Intestinal colonization and competitive exclusion of Campylobacter fetus subsp. jejuni in young chicks.

Colonization of Campylobacter fetus subsp. jejuni was investigated in monoxenic and holoxenic chicks. In monoxenic chicks, major colonization was found in the crop and ceca, with populations in the ceca consistently reaching 10(9) colony-forming-units/ml of cecal contents over the 28-day test period. Bacteremia was found in most chicks, but no significant gross pathological lesions were detected. In holoxenic chicks, major colonization occurred only in the ceca, and no evidence of bacteremia was detected. Colonization by native gut microflora sharply reduced subsequent colonization by C. fetus subsp. jejuni. The protective mechanism is perhaps the same as that protective against paratyphoid salmonellae and pathogenic strains of Escherichia coli.

Gastrointestinal colonization by salmonellae and pathogenic Escherichia coli in monoxenic and holoxenic chicks and poults.

Chicks monocolonized by either salmonellae or pathogenic strains of Escherichia coli had persistent and undiminished colonization of all levels of the gastrointestinal tract and frequently had bacteremia during test periods ranging to 35 days. Poults monocolonized by salmonellae or Arizona hinshawii 7:"1,7,8 developed a similar pattern of colonization. Conventionally reared chicks and poults had rather variable colonization by these pathogens, and it was most persistent in the ceca. Groups treated with a native protective microflora were infrequently colonized. Differences in colonization are explainable by lack of competing bacteria in the monocolonized group and by various degrees of protection provided by microflora colonizing the other groups.

Adherence of salmonellae and native gut microflora to the gastrointestinal mucosa of chicks.

Adherence of salmonellae to the mucosa of the cecum was demonstrated using scanning electron microscopy. In the absence of other microflora, adherence was also shown at all other levels of the alimentary tract tested. Comparative development of native gut microflora in the ceca was also investigated in chicks treated with selected fecal microflora and in untreated chicks using scanning electron microscopy. In the treated chicks, there was early colonization by adherent bacteria interconnected with fibers, forming a mat of microflora. This mat of microflora may be responsible for preventing colonization of salmonellae in the ceca.

Competitive exclusion of intestinal colonization of Escherichia coli in chicks.

A native gut microflora of chickens that protected chicks against Salmonella was evaluated against six pathogenic strains of Escherichia coli using similar methodology. Nalidixic-acid-resistant forms of the E. coli strains were derived for use in seeder-bird and individual-bird challenge tests. A substantial degree of exclusion of intestinal colonization of each of the six pathogenic strains of E. coli was secured in chicks that had been treated with native gut microflora. E. coli appeared to colonize chiefly the crop and cecum. Native gut microflora limited to a much lesser degree the "normal" E. coli present in the intestinal tract of test chicks. The mechanism of protection appears to be similar to that for Salmonella: native gut microflora and E. coli competed for sites of attachment.

The influence of lactobacilli on the competitive exclusion of paratyphoid salmonellae in chickens.

The competitive exclusion of salmonellae by native gut microflora was investigated by treating chicks with various avian lactobacilli. The evaluation of protection was based on the number of salmonellae adhering to the mucosa of the crop and the cecum, enumeration of salmonellae in fecal droppings, and enrichment of cloacal swabs and fecal droppings using both individual and seeder bird tests. Lactobacilli reduced the number of salmonellae adhering to the crop mucosa by 1 to 2 logs. Treatment with lactobacilli did not lower the number of chickens shedding salmonellae or reduce the number of salmonellae adhering to the mucosa of the cecum. Lactobacilli as a single bacterial treatment played a minor role in protecting the crop, but no protection of the cecum was demonstrated.

Reciprocal competitive exclusion of salmonella and Escherichia coli by native intestinal microflora of the chicken and turkey.

Both the native intestinal microflora of chickens that protected chicks against salmonellae and Escherichia coli and native turkey intestinal microflora were evaluated for their reciprocal protective capacity in both species against Salmonella typhimurium and a pathogenic strain of E. coli. Nalidixic-acid-resistant forms of the S. typhimurium and E. coli strains were used in seeder-bird and individual-bird challenge tests. Reciprocal protection was provided by native chicken and turkey intestinal microflora in chicks and poults against S. typhimurium and the pathogenic strain of E. coli. The chicken and turkey microflora appeared to be equally effective in protecting the two species from S. typhimurium, but protection against E. coli was somewhat greater in the chicken than in the turkey.

Effect of environmental temperature on susceptibility of young chickens to Salmonella typhimurium.

Day-old chickens kept in a cold environment (18 degrees to 22 degrees C) were more susceptible to a low and moderate challenge of Salmonella typhimurium than chickens similarly challenged and kept in a warm environment (32 degrees to 36 degrees C). Cold stress at 10 degrees C for 24 h when applied to 12-day-old chickens effectively increased the number of birds shedding organisms. However a similar cold stress on 20-day-old chickens resulted in a less dramatic increase in the number of birds shedding organisms. Of the 60 birds previously challenged with S. typhimurium and then subjected to cold stress, 16 birds recommenced shedding and 7 birds with no previous history of shedding began to shed organisms.