Date Published: June 2, 2008
Publisher: BioMed Central
Author(s): Sigbrit Mattsson, Per Wallgren.
Oedema disease is a severe disease, mainly affecting recently weaned pigs. It is caused by E. coli strains that express fimbriae F18 and produce verotoxin 2e, mainly belonging to serotype O138, O139 or O141. The aim of this study was to compare E. coli isolates within these serotypes with respect to diversity.
Faecal E. coli strains belonging to serotypes O138, O139 and O141 isolated during the period 1994–1998 from Swedish pigs aged less than 12 weeks were compared using a biochemical fingerprinting system. Aiming to compare the results obtained over time, also strains isolated during 1964–67 and 1975–80 were included in the study. The study comprised 129, 263 and 95 isolates of E. coli serotype O138, O139 and O141, respectively.
Biochemical phenotypes (BPTs) were defined. At each sampling occasion each herd could only contribute with one isolate per BPT. Consequently, all but one of identical BPTs identified at a specific sampling occasion was omitted. The final number of isolates from 1994–98 that was compared included 64, 182 and 41 isolates of serotypes O138, O139 and O141, respectively. Within each serotype, the dominating BPT included over 65% of the compared isolates, demonstrating a large dominance of one BPT per serotype. These dominating BPTs were also demonstrated in the material from the 1960ies and the 1970ies. Still, the presence of other common BPTs (especially within serotype O138 and O139) demonstrated a certain variation within serotype. In a herd severely affected by oedema disease, E. coli serotype O139 was easily demonstrated in diseased pigs but only rarely in apparently healthy weaners
The results obtained demonstrate the presence of dominating BPTs within the oedema disease inducing serotypes. A stability of these BPTs over time was observed, presumably at least partly due to a never-ending access to naïve pigs. Still, the presence of other common BPTs indicates a variation over time, which visualises the importance of monitoring for this. Such studies should focus on pigs affected by oedema disease, because oedema disease inducing strains of E. coli were only rarely demonstrated in healthy pigs in a herd affected by oedema disease.
Oedema disease is caused by E. coli strains that possess fimbrial adhesion factors enable to produce toxin . Most of these strains belong to a few serotypes and the fimbriae is often F18 (previously named F107) and produce verotoxin 2e (VT2e), also called shiga-like toxin IIe [2,3]. The E. coli bacteria multiply in the digestive tracts and colonize the small intestine [4,5]. Names like “oedema disease,” “bowel oedema” and “gut oedema” have been coined because oedema in the submucosa of the stomach and the mesocolon often are prominent features of the disease . The toxin may cause vascular lesions in the intestine, in the sub cutis and in the brain, leading to oedema in affected organs and to neurological symptoms . The production of VT2e is temperature dependent and most effective at 37°C, whereas the VT2e production is dramatically reduced at temperatures below 30°C or above 42°C .
Biochemical fingerprinting has frequently been used to measure the diversity of E. coli or coliforms in the gastrointestinal tracts of individual pigs at stressful situations such as weaning or allocation [17,18,32]. However, the method has also been successfully used when relationships between different isolates of specific bacteria have been investigated [33,34] and it has been used to update diagnostic panels for relevant serotypes in the national monitoring program for E. coli [29,27].
To conclude, the BPTs of E. coli that induce oedema disease appear to be rather few and also quite stable. Still a number of other BPTs are continuously present, which indicate a variation over time and calls for monitoring. Further, serotyping of E. coli strains isolated from pigs with oedema disease is still a valuable tool since new serotypes recently have been linked to the disease.
SM carried out the analysis performed and was the first author, PW made the study design in collaboration with SM and was the senior scientist. Both authors have contributed significantly to the work