Chlorotic streak disease in Queensland

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Completed projects final reports Pest, Disease and Weed Management

1995

Chlorotic streak disease in Queensland

Magarey, RC

http://hdl.handle.net/11079/763

Downloaded from Sugar Research Australia Ltd eLibrary

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BUREAU OF SUGAR EXPERIMENT STATIONS QUEENSLAND, AUSTRALIA

CHLOROTIC STREAK DISEASE IN QUEENSLAND by

R C Magarey TE95007

BSES Publication

Technical Reports TE95007 August 1995

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CONTENTS

Page No.

EXECUTIVE SUMMARY 1

1.0 INTRODUCTION 1

2.0 SYMPTOMS 1

3.0 HISTORY 1

4.0 NATURE OF THE DISEASE 2

4.1 Transmission and infection 2

4.2 Effect of chemicals on disease development 3

4.3 Vectors 3

4.4 Causal agent 3

5.0 ALTERNATIVE HOSTS 3

6.0 YIELD LOSS 4

6.1 Magnitude of losses 4

6.2 Components of yield loss 5

7.0 DISEASE INCIDENCE 5

7.1 Area diseased in Queensland crops 5

7.2 Disease incidence by district and mill area 6

8.0 CONTROL 7

8.1 Hot water treatment 7

8.2 Varietal resistance 7

8.2.1 Field test 7

8.2.2 Gravel hydroponic test 8

8.3 Recommended control measures 9

9.0 CURRENT PROBLEM SITUATIONS IN THE INDUSTRY 10

10.0 RESEARCH REQUIRED 10

11.0 DISCUSSION 10

12.0 CONCLUSION 11

13.0 REFERENCES 11

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EXECUTIVE SUMMARY

Chlorotic streak is a disease of unknown etiology affecting between 30-50,000 ha of caneland in Queensland annually. The disease is present in all canegrowing districts but is of greatest incidence in the Herbert River and Rocky Point mill areas. The disease is favoured by poor drainage and is spread by floodwaters. Yield losses of up to 40% have been recorded with the disease reducing germination, ratooning, stalk number, and stalk weight. It is likely to be reducing industry returns by $2-5m annually. Of concern is the likely increase of the disease with the return to wetter seasons in Queensland and with the increasing practice of re-cycling of irrigation tail waters in the Burdekin district. It is recommended that a varietal resistance screen be conducted to obtain disease ratings on current commercial varieties and that research into the causal agent be undertaken.

1.0 INTRODUCTION

Chlorotic streak disease is widespread in Queensland and is of particular concern in the low lying, poorly drained areas of a number of canegrowing districts. The causal agent is still unidentified even though the disease has been recognised for over 60 years. Some research suggests that the disease is caused by a virus but no conclusive evidence has been obtained. The disease is spread through flood and drainage water, and infects through the root system producing characteristic leaf symptoms. Significant yield losses are caused by the disease.

2.0 SYMPTOMS

Chlorotic streak is characterised by yellow to creamy-white leaf streaks with irregular wavy-margins. These streaks may be short or extend the full length of the leaf blade.

Streaks in the early stages of development are usually fragmented. Older streaks have a more yellow hue than younger ones and often have areas of necrosis along the centre of the streak. Death of leaf tissue at the tips and margins occurs in older leaves. Root temperature affects streak production and Sturgess (1962) found that 30°C was optimal for symptom development. In the field, leaf symptoms are often transient, probably as a result of variation in environmental conditions, including soil temperature. Internal stalk symptoms include a reddening of vascular bundles at the nodes; the reddening occurs right through the nodes penetrating a short distance into the internode.

3.0 HISTORY

Chlorotic streak was recognised concurrently in Java, Hawaii, and Australia in the 1929- 30 period. Named 'Pseudo-scald' in Australia, the first Australian record was in northern Queensland during the first disease survey of that district. The disease was apparently widespread from Cardwell north and endemic to the area (Bell, 1933). The disease was located soon after in the Proserpine mill area, and along the Maroochy River in the Moreton mill area (Bell, 1933).

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Careful disease inspections failed to locate the disease anywhere else and it seems likely that further findings may have resulted from transfer of the disease from infested areas.

The progress of the disease through Queensland is detailed in Table 1.

Table 1

The chronology of the finding of chlorotic streak disease in each sugarcane district of Queensland

Mill area of district First report Northern Queensland

Proserpine Moreton Rocky Point Maryborough Plane Creek

Mackay (Pleystowe) Bundaberg-Childers Invicta

Lower Burdekin (Inkerman)

1929 1929 1930 1946 1947 1953 1954 1955 1956 1960

In southern Queensland infested farms were initially quarantined in an attempt to prevent further spread but this proved useless. The first findings of chlorotic streak in each district were of limited distribution but rapid disease spread followed. The presence of alternative hosts, the lack of varietal resistance, and the ability of the pathogen to remain infectious in diseased soils all contributed to the lack of control achieved.

4.0 NATURE OF THE DISEASE

On a world basis, Queensland has been prominent in chlorotic streak research, particularly in the 1960s.

4.1 Transmission and infection

Research by Sturgess and Egan in the late 1950s and 1960s showed that the disease was transmitted by exposure of roots to contaminated water; that the minimum infection period for roots exposed to the disease was less than one hour; that the minimum incubation period was 12 days; that drainage waters from diseased fields could be infectious; that root inoculation within three days of ratooning led to high rates of transmission; that infectivity was maintained for at least 150 days in gravel hydroponic culture in the absence of host plants, while drying the gravel for five days eliminated the infectious agent; and that infested soil could remain infectious for up to 9 months in the absence of the host (Egan, 1961; Egan, 1963a and b; Egan, 1966; Hughes et al., 1967 and 1968; Sturgess, 1964).

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A number of attempts were made to transmit the disease by cane knife or other mechanical means but these failed (Bell, 1934; Hughes, 1940). Sturgess (1963) noted a low level of mechanical transmission when a hypodermic needle was used to inoculate roots with root extracts.

Early research showed that the disease rapidly infected healthy cane planted in low lying areas and Steindl (1955) suggested that inundation of the cane field, no matter how brief, leads to disease transmission if flood waters are contaminated. Sturgess (1964) found that waterlogging increased disease transmission when compared to plants growing in moist, but free draining soil.

4.2 Effect of chemicals on disease development

Initial experiments investigated the role of nutrients in symptom development, but none prevented disease development. Nutrients investigated include lithium, sodium, mercury, copper, boron, zinc, manganese, cobalt, barium, arsenic, bismuth, lead and iron (Bell, 1942).

Egan carried out experiments in the 1964-1970 period on the effect of various chemicals on transmission in gravel hydroponic culture. Dexon, nemagon, aureomycin and terramycin did not prevent transmission; terramycin possibly increased transmission. In contrast, the fungicides captan, PCNB (0.5%), and thiram (TMTD) (0.1%) greatly reduced transmission. Viral inhibitors (tri-sodium phosphate and milk) and benzalkonium chloride (Mirrol) reduced transmission considerably when plants were dipped in these chemicals after a two hour infection period (Hughes et al. 1965, 1967, 1968, 1969 and 1970).

4.3 Vectors

Vectors of the disease are unknown though extensive testing of common insects was undertaken in the 1930s and 1950s (Bell, 1938; Hitchcock, 1955). Insects tested included Perkinsiella saccharicida Kirk, Lophops saccharicida Kirk, Cicadella pathaon Kirk., Proutista lumholtzi Kirk, Phaenacantha australica Kirk, Saccharicoccus sacchari Ckll., Aphis sacchari Zehnt., Neomaskellia bergii Sign., Aphis maidis Fitch, and Tetranychus sp.

4.4 Causal agent

The causal agent has not been identified though some evidence suggests the disease has a viral origin. Sturgess (1963) suggested that the infectious agent could pass through a 0.5 mm aperture filter, and this was later confirmed by Egan (Anon, 1972). Recent unpublished BSES research has shown that ds-RNA may be associated with diseased leaves. No viral particles have been observed under the electron microscope.

5.0 ALTERNATIVE HOSTS

Egan (1965) and Hughes et al. (1968) reported that the following species were susceptible to chlorotic streak: Arundo donax, Brachiara mutica, Panicum maximum, Paspalum

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paniculatum, Pennisetum purpureum, Sorghum verticilliflorum, Sorghum almum, and Sorghum bicolor.

6.0 YIELD LOSS

6.1 Magnitude of losses

Immediately after the disease was recognised, yield loss trials were established. A summary of results up to the early 1960s is included in Table 2.

Table 2

Yield losses caused by chlorotic streak in Queensland experiments up to the early 1960s

Location Year Variety Yield loss References Pathology Plot, Brisbane

Northern Queensland Maroochy River Northern Queensland

1930 1930s 1948 late 1950s

Badila Badila POJ2878 Pindar P Q66 P Q67 P Pindar 1R Q66 1R Q67 1R

40%

(stalk number) 34%

25 t/ha (2 yr crop)

30%

17%

27%

10%

23%

16%

Bell, 1933 Hughes, 1948 Hughes, 1948 Egan, 1961 Egan, 1961

In two trials in the 1950s (Anon, 1960), yield losses varied from 13 to 36% in plant cane of seven varieties.

In more recent times Symington and Kaupilla (1982), using one row plots of Triton and Cassius, showed with multiple regression techniques that chlorotic streak caused yield losses of 16% in the 1981 season in the Macknade mill area. Nielsen et al. (1986), also working in the Macknade mill area, monitored disease levels and yield in 54 coplanted healthy and diseased strips of Triton and Cassius. They estimated a yield loss from chlorotic streak of 0.24% per each 1% of stools displaying disease symptoms. This would imply a maximum yield loss of 24%.

The disease is probably reducing sugar industry returns by $2-5m annually assuming a 2- 5% yield loss in diseased fields ($28/tonne cane sugar price).

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6.2 Components of yield loss

Smith (1952) stated that the use of diseased planting material may depress yield by up to 40%. The basis for these losses he attributed to germination and ratoon failures, increased susceptibility to drought, general unthriftiness, and a marked decrease in stalk number.

Overseas experience suggests that chlorotic streak may reduce stalk number, stalk length, stalk diameter, but not ccs (Wiehe, 1955).

7.0 DISEASE INCIDENCE

7.1 Area diseased in Queensland crops

Figures taken from Cane Pest and Disease Control Board (now Productivity Board) data from 1974-1991 give an idea of the amount of disease in Queensland crops. The average proportion of crops diseased for the period was 16.2%. The amount of disease in Queensland during the last 17 years has remained between 10-20%, with fluctuations arising from variable climatic conditions. High rainfall in the 1970s was associated with a higher incidence of the disease, while dry conditions in the mid-1980s led to lower disease levels. Disease figures for each year are presented in Figure1.

Figure 1 Percent of canelands in Queensland diseased with chlorotic streak:

1974-1991

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7.2 Disease incidence by district and mill area

The Herbert River district, low lying and with poor drainage, has the highest district disease incidence in the state, 34% in 1989-90. Figures for the other districts are included in Table 3.

Table 3

Chlorotic streak incidence in each district (average of 1989-90 incidence data), % area diseased

District Mossman Babinda

Innisfail Tully

Herbert Burdekin Central Southern

% Area diseased 27 10 34 9 13 11

When considering individual mill areas, Rocky Point, with 72% of crops diseased, has the highest mill area disease incidence. Mill areas showing low levels of disease include Pioneer, Kalamia, Inkerman, Fairymead and Millaquin-Qunaba. Data for all mill areas are included in Table 4.

Table 4

Chlorotic streak incidence in each mill area in the 1989 and 1990 seasons (% area diseased)

Board area 1989 1990 Mean

Mossman Hambledon Mulgrave Babinda

South Johnstone Mourilyan Tully Macknade Victoria Invicta Ayr Inkerman Proserpine Mackay Plane Creek Fairymead

Millaquin-Qunaba Bingera

Isis

Maryborough Moreton Rocky Point

0 28 36 24 4 3 23 31 27 24 0 0.5

17 14 0.8 0 0 0 0 0 58 69

24 40 36 29 4 3 22 52 35 55 0 0.4

23 14 1.0 0 0 0.2

0 0 35 76

12 34 36 28 4 3 23 42 31 40 0 0.5

20 14 0.9 0 0 0.1

0 0 47 73 8.0 CONTROL

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8.1 Hot water treatment

As early as 1930 it was known that hot water treatment of planting material at 52ôC for 20 mins could eliminate the disease (Bell, 1932). Extensive experiments into the effects of hot water continued in the late 1930s-early 1940s. It was found that temperatures as low as 45ôC for 20 mins were effective (Bell, 1938). Treatment of individual buds only at 52ôC for 20 mins failed (Bell, 1940) and it was concluded that the infectious agent occurred throughout the stalk tissue. Not every bud on a diseased stalk is infected however and disease-free plants can be propagated from lightly diseased planting material (Bell, 1939). Treatment of sections of stalk at 52ôC for 20 mins, with the shoot still attached, showed that chlorotic streak was eliminated from the treated portion and that a period of 18 hrs transpiration did not lead to re-infection of the treated section (Bell, 1940).

A hot water treatment of 50^oC for 30 mins is now a standard industry practice for the elimination of chlorotic streak from planting material. The regular supply of planting material (approved seed) from disease-free propagation plots is one of the main forms of disease control in areas where the disease is endemic.

8.2 Varietal resistance

There is currently no routine screening of varieties in the plant breeding program although a resistance screen is currently being developed. However, two methods for assessing differences in varietal reaction have been investigated, one based on infection rows and symptom development in the field, the second based on symptom development in a gravel hydroponic system.

8.2.1 Field test

A field trial with the majority of the commercial varieties of northern Queensland was planted at Babinda in May 1935, with diseased Badila in every third row. Varieties included Black Innes, Clark’s Seedling (HQ426), POJ 234, POJ 2364, Co 290, Uba, Q2, Q4, Q8, Q12, Q813, S. robustum (unidentified clone), B147, D1135 and S.J.4 (Bell, 1935). Little disease was evident during the plant crop but high disease levels became evident in some varieties in the first ratoon. Significant differences in disease levels were noted between varieties. Two further trials were planted in 1937 (Bell, 1939). Useful information was again obtained in the first ratoon crops. Data were collected on the total numbers of stools per plot and the number diseased. No disease ratings were calculated at that time. However, by selecting POJ234 and SJ4 as the resistant and susceptible standards (ratings of 1 and 9 respectively), the ratings for varieties included in two or more trials can be calculated; these are listed in Table 5.

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Table 5

Calculated resistance ratings on varieties from the 1935 and 1937 resistance trials Variety Trial 1 Trial 2 Trial 3 Mean

rating SJ4

HQ426 (Clark’s seedling) Q19

Badila Juno Hector Oramboo Q13 Q12 Q10 Q16 Korpi Q2 Q813 B147 POJ2364 X1 UBA X14 Co290 Q4 POJ234

9.0*

8.1 - 6.7

- - - - 6.8

- - - 5.7 4.3 2.7 3.4

- 2.6

- 1.0 1.0 1.0*

9.0*

- 7.7 8.5 8.6 7.1 7.6 6.0

- 5.6 6.0 6.7 4.4 2.7 3.9 3.1 2.2 1.0 2.0 2.0 1.0 1.0*

9.0*

7.6 7.5 6.4 4.3 5.8 4.3 5.1 4.4 5.4 4.6 3.7 3.4

- - 2.2 2.7 2.7 1.8 1.0

- 1.0*

9.0*

7.9 7.6 7.2 6.5 6.5 6.0 5.6 5.6 5.5 5.3 5.2 4.5 3.5 3.3 2.9 2.5 2.1 1.9 1.3 1.0 1.0*

Average diseased stools for susceptible standard: SJ4 = 83%

Average diseased stools for resistant standard: POJ234 = 0%

* Denotes standard ratings.

When trial 2 and trial 3 ratings were regressed, a high r-squared value was obtained suggesting that ratings were consistent between trials (Figure 2).

8.2.2 Gravel hydroponic test

Egan (1965) reported on a gravel hydroponic system for testing the resistance of a wide range of Saccharum germplasm. Galvanised troughs 180 x 40 x 20 cm deep containing nutrient solution and gravel were planted with varieties ranging from resistant to susceptible. Six stools each of two susceptible varieties were planted along with five stools of six other varieties. When the test canes produced 2-5 cms of stalk tissue, all shoots were ratooned 2 cms above the gravel and three diseased plants planted into each trough. Symptom development was monitored for 50 days and broad disease susceptibility ratings applied. Using this method, Egan (1965) noted that there was a wide range of resistance reactions in clones of each Saccharum species, including S.

spontaneum, S. robustum, S. edule, and S. officinarum.

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Figure 2 A linear regression of chlorotic streak ratings from two resistance trials

conducted in the 1930s

8.3 Recommended control measures

Recommended industry controls for chlorotic streak are:- (i) Regular use of clean planting material (approved seed).

(ii) Improved drainage.

(iii) Avoiding planting highly susceptible varieties in poorly drained or flood-prone areas.

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9.0 CURRENT PROBLEM SITUATIONS IN THE INDUSTRY

There are some areas of Queensland where chlorotic streak has historically been a problem. These include the Herbert River, low lying areas of northern Queensland, Rocky Point mill area and some poorly drained areas in central and southern districts. Significant yield losses occur regularly in some of these districts.

A more recent problem has developed in the Invicta mill area where irrigation drainage water has been reused. The use of tail water is attractive to farmers because it is cheaper than head water but high disease levels have resulted in some crops.

In January, 1991, record rainfall was recorded in the central district. Extensive flooding led to a high incidence of the disease in Q135. Chlorotic streak, coupled with the direct effects of waterlogging, resulted in very poor yields. With farmers unaware of the susceptibility of individual varieties, considerable yield losses have resulted form the planting of susceptible varieties in high disease risk areas.

10.0 RESEARCH REQUIRED

The following areas requiring research have been identified:

· Development of a suitable varietal resistance screen: The results could be used to advise farmers of the possible consequences of the disease on their property. The planting of susceptible varieties in problem areas could them be avoided. The resistance test used in the 1930s shows promise. Some account should be taken of when and how severe, symptoms occur in each variety.

· Investigate methods for inactivating the causal agent in recycled tailwater: This will be important in the Invicta mill area in the Burdekin district where chlorotic streak is a significant problem, large areas of irrigated caneland are being developed, and the use of re-cycled tailwater is being practised.

· Develop an effective assay and determine the identity of the causal agent: An understanding of the nature of the causal agent may make alternative control measures feasible.

11.0 DISCUSSION

Chlorotic streak remains a significant problem in some Queensland canegrowing districts, for instance the Herbert River and Rocky Point mill areas. However, yield losses are dependent on season. High rainfall, poor drainage, and flooding provide excellent conditions for disease transmission and high yield losses. Relatively dry seasons in recent times have reduced the area affected by chlorotic streak but with the return to wetter conditions, it is likely to become more important.

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A considerable amount of research has been undertaken in Queensland and this has led to the development of control measures. These include the hot water treatment of planting material (50^oC, 30 mins), the propagation of clean plant sources, and improved drainage.

In low lying areas where the disease is endemic , these control measures do not adequately control the disease during the crop cycle. Better control measures would reduce yield losses.

The nature of the causal agent remains a mystery. The lack of a suitable assay, and reliance on disease symptoms to indicate the presence of the disease, have hindered studies into the causal agent. Some evidence (passage through 0.5 µm filters, possible association of ds-RNA with diseased tissue, and inhibition of disease transmission with some viral inhibitors) suggests that the disease may be caused by a virus. Further research is required to confirm this. Of interest is some work recently undertaken in Tully, New York State, USA. Viruses transmitted in water, with no known vectors, were detected in a river draining undisturbed forest (Jacobi and Castello, 1991). A number of viruses belonging to the potex-, tombus, necro-, rhabdo-, and cucumo-virus groups have been detected in water from other rivers and appear to be transmitted in a similar way to chlorotic streak. Some unclassified plant viruses have also been detected in river water (Jacobi and Castello, 1991). Also to be considered is research conducted into the wheat disease, flame chlorosis, in Canada. A virus with no definite particle has been associated with a seedling wheat disease characterised by leaf chlorosis. The virus is transmitted by the fungus Pythium arrhenomanes (Haber et al., 1995), which spreads in floodwaters. A fungal transmitted virus with no detectable viral particle could fit with chlorotic streak observations in sugarcane, although passage through a 0.5 µm filter is not wholly consistant.

The importance of chlorotic streak may increase in some districts, particularly in the Burdekin River Irrigation Area (BRIA) if tail waters from flood irrigation are re-used.

Disease escalation under these conditions warrants careful monitoring.

12.0 CONCLUSION

Chlorotic streak is a disease associated with poorly drained areas and is endemic in many canegrowing areas of Queensland. The disease may reduce yields by up to 40% and is difficult to control due to rapid re-infection of crops planted with disease-free planting material. The disease is having a significant economic impact on the Queensland sugar industry and several aspects require further research.

13.0 REFERENCES

Anon. (1972) BSES Annual Report. p.54.

Anon. (1960) BSES Annual Report. p. 80-81.

Bell, A.F. (1932) BSES Annual Report. p.46.

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Bell, A.F. (1933) A new disease of Cane in North Queensland. Cane Growers’ Quarterly Bulletin. p. 42-46.

Egan, B.T. (1961) BSES Quarterly Bulletin, July, p.29.

Egan, B.T. (1963a) Studies with chlorotic streak. X. Rapid transmission by infection at ratooning. BSES Technical Communications. No.3.

Egan, B.T. (1963b) Studies with chlorotic streak disease of sugarcane x longevity of the pathogen in nutrient gravel cultures. BSES Technical Communications. No.4.

Egan, B.T. (1965) Host range and possible sources of resistance to chlorotic streak disease. Proc. Int. Soc. Sugar Cane Technol. 12: 1055-1059.

Egan, B.T. (1966) Studies with chlorotic streak. XIV. Infection and incubation periods of the pathogen. BSES Technical Communications.

Haber, S., Barr, D.J.S., Hiruki, C. and Tekauz, A. (1995) The link between cereal- associated Pythium isolates and flame chlorosis, a soil-transmitted virus-like disease of spring cereals and wild grasses. Canadian Journal of Botany (In Press).

Hitchcock, B.E. (1955) Investigations on insect transmission of two sugarcane diseases.

Proc. Q. Soc. Sugar Cane Technol., 22: 119-122.

Hughes, C.G. (1940) BSES Annual Report. p.19.

Hughes, C.G. (1948) The hot water treatment of plants on the farm. Cane Growers’

Quarterly Bulletin.

Hughes, C.G., Steindl, D.R.L. and Egan B.T. (1965) Chlorotic streak. BSES Annual Report. p. 69-71.

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Jacobi, V. and Castello, J.D. (1991). Isolation of tomato mosaic virus from waters draining forest stands in New York State. Phytopathology 81: 1112-1117.

Nielsen, P.J., Kaupilla, E.E. and Roach, B.T. (1986). An evaluation of the effect of chlorotic streak disease on sugarcane crops in the Herbert River district. Proc.

Aust. Soc. Sugarcane Technol. 1987 Conf., p. 135-140.

Smith, N.McD. (1952). BSES Cane Growers’ Quarterly Bulletin, January, p.90.

Steindl, D.R.L. (1955). BSES Annual Report. p.75.

Sturgess, O.W. (1962) Studies with chlorotic streak. VI. The influence of root

temperature on production of leaf symptoms. BSES Technical Communications.

No. 2.

Sturgess, O.W. (1963) Studies with chlorotic streak disease of sugarcane. VIII.

Transmission by mechanical methods. BSES Technical Communications. No. 3.

Sturgess, O.W. (1964) Studies with chlorotic streak. VII. Additional factors affecting transmission and the probable existence of a soil-borne vector. BSES Technical Communications. No.4.

Symington, W.M. and Kaupilla, E.E. (1982) Relationships between sugar yield, chlorotic streak disease, soil environment and crop factors in the Macknade mill area. Proc.

Aust. Soc. Sugarcane Technol., 1982 Conf., p.111-119.

Wiehe, P.O. (1955) Mauritius Sugar Ind. Res. Inst. Ann. Report. p. 47-50 (1954).