Search

Newly hatched chicks were vaccinated orally with a genetically defined Salmonella enteritidis aroA candidate, strain CVL30. In chickens immunized with 10(5) or 10(9) CFU and challenged by the intravenous route with 10(8) CFU of S. enteritidis 109 Nalr at 8 weeks old, there were similar reductions in colonization of the spleens, livers, and ceca of vaccinees compared with unvaccinated controls. Two groups of newly hatched female chicks were vaccinated orally with 10(9) CFU of strain CVL30, and one group was revaccinated intramuscularly with 10(9) CFU at 16 weeks old. When challenged intravenously with S. enteritidis 109 Nalr at 23 weeks old, there was a reduction in the colonization of spleens, livers, ovaries, and ceca compared with unvaccinated controls. Inclusion of the intramuscular booster gave increased protection to the ovary, although the vaccine strain was isolated on one occasion from a batch of eggs laid at 20 weeks old. In chickens immunized with 10(9) CFU of strain CVL30 and challenged orally with 10(9) CFU of S. enteritidis 109 Nalr, there was a reduction in intestinal shedding of the challenge strain from vaccines compared with unvaccinated controls. Circulating immunoglobulin G antibodies to lipopolysaccharide (LPS) were detected in unvaccinated controls within 7 to 10 days of oral challenge. In contrast, circulating immunoglobulin G antibodies to LPS in vaccinees were not altered by the oral challenge, which suggested that vaccination reduced or prevented invasion by the challenge strain from the gut or multiplication of the challenge strain in the tissues. Newly hatched chicks were vaccinated orally with ca. 10(9) CFU of strain CVL30, and 1 day later, the vaccines and unvaccinated controls were challenged orally with 10(5) or 10(9) CFU of S. enteritidis 109 Nalr. Colonization of the ceca and invasion from the gut by the S. enteritidis challenge strain was reduced in the vaccines up to 5 days postchallenge compared with controls. In a second trial, vaccinees and controls were challenged orally with 10(7) or 10(9) CFU of S. typhimurium 2391 Nalr. In contrast to the challenge with S. enteritidis, colonization of the ceca and invasion by the S. typhimurium strain were not greatly reduced.

Newly hatched chicks were dosed orally with a Salmonella typhimurium wild-type strain, an S. enteritidis wild-type strain, and a genetically defined S. enteritidis aroA vaccine candidate, strain CVL30. The S. typhimurium strain, 2391 Nalr, was virulent in newly hatched chicks and caused deaths in 7 of 20 chicks after an oral dose of 10(5) organisms. The S. enteritidis wild-type strain, LA5, caused death in 1 of 25 chicks and gross pathology including pericarditis and perihepatitis in 6 of the 24 survivors after an oral dose of 10(9) organisms. S. enteritidis aroA CVL30, attenuated by ca. 6.5 log10 in BALB/c mice, was nonvirulent when administered orally to chicks and did not cause morbidity. When newly hatched chicks were dosed, the pattern of invasion and colonization of the reticuloendothelial system by strain CVL30 was similar to that of its parent strain, LA5, irrespective of the dose. Oral inoculation of newly hatched chicks with < 10 organisms of S. enteritidis LA5 or CVL30 was followed by multiplication in the cecal contents. Within 3 days of hatching, the pH of the cecal contents was reduced from ca. 7 to 5. Samples of gut contents were inoculated in vitro. The S. enteritidis strains multiplied in samples taken from the ileum and duodenum irrespective of age but multiplied in the cecal samples from newly hatched chicks only. Invasion from the gut by S. enteritidis LA5 and CVL30 was both age and dose dependent.