Potato silver scurf, caused by Helminthosporium solani, is an important postharvest disease of economic significance. Control of H. solani has been accomplished primarily by postharvest applications of thiabendazole. However, many strains of H. solani have become resistant to thiabendazole, resulting in failure of disease control. Consequently, alternative control strategies are needed. This study showed that several salts significantly reduced silver scurf development on potato tuber at a concentration of 0.2 M and that the timing of application also influenced salt efficacy. Among the 23 tested salts, aluminum chloride was the only one reducing silver scurf severity when applied either 2, 4, or 7 days after H. solani inoculation. Aluminum lactate, potassium sorbate, sodium carbonate, sodium metabisulfite, and trisodium phosphate also markedly reduced silver scurf severity but only when applied 2 or 4 days after inoculation. Ammonium acetate, calcium chloride, sodium benzoate, sodium citrate, and sodium formate reduced disease severity by at least 50% when applied 2 days after H. solani inoculation. With the exception of calcium chloride and sodium formate, these salts also were shown to strongly inhibit H. solani mycelial growth or spore germination in vitro. Results of this study further demonstrate the possibility of using selected salts for the control of potato silver scurf.

Aluminum and bisulfite salts inhibit the growth of several fungi and bacteria, and their application effectively controls potato soft rot caused by Erwinia carotovora. In an effort to understand their inhibitory action, ultrastructural changes in Erwinia carotovora subsp. atroseptica after exposure (0 to 20 min) to different concentrations (0.05, 0.1, and 0.2 M) of these salts were examined by using transmission electron microscopy. Plasma membrane integrity was evaluated by using the SYTOX Green fluorochrome that penetrates only cells with altered membranes. Bacteria exposed to all aluminum chloride concentrations, especially 0.2 M, exhibited loosening of the cell walls, cell wall rupture, cytoplasmic aggregation, and an absence of extracellular vesicles. Sodium metabisulfite caused mainly a retraction of plasma membrane and cellular voids which were more pronounced with increasing concentration. Bacterial mortality was closely associated with SYTOX stain absorption when bacteria were exposed to either a high concentration (0.2 M) of aluminum chloride or prolonged exposure (20 min) to 0.05 M aluminum chloride or to a pH of 2.5. Bacteria exposed to lower concentrations of aluminum chloride (0.05 and 0.1 M) for 10 min or less, or to metabisulfite at all concentrations, did not exhibit significant stain absorption, suggesting that no membrane damage occurred or it was too weak to allow the penetration of the stain into the cell. While mortality caused by aluminum chloride involves membrane damage and subsequent cytoplasmic aggregation, sulfite exerts its effect intracellularly; it is transported across the membrane by free diffusion of molecular SO 2 with little damage to the cellular membrane.Aluminum and bisulfite salts are toxic to several microorganisms including fungi (7, 15, 16) and bacteria (1, 8). Aluminum chloride and sodium metabisulfite were shown to be toxic at low concentrations against Erwinia carotovora subsp. atroseptica and Erwinia carotovora subsp. carotovora (32a), gramnegative motile rod bacteria causing important economic losses in a wide variety of vegetable crops. Of particular interest, the application of these salts on potato tubers was effective in controlling soft rot caused by both bacteria (32a), a disease of high economic significance for the potato industry.Postulated mechanisms of sulfite toxicity or inhibition of microbial growth include reactions with protein disulfide groups (3,19,25), inhibition of enzyme activities by inactivating their cofactors (e.g., thiamine pyrophosphate) (31) or coenzymes (e.g., NAD) (20,25,27,29), and rapid depletion of ATP and ADP pools (14). Sulfites may also react with pyrimidine residues of nucleic acids (17, 26), which can lead to genetic damage and cell death. Mechanisms by which aluminum affects microorganisms include its binding to the cell wall causing impaired permeability (2, 9); its replacement of divalent metal complexes, chiefly Mg and Ca, in cells or cell membranes (1); and its complexion with ATP (6), DNA (32), and phosphates causing phos...

Soft rot caused by Pectobacterium sp. is a devastating disease affecting stored potato tubers, and there is a lack of effective means of controlling this disease. In this study, 21 organic and inorganic salts were tested for their ability to control soft rot in potato tubers. In the preventive treatment, significant control of soft rot was observed with AlCl3 (≥66%) and Na2S2O3 (≥57%) and to a lesser extent with Al lactate and Na benzoate (≥34%) and K sorbate and Na propionate (≥27%). However, only a moderate control was achieved by curative treatment with AlCl3 and Na2S2O3 (42%) and sodium benzoate (≥33%). Overall, the in vitro inhibitory activity of salts was attenuated in the presence of plant tissue (in vivo) to different degrees. The inhibitory action of the salts in the preventive treatment, whether effective or otherwise, showed an inverse linear relationship with water ionization capacity (pK') of the salt ions, whereas in the curative treatment, only the effective salts showed this inverse linear relationship. Salt-plant tissue interactions appear to play a central role in the attenuated inhibitory activity of salts in potato tuber through reduction in the availability of the inhibitory ions for salt-bacteria interactions. This study demonstrates that AlCl3, Na2S2O3, and Na benzoate have potential in controlling potato tuber soft rot and provides a general basis for understanding of specific salt-tissue interactions.

Twenty-one salts were tested for their effects on the growth of Pectobacterium carotovorum subsp. carotovorum and Pectobacterium atrosepticum. In liquid medium, 11 salts (0.2 M) exhibited strong inhibition of bacterial growth. The inhibitory action of salts relates to the water-ionizing capacity and the lipophilicity of their constituent ions.

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