Contribution of fimbriae and flagella ofSalmonella enteritidisto colonization and invasion of chicks

Abstract

Isogenic mutants of Salmonella enteritidis defective for the elaboration of fimbrial types SEF14, SEF17, SEF21 and flagella were used to study the contribution these organelles made to colonization, invasion and lateral transfer in young chicks. The caecum, liver and spleen were colonized within 24 h following oral inoculation of 1-day-old chicks with 10(5) wild-type S. enteritidis strain LA5. However, for some mutants, the numbers of organisms recovered from internal organs was reduced significantly, particularly at 24h post-inoculum, which supported the hypothesis that the organelles contribute to invasion and dissemination to internal organs. Specifically, mutations affecting SEF17, SEF21 and flagella contributed to a delay in colonization of the spleen, and those affecting SEF21 and flagella delayed colonization of the liver. Lower numbers of bacteria were recovered from the caecum with mutants deficient in elaboration of SEF21. Sentinel birds were colonized by LA5 or EAV40 (14s(-), 17(-), 21(-), fla(-)) directly from the environment within 2 days, although a consistent slight delay was observed with the multiple mutant. Overall, our data suggest a collective role for SEF17, SEF21 and flagella, but not SEF14, in the early stages of colonization and invasion of young chicks by S. enteritidis, but these surface appendages appear unnecessary for colonization of birds from their immediate environment.

Quantitative comparison of intestinal invasion of zoonotic serotypes of Salmonella enterica in poultry

“…However, it is possible that differences in intestinal invasiveness of Salmonella serotypes only lead to differences in the time needed to establish the generalized infection and not to differences in severity of infection. A report by Dibb-Fuller & Woodward (2000) could be taken as support for this because they showed that impairment of flagella and fimbriae function, and thereby a possible impairment of invasion in mutants of S. Enteritidis only leads to a delay in the establishment of the generalized infection measured as the time of colonization of internal organs. The particular ability of S. Enteritidis PT4 to infect the egg may not be related to invasion, but rather to unknown virulence determinants unique to this serotype (Keller et al, 1997).…”

Population Dynamics of Salmonella enterica Serotypes in Commercial Egg and Poultry Production

“…In S. Typhimurium, genes implicated in colonization include the type III secretion system genes of SPI-1 and SPI-2 (71), lpf and pef (78), and lipopolysaccharide biosynthesis genes (112). In S. Enteritidis, genes implicated in colonization include the type VI secretion system genes of SPI-19 (9) and the type III secretion system genes of SPI-2 (122), hilA (10), and the genes encoding fimbrial types SEF17 and SEF21 (34). However, given that the colonization mechanisms differ between hosts, between serovars, and even within an individual serovar, there is still much to understand related to colonization mechanisms employed by S. Heidelberg and S. Kentucky within the avian host.…”

Functional characterization of the FimH adhesin from Salmonella enterica serovar Enteritidis

“…Infection by Salmonella Enteritidis is initiated by the attachment and colonization of the gut mucosa, which seems to be an essential stage in the pathogenesis of salmonellosis. Increasing evidence suggests that bacterial fimbriae play an important role in these processes (De Buck et al, 2003;Dibb-Fuller et al, 1999;Dibb-Fuller & Woodward, 2000;Ewen et al, 1997;Naughton et al, 2001), although their exact role in the pathogenesis of Salmonella is still controversial (Rajashekara et al, 2000;.…”