Neonatal Diarrhea in Piglets – Part Two
Part two in Tonisity's four-part series on neonatal diarrhea in piglets; the most common symptom of disease in the baby pig.

In this second article, we discuss two of the main pathogens which can cause diarrhea during the first week of the piglet’s life, which are Enterotoxigenic Escherichia coli and Clostridium perfringens type C.

Enterotoxigenic Escherichia coli

In piglets, neonatal diarrhea refers to the diarrhea observed during the first week of life. It is often caused by a single pathogen (bacteria, virus…). One of these harmful bacteria is Escherichia coli (E. coli), a gram-negative, facultative anaerobic bacterium that is part of the normal intestinal flora (also called commensal intestinal flora). In healthy pigs, relatively small amounts of E. coli are present without any issues.

Among the different strains of E. coli that can be found in pig farms, one is called enterotoxigenic E. coli (ETEC). It is a pathogenic E. coli, causing different diseases, especially diarrhea in pigs. The diarrhea caused by ETEC is not specific and the pathological lesions are not severe. As healthy sows can carry ETEC, they can be a source of contamination through their faeces. Once some piglets are sick, they can contaminate the rest of the litter and their environment. It is common to find the same strain in a number of piglets as well as in several farrowing batches in the same room.

ETEC is one of the main causes of neonatal diarrhea in the swine industry. It is possible to control it by vaccinating gilts and sows and transfer the immunity to piglets via colostrum. It has also been found that some pigs are naturally resistant to colonisation by F4-positive E. coli and this resistance can be transferred to their offspring.

To cause diarrhea, ETEC must first multiply in the small intestine. For this, it will attach to the mucosa. It will then produce enterotoxins, which are going to disrupt the normal activity of the intestine. Some of these toxins will stimulate the production of chloride ions in the intestine, and depress the normal absorption of sodium and chloride ions by the enterocytes (intestinal absorptive cells). Other toxins will interfere with the secretion of bicarbonate.

The clinical signs of contamination with ETEC can be visible as early as early as a few hours after birth. The faeces are liquid, yellowish and the diarrhea incidence can be variable, from rather mild to abundant, watery diarrhea leading to severe dehydration and quick death. There are no specific lesions, but the small intestine is dilated with congestion of the intestinal wall.

Clostridium perfringens type C

Clostridium (C.) perfringens is an anaerobic bacterium; however it is oxygen tolerant. It is classified as a gram-positive, spore-forming rod and can be separated into five groups, called toxinotypes A to E, based on the production of the major toxin types (alpha, beta, epsilon, and iota). One of the C. perfringens, called type C (CpC), is able to produce alpha- and beta-toxin responsible for acute and haemorrhagic enteritis in new-born piglets.

Piglets with a well-established microflora are less sensitive to CpC. It also appears that because of low secretion of trypsin, and the presence of trypsin-inhibitors in colostrum, there is a slower degradation of the beta-toxin, which puts the new-born piglets at risk. Like for E. coli, the vaccination appears to help with resistance to the disease. In herds with low immunity, CpC can spread very fast and cause high mortality rates.

The clinical signs of contamination with C. perfringens can be visible usually from 12 hours after birth and during the first week of life but can still occur in the first three weeks of life. The faeces are showing signs of intestinal haemorrhage and under autopsy it can be observed mucosal necrosis in the small intestine as well as hyperaemia (excess of blood in the vessels). CpC is also able to attach to the villous epithelium in the beginning of the disease and upon histological observation it is usual to see such attachment to the damaged epithelium.

If you missed part one in the series, you can find it here. You can also find part three here and part four here.

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