Last week, I outlined four specious claims made by those attacking Rachel Carson and promoting DDT. (Visit that post to see links to articles in various national media outlets that swallowed these claims without any critical inspection. Sigh.)
Today, I’ll deal with their third bogus claim:
3. Mosquito resistance is not an issue. “Resistance” is not an issue since this mostly takes the form of avoidance and keeping mosquitoes away from human prey is the intended object anyway” (junkscience.com)
This is the heart of my objection to their “give us DDT and we’ll cure malaria” campaign. I’m not anti-pesticide or anti-DDT, I’m pro-IPM (Integrated Pest Management). IPM is a way of evaluating each pest situation individually, and making evidence-based choices for treatment.
My issue with the DDT fetishists, aside from their completely unwarranted attacks on Rachel Carson, is that they choose tactics FIRST, rather than evaluating each individual situation. This is like randomly prescribing drugs for a patient without any diagnosis. (Viagra for a bladder infection–bad idea.)
Not taking an IPM approach is a recipe for disaster–and this is how we get into insecticide resistance. I’ll start with some historic background, a brief discussion of how DDT works (and stops working when resistance evolves), and then get into the DDT evidence. It’s a complicated story, because resistance to DDT arose in several different ways.
The historic background
IPM originally was developed in the 50′s, as a response to insecticide resistance. If you look at some of the early papers from the late 40′s and 50′s, the optimism for DDT and its chemical relatives was incredibly high. It seemed like we could cure and kill anything. And it did work wonderfully…for a while.
For an excellent comprehensive review of the optimistic “veni, vidi, vici” attitude of the times, see “Golden Age of Insecticide Research” (1).
Two major problems quickly developed with synthetic pesticides: first, insects that had the metabolic ability to detoxify pesticides were quickly selected for and increased in the population. Classic Darwinian selection.
Second, “natural enemies,” or parasites and predators that acted as natural brakes on insect populations, were killed along with the mosquitoes. Oops.
To make things even worse, once an insect species becomes resistant to one pesticide, they often have “cross resistance” to other, newer pesticides. Note the rate of change increasing over time in this graph–that’s cross resistance at work.
Insect resistance happens because natural selection acts on rare, random mutations that happen to protect against harmful chemicals. Suddenly, these mutations are of value, and increase an insect’s chances of reproduction–and spreading that resistance in the population. From Doug Futuyma, a leading evolutionary biologist:
“The most effective strategy, based both on evolutionary models and on evidence, is to provide pest species with pesticide-free “refuges” in which susceptible genotypes can reproduce, thus preventing resistant genotypes from taking over. The intuitively appealing opposite strategy – trying to overwhelm the insect population with “saturation bombing” – simply hastens the evolution of resistance, because it increases the strength of natural selection.” (emphasis mine)
This is my primary objection to the pro-DDT folks–they don’t seem to have ANY understanding of resistance management, or natural selection. They present DDT as a cure-all solution. This is a sure-fire way to end up on the “pesticide treadmill“, and risks loosing the ability to use other pesticides to control malaria.
How do pesticides work–and stop working–through resistance?
Most pesticides are nerve poisons, although each different group has specific targets. (How pesticides work is a fascinating topic, and could have made my deadly dull organic chemistry classes a lot more lively, had we just discussed how to poison one another!)
Because books can (and have) been written about the many ways in which pesticides work, I’ll stick to just DDT’s mechanisms. Of necessity, I will grossly over-simplify for the molecular biology impaired
There have been 3 general modes of resistance to DDT:
1. Resistance due to metabolic detoxification
Insects with enzyme variations that can detoxify DDT quickly increase in a population through natural selection. Normal (unexposed to DDT) insect populations may also have an existing low level of these detoxifying enzymes, and then be selected for “over-expression”, where they overproduce the enzyme in enough quantities to quickly neutralize DDT.
Because these papers tend to be pretty heavy going for non-molecular biologists, I’ll just highlight one enzyme: Glutathione S-Transferase. This enzyme converts DDT to a non-toxic product. Do a Google search for this enzyme and “DDT” and you’ll get a sense of the volume of literature out there.
2. “kdr” (knockdown resistance)
This is the most well studied resistance mode in malarial mosquitoes. It is caused by a reduction in the sensitivity of the insect nervous system to the insecticide. For the most part, point mutations in sodium channel genes are the primary cause of knockdown resistance–in other words, single amino acid changes, the type of mistake that can quite easily happen in the DNA replication process. Not surprisingly, there are many different forms of kdr resistance, involving a slight change here or there on the ion gate gene sequence.
The literature is full of papers documenting kdr resistance across the globe–for brevity, I’ll simply send you to Google again, and tell you to search “DDT kdr”
3. Behavioral Resistance
This is where we come back to the junkscience.com misconceptions. They ignored the two major physiological resistance mechanisms I mentioned above, and focused on the “repellent” activities of DDT. This is a complex topic, and they have misunderstood it completely.
It’s important in an IPM strategy to know your pest–where do mosquitoes rest when they aren’t feeding? When do they feed? Many of the mosquito species important in malaria transmission are called “endophillic”; that’s a fancy way of saying they like to hang out indoors, in dark, enclosed areas. Like houses. So, spraying the interior walls of homes with DDT could be very effective for these species.
Except… not all mosquito species rest inside homes (Culex or Aedes do not, for example), so in areas where these species are the major vector, interior sprays won’t work.
The Junkscience people are partly correct; DDT does have a long lasting “irritancy” effect, where it provides a strong stimulation to take off and fly, making mosquitoes exit a treated house.
That sounds good, but this “bite and run” behavior means mosquitoes don’t rest on the treated walls. If they don’t rest on the inside wall, they don’t come in contact with the insecticide. The mozzies don’t die; and people are still bitten. There is abundant evidence from different parts of the world that DDT use created natural selection on endophillic species (usu. Anopheles), and resulted in altered behavior.
This was first described decades ago in Tanzania and Indonesia (4, 5). Some mosquitoes shifted their behavior to rest in bushes, or on the outsides of homes. Obviously, mosquitoes that have the “bite and run” trait will quickly increase in the population–since mosquitoes resting within a treated house are dead, and corpses rarely breed
In some cases, DDT irritancy can work for you–in this study, they conclude DDT will reduce mosquito/human contact. But they came to that conclusion after careful testing–not because of a political agenda. Note that the different species in the study cited had different responses to the DDT, as well. It’s not a one-size-fits-all solution.
Behavioral resistance continues to be a problem, and assessing the behavioral traits of a local population is an important first step to choosing an appropriate control.
This isn’t a mechanism of resistance, per se, but an unfortunate consequence. Sure, we can nuke mosquitoes with DDT. But we risk losing our chance to control insects with other pesticides if we overdo it with DDT.
In a recent study (3), malarial mosquitoes selected for DDT resistance also developed very high levels of cross-resistance to other pesticides–including malathion, permethrin, and bendiocarb. (Malathion is commonly sprayed in the US for mosquitoes.)
Unfortunately, the kdr trait confers cross-resistance to both the rapid paralytic and lethal actions of all known pyrethroids, as well as the pyrethrins and DDT(2). Most alarming, in field tests where the kdr resistance to DDT is present, the ability of pyrethroid-impregnated bed nets to prevent biting at night was compromised (“major loss of efficacy”).
I think it’s fair to say that the claim pro-DDT folks made, as outlined in my original post that “Mosquito resistance is not an issue” is well and truly dead.
I’ll close with a quote from one of my favorite authors, who is an entomologist with waaaaay more ‘street cred’ than me (she’s in the National Academy):
“The truth is that DDT is neither superhero nor supervillain — it’s just a tool. And if entomologists have learned anything in the last half-century of dealing with the million-plus species of insects in the world, it’s that there is no such thing as an all-purpose weapon when it comes to pest management. DDT may be useful in controlling malaria in some places in Africa, but it’s essential to determine whether target populations are resistant; if they are, then no amount of DDT will be effective….
Overselling a chemical’s capacity to solve a problem can do irretrievable harm not only by raising false hopes but by delaying the use of more effective long-term methods. So let’s drop the hyperbole and overblown rhetoric — it’s not what Africa needs. What’s needed is a recognition of the problem’s complexity and a willingness to use every available weapon to fight disease in an informed and rational way.”
- Read the rest of the excellent article by May Berenbaum, my favorite entomologist, about DDT
- A nice little PDF about insecticide resistance
- More about insecticide resistance
- An article about pesticide modes of action from Florida Extension
- “Re-reading silent spring”
- The big collection of all the posts so far from several blogs covering this topic
1. Casida & Quistad, 1998. Golden Age of Insecticide Research: Past, Present, or Future? Annual Review of Entomology 43: 1-16.
2. Soderlund, DM, Knipple, DC. 2003. The molecular biology of knockdown resistance to pyrethroid insecticides.
INSECT BIOCHEM MOLEC 33 (6): 563-577 doi:10.1016/S0965-1748(03)00023-7
3. T. S. MATAMBO, et al. 2007.Insecticide resistance in the malarial mosquito Anopheles arabiensis and association with the kdr mutation . Medical and Veterinary Entomology 21 (1), 97–102. doi:10.1111/j.1365-2915.2007.00671.x
4. Gerold J.L. 1977. Evaluation of some parameters of house-leaving behaviour of Anopheles gambinae Acta Leiden. 45: 79-90.
5. Sundavaraman S. 1958. The behaviour of A. sundaicus in relation to the application of residual insecticides in Tjilatjap, Indonesia. Ind. J. Malariol. 12: 129-156.
Hemingway & Ranson. 2000. Insecticide resistance in Insect Vectors of Human Disease. Annual Review of Entomology 45: 371-391.