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Seventy-five 25-day-old broilers were divided into three groups: group I unmedicated and challenged with E. coli O78:K80; group F infected and treated with 150 ppm of phosphomycin in their drinking water, and group C acted as a control. Their weights, feed intake, clinical signs, macroscopic lesions, E. coli reisolation, and serum biochemistry were compared. Group F showed fewer symptoms and gross lesions than those from group I while the average daily gain, bodyweight, and feed intake were similar to the control group. E. coli was reisolated in 32 per cent of the livers and spleens from group I, compared with 4 per cent of liver and 8 per cent of spleens from group F. There was an increase in the levels of total protein and globulins in group I but not in group F. These results provide evidence of the therapeutic efficacy of phosphomycin in the control of an experimental E. coli infection in broiler chickens.

Tight junctional structure and macromolecular permeability were tested in four three-week-old piglets, experimentally infected with the enterotoxigenic Escherichia coli (ETEC) strain 0149 K91 K88. Histologically, only minor microscopic evidence of inflammation and little or no architectural changes in the jejunal mucosa were observed. A significant decrease in tight junctional strand numbers occurred, without a concomitant decrease in tight junctional depth. The permeability of the porcine jejunal epithelium to horseradish peroxidase did not change after the ETEC infection.

The interactive effects of Eimeria tenella and Escherichia coli infection in chickens were investigated. Specific pathogen free chickens inoculated orally with E tenella and challenged four days later with E coli via the air sac showed more severe acute septicaemic lesions and subacute serositis than chickens given E coli alone. Moreover, caecal lesions induced by E tenella were more severe in chickens given both E tenella and E coli than in those given E tenella alone. In contrast, oral inoculation of E coli did not result in acute septicaemic lesions or subacute serositis and had no effect on the severity of the caecal lesions caused by E tenella.

SUMMARY The results of an investigation into 58 outbreaks of disease in pigs in which E. coli was considered significant are presented. A syndrome causing high mortality in baby piglets is described. The syndrome was consistently associated with certain serotypes of E. coli , and evidence is presented to suggest that they were of primary importance in its aetiology.

SUMMARY The serological examination of 797 E. coli strains isolated from cases of “coli-septicaemia” (243 strains) and other avian diseases is reported. Over 60 per cent of the strains from “coli-septicaemia” belonged to the serological O groups, O2, O78 or O1. The E. coli strains isolated from other avian diseases showed less serological uniformity, although over 18 per cent belonged to the O2 group. The results of pathogenicity tests using the common avian serotypes are described, and a syndrome resembling naturally occurring “coli-septicaemia” was reproduced by the intravenous inoculation of the E. coli serotypes most commonly isolated from field cases. The results of in vitro sensitivity tests showed that all E. coli strains tested were sensitive to furazolidone and that the incidence of tetracyclinc-resistant strains isolated from field outbreaks of disease had increased over the past 4 years. A small therapeutic trial in experimentally infected birds demonstrated the efficacy of furazolidone.

SUMMARY The development of coli-septicaemia was found to be accompanied by a complex physiological stress syndrome. This involved an increase in the weight of the spleen and adrenal glands and an increase in the ascorbic acid content of the blood, spleen and the bursa of Fabricius. An involution of the bursa occurred which was associated with increased bursal β-glucuronidase activity. Soon after infection rapid loss in body-weight occurred which was particularly marked among the relatively lighter birds. In certain cases it was possible to demonstrate a positive correlation between the severity of the pathological changes and growth rate in chicks surviving an infection. The phase of activity of the physiological defence mechanisms does not appear to persist subsequent to infection for longer than a week. During this period bacteraemia was suppressed. Antibody production was found to occur during the recovery period, 7 to 15 days after infection.

SUMMARY Twenty-one newborn piglets, the progeny of 5 gilts, were dosed by mouth with 3 strains of E. coli. When the 2 different serotypes G7 and E68 Type I were used all the piglets scoured and 11 of them died. The majority of the 25 controls inadvertently became infected later and 6 died. A ‘non-pathogenic’ strain given similarly to 7 piglets killed only 1 and failed to reproduce the same clinical syndrome. This experiment was spoiled by the intrusion of a ‘pathogenic’ serotype, but provided an opportunity for a study of the natural disease.

SUMMARY A litter of 14 piglets produced by hysterectomy and kept in strict isolation was divided into 3 groups. One group of 6 received E. coli serotype E68 Type I by month in varying doses when 12 hours old. Three piglets died and 3 scoured, but recovered. The size of the dose did not influence the severity of disease produced, 1000 organisms being sufficient to kill a piglet. The second group of 3 piglets received a supposedly non-pathogenic E. coli serotype (P50) by mouth in varying doses when 12 hours old and all these pigs scoured, but recovered. Four of the 5 control piglets remained healthy throughout the experiment. Subsequently at 6 days of age 3 of the surviving control piglets were given varying doses of E. coli serotype E68 Type 1. All 3 piglets died. Also at 6 days of age 2 of the 3 piglets which had received the supposedly non-pathogenic serotype (P50) when 12 hours old were given serotype E68 Type 1. Both piglets died. The experiments showed that a syndrome completely comparable to the field outbreak could be reproduced by dosing young piglets by mouth with a certain serotype of E. coli, but not with another. Some of the implications are discussed and suggestions are made for further investigations.