The Contribution of Eimeria Coinfection and Intestinal Inflammation to Cecal Colonization and Systemic Spread of Salmonella Typhimurium Deficient in Tetrathionate Reductase or Type III Secretion Systems Salmonella Pathogenicity Island 1 or 2.

Intestinal inflammation may provide a growth advantage for and enhance its systemic spread in chickens. triggers intestinal inflammation in the host by using type III secretion systems (T3SS) and produces the inflammatory end product tetrathionate. In mice, tetrathionate respiration confers a growth advantage for Typhimurium over the competitive microbiome in the inflamed intestine. Coccidia also promote intestinal inflammation and enhance intestinal growth and systemic spread in chickens. The objective of this study was to evaluate the contribution of inflammation, induced by spp. or Typhimurium, to colonization and dissemination in chickens. In addition, the fitness costs associated with defects in tetrathionate reductase and T3SS associated with Pathogenicity Island 1 or 2 (SPI-1 or SPI-2) were evaluated in competition experiments with wild-type strain, with or without coinfection. One-day-old specific-pathogen-free chickens were orally inoculated with a sham inoculum or with 4 × 10 oocysts cocktail of , , , and . At 6 days of age, birds were orally administered a 1:1 ratio of Typhimurium wild-type and mutant deficient in tetrathionate reductase, SPI-1, or SPI-2 (10 colony forming units/bird). Ceca, livers, and drumsticks were collected at 3, 7, 14, and 42 days after infection, for bacteriology. Intestinal inflammation was scored by histology. Significantly higher intestinal inflammation was observed in challenge groups compared with the control. However, there were no significant differences in intestinal inflammation scores between groups coinfected with both spp. and Typhimurium and birds infected with alone, and coinfection did not increase prevalence or abundance. Contrary to mouse studies, tetrathionate reductase did not enhance Typhimurium cecal colonization or systemic spread in chickens. SPI-1 and SPI-2 played a significant role in dissemination and cecal colonization in chickens, respectively.

Rimet CS ，Maurer JJ ，Berghaus RD ，Jordan BJ ，da Silva LHA ，Stabler LJ ，Johnson KK ，Tensa LR ，Segovia KM ，França MS ... -  《-》

Effects of infection of Eimeria tenella, E. acervulina, and E. maxima upon Salmonella typhimurium infection in chickens.

Three experiments were conducted to examine whether Salmonella typhimurium infection is enhanced by concurrent infection with Eimeria tenella, E. acervulina, or E. maxima. There were two groups in each experiment: birds infected with a daily oral dose of approximately 1 X 10(4) cfu of S. typhimurium for 5 days after coccidial infection and birds infected with S. typhimurium alone with the similar exposure schedule. Chickens were necropsied 7, 10, and 14 days after coccidial infection. The numbers of S. typhimurium in the contents of ceca and small intestine were counted, and numbers of chickens positive for S. typhimurium in the liver and bile were examined. In E. tenella infection, the S. typhimurium counts in the ceca and small intestine of concurrently infected chickens were significantly greater than those of birds infected with S. typhimurium alone. In E. acervulina infection, the S. typhimurium counts in the ceca of chickens killed 14 days after E. acervulina infection and the numbers of birds positive for S. typhimurium in the ceca of chickens killed 10 and 14 days after E. acervulina infection were significantly greater than those of chickens infected with S. typhimurium alone. In E. maxima infection, the numbers of birds positive for S. typhimurium in the ceca and liver of chickens killed 7 days after E. maxima infection were significantly greater than those of birds infected with S. typhimurium alone. Results of this study indicate that infection with E. acervulina or E. maxima is able to enhance S. typhimurium infection in chickens.

Takimoto H ，Baba E ，Fukata T ，Arakawa A ... -  《-》

The Salmonella pathogenicity island 1 and Salmonella pathogenicity island 2 type III secretion systems play a major role in pathogenesis of systemic disease and gastrointestinal tract colonization of Salmonella enterica serovar Typhimurium in the chicken.

Salmonella enterica serovar Typhimurium infection of chickens is a major public and animal health problem. In young chicks, S. Typhimurium infection results in severe systemic infection; in older chicks, infection results in prolonged gastrointestinal tract colonization. Here we determined the role of the Salmonella pathogenicity island 1 (SPI-1) and Salmonella pathogenicity island 2 (SPI-2) type III secretion systems in systemic infection and gastrointestinal tract colonization of the chicken though experimental infection of chicks with a S. Typhimurium strain with mutations in the genes encoding the secretion system machinery of SPI-1 (spaS) and SPI-2 (ssaU) that prevent secretion of effector proteins. In 1-day-old chicks, mutation of SPI-2 lead to a decrease in both systemic bacterial numbers and pathology, although no difference in gastrointestinal numbers was observed. Mutation of SPI-1 had little effect in 1-day old chicks. In 1-week-old animals the SPI-2 mutants could not be detected systemically and colonized the gastrointestinal tract only in low numbers in comparison with the parent strain, and was cleared in 1 week. The SPI-1 mutant showed greatly reduced levels of systemic infection, and colonized the gastrointestinal tract at a lower level than the parent strain. The findings show that the SPI-2 type III secretion system is required for systemic S. Typhimurium infection in both infection models, and that it plays a significant role in gastrointestinal colonization. The SPI-1 system is involved in both systemic infection and gastrointestinal colonization, but does not appear absolutely essential for either infection process.

Jones MA ，Hulme SD ，Barrow PA ，Wigley P ... -  《AVIAN PATHOLOGY》

Influence of coccidiosis on Salmonella colonization in broiler chickens under floor-pen conditions.

The influence of coccidiosis on colonization of Salmonella typhimurium in broiler chickens under floor pen conditions was studied by semiquantitative methods. Chickens of two groups, unmedicated and medicated with nicarbazin (125 ppm via the feed), were exposed to three species of Eimeria (Eimeria tenella, Eimeria maxima, and Eimeria acervulina) at 2, 3, and 4 wk of age and given S. typhimurium in the feed 2 days later. Salmonella typhimurium was isolated most often (100%) from ceca of chickens exposed at 3 wk of age. Birds in the unmedicated group were positive for S. typhimurium at a higher rate than those in the medicated group. Salmonella typhimurium was detected in livers only in a few unmedicated birds.

Arakawa A ，Fukata T ，Baba E ，McDougald LR ，Bailey JS ，Blankenship LC ... -  《-》

The invasion of Salmonella typhimurium into the cecal wall of chickens infected with Eimeria tenella.

The effect of concurrent Eimeria tenella and Salmonella typhimurium infections on the invasion of S. typhimurium into the cecal wall of chickens were studied. In the experiment 1) groups were composed of birds infected with a daily dose of 1 X 10(3) to 1 X 10(5) S. typhimurium for 5 days and birds infected with S. typhimurium as the same manner one day after having been infected with 20,000 E. tenella oocysts. Chickens were killed 7, 10 and 14 days after coccidial infection. The ceca were examined bacteriologically. The number of S. typhimurium in the cecal washings and cecal wall and the number of chickens positive for S. typhimurium in the ceca were significantly greater in the concurrent infections than in the S. typhimurium alone. In experiment 2) groups were composed of birds infected with E. tenella and S. typhimurium in the same manner as experiment 1) and birds infected with 2 X 10(6) to 2 X 10(7) S. typhimurium for 5 consecutive days. Chickens were killed 7, 10 and 14 (or 15) days after coccidial infection. The distribution of S. typhimurium in the ceca was examined by fluorescent antibody technique. In coccidia-infected chickens, intense, specific fluorescence was noted in the epithelia destructed by coccidia, around the coccidial oocysts parasitized in the epithelial cells, and in the lamina propria and submucosa. In S. typhimurium alone-infected chickens, specific fluorescence was also found in the epithelia, lamina propria and submucosa, but was only limited in the lumen and on the surface of epithelial linings. The results indicated that the invasion of S. typhimurium into the cecal wall was enhanced by E. tenella infection in chickens.

Hikasa Y ，Baba E ，Fukata T ，Arakawa A ... -  《-》