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Role of Deleterious Rhizobacteria as Minor Pathogens in Reducing Crop Growth. T. V. Suslow, Former graduate student, Department of Plant Pathology, University of California, Berkeley 94720; M. N. Schroth, professor, Department of Plant Pathology, University of California, Berkeley 94720. Phytopathology 72:111-115. Accepted for publication 19 March 1981. Copyright 1982 The American Phytopathological Society. DOI: 10.1094/Phyto-72-111.

Various strains of root-colonizing bacteria were pathogenic on sugar beet seedlings and were termed deleterious rhizobacteria (DRB). These DRB were a major component of the bacterial microflora of field-grown sugar beet roots. Pelleting DRB on sugar beet seed, at populations of 106 colony-forming units per seed, caused reduced seed germination, root distortions, root lesions, reduced root elongation, increased infection by root-colonizing fungi, and significantly decreased plant growth. These effects were observed in sterile polyester seed growth pouches containing Hoagland’s solution, in U.C. soil mix, and in field soil. Reductions in fresh and dry weight of sugar beet tops up to 48% (P = 0.05) were obtained with some strains. The genera of DRB that were tentatively identified included: Enterobacter, Klebsiella, Citrobacter, Flavobacterium, Achromobacter, and Arthrobacter. Three fluorescent Pseudomonas spp. were identified as similar to Pseudomonas cichorii and Pseudomonas viridiflava. Colonization of roots by DRB was determined by marking strains for resistance to rifampicin (rif) and nalidixic acid (nal) and reisolating on King’s medium B amended with the two antibiotics. Resistant rif-nal strains of DRB were reisolated from all lesions and areas of root distortion on inoculated plants. Coinoculation of sugar beet seed with strains of plant growth-promoting rhizobacteria (PGPR) and DRB resulted in inhibition of DRB colonization of roots and increased plant growth compared to inoculation with DRB alone. The mode of action of PGPR in increasing plant growth was in part related to the inhibition of DRB.