Africanized Killer Bees

Abstract

Patients stung multiple times by killer bees have signs and symptoms of a toxic envenomation, not allergic reactions. The author reviews the signs and symptoms, pathophysiology, and current management of toxic killer bee envenomations.The northward migration of large swarms of Africanized honeybees (AHBs), or “killer” bees, is responsible for a unique phenomenon that has not previously been experienced in the United States. More and more patients are coming to emergency departments and hospitals in the Southwest and South because of killer bee attacks. These patients, stung multiple times by the bees, have signs and symptoms of a toxic envenomation, not allergic reactions. Deaths from AHBs are a result of direct toxic effects, not anaphylaxis.1 The care of patients admitted to critical care units with toxic bee envenomations poses an unusual challenge for critical care nurses because this diagnosis is relatively new, and experience in caring for these patients is limited. These patients are critically ill, are at risk for serious complications related to their injury, and require complex nursing care. In this article, I review the signs and symptoms, pathophysiology, and current management of toxic AHB envenomations and present a case study of a patient who was attacked by a swarm of AHBs.Honeybees were transplanted from Africa (Tanzania) in 1956 to Brazil as part of a breeding program that would allow the European honeybees (EHB) to adapt to the hot South American climate and still maintain their normal production of honey. The African bees made less honey than did the European bees but tolerated the hot climate better. The project was intended to produce bees that made honey as EHB did but tolerated the extreme climate as the African bees did. In 1957, 26 swarms of the imported African bees escaped into the surrounding jungle and started breeding with the local wild bees. The local bees, which interbred with the imported bees, began to take on the more aggressive behaviors of the African honeybee, and became known as AHBs.2–4 Initially, it was assumed that hybridization would occur, but over time, the AHB characteristics have essentially replaced those of the EHB.5Two factors are responsible for the relentless migration of AHBs northward from Brazil into the United States. The first is their ability to fly longer distances than EHBs; the second is their unusually frequent swarming behavior.2,4 Swarming occurs as a result of hive overcrowding; normal honeybees reproduce at a rate that causes swarming 2 or 3 times per year; AHBs tend to swarm excessively, 6 to 12 times per year, planting new colonies at a rapid rate. AHBs were first found in the United States in Texas in 1990, spread to Arizona and New Mexico by 1993, and to California by 1994.1,6 By 1996, 4 fatal stinging attacks had been reported.7 Currently, AHBs are well established in Texas, New Mexico, Arizona, Nevada, and parts of southern California, and 2 samples of honeybees from Oklahoma were identified as AHBs by the Hayden Bee Research Center in Tucson, Ariz.2,8–11 Many experts think that AHBs will continue their migration, and it is probable that they will become endemic in the South, including Louisiana, Mississippi, Alabama, Florida, and parts of Georgia, representing a significant public health hazard.2,8 The first fatal attack in the United States occurred in Texas in 1993, and other fatal attacks have since been reported in Arizona and California.12 All attempts made to contain AHBs have, to date, been unsuccessful.The venom and morphology of EHBs and AHBs are similar. Although AHBs are about 10% smaller than EHBs, identifying AHBs accurately on the basis of visual inspection or conventional taxonomic indicators is difficult. Identification is usually based on computer analysis of morphometry, mitochondrial DNA alleles, and venom.2,8,12–16 Positive identification of the type of bee involved in an attack can take several days. All venom is composed primarily of proteins, peptides, and amines.1,4 The toxic components include phospholipids, bradykinin, histamine, acetylcholine, dopamine, and serotonin.1,2,17 The venom of AHBs is chemically similar to that of EHBs, although AHBs have a slightly smaller volume of venom than do EHBs.2,3,13 The lethal dose of bee venom from AHBs and EHBs is the same.18It is the behavior of the AHBs, which seems to be genetically modulated, that makes them different and dangerous.19 Several compounds, called pheromones, have been isolated primarily from AHBs and are regarded as mediators of this aggressive behavior.1,20 AHBs are considerably more aggressive than EHBs in pursuing victims, and AHBs may follow a victim for up to a quarter of a mile.3 If the victim can run more than a quarter of a mile, he or she may be able to outrun the bees because their pursuit is relatively slow.1,3 Also, AHBs tend to choose nesting locations close to populated areas, such as by homes and in yards, areas normal bees tend to avoid, making contact with people more likely. In addition, AHBs may be aggravated by minimal disturbances; the vibrations of a lawnmower, light-colored clothing, and perfume have been reported to provoke aggressive stinging behavior. Once disturbed, the colony may remain agitated for 24 hours, continuing attacking behavior.4,5,8,12The recommendation for anyone who is attacked by AHBs is to run to safety and to cover the eyes and mouth, if possible, because the bees will swarm into dark, moist openings.3,8,21 Diving underwater should be avoided because the bees may remain close by and may even crawl down a hollow tube used for breathing.3,5 Repellants do not seem to be helpful in deterring an AHB attack; Schmidt et al22 sprayed 3 different insect repellants on AHB colonies to determine if the repellants affected the bees’ attack behavior. Two had no effect and the other caused a greater attack response. Spraying the bees with soapy water neutralizes the bees either by making them unable to use their wings and fly or by killing them.3,10Although AHBs have an exceptionally high level of stinging behavior, the effect of the sting from a single AHB is almost identical to that of a sting by an EHB. The stinger is composed of 2 barbed lancets that are connected to the venom sac and supported by strong muscles. When the bee injects the stinger into the skin, the lancets alternately scissor their way into the victim, continuing to inject venom into the tissue even after the bee pulls away and subsequently dies18 (see FigureF1). The stinger continues to throb for 30 to 60 seconds, injecting additional venom and giving off alarm odors that mark the victim for other bees to attack.4The local reaction to the sting of an AHB consists of erythema, urticaria, and angioedema,23(p631) causing pain and pruritus. The systemic reaction is due to the large volume of venom injected during a massive AHB attack. Initial signs and symptoms include diffuse widespread edema, inflammation of the skin, headache, weakness and fatigue, and dizziness.23(p631) When the number of stings is greater than 50, nausea, vomiting, and diarrhea occur.2,4,13,24(p883) After the initial manifestations, hypotension, tachycardia, respiratory distress, acute renal failure, disseminated intravascular coagulation, and multiple organ dysfunction may develop.1,25Most researchers think that the reaction to AHB venom is not an allergic response, but instead is due to the toxic effects of the large quantity of injected bee venom. However, antibody studies suggest cross-reactivity between EHB and AHB venoms, so that a person allergic to an EHB sting would most likely experience the same allergic response to the sting of an AHB.3 Although a systemic toxic response can occur after as few as 50 simultaneous bee stings,13,23(p631),25 the lethal dose is considered to be 500 stings for children3 and up to 1100 bee stings for an adult, although some victims have survived a mass attack of 1000 or more stings.3,25 The estimated median lethal dose of venom per kilogram of body weight is the amount in 19 stings.4,18 The estimated dose of venom from 1000 stings, considered a fatal dose, is 1.3 mg/kg, or 90 mg of venom for an average adult; fatality appears to be related to the number of milligrams of venom per kilogram of body weight.2AHB venom contains vasoactive and hemolytic substances such as histamine, dopamine, serotonin, mellitin, kinins, and phospholipases, which are responsible for the effects reported with massive bee stings.1,2,26 The peptide mellitin, one of the major components of bee venom, inserts itself into the phospholipid layer of the cell membrane of red blood cells, white blood cells, platelets, and endothelial cells.4,8 In conjunction with a second component of the venom, phospholipid A, mellitin triggers the release of arachidonic acid, which causes cell membrane breakdown, damage of the vascular endothelium, and activation of the inflammatory response.17,26 Hyaluronidase, a third major component of the venom, breaks down connective tissue, increasing the spread and uptake of the venom components.4,17 The venom also contains small amounts of histamine, dopamine, and norepinephrine, responsible for hypotension, flushing, and dysrhythmias.2,17,23(p631)Massive injection of bee venom (envenomation) affects all organ systems. Acute renal failure may develop, often within 24 to 48 hours, and may be severe enough to require hemodialysis.25–27 Hypotension, intravascular hemolysis, rhabdomyolysis, and myoglobinuria from the muscle injury appear to be contributing factors, as well as the direct toxic effect of the massive quantities of injected venom.25 Activation of the inflammatory cascade, thromobcytopenia, and hemolysis can lead to the development of disseminated intravascular coagulation, resulting in significant bleeding. Liver damage contributes to the bleeding (because the liver’s ability to manufacture clotting factors is diminished) and to central nervous system changes. The ischemia and cell leakage produced by the venom is the basis for the development of adult respiratory distress syndrome and nausea, vomiting, and diarrhea.2,3,6,18 Because AHBs tend to invade the nose and mouth during mass attacks, stings of the mucous membranes and airway can result in upper airway obstruction, contributing to hypoxia and respiratory failure.2,5,13 The effects of the components of AHB venom are listed in Table 1.It may not be clear whether a person stung by AHBs is having an allergic reaction or a toxic reaction; however, initial treatment for a massive number of bee stings is the same regardless of the type of reaction. In the first few minutes, the 2 reactions cannot be distinguished from each other, and the first consideration is an allergic reaction. Initial treatment includes epinephrine, 1:1000, 0.3 to 0.5 mL given intramuscularly and diphenhydramine 50 mg intravenously or orally.2,27 Oxygenation by whatever method required to maintain saturations greater than 90% is an immediate priority. Aggressive fluid replacement is started if the patient is in shock or is vomiting or the development of rhabdomyolysis is probable. Histamine antagonists are given to treat the vascular effects of the venom.1,2 Steroids may be given to prevent a delayed hypersensitivity reaction, but they have a limited role in the management of acute toxic envenomation.1,2 Some sources3,8,23(p631),28 recommend removing the stingers still in the skin in the first minute by using the swiping method, that is, using a firm flat surface, like a credit card, to scrape the stinger off the skin. This method avoids accidentally injecting the remaining venom by pinching the stinger sac while attempting to remove the stinger.3,8,23(p631),28 However, because the stingers will continue to throb and inject their venom for 30 to 60 seconds even after the bee has pulled away, if multiple stings are evident, it may not be possible to remove the stingers within the time that it takes for them to empty into the patient on their own.4,8,28 The method of stinger removal is less relevant than the speed with which the stingers are removed. Hospital admission is recommended for patients who have been stung more than 50 times or who have indications of liver or kidney dysfunction, thrombocytopenia, or hemolysis.3,17 Currently, no antivenin is available; however, antibodies have been isolated from the serum of beekeepers and are being tested.6,24(p883) The circulating venom persists for many hours; it has been detected days later in victims of massive bee stings. Reports of delayed reactions to massive bee attacks are rare but have been reported. Initially, the stinging victim may appear to be in stable condition, with no laboratory abnormalities noted, but then the victim’s condition may deteriorate hours later.2,18 For this reason, patients with more than 50 bee stings should be monitored in the emergency department for at least 6 hours.18Once a patient who has been stung is hospitalized, ongoing care should include monitoring levels of creatinine, serum urea nitrogen, electrolytes, and myoglobin to assess renal function and the potential for rhabdomyolysis. The attack is considered a toxic envenomation rather than an allergic response when multiple bee stings are present and the level of creatine phosphokinase is elevated. Acid-base and oxygenation status must be monitored to detect the development of acute respiratory distress syndrome and acidosis. In patients with myoglobinuria, alkalinization of the urine and fluids may prevent the crystallization of myoglobin in the kidney tubules, which could lead to acute renal failure. Hemodialysis may be started to remove the low-molecular-weight components of the venom (eg, mellitin) or if acute renal failure develops. Continuous cardiac monitoring should be maintained because of the myocardial ischemia, cardiac dysrhythmias, and hyperkalemia that may be caused by the venom.2Patients admitted to the intensive care unit (ICU) with massive bee envenomations require the same complex and expert nursing care as any patient with multiorgan dysfunction. Because these patients are likely to be treated with mechanical ventilation and because adult respiratory distress syndrome may develop, frequent monitoring of oxygen saturation and respiratory status is required. Measures to reduce the potential for ventilator-associated pneumonia, such as elevating the head of the bed and a good oral care program, including careful suctioning above the endotracheal tube cuff, should be implemented. The use of proton pump inhibitors for stress ulcer prophylaxis has been linked to a reduction in ventilator-associated pneumonia and should be initiated for these patients.29Monitoring of electrolyte levels and maintaining normal values helps prevent the development of cardiac dysrhythmias. Careful control of serum levels of glucose in critically ill patients has improved outcomes and may confer a benefit to critically ill victims of bee attacks.30 Frequent monitoring of serum levels of glucose and intravenous administration of insulin should be considered in these patients. Because disseminated intravascular coagulation can develop in critically ill patients with multiorgan dysfunction, nurses should monitor coagulation indices and evaluate patients for any indications of gastrointestinal or other bleeding. Monitoring creatinine levels and daily measurement of fluid intake and output, including daily weight measurements, are necessary for patients at risk for renal failure and rhabdomyolysis.Adequate energy intake is required to prevent skin breakdown and promote healing, so enteral or parenteral nutrition should be considered early in the ICU course. Critically ill patients require frequent positioning and prophylaxis for deep vein thromboses.Emotional and spiritual support for the patient and the patient’s family is an essential part of nursing care. Being critically ill with an uncertain outcome can challenge the psychological resources of patients and their families. Additional support, information, and explanations from the nursing staff can be an important part of the healing process.An 88-year-old woman was checking on some vacant property she owned when she noticed a door to a shed that was normally locked was open. She entered the shed to check inside and was immediately attacked by a large swarm of bees. After getting a neighbor’s attention, she was able to walk about 45 m (150 ft) from where the attack began and then collapsed in the yard. The neighbor attempted to help the woman but was also attacked by the swarm of bees; he retreated into his house and called 911. When paramedics arrived at 10:03 AM, 4 minutes after dispatch, they found the woman down, with all exposed body parts thickly covered with bees. The scene was secured; the woman was sprayed with water in an attempt to protect her from the bees while additional rescuers arrived in full protective gear. The woman had the presence of mind to lean into the spray of water to assist in removing the bees. Initial observation indicated that she had sustained hundreds of bee stings to the head, face, neck, and upper and lower extremities. Once most of the bees were removed by the water, the paramedics were able to move the patient into an ambulance and assess her. She was alert and oriented, said she had no chest pain or shortness of breath, and had a severe hearing loss due to bees and stings located in her ear canal. Her airway was compromised because of numerous bees in her mouth and nose. The visible bees were immediately removed, and 100% oxygen by nonrebreather mask was started. The radial pulse was hard to locate and was weak and thready at a rate of 100/min by palpation, respirations were 28/min to 32/min, and blood pressure was initially unmeasurable. Two large-bore intravenous catheters were inserted, and a total of 400 mL of isotonic sodium chloride solution was infused as a bolus. Diphenhydramine 50 mg intravenously and methylprednisolone 125 mg intravenously were given at the scene before transport. Blood pressure was measured by palpation as 90 mm Hg. The patient was transported by air to the emergency department and was given 0.3 mL of epinephrine 1:1000 subcutaneously en route. She arrived in the emergency department at 10:45 AM, 43 minutes after the paramedics had reached her.Upon arrival in the emergency department, the patient’s blood pressure was 140/98 mm Hg, her pulse rate was 150/min with sinus tachycardia, respirations were 24/min, and oxygen saturation was 100% on a nonrebreather mask with 100% oxygen. She was moaning and complaining of pain but alert and cooperative. Her lungs were clear to auscultation. Swelling of the tongue was noted. The patient was given morphine sulfate 4 mg intravenously for pain, cimetidine 300 mg intravenously, and a tetanus immunization as a standard precaution. An electrocardiogram and a chest radiograph were obtained immediately. Blood samples were obtained for a complete blood cell count and measurement of prothrombin time, partial thromboplastin time, electrolyte levels, and creatinine level. A urinary catheter was inserted and drained clear yellow urine. No evidence of edema or cyanosis was noted on the extremities. The blood pressure remained stable. All stingers were carefully removed by swiping, as were some bees that were still tangled in her hair. The patient again complained of marked pain and was given an additional 10 mg of morphine sulfate intravenously. The results of the laboratory studies obtained in the emergency department are shown in Table 2. The patient was transferred to the ICU in stable but guarded condition about 2 hours after reaching the emergency department, not quite 3 hours after the bee attack had occurred. Blood pressure at the time of transfer was 190/110 mm Hg, heart rate was 105/min with sinus tachycardia and occasional premature atrial contractions, and respirations were 22/min. The emergency department staff estimated that the patient had sustained approximately 1000 bee stings.Her medical history included breast cancer 15 years earlier, hypertension, and a recent unexplained weight loss of 13 kg (29 lb). She had recently seen her primary care physician because she had had abdominal pain for the preceding 12 months; a computed tomography scan of the abdomen, done on an outpatient basis, did not show any intra-abdominal processes. A cause for the weight loss had not yet been determined at the time of AHB attack. She had been taking an oral meperidine preparation for the intermittent abdominal pain. She did not smoke or use alcohol.Computed tomography of the abdomen in the emergency department showed an ileus but no masses. After admission to the ICU, the patient was able to answer questions appropriately. More bee stingers were removed from her skin, and more dead bees were removed from her hair. She complained of pain to touch of the arms, neck, and lips. Her lips were swollen, but she was breathing easily, with no complaints of shortness of breath, and no stridor was present. She was able to rest and sleep but did become nauseated and vomited 150 mL of green fluid, which contained numerous dead bees. A central catheter was placed for fluid management. Her central venous pressure was 2 mm Hg. Pain was controlled with morphine sulfate. Cardiac monitoring was maintained. She was maintained on 5.45% dextrose in isotonic sodium chloride solution with 20 mmol of potassium at 100 mL/h to treat the low potassium and diphenhydramine 25 mg intravenously every 8 hours. In addition, a histamine2 blocker was administered every 8 hours intravenously. The patient vomited a second time several hours later, 200 mL of greenish fluid that still contained numerous bees. A bicarbonate infusion was started to alkalinize the urine in an effort to prevent crystallization of myoglobin and to protect her against the development of acute renal failure.During the night, the patient became disoriented and vomited a third time, 200 mL of greenish fluid, still containing numerous bees. She was given medication for the nausea after a fourth small emesis, this time without bees, and was able to rest for a while. She vomited a fifth time, 50 mL of green fluid, and was again disoriented, but she did reorient easily. She refused offers of pain medication, although she occasionally complained of discomfort from the bee stings.The patient’s condition appeared to stabilize. Her urine appeared slightly bloody, and her hands, feet, eyes, and lips were swollen, but she was breathing easily with no shortness of breath. Results of her laboratory tests are indicated in Table 2. Liver enzyme levels were elevated. Urine was positive for myoglobin. Her condition was stable enough for her to be transferred to a telemetry unit. Once there, she vomited again, 300 mL of yellow liquid mixed with food. She was given medication for nausea. No bees were noted in the vomitus. The patient was frequently disoriented and began having diarrhea and expelling flatus, which kept her awake during the night. Her upper extremities became more edematous and reddened, although she said she had no itching or discomfort. As the night progressed, respiratory distress developed; respirations increased to 24/min, and coarse crackles developed in both lung fields. The urine became a dark brown, and she complained of more severe abdominal cramping. Her blood pressure increased, and the cardiac monitor indicated that the rhythm changed to a multifocal atrial tachycardia. She was treated with furosemide 40 mg intravenously, 12.5 mg of meperidine intravenously, 5 mg of prochlorperazine intravenously, and a calcium channel blocker for the dysrhythmia. After treatment, her urine output improved, the color changed from dark brown to yellow, and her vital signs remained stable, except for spiking a fever (body temperature 38.6°C). The bicarbonate infusion was discontinued.By morning of the third day, the patient’s condition continued to deteriorate. Her abdomen was distended, the diarrhea continued, and she felt no relief from repeated intravenous doses of meperidine and prochlorperazine. Methylprednisolone 125 mg intravenously was also administered. Her white blood cell count increased to 22.4 × 109/L from 13.7 × 109/L, and her platelet count decreased to 101 × 109/L. Her heart rhythm changed from sinus tachycardia to atrial fibrillation with a heart rate up to 180/min. She was treated with a calcium channel blocker and then digitalis, which lowered the heart rate to about 130/min to 140/min. She was also given repeated doses of meperidine for pain. Her upper extremities, erythematous with purplish discolorations around the bee sting sites, began to leak serous drainage in marked amounts. By evening, the patient’s speech became slurred, and she had difficulty swallowing because of marked swelling of the tongue. The physician was notified; he examined her and ordered a transfer back to the ICU. Upon arrival in the ICU, the patient was pale, dry, and cool. Tympanic temperature was 35.3°C. Respirations were slow and shallow, and the monitor indicated a sinus tachycardia with a heart rate of 135/min. Oxygen saturation was 89% on 2 L per nasal cannula; the cannula was replaced by a nonrebreather mask with 100% oxygen, and the oxygen saturation increased to 90%. Central venous pressure was 1 mm Hg, so 5.45% dextrose in isotonic sodium chloride solution was administered at 200 mL/h through a warming device. Blood samples were obtained for culture and arterial blood gas analysis, and a bicarbonate infusion was restarted to treat a metabolic acidosis. The patient’s level of consciousness improved after fluid replacement and correction of the acidosis. A nasogastric tube was inserted to decompress the stomach and drained a small amount of brown fluid, positive for blood. Klebsiella pneumoniae was cultured from both the blood and urine specimens; appropriate antibiotics were started. Other laboratory values are noted in Table 2.By the morning of the fourth day, the patient’s respiratory rate had increased to 40/min to 50/min; her oxygen percentage had been decreased to 50% per Venturi mask, and she was maintaining an oxygen saturation of 100%. Her abdominal pain continued, and she was wincing at light palpation. She was intermittently confused, although still able to follow commands. A surgical consultation was obtained because of the increasing abdominal distention and continued pain, and with the family’s permission, she was prepared for surgery. Per the family’s request, a do-not-resuscitate order was written. The patient became hypotensive and oliguric. Her hemoglobin level decreased to 98 g/L (9.8 g/dL), hematocrit to 0.27, and platelet count to 24 × 109/L. Her screenings for disseminated intravascular coagulation came back positive. Liver enzyme levels were significantly elevated. Two units of packed red blood cells and 10 units of fresh frozen plasma were transfused, dopamine was administered to support blood pressure, and she was transferred to the operating room.During surgery, necrotic bowel was found throughout the abdomen. Because of the diffuse necrosis, nothing further was done, and surgery was ended. The patient’s family was informed of the extremely poor prognosis. Receiving mechanical ventilation and dopamine, the patient returned to the ICU from the operating room. Her blood pressure gradually decreased, her extremities became increasingly cyanotic and edematous, and the family requested that medications and the ventilatory support be withdrawn. The patient died early the next morning, less than 96 hours after the bee attack.The continued nausea, vomiting, and diarrhea, as well as the intestinal ischemia and necrosis, that occurred were attributed to the toxic effects of the bee venom. The rhabdomyolysis, liver injury, and hypotension were also most likely due to the effects of the bee venom. The patient’s discharge diagnoses included intestinal necrosis, toxic Hymenoptera bee envenomation, acute rhabdomyolysis, atrial fibrillation, and chronic vascular insufficiency to the bowel with weight loss and malnutrition. Ultimately, it was concluded that she died of complications related to the massive number of bee stings that she had sustained.