SLA Biomedical & Life Sciences Division Blog

The Bedbugs Aren’t Coming, They’re Already Here

Bedbugs (primarily Cimex lectularius, but occasionally in warmer climes the tropical version Cimex hemipterus)  are tiny (about ¼ inch) blood-sucking human parasites. They are  typically found living  in bedding, but are also found hidden in closets, thin cracks in headboards, floorboards, baseboards and walls. In short they are found anywhere that brings them in close proximity to the humans on which they feast. They generally come out at twilight (Romero, Potter & Haynes 2010), wait for their victims to drift off to sleep, and then puncture the skin with their proboscis to suck up the blood, while coincidentally injecting  a local anesthetic which masks the intrusion.

Bedbugs  have been around for tens of thousands of years (they have been found in the wrappings of Egyptian mummies) but  were once thought to have been almost completely wiped out in the United States , Canada, and most of the major economically advanced countries in Europe and Asia.

But now they have resurged to the point that they are found in all 50 US states and the Provinces of Canada, and virtually the major business cities and political capitals around the world (Benac 2010, Burleigh 2010,How & Yee 2010a, 2010b, Manuel 2010.

Most major city exterminators report now having a thriving practice in attempts to eliminate or control bedbugs, whereas as recently as ten years ago, their presence was an exception (Motoki 2010, Radcliffe 2010).  

While private homes do report infestations, the majority of calls for assistance come from places where there are multiple and often continuingly changing occupants of rooms and their furniture. Breakouts are most common in hotels, motels and college dormitories, but in recent years many reports have come in from hospitals,  movie theaters, and passenger seats on planes and trains (Anders, Brocker & Hamm 2010, ED Management Editors 2010, Johns Hopkins Medical Letter for Health After 50 Editors 2010, Mayo Clinic  Womens Healthsource Editors 2010, Von Drehle 2010, Yaguchi & Kasai 2010).

How has this come to happen? Answer 1: Mobility of victims & vermin

It takes only one person with bedbugs in  his or her suitcase or clothing to infest an entire hotel, a college dorm, or even a bus, but people rarely examine their own clothing or luggage for possible bedbug infestation, must less exterminate the bedbugs that are coming along for the ride by steam blasting them, or putting possibly odorous pest strips inside. (Chalupka 2010). Today,  when sales personnel and tourists can  visit a different country every day and sleep in a different time zone every night, there is an unprecedented opportunity for them to be unwitting carriers of bedbugs (Potter, Rosenberg & Henriksen 2011) .  

In addition, bedbugs can temporarily feast on other animals between human feedings, with the most recent temporary vector for them  turning out to be New York City pigeons (Haag-Wackernagel & Bircher 2010).

How has this come to happen? Answer 2: In the  decaying public housing sector, cockroaches stole the limelight away from bedbugs long enough for bedbugs to recover

One of the most fascinating articles dealing with this question is by Biehler (2009). Bedbugs used to be the number one insect pest of the interiors of communal housing or sleeping quarters. They were aggressively attacked and treated in a cooperative  effort by building managers and vigilant cooperating residents, often involving  a vigorous campaign of joint inspection, cleaning, and fumigation.

However, after the 1950s in the US at least, housing for the middle class and returning WWII veterans shifted from sometimes subsidized apartments in the cities, to individual private homes in the suburbs.

The  population that remained behind in public housing were often the poor and elderly.   The demographics of the poor in public housing also became more black and Hispanic, while the ownership or management often remained white,  and was in any case, affluent by comparison, and distant from “the projects” in terms of their personal home locations. There was a substantial breakdown in the sense of shared social responsibility for  keeping up the property. Housing units fell into greater and greater disrepair. Services like regularly scheduled fumigations and cooperative inspections for bedbugs fell by the wayside.

This did not end the need for exterminators, and in cities, public housing  projects provided one  of their greatest sources of revenue. However, the target pest species changed. For most of the latter 20^th century, the cockroach took precedence as insect public enemy number one (Ebeling 1965.  Meanwhile the diminished population of bedbugs began to rebuild its numbers.

How has this come to happen? Answer 3:  Pesticide Resistance on the Part of Both the Bedbug and the Apartment Dweller

Initially bedbug infested apartment buildings were evacuated for the better part of a day to allow for highly toxic, but also highly effective, hydrocyanic gas fumigation of the whole complex.  But in the 1950s and 1960s, localized spraying of DDT, organophosphates and organochlorines  in individual apartments took over as the technology of choice for extermination. The advantages of these liquid spray spot treatments were that whole buildings did not need to shut down, and to some degree, neighboring units in apartment complexes did not need to know about infestations, perhaps preserving privacy but also diminishing communal buy-in.

Eventually, insects of all types developed increasing resistance to these more common pesticides (Romero et al 2007) and a search for alternative pesticides developed in earnest. Several were in fact found, but at about the same time, apartment dwellers and public health officials began to worry that the chemical killing of the bedbugs presented almost as much of a chemical danger to residents as it did to the insects (Berg 2010).

Fortunately, for about 20 years the pyrethins , natural neurotoxins derived from chrysanthemums, which naturally biodegraded and had seemingly negligible toxicity to humans , served to keep down both cockroaches and the rising tide of bedbugs.

No longer, alas (Hirao & Tomita 2010, Iwamoto 2010, Seong et al 2009, Zhu et al 2010) and combinations of these mild toxins now often need to be combined with additional activating chemicals  in order to remain effective (Romero, Haynes & Potter 2009).

Taking off the chemical gloves in the fight against bedbugs

But owing to an increased concern about bedbugs transmitting some fairly serious diseases (Delaunay et al 2010), it now seems as if some new generation chemical agents, or retired chemical agents, are likely to be approved for deployment or redeployment.  The most likely candidate in the US and Canada is propoxur, which had been pulled off the market in 2007(Benac 2009), although certain folk remedies are being reinvestigated in Europe (Soukand, Kalle & Svanberg 2010).   

Nonetheless, public health officials whose concerns have in more recent years focused on potential toxicity to humans, are still urging more environmentally friendly Integrated Pest Management approaches that will limit blunt force chemical applications (Rossi & Jennings 2010). Heat treatment with live steam, and even flash freezing are now being tried against bedbugs with varying degrees of effectiveness (Benoit et al 2009, Watanabe 2010), often in combination or in alteration with chemical sprays.

Will a better understanding of bedbug biology lead to more innovative approaches?

If bedbugs have a weakness in their life cycle, it is in their reproductive behavior. Adult male bedbugs practice what is referred to as traumatic insemination on females (Reinhardt & Siva-Jothy 2007, Siva Jothy 2006, Stutt & Siva Jothy 2001).

Imagine that in order to have sex, male humans would have to slash open female stomach at roughly their navels, and then stuff their penis in and deposit their sperm, and hope they find their way to the uterus and ovaries. Indeed, this is a highly inefficient approach because it is estimated that it takes as many as 20 rapes to produce a successful pregnancy.

This is a rather dangerous proposition for  bedbug females and even for immature bedbug males which  are often homosexually raped (Ryne 2009). Not surprisingly some female bedbugs have evolved a special entry port which makes penetration bt violent males easier (Reinhardt, Naylor & Siva-Jothy 2003).

But other females and nymphs have developed certain chemical countersignals that forestall these violent mating attacks by the males, largely by confusing, alarming or even positively repelling them (Haraca, Ryne & Ignell 2010, Levin, Levinson & Maschwitz 1974, Siljander et al 2008, Morrow & Arnqvist 2003).

It is through chemically duplicating the bedbug's own sexually defensive sprays that we may one day hold the key to interrupting the further spread of bedbugs, by keeping bedbugs  from reproducing, by using  a kind of nontoxic but effective pheromone fog (Haynes, Goodman & Potter 2010).

Tony Stankus, FSLA [email protected], Life Sciences Librarian, Science Coordinator & Professor

University of Arkansas Libraries MULN 233 E

365 North McIlroy Avenue

Fayetteville AR 72701-4002

Voice: 479-409-0021

Fax: 479-575-4592

 

Anders, D., E. B. Brocker, and H. Hamm. 2010. Cimex lectularius - an unwelcome train attendant. European Journal of Dermatology 20 (2): 239-40.

Benac, Nancy. 2010. Bedbug bites becoming bigger battle. CMAJ 182 (15): 1606.

Benoit, J. B., G. Lopez-Martinez, N. M. Teets, S. A. Phillips, and D. L. Denlinger. 2009. Responses of the bed bug, Cimex lectularius, to temperature extremes and dehydration: Levels of tolerance, rapid cold hardening and expression of heat shock proteins. Medical and Veterinary Entomology 23 (4): 418-25.

Berg, R. 2010. Bed bugs: The pesticide dilemma. Journal of Environmental Health 72 (10): 32-5.

Biehler, D. D. 2009. Permeable homes: A historical political ecology of insects and pesticides in US public housing. Geoforum 40 (6): 1014-23.

Burleigh, Nina. 2010. Nightmare on bedbug street. Time 176 (9): 63-4.

Chalupka, S. 2010. Preventing bedbug infestation. AAOHN Journal 58 (11): 500-.

Cohen, P. R., J. A. Tschen, F. W. Robinson, and J. M. Gray. 2010. Recurrent episodes of painful and pruritic red skin lesions. American Journal of Clinical Dermatology 11 (1): 73-8.

Delaunay, P., V. Blanc, P. Del Giudice, A. Levy-Bencheton, O. Chosidow, P. Marty, and P. Brouqui. 2011. Bedbugs and infectious diseases. Clinical Infectious Diseases 52 (2): 200-10.

Ebeling, W. 1965. Cockroach control in public housing. Pest Control Operator News 25 (12): 21-24.

ED Management Editors 2010. EDs trying not to let the bed bugs bite. ED Manag 22 (9): 100-1.

Haag-Wackernagel, Daniel, and Andreas J. Bircher. 2010. Ectoparasites from feral pigeons affecting humans. Dermatology (Basel) 220 (1): 82-92.

Hawkins, C. N., and B. Barankin. 2010. Can you identify this condition? Canadian Family Physician 56 (6): 553,+.

Haynes, K. F., M. H. Goodman, and M. F. Potter. 2010. Bed bug deterrence. BMC Biology 8 .

Hirao, Motokazu, and Takashi Tomita. 2010. Insecticide resistance of bedbugs. Medical Entomology and Zoology 61 (3): 223-9.

How, Y. F., and C. Y. Lee. 2010a. Effects of life stages and feeding regimes on active movement behavior of the tropical bed bug, Cimex hemipterus (hemiptera: Cimicidae). Journal of Medical Entomology 47 (3): 305-12.

———. 2010b. Survey of bed bugs in infested premises in Malaysia and Singapore. Journal of Vector Ecology 35 (1): 89-94.

Iwamoto, Tatsuhiko. 2010. The present condition of bedbug management in the US: Some tips on promoting unification of laws regulating pesticides in Japan. Medical Entomology and Zoology 61 (3): 255-60.

Johns Hopkins Medical Letter for Health After 50 Editors. 2010. Don't let the bedbugs bite. Johns Hopkins Med Lett Health After 50 22 (2): 3.

Manuel, J. 2010. Invasion of the bedbugs. Environmental Health Perspectives 118 (10): A429-.

Mayo Clinic  Womens Healthsource Editors. 2010. I've heard that bedbugs have become a problem in hotels. How can I avoid them when I'm traveling? Mayo Clin Womens Healthsource 14 (8): 8.

Morrow, E.H., & G. Arnqvist. 2003. Proceedings of the Royal Society of London 270: 2377-2381.

Motoki, Mitsugu. 2010. Current status and problems of bedbug control in the pest-control industry. Medical Entomology and Zoology 61 (3): 251-3.

Pfeister, M. P.G. Koehler, & R.M. Pereira. 2009. Sexual conflict to the extreme: Traumatic insemination in bed bugs. American Entomologist 55: 244-249.

Radcliffe, Mark. 2010. Bedbugs and consultants are both bleeding us dry. Nurs Times 106 (34): 24.

Reinhardt, K., & M.T. Siva-Jothy.  2007. Biology of the bed bugs (Cimicidae). Annual Review of Entomology  52:351-374.

Reinhardt, K., R. Naylor, & R. Siva-Jothy. 2003. Reducing a cost of traumatic insemination: Female bedbugs evolve a unique organ. Proceedings of the Royal Society of London B Biological Sciences 270: 2371-2375.

Richard, S., P. Seng, P. Parola, D. Raoult, B. Davoust, and P. Brouqui. 2009. Detection of a new bacterium related to 'Candidatus midichloria mitochondrii' in bed bugs. Clinical Microbiology and Infection 15 : 84-5.

Romero, A., M. F. Potter, and K. F. Haynes. 2009. Evaluation of piperonyl butoxide as a deltamethrin synergist for pyrethroid-resistant bed bugs. Journal of Economic Entomology 102 (6): 2310-5.

Romero, Alvaro, Michael F. Potter, and Kenneth F. Haynes. 2010. Circadian rhythm of spontaneous locomotor activity in the bed bug, Cimex lectularius L. Journal of Insect Physiology 56 (11): 1516-22.

Rossi, L., and S. Jennings. 2010. Bed bugs: A public health problem in need of a collaborative solution. Journal of Environmental Health 72 (8): 34-5.

Ryne, C. 2009. Homosexual interactions in bed bugs: Alarm pheromones as male recognition signals. Animal Behaviour 78: 1471-1475.

Seong, K. M., D. Y. Lee, K. S. Yoon, D. H. Kwon, H. C. Kim, T. A. Klein, J. M. Clark, and S. H. Lee. 2010. Establishment of quantitative sequencing and filter contact vial bioassay for monitoring pyrethroid resistance in the common bed bug, Cimex lectularius. Journal of Medical Entomology 47 (4): 592-9.

Siljander, E., R. Gries, G. Khaskin & G. Gries. 2008. Identification of the airborne aggregation pheromone of the common bed bug, Cimex lectularius. Journal of Chemical Ecology 34: 708-718.

Siva-Jothy, M.T. 2001. Trauma, disease and collateral damage: Conflict in cimicids.  Philosophical Transactions of the Royal Society of London B Biological Sciences 361: 269-275.

Soukand, R., R. Kalle, and I. Svanberg. 2010. Uninvited guests: Traditional insect repellents in Estonia used against the clothes moth Tineola bisselliella, human flea Pulex irritans and bedbug Cimex lectularius. Journal of Insect Science 10 .

Straub, R. D., H. L. Salvaggio, D. R. Adams, and A. L. Zaenglein. 2009. Diffuse clusters of vesicles on the face and extremities of a 10-month-old girl. Pediatric Dermatology 26 (6): 747-8.

Tomita, Takashi. 2010. Insecticide resistance of bedbugs. Medical Entomology and Zoology 61 (3): 223-9.

Von Drehle, David. 2010. This really sucks. Time 176 (14): 36-8.

Watanabe, Mamoru. 2010. Insecticide susceptibility and effect of heat treatment on bedbug, Cimex lectularius. Medical Entomology and Zoology 61 (3): 239-44.

Yaguchi, Noboru, and Shinji Kasai. 2010. Current situation and problem of bedbug infestation in Tokyo, Japan: From public health officer's angle. Medical Entomology and Zoology 61 (3): 231-7.

Zhu, F., J. Wigginton, A. Romero, A. Moore, K. Ferguson, R. Palli, M. F. Potter, K. F. Haynes, and S. R. Palli. 2010. Widespread distribution of knockdown resistance mutations in the bed bug, Cimex lectularius (hemiptera: cimicidae), populations in the United States. Archives of Insect Biochemistry and Physiology 73 (4): 245-57.

Do Snake Venoms Evolve According to the Prey They Are Intended to Kill, Or Do Snakes Just Dial Up the Dosage or Concentration of Whatever Venom They Have to the Size of the Prey in their Sights?

Snake venoms are overwhelmingly composed  of dissolved protein  mixtures which typically exert their action on a victim in one of the following three ways, and sometimes in combination:

·        Hemotoxins. Depending on their mix of proteins, these can either cause the blood to clot precipitously, causing cardiovascular blockages (essentially heart attacks) in extreme cases, or alternatively, cause it to thin so quickly that the victim bleeds out.  This is one of the  modes of action of rattlesnake venoms.

 

·        Neurotoxins.  These disrupt either or both the voluntary and autonomic nervous system of the victim, rendering it incapable of escape, and in extreme cases, cause the victim to stop breathing or to convulse. This is the primary  mode of action of cobra venoms.

 

·         Tissue Necrotizers:  These basically break down the muscular and connective tissue at the site of the bite, and basically cause an ever expanding dead zone until the toxin is so diluted as to lose effect. Often the victim dies before this can happen. This is the mode of action of the fer-de-lance the most prominent perpetrator of poisonous snake bites in Latin America.

The popularity of proteomics and the wider availability of its instrumentation  leads to “venomics” & confirms evolutionary relationships & distinctions  among the many differing families  of poisonous snakes

 

Can you tell a venomous snake just by a chemical analysis of its venom?

The short, and historically most orthodox answer,  is, yes.

For most of the history of snake venom studies , the relatively small number of total analyses achieved indicated that most snakes tend to have signature venom protein mixes.

Now, given the widespread use of automated proteomics analyzers and advances in protein sequence informatics, much of this  old work is being confirmed with more  complete analyses of more venoms from more snakes and especially from differing families of snakes. Indeed, you can now search a variety of biomedical, chemical and pharmaceutical  databases under “Venomics” for on-point papers.

 And the new results can be extended to say that snakes that are in the same genus tend to have rather similar, if not always quite identical, cocktails of toxins.

Such variations as are found, are thought to be minor,  the results of random genetic drift, and to be incidental to the  study of  either the lineage, the  or day-to-day functioning of the snake.

There is  some thought that evolutionary relationships suggested by traditional morphological characters or modern genomics ,  can predict,  with reasonable certainty what venom toxins given families of snakes are likely to share, even before all their members are tested.

As a kind of real-world proof of the all-in-the-family nature  of protein toxins , consider that snake antivenoms (which work on biochemical recognition and disabling of venom proteins through binding them up)  work best when customized to the type of specific snake that does the biting. Such antitoxins are called monovalents, and are the treatment of choice whenever available.

But  given that maintaining a large and varied collection of monovalent antivenoms  is not always practical in areas where there are many possible different poisonous snakes which bite, some polyvalent vaccines have had to be developed which counteract, to some degree,  venoms from a variety of unrelated species.

Despite their polyvalent intent, their comparative effectiveness is positively correlated  with snakebites  that are evolutionarily related to the species from which the original pharmaceutical venom/vaccine was drawn.  In other words, antivenom that derives from a specific type of cobra,  is likely to work better with other persons bitten by somewhat different cobras, than it is to work on people bitten by rattlesnakes.

The prevalent theory is that the biosynthesis of toxins is likely to be highly conserved  over many generations and over differing populations of snake families  because their venom seems so central to the function of the snake, and that even incidental variations in toxins caused my random mutations could come at a cost to the snake in reduced prey killing capacity.

But  the dismissal of the significance of small differences in toxin blends within related snakes  is now being challenged,  and variations are being seen as having some meaningful function, and not just being blips in encoding that have no real life meaning to the snake.

Why have differing toxins within the same family of snakes? Couldn’t the snake just adjust the dosage to the size of the prey?

Differing types of snakes have differing quantities of venom available for hunting or defense, but certain general rules can predict among populations of the same snakes which will have more venom on average.

Generally, the older the snake of a given species is , the larger it is, and therefore the larger its storage and potential supply of venom for “envenomation, ”  when compared to younger and smaller snakes of the same species.

Furthermore female snakes generally have significantly more venom than males for two  readily  understood reasons: They are generally larger than males and have larger heads, and the head is where most of the venom production and storage is confined in all but a tiny handful of snake species.

But, it turns out that many adult snakes, whether large or small,  are actually thrifty in their use of venom.

They adjust the amount of venom to the size of their prey.  A mouse might get less venom per bite  than a gopher, for example.

Although as a general rule, given a choice between small and large prey , larger snakes will choose larger prey, and are willing to “spend the venom”  in order to get the larger meal.

The saw-scaled viper family and their venoms

A particularly  interesting comparison test of the venoms of four kinds of  saw-scaled vipers done by Barlow et al. (2009, cited below).

These four related viper species  are a genuine menace to public health in that they cause the majority of snakebite cases in North Africa and the adjacent Middle East.

 (The fact that some of them kill harmful vermin, may, of course be an offsetting factor, before deciding that they all should be wiped out indiscriminately.)

A comparison of the  electrophoretic separations of major toxin proteins  from the four different types of saw-scaled viper  showed that they were indeed, matching in the major protein bands,  something predictable owing to conventional thinking about the molecular evolution of snake venoms.

But there was a surprising amount of variation in the minor bands.

And this was also reflected in the fact that in the Middle East and in Northern Africa, saw scale viper antivenoms were markedly more effective against  Middle Eastern saw scale viper bites than they were against the bites of  the North African saw scale vipers that were presumed to be their evolutionarily closest relatives.

The drop off in effectiveness is notable in clinical terms and makes follow-up injections or IV drips of antivenom necessary more often in North Africa than they were in the Middle East.

A question arose:  Beyond any clinical significance, did these  variant protein toxins  have a purpose in the life of the snake?  Or, were they just the result of geographic isolation and random genetic drift?

Prey size vs. prey type: Which  plays a bigger role in the  evolution of venoms?

One competing theory of comparative venom toxicity  is that snakes within the same general family of snakes that prey on larger animals will eventually evolve   not only to produce more of the same general type of venom,  but also evolve higher, and therefore more potent concentrations of venom, with which to immobilize and kill their “big game.”

Its principal rival theory  is that differing prey  specialists within the same general family of snakes are more likely to require,  and eventually develop over succeeding generations venoms that gradually become more distinct, depending for success in killing prey, not so much on increasing the amount or the concentration of venom injected,   but rather on matching  the prey’s particular susceptibility to the venom.

Saw scale vipers represent a wonderful set of relatives upon which to test these competing outlooks.

Several types of saw scaled vipers have become small mammal specialists (usually eating rodents)  in terms of their prey.  Most of these are in the Middle East.

Others have a mixed diet of rodents and invertebrates.

(Most commonly in the Middle East and Africa, the invertebrates are various types of scorpions. )

Still others are almost exclusively scorpion feeders. These vipers are found only in North Africa.

It should be understood that even the biggest scorpions are but a fraction of the size and weight of the mice and rats typically consumed by either the rodent specialist,  or the mixed-diet-consuming saw scale  vipers.

Consequently “big game venom” should actually be more toxic to little game, because of its overall increased potency.

In other words, it may not be necessary to shoot a big-game venom cannon ball to kill a scorpion, but if it were to happen,  the cannon ball should surely be lethal to the scorpion.

Using ingenious methods, such as directly injecting carefully calibrated, matching fluid amounts of venom directly into  test scorpions from all four types of saw scale viper, and then seeing which venoms were, “ounce for ounce” more deadly, the team found something unexpected.

The “big game hunters”  of rats and mice, who would presumably need more toxicity to bring down their big game, actually  had venom that was notably less toxic to the small size game of scorpions, than the venom   of the mixed-bag-diet hunters.

And even more  intriguingly,   the mixed-bag-hunter venom was still less toxic to the scorpions than that of the specialized scorpion hunters.

The most toxic & effective venoms against the small game of scorpions, came from scorpion specialists, not from big-game or mixed-game specialists, who routinely had to knock down and kill bigger game.

In other words, the venom of North African scorpion specialists had become distinct enough through evolutionary adaptation to its prey, to make a difference in the life of its particular type of saw scale viper.

And maybe that distinction was now big enough to explain why Middle Eastern antivenom vaccines against North African saw scale vipers were seeing decreased efficiency.

Are the prey utterly without their own evolutionary defenses against specially  evolved snake venom?

This would seem to be the case, but in a number of settings, various ground squirrels, gophers and badgers, whose paths frequently intersect with predatory snakes like rattlers, seem to have grown immune to the local venom (see, for example Hayes, Lavin-Murcio & Kardong, 1995, cited below). This is also the case with some eels that live alongside sea snakes that hunt for eels (Heatwole & Pran, 1995).

Whether or not this leads to the evolutionary  alteration of the local snake venom to make if effective once again, has not yet been studied.

But in a particularly intriguing case, a poisonous sea snake that has become a fish egg eating specialists, and therefore has no need to immobilize and kill its prey (the eggs don’t run away and are not guarded by their parent fish) has actually evolved venom of greatly reduced toxicity, seeming to spare itself unnecessary toxin protein production (Li, Fry & Manjunatha Kini, 2005).

 

Tony Stankus [email protected] Life Sciences Librarian & Professor

University of Arkansas Libraries MULN 223 E

365 North McIIroy Avenue

Fayetteville, AR 72701-4002

Voice: 479-575-4031

Fax: 479-575-4592

 

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Will Global Warming & Increased CO2 Increase Crop Yields?

One of the few upsides  found when exploring  global warming scenarios is based on the assumption that  since green plants thrive on carbon dioxide (and there will be much more of it) for photosynthesis and since warmth tends more than cold to promote growth (and there will be more warmth), farmers who grow green plant crops should, on the whole,  thrive.  

This hypothesis has been tested in greenhouses with generally positive confirmations.

The problem with this overall proposition  is that it has run counter   to recent experience for most countries and crops, with China and plantains being  notable exceptions.  There is substantial agreement that world yields of wheat, rice, and corn (maize), as well as soybeans are trending down with increases in atmospheric CO2 and warmth.

Why would this be so?

Having More CO2 May Not Be All That Helpful If Other Inputs Do Not Match It

Having more CO2 may not help plants if they do not have access to increased water, nitrogen,  potash, and the right soil conditions, at the same time. It’s something like having more flour. By itself,  more flour does not mean you can bake a bigger cake. You also have to have baking powder, shortening, eggs, water, and other ingredients, or you are just going to get a modestly risen but  pasty  lump of dough.

Reports of Average Increases In Seasonal Temperature   Are Misleadingly Mild

Reports that on average, a region has an increase of 2 degree Fahrenheit over previous years , tend to smooth  over a number problems.

The first problem is that spikes of hot temperatures tend to occur more frequently, even if they do not last many days. It is not a case of each day being two degrees warmer; it is generally a case of more incidences of heat spells.

Location, Location, Location

Another poorly understood phenomenon is that temperature spikes tend to have more consequential effects  at the margins of the range  where a given crop can be cultivated. In other words, if  a region was on the borderline of being too hot for the crop, but the crop was still viable most of the time in the past, raises in the frequency of heat spells will tend to shut down the area altogether. This tends to have serious implications for farmers in those marginal regions  who depend largely on one cash crop. This is particularly the case in some of the poorest countries, and their farmers often have limited access to retool their operations to make them more viable with some sort of alternative crop.

Bad Timing

 A third problem is that the timing of heat waves is often at least as important as their duration.  Certain life stages in green plants  that reproduce sexually (which are most of the world’s cash crops) can be quite  temperature-sensitive.

This is particularly the case with pollen viability, pollen germinative ability, stigma viability, and ovule viability.

Given that an enormous number of crops are essentially providers of food as seeds ( grains, nuts) or  fruits with seeds (virtually all tree crops, and many vine crops) failures along these lines have immediate consequences for this year’s crop for the table, and may also diminish the amount and quality of seed for sowing for the follow-on crop.

Pollinator & Pest Problems Tend to Increase with  Spikes in Temperature

One consequence of timing  disruptions in plant life cycles caused by heat spikes  is that pollinators like bees,  butterflies, moths, and even birds, end up arriving too late or too early to do their jobs effectively.

Perversely,  reductions in killing frosts tend to allow more plant pests or their eggs  to overwinter and heat spikes may promote earlier  hatching or a higher rate of hatching success among  herbivores.

Both of these phenomena may extend to weeds that compete for resources with the crops.

It’s Not All Doom & Gloom

It is nonetheless worthwhile to consider that modern plant breeding has a  history of coming up with solutions to changes in climate, and, some colder regions that are now not notably crop productive may well experience a surge in productivity.

Whether either of these will offset downturn in crop yields owing to spikes in temperature,  may well be the most important plant science story of our time.

Tony Stankus [email protected] Life Sciences Librarian & Professor

University of Arkansas Libraries MULN 223-E

365 North McIlroy Avenue

Fayetteville, AR 72701-4002

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