Isolates of F. oxysporum collected from symptomless carnation cuttings from Australian carnation growers properties, together with isolates from national collections, were screened for pathogenicity and grouped according to vegetative compatibility and random amplified polymorphic DNA (RAPD) patterns. The collection of 82 Australian isolates sorted into 23 different vegetative compatibility groups (VCGs). Of 69 isolates tested for pathogenicity, 24 were pathogenic to carnations, while the remaining 45 were non-pathogenic. All pathogenic isolates were within two VCGs, one of which was also compatible with an isolate obtained from an international culture collection, and which is known to represent VCG 0021 and race 2. Race status of the two pathogenic VCGs remains unknown. The RAPD assay revealed distinct DNA banding patterns which could distinguish pathogenic from non-pathogenic isolates as well as differentiate between isolates from the two pathogenic VCGs.
Fusarium oxysporumSchlecht. causes vascular wilt in a broad range of host plants including carnations (Dianthus caryophyllus L.). This species of Fusarium
Field trials were conducted during 1982-85, to develop a comprehensive spray program for the control of bacterial canker (Pseudomonas syringae pv, syringae) of apricot and cherry. Five spray schedules were evaluated as measures to reduce disease levels. Copper hydroxide at 2.5 g/L in water was applied to apricot, and bordeaux mixture at 6 g copper sulfate + 8 g hydrated lime/L in water was applied to cherry, during autumn, winter and pre-bloom spring. The effectiveness of copper sprays in reducing epiphytic populations of the pathogen during post-bloom spring was also tested. Copper hydroxide was applied to apricot, and a foliar copper nutrient and copper hydroxide were applied to cherry at low concentrations. Most spray schedules tested significantly (P<0.05) reduced canker incidence relative to controls. Excellent control of epiphytic populations of the pathogen on apricot and cherry was achieved with copper sprays applied at post-bloom in spring. A spray schedule consisting of 2 autumn, 1 winter and 2 pre-bloom spring sprays with copper hydroxide on apricot or bordeaux mixture on cherry was successful in reducing canker (>67% reduction) and is recommended for control of the disease. Two applications of copper hydroxide at 1.0 g/L in water in post-bloom spring considerably reduced (>9 1 %) epiphytic populations (P. syringae pv. syringae) on apricot and cherry leaves. Later sprays are recommended for use in combination with the autumn-winter-spring (pre-bloom) spray schedule, especially under excessively wet and cool weather conditions in spring.
In a survey of the major stonefruit nurseries in Victoria during winter 1978 and 1979, Pseudomonas syringae pv. syringae, the causal organism of bacterial canker, was found to be present on most of the stonefruit material in all nurseries but was detected most frequently on apricot.
The epiphytic populations of P.s. pv. syringae on leaves, buds and shoots of apricot and cherry were assessed periodically between 1979 and 1983 by determining the proportion of trees bearing the bacterium or by counting numbers of bacteria. Populations consistently reached peak levels during spring and late autumn, with highest levels in spring. Populations were lowest during mid‐ to late summer. High proportions of tree contamination and high populations coincided with periods when maximum temperatures ranged from 19° to 25°C, and when rainfall was moderately high. The significance of these findings in the light of information from other studies on the seasonal variability of host susceptibility, and in relation to chemical control, is discussed.
There was no evidence of occurrence of P.s. pv. morsprunorum in Victoria.
The seasonal variation in susceptibility of buds, stems, leaves and fruit of apricot to Pseudomonas syringae pv. syringae, and sites through which infection occurs in apricot and cherry were studied. Infection of apricot and cherry occurred through buds, flowers, leaves, fruit and stems but not leaf scars through which natural infection can occur. Only stem and bud inoculations consistently led to the establishment of cankers. The proportion of buds showing infection was highest with inoculations made in late autumn and winter (May-July), and lowest with inoculations in summer (December-February). The number of stem inoculations, resulting in extensive cankers, was highest in late winter and spring (August-November) and lowest in summer and early autumn (December- March). Leaves and fruit were susceptible only during spring (September-November), when they were immature. The importance of these findings in relation to epidemiology and control of bacterial canker is discussed.
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