Submitted to: Meeting Abstract
Publication Type: Abstract only
Publication Acceptance Date: 2/4/2013
Publication Date: 2/5/2013
Citation: Beck, B.H., Farmer, B.D., Straus, D.L. 2013. Unlocking the secrets of columnaris disease [abstract]. 2013 Mid-Continent Warm Water Fish Culture Workshop, February 4-6, 2013, Mt. Magazine State Park, Paris, Arkansas. p.19. Interpretive Summary:
Technical Abstract: Columnaris disease, caused by the bacterial pathogen Flavobacterium columnare, continues to be a major problem worldwide and commonly leads to tremendous losses of both wild and cultured freshwater fish, particularly in intensively farmed aquaculture species such as channel catfish. Despite its ecologic and economic impacts, the fundamental molecular mechanisms of the host immune response to this pathogen remain unclear. While F. columnare can induce pathologic changes in numerous external tissues, the adhesion of F. columnare to the gill in particular is strongly associated with pathogen virulence and host susceptibility. Recently, in this regard, using next-generation gene profiling we found that a rhamnose-binding lectin (RBL; a family of molecules that bind sugar structures on bacteria) was dramatically upregulated in the gill of fish infected with F. columnare (as compared to naïve, unchallenged fish). Thus, in the present study we sought to further characterize and understand the RBL response in channel catfish. We first identified two distinct catfish families with differential susceptibilities to columnaris disease; one family was found to be completely resistant while the other was susceptible (0% mortality versus 20% respectively). Exclusively, in the susceptible family, we observed a strong upregulation in RBL that persisted for at least 24 h (P < 0.05). To elucidate whether RBL play a more direct role in columnaris disease development, we exposed channel catfish to different doses of the putative RBL ligands l-rhamnose and d-galactose, and found that these sugars protected channel catfish against columnaris disease, likely through competition with F. columnare binding of host RBL. Finally, we examined the role of nutritional status on RBL regulation and found that RBL expression was upregulated (>120-fold; P < 0.05) in fish fasted for 7 d (as compared to fish fed to satiation daily), yet expression levels returned to those of satiated fish within 4 h after re-feeding. Collectively, these findings highlight roles for RBL in the context of columnaris disease initiation and reveal new aspects linking RBL regulation to feed availability.