The saga of killer bees began about 60 years ago. The honey bees originally imported into Brazil from Europe performed poorly in the Brazilian tropical and subtropical environment. The bees produced little honey and were plagued with diseases, predators, and poor survival. In response, the government commissioned Dr. Warwick Kerr, known as “Varvique” to his colleagues and friends, to import some bees more suitable to the Brazilian climate. Kerr, a distinguished and talented bee scientist and geneticist, who is still active at age 92, did just that. He brought in and established in hives 48 queen African honey bees from the area around Pretoria, South Africa, and Tanzania, areas similar to parts of Brazil. They performed well in Brazil. While Kerr was away from the apiary one weekend, a visiting scientist opened the hive entrances, allowing 26 reproductive swarms to escape into the countryside. They thrived and reproduced vigorously in the wild. And they were wild, especially wild in their strong defensive attacks toward predators, people, pets, and livestock. Once liberated, the descendants of this original African bee stock began their rapid territorial expansion and arrived in south Texas in 1990. Throughout this trip northward, the wild African-derived bees moved through tropical areas, where they were highly adapted and displaced the poorly adapted honey bees originally brought in by the Spanish and Portuguese from the much colder Europe. The New World had no native honey bees, thus the honey bees present before the arrival of the bees from Africa were all best suited to European climates, not the warmer climates of much of South America and North America. The new African arrivals had to “fight” their way north, in the process stinging and defending themselves from predators and people unaccustomed to vigorously stinging bees. Consequently, the moving front of bees maintained its hot temper and tendency to attack right to Texas.
Warwick Kerr was politically progressive and an outspoken critic of the military dictatorship that came to rule Brazil after the African bees escaped and became known for their dispositions. In part to discredit Kerr, “his” bees were called abejas assinados by the authorities and press. In 1965, this catchy name was seized on by Time magazine and translated into English as “killer bees.” The name has stuck. Never mind that Kerr was doing his job, did it well, and continued to improve the bee’s genetics and management, such that Brazil went from the 27th-largest honey-producing nation in 1970 to the 5th largest in 1992 because of the bees from Africa.
HONEY AND STINGS. Those are what come to mind about honey bees. We like honey; it is familiar. We don’t like stings and think we know more than we’d like to know about them. The mechanical part of the slender stinger poking into the skin is the trivial part of a sting. It is the injected venom that counts. Honey bee venom is the best known of all insect venoms. Its chemical composition has been intensely studied since the 1950s and consists of two major proteins plus an assortment of other minor components. The main component, a small peptide found nowhere in nature except in the venoms of honey bees, is named melittin, a name derived from the scientific name for the honey bee Apis mellifera. Melittin is composed of 26 amino acids and comprises around half or so of the total venom. The first biological activity characterized for melittin was its striking ability to destroy red blood cells; thus it was labeled a “hemolysin” for this hemolytic activity. This became an unfortunate label, as melittin’s activity became pigeonholed in the minds of subsequent scientific investigators. In reality, melittin does much more than destroy blood cells: It causes pain and, in fact, is the only component in bee venom that causes the immediate sting pain; it greatly enhances the activity of the second-most abundant venom component, phospholipase, and it is a toxin that directly attacks the heart muscle. In hindsight, melittin would be better characterized as an algogen and cardiotoxin for its profound abilities to cause pain and poison the heart.
The second-largest component of honey bee venom, comprising around 20 percent of the total venom, is the protein enzyme phospholipase A2. Phospholipase destroys phospholipids, essential components of cellular membranes, in the process releasing lysophospholipids that indirectly initiate a variety of other reactions and contribute to producing minor pain. Phospholipase’s activity of attacking membrane phospholipids is greatly enhanced and synergized by trace amounts, even well below 1 percent, of melittin. How much activity phospholipase has in the absence of melittin is unclear.
In addition to melittin and phospholipase in honey bee venom are a gang of minor components, none of which comprises more than 4 percent of the total venom. The two most famous of these are apamin and mast-cell-degranulating peptide. Apamin was given its name from the genus name of honey bees, Apis (it couldn’t be named after the species name, mellifera, because that was already taken), and acts as a neurotoxin. Its only problem is that it acts in mammals mainly on the brain; yet, it is blocked by the brain’s protective blood-brain barrier. Thus, apamin in the venom is mostly ineffective against vertebrates. The other notorious component, the awkwardly named mast-cell-degranulating peptide (abbreviated MCD-peptide), is known mostly from its profound ability to cause mast cells in the body to degranulate. Degranulating mast cells release a cocktail of highly active components, including histamine, leukotrienes, cytokines, and a head-spinning number of other components. These components cause skin redness, swelling, rash, and a variety of other symptoms. Again, it is unclear how much this venom component contributes to the immediate sting reaction we experience when stung.
In almost any conversation about honey bee stings, the topic of bee sting allergy is mentioned, often with statements such as “My doctor told me I am deathly allergic to bees and might die if stung again.” Technically, this is correct if one considers 1 chance in 60,000 to be “might.” Granted, one’s chances of dying from a cow falling from the sky are less (a cow was actually recorded once falling out of an airplane) but chances of dying from a lightning strike are greater than from a bee sting. Far too much fear is generated relative to the risks of death from a bee sting.
Even more panic and fear permeate discussions of killer bee attacks. In these cases, the perceived threat is death directly from massive envenomation, not from a “possible” or “likely” lethal allergic reaction. Statistics show the contrary. In the United States, since the arrival of killer bees in 1990, only about six to eight toxic deaths from bee attacks have been carefully documented. The rest were deaths from allergic reactions. Leslie Boyer and I showed that a typical person can withstand six stings per pound of body weight and survive the bee attack without medical assistance. Ten stings per pound, in contrast, is lethal. Thus, a 170-pound person could survive 1,000 stings.10 If we halve that number to be safe, the person would not be at serious toxic risk with fewer than 500 stings. In contrast, death from an allergic reaction can be caused by 1 sting or by 100 stings. When carefully investigated, the majority of deaths blamed on massive bee attacks are allergic deaths, not toxic deaths. A take-away message for medical-treating personnel is to pay attention to allergic problems in massive bee attacks.
An urgent need for an antivenom to combat toxic envenomations became apparent after the arrival of killer bees in the United States. The idea was to produce an antivenom that would neutralize the venom toxins and save lives, just as antivenoms to snake bites and scorpion stings save lives. Attempts to generate protective antibodies in animals, as with snake venoms, failed with honey bees. Antibodies were nicely raised against the major allergenic components of honey bee venom, including phospholipase and hyaluronidase, but these antibodies did not protect mice from lethal doses of venom. Throughout these investigations, nobody asked how honey bee venom actually killed. My hunch was that melittin, the small peptide that does not readily induce antibody generation, was the major cause. Because animal- or even beekeeper-generated antibodies to melittin were not produced in meaningful levels, the melittin in venom challenges would not be neutralized. The bee venom components melittin, phospholipase, and apamin were individually tested for lethality. Apamin had low lethality and was present in only small amounts in ho
ney bee venom, so it was ruled out as a killing factor. Phospholipase alone was the most lethal bee venom component, but it is present in quantities only about one-third those of melittin.
The answer to who’s the guilty party in honey bee venom that kills the victim came from a recombination experiment in which pure melittin and pure phospholipase were recombined in the natural 3:1 ratio found in honey bee venom. The combined two components had the same killing power as the melittin alone. In other words, the phospholipase was contributing no more than any inert protein to the overall lethality and was not enhancing the activity of the melittin. The two were operating independently. Autopsies revealed that phospholipase kills by congesting the lungs with fluid and blood, and melittin kills by stopping the heartbeat. The combination of the two stopped the heart and left the lungs clear.11 The answer to what kills in honey bee venom is melittin, and because it could not be neutralized by current antivenoms that lack antibodies to melittin, the antivenom did not work.
With the arrival of the new bee on the block came questions about how the stings and venom of this new bee differed from those of our ordinary honey bees. Emotionally satisfying expectations were that killer bee stings and venom would hurt more and be more toxic than ordinary familiar bees. In contrast, honey bee defenders claimed with an air of confidence that the two were the same. These statements were simply wishful thinking based on no evidence whatsoever. With the aid of my colleagues Michael Schumacher, an allergist, and Ned Egen, a bioengineer, we decided to investigate these questions. The venoms of killer and domestic bees were similar, differing mainly in the relative ratios of melittin and phospholipase, and had the identical LD50 values to mice.12 Perhaps counterintuitively, domestic honey bee stings hurt more. The reason appeared to be because killer bee venom contained less melittin, the pain-inducing component, than domestic bee venom, and not because killer bees contained less venom. Although they are smaller, killer bees produce about the same quantity of venom as domestic bees. When analyses were extended to other species of honey bees, the results revealed that the venoms of giant honey bees, eastern hive bees, dwarf honey bees, and three strikingly different races of western hive bees all had identical lethalities to mice.11 The venoms mainly differed in the amount produced by the various bees, with giant honey bees producing eight times as much venom as dwarf honey bees. So, in the end, the venoms of all honey bee species are extraordinarily similar and the experts guessed right that the stings and venoms of killer and domestic bees are the same.
I DON’T RECALL MY FIRST honey bee sting. I also don’t know how many honey bee stings I have received. The number is probably about a thousand, a number seemingly low for someone who has specialized in killer bees for a quarter century. The reasons for the low number are that bee stings are boring, I don’t like being stung, and I take precautions. Why boring? Just as eating lots of Halloween candy gets boring after a few days, getting stung by the same species gets boring after a while. The greatest number of stings I ever received at a time occurred from being too casual during a beekeeping operation. I and a helper were moving hives by picking up each hive and carrying it to the new location a few meters away. We had on bee suits and veils but left off the heavy bee gloves as they impeded dexterity. Big mistake. While we were moving a hive, the bottom fell off, just as we got it to carrying height. The whole hive was at risk of falling to the ground and disintegrating. We grabbed the bottom of the exposed hive body to lift it. Unfortunately, about a hundred bees were in a cluster between the hive and my left hand. Squish, sting. Many stings. About 50 in all. We saved the hive. Yes, the stings hurt, but not enough to drop the hive. After five minutes of language best not heard by young children, all was well, save the swelling of the hand for the next day.
My scariest experience with stinging bees occurred in Costa Rica with newly arrived killer bees. I was with my technician who had grown up in a beekeeping family that also operated a beekeeping supply store and beyond doubt had experience, skill, and confidence surpassing that of anybody I knew. We had on bee suits. The day was not optimal. A storm was brewing on the horizon. As we approached within 25 meters, a batch of no-nonsense bees greeted us. A few breached Steve’s armor and got inside his veil. In the process of trying to dislodge those bees, he knocked his pith helmet akilter and more bees entered. He panicked and fled. Then, not knowing what to do, I fled right behind him. Lesson learned—don’t ever work killer bees with a two-piece veil consisting of hat and veil; always use a one-piece veil, preferably one without a hat that can get bumped.
I am often asked what my worst honey bee sting was. Until recently, my answer was “a sting to the nose or upper lip.” A peculiar response to a sting to the nose is that it always seems to cause a series of sneezes. Nobody knows why. Perhaps to sneeze out a bee inside the nose. Stings to the nose or lips really hurt. To make matters worse, stings to the lip invariably swell, irrespective of any “allergy.” My most humorous experience (to my colleagues, not to me) occurred in Costa Rica. We came across a nest of a social wasp in the genus Polybia, known for its defensiveness. About 10 centimeters away on the same branch as the Polybia nest was a small three-wasp nest of Mischocyttarus. The little nest was built there to gain benefit from the protection of the nearby “big sister” species. I wanted to identify the small wasp by capturing one of the inhabitants of the tiny satellite nest. The objective was to do this while avoiding arousing the big nest. I attempted to suck one of the docile little wasps into my aspirator. Instead, the little rascal flew off the nest and stung the right side of my upper lip. That night at dinner I was kidded for having a fat right upper lip. The next day it was back to the honey bees, only this time a bee got into my bee veil and stung the left side of my upper lip. At dinner, the chiding was that now I made my swollen lip symmetrical.
Back to my worst honey bee sting. The actual worst sting occurred while I was innocently riding a tandem bicycle with my wife. My mouth was open to get more air. In flew a honey bee and stung my tongue. Extreme pain. Pain much worse than biting one’s tongue. This pain truly hurt. It really hurt. Far more than any other honey bee sting. I had to stop, get off the bicycle, and sit on a rock, face in hands. Three minutes of eternity later I could sort of resume riding. Lesson: keep your mouth shut while riding a bicycle.
The difference in sting pain, depending on sting location, is one reason the sting pain scale has only four levels. A superficial honey bee sting to the back of the hand might only rate a 1.5, whereas a sting to the tongue might be a 3. Overall, when combining the values for a different location, an average value of 2 is obtained.
Michael Smith, a Cornell University graduate student, noticed my comments about the differences in the intensity of pain, depending on sting location, and decided to test the subject more thoroughly. In my own experiences, I had simply recorded the pain level and noted the location of the sting. I had never stung myself in various locations or systematically designed stings. I simply recorded what came naturally. Michael, a tall, lean fellow with fluffy red hair and a sense of humor, decided to systematically test pain levels of honey bee stings placed in a random order on 25 different body locations. To increase precision and control variables of bee age and amount of venom delivered, he took bees from the same cohort of guard bees from the hive entrance, placed them on the indicated location, allowed them to sting for 60 seconds, and recorded the pain on a scale of 1 to 10. He received three test stings plus two calibration stings daily over 6 weeks until he accumulated a total of three stings to each location. The chosen locations included some expected locations, such as to the upper arm, forearm, wrist, middle finger, thigh, calf, top of foot, middle toe, lower back, neck, skull, upper lip, and nose. Also included were some nontraditional locations, including buttocks, nipple, scrotum, and penis. As one might well imagine, the latter locations received much public attention. Michael’s results ranged from pain ratings of 2.3 to 9.0 and were much as I had expected and experienced. The lowest pain ratings were toes, upper arm
, and various other locations on arms and legs. Not surprisingly nose, upper lip, and palm of hand were among the highest pain inducers. The taboo sites were right up there near the top, with the exception of nipple, which was one-third the way down.13 Michael’s study took honey bee sting pain science to a new high.
Honey Bees and Humans: An Evolutionary Symbiosis
A SYMBIOSIS IS A relationship between two different types of organisms that, on the whole, benefits both members. We think of dogs and people, humans and sheep, and some bacteria in our gut as symbiotic. Dogs provide early warning of threats, defend us, help us herd our sheep, and keep us company. We benefit dogs by feeding them, giving them a home, and protecting them. On balance, both dogs and people benefit. The same goes for the sheep-human relationship: sheep provide us wool and meat; we provide protection and pastures for sheep. In our digestive systems are bacteria that synthesize vitamin K. In trade for receiving valuable vitamin K, we provide the bacteria food and a nice home. Symbioses not involving a human are common in nature. A classic example is bees and flowers. The plants benefit from sex, that is, getting sex via bees transporting male pollen to female floral stigmas. The bees benefit by getting food and sometimes other resources. We do not usually think of symbioses as involving stinging insects, other than bees and flowers. For example, we do not think of fire ants as friends or symbionts of us (or anything else, save aphids and other honeydew producers). One exception to our view of symbiosis between stinging insects and another species springs to mind. That exception is the mutually beneficial relationship between bullhorn acacia ants and acacia plants. The plants provide homes in the form of swollen thorns for the ants and food bodies that the ants eat. The ants provide protection from herbivores, such as cows, caterpillars, or leaf beetles and competing plants by stinging herbivores and chewing off plant competitors.
The Sting of the Wild Page 24