LB9 (GenBank: JQ864377.1) matching 99% identity. This explains the relatively high number of total bacterial colonies recovered from mushroom tissue treated with Bdellovibrio, despite the reduction in the dark lesions characteristic of P. tolaasii infection: Bdellovibrio predation rapidly reduces P. tolaasii population numbers on the mushroom surface, but does not necessarily reduce those of other non-disease

causing, likely mushroom-indigenous species, such as the Enterobacter isolated in this study. The King’s Medium B in which P. tolaasii 2192T and B. bacteriovorus HD100 were added to the surface of the PD173074 in vitro mushroom during test inoculations, and the cell-lysate debris left behind after P. tolaasii death due to predation, may then allow these indigenous Enterobacter to occupy the niche caused by Bdellovibrio predation of P. tolaasii. selleck chemicals Discussion We showed

that B. bacteriovorus HD100 is a predator of P. tolaasii 2192T in vitro and in vivo (in funga), suppressing population growth LXH254 mw of the strain over a 24-hour period where 4 × 106 or 1.6 × 107 PFU B. bacteriovorus HD100 were added to pathogen on post-harvest mushrooms (Figures 1 and 4). P. tolaasii is a difficult pathogen to control in mushroom grow-houses due to its ability to persist in nutrient-poor soils and the ease with which it spreads through mushroom compost, through flagellar swimming, and via the hands of pickers during the manual harvesting process [8]. Furthermore, commensal bacterial species in the mushroom casing soil play a key role in mushroom growth initiation, and therefore any treatment to prevent or treat P. tolaasii infection must not result in a completely sterile growth environment, which may result from broad antibiotic or antiseptic treatment. Thus it is beneficial to explore post-harvest anti- P. tolaasii treatments, such as this study with B. bacteriovorus. Our SEM images confirmed that B. bacteriovorus HD100 survived on the post-harvest supermarket mushroom surfaces after 48 hours, and was therefore unaffected by any

pre-treatment of those mushrooms for commercial purposes to promote growth and extend shelf-life in the film-covered plastic trays they were sold in (Figure 3c). B. bacteriovorus is therefore a viable treatment for bacterial Aurora Kinase diseases of mushrooms, such as brown blotch disease. Previous studies of mushroom infections have found that a ‘threshold’ number of P. tolaasii cells are required for the initiation of infection, which includes production of tolaasin, the chemical mediator of the brown blotch symptom development [8]. We found that when B. bacteriovorus HD100 was applied to the surface of post-harvest, commercially grown mushrooms before or after inoculation with P. tolaasii, both the intensity of the brown blotch symptoms of disease and the number of P. tolaasii 2192T present the mushroom surface were significantly reduced (Figures 2 and 4), supporting the threshold hypothesis.