‘The idea of using a form of poison which could not possibly be discovered by any chemical test was just such a one as would occur to a clever and ruthless man who had had an Eastern training. The rapidity with which such a poison would take effect would also, from his point of view, be an advantage. It would be a sharp-eyed coroner, indeed, who could distinguish the two little dark punctures which would show where the poison fangs had done their work.’
Sherlock Holmes, in Arthur Conan Doyle, The Speckled Band
Primo Levi was taken with the way an insect “in a brain weighing the fraction of a milligram . . . can store the crafts of the weaver, the ceramicist, the miner, the murderer by poison, the trapper and the wet nurse.” Harm is done automatically, and the venomous animals have no need to think, because venom is generated at the molecular level.
Almost every group of animals, other than the birds, has at least one member that carries a venom. The male platypus is the only mammal, and the Gila monster may be the only lizard, but the rest of the animal kingdom is scattered with individuals with a poisonous defense. The Crown of Thorns starfish, cone shells, the cane toad, and a Brazilian caterpillar, Lonomia obliqua, deadlier than most snakes, are all out there, along with many others.
The Oxford English Dictionary lists three interesting words—well, it lists many, but three that are germane to this book: toxicomania, a morbid craving for poisons, and toxiphobia or toxicophobia, both meaning “a fear of poisons.” As a rule, toxicomanes are rare, if only because they tend to disappear soon after discovery, but toxicophobes last rather longer.
Australia, regarded by many of the fearful as the home of fearsome animals, sees 1,800 road deaths a year, 120 knife and 60 gun deaths, four from snakes, two each from bees, sharks, and lightning, one from crocodile attack, and none from spider bites. Of course, before antivenoms were developed, there were many more poison deaths, but snakes have traditionally fascinated. In the nineteenth century, the rattlesnake captured the morbid imagination of Americans, but there are now about 12 snake deaths each year in the United States.
Exotic Indian snakes such as the one Holmes refers to in The Speckled Band sent frissons of fear down the spines of nineteenth-century Britons. Their fear was helped along by the writings of men like Sir Joseph Fayrer (1824–1907), who made a long and patient study of poisonous animals in India. A snippet caught my eye, a report in The Lancet, December 17, 1870, of 11,416 cases of snakebite, including “6,645 in Bengal, Assam and Orissa, 1,995 in the NW Provinces, 755 in the Punjab, and 1,205 in Oude.” “Dr. Fayrer thinks there must be 20,000 deaths annually in the whole of Hindoostan.”
Fayrer began as a naval surgeon, studying with T. H. Huxley, and probably met Edward Pritchard at this time, as both were attached at least nominally to HMS Victory, but by 1850, Fayrer was serving in Bengal. By 1859, he was professor of surgery at the Medical College of Calcutta, and he accompanied the then Prince of Wales on a tour of India. His Thanatophidia of India (1872, 1874) was cited by Charles Darwin when he wrote on venoms and their effects on the carnivorous sundew plant, Drosera. Sadly, according to Holmes scholars, Conan Doyle seems not to have consulted Fayrer’s work, so the snake in The Speckled Band does not appear to be a recognizable species.
It was Fayrer who persuaded Huxley to join the Royal Navy, setting him on the path that would bring him to Australia with John MacGillivray (appropriately, they sailed on HMS Rattlesnake), where he met the future Mrs. Huxley, with whom he would found a famous dynasty, while gaining fame as Darwin’s bulldog and countering the venom of the lowbrow divines who were appalled by the awful ideas of evolution that Darwin was putting about. In 1866, Fayrer invited Huxley to India to explore linguistics with him, but Huxley declined and Fayrer turned to poisonous snakes in a work “illustrated in colour by Hindu artists,” and made generations of British even more fearful of snakes.
Readers of Kipling’s Rikki Tikki Tavi, or of Herford’s poem “The Mongoos,” would know at least one way to be secure from snakes: keep a mongoose. Of course, any number of islands have suffered ecological damage from the mongoose, but it is certainly effective at killing snakes when there are no endangered bird species to chomp, and this raises the question: how does the mongoose manage against the snake?
Snake venom varies, but as a rule it contains one of those poisons that interferes with acetylcholine, like Botox or nerve gases. Snakes have a differently shaped acetylcholine receptor, and so, it turns out, does the mongoose.
Snakes’ venom does not protect them from all predators, however, and monitor lizards are partial to the occasional meal of snake. A monitor’s presence was usually a good early warning sign of the presence of a more unwelcome reptile. Horatio, Lord Nelson, had one such encounter on his travels.
He had ordered his hammock to be slung under some trees, being excessively fatigued, and was sleeping, when a monitory lizard passed across his face. The Indians happily observed the reptile; and knowing what it indicated, awoke him. He started up, and found one of the deadliest serpents of the country coiled up at his feet. He suffered from poison of another kind; for drinking at a spring in which some boughs of the manchineel had been thrown, the effects were so severe as, in the opinion of some of his friends, to inflict a lasting injury upon his constitution.
Robert Southey, The Life of Horatio Lord Nelson, 1813
The manchineel, or mancanilla (Hippomane mancinella), claimed many unsuspecting victims. Basil Ringrose was a buccaneer in the Caribbean, and he wrote in his journal of an incident on the island of Cayboa in the Gulf of Panama in 1679. “I was washing myself, and standing under a mancanilla tree, a small shower of rain happened to fall on the tree and from thence dropped upon my skin. These drops caused me to break out all over my body into red spots, of which I was not well for the space of a week after.”
The mancanilla is a tree reaching some 40 to 50 feet, mostly found on sandy seashores in South America, Venezuela, Panama, and the islands of the West Indies. Merely sleeping in its shade was said to be enough to kill, perhaps in the way Ringrose described. Five years later, John Esquemeling mentions the death of another and less lucky buccaneer, William Stephens: “It was commonly believed that he poisoned himself with man-canilla in Golfo Dulce, for he had never been in health since that time.”
It was not just the strange trees and animals that travelers had to learn about the hard way, many times over. There was always the risk that food known to be innocuous in one place may not be so in another. Xenophon describes an unfortunate experience he and his troops shared when they tried honey that the industrious local bees had made from Azalea pontica:
Here, generally speaking, there was nothing to excite their wonderment, but the numbers of bee-hives were indeed astonishing, and so were certain properties of the honey. The effect upon the soldiers who tasted the combs was, that they all went for the nonce quite off their heads, and suffered from vomiting and diarrhoea, with a total inability to stand steady on their legs. A small dose produced a condition not unlike violent drunkenness, a large one an attack very like a fit of madness, and some dropped down, apparently at death’s door. So they lay, hundreds of them, as if there had been a great defeat, a prey to the cruellest despondency. But the next day, none had died; and almost at the same hour of the day at which they had eaten they recovered their senses, and on the third or fourth day got on their legs again like convalescents after a severe course of medical treatment.
Xenophon, Anabasis, c. 360 BC
Forewarned is forearmed, but sometimes experienced advice was ignored. In this account, the almiranta is the second ship of a fleet, the capitana the flagship.
There was in the almiranta an honest sailor called Saabedra, very experienced in the coast of Havannah and New Spain who said to Luis Baes and to me ‘Notice Gentlemen that much of this fish is jaundiced, namely that which has black teeth, and it is pure poison, do not eat it but throw it into the sea and only eat that which has white teeth;’ this was done and having cleaned out some of those with black teeth they were eaten by two cats and two young pigs and they all died within two days. They gave this advice at once to the people of the capitana, but they called us gluttons, as if we wanted them for ourselves.
Pedro Fernandez de Quiros, The Discovery of Australia, 1607
De Quiros goes on to explain how the seamen on the capitana ate the poisonous fish, then sent a boat at midnight, calling for priest and surgeon,
. . . for all the men were prostrate on the upper deck, asking for confession because they were dying. They went and did their duty and the surgeon took a jar of oil and gave it to the sick to drink and they vomited the food. The remedy was opportune for if they had delayed it would have done the same as to the cats and pigs; this poison closes the ducts of the faeces and urine and at once produces dementia, and there were some who did not come to themselves for more than a fortnight.
Pedro Fernandez de Quiros, The Discovery of Australia, 1607
Poison from fish, and from seafood in general, is a major topic, and one where ideas are changing all the time. Take, for example, the puffer fish, with its poison known as tetrodotoxin (TTX). This is a potent neurotoxin. In technical terms, it blocks voltage-gated sodium channels on the surface of a cell membrane. The molecule mimics the hydrated sodium ion, enters the gate, and binds to it. A hydrated sodium ion lets go in nanoseconds, while TTX holds on for tens of seconds. It has the same organizational effect as jamming elephants in all the gateways of a football stadium.
The TTX effectively blocks all sodium movement, and a single milligram is enough to kill an adult human. Tetrodotoxin is exquisitely well-designed. The molecule fits very exactly, and binds to no less than six sites on the sodium ion channel. Treatment normally comes down to artificial respiration and gastric lavage with activated charcoal.
TTX is a highly efficient killer and strangely spread among living things. A number of fish—Fugu, Tetraodon, Arothron, Chelonodon, and Takifugu—all store TTX and related analog in their tissues, but TTX turns up also in the blue-ringed octopus, seastars, crabs, marine snails and molluscs, flatworms, ribbon-worms, and even marine algae. On land, some frogs, newts, and salamanders carry the same venom.
The scattered distribution of such a perfect killer molecule in unrelated groups of living things says something to biologists. It goes against all probability that such a diverse group of animals (and even algae) could have evolved the same poison. What is far more likely is that some smaller organism, down at the bottom of the food chain, makes the toxin, which others collect; a theory supported by the fact that puffer fish grown in culture do not contain TTX until they are given tissue from a TTX-producing fish to eat.
A single-point mutation in the sodium ion channel is enough to make the puffer fish immune to TTX. The mutation clearly does not affect the operation of the channel too much, but it makes the fish immune to something that up until then had poisoned its environment. Current thinking identifies the culprits making the toxin as bacteria or something of a bacterial size range.
There are other small poisoners in the sea aside from the mysterious sources of TTX. Filter-feeding bivalves survive by straining tiny plankton from the sea as it washes past them. When there is an algal bloom, the bivalves can take on significant loads of whatever toxins the plankton happen to be carrying. These toxins are not a great problem for the bivalves, however, since they have eons of evolutionary filtering behind them. In fact, the toxins can be a definite advantage, because casual shellfish eaters such as humans do not have the same immunity.
Shellfish poisoning takes several forms: paralytic shellfish poisoning is self-explanatory, and, as you might expect, the toxins work by binding to sodium channels in nerves. Interestingly, the target sites are the same as for TTX. The diarrheic form is triggered by toxins from dinoflagellates, and it usually sets in within 30 minutes, causing cramps, chills, nausea, and diarrhea. It appears to be nonfatal, although the toxins may cause stomach tumors in the longer term. Then there is amnesic shellfish poisoning caused by domoic acid, a toxin from diatoms that can also be found in fish and crabs in some localities. In this case, the memory loss that gives this form of poisoning its name can last up to several years.
Dinoflagellate toxin can be found in many shapes, sizes, and species. Ciguatoxin, for example, is a secondary reason for avoiding moray eels whenever possible: apart from their bite, their flesh is loaded with this poison. Just a few years ago, nobody knew where the toxin came from. Some fishermen believed it developed in the intestines of fish that were not processed immediately, but fish that had been frozen immediately after they left the water were still found to be toxic. Another theory suggests the ciguatoxic fish became toxic by eating puffer fish, but cigua-toxin and tetrodotoxin are quite different.
It is now generally held that a single-celled organism, a dinoflagellate called Gambierdiscus toxicus, puts the toxin into circulation through the food chain. In 2001, after ten years of work by more than 100 researchers, the full chemical process of ciguatoxin synthesis, all 90 steps of it, was completed, a process that, in passing, was laid at the door of this tiny organism. Ciguatoxin claims 20,000 victims each year, and the toxin is known from more than 400 fish. The distribution of the toxin can be surprisingly patchy, with ciguatoxic fish sometimes coming from one side of a small island, but not the other.
A poisoned food chain lay behind a peculiar disease found only on the island of Guam, east of the Philippines, halfway between Japan and Australia. In the early 1950s, the local population was suddenly struck with a form of amyotrophic lateral sclerosis (ALS), or Lou Gehrig’s disease, at a rate roughly 100 times the global average. The symptoms included paralysis, tremors, and rigidity, similar to parkinsonism, and an Alzheimer-like dementia, so the condition was dubbed parkinsonism-dementia complex (PDC) or ALS-PDC. There was no single standard form of the condition, and no two cases were the same.
The local Chamorro population called the disease lytico-bodig, lytico being paralysis, and bodig parkinsonism. In recent times, lytico-bodig has been dying out, threatening to disappear before a cause could be identified. Once more, an unexplained disease might disappear, only to lie low and break forth again, perhaps in a more dangerous form, somewhere else. More importantly, lytico-bodig might hold some of the clues that would allow medical workers to unravel the secrets of Parkinson’s disease and other similar conditions.
A neurotoxin in the food supply was the main suspect, because the disease affected only Chamorros. Cycad seeds were the most likely source of the neurotoxin. In the traditional Chamorro diet, the seeds of Cycas sp.,* a tree native to Guam, are ground into flour called fadang or federico. The Chamorros are well aware of the toxicity of the seeds and rinse the flour several times before cooking it. The washing is an old practice, and Oliver Sacks found a reference to it in the works of Louis de Freycinet, a French explorer who called in at Guam in 1819. By all reports, fadang is delicious, but why was lytico-bodig only a problem among the Chamorro of Guam, and even then, only among the traditional people of Umatac?
* The use above of “Cycas sp.” is deliberate: what was once Cycas circinalis is now known as Cycas micronesica in the Cycas rumphii complex, and all three names may be encountered in a single document.
Guam is part of Micronesia, a region of the Pacific where people from different islands are immediately recognizable. This is a consequence of most populations originating in small bands, together with later rises and falls in numbers. These genetic distillations, known technically as the “founder” and “bottleneck” effects, can produce populations where large numbers of members share rare genes. In this part of the world, therefore, it is quite possible lytico-bodig could be inherited in some similar genetic mischance, but there was still a nagging suspicion that the cycads were somehow involved. Straight genetics could be ruled out, as it seemed to be only the elderly who were developing the disease. This was another puzzle: as the old sufferers died out, they were not being replaced by younger victims—almost nobody born after 1960 developed lytico-bodig. Over time, mineral deficiencies and parasites were ruled out, leaving neurotoxins as the prime suspects, but working out how these poisons entered the diet took a little longer.
Hunting is part of the Micronesian culture, and a wander in the rainforest or the mangroves on any island is all too often accompanied by the crack of rifles. At the end of the Japanese occupation, after World War II, America took over and the area became known officially as the Caroline Islands. Rifles were readily available, and far more efficient than the snares the Chamorros had previously used to catch food. Prized delicacies such as fruit bats were now available at the squeeze of a trigger. Until, that is, the bats were almost entirely shot out. One of Guam’s two bat species vanished by the mid-1970s; the other dwindled to fewer than 100 individuals, and Guam bats were taken off the menu.
People were still eating bats, but now they were imported from Samoa, and as the local bats grew scarcer, so did cases of lytico-bodig. Conclusion: there was something in the local bats where occasional eating caused no real harm but the more often they appeared on the menu, the more people got sick. Whatever it was, the bats from Samoa did not have it—and Samoa is cycad-free.
So now it appears the mystery disease was a simple case of poisoning, but that still leaves the problem of identifying the toxin that the Guam bats held in their flesh. It may well have come from the cycads, but the bats would have to be bioaccumulating or building up its levels in their bodies. The most likely suspect is a known neurotoxin, cycasin, but it is water-soluble and so unlikely to accumulate in the bats’ tissues. Whatever it was, the unfortunate bats of Guam may have left a spiteful legacy to their predators. It was just the bats’ bad luck that the legacy was not associated with a warning color or bitter taste that might have educated the predators sooner.
Roger Ascham called his 1545 treatise on archery Toxophily, meaning “the love of archery.” The similarity between tox-ophily and toxic is not mere chance, and the overlap starts with the Greek word, toxon, meaning “bow,” from which we got toxicon, “having to do with the bow,” in the form of toxicon pharmakon, poison for putting on arrows.
Hunters throughout the ages have taken a leaf out of nature’s book and used poison as a weapon, because their prey would remain maddeningly out of reach of conventional weapons. All too often a tasty meal would last be seen scampering up a trunk and out onto a slim branch, where it could snigger derisively at its pursuers. A pursuer who had a poison dart or a poison arrow, however, only needed to wing his target, then wait for it to fall off that safe branch and into range of a big stick.
The only drawback for the hunters was the risk that some of the poison might remain in the meat, but, with luck, the poison’s effect was in some way reduced in passing through the animal or in cooking, or maybe the toxin was less poisonous when swallowed.
As well as worrying about the food their local guides provided for them, travelers and explorers always feared these locals using poison weapons against them. William Dampier sailed the northern coast of Australia in the late seventeenth century, and wrote in 1699: “My young man, who had been struck through the cheek by one of their lances, was afraid it had been poisoned, but I did not think that likely. His wound was very painful to him, being made with a blunt weapon; but he soon recovered of it.” Sir Joseph Banks, some 70 years later, had much the same fears on Australia’s east coast. Here he describes, in his usual eccentric spelling, how they came on an Aboriginal camp, and how it was looted:
We however thought it no improper measure to take away with us all the lances which we could find about the houses, amounting in number to forty or fifty. They were of various lenghs, from 15 to 6 feet in lengh; both those which were thrown at us and all we found except one had 4 prongs headed with very sharp fish bones, which were besmeard with a greenish colourd gum that at first gave me some suspicions of Poison. . . . Upon examining the lances we had taken from them we found that the very most of them had been usd in striking fish, at least we concluded so from sea weed which was found stuck in among the four prongs.
Sir Joseph Banks, Journal, 1770
There was, however, one part of the world where deadly poisons were indeed used as a regular thing by hunters, and this was South America, though the story of how Europeans discovered this is a little convoluted. Certain French scientists, perhaps more out of bloody-mindedness than any exercise of logic, argued that the Earth was like a rugby football on its end, as opposed to the logical English view, put forward by Isaac Newton, of our world as an oblate spheroid, a bit like a sat-upon and under-inflated soccer ball.
Newton’s model arose from careful analytical thought, but the French were determined to prove their theorem. To do this, they needed to measure a degree of latitude as far north as possible, and again as close to the equator as possible, so two expeditions were sent forth. One went to Lapland, and had some creditable scientists among it who did creditable things, but the one that went to South America was a mixed bunch, and some of them did incredible things. One such was Charles-Marie de la Condamine, who would spend ten years in South America in all.
During this time, Condamine saw tribesmen using blowpipes to hunt, and inspected and analyzed the poisoned arrows, reporting that the poison was “so active that, when it is fresh, it will kill in less than a minute, any animal whose blood it entered.” This was curare, and, in another time, its discovery might have changed warfare. As it was, Condamine made a more influential discovery for warriors, one that provided quiet boots and excellent non-slip knife handles for commandos, suits for frogmen and tires for motor transport. In short, he discovered caoutchouc, as he named it, but it was given a more practical English name by Joseph Priestley. Based on its use to rub pencil marks off paper, he called it rubber. Curare came back from South America to Europe at the same time. Eventually, it would be used in medicine, even as the Amazonian hunters continued using it for its original purpose. It was left out of the armory, however, because there were much better poisons to use in war.
Many of the indigenous hunters around the world used stupefiers, a practice that is now being used to devastating effect by modern-day hunters seeking live fish for the gourmet seafood trade. They squirt cyanide into a coral reef in order to stupefy fish and catch them alive, but the poison hits more than the fish. Slowly, piece by piece, the reef is killed by this sort of “hunting.” The original users of this method would only have used stupefiers to stun the fish in a stream, without any lasting harm to the ecosystem.
A “hunting and gathering” poison from the rainforest can now be found in the suburban garden as a pesticide. In Central and South America, rotenone, in the form of extracts of the ground-up root of Jamaica dogwood (Piscidia erythrina) and other plants, has been widely used to poison fish. Rotenone kills insects as well, and it has been used in agriculture to control lice, fleas, and assorted larvae. It seemed to be safe when swallowed by birds and mammals, and it has even shown some interesting anti-cancer effects.
Problems can arise when it is sprayed, however, because inhalation of rotenone is by no means the same thing as swallowing it. The digestive tract is much more ferocious to chemicals than the lining of the lungs, which may usher the offensive molecules gently into the bloodstream, unchanged. Recently, when rats were regularly injected with rotenone over a period of some weeks, they developed symptoms resembling those of Parkinson’s disease, including difficulty in walking and shakiness of the extremities—and their brain cells showed some protein deposits. It remains to be seen whether this means rotenone is more dangerous than we thought, or whether it simply causes rats to mimic parkinsonism, but there is every chance this discovery may be a boon to medical researchers if it gives them a way of inducing the symptoms they seek to cure.
The use of poisons to catch things remains normal practice for entomologists, although they are not so concerned with their catch being alive. They will sometimes spread sheets under a rainforest tree, for example, and fog it with insecticide, so thousands of dead insects rain down, adding a little more to our knowledge of the many species that are being endangered as the rainforests disappear. I intend no irony here: the lost insects will soon be replaced by others of their species in other trees, and there is really no other way to know what species are there, other than by dislodging them.
The world’s rainforests are dying in many ways: in some parts of the Amazon basin, the main cause is road-building for the benefit of hunters of gold, one of the few metals that seems to be entirely nonpoisonous. The yellow metal is almost inert, but of the two most common methods of extracting it from the environment, one uses cyanide while the second uses mercury. Both poison rivers in rainforests and elsewhere.
The gold miners who use mercury rely on the process of amalgamation, in its original meaning, where other solid metals are dissolved into liquid mercury. When the amalgam is later heated, the mercury evaporates, leaving behind the gold or other absorbed metal. In theory, all of the evaporated mercury is condensed and recovered—in reality, mercury escapes into the ecosystem at every stage in the process.
If gold seems to be nontoxic, the same cannot be said for silver, and there is even a name for the condition it causes. “Argyria” is a blue-black deposit of silver in the skin that can be localized in areas where repeated contact is made with silver dust or silver salts. Occasionally, silver can be inhaled, but however absorbed, it often ends up in the eye as a gray-blue layer of silver sulfide, or as the aforementioned skin discoloration. Either way, once it gets in, it does not get out again. These days, the most spectacular cases are seen in people taking “colloidal silver” as an alternative medicine. Other victims make silver nitrate or silver decorative objects, or engage in silver mining and plating.
As we saw in the Guam bats, animals can also acquire poisons, and monarch butterflies have a well-known trick of eating milkweed, Asclepia syriaca, which is full of cardiac glycosides. The monarchs can tolerate this, but the bluejays that might otherwise eat them find the butterflies repulsive, on account of the diet they chose as caterpillars.
Cardiac glycosides are found in oleanders and foxgloves, and they include the useful drug digitalis. These are classed as carde-nolides, but there is another subclass known as bufadienolides. This class can be found in a number of South African plants, like the Cape honey flower (Melianthus comosus) and Cape tulips (Homeria spp.) and also the mother-of-millions (Bryophyllum spp. ), introduced to Australia from southern and eastern Africa and Madagascar.
While poisons often teach us stern lessons, we can still be slow to learn. Even though Bryophyllum became a noxious weed in Australia and poisoned livestock over large areas, it is commerically available in the United States and Canada as an ornamental plant, despite being recognized as invasive. It can only be a matter of time before it causes problems. The plant kills grazing stock, pulling it out of the ground doesn’t kill it, and burning it releases toxic fumes.
And then there is the scarlet-bodied wasp moth of Florida. These moths take nine hours to mate, and during this time, the entangled couple would make a tasty morsel for a bat or spider, which probably accounts for the male moth’s ploy of dining healthily on the poisonous dogfennel plant before mating. Actually, he doesn’t so much dine as vomit on the plant, dissolving the fibers into a nice toxic soup that he absorbs into a pouch on his front. Now he is safe from predators, but his mate is not.
Picture a Lepidopteran Lothario, tanked up with toxic juice and in search of a mate. Soon, he finds one, but before the serious business starts, he showers her with toxins that she, in turn, later passes on to the eggs, thus protecting the next generation as well. No spider or bat wants to know about such a toxin-spattered morsel.
Toxins can play another role in mating, one that shows the strange logic that sometimes applies in the evolutionary game, where anything goes, as long as it results in more offspring. Fruitfly semen contains chemicals, some similar to spider toxin, that induce egg production in females and delay subsequent mating with another male. The effect of this is to make it more likely that a given mating will produce fertilized eggs with the toxic male’s genes.
There is just one minor snag: the chemicals also reduce the female fruitfly’s life span. But as long as she has laid his eggs by the time she dies (and she will have), the male has no concerns about her shorter life. There has even been an elegant experiment, where females and males are bred monogamously for a few generations and, by simple selection, the semen ceases to be toxic. The male’s genes get an advantage from toxic semen in a promiscuous situation, but in monogamy the male with non-toxic semen produces more offspring from his single female. Under those conditions, the cost of the toxic semen outweighs the advantage it confers.
You could be excused from thinking that very little in the natural world could be smaller or more lethal to its recipient than toxic fruitfly semen, but the world’s best poisoners are very, very, very small. There is no place to hide from these poisoners.