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Pregnant swine were vaccinated with 1 of 2 enteropathogenic strains of Escherichia coli, and their pigs were challenge inoculated with the homologous strain 1.5 hours after the entire litter was born. Seventeen sows were vaccinated orally by feeding viable cultures on 3 consecutive days, 6 sows were given 2 intramuscular (IM) injections of viable cultures at 10- to 14-day intervals, 6 sows were given 2 IM injections fo formolized cultures at 10- to 14-day intervals, and 12 sows were not vaccinated. The pigs from sows which had been orally vaccinated with viable cultures were protected during the 10-day observation period against diarrhea, as well as against death, when the newborn pigs were challenge inoculated with the homologous strain. Most of the pigs from sows which had been vaccinated IM were protected against death, but few neonates were protected against the diarrheal effects of challenge exposure with the homologous strain. Challenge-inoculated pigs suckling nonvaccinated sows had diarrhea and became dehydrated, and many died. Fewer viable E coli were usually recovered from the homogenized intestinal contents or intestinal segments of newborn pigs which did not have diarrhea than from similar specimens of diarrheal pigs. Microscopic examination of segments of the small intestine revealed that large numbers of E coli were closely associated with the ileal mucosa of newborn pigs killed in the acute phase of neonatal enteric colibacillosis caused by either strain, but organisms were not detected in this location in the pigs which remained normal after challenge exposure. It is concluded that swine which have been vaccinated by feeding large numbers of viable E coli late in gestation can provide good protection to their suckling pigs against the effects of challenge inoculation with the homologous enteropathogenic strain.

Two siblings with a congenital syndrome of secretory diarrhea and seizures developed progressive skin rash, alopecia, and mucocutaneous candidiasis while receiving biotin-free total parenteral nutrition. Abnormally low urinary biotin excretion was associated with these clinical findings, but the serum concentration of biotin was within the normal range. There was also increased urinary excretion of lactic acid, 3-hydroxyisovaleric acid, 3-hydroxypropionic acid, and 3-methylcrotonylglycine. The younger of the two children subsequently died with severe metabolic acidosis. In the oder sibling, intravenous treatment with biotin (200 micrograms/day) resulted in resolution of the organic aciduria. A larger dose (10 mg/day) appeared to be required for rapid improvement in the skin lesions. These cases suggest that clinically significant biotin deficiency can occur in patients with chronic diarrhea receiving biotin-free total parenteral nutrition.

The onset of fecal shedding, serogroup involvement, and association of hemolytic Escherichia coli with the postweaning diarrhea syndrome were studied in swine. The only E coli O antigen, detected by slide agglutination with the antisera used, was O157; K antigens were not detected. The ligated intestinal loop test (LILT) was used for enterotoxigenicity testing. All O157 serogroup isolates (n = 9) were hemolytic, and 89% (8 of 9) were LILT positive. Of all hemolytic isolates tested, 59% (10 of 17) were LILT positive. Twenty-seven nonhemolytic isolates were tested for enterotoxigenicity; of these, 45% (12) were LILT positive. The onset of postweaning diarrhea coincided with the modal onset of hemolytic E coli shedding at postweaning day 7. At postweaning day 7, hemolytic E coli shedding was concurrently associated with diarrhea (P less than 0.0005), whereas later during the postweaning period, this was not the situation.

Nine gnotobiotic pigs derived from one gilt were fed bacteria-free filtrates prepared from: 1) cultures of an enteropathogenic strain of Escherichia coli 09:K.:NM (Strain 340), 2) cultures of a nonenteropathogenic strain of E. coli 08.K..H16 (Strain CDC-1466-56), and 3) uninoculated culture medium. Diarrhea was observed initially two to four hours after feeding the filtrate prepared from the enteropathogenic E. coli. The duration of diarrhea was five to ten hours. No diarrhea was observed after feeding filtrate prepared from uninoculated medium or cultures of nonenteropathogenic E. coli. The pH values of the feces increased with the onset of diarrhea and decreased to normal after diarrhea stopped. No histopathological lesions were found.

The immune response of orally infected and parenterally vaccinated (E. COLI 08:K.:H21) gnotobiotic pigs was studied by bactericidal and indirect hemagglutination test methods. The bacterial agglutination test proved to be of no value in this study. The results demonstrated that antibody was detectable within 8 days following oral infection, but the titers remained very low until after the pigs were vaccinated intravenously. The titers of the sera were markedly increased following intravenous vaccination. There was no detectable absorption of antibody from the gut of gnotobiotic pigs fed immune serum at 4 to 6 days of age and no detectable difference between the immune response of these pigs and those not fed serum.

The protective effect of orally administered immune (E. COLI 08:K.:H21) serum was demonstrated in experimentally infected gnotobiotic pigs. The temporary protective effect of the immune serum and the correlation of protection with IN VITRO antibody determinations were discussed. The results indicated that the protective action of the immune serum is apparently not dependent upon the complement-antibody bactericidal system. It was suggested that the most plausible mechanism of action of the immune serum was the inactivation of endotoxin in the lumen of the intestine.

The effects of orally and/or parenterally administered immune serums were evaluated in 36 gnotobiotic pigs infected with an enteropathogenic strain of Escherichia coli. Pigs were euthanatized at predetermined time intervals between 6 and 48 hours prostinfection. The results were evaluated on the basis of: 1) clinical observations, 2) necropsy observations, 3) counts of viable E. coli in segments of the small intestine, 4) attempts to isolate E. coli from the heart, liver, and bile, 5) microscopic examination of fixed intestinal sections to determine the location of E. coli and morphologic evidence of the host response, and 6) determination of the pH of the various portions portions of the gastrointestinal tract. Orally administered immune serum completely protected the pigs from fluid loss and diarrhea. Parenterally administered serum did not protect against fluid loss into the intestinal lumen but diarrhea was not observed. The pH of the contents of the lumen of the cecum and colon was markedly elevated simultaneously with the accumulation of fluids and incompletely digested milk. The results of microscopic examination of tissues as well as other determinations did not reveal the mechanism of fluid loss nor the mechanism of protection afforded by orally administered immune serum. The results support the contention that continuous adequate levels of appropriate antibodies in the lumen of the intestinal tract aŕe a significant deterrant to the establishment of colibacillosis in baby pigs.

Four gnotobiotic pigs were infected with an enteropathogenic strain of Escherichia coli, and 4 were infected with a nonenteropathogenic strain of E. coli. Pigs killed in pairs at 6, 12, 24, and 48 hours PI. Four pigs were maintained as germfree controls. The discussions were based on the results of 1) clinical observations, 2) necropsy observations, 3) counts of viable E. coli in segments of the small intestine, 4) attempts to isolate E. coli from the heart, liver, and bile, 5) microscopic examination of fixed intestinal sections to determine the location of E. coli and morphologic evidence of the host response, and (6) determinations of the pH of the contents of the various portions of the gastrointestinal tract. No diarrhea, fluid accumulation, or impairment of the digestive capacity were noted in the pigs infected with the nonenteropathogenic strain of E. coli. The number of viable E. coli detected in the respective segments of the homogenized small intestine was similar in pigs infected with either strain. Diarrhea occurred continuously starting 18 hours PI in the pigs infected with the enteropathogenic strain and killed 24 or 48 hours PI. The pH of the contents of the cecum and colon became markedly more alkaline simultaneously with the increase in the heterogeneity and fluid content of the cecum and colon and thus appeared to correlate well with the onset of the clinical diarrhea. No enteritis was detected grossly or microscopically. The characteristics that determine the enteropathogenicity of a strain of E. coli could not be defined from the results, but it was noted that the host response appeared to be quite similar to that of infant rabbits experimentally infected with Vibrio cholera.

Tissues from three groups of pigs (germfree, Escherichia coli monocontaminated, and healthy conventional pigs) were collected at intervals between 24 minutes and 7 hours 12 minutes after death. Histological differences between the three groups were present in the alimentary mucosa and were most striking in the ileum and colon.Autolytic change was detected only in the digestive system and the sequence of autolytic events was similar in all groups. The time of onset and rate of progress differed markedly between groups and between segments of the alimentary canal. In the conventional group, autolysis started quickly and progressed rapidly. In the germfree group it was later in onset and slower in progress. The E. coli infected group was intermediate. The initial visible change occurred in the small intestine. The morphological differences and autolytic changes were described.

The successful experimental production of colibacillosis in young gnotobiotic pigs by the oral administration of E. COLI (08:K.:H21 was accomplished. Colibacillosis was not produced in gnotobiotic pigs infected with either of the 2 other strains of E.COLI employed.Necropsy observations were presented and discussed. Emphasis was placed on the absence of grossly visible enteritis in pigs that died in the acute phase of the disease. The gross appearance of the intestinal tract changed some hours after death to resemble that associated with enteritis.Bacteremia was detected in the gnotobiotic pigs orally infected with each of the 3 strains of E. COLI, and the special characteristics of the colostrum-deprived pig were stressed as important factors in these findings.