Diarrhea associated with Escherichia coli can occur in young piglets within a few days of birth through well after weaning. Occasional cases of septicemia are attributable to E. coli. Edema disease, a unique form of colibacillosis, is presented separately (see Edema disease).
Colibacillosis affects pigs in all major swine-raising countries. There are many different types of E. coli, each of which may possess several of many virulence factors. Many outbreaks occur within the first week after birth. Others occur later during the nursing period. Still others occur about 1-2 weeks after weaning or following abrupt changes in environment or nutrition.
Colibacillosis has been recognized as an important diarrheal disease of pigs for over fifty years. For many years treatment and control were largely empirical. Recurring losses, as well as the importance of E. coli in other species including man, stimulated research on the disease. Research has largely paralleled development of confinement rearing. Advances in molecular biology have simplified specific identification of pathogenic coliforms and their genes related to virulence.
The coliform responsible for several recently reported food poisonings of people, O157:H7, does not appear to cause disease in swine nor is this serotype common in swine.
Pathogenic strains of E. coli are easily isolated, Gram-negative, flagellated bacilli. Most pathogenic strains form smooth to mucoid colonies; some are beta-hemolytic. Virulence factors include fimbria (pili), enterotoxins (exotoxins), endotoxins, and capsules. Fimbria are the small hair-like processes on the bacterial surface that allow attachment to specific receptors on the surface of mucosal enterocytes of the small intestine (colonization). Pathogenic strains also produce one or more enterotoxins, which are exotoxins elaborated locally in the small intestine that can have either local or systemic effects. These strains are termed enterotoxigenic E. coli (ETEC).
There are five common, antigenically distinct pilus types found in pigs: F4 (K88), F5 (K99), F41, F6 (987P) and F18. The first four pilus types mediate adhesion in neonates. F18 is not associated with neonatal colibacillosis but is common in postweaning colibacillosis as is F4. Some strains have the ability to erode epithelium and are termed attaching and effacing E. coli (AEEC).
The toxins elaborated by pathogenic E. coli in swine (ETEC) are labile toxin (LT), stable toxin A (StA), stable toxin B (StB), and verotoxin (shiga-like toxin, SLT). The first three act locally causing hypersecretion of fluid from the intestine while verotoxin is responsible for the systemic vascular effects of edema disease (discussed separately).
In summary, there are many strains and types of E. coli present in swine and their environment. Enteropathogenic E. coli require the presence of both fimbria-mediated adhesion to enterocytes as well as elaboration of one or more toxins.
Potentially pathogenic E. coli are present in the intestinal tract and feces of many normal swine. Dams often act as immune carriers. Continuous farrowing, accompanied by poor sanitation and chilling, can increase the risk of colibacillosis. E. coli organisms contaminate the skin and mammary glands of dams and are ingested by nursing piglets. Piglets with little colostral or inherent immunity (enterocyte receptors for certain pilus types are not present in all genetic lines of swine) sicken first. Pathogenic coliforms are magnified by fecal shedding to further increase exposure of littermates. Disease occurrence and severity is related to dose ingested and the level of immunity derived from colostral immunity.
Pathogenic coliforms survive in contaminated buildings and can infect successive litters of pigs. Once present, E. coli tend to persist unless vigorous efforts are given to maintaining sanitation, husbandry, and environment.
Ingested pathogenic E. coli adhere to receptors on microvilli of enterocytes via pili. There they colonize, proliferate, and elaborate enterotoxins that cause excessive secretion of fluid and electrolytes by crypt epithelial cells which markedly exceeds absorptive capacity resulting in a net flow of tissue fluids into the lumen. Up to 40% of a piglet’s weight may be lost as fluid passed into the intestine. The enterotoxins, endotoxin, and/or adhesins may damage the microvilli and enterocytes as well. This reduces the absorption of electrolytes, water and endogenous secretions from the lumen. The large intestine, sometimes also affected, is unable to absorb the excess fluid and diarrhea results. Damage to epithelial cells sometimes leads to septicemia. Diarrhea usually continues until death results from dehydration and metabolic acidosis or from terminal septicemia.
Post-weaning colibacillosis is similar but with one additional consideration. Verotoxigenic strains elaborate verotoxin (shiga-like toxin) which has systemic effects on endothelium of blood vessels (edema disease). These strains are sometimes hemolytic on blood agar.
Whether piglets contract colibacillosis depends on a balance between the number and virulence of pathogenic E. coli in the intestine, the pigs’ resistance to the disease, and environmental factors (temperature, humidity, sanitation, etc.). Neonatal piglets have incompletely developed immune systems and limited innate resistance. They are largely dependent on antibodies supplied in colostrum and milk. Anything that prevents piglets from obtaining colostrum leaves them susceptible to colibacillosis.
If purchased gilts farrow before they have developed antibodies to endemically present pathogenic E. coli, their colostrum and milk may not contain enough antibodies to protect their piglets. Also, as the nursing period progresses, piglets get less milk and the milk contains fewer antibodies. Chilling of piglets impairs intestinal motility and lowers resistance to infection. Massive exposure can overwhelm resistance. In recently weaned pigs, absence of milk antibodies and the different type of feed may contribute to outbreaks of colibacillosis.
Colibacillosis usually is signaled by the appearance of diarrhea. Piglets from gilts may be more severely affected than piglets nursing sows. The severity of the diarrhea varies. The hypersecretory diarrhea usually has an alkaline pH but varies in color. It may be clear and watery, especially in neonates, but may be white or yellow, influenced by type of ingesta and duration of the disease. Sick pigs occasionally vomit but vomiting is not as prominent as with transmissible gastroenteritis (TGE).
As diarrhea continues, there is progressive dehydration and the hair coat becomes roughened. Body temperature often is subnormal. Shivering often is noted unless an adequate supplementary heat source, such as heat lamps, is available. Signs are similar in pigs of various ages but tend to be more severe in younger pigs. Death losses can be severe if husbandry and environmental conditions are poor. Diarrhea tends to persist until intervention is accomplished.
E. coli is one of the most common causes of neonatal septicemia and polyserositis. Often, strains associated with septicemia are not enteropathogenic.
Dehydration is the most obvious clinical sign. The small intestine and colon may contain excess watery fluid or may be distended and gas-filled. There may be mild reddening and congestion of the stomach. Lesions often are surprisingly mild, especially in very young piglets. However, in outbreaks caused by certain pathogenic strains, usually in older postweaned pigs, there can be marked congestion of the gastrointestinal tract.
Microscopy of the mucosa of the small intestine reveals many coliforms adhered to microvilli of intestinal epithelial cells. Villi usually are intact. With some strains of E. coli, there may be necrosis of some villi and microvascular thrombosis in the lamina propria.
E. coli is a common cause of septicemia in neonates. In those cases, there is fibrinous polyserositis and arthritis.
Typical signs and lesions are useful but not definitive. The isolation of a uniform and high population of smooth, mucoid, or hemolytic E. coli from the small intestine is suggestive of colibacillosis. Diagnostic labs often use one of the following methods to more specifically identify the pathogenic E. coli:
- A slide agglutination test can identify the serogroup but does not confirm pathogenicity.
- Adhesin(s) can be identified using monoclonal antibodies.
- A polymerase chain reaction (PCR) can identify the pathogen genetically.
Genotyping by multiplex PCR is widely practiced to determine specific pilus and toxin genes present in the isolate.
Diagnostic methods do not identify important contributing factors such as chilling, poor sanitation or starvation. These often must be corrected if prevention or treatment is to be successful.
Colibacillosis has to be differentiated from other diarrheal diseases of young pigs. These include transmissible gastroenteritis (TGE), rotaviral infection, coccidiosis and Strongyloides parasitism. Starvation is also a major differential diagnosis.
As E. coli are commonly found in the small intestine of both normal and diseased pigs, microscopic examination of small intestinal sections can be useful in distinguishing the significance of the infection. Dense colonization of the brush border with adherent E. colishould be expected in most cases of colibacillosis with additional erosive or congestive changes present depending on the toxins that have been elaborated.
Many experienced veterinarians believe that colibacillosis is related largely to problems in housing and management which cause the disease secondarily. More detailed information on housing and management is available elsewhere. A few general guidelines on prevention and treatment follow:
Insofar as is possible, breeding stock should be obtained from a single source with no problems of colibacillosis. Dams should be acclimatized together for 3-6 weeks prior to breeding and during gestation so they can develop immunity to endemically occurring pathogens. This allows for the production of an adequate amount of specific antibodies in colostrum and milk.
It often is worthwhile to try to enhance the immunity of sows by using vaccines made from bacterial pili or toxins or both. Pregnant dams often are vaccinated twice at 2-3 week intervals prior to farrowing. A recent analysis of the value of vaccination, based on data from a National Animal Health Monitoring System (NAHMS) national survey, predicts that E. coli vaccination of sows would be cost effective for producers.
Another method of increasing colostral antibodies is feeding some farrowing house waste to sows during late gestation. Waste should include any pathogens present in the farrowing house and will stimulate formation of antibodies against them. Oral vaccination of sows with virulent E. coli cultured in milk was quite useful prior to the development of commercial injectable vaccines.
Use of the all in/all out system of raising piglets is recommended. Farrowing should occur in a facility thoroughly cleaned, disinfected, and dried between farrowings. The build-up of pathogens can be minimized by a vigorous, ongoing sanitation program.
The farrowing facility should be designed to provide a dry, comfortable environment for both dams and piglets. This requires lower temperatures (~70° F) for sows and areas warmed (to ~90° F) for small piglets. Stresses on piglets should be minimized.
When precautionary efforts fail, a system should be available to treat piglets immediately if signs of colibacillosis appear. Antimicrobials can be administered to neonates orally or by injection. Due to the contagious nature of the organism, when treating sick pigs before weaning, all pigs (including those not scouring) in the litter also need to be treated at the same time. Weanlings can be given antibiotics in water. Antimicrobial sensitivity data is quite useful in selection of an appropriate antimicrobial. Oral electrolyte replacement solutions sometimes are used to help control dehydration. Various products may aid in prevention of postweaning colibacillosis. Plasma proteins, zinc oxide, organic acids, and probiotics are commonly used.
Some swine are genetically resistant to certain fimbriae of pathogenic E. coli. Breeding for genetically related resistance eventually may help control some forms of colibacillosis.