Malevolent Design - How The Malevolent Designer Perfected The Mosquito As Its Favourite Parasite Delivery System

Thermal image of human bodies

Photo Credit: Ildar Abulkhanov via iStock

Mosquitoes sense infrared from body heat to help track humans down | The Current

To an intelligent [sic] design creationists it must seem that the mosquito is the divine malevolence's delivery system of choice for getting its parasites into as many people as possible to maximise the suffering in the world.

There are others of course, such as the tsetse fly that delivers the parasite that causes sleeping sickness to humans and their cattle, which is probably the major reason Africans never developed agriculture, and ticks do their bit in spreading diseases too, but none are as effective as the mosquito which is responsible for transmitting parasites that cause the deaths of half a million or more people annually.

The World Health Organization has estimated that malaria alone causes 400,000 deaths a year, mostly children, then there is dengue, yellow fever, zika and several other diseases transmitted by the female mosquito when she takes a blood meal. To keep the blood flowing she first injects saliva which contains an anticoagulant. It also contains viruses and microorganisms such as Plasmodium falciparum.

What viruses and parasites are female mosquitoes the vectors for and how do these affect the human population? Female mosquitoes are notorious vectors for several viruses and parasites that significantly impact human health. Here’s an overview of the main pathogens they transmit and their effects on the human population:

1. Malaria
   • Pathogen: Plasmodium parasites (primarily Plasmodium falciparum, P. vivax, P. ovale, and P. malariae)
   • Vector: Anopheles mosquitoes
   • Effect on Humans: Malaria is one of the deadliest diseases transmitted by mosquitoes, causing symptoms like fever, chills, and flu-like illness. Severe cases can lead to anemia, cerebral malaria, and death. Malaria remains a major public health problem, particularly in sub-Saharan Africa, causing over 600,000 deaths annually, most of which are children under five years old.
   
   
2. Dengue Fever
   • Pathogen: Dengue virus (DENV), which has four serotypes (DENV-1 to DENV-4)
   • Vector: Aedes aegypti and Aedes albopictus mosquitoes
   • Effect on Humans: Dengue fever causes high fever, severe headache, pain behind the eyes, joint and muscle pain, and rash. Severe forms, such as dengue hemorrhagic fever and dengue shock syndrome, can be fatal. Dengue is a major cause of illness in tropical and subtropical regions, with an estimated 100 million cases occurring annually.
   
   
3. Zika Virus
   • Pathogen: Zika virus (ZIKV)
   • Vector: Aedes aegypti and Aedes albopictus mosquitoes
   • Effect on Humans: Zika virus usually causes mild symptoms like fever, rash, and joint pain. However, it can cause severe birth defects, particularly microcephaly, when a pregnant woman is infected. Zika outbreaks have occurred in Africa, Southeast Asia, and the Pacific Islands, with the most notable outbreak occurring in Brazil in 2015-2016.
   
   
4. Chikungunya
   • Pathogen: Chikungunya virus (CHIKV)
   • Vector: Aedes aegypti and Aedes albopictus mosquitoes
   • Effect on Humans: Chikungunya causes fever and severe joint pain, often leading to chronic pain that can last for months or even years. The disease is rarely fatal, but it significantly impacts quality of life. It has caused numerous outbreaks in Africa, Asia, and the Americas.
   
   
5. Yellow Fever
   • Pathogen: Yellow fever virus (YFV)
   • Vector: Aedes aegypti mosquitoes
   • Effect on Humans: Yellow fever can range from mild symptoms like fever and muscle pain to severe liver disease with bleeding and jaundice, often leading to death. The disease is endemic in tropical areas of Africa and Central and South America, and despite the availability of a vaccine, it still causes significant mortality in unvaccinated populations.
   
   
6. West Nile Virus
   • Pathogen: West Nile virus (WNV)
   • Vector: Culex species mosquitoes
   • Effect on Humans: West Nile virus can cause a range of symptoms, from mild fever to severe neurological diseases such as encephalitis and meningitis. While most infections are asymptomatic, severe cases can lead to long-term neurological damage or death. The virus is prevalent in Africa, Europe, the Middle East, and the Americas.
   
   
7. Lymphatic Filariasis (Elephantiasis)
   • Pathogen: Wuchereria bancrofti, Brugia malayi, and Brugia timori (parasitic worms)
   • Vector: Culex, Anopheles, and Aedes mosquitoes
   • Effect on Humans: Lymphatic filariasis is a debilitating disease that causes lymphedema (swelling due to lymphatic system blockage), leading to severe disability and social stigma. The condition, known as elephantiasis, causes the enlargement and hardening of limbs and genitals. It affects millions of people, primarily in tropical and subtropical regions.
   
   
8. Rift Valley Fever
   • Pathogen: Rift Valley fever virus (RVFV)
   • Vector: Various mosquito species, including Aedes and Culex
   • Effect on Humans: Rift Valley fever primarily affects animals, but humans can also contract the virus, leading to symptoms like fever, muscle pain, and in severe cases, hemorrhagic fever, encephalitis, or blindness. Outbreaks are often associated with heavy rainfall and flooding, particularly in sub-Saharan Africa.
   
   
9. Japanese Encephalitis
   • Pathogen: Japanese encephalitis virus (JEV)
   • Vector: Culex species mosquitoes
   • Effect on Humans: Japanese encephalitis causes inflammation of the brain, leading to symptoms like fever, headache, vomiting, and neurological symptoms, including seizures and paralysis. It can be fatal or cause permanent neurological damage. The disease is endemic in parts of Asia and the Western Pacific.

Public Health Impact
The diseases transmitted by female mosquitoes have a profound impact on public health worldwide, particularly in tropical and subtropical regions. The economic burden includes the cost of medical treatment, lost productivity, and vector control programs. These diseases also contribute to poverty and hinder economic development in affected regions.

Efforts to combat mosquito-borne diseases include widespread vaccination campaigns (where vaccines are available), distribution of insecticide-treated bed nets, indoor residual spraying, and public health campaigns to reduce mosquito breeding sites. However, the control and eradication of these diseases remain challenging due to factors like insecticide resistance, climate change, and the rapid urbanization of tropical areas.

It is this act of injecting saliva which make the female mosquito such a dangerous insect, together with the fact that it seems to have salivary glands designed to contain the viruses and parasites.

But of course, to be really effective, the female mosquito must first find a victim. How she does this is the subject of a paper by A team led by researchers at the University of California Santa Barbara recently published, open access, in Nature and explained in a UC Sata Barbara News release:

Mosquitoes sense infrared from body heat to help track humans down

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While a mosquito bite is often no more than a temporary bother, in many parts of the world it can be scary. One mosquito species, Aedes aegypti, spreads the viruses that cause over 100,000,000 cases of dengue, yellow fever, Zika and other diseases every year. Another, Anopheles gambiae, spreads the parasite that causes malaria. The World Health Organization estimates that malaria alone causes more than 400,000 deaths every year. Indeed, their capacity to transmit disease has earned mosquitoes the title of deadliest animal.

Male mosquitoes are harmless, but females need blood for egg development. It’s no surprise that there’s over 100 years of rigorous research on how they find their hosts. Over that time, scientists have discovered there is no one single cue that these insects rely on. Instead, they integrate information from many different senses across various distances.

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A team led by researchers at UC Santa Barbara has added another sense to the mosquito’s documented repertoire: infrared detection. Infrared radiation from a source roughly the temperature of human skin doubled the insects’ overall host-seeking behavior when combined with \(\small \ce{CO2}\) and human odor. The mosquitoes overwhelmingly navigated toward this infrared source while host seeking. The researchers also discovered where this infrared detector is located and how it works on a morphological and biochemical level. The results are detailed in the journal Nature.

The mosquito we study, Aedes aegypti, is exceptionally skilled at finding human hosts. This work sheds new light on how they achieve this.

Dr. Nicolas DeBeaubien, co-lead author
Department of Molecular, Cellular, and Developmental Biology
University of California, Santa Barbara, CA, USA.

Guided by thermal infrared

It is well established that mosquitoes like Aedes aegypti use multiple cues to home in on hosts from a distance.

These include \(\small \ce{CO2}\) from our exhaled breath, odors, vision, [convection] heat from our skin, and humidity from our bodies. However, each of these cues have limitations.

Dr. Avinash Chandel, co-lead author
Department of Molecular, Cellular, and Developmental Biology
University of California, Santa Barbara, CA, USA.

The insects have poor vision, and a strong wind or rapid movement of the human host can throw off their tracking of the chemical senses. So the authors wondered if mosquitoes could detect a more reliable directional cue, like infrared radiation.

Within about 10 cm, these insects can detect the heat rising from our skin. And they can directly sense the temperature of our skin once they land. These two senses correspond to two of the three kinds of heat transfer: convection, heat carried away by a medium like air, and conduction, heat via direct touch. But energy from heat can also travel longer distances when converted into electromagnetic waves, generally in the infrared (IR) range of the spectrum. The IR can then heat whatever it hits. Animals like pit vipers can sense thermal IR from warm prey, and the team wondered whether mosquitoes, like Aedes aegypti, could as well.

The researchers put female mosquitoes in a cage and measured their host-seeking activity in two zones. Each zone was exposed to human odors and \(\small \ce{CO2}\) at the same concentration that we exhale. However, only one zone was also exposed to IR from a source at skin temperature. A barrier separated the source from the chamber prevented heat exchange through conduction and convection. They then counted how many mosquitoes began probing as if they were searching for a vein.

Adding thermal IR from a 34º Celcius source (about skin temperature) doubled the insects’ host-seeking activity. This makes infrared radiation a newly documented sense that mosquitoes use to locate us. And the team discovered it remains effective up to about 70 cm (2.5 feet).

What struck me most about this work was just how strong of a cue IR ended up being. Once we got all the parameters just right, the results were undeniably clear.

Dr. Nicolas DeBeaubien.

Previous studies didn’t observe any effect of thermal infrared on mosquito behavior, but senior author Craig Montell suspects this comes down to methodology. An assiduous scientist might try to isolate the effect of thermal IR on insects by only presenting an infrared signal without any other cues. “But any single cue alone doesn’t stimulate host-seeking activity. It’s only in the context of other cues, such as elevated \(\small \ce{CO2}\) and human odor that IR makes a difference,” said Montell, the Duggan and Distinguished Professor of Molecular, Cellular, and Developmental Biology. In fact, his team found the same thing in tests with only IR: infrared alone has no impact.

A trick for sensing infrared

It isn’t possible for mosquitoes to detect thermal infrared radiation the same way they would detect visible light. The energy of IR is far too low to activate the rhodopsin proteins that detect visible light in animal eyes. Electromagnetic radiation with a wavelength longer than about 700 nanometers won’t activate rhodopsin, and IR generated from body heat is around 9,300 nm. In fact, no known protein is activated by radiation with such long wavelengths, Montell said. But there is another way to detect IR.

Consider heat emitted by the sun. The heat is converted into IR, which streams through empty space. When the IR reaches Earth, it hits atoms in the atmosphere, transferring energy and warming the planet. “You have heat converted into electromagnetic waves, which is being converted back into heat,” Montell said. He noted that the IR coming from the sun has a different wavelength from the IR generated by our body heat, since the wavelength depends on the temperature of the source.

The authors thought that perhaps our body heat, which generates IR, might then hit certain neurons in the mosquito, activating them by heating them up. That would enable the mosquitoes to detect the radiation indirectly.

Scientists have known that the tips of a mosquito’s antennae have heat-sensing neurons. And the team discovered that removing these tips eliminated the mosquitoes’ ability to detect IR.

Indeed, another lab found the temperature-sensitive protein, TRPA1, in the end of the antenna. And the UCSB team observed that animals without a functional trpA1 gene, which codes for the protein, couldn’t detect IR.

Pits at the end of the mosquito’s antennae shield the peg-like structures that detect thermal IR.

Photo Credit: deBeaubien and Chandel et al.

The tip of each antenna has peg-in-pit structures that are well adapted to sensing radiation. The pit shields the peg from conductive and convective heat, enabling the highly directional IR radiation to enter and warm up the structure. The mosquito then uses TRPA1 — essentially a temperature sensor — to detect infrared radiation.

Diving into the biochemistry

The activity of the heat-activated TRPA1 channel alone might not fully explain the range over which mosquitoes were able to detect IR. A sensor that exclusively relied on this protein may not be useful at the 70 cm range the team had observed. At this distance there likely isn’t sufficient IR collected by the peg-in-pit structure to heat it enough to activate TRPA1.

Fortunately, Montell’s group thought there might be more sensitive temperature receptors based on their previous work on fruit flies in 2011. They had found a few proteins in the rhodopsin family that were quite sensitive to small increases in temperature. Although rhodopsins were originally thought of exclusively as light detectors, Montell’s group found that certain rhodopsins can be triggered by a variety of stimuli. They discovered that proteins in this group are quite versatile, involved not just in vision, but also in taste and temperature sensing. Upon further investigation, the researchers discovered that two of the 10 rhodopsins found in mosquitoes are expressed in the same antennal neurons as TRPA1.

Knocking out TRPA1 eliminated the mosquito’s sensitivity to IR. But insects with faults in either of the rhodopsins, Op1 or Op2, were unaffected. Even knocking out both the rhodopsins together didn’t entirely eliminate the animal’s sensitivity to IR, although it significantly weakened the sense.

Their results indicated that more intense thermal IR — like what a mosquito would experience at closer range (for example, around 1 foot) — directly activates TRPA1. Meanwhile, Op1 and Op2 can get activated at lower levels of thermal IR, and then indirectly trigger TRPA1. Since our skin temperature is constant, extending the sensitivity of TRPA1 effectively extends the range of the mosquito’s IR sensor to around 2.5 ft.

A tactical advantage

Half the world’s population is at risk for mosquito-borne diseases, and about a billion people get infected every year, Chandel said. What’s more, climate change and worldwide travel have extended the ranges of Aedes aegypti beyond tropical and subtropical countries. These mosquitoes are now present in places in the US where they were never found just a few years ago, including California.

The team’s discovery could provide a way to improve methods for suppressing mosquito populations. For instance, incorporating thermal IR from sources around skin temperature could make mosquito traps more effective. The findings also help explain why loose-fitting clothing is particularly good at preventing bites. Not only does it block the mosquito from reaching our skin, it also allows the IR to dissipate between our skin and the clothing so the mosquitoes cannot detect it.

Loose fitting clothing lets through less IR.

Photo Credit: deBeaubien and Chandel et al.

Despite their diminutive size, mosquitoes are responsible for more human deaths than any other animal. Our research enhances the understanding of how mosquitoes target humans and offers new possibilities for controlling the transmission of mosquito-borne diseases.

Dr. Nicolas DeBeaubien

In addition to the Montell team, Vincent Salgado, formerly at BASF, and his student, Andreas Krumhotz, contributed to this study.

The technical details will tell creationists just how clever their favourite malevolence has been in its mosquito design:

Abstract
Mosquito-borne diseases affect hundreds of millions of people annually and disproportionately impact the developing world^1,2. One mosquito species, Aedes aegypti, is a primary vector of viruses that cause dengue, yellow fever and Zika. The attraction of Ae. aegypti female mosquitos to humans requires integrating multiple cues, including \(\small \ce{CO2}\) from breath, organic odours from skin and visual cues, all sensed at mid and long ranges, and other cues sensed at very close range^3,4,5,6. Here we identify a cue that Ae. aegypti use as part of their sensory arsenal to find humans. We demonstrate that Ae. aegypti sense the infrared (IR) radiation emanating from their targets and use this information in combination with other cues for highly effective mid-range navigation. Detection of thermal IR requires the heat-activated channel TRPA1, which is expressed in neurons at the tip of the antenna. Two opsins are co-expressed with TRPA1 in these neurons and promote the detection of lower IR intensities. We propose that radiant energy causes local heating at the end of the antenna, thereby activating temperature-sensitive receptors in thermosensory neurons. The realization that thermal IR radiation is an outstanding mid-range directional cue expands our understanding as to how mosquitoes are exquisitely effective in locating hosts.

Main
Aedes aegypti is an invasive mosquito species that transmits flaviviruses, impacting a growing proportion of the world’s population^1,2. As female mosquitoes blood feed multiple times, they often shuttle viruses causing diseases ranging from dengue to yellow fever, Zika and chikungunya2. Ae. aegypti integrate multiple sensory cues to locate and navigate towards humans^3,4,5,6 (Fig. 1a). Integration is essential as any single stimulus is inadequate to differentiate humans from other targets. Detection of exhaled \(\small \ce{CO2}\) elevates their locomotor activity and increases their responsiveness to other host-derived stimuli, such as visual cues^3,4,5,6. However, Ae. aegypti has poor visual acuity, limiting its usefulness in discriminating between people and other hosts⁷. Organic olfactory cues are particularly important for finding humans. However, the efficacy of \(\small \ce{CO2}\) and olfactory cues in providing directional information is limited by air-current disturbances that exceed the mosquito’s flight speed, or if the host is moving quickly⁸. When mosquitoes are very close to the skin surface, they detect moisture and convective body heat^4,9.

Fig. 1: Set-up for testing IR radiation as a potential host-associated cue.

a, Known host-associated sensory cues. b, Modes of thermal energy transfer: convection, conduction and IR radiation. The peak emission wavelength (λ^M) of emitting bodies at 34 °C is around 9.4 µm. c, The host-associated cues presented during the assay: human odour, 5% (v/v) \(\small \ce{CO2}\) and heat in the form of IR radiation. Assay cages were 4 cm from the arena wall that housed the Peltier device to mitigate the effect of convective cues. Human odour was applied uniformly on the outside of the mesh of the assay cage from a used nitrile glove. \(\small \ce{CO2}\) was delivered through perforated tubing, which formed a perimeter around both the control and IR zones. d, The Peltier device housing. An IR-transparent polyethylene (PE) film blocked convective cues from reaching the mosquitoes. e, Schematic of the behavioural assay. Mosquitoes were presented with IR and their host-seeking behaviour was video recorded for 5 min. f, Representative video frame taken from an experiment in which females were exposed to human odour and 5% \(\small \ce{CO2}\). One zone was exposed to 34 °C radiant heat from a Peltier device. The Peltier device behind the other zone was off, and equilibrated to the ambient temperature (temp.) (29.5 °C). The position of each host-seeking mosquito was recorded during the experimental window. In all of the experiments in which \(\small \ce{CO2}\) was provided, it was applied using the indicated time series (in seconds) unless otherwise stated. g, The PI, calculated from the indicated formula, using the total number of host-seeking observations in each zone during the 5 min experiment. PI < 0 indicates preference for zone 1; PI > 0 indicates preference for zone 2.

Thermal energy is transferred through conduction, convection and radiation (Fig. 1b). Mosquito attraction to heat depends at least in part on the antenna^10,11. The terminal antennal segment contains neurons that respond to cooling and warming^12,13,14,15. Conduction requires contact and is not useful during host-seeking flight. Convective currents move upwards and are sensed only at distances of less than 10 cm (ref. ¹⁶). Detecting convective heat from hosts at short range is promoted by a general attraction to warmth, and by avoiding both cool and very hot temperatures¹⁷. Elimination of either of two ionotropic receptors from cooling-responsive neurons impairs attraction to convection heat^14,18. Moreover, disruption of the Aedes TRPA1 channel impairs avoidance of very hot temperatures at close range (50−60 °C), but does not impair the responses to surfaces ≤45 °C (ref. ¹⁷). The neurons that depend on TRPA1 for avoiding noxious heat remain to be identified. In Anopheles gambiae, trpA1 is expressed at the antennal tip15, although its thermosensory role is unclear.

Conductive heat requires contact, and convective heat is sensed at close range16. Thus, if mosquitoes sense thermal IR radiation, then surface body temperature could be detected at greater distances, as radiant heat is not limited by the physical constraints of convection and conduction. Thermal IR emitted by humans (~34 °C skin surface) has a peak emission wavelength of around 9.4 μm, with 90% of its energy between 3–30 μm (ref. ¹⁹). This electromagnetic radiation is much lower energy than the ~300–700 nm wavelengths that activate rhodopsins²⁰. Thus, if mosquitoes detect thermal IR, this sensation should not rely on phototransduction.

Few animals are thought to sense IR for navigation or sensing prey. These include rattlesnakes^21,22, certain beetles^23,24, western conifer seed bugs²⁵, kissing bugs and ticks^26,27. By contrast, it has been reported that mosquitoes, including Ae. aegypti, are not attracted to IR^9,28,29 However, in these studies, thermal IR was presented alone rather than in the presence of other host-associated stimuli^9,28,29. Given the importance of multisensory integration in host seeking^3,4,5,6, we wondered whether mosquitoes might exhibit attraction to thermal IR, but only in combination with other host cues.

[…]

Discussion
The finding that thermal IR is an important cue that Ae. aegypti females use to find their targets counters reports that Ae. aegypti do not respond behaviourally to thermal IR^9,28,29. However, previous research examined IR in isolation. Ae. aegypti require multisensory integration to home in on people, and individual human-associated cues, such as IR, \(\small \ce{CO2}\) plumes and organic odours, have little efficacy in stimulating host-seeking behaviour on their own^3,4,5,6. Our finding that IR is used in combination with other cues adds critical breadth to the Aedes toolkit—allowing them to home in on humans from mid-range distance in varied and dynamic environments.

The thermal IR that emanates from surface body temperature is far lower in energy than the longest wavelengths that activate visual pigments²⁰. Rather than detecting photons directly, a more plausible mechanism for thermal IR detection is that the radiant energy warms dendrites in coeloconic sensilla near to the tip of the antenna, which in turn activates thermosensitive receptors. In support of this model, removal of the distal portion of the antenna, which contains heat-sensitive neurons^12,13,15, eliminates IR attraction. While past research reports that the coeloconic sensilla at the distal end of the antenna sense convective heat¹³, the design of the thermosensitive peg-in-pit coeloconic sensilla at the antennal tip is more consistent with a sensor of radiant than of convective heat. Located in a pit, the neurons would be largely protected from convective currents, and would receive radiant heat preferentially from the direction of the pit aperture. Directionality is important for a radiant heat sensor, but would reduce the sensitivity of a convective heat sensor. Nevertheless, at very close range, the neurons in peg-in-pit sensilla would also be activated by convection heat.

We propose that IR impinging on the peg-in-pit sensilla is partially absorbed by the cuticle, and then energy is transferred to the endolymph through conduction. Some IR might also penetrate the cuticle and directly warm the endolymph. We found that the heat-activated TRPA1 channel is expressed in neurons at the antennal tip and is required for responding to IR. By contrast, trpA1 mutants display normal attraction to conductive/convective heat in the temperature range of human skin¹⁷. In the presence of conductive/convective heat, the role for TRPA1 is to help to avoid ≥50 °C conditions (ref. ¹⁷), even though TRPA1 is activated with a threshold of only around 32 °C (ref. ⁴¹). The anatomical location for this close-range TRPA1 function appears to be distinct from IR sensation. Our data support the model that TRPA1 senses IR at mid-range distances (~0.7 m) through the ‘warming neurons’ in the peg-in-pit sensilla.

Two opsins (op1, op2) and trpA1 are co-expressed at the end of the antenna, and mutations eliminating these opsins reduce IR sensation, but only at lower intensities of radiant heat. We propose that contributions of both opsins and TRPA1 to detecting radiant heat endows mosquitoes with a greater dynamic range for sensing radiant heating. We suggest that, at higher IR intensities, the radiant heat is sufficient to directly activate TRPA1, while, at lower levels of thermal IR, activation of the opsins initiates a cascade that amplifies the signal and indirectly activates TRPA1.

In conclusion, thermal IR represents an important mid-range cue that is used by Ae. aegypti to couple longer- and shorter-range cues. As An. stephensi are also attracted to thermal IR, we speculate that detection of the IR may be widely used among blood-feeding mosquitoes to home in on warm-blooded hosts. Finally, the finding that thermal IR is an effective host-seeking cue raises the possibility of developing strategies to interfere with this attraction, and the opportunity to devise more effective mosquito baits (Supplementary Discussion).

Chandel, A., DeBeaubien, N.A., Ganguly, A. et al.
Thermal infrared directs host-seeking behaviour in Aedes aegypti mosquitoes. Nature (2024). https://doi.org/10.1038/s41586-024-07848-5

Copyright: © 2024 The authors.
Published by Springer Nature Ltd. Open access.
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)

Clearly, if we assume for the sake of argument that intelligent [sic] design creationism has any merit, a great deal of design perfection has gone into designing the ways in which mosquitoes find their victims and deliver their cargo of infectious parasites. Just in case any creationists feel tempted to suggest that delivering parasites to warm-blooded animals like humans was not the design purpose of mosquitoes, it should be pointed out that their putative designer is allegedly both omniscient and omnipotent so anything it designs is designed in full knowledge of what it will do and, if in the unlikely event of undesired outcome, scrapping the design and starting again should be well within the designer's capability, so we have to assume any outcome was intentional and the purpose of the design.

And of course, we can dismiss the traditional creationist excuse of 'genetic entropy' causing 'devolution' [sic] as Michael J Behe's excuse for parasites, since the clever design for finding a blood meal is distinctly advantageous for the mosquito and can't possibly be described as 'devolution'.

If we don't assume intelligent design, however, we are left with a mindless evolutionary process with no plan and no intent, malevolent or otherwise. We are left with a full and complete explanation of how and why mosquitoes have these abilities and why they infect us with parasites, so increasing the suffering in the world - there is no benevolent god organising it.

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The Malevolent Designer: Why Nature's God is Not Good

This book presents the reader with multiple examples of why, even if we accept Creationism's putative intelligent designer, any such entity can only be regarded as malevolent, designing ever-more ingenious ways to make life difficult for living things, including humans, for no other reason than the sheer pleasure of doing so. This putative creator has also given other creatures much better things like immune systems, eyesight and ability to regenerate limbs that it could have given to all its creation, including humans, but chose not to. This book will leave creationists with the dilemma of explaining why evolution by natural selection is the only plausible explanation for so many nasty little parasites that doesn't leave their creator looking like an ingenious, sadistic, misanthropic, malevolence finding ever more ways to increase pain and suffering in the world, and not the omnibenevolent, maximally good god that Creationists of all Abrahamic religions believe created everything. As with a previous book by this author, "The Unintelligent Designer: Refuting the Intelligent Design Hoax", this book comprehensively refutes any notion of intelligent design by anything resembling a loving, intelligent and maximally good god. Such evil could not exist in a universe created by such a god. Evil exists, therefore a maximally good, all-knowing, all-loving god does not.

Illustrated by Catherine Webber-Hounslow.

Available in Hardcover, Paperback or ebook for Kindle

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The Unintelligent Designer: Refuting The Intelligent Design Hoax

ID is not a problem for science; rather science is a problem for ID. This book shows why. It exposes the fallacy of Intelligent Design by showing that, when examined in detail, biological systems are anything but intelligently designed. They show no signs of a plan and are quite ludicrously complex for whatever can be described as a purpose. The Intelligent Design movement relies on almost total ignorance of biological science and seemingly limitless credulity in its target marks. Its only real appeal appears to be to those who find science too difficult or too much trouble to learn yet want their opinions to be regarded as at least as important as those of scientists and experts in their fields.

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Malevolent Designer - A Newly-Discovered Fish Parasite

Red lipped Blenny, a tropical marine species in which the researchers discovered the ichthyocolids.

Photo: François Libert

Red-lipped Blenny.

Credit to Matthew Hoelscher.
CC BY-SA 2.0 DEED

Previously uncharacterized parasite uncovered in fish worldwide

Parasites present creationists with an insurmountable problem, especially those who equate the putative designer with the Abrahamic, supposedly omnibenevolent, god of the Bible, Torah and Qur'an.

It is a problem for creationism because there is no way the design of parasites, which appear to have only two functions - Making their hosts sick, so increasing the suffering in the world, and producing more parasites to make more hosts sick - can't possibly be the work of an omnibenevolent designer, and the inevitable resulting arms races between parasite and host are not the act of an intelligent designer.

The traditional explanation offered by creationists, particularly those with only a rudimentary grasp of the subject is to blame 'devolution' [sic] caused by 'genetic entropy' which was made possible by 'Sin' following the mythical 'Fall' as an organism evolves away from some assumed initial perfection at 'creation'. Apart from betraying the religious fundamentalism dressed in a grubby lab coat, that is 'intelligent design' creationism, this is scientifically nonsensical and counter factual, of course.

Covidiot News - How Regular Vaccine Boosters Are Giving Even More Protection.

Health-care workers received the first doses of the COVID-19 vaccine in December 2020. Repeat booster vaccination with updated versions of the vaccine promotes antibodies against a wide range of variants, as well as related coronaviruses.

Repeat COVID-19 vaccinations elicit antibodies that neutralize variants, other viruses – Washington University School of Medicine in St. Louis

A new study has shown that regular boosters of the COVID-19 vaccines against each new variant, give protection against a broad range of variants probably including variants yet to emerge, as well as related viruses.

This was the conclusion of a study by researchers at Washington University School of Medicine in St. Louis. The concern had been that, like the flu vaccines, earlier vaccinations tend to inhibit the formation of newer antibodies, but the study showed that not only are antibodies raised to the new variant but repeated vaccinations 'train' the immune system to produce a broad spectrum of antibodies.

This very welcome news to someone who has just had his 7th booster but still contracted a mild infection at the end of last summer on a trip to France, especially as we're going to Czechia in a few days’ time.

The research findings are the subject of a pre-edited paper in nature which is sadly behind a paywall, so we only have the Abstract. However, the researchers have provided more detail in a Washington University news release:

Malevolent Design - How a Bacterium Carries a Virus That Selectively Kills Male Insects And Only Allows Infected Females To Breed

How does a virus hijack insect sperm to control disease vectors and pests? | Penn State University

Wolbachia are a genus of bacteria that form a symbiotic relationship with about 50% of arthropod species, including insects and spiders but they can also manipulate the species for their own ends (in terms of breeding success). They are aided in this by a virus which is incorporated in their genome which has been shown to join forces with Wolbachia to ensure their own reproductive success in the form of females infected with the virus-bearing Wolbachia.

So completely have Wolbachia integrated with insects that one species of fruit fly has the entire Wolbachia genome incorporated into its own genome, making it, biologically, both bacterium and fruit fly.

One way Wolbachia ensure their own survival at the expense of the species of insect they infect is by making the sperm and egg incompatible if the female is not also a carrier of the right species of Wolbachia. And, to be on the safe side, two proteins produced by the virus break the sperm's DNA so any resulting embryo will be defective and will fail to develop. This ensures that only the females carrying the infection can breed, so increasing the Wolbachia and its virus in the gene pool.

The team who discovered this nasty little virus and how it acts selfishly, was co-led by Professor Seth R. Bordenstein, of the One Health Microbiome Center at Pennsylvania State University. They have published their findings in Science and described it in a Penn State News item.

But first, a little background on Wolbachia:

Creationism in Crisis - How Genomic Imprinting Evolved - Unintelligently

Microscopic fluorescence image of a C.tropicalis mother worm. The worm carries eggs loaded with a toxin (red) which is expressed from a Toxin-Antidote selfish genetic element only when it was maternally inherited.

© Pinelopi Pliota/IMBA

Revealing the evolutionary origin of genomic imprinting 

Caenorhabditis elegans

Genomic imprinting is the process by which genes are suppressed by epigenetic settings that differ depending on whether the genes come from the father or the mother in a sexually-reproducing species.

This is an example of the sort of Heath Robinson machine which a natural, mindless evolutionary process can and does produce and which distinguishes evolved systems from intelligently designed processes. It comes from the fact that multicellular organism uses the same method to replicate their cells as their single-celled ancestors used, yet only need a small selection of the genes depending on how specialised the particular cells are.

But the reason for genomic imprinting involves something even more embarrassing to any creationists who understand it - it probably evolved out of an arms race not between the organism and a foreign parasite but between the organism and one of its genes that had gone rogue and turned into a 'jumping' gene or 'selfish genetic element':

What exactly are 'selfish genetic elements' and what do they do? Selfish genetic elements are DNA sequences that have evolved to enhance their own transmission to the next generation, often at the expense of the organism's overall fitness. These elements can manipulate various cellular and reproductive processes to increase their own propagation within a population, sometimes even if it is detrimental to the host organism.

One well-known example of selfish genetic elements is transposable elements, also known as jumping genes. These DNA sequences have the ability to move or copy themselves within the genome, potentially disrupting genes or regulatory sequences in the process. While transposable elements can sometimes contribute to genetic variation and evolution, they can also cause harmful mutations or genomic instability.

Another example of selfish genetic elements is meiotic drive elements. These elements bias their own transmission during meiosis, the process by which gametes (sperm and eggs) are formed. Meiotic drive can result in the preferential transmission of one allele (variant of a gene) over another, leading to distortions in genetic inheritance patterns within a population.

Selfish genetic elements can have significant implications for evolutionary processes, population genetics, and genome stability. They can influence patterns of genetic diversity, contribute to speciation, and even drive the evolution of complex biological systems. However, they can also pose challenges for organisms by causing genetic disorders or reducing overall reproductive success.

In the case of the nematode, Caenorhabditis elegans, this arms race has produced a truly bizarre result, and something only an unintelligent, mindless designer, or a malevolent designer, could come up with, known as toxic ascaris, or TAs:

Unintelligent Design - The Heath-Robinson Workaround For A Design Fault In The Immune System

A dendritic cell, one of the cells of the innate immune system where cGAS plays a major role.

©EPFL/iStock photos (Design Cells)

The “switch” that keeps the immune system from attacking the body - EPFL

A Machine for Testing Golf Drivers - William Heath-Robinson

A characteristic of designs by creationism's putative intelligent designer, is the needless complexity which often arises because earlier solutions were suboptimal and either didn't work very well or tended to cause problems that needed to be mitigated with another layer of (often suboptimal) complexity.

This is also a characteristic of systems 'designed' by a mindless natural process with no power or mechanism for scrapping a suboptimal design and starting again and no ability to predict the future and design for problems which will arise later.

In fact, what creationists think is evidence of a supreme intelligence, more often seems to resemble the designs of the British cartoonist and eccentric designer, William Heath-Robinson, who was famous for his machines designed to solve every-day problem, which were invariably far more complex than they need have been, and which incorporated everyday objects such as umbrellas, full coal-scuttles for counter-weights, lengths of knotted string and stepladders balanced on upright pianos to give them enough height. Take away any of these unlikely components and the whole machine would fail, in an almost perfect metaphor for how evolution can exapt pre-exiting structures from other processes and structures for novel functions, to give the appearance of irreducible complexity.

And yet they work, or at least look as though they would if anyone ever made one.

An example of a Heath-Robinson machine in mammalian 'design' was revealed by a scientists working at the Swiss École polytechnique fédérale de Lausanne (EPFL), who have discovered how the body prevents the immune system from attacking itself.

But, as the very many auto-immune diseases show, this system is far from perfect and frequently fails, sometime with serious, even fatal, consequences.

But the whole immune system is only needed because something designed pathogens such as bacteria, viruses and other parasites, apparently to attack us and make us sick in the first place. Parasites are a source of conflict for creationists who have to believe both that the putative designer god is the only entity capable of designing living things, and that something else created parasites because their god wouldn't do such a thing, and both that their god is omnipotent, but powerless against that other designer.

So, what is this mechanism the EPFL researchers have discovered?

Their findings are the subject of an open access paper in Nature and is explained in an EPFL news release:

Malevolent Designer News - How Creationism's Divine Malevolence Is Adapting The Avian Flu Virus to Kill Marine Mammals

Dead elephant seals line a beach in Argentina in fall 2023.

Photo: Ralph Vanstreels/UC Davis

Avian Influenza Virus Is Adapting to Spread to Marine Mammals | UC Davis

Elephant seals lie dead on a beach in Argentina following an outbreak of avian influenza in the region.

Photo: Maxi Jonas.

As an example of creationist double-think and intellectual bankruptcy, their attitude toward parasites like viruses is a classic:

• "Only God is capable of designing organisms, so "Look at the trees!" and "What about irreducible complexity?"
• "Something else created parasites like bacteria, worms and viruses, because God wouldn't do something like that!"

Simultaneously committing blasphemy and refuting their own argument from teleology!

I wonder then how that rarest of animals, the intellectually honest creationist copes with the news that the creator of the avian flu virus, H5N1, is in the process of adapting it to kill marine mammals such as elephant seals, just as it adapted the SARS-CoV-2 virus from a bat virus to one that could kill humans and cause economic collapse.

Evidence that it is doing so, if you believe viruses are created and don't evolve naturally, which dogma forbids a creationist from believing, comes in the form of a study by scientists from University of California, Davis, and the National Institute of Agricultural Technology (INTA) in Argentina. The study, the first genomic characterization of H5N1 in marine wildlife on the Atlantic shore of South America, is published in the journal Emerging Infectious Diseases and is described in a UC Davis news release:

Malevolent Designer News - How Creationism's Favourite Sadist May Use Climate Change To Increase The Suffering In The World

Nematode movement

Parasitic worms cause huge economic loss to farmers and can infest humans too.

Temperature, humidity may drive future transmission of parasitic worm infections | Penn State University

Creationists who believe nothing happens unless their invisible magic god wants it to have to have all manner of intellectual gymnastics to avoid giving it credit for all the nasty things to be found in nature, such as parasitic worms.

Their favourite strategy is the old trick of believing two mutually exclusive ideas simultaneously - that only their god is capable of designing living systems, so anything too complex for them to understand must have been created by it, whilst simultaneously believing that all pathogens are created by another entity, called 'Sin', no matter how complex or difficult to understand they may be.

And of course, they are forbidden by dogma to believe in more than one creator and must believe, also by dogma, that that creator is omni-everything - omnibenevolent, omniscient and omnipotent - so they have to believe that whatever its designs do, they were designed to do it, and whatever the future may bring, they were aware of that whilst designing their creations.

What percentage of the surface of Earth is habitable to humans without special equipment? Approximately 29% of the Earth's surface is comprised of land, which is habitable to humans without special equipment. The remaining 71% is covered by water, primarily in the form of oceans, which generally require specialized equipment for prolonged habitation. Therefore, without considering other factors such as climate, terrain, and resources, roughly 29% of Earth's surface is habitable to humans without special equipment.

That means, creationists have no choice but to accept that the results of climate change were part of their designer creator's plan, as was the response of their creations to it. And one of those responses to climate change may be an increase in parasitic worms in parts of the world they have not been prevalent in before.

Many of these worms are, or have been, confined to the tropics and sub-tropical zones, and the northern and southern part of the world, where most advanced economies are based, have been relatively free from them. But, as Earth gets warmer, the 'habitable zone' for parasitic worms expands to incorporate more of the advanced economies, but the habitable zone for humans shrinks even further.

This is the prediction of a team of researchers from the Center for Infectious Disease Dynamics and Department of Biology, The Pennsylvania State University (PennState), Pennsylvania, USA, and Dipartimento di Elettronica, Informazione e Bioingegneria, Politecnico di Milano, Milano, Italy, led by Professor Isabella Cattadori and Dr. Chiara Vanalli of PennState, who have just published their findings, open access, in the journal Ecology Letters. Their work is explained in a PennState news release:

Malevolent Designer News - How Bacterial Pathogens Are Cleverly Designed to Invade Their Victim's Body

The exceptional secretion mechanism of Tc Toxins.

MPI MOPH

Functional model for Yen-Tc toxicity. Following ingestion of the Tc, it is likely that the surface-bound chitinases bind to and/or degrade the chitin-rich peritrophic membrane of the insect midgut. Cell surface recognition is likely facilitated by motifs within the A subunits prior to internalization. Similarities to the well characterized bacterial binary toxin systems (e.g., anthrax, cholera, diphtheria) suggest a mechanism involving receptor-mediated endocytosis followed by pore formation and translocation of the B and/or C components into the cytosol (I), although alternative mechanisms (e.g., II, III) cannot be ruled out.

Landsberg, MJ., Jones, SA., Rothnagel R., et al (2011)

24-01-18 | Max Planck Institute of Molecular Physiology

Imagine you're in charge of an invading army laying siege to your enemy's outer defences. How do you neutralise them?

One way would be to send a small group of soldiers, packed with high explosives and deadly toxins on a kamikaze mission into the defences, with instructions to detonate their explosives and so spread the toxins when inside to destroy the defences and kill the defenders. You could improve on that by removing any temptation the suicide bombers might have to not detonate their defences by automating the trigger to fire as soon as they encountered the defender.

That's exactly what a team at the Max Planck Institute for Molecular Physiology (MPI MOPH), Dortmund, Germany, have found bacteria use to gain access to their victim’s body and make their hosts sick and die. The team, led by Stefan Raunser, Director of MPI MOPH, have published their findings, open access, in Nature Microbiology. Their work is described in a MPI MOPH press release:

Creationism in Crisis - When Creationists Believe The Universe Was Being Made From Nothing, People Were Chewing Gum and Eating Trout, Deer And Nuts In Scandinavia

Photo from the excavation site Huseby Klev at the Swedish west coast.

Photo: Bengt Nordquist

The plastelina casts for one of the chewing gums from Huseby Klev. The cast captures the teeth imprints from each side.

Photo: Verner Alexandersen.

Ancient chewing gum reveals stone age diet - Stockholm University

How could the Bible's authors possibly have known what people were doing in Scandinavia when they didn’t even know where Scandinavia was because they thought Earth was a small flat place with a dome over it to keep the water above the sky out, centred on the Middle East?

The answer is that they couldn't of course. Had they done so, they would have concocted much less parochial tales about the things they didn't understand and would have known that Earth was much older than the few thousand years they imagined.

But now we know much better than they did. For example, modern science is able to take the resin people were chewing on (probably to make glue from it) and analyse the DNA in it to see what they had been eating and what organisms they had living in their mouths. It turns out that just about the time when the Bible's authors were setting their creation tale, people in Scandinavia were eating trout, deer and hazelnuts, and suffering from pathogenic bacteria, oblivious of the creation allegedly going on far away in the Canaanite Hills.

Although creationists now tell us that pathogens and other parasites didn't exist before the supposed 'Fall' and must have been made since by a thing called 'Sin', there is no biblical support for this modern invention which has been hurriedly cobbled together to defend the alleged creator god from the charge of malevolence in the design of pathogens which do nothing other than make more copies of themselves and add to the suffering in the world.

Embarrassingly for those creationist apologists, the same study presents compelling evidence of commensal and pathogenic organisms in the mouths of these Scandinavians, just as there are today in modern humans, including bacteria that cause teeth to fall out.

How scientists discovered this is the subject of an open access paper in Scientific Reports and a news release from Stockholm University:

Unintelligent Design - Another Ludicrously Complex Arms Race, This Time Between Plants And A Predatory Fungus

Gray Mold, Botrytis cinerea, on green tomatoes

Discovery: plants use “trojan horse” to fight mold invasions | News Running epigenetics a close second for the most obvious evidence on unintelligent design in nature is the ubiquitous arms race; Arms races are a major component of evolutionary biology, easily understandable in terms of evolution by natural selection. One organism (call it Organism A) predates on, or parasitises another (call it Organism B); this creates an advantage for Organism B in avoiding being eaten of serving as the host of Organism A, so any functional defense mechanism is selected for by natural selection. This in turn creates an advantage for Organism A to evolve a mechanism for overcoming Organism B's defences, and so on until a state of equilibrium is achieved in which either one or the other organism is no longer able to evolve further.

This can lead to some extreme adaptations such as the stupidly long neck and legs of the giraffe which is a response to acacia trees evolving longer trunks to place their leaves, flowers and seeds beyond the reach of giraffes. In the process, acacia trees need to produce masses of cellulose to build the trunk and pump water much higher against gravity than if they were low-growing bushes, and giraffes have to maintain a very high blood pressure to keep their brain supplied with oxygen while drinking water places them at risk of predation by lions because they can't stand up and raise their heads quickly or they will lose consciousness. And they need the additional complexity of special valves in their neck veins to maintain a high blood pressure to their brain.

Now, take away acacia trees (imagine a sudden virus that wipes them out) and the giraffe is no longer superbly adapted for its environment; instead, it is severely handicapped, and might even find feeding from an alternative source difficult.

Another arms race can be seen at the moment is where the SARS-CoV-2 virus is evolving new variants every few months in response to growing herd immunity in its hosts, the human population, due to vaccinations and sub-lethal infections. The virus is getting better at evading our antibodies for long enough for us to pass on the infection to someone else and is tending to be less lethal, so we survive to infect others, even being asymptomatic. Gradually the virus will evolve to become a relatively mild infection that most of us will catch as often as we catch the common cold, and only especially vulnerable people will be made seriously ill by it.

These are just two examples of hundreds of similar arms races in nature; there are even arms races between sexes of the same species as females evolve strategies to retain the ability to only mate with a male of her choice, while males evolve strategies to deprive her of that ability.

But how on Earth can this be explained in terms of design by a single designer, or, including the creationists fallback excuse for parasites, two designers - their supposedly omnipotent, omniscient god and 'Sin'? Would not an omnipotent, omniscient god know in advance what Sin's next response would be and create a design that it couldn't overcome, so an arms race never started in the first place? Or are we to believe that creationism’s god and this 'Sin' thing are equal in all things yet able to conceal their next move from something all-knowing, but powerless to stop its rival? In other words, neither omniscient nor omnipotent.

The notion of intelligent design is quite simply incompatible with the evidence of arms races, for which evolution provides a ready answer.

I have devoted the whole of chapter 3 to arms races in nature in my popular, illustrated book, The Unintelligent Designer: Refuting The Intelligent Design Hoax, but what it doesn't include is this recently discovered arms race between plants and a parasitic fungus, Botrytis cinerea, or gray mold.