Intestinal colonisation in the chicken by food‐poisoningsalmonellaserotypes; Microbial characteristics associated with faecal excretion

Abstract

SUMMARYFollowing oral inoculation of newly-hatched or three-week-old chickens, Salmonella organisms persisted longest in the caeca and they were also present for a shorter time in the crop. S. cholerae-suis, E. coli K12 and Saccharomyces cerevisiae did not colonise the alimentary tract when inoculated orally, but they persisted longer in the caeca than in other regions of the gut. This suggested that preferential localisation of Salmonella in the caeca may be the result of non-specific or host factors. This may include the slow rate of flow of contents through this organ which would allow greater microbial multiplication and persistence. Some Salmonella strains, particularly S. typhimurium, inoculated orally into three-week-old chickens were isolated in greater numbers from homogenates of the crop wall and, much less frequently, from the caecal wall, than from the luminal contents of these organs. None of the strains associated with the crop wall to the same extent as did lactobacilli.After oral inoculation of food-poisoning Salmonella serotypes the number of chickens excreting Salmonellae in their faeces gradually declined over a period of at least 4 weeks. In contrast, host adapted serotypes such as S. cholerae-suis and S. abortus-ovis were not excreted for longer than a few days. By testing mutants of S. typhimurium and S. infantis which were devoid of easily recognised characteristics it was concluded that neither flagellar (H) antigens, somatic (O) antigens, mannose-sensitive haemagglutinins nor the possession of the virulenceassociated 85 kilobase plasmid of S. typhimurium, were essential for colonisation (persistent faecal excretion). However, a mutant of S. infantis which was created by nitroso-guanidine treatment still possessed flagellar and somatic antigens and haemagglutinins and yet did not colonise the alimentary tract, indicating that an unidentified microbial factor was essential for colonisation.

Further studies on the inhibition of colonization of the chicken alimentary tract withSalmonella typhimuriumby pre–colonization with an avirulent mutant

“…S. infantis 1326/28 Spcr was selected for this purpose [3]. The challenge strains (7 serotypes) are shown in A. BERCHIERI AND P. A. BARROW faecal excretion of the challenge strain F98 Nalr was examined.…”

“…The rough mutant of F98 was prepared by selecting for a bacteriophage resistant mutant using a phage isolated from sewage as described by Barrow, Simpson and Lovell [3]. This was made Sper, while the fully virulent strain was made resistant to nalidixic acid (Nalr), by the method of Smith and Tucker [2].…”

“…Chickens infected at this time with salmonella serotypes characteristic of human food-poisoning excrete organisms in the faeces in greater numbers and for longer than do chickens infected when they are older [1][2][3]. This increase in resistance is explained by the gradual acquisition by the chickens of the microorganisms that constitute its normal intestinal microflora [4][5][6][7].…”

Modulation of cytokine gene expression by selectedLactobacillusisolates in the ileum, caecal tonsils and spleen ofSalmonella-challenged broilers

“…The gastrointestinal tract is the first site encountered by orally ingested pathogens, with the ileum and caecum being the major sites of colonization in chickens (Barrow et al, 1988). The infection of Salmonella Typhimurium in animals is a progressive process, which starts from colonization of the intestines followed by spreading to internal organs, such as the spleen and liver (Côté et al, 2004).…”

Scientific Opinion on the public health risks of table eggs due to deterioration and development of pathogens

“…In the paratyphoidal diseases, infection is largely confined to the gastrointestinal tract and is accompanied by faecal excretion (Shivaprasad et al, 2013). Some Salmonella serovars responsible for paratyphoid infection (such as S. Infantis and S. Montevideo) are less invasive but able to achieve a more extensive gastrointestinal colonization, therefore shedding larger numbers of bacteria over longer periods (Barrow et al, 1988).…”