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Mundulla Yellows (MY): Proof of Cause(s) at Last

Kevin Handreck

In two very recent scientific papers, scientists of the Victorian Department of Primary Industries and University of Melbourne have, in my view, provided conclusive proof that Mundulla Yellows is not caused by any pathogen, but by various imbalances in soil properties This is very thorough research of the highest quality.

The papers are:
  • Investigating the presence of biotic agents associated with Mundulla Yellows (JE Luck, R Crnov, B Czerniakowski, IW Smith and JR Moran) Plant Disease 90:404-410 (2006).
  • Soil properties associated with the tree decline 'Mundulla Yellows' (B Czerniakowski, R Crnov, IW Smith and JE Luck) Plant Soil DOI10.1007/s11104-006-9005-7 (2006).

The scientists found study sites in both South Australia and Victoria where there were Eucalyptus trees showing both MY symptoms and nearby others that were not showing symptoms.

To see if there was any biotic cause, they did the following:

  1. Grafted branch pieces (scions) from both asymptomatic and symptomatic E.camaldulensis trees onto unaffected E. camaldulensis rootstocks. All successful grafts produced healthy new growth, irrespective of the symptoms on the scion material used. They have now been monitored for almost 2 years and they will be monitored for a further 3 years, but the evidence so far does not support any conclusion that any disease-causing organism is present.

  2. Seed from asymptomatic E.camaldulensis trees was germinated in soil collected from under both symptomatic and asymptomatic trees. The seeds were either sterilised in a microwave oven or left untreated before sowing. Seedlings growing in the soil from asymptomatic trees were all green and healthy. Those in soil from symptomatic trees emerged yellow. The conclusion from these studies is clearly that non-biotic factors are producing MY.

  3. All investingations aimed at detecting virus or viroid particles, fungi, bacteria or phytoplasmas gave negative results. One symptomatic tree has an elevated level of a nematode present in the soil around its roots, but not an elevated level on the roots themselves. This was interpreted as not supporting a primary role for nematodes in MY.

  4. Insect sampling over two seasons did not show any difference in insect populations between symptomatic and asymptomatic trees.

So the conclusion from these thorough, multi-disiplinary studies is that there is no evidence for the association with MY of any biological agent. This is consistent with the inability of the South Australian research group led by Professor Randles to find any biotic agent associated with MY.

Therefore, the cause(s) must be non-biotic, with the proof as follows:

Soil samples from under symptomatic and asymptomatic trees were analysed by a complete range of standard soil tests: pH, salinity, exchangeable cations, available trace elements and ions dissolved in the water in the soils.

Soil (sampled separately at depths of 0-10 cm and 10-30 cm) from under symptomatic and asymptomatic trees had several key properties that were highly significantly different, as shown in the table.

Soil propertySymptomatic (MY) treesAsymptomatic trees
pH7.8 to 8.9 (highly alkaline)5.1 to 7.1 (acidic to neutral)
Salinity of 1:5 water extract (dS/m)0.22 to 0.88 (high)0.08 to 0.17 (low)
Moisture content (%)10 to 212.1 to 13
Total cations (meq%)30 to 433.1 to 20
Exchangeable calcium (meq%)26 to 380.5 to 13
Available iron (mg/kg)8 to 2450 to 390
Available manganese2.4 to 5.63.3 to 15
Boron (mg/kg)2 to 4.30.5 to 2.8
Carbonate and bicarbonate in soil water (mg/L)360 to 55915 to 224
Nitrate in soil water (mg/L)13 to 4230.0 to 31

You do not need to be a soil scientist to see that there is a huge difference in most of these properties between the soils on which symptomatic and asymptomatic trees were growing. The soils from under MY trees had much higher pH values, higher salinity, higher moisture content, higher total cations (hence had a higher clay content), higher exchangeable calcium, much higher carbonate and bicarbonate concentrations in the soil water, higher nitrate and much lower concentrations of available iron (especially) and manganese.

Analysis of youngest mature leaves from symptomatic and asymptomatic trees gave mixed results. Thus, at SA sites, MY leaves had only half the iron concentrations of those in leaves from asymptomatic trees, but in Victoria, iron concentrations were about the same in each. In conjunction with the information about bicarbonate levels given in the Table, I would interpret this as still being consistent with iron deficiency in the MY trees, with bicarbonate interfering with iron use in the leaves. MY tree leaves had higher chloride concentrations than in the leaves from asymptomatic trees.

Proof that what we see as symptoms on MY trees (chlorotic (interveinal yellowing on) youngest leaves, death of tips and dying back from tips) is largely iron deficiency was provided by the fact that MY trees sprayed with iron lost their symptoms and started to grow normally. Another supporting piece of evidence was that the soil under one tree that had only one branch with MY symptoms had a higher pH and salinity right under that branch (and hence around its supporting roots) than under all the other parts of the tree.

But why have these trees that have long grown in these areas started to show symptoms over the last 40 years? The authors conclude that it is due to a complex interaction between soil properties: at some sites earthworks have increased the lime content of the soil; at other sites, accumulation of salt in the root area, soil compaction, the formation of impermeable soil layers and increased soil sodicity may contribute to the problem.

While the major symptom is of iron deficiency, at many sites chloride toxicity (from higher salinity) looks to be part of the syndrome. Manganese deficiency and other micronutrient deficiencies and toxicities are also possible contributors at some sites. In a private communication, Dr Luck has told me that other deficiencies and toxicities have been implicated in other Australian states. For example, in Western Australia, Canberra and Tasmania MY-like symptoms have been observed in eucalypts on neutral or acidic soils with various nutrient imbalances and toxicities. A paper is in preparation.

The authors of these two papers did not comment on or investigate the claims of JA McNamara (Australian Biology, 16:94-107, 2003) that MY is caused by poisoning by herbicide(s) such as simazine. The Victorian scientists do not have any evidence that enables them to comment on this.

From the newsletter of the South Australian Region of the Australian Plants Society, November 2006.

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