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Phellinus noxius is a fungus that causes brown root rot disease in tree and shrub species of subtropical and tropical regions. It has infected and rapidly killed hundreds of important tree and shrub species in these regions. It is widespread in the Pacific Region including all the island states of American Samoa, the Federated States of Micronesia (Chuuk, Kosrae, Pohnpei, and Yap), the Republic of Palau, the Commonwealth of the Northern Mariana Islands (Islands of Rota and Saipan), and Guam. This report explains how to detect brown root rot disease and its causal pathogen (P. noxius) by recognizing the signs and symptoms of the disease as well as using molecular techniques. It discusses several characteristics of P. noxius that make it such a destructive pathogen in the areas where it occurs and explains how the hot, humid, and sometimes stormy conditions that occur on these islands contribute significantly to disease spread and development. This publication also describes multiple approaches that have been attempted to control this fungus along with science-based information for consideration when trying to manage the pathogen.

The redbay ambrosia beetle Xyleborus glabratus Eichhoff is a non‐native vector of the pathogen that causes laurel wilt, a deadly disease of trees in the family Lauraceae in the southeastern U.S.A. Concern exists that X. glabratus and its fungal symbiont could be transported to the western U.S.A. and cause damage to California bay laurel Umbellularia californica (Hook. & Arn.) Nutt. in California and Washington. The present study evaluated in‐flight attraction, attack density and emergence of X. glabratus and another invasive ambrosia beetle Xylosandrus crassiusculus (Motschulsky) on cut bolts of California bay laurel and eight related tree species in an infested forest in South Carolina. Xylosandrus crassiusculus is not a vector of the laurel wilt pathogen but is a pest of nursery and ornamental trees. Mean catch of X. glabratus on California bay laurel bolts was not significantly different from catches on bolts of known X. glabratus hosts sassafras Sassafras albidum (Nutt.) Nees and swampbay Persea palustris (Raf.) Sarg. Mean attack density and adult emergence of both beetle species from California bay laurel was equal to or greater than all other tree species tested. Both beetle species readily produced brood in California bay laurel bolts. The results obtained in the present study suggest that California bay laurel may be negatively impacted by both of these invasive ambrosia beetles if they become established in the tree's native range.

Background Development and application of DNA-based methods to distinguish highly virulent isolates of Fusarium oxysporum f. sp. koae [Fo koae; cause of koa wilt disease on Acacia koa (koa)] will help disease management through early detection, enhanced monitoring, and improved disease resistance-breeding programs. Results This study presents whole genome analyses of one highly virulent Fo koae isolate and one non-pathogenic F. oxysporum (Fo) isolate. These analyses allowed for the identification of putative lineage-specific DNA and predicted genes necessary for disease development on koa. Using putative chromosomes and predicted gene comparisons, Fo koae-exclusive, virulence genes were identified. The putative lineage-specific DNA included identified genes encoding products secreted in xylem (e. g., SIX1 and SIX6) that may be necessary for disease development on koa. Unique genes from Fo koae were used to develop pathogen-specific PCR primers. These diagnostic primers allowed target amplification in the characterized highly virulent Fo koae isolates but did not allow product amplification in low-virulence or non-pathogenic isolates of Fo. Thus, primers developed in this study will be useful for early detection and monitoring of highly virulent strains of Fo koae. Isolate verification is also important for disease resistance-breeding programs that require a diverse set of highly virulent Fo koae isolates for their disease-screening assays to develop disease-resistant koa. Conclusions These results provide the framework for understanding the pathogen genes necessary for koa wilt disease and the genetic variation of Fo koae populations across the Hawaiian Islands.

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