
Fire blight Erwinia amylovora on pear shoots
(Photo: J.L. Vanneste)
Streptomycin management strategy
(Revised February 2005)
Introduction
The goals of these guidelines are to preserve the efficacy of streptomycin where it has not been compromised by the development of resistance, and to limit the development and the spread of streptomycin resistance in plant pathogenic and commensal bacteria where such resistance has already developed. Streptomycin is an aminoglycoside that kills bacteria by interfering with protein synthesis. It is the only antibiotic used in New Zealand for the control of plant pathogenic bacteria. There are only limited alternatives to the use of this antibiotic for bacterial disease control, the most frequently used being copper-based compounds. Use of these compounds can lead to copper resistance and to plant toxicity.
Streptomycin product perspective
Only one product containing streptomycin, Keystrepto™, is on the market in New Zealand. It is formulated as streptomycin sulphate and is registered for the control of a relatively narrow range of plant bacterial diseases (Table 1). Resistance to streptomycin has been reported both overseas and in New Zealand. Streptomycin binds to the bacterial ribosome, interfering with peptide synthesis. Resistance can result from either a modification of the ribosome or a modification of the antibiotic itself. Non-antibiotic products, such as biological control agents, that can help to control or limit the incidence of bacterial diseases are also becoming available overseas and in New Zealand.
| Pathogen | Disease | Crop |
|---|---|---|
| Erwinia amylovora | fire blight | Apple, pear and nashi |
| Pseudomonas syringae pv. syringae | bacterial blast | Stone fruit |
| Xanthomonas arboricola pv. pruni | bacterial spot | Stone fruit |
| Pseudomonas syringae pv. tomato | tomato speck | Tomato |
| Pseudomonas syringae pv. syringae | Tomato | |
| Xanthomonas campestris pv. vesicatoria | bacterial spot | Tomato |
| Clavibacter michiganensis pv. michiganensis | bacterial canker and wilt | Tomato |
Current status of streptomycin resistance
Development of resistance to streptomycin in plant pathogens and in other plant-associated bacteria seems to be relatively common. Such a resistance has been found in New Zealand. Resistance to streptomycin results either from an enzymatic modification of streptomycin (preventing it from binding to the bacterial ribosome) or from the modification of the ribosomal protein S12, which is the target molecule in the bacterial ribosome. Modification of the target molecule results from a point mutation in the gene rpsL which codes for the protein S12. Such a mutation makes bacteria resistant to extremely high levels of streptomycin (over ten times the recommended levels), but the resistance cannot be easily transferred to other bacteria. It is usually transferred only during bacterial division. Bacteria that are able to enzymatically inactivate streptomycin have usually acquired this capability through the acquisition of genes, which code for the enzyme(s) necessary to inactivate streptomycin. These genes are carried by genetic elements, such as plasmids or transposons, that can be transferred and can confer resistance to other bacteria including bacteria from other species or other genera. Those bacteria are resistant to lower levels of streptomycin than bacteria that have a mutation in the rpsL gene.
Strains of Erwinia amylovora, the fire blight pathogen, resistant to streptomycin have been isolated from Hawke's Bay (Thomson et al. 1993). All strains of E. amylovora that have been isolated from New Zealand were found to carry a mutation in the rpsL gene (Vanneste & Voyle 2001). Several years of monitoring failed to find resistance to streptomycin in other regions. However, no survey has been conducted since 2000.
Some strains of Pseudomonas syringae pv. syringae isolated from apple orchards in Hawke's Bay and stone fruit orchards in Otago have been found to be resistant to streptomycin (Vanneste & Voyle 2001). These strains have acquired the genes strA and strB, which are carried on a plasmid or on a transposon (Vanneste & Voyle 2001). In some cases this resistance seems to be linked to copper resistance (Vanneste & Voyle 2003). Since no formal survey has been carried out, the current status of streptomycin resistance in P. syringae in New Zealand is unknown. No information is available on bacterial pathogens of tomato.
Overseas, streptomycin resistance has been detected for most if not all the pathogens targeted by this antibiotic, and in particular for E. amylovora, Erwinia carotorovora, P. syringae pv. syringae, P. syringae pv. papulans, Pseudomonas cichorii, Pseudomonas lachrymans, Xanthomonas campestris pv. vesicatoria and Xanthomonas diffenbachiae (McManus et al. 2002). Streptomycin resistant strains of E. amylovora have been detected in the USA (California, Idaho, Michigan, Missouri, Oregon and Washington) and in Israel (Psallidas & Tsiantos 2000). In contrast to the situation found in New Zealand, strains of E. amylovora carrying the genes strA, strB, have been isolated on several occasions in the USA (Jones & Schnabel, 2000). Streptomycin-resistant strains of X. campestris pv. vesicatoria, which causes bacterial spot on tomato, have been isolated in the USA (California, Florida Georgia and Pennsylvania) since the early 1960s (Stall & Thayer 1962). It has also been found in Argentina, Brazil and Taiwan (McManus et al. 2002). Isolation from Canada of streptomycin-resistant strains of P. syringae has been documented since the late 1970s (de Boer 1980). This was the time when the isolation of streptomycin-resistant strains of the same pathogen was being recorded in New Zealand (Young 1977). Streptomycin-resistant strains of P. syringae have also been isolated in the USA (Michigan, New York, Oklahoma and Oregon) (McManus et al. 2002).
Resistance management strategy
Observe manufacturers' recommendations on application rate and timing and observe maximum numbers of applications for specific crops (Table 2). Use streptomycin only when climatic conditions are favourable for disease development and the target pathogen is present. Do not use for emergency disease management when high disease levels have already developed. When other compounds are available they should be used in preference to streptomycin. At the first sign of lack of efficacy, the use of streptomycin should be suspended until the presence or absence of resistant strains of the pathogen can be confirmed. This will require the determination of streptomycin resistance status by a microbiology laboratory. Since streptomycin can kill epiphytic bacteria that otherwise compete with the pathogen for space and nutrients, the use of streptomycin on crops affected by streptomycin-resistant strains of the pathogen can increase development of the disease.
| Crop | Disease | Recommendations |
|---|---|---|
| Apples, pears | Fire blight | Use no more than three times over the bloom period. Use only when climatic risk and level of inoculum are high. Periods of high disease risk should be determined with the help of computer programmes such as Maryblight or Cougar blight. |
| Stonefruit | Bacterial blast and bacterial spot | Use no more than three times over the period from green tip to mid-December. Use in autumn, but only if severe symptoms were detected during the growing season. Stop using streptomycin as soon as lack of control is suspected. Do not use streptomycin if streptomycin resistance has been previously detected in the orchard (Streptomycin resistant strains of these pathogens can survive in the orchard for a very long time). |
| Tomato seedlings | Bacterial speck, spot, canker and wilt | Each lot of plants should not be sprayed more than three times with streptomycin. Disinfect the glasshouse (including substrate and equipment) between each lot of plants to reduce the risk of carry over of streptomycin resistant strains. Use disease free seeds or treated seeds whenever possible. |
Implementation recommendations
Label directions for use of streptomycin should include an appropriate statement about resistance management and recommendations about the maximum number of treatments that should be applied for each of the pathogens targeted. The only streptomycin product available in New Zealand for the treatment of plant bacterial pathogens does not currently have a statement about resistance management.
Reference
De Boer SH 1980. Leaf spot of cherry laurel caused by Pseudomonas syringae. Canadian Journal of Plant Pathology 2: 235-238.
Jones AL, Schnabel EL 2000. The development of streptomycin resistant strains of Erwinia amylovora. In: Vanneste JL ed. Fire blight – The Disease and its Causative Agent, Erwinia amylovora. CABI Publishing, Wallingford, United Kingdom. Pp. 235-251.
McManus PS, Stockwell VO, Sundin GW, Jones AL 2002. Antibiotic use in plant agriculture. Annual Reviews in Phytopathology 40: 443-465.
Psallidas PG, Tsiantos J 2000. Chemical control of fire blight. In: Vanneste JL ed. Fire blight – The Disease and its Causative Agent, Erwinia amylovora. CABI Publishing, Wallingford, United Kingdom. Pp. 199-234.
Stall RE, Thayer PL 1962. Streptomycin resistance of the bacterial spot pathogen and control with streptomycin. Plant Disease Reporter 46:389-392.
Thomson SV, Gouk SC, Vanneste JL, Hale CN, Clark RG 1993. The presence of streptomycin resistance in pathogenic and epiphytic bacteria isolated in apple orchards in New Zealand. Acta Horticulturae 489: 672-672.
Vanneste JL, Voyle MD 2003. Genetic basis of copper resistance in New Zealand strains of Pseudomonas syringae. New Zealand Plant Protection 56: 109-112.
Vanneste JL, Voyle MD 2001. Characterisation of transposon genes and mutations which confer streptomycin resistance in bacterial strains isolated from New Zealand orchards. Acta Horticulturae 590: 493-495.
Young JM 1977. Resistance to streptomycin in Pseudomonas syringae from apricot. New Zealand Journal of Agricultural Research 20: 249-251.
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from Pesticide Resistance: Prevention and Management Strategies 2005
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