Thornton J C, Garduño R A, Newman S G, Kay W W
Department of Biochemistry and Microbiology, University of Victoria, British Columbia, Canada.
Microb Pathog. 1991 Aug;11(2):85-99. doi: 10.1016/0882-4010(91)90002-r.
A slow-growing, aminoglycoside-resistant mutant and a rapidly-growing pseudo-revertant were isolated from Aeromonas salmonicida, the causative agent of salmonid furunculosis. These mutants continued to elicit a variety of classical virulence factors associated with A. salmonicida pathogenesis. They differed morphologically from the wild-type and from one another with respect to A-layer organization, membrane antagonist sensitivity and particularly to aerobic metabolism. Both mutants were drastically altered in the architecture of the 2D crystalline surface array (A-layer), although both were similar to wild-type with respect to cell surface composition. The slow-growing, antibiotic-resistant mutant differed significantly from the wild-type by the apparent loss of virtually all aerobic metabolism; the pseudo-revertant had partially recovered the ability to aerobically metabolize certain carbon sources. Both mutants were avirulent and incapable of tissue persistence. The rapidly-growing, antibiotic-sensitive pseudo-revertant, when administered either intraperitoneally or by immersion, effectively protected salmonid fish from challenge by a heterologous virulent stain suggesting its candidature as a live, attenuated furunculosis vaccine.
