Messing with BedBugs’ Genes Could Carry Other Risks?

Bed Bugs Will Outlive All Of Us Unless We Screw With Their Genes

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photo:  Bluejake/Sara Bibi/Gothamist

Bed bugs, like cockroaches and new seasons of The Bachelor, seem impossible to eradicate from the face of the Earth, no matter how many exterminators our landlords call to spray that one time and then never, ever again. But Science says there’s some small hope for the extinction of a moviegoer’s biggest fear—screwing with their genome.

Scientists have managed to map the genome of the common bed bug, revealing some fun things about the little suckers. For instance, bed bugs are actually able to break down toxins, like the ones an exterminator might use, to render them harmless, allowing them to survive even when you try to whack them with bug killer. They’ve also been MUTATING, producing genes that make them resistant to certain insecticides and making it all the more difficult to eradicate an infestation. Another fun fact is that bugs’ genes vary from location to location—a Brooklyn bed bug will have a different genetic sequence from a Queens bed bug, though both are equally disgusting.

Bed bugs also inbreed, and their sex is quite violent. This violent sex has been well-documented, and for those of you who have not yet seen Isabella Rossellini’s bed bug porno, you’re welcome, and sorry:

The takeaway here is that bed bugs have been able to hold us hostage for a long time, but scientists might be able to murder them, provided they make a few genetic tweaks. First, though, let’s kill all the mosquitoes.

[A. Steiner:  So…..Messing with Genes Could Carry Other Risks – YES!]

#SayNOtoPESTICIDES!

Genome of BedBug shows close relationships to Kissing Bug, one of several vectors for deadly Chagas disease, and the body louse. Both have tight associations with humans.

February 2, 2016 | News from Weill Cornell Medical College

Researchers Sequence First Bedbug Genome.  Scientists have assembled the first complete genome of one of humanity’s oldest and least-loved companions: the bedbug. The new work, led by researchers at the American Museum of Natural History and Weill Cornell Medicine, and published Feb. 2 in Nature Communications, could help combat pesticide resistance in the unwelcome parasite. The data also provides a rich genetic resource for mapping bedbug activity in human hosts and in cities, including subways.

male and female bedbugs – both fed and unfed – comparison with apple seeds

“Bedbugs are one of New York City’s most iconic living fossils, along with cockroaches, meaning that their outward appearance has hardly changed throughout their long lineage,” said one of the paper’s corresponding authors Dr. George Amato, director of the museum’s Sackler Institute for Comparative Genomics. “But despite their static look, we know that they continue to evolve, mostly in ways that make it harder for humans to dissociate with them. This work gives us the genetic basis to explore the bedbug’s basic biology and its adaptation to dense human environments.”

The common bedbug (Cimex lectularius) has been coupled with humans for thousands of years. This species is found in temperate regions and prefers to feed on human blood. In recent decades, the prevalence of heated homes and global air travel has accelerated infestations in urban areas, where bedbugs have constant access to blood meals and opportunities to migrate to new hosts. A resurgence in bedbug infestations since the late 1990s is largely associated with the evolution of the insects’ resistance to known pesticides, many of which are not suitable for indoor application.

“Bedbugs all but vanished from human lives in the 1940s because of the widespread use of DDT, but unfortunately, overuse contributed to resistance issues quite soon after that in bedbugs and other insect pests,” said Louis Sorkin, an author on the paper and a senior scientific assistant in the Museum’s Division of Invertebrate Zoology. “Today, a very high percentage of bedbugs have genetic mutations that make them resistant to the insecticides that were commonly used to battle these urban pests. This makes the control of bedbugs extremely labor intensive.”

The researchers extracted DNA and RNA from preserved and living collections, including samples from a population that was first collected in 1973 and has been maintained by museum staff members since then. RNA was sampled from males and females representing each of the bug’s six life stages, before and after blood meals, in order to paint a full picture of the bedbug genome.

When compared with 20 other arthropod genomes, the genome of the common bedbug shows close relationships to the kissing bug (Rhodnius prolixus), one of several vectors for Chagas disease, and the body louse (Pediculus humanus), which both have tight associations with humans.

Click here to read complete article.

 

SayNOtoPESTICIDES!

Bed Bugs show resistance to pesticides: What to do now? Build a wall!

Why chemicals used to fight bed bugs aren’t working any longer was revealed in a new study that compared today’s bed bugs with those that have been isolated in a lab for 30 years.

February 1, 2016 | by Lonnie Shekhtman  | The Christian Science Monitor

The chemicals used to fight bed bug infestations are no longer working, say scientists from Virginia Polytechnic Institute and New Mexico State University. The tiny pests have developed a resistance to the most commonly used type of insecticides, called neonicotinoids, or neonics, which is part of the reason there has been a resurgence of them in the last couple of decades.

“While we all want a powerful tool to fight bed bug infestations, what we are using as a chemical intervention is not working as effectively it was designed and, in turn, people are spending a lot of money on products that aren’t working,” Troy Anderson, an assistant professor of entomology in the Virginia Tech College of Agriculture and Life Sciences, said in an announcement last week.

In an experiment, researchers compared bed bugs from homes in Cincinnati and Michigan that had been previously exposed to neonics with those that a researcher has kept isolated in a lab for 30 years, dating back to a time before the insecticides were used commercially.

In results published Thursday in the Journal of Medical Entomology, Dr. Anderson and Alvaro Romero, an assistant professor of entomology at New Mexico State University, reported that the bed bugs that had been isolated in a lab for 30 years died when treated with a small amount of neonics. Those collected from homes in Cincinnati and Michigan showed much higher resistance to the chemical treatment.

The team also tested bedbugs from New Jersey that were already resistant to pyrethroids, another class of widely used insecticides often mixed with neonics, but had been isolated from neonics since 2008. Those bugs were more susceptible to the insecticides than the ones from Cincinnati and Michigan, but not as much as the isolated bedbugs.

“Companies need to be vigilant for hints of declining performance of products that contain neonicotinoids,” Dr. Romero said in a study announcement.

“For example, bed bugs persisting on previously treated surfaces might be an indication of resistance. In these cases, laboratory confirmation of resistance is advised, and if resistance is detected, products with different modes of action need to be considered, along with the use of non-chemical methods,” he said.

Bed bugs are particularly burdensome in apartment buildings, where they can spread to many units. They are also more problematic for low-income, elderly, and disabled people who can’t spot the tiny red bug and often don’t have the means to get rid of them, say researchers from Virginia Tech.

Bed bugs thrive in beds, couches, and around electrical outlets and cause hundreds of bites a night.

“When well-off people get bed bugs, it’s an inconvenience. But when low-income families get them, there aren’t many options,” said Molly Stedfast, who worked with bed bugs as a graduate entomology student at Virginia Tech in 2013.

“Those who can’t afford the treatments,” she says, often end up living with bed bugs for a long time.

Virginia Tech’s pest lab recommends a nontoxic, non-neonic treatment that can be applied to the inside perimeter of an apartment. The treatment is diatomaceous earth, a dust made from fossilized remains of diatoms, a type of hard-shelled algae. Researchers said this dust has been used to control pests for more than a century. It clings to the bed bugs as they walk through it, absorbs moisture, and kills them via dehydration.

“We treat the perimeter of the apartment to isolate infestations in one unit and not allow them to spread. It is a lot less expensive to treat one apartment than every unit in the building,” said Dini Miller, a professor of entomology at Virginia Tech.

#SayNOtoPESTICIDES!

Announcement: Bedbug Genome Assembled

Bed_Bugs_CommentarayScientists have assembled the first complete genome of bedbugs, which existed in some form even before humans were around to invent beds.

February 2, 2016 | by Elizabeth Kolbert | The New Yorker

In the great contest that is life, the common bedbug, Cimex lectularius, qualifies as a winner. This is true not just in the Donald Trumpian sense of being extremely difficult to get rid of but in the long-term evolutionary sense of surviving multiple geological epochs. A creature that looked very much like a bedbug was scuttling around during the time of the dinosaurs; a sort of proto-bedbug has been found in amber that’s almost a hundred million years old. It’s not clear what that bug fed on, but it’s believed that long before modern humans—and therefore beds—existed, Cimex lectularius sucked on bats’ blood. When humans took to living in caves, bedbugs descended from the bats and began feeding on people. (There are still bedbugs that prefer bats, and scientists have proposed that the lineage that prefers humans is in the process of becoming a separate species.)

Today, researchers from the American Museum of Natural History and Weill Cornell Medicine announced that they had assembled the complete genome of Cimex lectularius. The same team is working on the cockroach genome; both projects are part of an effort to better understand so-called “living fossils.” A paper on the bedbug genome is appearing today in the journal Nature Communications.

“Bedbugs are one of New York City’s most iconic living fossils,” George Amato, one of the paper’s authors and the director of the museum’s Sackler Institute for Comparative Genomics, noted. The bedbug genome turns out to consist of almost seven hundred million base pairs. This is significantly larger than the fruit-fly genome (a hundred and twenty million base pairs), but not nearly as large as the locust genome (six billion base pairs). In addition to sequencing the bedbug’s genome, the researchers also looked at gene expression over the bug’s life cycle, which spans five instar stages. From this, they concluded that the “first blood meal of the bedbug is the most dynamic period of the bedbug’s transcriptional activity.”

Bedbugs are so-called true bugs. Members of this group also include cicadas, aphids, and leafhoppers, and all share a common arrangement of mouthparts. As anyone who has suffered an infestation knows, bedbugs use their mouthparts, or proboscises, to seek out blood vessels. Then they inject anticoagulants into their victims, to prevent themselves from, in effect, choking. The researchers found that bedbugs possess several classes of genes that code for anticoagulant proteins, including for proteins usually associated with snake venom. This doesn’t mean that bedbugs are any more closely related to snakes than other insects, just that they’ve come up with some of the same strategies.

“What we’re really finding is a structural motif—something about the sequence of amino acids that is probably involved in preventing blood from clotting in the same way a snake venom protein is, but doesn’t share an evolutionary history,” Mark Siddall, another author of the paper and a curator at the Museum of Natural History, explained.

The ancient Greeks were already complaining about bedbugs in the fifth century B.C.; references to bedbugs appear in Aristophanes and then in Aristotle. The bugs seem to have travelled with humans along ancient trade routes; by the seventh century A.D., they were in China, and by the eleventh century in Germany. From Europe, bedbugs migrated to North America and Australia with the colonists.

Bedbugs suffered a population crash in the mid-twentieth century, with the introduction of pesticides like D.D.T. But they have since evolved resistance to many of the chemicals used against them, and their numbers have roared—or, if you prefer, snuck—back up. A recent study by researchers at Virginia Tech and New Mexico State University found that bedbugs have already evolved resistance to neonicotinoids, a class of pesticides that has been in use for only twenty years or so. (The study shows that it takes something like five hundred times the amount of neonicotinoids to kill bedbugs from populations that have been exposed to the chemicals as it takes to kill bugs from populations that have never been exposed.) The researchers who put together the bedbug genome identified several genes that may be involved in pesticide resistance; this information could potentially be used to create more effective bug killers.

“It turns a light on for people to begin in a logical way to explore these areas that we’ve identified,” Amato said.

By combining the information from the genome with information from DNA swabs taken from New York City subway stations, the researchers were also able to map relationships among the city’s bedbug populations. This effort suggests that even bedbugs have a hard time getting across Manhattan.

“We found more north-south connectivity for the bedbugs than we found east-west,” Siddall observed. “And that’s reflecting what we already know to be true.”

Trending today: #Bedbugs are developing a strong resistance to most common insecticides

February 2, 2016 | by Ryan Biek | Newsy

Bedbugs are reportedly building up a strong resistance to some of the most powerful insecticides due to overuse, which means we might need to turn to non-chemical solutions to get rid of them.

Researchers from Virginia Tech and New Mexico State University tested the most common class of insecticide called neonicotinoids, or neonics, which is often combined with pyrethroids in commercial treatments for bedbugs.

Bedbugs are developing a strong resistance to most common insecticides photo

They took a group of bedbugs that came from homes in Ohio and Michigan, which had previously been exposed to neonics, and compared those bedbugs to a population that has been kept in isolation for 30 years, before the insecticide was used.

A third group of bedbugs that was resistant to pyrethroids but never exposed to neonics was also included in the study.

Depending on the specific types of neonic tested, the Ohio and Michigan bedbugs were hundreds to tens of thousands of times more resistant than the isolated group.

The third group’s results were in the middle: more resistant than the isolated group but less resistant than the Ohio and Michigan bedbugs.

Because that third group had never been exposed to neonics, the researchers believe the bedbugs may have a pre-existing resistance mechanism.

The researchers said more non-chemical methods need to be used to combat bedbug infestations. However, they noted the most resistant bedbugs in the study only came from two areas, and not all of the U.S. may be facing this level of resistance.

Zika has nothing on deadly Chagas disease. Chagas disease is a much bigger problem.

February 1, 2016 | by Cal Crilly | Global Research

“Although a causal link between Zika infection in pregnancy and microcephaly has not, and I must emphasize, has not been established, the circumstantial evidence is suggestive and extremely worrisome,” WHO Director-General Margaret Chan said, reported by Reuters. “An increased occurrence of neurological symptoms, noted in some countries coincident with arrival of the virus, adds to the concern.”

Pesticides in Brazil and Pernambuco state are more likely to be the cause of microcephaly and birth defects than Zika virus and the links below speak for themselves.

“The farmers of Brazil have become the world’s top exporters of sugar, orange juice, coffee, beef, poultry and soybeans. They’ve also earned a more dubious distinction: In 2012, Brazil passed the United States as the largest buyer of pesticides.

This rapid growth has made Brazil an enticing market for pesticides banned or phased out in richer nations because of health or environmental risks.”

Why Brazil has a big appetite for risky pesticides

“According to the latest figures available from Brazil’s health ministry, published on 20 January, 3,893 cases of microcephaly have been recorded since the start of 2015. Pernambuco accounts for 1,306 of those, around a third of the total. In 2014, there were 150 cases across the whole of Brazil.” [1]

City at centre of Brazil’s Zika epidemic reeling from disease’s insidious effects

The most obvious cause of birth defects in this area is direct contact and absorption of pesticides.

“A study of pesticide use on tomatoes in the Northern State of Pernambuco, Brazil, indicates high exposure to pesticide workers and poor application methods which threaten the ecology of the area.”

“Women washed the pesticide application equipment, generally in the work environment, without protective clothing or without observing the recommended three-fold washing process. [2]

Poisoning assessment

Many of the pesticides used were hazardous organochlorine and OP insecticides. Of the workers interviewed, 13% suffered some type of acute poisoning that required first-aid treatment; 28% reported nausea during application of pesticides; and the majority experienced some symptoms immediately after exposure. 36% reported health problems related to the immune system (frequent itching of skin, eyes, and nose; or fever); 36%, skeletal/muscular problems (pains in joints); 33%, central and peripheral nervous system problems (dizziness, numbness in superior limbs, alterations in sleep patterns, and vomiting); 28%, digestive system problems; 25%, sensory organ problems; 18%, cardiovascular problems; 13%, respiratory system problems; and 11%, with urinary-genital system problems

Reproductive effects

Of the women workers, 32% reported being pregnant more than five times, 53% reported having prenatal examinations, 97% reported that they were not poisoned by pesticides during pregnancy. Almost three-quarters of the women (71%) reported miscarriages, and 11% reported having mentally and/or physically impaired offspring.

Neuro-psychological symptoms

Symptoms of minor psychiatric disturbances were observed in 44% of women and 56% of men surveyed (in the general Brazilian population, the prevalence is 5% to 15%)”

“The results of the laboratory analysis showed the maximum residue limits (MRLs) are regularly exceeded: methamidophos in 25% of the samples, and ETU in 78%. ETU can cause goitres (a condition in which the thyroid gland is enlarged), birth defects and cancer in exposed experimental animals. ETU has been classified as a probable human carcinogen by the US EPA. The organochlorine insecticide, endosulfan, which is banned for use on tomatoes was detected in 28% of samples at levels of up to 510 parts per billion.”

“It is important to introduce education on the hazards of pesticides and good agricultural practices in the school curriculum as many children accompany their family members into the fields”

Tomato production in Brazil:  Poor working conditions and high residues threaten safety

“Pesticides were found in the milk from 11 farms and one milk cooler (Fig.1), totalizing 12 positives milk samples. The main pesticide was fenthion, detected in four samples of 12 (33.33%), followed by dimethoate (25%), coumaphos (8.33%) and malathion (8.33%). In CB group, the pesticides detected were carbofuran (25%), aldicarb (16.67%) and carbaryl (8.33%). In some samples, two or more active principals were detected, what explains percentages over 100%. The frequency of pesticides found in this study is in agreement with Araújo et al. (2000) that noted that the most pesticides commonly used in Pernambuco are from OP class, followed by CB and pyrethroids.” [3]

Organophosphorus and carbamates residues in milk and feedstuff supplied to dairy cattle

“It is very well known that acute or chronic increase of retinoic acid (RA)levels leads to teratogenic effects during human pregnancy and in experimental models.

The characteristic features displayed by RA embryopathy in humans include brain abnormalities such as microcephaly, microphtalmia and impairment of hindbrain development; abnormal external and middle ears (microtia or anotia), mandibular and mid facial underdevelopment, and cleft palate. Many craniofacial malformations can be attributed to defects in cranial neural crest cells.” [4]

Pesticides Used in South American GMO-Based Agriculture

“There has been ongoing controversy regarding the possible adverse effects of glyphosate on the environment and on human health. Reports of neural defects and craniofacial malformations from regions where glyphosate-based herbicides (GBH)…” [5]

Glyphosate-Based Herbicides Produce Teratogenic Effects on Vertebrates by Impairing Retinoic Acid Signaling

“The report says that national consumption of agrochemicals is equivalent to 5.2 litres of agrochemicals per year for each inhabitant. Agrochemical sales increased from USD 2 billion in 2001 to 8.5 billion in 2011. The report names GM crops as a key cause of the trend: “Importantly, the release of transgenic seeds in Brazil was one of the factors responsible for putting the country in first place in the ranking of agrochemical consumption – since the cultivation of these modified seeds requires the use of large quantities of these products.” [6]

The report continues:

“The cropping pattern with the intensive use of pesticides generates major harms, including environmental pollution and poisoning of workers and the population in general. Acute pesticide poisoning is the best known effect and affects especially those exposed in the workplace (occupational exposure). This is characterized by effects such as irritation of the skin and eyes, itching, cramps, vomiting, diarrhea, spasms, breathing difficulties, seizures and death.

“Already chronic poisoning may affect the whole population, as this is due to multiple exposures to pesticides, that is, the presence of pesticide residues in food and the environment, usually at low doses. Adverse effects of chronic exposure to pesticides may appear long after the exposure, and so are difficult to correlate with the agent. Among the effects that can be associated with chronic exposure to pesticide active ingredients are infertility, impotence, abortions, malformations, neurotoxicity, hormonal disruption, effects on the immune system, and cancer.”

Brazil’s National Cancer Institute Names GM Crops as Cause of Massive Pesticide Us [7]

Health information systems and pesticide poisoning at Pernambuco [8]

Most of this is not new, with Pernambuco it’s just concentrated.

The Long Battle Over Pesticides, Birth Defects and Mental Impairment

There may be links with mosquitos and Zika virus but time will tell, if they manage to reduce the mosquito problem with more insecticides that may be a good thing but if birth defects keep rising in these areas it will be the pesticide use to blame.

If that happens we might have to start thinking about what on earth we are doing?

#SayNOtoPESTICIDES!

Bed Bugs in the US have developed extreme tolerance to popular insecticides … Uh oh. So why use them?

VA_Tech_BedBugJanuary 29, 2016 | by Peter Dockrill | Science Alert

Scientists have discovered that popular chemicals used to eradicate the common bed bug (Cimex lectularius) may have become virtually ineffective, as the insects have developed extremely high levels of resistance to the poisons.

According to the researchers, their study is the first to demonstrate that overuse of certain insecticides has fuelled bed bugs’ resistance mechanisms, and it could mean that we need to develop new ways of controlling or eliminating the pests.

“While we all want a powerful tool to fight bed bug infestations, what we are using as a chemical intervention is not working as effectively it was designed and, in turn, people are spending a lot of money on products that aren’t working,” said entomologist Troy Anderson from Virginia Tech.

To examine whether a commonly used class of insecticides called neonicotinoids (aka neonics) were doing their job, the researchers compared bed bugs that had been exposed to the chemicals with a colony of isolated insects that hadn’t.

The team collected exposed bed bugs from houses in two US cities – Cincinnati and Michigan – and sourced the unexposed insects from a laboratory colony that had been kept in isolation from before the insecticide was used (some 30 years ago).

They found dramatically different levels of resistance to neonicotinoids depending on the history of exposure. It took just 0.3 nanograms of a neonicotinoid called acetamiprid to kill 50 percent of bed bugs from the isolated colony, but required more than 10,000 nanograms to kill 50 percent of the insects from Michigan and Cincinnati.

For another chemical called imidacloprid, 2.3 nanograms killed 50 percent of the isolated bed bugs, but it took 1,064 nanograms and 365 nanograms to kill half the Michigan and Cincinnati populations, respectively.

All up, the exposed bugs taken from homes demonstrated between 163 and 33,333 times the resistance to four types of neonicotinoids. A third population of bed bugs that hadn’t been exposed to neonicotinoids since 2008 showed moderate levels of resistance in the tests.

According to the researchers, when bed bugs are exposed to insecticides, they produce detoxifying enzymes to counter the poisons, which can clearly become quite powerful in negating the effects of neonicotinoids.

The findings, reported in the Journal of Medical Entymology, don’t mean that bugs all over the US or the rest of the world would have developed equal levels of resistance to those extracted from Michigan and Cincinnati, but they do suggest that insects with exposure to insecticides are getting better at resisting them – and in some cases, by a dramatic degree.

“We need to emphasise that we need to use different tools – we can’t depend totally on chemicals. We need to incorporate other alternatives,” Alvaro Romero, one of the researchers from New Mexico State University, told Matt McGrath at the BBC.

Romero says non-chemical solutions currently being looked at by the pest control industry include heat, vapour, and encasement methods of killing bed bugs, but he also acknowledges there’s no quick fix to the resistance phenomenon they’ve discovered.

[Heat, vapour and encasement methods of killing bed bugs DO NOT WORK.  Bed bugs scatter and hide and can stay undercover for 12 months without eating – only to return in full force.  ~A. Steiner~]

“It’s a very complex problem and we are going to have bed bugs for many years because of this problem with insecticides,” Romero told the BBC, “and then there is a social context that makes eradication and control very difficult.”

SayNOtoPESTICIDES!

Rise of the SUPER PESTS: Bed Bugs are resistant to common insecticides. Use of non-chemical methods need to be considered to eradicate Bed Bugs.

  • Scientists tested resistance of four populations to neonicotinoids 
  • They found bugs in Michigan and Cincinnati were resistant to certain types 
  • This means sprays used to kill the bugs aren’t very effective
  • Rise in infestations blamed on travelling, as bugs hitch a ride on clothes

January 28, 2016 | by Sarah Griffiths | MailOnline

They live in the cracks and crevices of beds and crawl out a night to suck blood by detecting our body heat and carbon dioxide.

Now the much loathed bed bug is threatening to become even more of a pest because it is resistant to a common insecticide, scientists warn.

Exotic holidays have been blamed for the recent resurgence of bed bugs in homes as they hitch a ride on clothing or in luggage.

The blood-sucking bed bug (pictured) that's attracted to our body heat and carbon dioxide is threatening to become even more of a pest because it is resistant to a common insecticide, scientists warn.

The blood-sucking bed bug (pictured) that’s attracted to our body heat and carbon dioxide is threatening to become even more of a pest because it is resistant to a common insecticide, scientists warn.

The research has found the parasites have developed a tolerance to neonicotinoids, or neonics, because of their widespread use.

“people are spending a lot of money on products that aren’t working”

It is the first study to show the overuse of certain insecticides has led to an increased resistance to the compounds, making them much less effective than advertised.

In the US alone, millions of dollars are spent on the most widely used commercial chemicals to kill bedbugs, but their overuse has led to an increased resistance to the compounds.

Assistant professor Troy Anderson, from Virginia Tech College of Agriculture and Life Sciences said: ‘While we all want a powerful tool to fight bed bug infestations, what we are using as a chemical intervention is not working as effectively it was designed and, in turn, people are spending a lot of money on products that aren’t working.

New research has found the parasites have developed a tolerance to neonicotinoids, or neonics, because of their widespread use. A stock image of  fumigation is pictured

New research has found the parasites have developed a tolerance to neonicotinoids, or neonics, because of their widespread use. A stock image of fumigation is pictured.

WHERE INFESTATIONS BEGIN

In 2014, genetic tests revealed that a single undetected pregnant bed bug is all it takes to start an entire infestation.

A DNA study at Sheffield University showed colonies of bed bugs come from a common ancestor or a few of the female bed bugs.

The pregnant bed bug could rapidly create a colony of thousands that feed on humans.

Researchers told the BBC that bed bugs’ ability to generate a new colony from such small numbers might be a ‘clue to their recent success’.

‘If you just miss one, they can grow very quickly,’ Professor Roger Butlin said, adding it takes only a few weeks for this to happen.

Bed bugs are capable of surviving without feeding for a month as they wait for a human.

In the late 1880s, an estimated 75 per cent of households were affected, but by the outbreak of World War II, that figure had dwindled to 25 per cent,

Their recent resurgence has been blamed by some experts on resistance to commonly used insecticides and international travel.

‘Unfortunately, the insecticides we were hoping would help solve some of our bed bug problems are no longer as effective as they used to be, so we need to re-evaluate some of our strategies for fighting them.’

Products developed to eradicate infestations in recent years combine both neonics with pyrethroids – another class of insecticide.

Assistant Professor Dr Alvaro Romero from New Mexico State University added: ‘If resistance is detected, products with different modes of action need to be considered, along with the use of non-chemical methods.

‘Companies need to be vigilant for hints of declining performance of products that contain neonicotinoids.

‘For example, bed bugs persisting on previously treated surfaces might be an indication of resistance.

‘In these cases, laboratory confirmation of resistance is advised, and if resistance is detected, products with different modes of action need to be considered, along with the use of non-chemical methods.’

The study, published in the Journal of Medical Entomology, is the first to confirm the resistance.

Researchers collected bed bugs from homes in Cincinnati and Michigan and exposed them to four different neonics: acetamiprid, dinotefuran, imidacloprid and thiamethoxam.

In the US alone, millions of dollars are spent on the most widely used commercial chemicals to kill bedbugs (microscopic image shown) but their overuse has led to an increased resistance to the compounds.

They also used the chemicals on a bed bug colony kept free of insecticide exposure for more than 30 years and to a pyrethroid-resistant population from Jersey City that had not been exposed to neonics since they were collected in 2008.

Those that hadn’t been exposed to the neonics died after contact with very small amounts of the pesticide, while the Jersey City bed bugs showed moderate resistance to acetamiprid and dinotefuran, but not to imidacloprid or thiamethoxam.

The Jersey City colony’s resistance could be due to pre-existing resistance mechanisms.

When exposed to insecticides, bed bugs produce ‘detoxifying enzymes’ to counter them.

Researchers collected bed bugs from homes in Cincinnati and Michigan and exposed them to four different neonics - acetamiprid, dinotefuran, imidacloprid and thiamethoxam. A stock image of fumegation is shown

Researchers collected bed bugs from homes in Cincinnati and Michigan and exposed them to four different neonics – acetamiprid, dinotefuran, imidacloprid and thiamethoxam. A stock image of fumegation is shown

THE CHEMICALS AND BED BUGS

The levels of detoxifying enzymes in the Jersey City bed bugs were higher than those of the susceptible Harlan population.

The Michigan and Cincinnati bed bugs, which were collected after combinations of pyrethroids and neonicotinoids were introduced, had even higher levels of resistance to neonics.

It only took 0.3 nanograms of acetamiprid to kill 50% of the non-resistant bed bugs from Dr Harlan’s lab, but it took more than 10,000 nanograms to kill 50% of the Michigan and Cincinnati bed bugs.

Just 2.3 nanograms of imidacloprid was enough to kill 50% t of the Harlan bed bugs, but it took 1,064 and 365 nanograms to kill the Michigan and Cincinnati bed bugs.

The numbers were similar for dinotefuran and thiamethoxam.

Compared to the Harlan control group, the Michigan bed bugs were 462 times more resistant to imidacloprid, 198 times more resistant to dinotefuran, 546 times more resistant to thiamethoxam, and 33,333 times more resistant to acetamiprid.

The Cincinnati bed bugs were 163 times more resistant to imidacloprid, 226 times more resistant to thiamethoxam, 358 times more resistant to dinotefuran, and 33,333 times more resistant to acetamiprid.

The levels of detoxifying enzymes in the Jersey City bed bugs were higher than those of the susceptible Harlan population.

Professor Romero explained: ‘Elevated levels of detoxifying enzymes induced by other classes of insecticides might affect the performance of newer insecticides.’

The Michigan and Cincinnati bed bugs, which were collected after combinations of pyrethroids and neonicotinoids were introduced, had even higher levels of resistance to neonics.

It only took 0.3 nanograms of acetamiprid to kill 50 per cent of the non-resistant bed bugs from Dr Harlan’s lab, but it took more than 10,000 nanograms to kill 50 per cent of the Michigan and Cincinnati bed bugs.

Just 2.3 nanograms of imidacloprid was enough to kill 50 per cent of the Harlan bed bugs, but it took 1,064 and 365 nanograms to kill the Michigan and Cincinnati bed bugs, respectively.

The numbers were similar for dinotefuran and thiamethoxam.

Compared to the Harlan control group, the Michigan bed bugs were 462 times more resistant to imidacloprid, 198 times more resistant to dinotefuran, 546 times more resistant to thiamethoxam, and 33,333 times more resistant to acetamiprid.

The Cincinnati bed bugs were 163 times more resistant to imidacloprid, 226 times more resistant to thiamethoxam, 358 times more resistant to dinotefuran, and 33,333 times more resistant to acetamiprid.

SayNOtoPESTICIDES!

Bed Bugs have Developed Resistance to most widely used Insecticide, Neonicotinoids.

If neonicotinoids no longer work against the elusive and resilient creatures, bed bugs will continue to thrive despite exterminators’ efforts.

Bed bugs are most often found in human dwellings such as apartments, condominiums, single-family homes, hotels, motels, movie theaters, libraries, dormitories, trains, buses, planes, workplace, waiting rooms and the list goes on.

“different modes … need to be considered, along with the use of non-chemical methods.”

January 28, 2016 | by Mahita Gajanan | The Guardian

Bed bugs have developed a resistance to neonicotinoids, a group of the most widely used insecticides, according to a new study published in the Journal of Medical Entomology.

Products developed over the past few years to control bed bugs combine neonicotinoids, or neonics, with pyrethroids, another class of insecticide.

The newly found resistance to neonics has real implications for people who need to control the pest, which are most often found in human dwellings such as apartments or condominiums, single-family homes and hotels or motels, according to the 2015 Bugs Without Borders Survey. Neonics are the most commonly used insecticide to fight the already elusive and resilient bed bugs, and if they no longer work, bed bugs will continue to thrive despite exterminators’ efforts.

Study authors Alvaro Romero, from New Mexico State University, and Troy Anderson, from Virginia Tech, discovered the resistance by collecting bed bugs from human dwellings in Cincinnati and Michigan and exposing them to four different neonics: acetamiprid, dinotefuran, imidacloprid and thiamethoxam.

Romero and Anderson applied the same neonics to a bed bug colony kept by entomologist Harold Harlan for more than 30 years without exposure to insecticide, and to a pyrethroid-resistant population from Jersey City, New Jersey, that had not been exposed to neonics since 2008.

Harlan’s bed bugs died after exposure to small amounts of neonics. The Jersey City bed bugs died when exposed to imidacloprid and thiamethoxam but resisted the other two neonics.

According to Romero and Anderson, the neonic resistance in the Jersey City bed bugs could be credited to pre-existing resistance mechanisms. Bed bugs produce “detoxifying enzymes” to counter exposure to insecticides, and the researchers found that the Jersey City bed bugs had higher levels of the enzymes than did the Harlan bed bugs.

“Elevated levels of detoxifying enzymes induced by other classes of insecticides might affect the performance of newer insecticides,” Romero said.

The bed bugs collected from Cincinnati and Michigan proved to be tougher, with a much higher resistance to neonics than the Harlan and Jersey City bed bugs. Compared with Harlan’s bed bugs, the Michigan creatures were 462 times more resistant to imidacloprid, 198 times more resistant to dinotefuran, 546 times more resistant to thiamethoxam and 33,333 times more resistant to acetamiprid.

Similarly, the Cincinnati bed bugs were 163 times more resistant to imidacloprid, 358 times more resistant to dinotefuran, 226 times more resistant to thiamethoxam and 33,333 times more resistant to acetamiprid.

Romero said insecticide companies should be “vigilant for hints of declining performance of products that contain neonicotinoids”.

“For example, bed bugs persisting on previously treated surfaces might be an indication of resistance,” he said. “In these cases, laboratory confirmation of resistance is advised, and if resistance is detected, products with different modes of action need to be considered, along with the use of non-chemical methods.”

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