Aphelenchoides rutgersi was axenically cultured in modified Soytone, yeast extract, lyophilized chick embryo extract medium (3% ST:2% YE:20% CEE-L, w/v:w/v:v/v). Earlier formulations used 10% CEE, v/v, before the manufacturer changed the preparation. After reestablishing A. rutgersi in medium that permitted continuous subcultivadon and reproduction, a second medium was tested that contained 0.5% sucrose and 0.5% Lipid Concentrate. The commercially available Lipid Concentrate made it possible to incorporate nonaqueous soluble chemicals into the medium. In addition, 0.1% Fast Green #3 was added to both media to visually demonstrate active ingestion of nutriment.

A 2-year study was conducted on Merion Kentucky bluegrass turf (Poa pratensis) to identify potential relationships among seasonal population dynamics of nematodes, chemical applications, thatch, tillering, dollar spot caused by Sclerotinia homoeocarpa, clipping weight, and other factors. Numbers of Tylenchorhynchus maximus determined during June were inversely related to the wet weight of grass from May. One or more monthly counts of Paratylenchus hamatus, Criconemella rusium, and T. maximus negatively correlated with the numbers of spring tillers. Applications of benomyl, used for dollar spot control, decreased numbers of T. maximus and free-living nematodes, and this chemical was associated with acidification of the thatch. Hoplolaimus galeatus levels were associated with an estimated 8% increase in the severity of dollar spot.

Hemicycliophora ritteri and Paratrichodorus minor were associated in high numbers with a previously unknown "dieback disease" of cranberry. Chemical treatment with nematicides and fungicides failed to control this disease. There were no correlations (P ≤ 0.05) among nematode numbers and yields of good or rotten berries, and with disease ratings. Nematodes were apparently not involved in the etiology of this dieback disease.

A metal detector was used to relocate steel pins marking the boundaries of semipermanent plots in cranberry bogs and turfgrass where continuous use precluded the placement of permanent wooden stakes.

The progression of events in the development of pine wilt disease following the invasion by Bursaphelenchus xylophilus is reviewed from early migration through pine tissues until symptom development on foliage. Disease resistance in pines, especially the hypersensitive reaction that is successful in controlling many potential pests and pathogens, is explored. Pathologies resulting from the activities of pinewood nematode include cortical trails and cavities; formation of cambial gaps and traumatic resin cysts; browning and death of cortex, phloem, cambium, and ray tissues; granulation and shrinkage of cell cytoplasm in rays; and destruction of resin canal epithelial and ray parenchyma cells. Death of parenchyma, production of toxins, and leakage of oleoresins and other material into tracheids are typical of the hypersensitive reaction occurring in pines following migration of small numbers of pinewood nematodes. The hypothesis presented is that a spreading hypersensitive reaction results in some of the observed pathologies and symptoms and eventually causes pine death. The growth-differentiation balance hypothesis is used to help explain predisposition, oleoresin production and toxicity, susceptibility and resistance, and the effects of variation in climate on host pines as related to pinewilt disease.

Percentage and rate of mortality in 2-4-year-old conifers depended upon the numbers of pinewood nematodes Bursaphelenchus xylophilus inoculated into their stems. In addition, percentage of conifer mortality was greater for spring inoculations when cambial activity was greater than for late summer and fall inoculations. Gross and histological examination of stems revealed destruction of the cambial layer, including fusiform and ray intitials and their derivatives. These data suggest that cambial and ray destruction causes tree death through blockage of tracheids by gas, oleoresin, or metabolites from dying ray tissues.