The Infection Process of Yersinia ruckeri: Reviewing the Pieces of the Jigsaw Puzzle

Abstract

Finding the keys to understanding the infectious process of Yersinia ruckeri was not a priority for many years due to the prompt development of an effective biotype 1 vaccine which was used mainly in Europe and USA. However, the gradual emergence of outbreaks in vaccinated fish, which have been reported since 2003, has awakened interest in the mechanism of virulence in this pathogen. Thus, during the last two decades, a large number of studies have considerably enriched our knowledge of many aspects of the pathogen and its interaction with the host. By means of both conventional and a variety of novel strategies, such as cell GFP tagging, bioluminescence imaging and optical projection tomography, it has been possible to determine three putative Y. ruckeri infection routes, the main point of entry for the bacterium being the gill lamellae. Moreover, a wide range of potential virulence factors have been highlighted by specific gene mutagenesis strategies or genome-wide transposon/plasmid insertion-based screening approaches, such us in vivo expression technology (IVET) and signature tagged mutagenesis (STM). Finally, recent proteomic and whole genomic analyses have allowed many of the genes and systems that are potentially implicated in the organism's pathogenicity and its adaptation to the host environmental conditions to be elucidated. Altogether, these studies contribute to a better understanding of the infectious process of Y. ruckeri in fish, which is crucial for the development of more effective strategies for preventing or treating enteric redmouth disease (ERM).

The repeat structure of two paralogous genes, Yersinia ruckeri invasin (yrInv) and a “Y. ruckeri invasin-like molecule”, (yrIlm) sheds light on the evolution of adhesive capacities of a fish pathogen

“…This might be explained by the early success of the ERM vaccine in the 1960s, the complex taxonomy and the limited amount of research on different Y. ruckeri serotypes (Barnes, 2011). However, one thing is clear: virulence of Y. ruckeri is influenced by several factors, such as iron availability, temperature, pH and osmolarity (Guijarro et al, 2018). Furthermore, it is believed that the virulence mechanism and virulence determinants of Y. ruckeri are similar to other members of the Enterobacteriaceae family (Fernández et al, 2007a).…”

“…In contrast, STM is used to screen for Y. ruckeri mutants that survive in vitro, but not in vivo, meaning that the inactivated gene is required for survival or infection. Other techniques, especially those developed in recent years, are based on prediction of the role of virulence factors, and they include proteomic, transcriptomic and genomic analyses (Guijarro et al, 2018;. Although these methods have several limitations, they have helped understand the pathogenesis of Y. ruckeri infection (Guijarro et al, 2018).…”

Effects of siRNA silencing on the susceptibility of the fish cell line CHSE-214 to Yersinia ruckeri

“…Interestingly; while Y. ruckeri does not harbour a YadA equivalent, it is known to harbour two homologs of invasin: Y. ruckeri invasin (YrInv) and Y. ruckeri invasin-like molecule (YrIlm) [3]. Furthermore, several isolates of Y. ruckeri belonging to the O1 serotype also carry a cluster of fimbrial gene homologous to the STF cluster of S. typhimurium [10,11]. However, this cluster is absent from the ATCC 29473 type strain studied here [11].…”

“…Among the proteins carried on SPI-1 is the chaperon Invasion protein B (InvB); SPI-1 is known to play a role in the intracellular invasion of S. enterica [15] so the Ysa of Y. ruckeri could plausibly be involved in intracellular invasion of Y. ruckeri. However, our knowledge of Ysa T3SS, and that of Y. ruckeri in particular is still very incomplete [10] and no conclusion is currently possible.…”

Effects of siRNA silencing on the susceptibility of the fish cell line CHSE-214 toYersinia ruckeri

“…Among the proteins carried on the SPI-1 is the chaperon Invasion protein B (InvB) and the SPI-1 is known to play a role in the intracellular invasion of S. enterica (15, 16) so the Ysa of Y. ruckeri could plausibly be involved in intracellular invasion of Y. ruckeri. However, our knowledge of the Ysa T3SS, and that of Y. ruckeri in particular is still incomplete (17) and no conclusion is currently possible.…”