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Australian Lucerne Yellows Disease – Pathogen, vector and control by Geoff Gurr, Leigh Pilkington, Murray Fletcher, Eric Elliott, Alex Nikandrow, Karen Gibb
September 2005
RIRDC Publication No 05/033 RIRDC Project No US-85A
Three newly-sown lucerne stands in the Mid Lachlan Valley region of New South Wales, Australia were sampled over 50 weeks for ALuY disease distribution and severity. Leafhopper populations were also monitored. Symptoms developed in all three stands within 32 weeks of sowing. There were statistically significant spatial patterns in the density of symptomatic plants for two dates at two sites. Two possible insect vectors, the spotted leafhopper (Austroagallia torrida) and the large green jassid (Batracomorphus angustatus) were more numerous in some sections of crop-margins at two sites. These two species and a third possible insect vector, the common brown leafhopper (Orosius argentatus) each had a statistically significant spatial and temporal correlation with symptomatic plant numbers for at least one site-date. The same leafhoppers were present in South Australia.
Two border treatment experiments evaluated the effect of crop-margin treatments on leafhopper movement into and from the stand. The second border treatment experiment examined also the treatment effect on ALuY disease incidence. Treatment with insecticide or herbicide significantly reduced the overall movement of leafhoppers. In addition, the insecticide treatment lowered the incidence of disease expression in adjacent lucerne. Results suggest that there is scope for management of this plant disease by reducing immigration of leafhopper vectors into lucerne from non-crop vegetation.
The spotted leafhopper, large green jassid and the common brown leafhopper were used in transmission tests to determine their vector status for the phytoplasmas associated with ALuY.
Caged, seed-grown lucerne plants were monitored for foliar symptom expression after feeding by leafhoppers transferred from ALuY symptomatic lucerne plants. Twelve of 25 plants developed phytoplasma disease-like symptoms including stunting and yellowing. The most pronounced foliar symptoms were displayed by five plants that had been fed on by the common brown leafhopper and four plants that had been fed on by spotted leafhopper. Only one plant, fed on by the common brown leafhopper, showed the distinctive root symptoms of ALuY. Molecular tests detected a phytoplasma in one plant each from the batches that had been fed upon by each leafhopper species. The phytoplasma detected from the plant that had been fed on by spotted leafhopper was shown by DNA analysis to be tomato big bud (TBB), a separate phytoplasma that causes witches’ broom and phyllody in lucerne. Electron microscopy detected an unidentified phytoplasma in two plants fed on by the common brown leafhopper and one by spotted leafhopper. Molecular tests failed to detect phytoplasma DNA from any of the leafhopper species used in transmission tests or from specimens sampled from lucerne crops. The common brown leafhopper is considered the most likely vector for the ALuY pathogen though the large green jassid cannot be ruled out. The spotted leafhopper is shown to be a vector for TBB phytoplasma.
Diseased plants within an
established irrigated lucerne stand in the mid Lachlan Valley were used
to assess the effect of several treatments on Australian lucerne yellows
(ALuY) disease. Treatments included applications of supplementary water,
multi-nutrients, potash, tetracycline antibiotic and a nil control. After
12 weeks, the plants in five of the ten blocks were harvested and fresh
weight, dry weight and symptom severity were recorded. Two weeks later,
the remaining plants were harvested and the same parameters, except fresh
weight, as well as seed yield and seed germination rate were measured.
Supplementary water resulted in a modest but statistically significant
increase of seed yield though effects on other measures of plant health
were not significant. Other treatments had no significant effect so the
scope for effective management of this disease via symptom alleviation
or antibiotic treatment appears limited.
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