By K.H. Tan
Retired Professor of Entomology
“Neonicotinoids – from zero to hero in insecticide chemistry” was just reported in 2008 (Jeschke, P. and Nauen, R., 2008). They belong to a new novel class of insecticides that are very potent agonists acting selectively on specific molecular target sites (nicotinic acetylcholine receptors) of insect nervous system; and have made a significant impact on insect pest control. These compounds have low toxicity to mammals, which have a nervous system in which entirely different muscarinic acetylcholine receptors that are unaffected by the neonicotinoids, predominate. Imidacloprid, a potent neonicotinoid, was first commercialized in 1991 and since then has been used extensively especially in the control of insect pests in the agriculture, health and veterinary sectors.
Imidacloprid, like any other insecticide, when used judiciously is beneficial in integrated pest management (IPM) programs. But when used extensively and intensively, it will give rise to many problems such as pest resurgence and resistance, besides eliminating natural enemies and pollinators as well as causing environmental contamination. Here, I trace the development of resistance in the brown planthopper (BPH), Nilaparvata lugens Stål. to imidacloprid.
It was in the late 1990s when the brown planthopper was reported to have developed resistance to orgnanophospate insecticide (Karunaratne, et al., 1999) that rice farmers began to rely more on imidacloprid. In 2006, it was reported that for control of the brown planhopper, imidacloprid has been used for a few years but there was no obvious build-up of resistance in the field population studied; and a field collected strain developed a 250-fold resistance was induced after 37 generations in the laboratory (Liu and Han, 2006). However, over a relatively short period of several years of usage, field resistance had developed against imidacloprid was first observed in Thailand in 2003, and since then it has been found in other Asian countries like China, Japan and Vietnam (Matsumura et al, 2008). Additionally, a test was conducted using two diagnostic doses of imidacloprid on samples collected from China, India, Indonesia, Malaysia, Thailand and Vietnam during 2005 and 2006. It was shown that of 12 samples collected in 2005, only two late season samples collected from India had reduced mortality, while the rest remained susceptible to imidacloprid. But in 2006, all the 13 samples collected had reduced mortality with one of them having a 100-fold resistance compared with the susceptible strain (Gorman et al., 2008).
The detoxification of imidacloprid by P450-oxygenases may be an important resistance mechanism in the brown planthopper (Liu et al., 2003); and it is not unexpected. The reason being that insects possess three important classes of enzymes – esterases, oxygenases and S-gluthaione transferases, that specifically cater for the detoxification of a large array of endogenous and exogenous toxic chemicals. It is this process involving esterases that also allows some insect pest species to develop resistance to its own hormone/juvenoids that are applied as insecticides during their control programs. In my opinion, if an insect can develop resistance to its own hormone when applied as a control measure, development of resistance to a particular insecticide/insecticidal toxin is inevitable whenever there is a high selection pressure applied to a natural population of an insect species via intensive and/or prophylactic applications.
As a result of a very high level of resistance developed in field populations of the brown planthopper in China, imidacloprid is likely to be withdrawn for use in field application in 2009. Similar, action will soon follow in other Asian countries when high resistance has been detected. As such, it is unfortunate that imidacloprid, a novel insecticide for the brown planthopper, will soon disappear from the farmers shelves, i.e. “from hero to zero in the control of brown planthopper” in a relatively short span of time.
- Jeschke, P. and Nauen, R. 2008. Neonicotinoids – from zero to hero in insecticide chemistry. Pest Manag. Sci. 64: 1084-1098.
- Karunaratne,S.H.P.P., Small, G.J. and Hemmingway, J. 1999. Characterization of the elevated esterase-associated insecticide resistance mechanism in Nilaparvata lugens (Stal) and other planthopper species. Instnat. J. Pest Manag. 45: 225-230.
- Liu, Z. And Han, Z. 2006. Fitness costs of laboratory-selected imidacloprid resistance in the brown planthopper, Nilaparvata lugens Stal. Pest Manag. Sci. 62: 279-282.
- Matsumura, M., Takeuchi, H., Satoh, M., Sanada-Morimura, S., Otuka, A., Wanate, T., and Van Thanh, D. 2008. Species-specific insectidice resistance to imidacloprid and fipronil in the rice planthoppers Nilarparvata lugens and Sogatella furcifera in East and South-east Asia. Pest Manag. Sci. 64: 1115-1121.
- Gorman, K., Liu,Z ., Denholm, I., Bruggen, K-U, and Nauen, R. 2008. Neonicotinoid resistance in rice brown planthopper, Nilaparvata lugens. Pest Manag. Sci. 64: 1122-1125.
- 6. Liu, Z., Han, Z., Wang,Y., Zhang, L., Zhang, H., and Liu, C. 2003. Selection for imidacloprid resistance in Nilaparvata lugens: cross-resistance patterns and posible mechanisms. Pest Manag. Sci. 59:1355-1359.