More tales of CIN-1: PBO and deltamethrin

CIN-1 is a strain of bed bugs maintained at the University of Kentucky—one imagines for the purposes of inquiry into the supernatural limits of its invincibility.

Its provenance is the beleaguered city of Cincinnati, c. 2005.

Cincinnati, the city where bed bugs are run over by cars.1

I am sure you have read about CIN-1 already; it’s the (let’s say villainous) star of numerous research articles out of the University of Kentucky. Indeed there are other pyrethroid resistant strains in the University of Kentucky lab, but with every new article I find myself thinking, what fresh adventures in death and survival, CIN-1?2

Romero, A., Potter, M.F. & Haynes, K.F., 2009. Evaluation of Piperonyl Butoxide as a Deltamethrin Synergist for Pyrethroid-Resistant Bed Bugs. Journal of Economic Entomology, 102, 2310-2315.  

This new study looks at the role of piperonyl butoxide (PBO) in improving the effectiveness of deltamethrin. To the extent that pyrethroids remain the principal class of chemicals used against pyrethroid-resistant bed bugs (that is essentially the difficult situation we are in), it becomes crucial to figure out what resistance management strategies may be useful.

Here we can look back at the explanation of the mechanisms of resistance we got from Alvaro Romero earlier this year:

Alvaro Romero: Insects and various other arthropods have the potential to reduce the toxic effect of pyrethroids by becoming insensitive to them (mechanism known as target site insensitivity), by limiting penetration of the insecticide through their cuticle (skin), or by breaking down the insecticides with enzymes before the chemicals reach their target. Some of these resistance mechanisms have already been recognized in bed bugs.

PBO is a pesticide synergist; it increases pyrethroid toxicity by inhibiting P450s, the enzymatic systems that may be responsible for the bed bug’s metabolism of pyrethroids.

However, if resistance is not due to P450-dependent metabolism as indicated by PBO synergism, then presumably other mechanisms of resistance would be operating:

The level of synergism of pyrethroids with PBO is greater when P450s are responsible for conferring insecticide resistance (Kasai et al. 1998, Wu et al. 1998). Synergism with PBO has been proposed to increase the efficacy of pyrethroids against bed bug infestations that are difficult to control. Nevertheless, currently there is no adequate evidence about the effectiveness of these mixtures against resistant bed bugs. In this study we show P450s mediated detoxification in deltamethrin-resistant bed bugs.

First of all, for CIN-1 bed bugs, dry residues of deltamethrin alone do not cause greater than 50% mortality.

In tests with technical-grade deltamethrin dry residues, CIN-1 bed bugs that were pre-treated with PBO saw their resistance ratio (RR = LC50 of resistant strain divided by LC50 of susceptible strain; LC50 = “concentration that kills 50% of individuals at 24 h”) decrease from >2,588 to 174. When they were topically treated with deltamethrin (this might be analogous to directly spraying bed bugs), the highest exposure dose killed 72.5% of the PBO-pre-treated bed bugs.

In tests with formulated deltamethrin (Suspend) plus PBO (Exponent) or synergized pyrethrins (Kicker):

The rate of mortality of bed bugs exposed to Suspend, measured by LT50 values, was much slower in CIN-1 (LT50 = 15.2 d) and WOR-1 [a deltamethrin-resistant bed bug strain from Worcester, MA-RC] (LT50 = 5.4 d) than in the susceptible strain Fort Dix (100% mortality after 5 h exposure; data not shown). [...] The mixture of Suspend and Kicker required 36% less time than Suspend alone to cause 50% mortality in CIN-1 (9.7 and 15.2 d, respectively) and 50% less time in WOR-1 (2.7 and 5.4 d) (Table 2); however, significant differences between the two treatments were observed only in WOR-1 (Table 3).

LT50 = time to kill 50% of the exposed bed bugs.

Here’s Table 3 showing the differences between treatments for CIN-1 were not significant:

comparison of Suspend treatments.png

So, what is going on that PBO does not significantly improve the performance of formulated deltamethrin?

Lack of enhancement of mortality with dry residues of deltamethrin by PBO against CIN-1, a pyrethroid-resistant strain, indicates that addition of PBO, either alone or in combination with pyrethrins, is not a comprehensive solution to deltamethrin resistance. Dry residues of piperonyl butoxide synergized-pyrethroid formulations might only be effective against susceptible bed bugs or against pyrethroid-resistant bed bugs in which P450s are primarily responsible for the detoxification of the insecticide. Presence of a kdr-like insensitivity or any other resistance mechanism that is not inhibited by PBO might limit the effectiveness of dry residues of synergized pyrethroids against resistant bed bugs.

I’ve stopped thinking about the sorry pesticide that is deltamethrin. Instead, I worry about whatever comes next.

  1. Don’t get offended, please, just some pot/kettle humor between Great American Bed Bug Cities. []
  2. We can review: we know that CIN-1 bed bugs will cross a deltamethrin barrier to feed, but will avoid resting on deltamethrin-treated surfaces — and yet if it’s an established harborage we’re talking about, it doesn’t much matter to them if it’s been treated with deltamethrin or not. Nonetheless, in spite of their extraordinary resistance to pyrethroids (and DDT, mais oui!), Tempo Dust will knock them out within 24 hours. And while we catalogue these CIN-1 features, let me remind you that there are reportedly two tested pyrethroid-resistant strains that can be killed by a 4-month-old dry residue of chlorfenapyr (which we already know they do not avoid). CIN-1, surely, no? Otherwise it wouldn’t really be anything to brag about. And that goes double for the reported Section 18-supporting propoxur trial. []

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