In vitro studies were conducted into the activity of 22 fungicides against Phaeomoniella chlamydospora, the cause of Petri disease(1). Mycelial growth of the pathogen was inhibited by the DMI fungicides, cyproconazole, bitertanol, tebuconazole, fenarimol, myclobutanil and prochloraz, which gave EC50 values of less than 0.2 mg l-1; by the benzimidazole fungicides, benomyl, carbendazim and thiophanate methyl, which gave EC50 values of less than 0.4 mg l-1; by the anilopyrimidines, pyrimethanil and cyprodinil/fludioxonil, which gave EC50 values of less than 0.02 mg l-1. The same fungicides had different effects on germination of conidia. All the DMI fungicides tested were relatively ineffective with EC50 values greater than 15 mg l-1 for germination. Of the benzimidazoles, only benomyl was relatively effective at reducing germination, with an EC50 value of 0.09 mg l-1, whereas the anilopyrimidines, alone or combined with phenylpyrrole, were effective with EC50 values of less than 0.1 mg l-1. Kresoxim-methyl, which is locally systemic, was effective at inhibiting mycelial growth and germination with EC50 values of 0.086 and 0.11 mg l-1 respectively. Of the contact fungicides tested, most were effective at reducing germination of P. chlamydospora conidia, since their EC50 values were much lower than the recommended field rates, but these fungicides were also much less effective at reducing mycelial growth, for which their EC50 values were up to 400 times greater. The disinfectant, hydroxyquinolene sulphate was highly effective at reducing germination but less effective against mycelial growth, with EC50 values of 0.002 and 8.5 mg l-1 respectively. The potential role of these fungicides for disease management in the nursery and vineyard is discussed.