumstance exactly: medication given days BEFORE clinical signs reduces the outbreak, and medication given after them does nothing, because the toxin is already bound to its receptors. That is a real treatment with a window that closes before the disease is visible.
C8 Vaccine availability
Availability of effective vaccines or bacterins
Available, or not needed: Effective vaccines are widely available in the US or secured for national outbreak response, or the disease does not clinically or economically justify vaccinating
CONFIRMED by Eric. The assignment reached this level from the evidence, and he has reviewed and ratified it.
Confirmed by Eric. CONFIRMED. "c8l1, agree with assessment - I am not aware of the vaccine at all, and am sure is not currently available in US. but if there is evidence it is available and works, L1 is correct (and in most farms it is not needed anyway)"
Basis. ch49 49.5.6.3: "A commercial injectable vaccine based on genetically modified recombinant Stx2e that showed reduction of mortality due to ED is licensed in several countries. 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, and provide immunity for at least 105 days post vaccination." A second recombinant Stx2e vaccine given at 2 days of age protected "from 21 days to at least 112 days post vaccination". A 2022 systematic review and meta-analysis found vaccinated pigs "showed lower clinical signs, reduced mortality, and increased weight gain".
How this level was decided
Level 1 on the first clause -- an effective vaccine exists, is commercially licensed, and a meta-analysis confirms it cuts clinical signs and mortality and improves weight gain. FLAGGED FOR ERIC AS A GEOGRAPHY QUESTION HE MAY NEED TO SETTLE, and it is the same shape as the label question he ruled on for tiamulin: the chapter says the product is "licensed in several countries" and does not name them, and C8 level 1 requires effective vaccines to be widely available IN THE US. If the recombinant Stx2e vaccine is not US-licensed, this cell is level 3 -- an effective vaccine has been developed and the US cannot buy it.
Levels and evidence are generated from data/assignments/ecoli_edema_disease.yml; the overview is authored in data/overviews/ecoli_edema_disease.md. Do not hand-edit this page — corrections go in data/assignments/CORRECTIONS.yml.
Quoted material marked Basis is from Zimmerman JJ, Karriker LA, Ramirez A, Schwartz KJ, Stevenson GW, Zhang J, eds. Diseases of Swine, 12th edition. Hoboken: Wiley Blackwell, 2025 — except where another source is named in the quotation itself.