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<i>Yersinia ruckeri</i> causes outbreaks of enteric redmouth disease in salmon aquaculture all over the world. The transient antibiotic tolerance exhibited by bacterial persisters is commonly thought to be responsible for outbreaks; however, the molecular factors underlying this behavior have not been explored in <i>Y. ruckeri</i>. In this study, we investigated the participation of the RNA chaperone Hfq from <i>Y. ruckeri</i> in antibiotic persistence. Cultures of the <i>hfq</i>-knockout mutant (Δ<i>hfq</i>) exhibited faster replication, increased ATP levels and a more reductive environment than the wild type. The growth curves of bacteria exposed to sublethal concentrations of ampicillin, oxolinic acid, ciprofloxacin and polymyxin B revealed a greater susceptibility for the Δ<i>hfq</i> strain. The time-kill curves of bacteria treated with the antibiotics mentioned above and florfenicol, using inoculums from exponential, stationary and biofilm cultures, demonstrated that the Δ<i>hfq</i> strain has significant defects in persister cells production. To shed more light on the role of Hfq in antibiotic persistence, we analyzed its dependence on the (p)ppGpp synthetase RelA by determining the persister cells production in the absence of the <i>relA</i> gene. The Δ<i>relA</i> and Δ<i>relA</i>Δ<i>hfq</i> strains displayed similar defects in persister cells formation, but higher than Δ<i>hfq</i> strain. Similarly, stationary cultures of the Δ<i>relA</i> and Δ<i>relA</i>Δ<i>hfq</i> strains exhibited comparable levels of ATP but higher than that of the Δ<i>hfq</i> strain, indicating that <i>relA</i> is epistatic over <i>hfq</i>. Taken together, our findings provide valuable information on antibiotic persistence in <i>Y. ruckeri</i>, shedding light on the participation of Hfq in the persistence phenomenon.