Diarrhoea Neonatal (Scours)
Age affected: Newborn, human risk.
Causes: E. coli; clostridial infection; TGE; epidemic diarrhoea; rotavirus.
Effects: Watery diarrhoea within 48 hours of birth, stunting, death.
The gut of the newborn pig is sterile but is rapidly colonised by bacteria. Antibodies found in colostrum and later in milk protect against any damaging effects of these bacteria in normal piglets. Piglets which do not receive colostrum and those born from non-immune sows may develop disease. One of the first bacteria to colonise the neonatal piglet is Escherichia coli. The strains of E. coli responsible for neonatal diarrhoea adhere to the cells lining the small intestine by means of fimbriae (hair-like processes), most often the K99 or F5 fimbriae, and secrete an enterotoxin (usually Heat Stable Toxin, ST) which causes loss of chloride ions, the secretion of fluid followed by diarrhoea. Diarrhoea and loss of fluid are particularly important in neonatal piglets as water forms a large part of their body mass and the only source is sow's milk. The next organisms to colonise are the clostridia, C. perfringens type A and type C and possibly, C. difficile. They may be followed by rotavirus, the viruses of Transmissible Gastroenteritis or Porcine Epidemic Diarrhoea and coccidia which multiply in the cells lining the small intestine, destroy absorptive cells and produce atrophy of the intestinal wall (finger-like processes) and give rise to diarrhoea.
Mode of transmission
The sources of infection in neonatal diarrhoea are affected piglets, the piglet environment and the faeces of the sow. Each of the agents mentioned can occur in small numbers in the faeces of the sow, although adult animals are unaffected by the coccidia, rotavirus, E. coli and clostridial strains concerned because of immunity. Piglet to piglet transmission is most common within a pen or house but the most important agents (E. coli and the clostridia) can also persist in the environment for months in the absence of thorough cleaning. New strains of all the agents can be introduced to a farm with carrier pigs.
Neonatal diarrhoea (scouring) occurs in piglets aged 0-4 days and can begin within 12 hours of birth. Affected piglets may suck but often stand with drooping tails, appear shrunken and have a dull skin with erect coat hairs. Dehydration results in sunken eyes and makes the hips and backbone more prominent. The diarrhoeic faeces may be difficult to see on casual inspection as it is often pale in colour. Dried crusts of diarrhoeic faeces may be seen on the thighs or perineum and there may also be scalding about the anus. Affected pigs may either enter a coma and die, or recover without subsequent loss of condition after 3-6 days or remain stunted. Diarrhoeic faeces may be present in creeps and on the bars of slatted floors. Blood-stained diarrhoea may occur after 36-48 hours when clostridia are involved. Outbreaks of neonatal diarrhoea occur in successive litters, particularly those of gilts or newly purchased sows. In some cases up to 70% of all piglets born may be affected. Seventy percent of piglets affected with diarrhoea in the first few days of life may die. Mortality rates from diarrhoea then decrease rapidly until less than 10% occurs in affected pigs over 2 weeks of age.
The presence of neonatal diarrhoea in piglets is confirmed by inspection of the piglets and the pen. Dehydrated piglets often have diarrhoea, but it may be necessary to examine piglets individually to confirm diarrhoea in very young glitters and early cases in older piglets. Rectal temperatures are usually normal, and insertion of a thermometer or a swab often confirms the presence of diarrhoea and provides a sample for laboratory examination. Scalding of the anus or drying crusts of faeces on the thighs may indicate the past presence of diarrhoea. The sow may develop agalactia or even mastitis following reduction in sucking by the litter and this may also draw attention to the problem. The cause of the diarrhoea is difficult to identify by clinical means alone, although the bloody faeces of C. perfringens Type C and the associated mortality is distinctive. Laboratory examination of faecal samples from live pigs or the intestines of dead pigs (in some cases freshly-killed) is required to confirm the actual cause. The usual cause is enterotoxigenic E. coli producing K99 (F5) or 987 P (F6) fimbriae, but C. perfringens type A or type C, possibly C. difficile, and later rotavirus, coccidia or TGE and PED may be present. The mortality associated with PED and TGE and their effects on the remainder of the herd is suggestive of their presence.
Post-mortem findings of a dehydrated carcase, usually with faecal pasting on the hindquarters, a dark liver, milk curd in the stomach, a dilated, flaccid and fluid-filled small intestine and fluid contents of the large intestine confirm the presence of neonatal diarrhoea in pigs which have died. When E. coli is responsible, the intestine is not reddened, or only mildly so, but in C. perfringens Type C it is an intense red with bloody contents and in C. difficile infection, there is marked oedema of the large intestinal mesentery and thickening of the intestine. Freshly killed piglets are necessary for the full range of pathological examinations because of the rapid degeneration of the gut after death. In freshly-killed animals with E. coli infections the villi are intact in the early stages of infection, in contrast to the situation with the other agents. The bacteria may be isolated in culture, the coccidia seen by microscopy and the viruses demonstrated using antibody tests such as ELISA or by RT-PCR.
Treatment and prevention
Neonatal diarrhoea can be treated by individual oral dosing with antimicrobial for 3-5 days. As most neonatal diarrhoea is caused by E. coli, ampicillin, amoxicillin, neomycin, apramycin, tetracyclines, trimethoprim sulphonamide, spectinomycin, fluoroquinolones, gentamicin and cephalothin or ceftiofur (where registered) can all be used. Where treatment is ineffective, post-mortem examination and laboratory tests are required to confirm that E. coli is the sole cause and whether or not it is sensitive to the antimicrobial used. Penicillin, ampicillin and amoxicillin may be required for clostridial disease and the viral conditions do not respond. Electrolyte solutions with glucose: glycine should be available in all cases or be given if piglets cannot yet drink and environmental temperatures should be corrected. Neonatal diarrhoea caused by E. coli can be prevented by vaccinating the sow and ensuring that the litter receive colostrum. Most vaccines consist of killed E. coli and contain mixed pathogenic serotypes, strains carrying pathogenic determinants and enterotoxin antigens or the purified pathogenic determinants themselves. Some also contain clostridial antigens. All-in, all-out management should be practised in farrowing houses with thorough disinfection between batches. Correct environmental temperatures should be maintained.
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