The University of Kentucky announced yesterday that knockdown resistance (kdr-type) mutations, conferring resistance to synthetic pyrethroid pesticides, are widely prevalent in U.S. bed bug populations. The study, forthcoming1 in Archives of Insect Biochemistry and Physiology, finds that one or two of two previously identified genetic mutations (briefly discussed here) are present in a majority of U.S. bed bug populations.
From the press release:
Fang Zhu, a post-doctoral fellow at UK along with fellow UK entomologists Mike Potter, Ken Haynes and Reddy Palli and several students, analyzed 110 bed bug populations from across the United States and found 88 percent of them had one or two genetic mutations. These mutations produce what is known as knockdown resistance, meaning the insecticide is not able to kill bed bugs.
“We need alternative insecticides to fight this bug,” Potter said, “Unfortunately today’s products are not as effective as ones we had previously. Non-chemical measures are important but are seldom completely effective and can be laborious and expensive. History has taught us insecticides are a crucial part of the bed bug solution.”
Data from this study will help pest management professionals make future decisions.
“The methods and primers developed by this group could be used to tell pest control professionals whether or not pyrethroids work on certain bed bugs by looking for these genetic mutations in the bugs’ DNA,” Palli said. “If it’s a target-site mutation, like the majority of these, spraying probably would be ineffective, but if it has another type of resistance, we could possibly add synergists to the current insecticide to help fight them.”
kdr-type mutations cause resistance at the pesticide target site via a mechanism of nerve insensitivity. (For an accessible explanation of pesticide resistance, I refer you to our interview with Dr. Alvaro Romero last year.)
For organochlorines and pyrethroids, these target sites are nerve sodium channels. Thus, DDT resistance can lead to pyrethroid resistance, as both pesticide classes act on the same target site.
As this study is not yet available, I reached out to the University of Kentucky researchers for clarification of the potential meanings of these findings.
New York vs Bed Bugs: Your study shows that the two mutations identified by Yoon et al. (2008) in a NYC population are actually widely prevalent in the United States?
Reddy Palli: Correct, more than 80% of populations showed the presence of one of these mutations.
New York vs Bed Bugs: In the press release you indicate that pest management professionals might use this information to determine a course of action. Can you confirm if UKY’s NYC and Cincinnati bed bug populations are among those with kdr mutations in your study?
Mike Potter: Some of the populations we tested from Cincinnati had one or both mutations while a few others did not (both of the latter still showed high resistance to pyrethroids in bioassays, however, suggesting that other resistance mechanisms may be involved). As far as the NYC populations we tested, all (12) had one or both mutations for pyrethroid resistance.
New York vs Bed Bugs: Are kdr mutations predictive of cross-resistance with other pesticide classes? I note that DDT conferring resistance on modern populations is stated as a possibility (but does this require further investigation?), but what of other possible cross-resistance possibilities?
Reddy Palli: Insecticides (eg. DTT, BHC) that use sodium channel as a target site likely show resistance. As you say, this requires further investigation. Insecticides (eg. Phantom and Propoxur) that work through target sites other than sodium channels may work fine on these resistant populations.
Mike Potter: Unfortunately, we just don’t have too many of these presently that have residual activity as a dry deposit other than products like Phantom (chlorfenapyr), desiccant dusts (e.g., silica gel, DE), and to a degree, the IGRs. Propoxur would be another but the decision to grant it a Section 18 emergency exemption is up to EPA.
New York vs Bed Bugs: I think the public may misinterpret this study as confirmation that “pesticides don’t work” — which is not really the case.
Mike Potter: I think it may be a bit too strong of a statement to conclude that pyrethroids “don’t work” on most of the bed bug populations in US, as we often do kill a percentage of the individuals we test in the laboratory, especially when they are contacted directly with the wet spray deposit. Dry residues typically kill far fewer and we know this to be important for optimal performance of products in the field. Reports from many pest control firms further indicate the pyrethroid products are not performing as well as they would like. Some companies continue to believe that they are working ok, but generally these companies are also incorporating additional treatment measures such as the use of contact killers (Sterifab, Bedlam, Phantom aerosol, etc.), steam, encasement of beds, etc., making it hard to know what specifically is working.
I thank Dr. Palli and Dr. Potter for so kindly taking the time to answer my questions.
This is most definitely bad news; however, we have been expecting as much and indeed researchers at the University of Kentucky have been warning of widespread pyrethroid resistance for years. Having this confirmed, on this scale, is still a blow. The urgency of having options to enable the most basic resistance management countermeasures should be obvious.
Perhaps I should remind you that today is the last day of the public comment period for Ohio’s Section 18 propoxur exemption request under consideration by EPA.
- 4/10 – the article has been published: Zhu, Fang, John Wigginton, Alvaro Romero, Ali Moore, Kimberly Ferguson, Roshan Palli, Michael F. Potter, Kenneth F. Haynes, and Subba R. Palli. 2010. Widespread distribution of knockdown resistance mutations in the bed bug, Cimex lectularius (Hemiptera: Cimicidae), populations in the United States. Archives of Insect Biochemistry and Physiology 73, no. 4: 245-257. doi:10.1002/arch.20355. [↩]