Physics Is Not Immune: Testing Whether Bed Bugs Can Evolve Heat Resistance

1. Introduction: a claim, not a law

Heat treatment is sold with a promise no chemical method can make: that the insects cannot become resistant to it. This journal's article on thermal disinfestation examined the time and temperature requirements and did not examine that promise.

1.1 Could potentially select them

Which is the form of the worry, and it is a question about evolution rather than about physics.²

1.2 What this article argues

That the claim was tested and the answer is bounded rather than absolute, that survivors are explained by escape and incomplete heating rather than by tolerance, and that one route to heat resistance remains untested in this species. Sections 7, 21 and 24 are the case.

2. Why the question is reasonable

Because a treatment that fails partially applies selection pressure.

The abiotic challenges in achieving lethal temperatures in harbourage areas, combined with the ability of bed bugs to respond behaviourally or physiologically to sublethal exposure, could theoretically select them for increased heat resistance.⁶

2.1 Which is the standard structure of a resistance problem

Incomplete kill, survivors with some heritable advantage, repetition. Our rotation and mixture articles described exactly that sequence for compounds.

2.1b And the physics argument does not answer it

Protein denaturation is a physical process and no organism repeals it. But the temperature at which an animal's proteins fail, and the speed at which it repairs damage below that temperature, are biological quantities with heritable variation like any other.

So the claim that resistance to heat is impossible confuses the mechanism of death with the threshold at which it occurs. The first is physics and the second is physiology, and only the second matters for whether the treatment works.

2.2 And heat treatments are frequently incomplete

Which our thermal article established from the time-and-temperature side, before any question of biology arises.

3. And the precedents in other arthropods

There are several.

Heat exposing one laboratory fly species resulted in greater temperature resistance within a few generations of selection; plastic temperature tolerance traits were shown to be selectable in a mosquito reared at different temperatures; and a springtail significantly increased expression of heat shock protein family members after exposure to non-lethal high temperatures, which is heat hardening.⁶

3.1 So the trait is evolvable in arthropods generally

Which removes any presumption that it could not happen here.⁶

4. One of which should worry us more than the others

And it is the one we had not considered before reading this.

A greenhouse mite was selected for resistance to a pesticide and also showed some cross-resistance to heat exposure due to increased expression of heat shock proteins.⁶

4.1 Chemical selection producing thermal tolerance

Without heat ever being applied as the selecting agent.⁶

4.1b And the direction of that cross-resistance is worth pausing on

Our articles on cross-resistance have all concerned one compound conferring survival against another compound, with mode of action as the organising principle. This is a compound conferring survival against a physical stressor, which no mode-of-action scheme predicts.⁶

4.2 We return to this at §24

Because it changes where the risk would come from, and nobody appears to have looked for it in this species.

5. The three explanations for a survivor

Bed bugs may be present after a heat treatment due to abiotic factors associated with the inability to achieve lethal temperatures in harbourage areas for a sufficient time period, re-infestation from insects that escaped to cooler areas during the treatment, or development of physiological resistance allowing them to survive heat exposure.⁴

5.0b And only one of them is about the insect

The first is about the equipment and the building, the second about the building and the treatment's design, and only the third is a claim about biology. Two thirds of the explanation space belongs to the operator.⁴

5.1 The three are not mutually exclusive

And distinguishing them requires testing the third directly, which is what §6 describes.

6. The selection experiment

Which asked the question in the only way it can be asked.

The study set out to determine whether bed bugs could be selected for heat resistance under a laboratory selection regime, and whether populations with various heat exposure histories, insecticide resistance profiles and geographic origins have differential temperature tolerances, using two exposure techniques described as step-function and ramp-function.¹

6.1 Two exposure shapes

A step imposes the target temperature abruptly; a ramp approaches it gradually, which is closer to how a room heats.¹

6.2 That second design choice matters

Because §20 reports that the animals respond behaviourally to rising temperature, so the shape of the rise is not incidental to what happens.

That observation is ours.

7. What it found

Selection experiments found an initial increase in bed bug survivorship; however, survivorship did not increase past the fourth generation.¹

7.1 With the conclusion stated carefully

That based on these outcomes, the ability of bed bugs to develop heat resistance appears to be limited.¹

7.2 Limited is not absent

And the abstract's first clause reports a real response before the plateau, which the headline finding is easy to read past.¹

8. Reading the plateau

Our interpretation, and we hold it loosely.

A response that rises and then stops is what happens when selection exhausts the standing genetic variation available for a trait. The population contained some heritable variation in heat survival, selection concentrated it within four generations, and there was nothing further to concentrate.

8.1 Which would make the limit a property of that starting population

Rather than of the species, and a different founding population with different variation might plateau elsewhere.

8.1b Which is testable and was not tested

Selecting from several independently founded populations would show whether the plateau sits at a common value or at a population-specific one, and the first would point at a physiological ceiling while the second would point at exhausted variation.

8.2 And new variation can arrive by mutation

On a timescale far longer than four generations, which is the reason we would not treat a plateau as a ceiling that holds forever.

8.3 Neither point is made by our source

Which reports the plateau and does not interpret its cause, and we may be reading more into the shape than the data supports.¹

9. And the population comparison

The second half of the study.

The step-function technique revealed non-significant variation in heat tolerance between populations and the ramp-function technique provided similar results.¹

9.1 Across populations differing in heat exposure history

Which is the field version of the selection experiment: populations that had actually been heated in buildings, compared with those that had not.¹

9.1b Which is the more convincing half of the study

A laboratory selection line is an artificial population under an artificial regime. Field populations that have actually been heat treated in buildings, compared against those that have not, test the thing anybody actually cares about.

That the two approaches agreed is what gives the conclusion its weight, and it is our reading rather than a point the abstract makes.¹

9.2 And differing in insecticide resistance profile

Which is the closest available test of the cross-resistance route in §4, and it found nothing. That is a real piece of reassurance and we note it before §24 raises the question again.¹

10. The baseline tolerance

In response to heat stress, fewer than 20% of the bugs survived a 1-h exposure to 46°C, and nearly all were killed at 48°C.³

10.0b The exposure duration is part of the figure

Both numbers are for a one-hour exposure. A shorter exposure at the same temperature kills less and a longer one kills more, which is why our thermal article treated time and temperature as a single specification rather than as a threshold.³

10.1 Which is the window thermal treatment works in

Two degrees between substantial survival and near-complete kill.³

11. Three attempts to induce more

Made in the same study.

Dehydration, heat acclimation at 30 degrees for two weeks, and rapid heat hardening at 37 degrees for one hour.³

11.0b Each targets a different physiology

Dehydration acts through osmolytes, prolonged acclimation through sustained gene expression, and a brief pre-exposure through the rapid response described in section 15.³

11.1 Each is a standard induction protocol

Corresponding to the mechanisms that produce induced tolerance in other species.⁶

12. All of which failed

Dehydration, heat acclimation at 30°C for 2 weeks and rapid heat hardening at 37°C for 1 h all failed to improve heat tolerance.³

12.0b And the failure of acclimation is the surprising one

Two weeks at 30 degrees is a long exposure to a temperature the animal tolerates comfortably, and in many insects that is precisely the regime that shifts the upper limit upward. Here it moved nothing.³

12.1 Three routes, none of which works in this animal

Which is a stronger result than any single negative, because the three act through different physiology.³

13. The asymmetry with cold

Neither cold acclimation at 4 degrees for two weeks nor dehydration enhanced cold tolerance. However, bed bugs have the capacity for rapid cold hardening, i.e. a 1-h exposure to 0°C improved their subsequent tolerance of −14 and −16°C.³

13.1 An hour at zero buys real protection downward

And an hour at 37 buys nothing upward.³

13.2 With a separate cold finding worth recording

The supercooling point was approximately minus 20 degrees, yet all were killed by a direct one-hour exposure to minus 16, so the species cannot tolerate freezing and is killed at temperatures well above its supercooling point.³

14. Which is the most interesting physiological fact here

Our assessment.

The animal has an inducible protective response in one thermal direction and not the other, tested within the same study, in the same population.³

14.0b And the cold result has its own oddity

Two weeks at 4 degrees did nothing while one hour at zero did something, which is the reverse of what a dose-response intuition would predict. Rapid cold hardening is a distinct physiological mechanism triggered by a sharp drop rather than a cumulative one, and the study's design separates the two cleanly.³

14.1 So the absence of heat hardening is not general inflexibility

It is specific to heat, which makes it a fact about this particular physiology rather than about insects being unable to adjust.

14.2 And it has an ecological reading

A species living in and on a warm-blooded host in heated buildings encounters cold excursions when a building fails or an item is moved outdoors. It does not, in its evolutionary history, encounter 46 degrees.

That is ours and it is speculation, offered because the asymmetry otherwise looks arbitrary.

15. The heat shock proteins

Which are the obvious candidate mechanism and were looked for.

Experiments revealed that named heat shock protein genes, two in the 70 kilodalton family and a putative small one, were significantly up-regulated 15 min, 2, and 4 h post-heat exposure and decreased back to baseline levels by 24 h.⁶

15.0b What a heat shock protein does

Broadly, it binds proteins that heat has begun to unfold and either holds them stable or assists them back into shape, which is why the family is the standard mechanism wherever thermal tolerance is found in other organisms.⁶

So finding the response present and the tolerance absent is the informative combination: the candidate mechanism exists in this animal and does not deliver the outcome it delivers elsewhere.

15.1 So the machinery exists and responds

Rapidly, and transiently.⁶

16. Which are present and do not confer survival

The authors' own reading of the whole picture.

These results suggest that bed bugs do not survive heat treatments due to the development of greater thermo-tolerance.⁵

16.1 The response is recovery rather than protection

The genes are described as implicated in heat induced stress recovery, which is repair after survivable damage rather than a mechanism for surviving a lethal exposure.⁶

17. So what explains the survivors

The first two items in §5.

Harbourages that never reached lethal temperature for long enough, and animals that left before they did.⁴

17.1 Which is where the remaining sections go

Sections 18 to 21 deal with the escape route and §22 with what happens to the animals that neither die nor escape cleanly.

18. The detection ability

Which is better than we expected.

When bed bugs are close to heated objects, at less than 3 centimetres, they can detect temperature differences of 2.0 °C.⁵

18.0b Which is a capability built for finding a host

A sleeping human is a warm object a few centimetres from a harbourage, and an animal that locates one by temperature gradient needs exactly the resolution reported here. The sensitivity is not an adaptation to treatment; it is the feeding apparatus.⁵

18.1 And they orient to heat at short range

Placed in an arena at room temperature they detect and orient towards a heated coil ranging from 28 to 48 degrees at 10 to 30 millimetres away.⁶

19. And the attraction paradox

Which is the part that makes this species difficult.

Bed bugs are attracted to heated objects as the temperature of the object increases to a maximum of 48.0 °C, while on a temperature gradient they preferentially rest in areas heated to 28 to 29 degrees.⁵

19.1 Attracted up to the temperature that kills them

Because heat is the host cue, and a host does not reach 48 degrees.⁵

19.1b And the resting preference sits well below both

Twenty-eight to twenty-nine degrees is where they choose to be when nothing is forcing them, which is warmer than a room and cooler than a host.⁵

19.2 Which is a sensory system working correctly in a novel situation

Our reading, and it is the same structure as the light trap and pheromone problems our other articles describe: a cue that was reliable until people started producing it artificially.

20. The dispersal temperature

And this is the operationally important number.

When harborage top temperatures approach 40.0-43.0 °C, bed bugs will disperse in search for cooler areas.⁶

20.0b And it is measured at the harbourage rather than the room

Harbourage top temperature is the quantity reported, which is the surface the animals are under rather than the air a thermostat reads. Those diverge by exactly the amount that makes heat treatment difficult.⁶

20.1 Which is below the lethal range

Section 10 puts substantial mortality at 46 and near-complete kill at 48. The animals begin leaving several degrees before that.³⁶

21. Which makes failure a containment problem

Our conclusion, and it is the practical centre of the article.

A treatment that heats a room to lethal temperature also heats it through a range in which the occupants actively move away, using a sensory system that resolves two degrees at close range.⁵⁶

21.1 So the animals are not enduring the treatment

They are responding to it, and whether they succeed depends on whether anywhere cooler is reachable.

21.1b And it explains why the method is sold with containment measures

Fans to move air into voids, sensors placed in harbourage rather than in the room, and treatment of adjoining spaces are all standard, and each addresses escape or incomplete heating rather than tolerance.

The practice, in other words, already assumes the answer this article arrives at. What it has not generally done is say so, which leaves the resistance claim doing work the containment measures are actually doing.

21.2 Which turns the question into one about the building

Wall voids, adjoining units, the far side of a partition: our article on bed bug dispersal in apartments described the routes, and this supplies the stimulus that drives animals into them.

21.3 And it makes ramp rate a variable worth attention

A slow approach to lethal temperature gives more time in the dispersal window than a fast one. We found no study testing that, and §6.1 notes the selection work used both shapes for a different purpose.

22. Sublethal exposure damages the population

Which is the other half of the picture.

Experimental populations exposed to 34, 36 or 38 degrees for two or three weeks suffered significant mortality during exposure, and among survivors egg production, egg hatching, moulting success and offspring proliferation decreased significantly in a subsequent seven week recovery period at 22 degrees.⁴

22.0b Which suggests a treatment option nobody sells

Sustained moderate heat, well below the lethal range, degrades the population over weeks rather than killing it in a day. That is not a service a contractor can offer, because it requires a building to be held warm for a fortnight, but it is a description of what a chronically overheated space does to an infestation.⁴

Which our article on indoor thermal refugia should be read against: the same heat that makes a building habitable year-round for these species has a range above which it starts working the other way.

22.1 And shorter exposures do the same

Adults exposed to sublethal temperatures of 35.5 to 40 degrees over three to nine days showed lower fecundity, higher mortality and lower egg hatch rates, particularly at longer durations and higher temperatures.⁴

22.2 The selection study found the same direction

Reporting that sublethal exposure to heat significantly reduced feeding and in some cases inhibited development.¹

23. Which runs against the usual sublethal worry

Our observation.

In our resistance articles, sublethal exposure is the mechanism by which selection proceeds: the survivors carry the advantage forward. Here sublethal exposure reduces the reproductive output of the survivors themselves.

23.1 A partial heat treatment weakens the population it fails to kill

Which is not true of a partial insecticide application.⁴

23.1b And the effect persisted well past the exposure

The reproductive deficits were measured over a seven-week recovery period at 22 degrees, so the damage is not a transient depression during the heat but a lasting change in what the survivors produce.⁴

23.2 Though it does not eliminate the selection argument

Reduced fecundity across survivors still leaves relative differences between them, and selection acts on the relative rather than the absolute. The damage lowers the population; it does not switch off the sorting.

That qualification is ours and we think it is the honest form of §23.1.

24. The route nobody has closed

A greenhouse mite selected for a pesticide acquired cross-resistance to heat through increased heat shock protein expression.⁶

24.1 Bed bug populations are under continuous chemical selection

Which our layered resistance article documented at length, across several mechanisms and compound classes.

24.2 So the selecting agent for a thermal trait need not be heat

And a population that has never been heat treated could in principle arrive with a heat phenotype acquired elsewhere.

24.3 With the counter-evidence stated fairly

The population comparison in §9 included strains differing in insecticide resistance profile and found non-significant variation in heat tolerance, which is the most direct available test and points the other way.¹

25. Why that matters here specifically

Because the two methods are used in sequence.

A property treated chemically for years and then heat treated is the exact case where a chemically-acquired thermal trait would first appear, and that sequence is the ordinary history of a bed bug infestation in this city.

25.1 We are not predicting it

Section 24.3 is the best evidence available and it found nothing. We are noting that the question has been asked once, in one study, as a secondary objective.¹

26. What we would say to a client

That resistance to heat has been tested for and appears limited, that no population difference has been found, and that the reasons a heat treatment fails are almost always that somewhere did not get hot enough or that the animals moved somewhere that did not.¹⁴

26.0b And it changes what a failed treatment means

A client whose heat treatment failed has usually been told the infestation was worse than expected. The literature says the likelier explanations are a cold spot and an escape route, both of which are findable and fixable before a second attempt.

26.1 Which is more useful than the usual formulation

Because it tells them what to ask about: coverage, monitoring of harbourage temperature, and containment of adjoining spaces.

27. And what we would not say

That resistance to heat is impossible.

The selection experiment produced an increase before it stopped, the study describes the ability as limited rather than absent, and the mite precedent shows a route that has been checked once in this species.¹⁶

27.0b And the useful claim is available without it

That heat resistance has been looked for and not found, in a laboratory line and across field populations, is a stronger thing to be able to say than an assertion about what is possible, because it is checkable and it is true.¹

27.1 Impossible is a stronger word than anybody has earned

And our articles on statistic provenance and on guarantee language both concern claims that grew firmer as they were repeated.

28. Our own position

The disclosure.

Heat treatment is a premium service and the resistance-proof claim is part of what justifies its price. This article says the claim is roughly right, overstated at the edges, and rests on a small evidence base.

28.1 Which is a mild correction rather than a reversal

The method works, the evidence supports its central premise, and the failure modes are the ones our thermal article already described.

29. A note on who funded the study

Which we record as a matter of practice.

The selection study's acknowledgements name an industry-linked foundation and a named company, with a declaration that the company's involvement does not alter the authors' adherence to the journal's policies.²

29.1 A study asking whether the industry's premium method can be defeated

Funded in part by industry sources, reporting that it largely cannot, with the funding declared.²

29.1b And the result runs toward the funder's interest

Which is the configuration that warrants recording rather than the reverse. A finding against a funder's interest needs no such note.

29.2 We are not impugning it

Declared industry funding of applied entomology is normal, the finding is a negative result that was published, and the alternative is that nobody asks the question at all. We note it because our article on trial provenance would note it about anybody else.

30. The Manitoba position

30.1 Why this matters more here

Our articles on multi-unit housing describe bed bugs as the dominant treatment problem in this city's apartment stock, and heat is the method most often proposed when chemical treatment has failed repeatedly.

30.1b And the sequence here is the one §25 describes

Chemical treatment first, repeatedly, often by several operators over years, with heat proposed once that has failed. If the chemical-to-thermal route exists, this city's apartment stock is where it would be found.

30.2 What we could not find

Any local data on heat treatment outcomes, any Canadian study of thermal tolerance in this species, and any record of harbourage temperature monitoring practice by contractors here.

30.3 With one climate observation

Section 13.2 reports the species cannot tolerate freezing and dies well above its supercooling point, which is relevant to the local practice of leaving infested items outdoors in winter.³

31. Limitations and open questions

The central finding rests on one study. A single selection experiment, read as its abstract and introduction rather than in full, and we did not see the selection protocol, the number of lines, the population sizes or the survivorship figures.¹²

That is the most important limitation because §§7 to 9 carry the article's answer and we have the conclusions without the data behind them.

Four generations is a short selection experiment. The plateau is reported at generation four and we do not know how many generations were run in total.¹

The tolerance work is from 2009. Predating the widespread adoption of thermal remediation, so the populations tested had no heat exposure history to speak of.³

Two sources reach us as abstracts of the same paper. The escape behaviour work is cited here through a bibliographic record and a publisher extract rather than the full text.⁵⁶

And the sublethal figures come through a citing paper. The fecundity and hatching results are quoted in another paper's discussion rather than read in the original study.⁴

Sections 6.2, 8, 14, 19.2, 21, 23, 24, 25 and 27 are our reasoning. The reading of the plateau as exhausted standing variation, the ecological account of the cold-heat asymmetry, the containment framing, the qualification to the sublethal argument and the chemical-to-thermal route are ours rather than sourced positions.

32. Conclusion

The claim that insects cannot become resistant to heat is empirical, and somebody tested it. A selection experiment found an initial increase in bed bug survivorship which did not increase past the fourth generation, found non-significant variation in heat tolerance between populations differing in heat exposure history, insecticide resistance profile and geographic origin, and concluded that the ability to develop heat resistance appears limited.¹ Limited is the authors' word and it is not the same as absent. Earlier work found fewer than 20 per cent surviving an hour at 46 degrees and nearly all killed at 48, with dehydration, two weeks at 30 degrees and an hour at 37 all failing to improve heat tolerance, while an hour at zero measurably improved cold survival in the same animals.³ The protective flexibility runs downward and not upward.

Heat shock proteins are upregulated within fifteen minutes and return to baseline by twenty-four hours, and the authors read them as recovery from survivable damage rather than as a survival mechanism, concluding that bed bugs do not survive heat treatments through greater thermotolerance.⁶⁵ What explains survivors is the other two possibilities: harbourages that never got hot enough, and animals that left. They detect two degree differences within three centimetres, they are attracted to heated objects right up to 48 degrees because heat is how they find a host, and they disperse when harbourage temperatures approach 40 to 43, which is several degrees below the lethal range.⁵⁶ A heat treatment therefore passes its occupants through a window in which they actively leave, and whether that matters depends on whether anywhere cooler is reachable. Failure is a containment problem.

Two things temper the reassurance. Sublethal heat damages the survivors, reducing fecundity, hatching and moulting success, which is the opposite of the usual sublethal selection story, though it lowers the population without switching off the sorting between individuals.⁴ And a greenhouse mite selected for a pesticide acquired cross-resistance to heat through heat shock protein expression, which means the selecting agent for a thermal trait need not be heat.⁶ Bed bug populations are under continuous chemical selection and are then heat treated, which is exactly the sequence in which such a trait would first show up. One study looked for it as a secondary objective and found nothing. That is the best evidence available and it is one study.

References

1. Bed bugs exhibit limited ability to develop heat resistance. Open-access journal article, read as its published abstract. Source for the study's two stated goals, namely determining whether bed bugs could be selected for heat resistance under a laboratory selection regime and whether populations with various heat exposure histories, insecticide resistance profiles and geographic origins have differential temperature tolerances, using step-function and ramp-function exposure techniques; for the finding that selection experiments produced an initial increase in survivorship which did not increase past the fourth generation; for the finding that sublethal exposure to heat significantly reduced feeding and in some cases inhibited development; for the finding that the step-function technique revealed non-significant variation in heat tolerance between populations with the ramp-function technique providing similar results; and for the conclusion that based on these outcomes the ability of bed bugs to develop heat resistance appears to be limited. https://journals.plos.org/plosone/article?id=10.1371%2Fjournal.pone.0211677
2. Printable full text of the same article, read as extracts of its introduction and acknowledgements. Source for the statement of the underlying worry, namely that although bed bugs do not display heat hardening, repeated sublethal heat exposure could potentially select them for heat resistance, which would be problematic for the use of thermal remediation for their control; for the note that a springtail species significantly increased expression of heat shock protein family members after exposure to non-lethal high temperatures; and for the acknowledgement naming an industry-linked foundation and a named company as supporting the work, with a declaration that this does not alter the authors' adherence to the journal's policies. https://journals.plos.org/plosone/article/file?type=printable&id=10.1371/journal.pone.0211677
3. Responses of the bed bug to temperature extremes and dehydration: levels of tolerance, rapid cold hardening and expression of heat shock proteins. Journal article in a medical and veterinary entomology title, read as its published abstract. Source for the finding that fewer than 20 per cent of bugs survived a one-hour exposure to 46 degrees and nearly all were killed at 48; for the finding that dehydration, heat acclimation at 30 degrees for two weeks and rapid heat hardening at 37 degrees for one hour all failed to improve heat tolerance; for the cold results that the supercooling point was approximately minus 20 degrees yet all were killed by a direct one-hour exposure to minus 16, so that the species cannot tolerate freezing and is killed at temperatures well above its supercooling point; that neither cold acclimation at 4 degrees for two weeks nor dehydration enhanced cold tolerance; and that the species does have the capacity for rapid cold hardening, with a one-hour exposure to zero improving subsequent tolerance of minus 14 and minus 16 degrees. https://resjournals.onlinelibrary.wiley.com/doi/10.1111/j.1365-2915.2009.00832.x
4. Record for the same temperature-extremes paper on a research-sharing platform, displaying material from papers citing it. Used for statements made in other work rather than for the paper itself, which we flag. Source for the enumeration of three explanations for bed bugs being present after a heat treatment, namely abiotic factors associated with inability to achieve lethal temperatures in harbourage areas for sufficient time, re-infestation from insects that escaped to cooler areas during treatment, or development of physiological resistance; for the note that other studies have not found changes in survival at high temperatures up to 48 degrees after previous exposure to sublethal elevated temperatures; and for the reported findings of a separate study that experimental populations exposed to 34, 36 or 38 degrees for two or three weeks suffered significant mortality during exposure, that among survivors egg production, egg hatching, moulting success and offspring proliferation decreased significantly over a subsequent seven-week recovery period at 22 degrees, and that adults exposed to sublethal temperatures of 35.5 to 40 degrees over three to nine days showed lower fecundity, higher mortality and lower egg hatch rates. https://www.researchgate.net/publication/40034773_Responses_of_the_bed_bug_Cimex_lectularius_to_temperature_extremes_and_dehydration_Levels_of_tolerance_rapid_cold_hardening_and_expression_of_heat_shock_proteins
5. Characterization of heat exposure-associated escape behaviors and heat shock protein gene expression in bed bugs. Journal article in a pest management title, read as a publisher extract. Source for the statement that when bed bugs are close to heated objects, at less than 3 centimetres, they can detect temperature differences of 2.0 degrees; for the statement that they are attracted to heated objects as the object's temperature increases to a maximum of 48.0 degrees and that on a temperature gradient they preferentially rest in areas heated to 28 to 29 degrees; for the note that how bed bug behaviour changes in response to rising temperatures inside harbourage locations had not previously been determined; and for the reading that the results suggest bed bugs do not survive heat treatments due to the development of greater thermo-tolerance. https://scijournals.onlinelibrary.wiley.com/doi/epdf/10.1002/ps.6620
6. Bibliographic record and abstract for the escape behaviour study, in a biomedical literature database, together with introduction material from the selection study carried in the same search context. Source for the finding that when harbourage top temperatures approach 40.0 to 43.0 degrees bed bugs will disperse in search of cooler areas; for the result that two named 70 kilodalton heat shock protein genes and a putative small one were significantly upregulated at 15 minutes, 2 hours and 4 hours post-exposure and decreased back to baseline by 24 hours, with those genes implicated in heat induced stress recovery; for the statement that the abiotic challenges in achieving lethal temperatures in harbourages, combined with behavioural or physiological responses to sublethal exposure, could theoretically select for increased heat resistance; for the precedents that heat exposing one laboratory fly species produced greater temperature resistance within a few generations of selection and that plastic temperature tolerance traits were selectable in a mosquito reared at different temperatures; for the report that a greenhouse mite selected for resistance to a named pesticide also showed some cross-resistance to heat exposure due to increased expression of heat shock proteins; and for the observation that bed bugs placed in an arena at room temperature detect and orient towards a heated coil ranging from 28 to 48 degrees at 10 to 30 millimetres away. https://pubmed.ncbi.nlm.nih.gov/34468070/