Escherichia coli (non-enteric infections)
LEVELS: Highly unlikely; No human illness; Already in the herd; Laboratory-dependent; Minor; Negligible; Some; Available, or not needed
| Register id | ecoli_nonenteric_infection |
| Type | bacteria |
| Scientific name | Escherichia coli |
| NCBI taxid | 562 |
| Evidence | 2 document(s) |
| Assigned | 2026-09-04, against criteria version 093366e352a2 |
Overview
This entry groups the Escherichia coli infections of pigs that are not gut disease: coliform mastitis in the sow, urinary tract infection, and septicaemia caused by extraintestinal pathogenic E. coli. What they share is that they are not contagious. The bacteria are already present — in the sow's own intestine, or in faecal and environmental contamination of the teats and urethra — and disease follows when they invade tissue rather than when they are passed from one pig to another. Coliform mastitis is reported worldwide at an average herd-level incidence of 13%, and up to 80% of sows that fail to milk properly have visible mastitis; the real cost falls on the piglets, which lose growth or die because a painful udder stops the sow feeding them. Urinary infection is very common in sows — studies report 16–58%, and cystitis was found in 46% of culled sows — and affected sows wean smaller litters and take longer to breed back. Because the source is endogenous, control is about hygiene, water intake and sow condition rather than exclusion.
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, no evidence that the pig strains are a significance source of human infections"
Basis. ch49 49.3, the whole public health section for the chapter, and it is about ONE pathotype: EHEC, "particularly EHEC O157:H7, O26, and other non-O157 serogroups", which "may be sporadically present in the intestines and feces of pigs". "PIGS ARE NOT CONSIDERED A MAJOR SOURCE OF O157 EHEC, AS THE PREVALENCE RATE IS TYPICALLY VERY LOW." The section says nothing about extraintestinal pathogenic E. coli. The chapter's only statement bearing on this entry is 49.2.1.4: "ExPEC is a heterogeneous group of E. coli, which normally inhabit the intestinal tract that can occasionally cause bacteremia leading to septicemia and colonization of extraintestinal niches... Commensal E. coli, which are part of the normal intestinal microbiota, constitute an important reservoir of extraintestinal virulence factors and can be the origin of ExPEC strains."
How this level was decided
INFERRED FROM A STRUCTURED SILENCE, and this is the entry where that silence is thinnest. The chapter gives the human question a section of its own and uses it entirely on EHEC, saying nothing about ExPEC as a human risk, so on the folder the answer is level 1. FLAGGED HONESTLY: ExPEC is a recognised HUMAN pathotype -- it is the cause of most human urinary tract infection and a major cause of human sepsis -- and whether food animals are a source of human ExPEC is an active research question that this chapter does not engage with. The register entry is pig ExPEC and the chapter is silent on transmission, so level 1 records what is held rather than a settled negative. NOTE ON WHAT THIS ENTRY IS: the register unit covers the four non-enteric syndromes of chapter 49 -- E. coli causing fatal shock (49.6), systemic infection and septicaemia (49.7), coliform mastitis (49.8), and nonspecific urinary tract infection (49.9). The agent is extraintestinal pathogenic E. coli, ExPEC, plus ETEC invading secondarily.
C2 Zoonotic impact
Severity of human illness caused by the agent
No human illness: Agent does not cause illness in people
CONFIRMED by Eric. The assignment reached this level from the evidence, and he has reviewed and ratified it.
Confirmed by Eric. CONFIRMED. "c2l1, no evidence that the pig strains are a significance source of human infections"
Basis. No human illness attributable to porcine ExPEC is described anywhere in chapter 49.
How this level was decided
RE-SCORED 2026-09-04. C2 now grades the severity of the illness the agent causes in a person, independent of how the person was exposed -- the 2026-09-01 pig-attribution reading is reversed, and C1 alone carries the source question. FLAG. Human ExPEC causes urinary tract infection and sepsis, so the genus plainly sickens people, but the registered agent is the porcine non-enteric pathotype and the folder does not grade human illness.
PREVIOUS ANSWER, written under the pig-attribution reading: INFERRED, following C1. Under C2 as rescoped, level 1 means pigs are not a source of human illness with this agent, and nothing in the folder says otherwise. FLAGGED WITH C1: if pig ExPEC were shown to reach people, the severity would not be trivial -- human ExPEC causes urosepsis and bacteraemia -- so this is the cell that would move furthest if the evidence base changed.
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 49.4.3, stated outright: "In contrast, infections caused by ExPEC and E. coli causing CM and UTI DO NOT BEHAVE AS COMMUNICABLE DISEASES. Mixed infections by more than one strain are frequent and are acquired by invasion of preexisting intestinal bacteria in the case of ExPEC, and from fecal or environmental contamination of the teats and urethra in the case of CM and UTI, respectively." 49.9: "nonspecific UTI behaves like a noncontagious infectious disease of endogenous origin, where the fecal microbiota is a reservoir for this extraintestinal infection." 49.7: "The intestine is considered the major route of E. coli invasion."
How this level was decided
Level 1, and this is the cleanest level 1 in the batch because the chapter denies communicability in terms. These are not infections a pig catches; they are the pig's own gut flora getting somewhere it should not be -- through the intestinal wall in septicaemia, up the teat canal in mastitis, up the urethra in cystitis. There is no introduction event to prevent because there is no introduction. NOTE the consequence for control, which the chapter draws: prevention is colostrum intake, farrowing hygiene, water intake and housing, not biosecurity.
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
Basis. ch49 49.7.4: "Systemic colibacillosis should be suspected with the appearance of the clinical signs and lesions described above, especially when observed in pigs under 4 days of age... In older suckling and especially weanling pigs with polyserositis, differentials should include G. parasuis, Mycoplasma hyorhinis, and S. suis. Diagnosis is confirmed by isolation of the organism in pure culture or by the predominance in extraintestinal organs." 49.8.4, on coliform mastitis: "A RELIABLE RAPID TEST FOR USE ON THE FARM IS NOT AVAILABLE... Because mastitis is a local process, samples must be taken from individual complexes and not pooled." 49.9.2, on UTI: "In the vast majority of nonspecific UTI cases, there are no clinical signs." 49.9.4: "Clinical examination of the animal is of little value in the diagnosis of UTI, which requires laboratory confirmation... in dead sows, histopathology is the gold standard."
How this level was decided
Level 2, and every one of the four syndromes fails the level 1 test for a different reason. Polyserositis in a weaner points at three other bacteria before it points here. Coliform mastitis has no farm-side test and must be sampled gland by gland rather than pooled. Urinary tract infection is usually silent and needs urinalysis and culture in the live sow or histopathology in the dead one. But once the sample is taken, the work is ordinary bacteriology on ordinary media at a regional laboratory, which is level 2. NOTE the interpretive difficulty the chapter records for UTI: the vagina and distal urethra carry normal flora, so infection is separated from contamination by quantifying the bacteria in the urine.
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
Corrected by Eric from L3 Moderate. Reason: "c5l2, we will downgrade. It is tricky because virtually no microbiology is done on mastitis cases and many other septic diseases are also just discounted as 'one of those things' and not worked up in lab so we don't really know the prevalence in the field."
Basis. ch49 49.8: coliform mastitis "is reported worldwide with an average incidence of 13% at the herd level", and "The most important adverse economic effect of CM in sows is the mortality and growth retardation in piglets due to pain in affected teats and dysgalactia." "Up to 80% of dysgalactic sows may have gross lesions of mastitis." 49.4.2: UTI prevalence studies range "from 15.8 to 58%", and "cystitis was diagnosed histologically in 45.94% of culled sows". 49.9.2: "Sows with a significant bacteriuria tend to wean small litters, have increased intervals between litters, show a lower fertility rate, and exhibit an inferior body condition", and pyelonephritis "may lead to the death or early culling of sows". 49.7: septicaemia "occurs sporadically or rarely as small outbreaks".
How this level was decided
Level 3, ONE LEVEL ABOVE THE OTHER THREE E. COLI ENTRIES, and the justification is that this entry attacks the sow rather than the piglet. Coliform mastitis runs at 13% herd incidence and takes the milk away from a whole litter. Urinary tract infection is found in a sixth to more than half of sows depending on the method, cystitis in 46% of CULLED sows, and it costs smaller litters, longer intervals between them, lower fertility, poorer condition, and premature culling or death from pyelonephritis. Sow longevity and reproductive output are where a breeding herd makes its money, so losses of that kind measurably increase cost of production while remaining manageable within normal operations. FLAGGED as the judgment most worth Eric's eye in this batch: the chapter gives dollar figures for neonatal diarrhoea and PWD and none for these syndromes, so level 3 rests on the prevalence and the mechanism rather than on a costing.
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 in sections 49.6 to 49.9. These are endogenous, non-communicable conditions of individual pigs and sows, occurring worldwide.
How this level was decided
INFERRED. Under the standing note SCORING/market_impact, conditions arising from a pig's own gut flora, diagnosed routinely in US herds and never notifiable, have no route to pork supply or demand. 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 49.7.5, on septicaemia: "treatment may be useful in subacute cases of infection but is mostly ineffective after the appearance of clinical signs." 49.8.6, on coliform mastitis: "therapeutic measures are usually not undertaken before the sow shows signs of dysgalactia. Thus, treatment may at best shorten the period of underfeeding of the piglets. Antimicrobial therapy is complicated by the heterogeneous pattern of antimicrobial susceptibility of individual isolates not only within a herd but also within a sow. THEREFORE, SENSITIVITY TESTING IS OF LITTLE VALUE IN INDIVIDUAL CASES." Amoxicillin, tylosin, potentiated sulfonamides, enrofloxacin and cefquinome are named as effective, with meloxicam indicated. 49.9.6, on UTI: "Treatment of urogenital infections of swine can be frustrating... Prolonged parenteral treatment may be recommended, although subclinical UTI often persists after treatment."
How this level was decided
Level 2, and the chapter says "treatment exists but is inconsistent" three separate times in three different sections. Effective drugs are named for mastitis and used for all three syndromes, so this is not level 3. What holds it off level 1 is that every syndrome defeats treatment in its own way: septicaemia is past saving once signs appear, mastitis is recognised too late to do more than shorten the piglets' hunger and carries susceptibility so heterogeneous that the chapter says testing is of little value even within one sow, and urinary infection frequently persists subclinically after a prolonged course.
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
Corrected by Eric from L2 Available but inconsistent. Reason: "c8l1, downgraded. I don't think there is a specific e.coli with a claim to prevent mastitis or septicemia, this is a different e.coli and toxin potential than other e.coli's in diarrhea vaccines. i don't think they work for mastitis and septicemia. similar situation in dairy cow mastitis - coliform mastitis is a recognized problem and in fact there was a J5 antigen vaccine made to combat it but i don't think ever captured much market. there seems to be important cofactors that allow e.coli to become septic and wisdom is to fix these, rather than trying to find a vaccine"
Basis. ch49 49.7.5: "Vaccination is rarely considered for the control of septicemia due to E. coli. However, in the case of small outbreaks of septicemia, careful monitoring of the causative serogroup(s), production of an autovaccine, and its administration to the pregnant sows might be beneficial." 49.8.5, on coliform mastitis: "An episode of CM apparently does not result in protection against homologous reinfection." No vaccine is described for coliform mastitis or for urinary tract infection.
How this level was decided
Level 2 on the first clause, and narrowly. Autogenous bacterins are a recognised option for the one syndrome where a serogroup can be identified and given to pregnant sows, so a vaccine of a kind exists and its protection is plainly inconsistent -- the chapter says vaccination is rarely considered at all. FLAGGED AS A LEVEL 2 OR 3 JUDGMENT, because the autogenous route covers only septicaemia, which is the rarest of the four syndromes, and nothing exists for the two that carry the cost. The chapter also records the reason a mastitis vaccine would be hard: natural infection confers no protection against reinfection by the same strain, so there is no immunity to imitate.
Levels and evidence are generated from data/assignments/ecoli_nonenteric_infection.yml; the overview is authored in data/overviews/ecoli_nonenteric_infection.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.