Age affected: Weaners.
Causes: Overfeeding; dietary factors; E. coli; poor hygiene.
Effects: Sudden death, jowl swelling, nervous signs.
Oedema disease is caused by pathogenic strains of Escherichia coli, a Gram-negative rod or coccobacillus which has flagellae, F18 fimbriae (filamentous adhesins) in two forms, F18ab and F18ac and VTIIe, VT2e, SLT IIe or SLT2e toxin (the same thing).
It grows aerobically and anaerobically on a wide variety of media. E. coli can survive drying for months, is killed by heating to 66°C for 30 minutes and by most disinfectants. It is sensitive to many antimicrobials but resistance has been recorded. The E. coli strains responsible usually belong to serotype 0139: K12: H1, 0138 K81 NW, 0141 K85 ab H4 and 0141 K85 ac H4. These pathogenic E. coli multiply throughout the small intestine and adhere to the epithelial (lining) cells by means of the F18 fimbriae.
Adherence of the E. coli (and subsequent toxin production) is dependent on the presence of the receptors in the intestine and is under genetic control. Levels of the E. coli responsible are greatest 2 days post-infection.
Toxin is produced and absorbed to the smooth muscle cells of the arterioles to cause hypertension, following which the sub-mucosal arterioles are damaged. These changes are responsible for the oedema and for the nervous signs and central nervous system lesions. Recovery from infection may be accompanied by the development of antibody to both F18 fimbriae and to a lesser extent to VT2e.
Mode of transmission
The toxigenic E. coli strains responsible are present in the faeces of affected and carrier pigs and are ingested by other animals in contaminated feed or water and directly from the floor. Infection may also result from dusty material containing dried organisms in inadequately cleaned pens. The disease only affects pigs which are genetically-susceptible. Introduction of the disease to a farm may result from the introduction of genetically-susceptible stock or to introduction of the E. coli strains concerned in carrier pigs, transport or implements and clothing.
The disease occurs within 10 days of weaning or dietary change and affects the better piglets in the group. Outbreaks commence with one or more pigs being found dead and others developing varying degrees of nervous disturbance.
Affected pigs appear dull, may appear blind and may show head pressing. General incoordination and loss of balance occur later and may be noted at feeding time. Affected animals lag behind others and are less able to reach feed. Lateral recumbency with paddling movements leading to coma and death, normally follows within 4-36 hours or the onset of clinical signs. Affected pigs may have oedema of the eyelids, nose and ears and early cases may have a peculiar, squeaky voice. Body temperature may reach 40°C (104°F), early in the disease but rectal temperature is often normal when clinical signs develop. Neither constipation, nor diarrhoea, is a constant feature. Affected pigs often die but may recover completely, apart from a check in growth or remain with a head tilt, gait disturbance or paralysis. Oedema disease has occurred in sows as inappetence and progressive locomotor disturbance, leading within hours or days to loss of control of the hind limbs and eventual recumbency.
Clinical signs of dullness, blindness and head pressing, oedema of the eyelids and death within 10 days of weaning in 30% of pigs, suggest oedema disease. ELISAs can detect VT2e in faeces and recombinant BT2e can detect antibody in serum from groups of pigs within 2-3 months of infection.
Dead animals are in good condition with full stomachs and oedema of the eyelids and face. Oedema is present in the greater curvature of the stomach, between the mucosa and the muscle layers. Jelly-like areas of oedema may be present in the mescocolon, larynx and the kidney capsule.
Oedema disappears rapidly once the carcase is opening. Microscopical findings confirm the presence of oedema in the stomach wall and of perivascular spaces in the brain. Encephalomalacia (destruction of areas of brain) is seen in chronic cases. Degeneration and necrosis in arteries and arterioles is the cause.
Proliferative arteriopathy (blood vessel blockage by the lining cells) is present in pigs when have died after several days’ illness. The isolation of serotypes of E. coli, such as 0139 K81, 0139 K12 and 0141 K58 from the small intestine, provides additional evidence and the identification of genes for VT2e and F18 using DNA probes or by PCR is confirmatory.
Treatment and prevention
Affected pigs unable to walk after 3 days should be killed. Antimicrobial injection is rarely of value to individuals but therapy may be of value to the group. The antimicrobials used for injection or in water are: ampicillin, amoxicillin, apramycin, neomycin, tetracyclines, trimethoprim: sulphonamide, spectinomycin, gentamicin and cephalothin or ceftiofur (where registered).
Treatment for 3-5 days should begin when clinical signs are notes. In-feed medication with chlortetracycline, oxytetracycline, apramycin, neomycin, sulphonamide, trimethoprim: sulphonamide and enrofloxacin is given for 10 days. Antimicrobial treatment in the drinking water or feed during the period of risk will control.
Zinc oxide reduces the incidence. Oedema disease can be prevented by limiting the feed in recently weaned pigs or by increasing roughage, use of acidifiers, correction of environmental problems and weaning by removal of the sow. Weaning with scrupulous attention to hygiene and environment, with frequent small feeds of digestible rations after weaning, may prevent the disease.
Immunisation of pigs with F18 fimbriae is protective and commercial vaccines are available. Genetically resistant strains of pig are known. Eradication is possible by depopulation, leaving empty for 4 weeks, removal of contaminated soil and material, cleaning and disinfecting using formalin in buildings and lime in the slurry channels. Restock with clean animals after 3 weeks.