Key take-aways 

  • Common and costly: One of the most frequent nursery diseases worldwide; hits herd performance and treatment budgets across production systems. 
  • When it strikes: Typically 3-10 days (up to about 2 weeks) after weaning; sudden group‑wide watery scour, dehydration, growth check. 
  • Main culprit: Enterotoxigenic E. coli (ETEC) with F4 or F18 fimbriae + LT/ST toxins drives classic PWD. 
  • But not always E. coli: Substantial share of diarrhoea outbreaks show low/no high‑level ETEC; rotavirus A frequently detected in ZnO‑free field cases. 
  • Strain shift alert: Recent US surveillance – F18 strains now outnumber F4; rising hybrid F18:LT:STa:STb:Stx2e links PWD with oedema disease risk. 
  • Resistance pressure: Nursery E. coli show worrying multidrug resistance; culture & susceptibility testing before mass medication is increasingly essential. 
  • ZnO era ending: Therapeutic zinc oxide once a cornerstone; phased out EU‑wide (June 2022) and further tightened nationally – some farms report renewed scour pressure post‑withdrawal. 
  • High‑impact hygiene moves: All‑in/all‑out flow, thorough cleaning/drying, effective disinfection, and easily sanitised (slatted) flooring reduce PWD risk. 
  • Cut weaning stress: Warm, draft‑free pens; minimal mixing; good colostrum start; encourage early creep feed intake to smooth diet transition. 
  • Nutrition levers: Lower crude protein (balance amino acids), reduce diet acid‑binding capacity, add organic acids, use highly digestible ingredients, manage DON/mycotoxins. 
  • Gut‑health adjuncts: Probiotics, prebiotics/fibre and phytogenics (e.g. horseradish/essential oils) show protective effects in some commercial herds; results farm‑specific. 
  • Therapy today: Use short, targeted antimicrobial courses guided by lab results; combine with aggressive oral rehydration, warmth, and improved hygiene. 
  • New tools coming: Feed “receptor analogue” decoys blocking F18/F4 adhesion show promising protection in trials; watch commercial rollout. 
  • Phage potential: Acid‑protected bacteriophage cocktails can sharply reduce ETEC counts in models – an emerging antibiotic alternative under development. 
  • Track and adapt: Monitor local E. coli virotypes and AMR trends; log scour scores post‑ZnO to benchmark interventions and refine control plans. 

Definition and impact of post-weaning diarrhoea (PWD) 

Post-weaning diarrhoea (PWD) is a common disease syndrome affecting piglets within about 2 weeks after weaning. It is characterised by sudden onset of watery diarrhoea, dehydration, loss of body weight in surviving piglets, and in severe cases significant mortality. PWD is considered one of the most frequent and costly diseases in pig production worldwide. Economic losses arise from increased piglet deaths, veterinary treatment costs, and stunted growth of recovered pigs. Mortality rates in outbreaks vary, but in poorly managed or untreated cases up to 20-25% of affected piglets may die. Even subclinical or short bouts of diarrhoea can reduce growth rates and feed efficiency. Because weaning is a universally stressful period for piglets, PWD is a global concern wherever pigs are raised. 

Causes and pathogens of Post-weaning diarrhoea in pigs (Enterotoxigenic E. coli) 

PWD has a multifactorial origin, but the primary identified cause is infection with enterotoxigenic Escherichia coli (ETEC) bacteria. These pathogenic E. coli strains colonise the small intestine using hair-like fimbriae (typically F4 [K88] or F18 in post-weaning pigs) and produce enterotoxins – notably heat-labile toxin (LT) and heat-stable toxins (STa, STb) – that induce fluid secretion and diarrhoea. This condition is often called “post-weaning colibacillosis,” reflecting the central role of E. coli. In fact, pig veterinarians and farmers traditionally use “PWD” and “coli diarrhoea” interchangeably. 

However, not all cases of post-weaning diarrhoea are caused by E. coli. Recent field studies have shown that in a substantial portion of PWD outbreaks, ETEC cannot be detected at significant levels. For example, a European survey of 873 diarrhoeic pigs found no ETEC in about 40% of affected herds. In such cases, other pathogens or non-infectious factors may be involved. Other infectious agents that can occasionally cause similar post-weaning diarrhoea include enteropathogenic E. coli (EPEC) and (more rarely) Salmonella species. The role of rotaviruses (especially Rotavirus A and C) in PWD is still debated – some outbreaks have high rotavirus levels, but it’s unclear if rotavirus alone triggers PWD or simply co-infects piglets already predisposed to diarrhoea. In many herds, PWD is multifactorial, arising from a combination of mild infections and management/diet factors rather than a single pathogen. There is growing evidence that post-weaning intestinal upset can occur with no specific infectious agent, due to post-weaning diet changes, gut microbial imbalances, and weaning stress. Overall, E. coli remains the pivotal pathogen in classic PWD, but veterinarians should consider differential diagnoses (such as viral or parasitic diarrhoea) when ETEC is not identified. 

Clinical signs of Post-weaning diarrhoea in pigs

Post-weaning diarrhoea typically appears 3 to 10 days after weaning, often peaking around the end of the first week post-weaning. The clinical hallmark is a profuse, watery diarrhoea that is usually non-bloody. Faeces are often greyish or brown, watery in consistency, and may cause soiling of the piglet’s hindquarters and tail. Mucus or blood in the stool is uncommon in PWD – if blood is present, other causes like swine dysentery or Lawsonia infection might be suspected. Affected piglets quickly show signs of dehydration (sunken eyes, reduced skin elasticity) and may appear hollow-flanked and weak. In many cases the diarrhoea is self-limiting and lasts 3-5 days before resolving as piglets develop some immunity. However, under poor husbandry conditions or virulent infections, diarrhoea may persist and piglets can become severely dehydrated and acidotic. Early PWD generally does not cause fever (body temperatures often normal or even below normal due to dehydration), though mild fever up to about 40°C has been reported in some outbreaks. Affected piglets often have reduced appetite and huddle due to chilling (from fluid loss and wetness). If PWD is uncomplicated, mortality is usually relatively low (under 10% of affected pigs). Nonetheless, even transient diarrhoea can cause growth checks – survivors of PWD outbreaks may be permanently stunted or take longer to reach market weight. 

Diagnosis of Post-weaning diarrhoea in pigs

Diagnosis of post-weaning diarrhoea is based on the age and clinical presentation, combined with laboratory testing to confirm the causative agent. Clinically, a diagnosis of PWD is suspected when multiple recently weaned piglets develop sudden watery diarrhoea within the first 1-2 weeks post-weaning. This temporal pattern and the absence of blood in faeces help distinguish PWD from neonatal diarrhoea or later-stage grower diseases. For a definitive diagnosis and to guide treatment, veterinarians often submit samples to a lab to identify E. coli and other pathogens. Bacteriological culture and PCR tests are used to detect ETEC strains and their virulence factors. Typically, laboratories will confirm if heavy growth of β-haemolytic E. coli is present and test for fimbrial antigens (F4, F18, etc.) or toxin genes. A pure culture of E. coli from the small intestine of a freshly dead piglet, especially one showing appropriate toxin genes, strongly supports enteric colibacillosis. Modern PCR assays can quantify the load of ETEC (e.g. copy numbers of fimbrial genes), which helps distinguish incidental findings from a true etiological role. If no ETEC is detected, labs will look for rotaviruses, Isospora suis (coccidia), Clostridium perfringens, and other causes of piglet diarrhoea. It’s important to interpret lab results in context – low levels of E. coli or presence of rotavirus might not fully explain an outbreak. In practice, veterinarians often initiate treatment based on clinical diagnosis (especially in severe outbreaks) while awaiting lab confirmation. Post-mortem examinations can also support the diagnosis: piglets that died from PWD often have dilated, fluid-filled small intestines with intact villi and minimal intestinal lesions (consistent with a secretory diarrhoea), and dehydration of the carcass. 

Transmission and risk factors of Post-weaning diarrhoea in pigs

Post-weaning E. coli diarrhoea is primarily spread via the faecal-oral route. The E. coli strains that cause PWD are typically already present in the farm environment or carried in the gut of healthy older pigs. At weaning, piglets are exposed to these bacteria through contaminated pen floors, feeders, and the general environment (often seeded by faeces of previous weaned groups). Piglets that carry pathogenic E. coli can also infect their pen-mates by direct faecal contact. The stress of weaning – including mixing of litters, transport, and a new diet – often triggers increased shedding of pathogens and greater susceptibility in naive piglets. E. coli can survive well in manure and dust, so inadequate cleaning between batches or continuous-flow rearing allows the bacteria to persist and accumulate. Older pigs that have recovered from PWD may remain carriers of the organism and introduce it to younger groups if age segregation is poor. Thus, high infection pressure (many bacteria in the environment) is a major risk factor for PWD outbreaks. 

Aside from exposure to the bacteria, several predisposing factors make post-weaning piglets especially vulnerable to diarrhoea: 

  • Weaning stress and immunity: Weaning typically occurs at 3–4 weeks of age on commercial farms, which is an abrupt separation from the sow’s milk. Maternal milk contains antibodies (IgA) that help suppress intestinal E. coli. After weaning, this lactogenic immunity disappears within days, leaving piglets immunologically naïve in the gut. At the same time, piglets experience stress from transport, mixing with unfamiliar pigs, and adapting to a new pen environment. These stressors elevate cortisol levels and temporarily suppress the piglet’s immune defenses, reducing the ability to cope with pathogens. 
  • Diet change: The transition from easily digestible sow’s milk to a solid, plant-based diet is a key factor in PWD. Piglets often go off-feed (anorexia) for a day or two post-weaning, causing undigested feed to accumulate once they resume eating. The new diets typically contain higher levels of plant proteins, complex carbohydrates, and anti-nutritional factors that piglets’ immature digestive systems struggle to process. This leads to indigestion and nutrients lingering in the gut lumen, which in turn feed bacteria like E. coli. Weaning-induced anorexia also results in villous atrophy in the small intestine (the intestinal villi shrink due to lack of enteral nutrition), reducing the piglet’s absorptive capacity. The combination of gut mucosal damage and abundant nutrients creates ideal conditions for E. coli to proliferate and attach to the gut lining. Furthermore, within a few days of weaning the stomach pH of piglets rises (becomes less acidic) because milk intake stops and acid secretion is initially low. A higher gastric pH means less killing of bacteria in the stomach, so more pathogens survive into the intestines. Research has shown that post-weaning piglets often have significantly higher stomach and small intestine pH, facilitating E. coli colonisation. 
  • Intestinal microflora changes: The removal of milk and its lactose, along with reduced feed intake, also alters the piglet’s gut microbiome. Beneficial bacteria that thrived on milk (like lactobacilli and bifidobacteria) decrease, while opportunistic Enterobacteriaceae (such as E. coli) increase in number. This dysbiosis can compromise gut health. If the beneficial commensals are depleted, pathogenic E. coli face less competition and can more easily dominate the gut ecosystem, contributing to diarrhoea. 
  • Environmental and management factors: Husbandry conditions around weaning can greatly influence PWD outcomes. Chilling is a known risk factor – if the ambient temperature in the nursery falls too low for young pigs, their intestinal motility slows down and immunity is impaired, allowing bacteria to proliferate. For instance, colder pen temperatures have been correlated with more severe and prolonged diarrhoea. Overcrowding and poor sanitation also raise the risk of PWD outbreaks by increasing exposure to pathogens and stress. In contrast, farms that practice strict all-in/all-out management (keeping each weaning group separate and fully cleaning facilities between batches) tend to have fewer PWD issues, because this breaks the cycle of transmission. A recent study in Austria found that implementing all-in/all-out in nursery rooms and thoroughly cleaning (often associated with fully slatted flooring designs) was strongly associated with lower PWD incidence. In that study, farms with continuous flow or partial hygiene measures had more frequent diarrhoea cases. Other management-related risk factors include mixing piglets from many sources (increases pathogen spread), a history of neonatal diarrhoea in the farrowing house (indicating presence of virulent E. coli early on), and early weaning of very light-weight piglets (which may have underdeveloped immunity). All these factors interplay to determine whether an E. coli challenge at weaning turns into a full-blown diarrhoea outbreak or just a mild, transient upset. 

Treatment of Post-weaning diarrhoea in pigs and the impact of antibiotic/ZnO restrictions 

The traditional treatment for post-weaning diarrhoea caused by E. coli has been antimicrobial therapy combined with supportive care. At the first signs of an outbreak, veterinarians often administer broad-spectrum antibiotics to affected piglets (for example, oral neomycin, gentamicin, trimethoprim-sulfa, or amoxicillin, depending on the region and antibiotic sensitivity results). In many cases, medication is delivered via the drinking water or feed to treat the whole group, as PWD tends to spread rapidly. Prompt antibiotic treatment usually reduces piglet mortality and shortens the course of diarrhoea. Alongside antimicrobials, supportive measures are important: providing easily accessible clean water and oral rehydration solutions, keeping piglets warm and dry (to counteract dehydration and energy loss), and offering highly digestible feed to encourage intake and recovery. Severely dehydrated pigs may require injectable electrolytes or even hospitalization for intravenous fluids in extreme cases, though on-farm this is rare. 

Global shifts in antibiotic use: In recent years, the routine use of antibiotics for PWD has come under scrutiny due to rising antimicrobial resistance (AMR). Studies have documented that E. coli isolated from piglets with diarrhoea often harbour resistance to multiple antibiotic classes. This makes choosing an effective drug more challenging and raises public health concerns. Notably, E. coli resistance to historically used drugs like tetracyclines, sulfonamides, and even newer cephalosporins has been observed.  

Zinc oxide (ZnO) ban and its consequences: For decades, in-feed zinc oxide at high doses was a cornerstone of PWD prevention and treatment, especially in Europe. Pharmaceutical-grade ZnO (typically given at 2,000–3,000 ppm in piglet feed for two weeks post-weaning) is very effective at reducing post-weaning diarrhoea. Unlike antibiotics, zinc oxide doesn’t target E. coli via a specific bactericidal mechanism; rather, it improves gut health through multiple pathways (e.g. strengthening the intestinal barrier, reducing gut inflammation, and altering the gut microbiota in beneficial ways). This made ZnO a valuable tool to control diarrhoea without selecting for bacterial resistance. However, prolonged heavy use of ZnO raised environmental and health concerns.  

Current treatment approaches: Given these restrictions, treatment of PWD now focuses on strategic antibiotic use and non-antibiotic adjuncts. When an outbreak occurs, veterinarians will often perform antibiotic sensitivity testing on E. coli isolates to choose an effective drug, since empirical choices have become less reliable with resistance. The duration of treatment is kept as short as possible, and only sick groups are medicated (no blanket prophylaxis). Supportive care (warm, dry housing and oral rehydration) is critical. If available, some farms use oral vaccines or immune serum products at weaning (see below), but these are more preventive. Overall, the trend is toward reducing antibiotic reliance and using an integrated approach to manage PWD through improved hygiene, nutrition, and targeted interventions. 

Integrated prevention strategies of Post-weaning diarrhoea in pigs

Preventing post-weaning diarrhoea requires a holistic approach addressing sanitation, pig management, and nutrition. No single measure is 100% effective by itself; successful control comes from combining multiple strategies that collectively reduce the pigs’ stress and pathogen exposure. Key components of an integrated PWD prevention program include: 

  • Hygiene and biosecurity: Rigorous hygiene is fundamental. Nurseries should be run on an all-in/all-out basis, where each batch of pigs is moved out completely, then the room is thoroughly cleaned, disinfected, and left empty (dry) for a period before new weaners enter. This breaks the cycle of infection between groups. 
  • Environmental management: Stress reduction at weaning is critical. Provide a warm, draft-free environment for weaned pigs, since chilling exacerbates diarrhoea. The nursery temperature should be around 28–30°C at weaning and then gradually reduced, ensuring piglets can pile together for warmth but are not cold-stressed.  
  • Nutritional strategies: The composition and presentation of the weaner diet have a profound effect on PWD risk. A common approach is to reduce the crude protein level of the diet without sacrificing essential amino acids (this is done by using highly digestible protein sources and supplementing amino acids).  Acidifying the feed is another proven strategy: organic acids (like citric, fumaric, or formic acid) or acid salts are often added to weaner diets to lower the gut pH and create an unfavourable environment for E. coli. Many piglet diets now also include feed additives aimed at gut health, such as zinc alternatives (e.g. lower-dose organic zinc, or zinc in chelated form which may allow efficacy at lower inclusion), and phytochemicals.  
  • Proactive health measures: Without prophylactic antibiotics, farms have turned to natural or management-based prophylaxis. One such measure is providing probiotics to newly weaned pigs. Direct-fed microbials (e.g. certain strains of Lactobacillus, Enterococcus, or Bacillus bacteria or yeast) can help stabilize the gut flora and competitively exclude pathogens. Some farms also use plant extracts and essential oils (phytogenics) as natural antimicrobials and anti-inflammatories in feed. Vaccination of piglets is another proactive strategy, though historically it’s been challenging for PWD (see next section for new vaccine developments). Currently, commercial vaccines for E. coli are mostly given to sows pre-farrowing to protect piglets via colostrum (this helps with neonatal diarrhoea, but maternal antibodies wane by post-weaning). Nonetheless, ensuring piglets get adequate colostrum intake and are in good health at weaning provides them with a stronger baseline immunity. Good creep feeding practices (exposing piglets to dry feed before weaning) can also smooth the transition onto feed and lessen the growth check after weaning, indirectly reducing the risk of diarrhoea. 

Emerging innovations in Post-weaning diarrhoea in pigs and future solutions 

The challenges posed by antibiotic resistance and the ZnO ban have spurred research into new methods to combat PWD. Several promising innovations are on the horizon for controlling E. coli diarrhoea in pigs: 

  • Vaccines for weaned pigs: While sow vaccination against E. coli (to boost colostral antibodies) has long been used for neonatal scour prevention, attention is now turning to vaccinating piglets themselves against PWD. Oral vaccines are considered the most effective route for intestinal protection because they stimulate local gut immunity (secretory IgA antibodies).  Additionally, subunit vaccines (oral vaccines made of purified fimbriae proteins or toxoids rather than live bacteria) are being explored.  
  • Receptor analogues (decoy molecules): A novel strategy that has shown great promise is the use of receptor analogues in feed. This approach involves feeding piglets molecules that mimic the specific receptors on the intestinal lining to which ETEC bacteria bind. If the E. coli bacteria attach to these decoy molecules instead of the pig’s intestinal cells, they are flushed out without causing disease. 
  • Bacteriophage therapy: Bacteriophages are viruses that infect and kill bacteria. Phage therapy for E. coli in pigs is an exciting area of research as an alternative to chemical antibiotics. Phages are very specific to their bacterial hosts, so a phage that targets ETEC could, in theory, eliminate pathogenic E. coli in the pig’s gut without disturbing other bacteria. Researchers have begun isolating phages that infect the common ETEC serotypes.  
  • Immunotherapeutics (passive immunity and antibody derivatives): Another innovation focuses on using antibodies or fragments of antibodies to neutralise E. coli in the gut. An example is the development of VHH antibodies (also known as nanobodies). VHHs are special single-domain antibody fragments derived from camelids (like llamas) that can be engineered to bind specifically to antigens – in this case, ETEC fimbriae or toxins. Scientists have created VHH that bind strongly to F4 and F18 fimbriae of E. coli. Similarly, some companies are exploring spray-dried egg yolk antibodies (IgY) against ETEC – hens are hyperimmunised with ETEC antigens, and the IgY antibodies extracted from their eggs can be fed to piglets to bind E. coli. These passive immunity approaches don’t induce the pig’s own immune response, but they can bridge the gap during the critical post-weaning window. 
  • Genetic resistance in pigs: A more long-term innovation is breeding pigs that are genetically resistant to ETEC. It’s known that pigs must express certain receptors on their intestinal cells for ETEC bacteria to attach.  
  • Other novel interventions: Additional innovations under exploration include bacteriocins (small antibacterial peptides produced by benign bacteria that could be given to pigs to suppress E. coli), engineered probiotics (probiotic bacteria designed to secrete anti-E. coli enzymes or factors), and small molecule inhibitors that block E. coli quorum sensing or toxin production. Research is also looking at immunomodulators that could be given at weaningto boost the pig’s own gut immune response. While these are in early stages, they underscore the variety of creative approaches scientists and veterinarians are pursuing to tackle PWD in the post-antibiotic era. 

Many of these emerging solutions are in experimental or trial phases as of 2025. It’s likely that the future of PWD control will involve using several of them in combination.  

Global occurrence, strain variation and prevalence of Post-weaning diarrhoea in pigs

Post-weaning diarrhoea due to E. coli is truly a global issue, affecting pig farms on every continent. It tends to be a disease of intensive pig production – wherever large numbers of pigs are weaned in batches at a young age, PWD has the potential to emerge. Surveys confirm that PWD remains one of the most significant enteric diseases of swine worldwide (Paiva et al., 2025). However, the prevalence of PWD outbreaks can vary widely between regions and farm systems, depending on management practices and prevalent E. coli strains. 

In terms of geographical occurrence, PWD is reported in all major pork-producing regions (Europe, North and South America, Asia, etc.). For instance, countries like Denmark and The Netherlands (with very early weaning and historically heavy ZnO use) have documented PWD as a leading post-weaning problem for decades. After the removal of ZnO in the EU, veterinarians in Europe noted a rise in cases (as mentioned earlier). In contrast, some regions with later weaning ages or smaller-scale farming may see fewer severe outbreaks. Nonetheless, even smallholder farms in developing countries experience PWD if weaning is not managed well – though it may be under-reported in those settings. 

When it comes to strain variation of E. coli, there are important differences in the types of E. coli causing PWD across the world and even over time. The two primary fimbrial types in weaned pig diarrhoea are F4 (K88) and F18. Historically, F4^+ ETEC was notorious for causing devastating diarrhoea in very young pigs (including pre- and post-weaning) especially if colostral immunity was lacking; these infections could kill many piglets in an outbreak. F18^+ strains tend to be associated with slightly older nursery pigs and are also linked to oedema disease. A recent comprehensive study of E. coli isolates from PWD cases in the United States (2010–2023) illustrates current patterns: about 70% of the isolates possessed F18 fimbriae, whereas ~26% had F4 fimbriae, with only a tiny fraction carrying F5 or other adhesins. This indicates F18 strains have become very prevalent in PWD situations (possibly as farms started controlling F4 with sow vaccination and other measures, F18 emerged more).  

Prevalence on farms: Within a farm, the prevalence of PWD (proportion of piglets affected) can range widely. Some farms experience sporadic mild cases (only a few pigs with loose stool), while others suffer explosive outbreaks where nearly the entire group scours. Nielsen et al. (2023) documented PWD outbreaks in Danish herds (without ZnO) with diarrhoea prevalence ranging from 10% up to 94% of piglets in the group. Typically, if PWD is going to occur, at least 20–50% of pigs break with diarrhoea, but mortality is much lower (often <5–10% with treatment). These numbers can worsen in the absence of interventions. Importantly, the farm-to-farm variation in PWD prevalence highlights the influence of management: farms with very good weaning protocols and hygiene may keep incidence near zero, whereas those with suboptimal conditions struggle with frequent cases. 

Looking at global trends, there is some anecdotal evidence that PWD problems have increased in regions enforcing antibiotic reduction. For example, European practitioners report more PWD cases post-2022 (ZnO ban), and China has also noted PWD challenges as they attempt to reduce colistin usage. Conversely, countries that still allow certain in-feed antibiotics (like carbadox in some North American systems) or ZnO may have somewhat fewer issues, though they face other pressures to eliminate those tools eventually. The E. coli strains themselves also evolve: vaccination and other pressures may change the dominant strains over time (for instance, if an oral vaccine against F4 is widely used, we might see more F18 or non-vaccine strains emerging). 

FAQ – Frequently asked questions about post-weaning diarrhoea in pigs

Q: When do piglets typically get post-weaning diarrhoea and what are the signs? 

A: PWD usually strikes within the first 3–10 days after piglets are weaned. Farmers often notice it about a week post-weaning. The main sign is watery diarrhoea – the pen floor or mat will be wet and you may see grey, brown, or yellowish loose stools. Unlike some other diarrhoeas, there’s usually no blood in the faeces. Affected piglets look dehydrated (shrunken eyes, tucked-up abdomen) and might be a bit thin or gaunt. They may also appear depressed, eat less feed, and huddle together if they feel cold. In most cases, piglets remain bright but just scouring; however, if it’s severe, some piglets can become very weak or even die from dehydration. You might notice a stunted, “poor-doing” group if PWD has caused growth checks. Typically, a large percentage of the group breaks with diarrhoea around the same time, which is a key indicator that it’s post-weaning scour. 

Q: What causes post-weaning diarrhoea? 

A: The primary cause of PWD is a bacterial infection by enterotoxigenic Escherichia coli (ETEC). These are strains of E. coli that produce specific toxins in the gut, causing the piglet to secrete fluid and develop diarrhoea. They often are called “coli” or “colibacillosis.” The stress of weaning (coming off the sow’s milk and onto solid feed) creates conditions that let E. coli flourish in the intestines. Piglets no longer get protective antibodies from sow’s milk at this stage, and the sudden diet change can upset their digestion, both of which let E. coli bacteria multiply rapidly. While E. coli is the main culprit, it’s often a combination of factors that leads to an outbreak – for example, chilling, overcrowding, or not enough hygiene can all increase the risk. Occasionally, other germs like rotavirus or Salmonella might be involved, but if you have piglets with diarrhoea right after weaning, E. coli is the first thing we suspect. 

Q: How is PWD different from other pig diarrhoeas, and how is it possible to confirm it is E. coli? 

A: PWD is specifically diarrhoea affecting recently weaned pigs (roughly 3–10 weeks old). This sets it apart from neonatal piglet scours (which hit newborns and are often due to E. coli F5/K99, Clostridium, or viral causes) and from grower/finisher diarrhoeas (like swine dysentery or ileitis, which occur in older pigs and often have blood or necrotic stool). In PWD, piglets are a few weeks old, there’s no blood in the diarrhoea, and it coincides with the weaning period. To confirm E. coli as the cause, a vet can take fecal samples or dead piglets to a lab. The lab will culture the bacteria and identify if it’s an enterotoxigenic E. coli (they have tests to detect the toxin genes and the fimbriae like F4 or F18). If they find a heavy growth of ETEC matching the history, that confirms “post-weaning colibacillosis.” Often, vets will treat based on the characteristic signs and age, but lab confirmation helps, especially to do an antibiotic sensitivity test. It’s also useful to rule out other causes – for instance, checking for rotavirus or coccidial oocysts in the feces can tell you if those are playing a role. But in practice, the timing (right after weaning) and watery nature of the scour are strong clues. 

Q: How do piglets get infected with E. coli? 

A: E. coli that cause PWD are usually already present on the farm. Piglets often ingest the bacteria from their environment. After weaning, they’re moved into nursery pens that might have residual bacteria on floors or feeders if not thoroughly cleaned. Also, piglets from different litters are mixed, so a piglet carrying a pathogenic E. coli strain can spread it to pen-mates. The bacteria spread through faeces – one piglet starts shedding E. coli in its diarrhoea, and others swallow those germs (by nosing the floor, feeders, or each other) and then get sick. E. coli can survive in manure, on boots, equipment, even carried in on flies or dust. Sometimes older pigs in the barn are carriers; they might not show signs but can shed the bacteria that younger pigs pick up. Essentially, anything contaminated with feces from an infected pig can transmit the bug. This is why cleaning and disinfection between batches, and limiting direct contact between different age groups, is important to break the cycle. 

Q: What treatments are available for post-weaning diarrhoea? 

A: The main treatment has been antibiotics to kill the E. coli bacteria, along with supportive care. Common antibiotics used include things like neomycin, gentamicin, trimethoprim-sulfa, or others, often given in water or sometimes by injection for a few days. A vet will choose an appropriate antibiotic (ideally based on lab sensitivity results, because E. coli on some farms are resistant to certain drugs). Early treatment is important – if you medicate right when pigs start scouring, you can prevent deaths and help them recover faster. Supportive care means making sure the piglets don’t get dehydrated: providing electrolytes in water, making water easy to access, and keeping the piglets warm. Many farmers will increase the temperature in the room a bit for scouring piglets and give high-energy electrolytes to drink. With those steps, typically the diarrhoea will subside in a few days. It’s also critical to remove and properly dispose of dead pigs and to clean up the pens, because that reduces the infection pressure. One thing to note: in the EU and some other places, we can’t use preventive antibiotics anymore, so we only treat pigs that are actually sick. Also, high-dose zinc oxide in feed was commonly used as a “treatment” or preventative in the past – it helped a lot to reduce diarrhoea – but it’s now banned in the EU due to environmental concerns. So, treatment now focuses more on prompt therapeutic antibiotics and nursing care. In very severe outbreaks, some farmers will feed a bland diet (like more cooked rice or a gruel) for a short period to help piglets recover. 

Q: How can PWD be prevented, especially now that antibiotics and zinc are restricted? 

A: Prevention is all about management and alternatives. First, hygiene is your best friend: thoroughly clean and disinfect the nursery pens between groups of piglets. If you can leave the room empty (dry) for a few days, that helps kill off E. coli in the environment. Using an all-in/all-out system by age group is ideal. Second, ensure the weaning process is as smooth as possible – wean at a consistent age (at least 21 days, preferably closer to 28 days if feasible) and make sure piglets are healthy and robust (good birth weights, no concurrent diseases) going into the nursery. Try to minimise stress: keep temperature and ventilation at comfort levels, avoid mixing piglets from too many sources, and don’t overstock the pens. Providing creep feed before weaning can get piglets used to solid food; that way they maintain better feed intake after weaning which is key to preventing gut upsets. Nutrition is critical: use a high-quality weaner diet that is easy to digest (e.g. include cooked cereals, animal proteins like plasma or fish meal, and not too much crude protein overall). High protein diets canmake PWD worse, so some farms have successfully reduced protein % and added synthetic amino acids to compensate. Many producers now add acidifiers (organic acids) to feed or water to keep stomach pH low and inhibit E. coli. Also consider feed additives like probiotics (beneficial bacteria), prebiotics, or essential oils (like oregano oil, etc.) – these can help balance gut flora and have mild anti-E. coli effects. Since we can’t use zinc oxide at high doses anymore in the EU, these feed-based strategies have become more popular. On the health side, make sure piglets get ample colostrum right after birth – that gives them the best start and some immunity. While maternal antibodies won’t last until after weaning, healthier piglets cope better with stress. Some farms are trying oral vaccines for E. coli at weaning or before weaning; if available, that might reduce the incidence or severity of PWD (results have been mixed, but it’s a promising area). In summary, prevention now relies on excellent sanitation, careful weaning management, and nutritional adjustments to protect the gut – essentially strengthening the piglets’ defenses and reducing exposure to the bugs. 

Q: Is there a vaccine for post-weaning E. coli diarrhoea? 

A: There isn’t a perfect widely-used vaccine yet, but there are a couple of options and more in development. For years, we’ve vaccinated sows (mother pigs) for E. coli; those vaccines raise antibodies in the sow’s milk to protect piglets while they are nursing. That works well for neonatal E. coli scours, but those antibodies drop off after weaning, so they don’t directly prevent PWD. Recently, however, live oral vaccines given to piglets have been introduced. In Europe, for example, there’s an oral vaccine that contains live E. coli strains with F4 and F18 fimbriae (but made harmless). Piglets can be given this around 2–3 weeks of age (even a few days before weaning), and it helps them build immunity in their gut to those ETEC strains. The idea is that when they encounter real pathogenic E. coli after weaning, their immune system can fight it off. Similarly in North America, there are oral vaccines targeting F18 (for oedema disease) and F4. These vaccines are fairly new and management needs to be just right (you shouldn’t give antibiotics around the vaccine period, or it might kill the vaccine bacteria, and the piglets need to be old enough to respond but ideally before they are exposed to the farm’s E. coli). The effectiveness in the field has been promising, but they may not eliminate PWD entirely – rather, they reduce the severity and losses. Researchers are also working on other vaccines, like non-living oral vaccines and improved formulations that can be given even when piglets still have some maternal antibodies. There’s hope that in the future we might vaccinate piglets like we do for some other diseases and get solid immunity against PWD. For now, if a farm is struggling with heavy losses due to E. coli post-weaning, they might try using one of these oral vaccines as part of the strategy, in consultation with their vet. It’s one tool among many, and ongoing research will hopefully give us even better vaccines. 

Q: Can we breed pigs that are less susceptible to PWD? 

A: Yes, this is actually a known possibility. The ability of E. coli to cause disease in a pig depends on the pig having the right receptor in its gut for the bacteria to attach. Some pigs naturally lack the receptors for F4 or F18 E. coli. For instance, pigs with a certain gene variant (FUT1 gene) do not express the receptor for F18, so they are essentially immune to F18 E. coli – they won’t get edema disease or PWD from those strains. Similarly, there are pigs that don’t have receptors for F4 E. coli. Breeding for these traits is feasible: there are genetic tests to identify pigs that are “resistant” to F18. Some breeding companies have worked on incorporating these genes so that a percentage of their pigs are less susceptible. The challenge is that you need to balance this with other important traits (growth, litter size, etc.). Also, a pig that’s resistant to F18 could still get diarrhoea from an F4 E. coli if it has that receptor, and vice versa. So, in practice, we don’t yet have commercial herds that are fully PWD-proof. But it’s a very interesting area – if through gene editing or selective breeding we could produce pigs that simply don’t have the lock-and-key for these bacteria, it would be a permanent solution. It’s likely something for the long term. In the meantime, some producers can select breeding stock that tested negative for the F18 receptor to reduce problems with edema disease. This genetic approach will probably complement other measures – it won’t solve PWD alone unless all pigs on the farm are fixed for resistance genes, which could be many generations of breeding effort.