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46 BITES, VENOMS, STINGS, AND MARINE POISONINGS

46 BITES, VENOMS, STINGS, AND MARINE POISONINGS
Harrison’s Manual of Medicine

46

BITES, VENOMS, STINGS, AND MARINE POISONINGS

Mammalian Bites
Venomous Snakebites
Marine Envenomations
Marine Poisonings
Arthropod Bites and Stings
Tick Bites and Tick Paralysis
Bibliography

MAMMALIAN BITES
Between 1 and 2 million mammalian animal-bite wounds are sustained in the U.S. each year; the vast majority are inflicted by pet dogs and cats. A significant number result in infection, which may be life-threatening. The microbiology of bite-wound infections generally reflects the oropharyngeal flora of the biting animal, although organisms from the soil, the skin of the animal or victim, or the animal’s feces may also be involved.
DOG BITES   Dogs account for ~80% of bite wounds, and 15–20% of dog-bite wounds become infected. Infection typically manifests 8–24 h after the bite, with pain, cellulitis, and a purulent, sometimes foul-smelling discharge. Fever, lymphadenopathy, and lymphangitis may occur. If the dog’s tooth penetrates synovium or bone, septic arthritis or osteomyelitis may develop. While infection usually remains localized, systemic spread (e.g., bacteremia, endocarditis, brain abscess) can take place. Dissemination is most likely in pts with poor lymphatic drainage of the affected area or with systemic immunocompromise.
The microbiology of dog-bite wound infections is usually mixed and includes staphylococci, a-hemolytic streptococci, Pasteurella multocida, Eikenella corrodens, and Capnocytophaga canimorsus (formerly designated DF-2). Anaerobes (Actinomyces, Fusobacterium, Prevotella, and Porphyromonas spp.) are often present as well. Infection with C. canimorsus can be fulminant, presenting as sepsis syndrome, DIC, and renal failure, particularly in pts who are splenectomized, have hepatic dysfunction, or are otherwise immunosuppressed. This fastidious, thin gram-negative rod is occasionally seen within PMNs on Wright-stained smears of peripheral blood from septic pts. In addition to bacterial infections, dog bites may transmit rabies (Chap. 107) and may lead to tetanus intoxication (Chap. 95).
CAT BITES   More than half of cat bites and scratches result in infection due to deep tissue penetration of narrow, sharp feline incisors. Accordingly, cat bites are more likely than dog bites to cause septic arthritis or osteomyelitis, sequelae that are particularly likely following bites over joints (especially those involving the hand). The microflora of cat-bite infections is usually mixed, reflecting the feline oral flora, although P. multocida is the most important pathogen. Infection with P. multocida can cause rapidly advancing, painful inflammation that may manifest only a few hours after the bite as well as purulent or serosanguineous discharge. A mixed bacterial flora is often present, and dissemination may occur. Like dog bites, cat bites may transmit rabies or may lead to tetanus intoxication. Cat bites and scratches may also transmit Bartonella henselae, the agent of cat-scratch disease, as well as tularemia (Chap. 94).
OTHER ANIMAL BITES   Bite infections from other species reflect the oral flora of the biting animal. Bites from nonhuman primates contain bacteria similar to those found in human bites. Bites from Old World monkeys (Macaca spp.) may transmit herpes B virus (Herpesvirus simiae), which can cause CNS infection with high mortality.
Bites from small rodents and the animals that prey on them may transmit rat-bite fever, caused by Streptobacillus moniliformis (in the U.S.) or Spirillum minor (in Asia). Infection with S. moniliformis manifests as fever, chills, myalgias, headache, and migratory arthralgias, which are followed by a maculopapular rash 3–10 days after the bite (most often after the bite has healed). Complications can include metastatic abscesses, endocarditis, meningitis, or pneumonia. Diagnosis can be made by culture on enriched media and serologic testing. Infection with S. minor causes local inflammation, pain, and regional lymphadenopathy 1–4 weeks after the bite, with evolution into a systemic illness. Diagnosis can be made by detection of spirochetes on microscopic examination.
HUMAN BITES   Human bites are categorized as occlusional injuries, which are inflicted by actual biting, or clenched-fist injuries, which may result when the fist of one individual strikes the teeth of another. Human-bite wounds become infected more frequently than bite wounds from other animals. Clenched-fist injuries are particularly prone to serious infection due to spread and sequestration of oral flora along deep tissue planes as the fingers are extended after the bite. The flora of human-bite wounds is diverse, including viridans streptococci, Staphylococcus aureus, E. corrodens, and Haemophilus influenzae. Anaerobic species are isolated from 50% of human-bite wounds and include Fusobacterium nucleatum as well as Prevotella, Porphyromonas, and Peptostreptococcus spp.

TREATMENT
Initial Assessment
Elicit a careful history including the type of animal responsible, whether or not the attack was provoked, and the time elapsed since the injury. Contact public health authorities if rabies is a consideration. Consider domestic abuse if confronted with suspicious human-bite wounds. Obtain details regarding possible antibiotic allergies, systemic immunosuppression, and immunization history. Assess the type of wound (e.g., puncture, laceration, crush injury, scratch); its depth; and the possibility of injury to joints, tendons, nerves, or bone. In addition to conducting a general physical examination, carefully examine the bite site for evidence of infection, including redness, exudate, foul odor, lymphangitis, or lymphadenopathy. Because of their potentially debilitating consequences, hand injuries warrant consultation with a hand surgeon. Obtain radiographs if bony injury or retained tooth fragments are suspected. Stain (Gram’s) and culture drainage and/or tissue specimens from all infected wounds; include specimens for anaerobic culture. For bites of animals other than dogs or cats, staining (Gram’s) and culture from an uninfected- appearing wound may be of use, since the flora causing infections of these bites is less predictable. A WBC count and blood cultures should be performed if systemic infection is suspected.
Wound Management
Wound closure is controversial in bite injuries. After thorough cleansing, facial wounds are usually sutured for cosmetic reasons and because the abundant facial blood supply and absence of dependent edema lessen the risk of infection there. For wounds elsewhere, many authorities do not attempt primary closure, preferring instead to irrigate copiously, debride devitalized tissue, remove foreign bodies, and approximate the margins. Delayed primary closure may be undertaken after the risk of infection has passed. Puncture wounds due to cat bites should not be sutured because of their high risk of infection.
Antibiotic Therapy
Presumptive or Prophylactic Therapy All human and nonhuman primate bites and most cat bites (especially those on the hand) merit prophylactic antibiotic therapy because of high infection rates (Table 46-1). Antibiotic therapy for other bite injuries <8 h old is controversial, although one meta- analysis of prophylaxis of dog-bite wounds showed a 50% reduction in the rate of infection. Factors favoring empirical therapy include the presence of severe and/or extensive wounds; bites involving joints, hands, or genitals; host immunocompromise, including that due to liver disease or splenectomy; and impaired lymphatic drainage of the bite site. When given, prophylaxis should continue for 3–5 days.

Table 46-1 Management of Wound Infections Following Animal Bites

Therapy for Infected Bite Wounds Antibiotics should certainly be used for all established bite-wound infections and should target likely pathogens (Table 46-1). Initial treatment is usually continued for 10–14 days. Elevation and immobilization of the site of injury are important adjunctive measures. Therapeutic response must be carefully monitored. If treatment fails, alternative diagnoses (such as osteomyelitis or septic arthritis) should be considered, surgical evaluation performed for possible drainage or debridement, and a longer (several-week) course of antibiotic therapy planned.
C. canimorsus sepsis requires a 2-week course of IV penicillin G (2 × 106 U q4h); cephalosporins and quinolones are alternative agents. Serious P. multocida infection should also be treated with IV penicillin G; alternative agents with which there is less clinical experience include second- or third- generation cephalosporins and ciprofloxacin.
A tetanus booster immunization should be given for pts previously immunized but not boosted within 5 years. Pts not previously immunized should undergo primary immunization and should also receive tetanus immune globulin. Rabies prophylaxis includes administration of rabies immune globulin (infiltrated both around the wound site and intramuscularly) as well as rabies vaccine and should be given in consultation with local and regional public health authorities.

VENOMOUS SNAKEBITES
ETIOLOGY AND EPIDEMIOLOGY   Venomous snakebites are rare in most developed countries (Table 46-2). Worldwide, 30,000 to 40,000 people die from these injuries each year. Poisonous snakes indigenous to the U.S. include the rattlesnake, the copperhead, the coral snake, and the water moccasin. Eastern and western diamondback rattlesnakes (Crotalus adamanteus and C. atrox, respectively) are responsible for most deaths from snakebite in the U.S. Snake venoms are complex mixtures of enzymes and other substances that can activate the coagulation cascade or induce proteolysis or neurotoxicity. Most snake venoms have multisystem effects in their victims. The overall mortality rate for venomous snakebite is <1% among U.S. victims who receive antivenom.

Table 46-2 Venomous Snakes of the World

TREATMENT
Field Management
Prehospital measures should focus on delivering the victim to definitive care as soon as possible. The victim should be as inactive as is feasible in order to minimize systemic spread of the venom. After viperid bites, local suction to remove venom may be beneficial if applied within 3–5 min and should be continued for at least 30 min. A mechanical suction device should be used; mouth-to-wound suction should be avoided. If the victim is >60 min from medical care, a proximal lymphatic-occlusive constriction band may also limit the spread of venom if applied so as not to interfere with arterial flow within 30 min after the bite. A bitten extremity should be splinted, if possible, and kept at heart level. Incisions into the bite wound, cooling, giving alcoholic beverages to the victim, and electric shock should all be avoided.
Hospital Management
The victim should be closely monitored (vital signs, cardiac rhythm, O2 saturation). The level of erythema and swelling should be marked and limb circumference measured every 15 min. IV access with a large-bore catheter should be established in an unaffected extremity. Shock should be treated initially with fluid resuscitation (normal saline or Ringer’s lactate, up to 20–40 mL/kg of body weight). If hypotension persists, 5% albumin (10–20 mL/ kg) should be tried next, followed by a dopamine infusion. Central hemodynamic monitoring may be helpful but must be instituted with great care if coagulopathy is present.
Blood for laboratory testing should be drawn as soon as possible, with a CBC, an assessment of renal and hepatic function, coagulation studies, and typing and cross-matching. Urine should be tested for blood or myoglobin. In severe cases, arterial blood gas studies, ECG, and CXR should also be done.
Attempts to locate an appropriate and specific antivenom should begin early in all cases of known venomous snakebite, regardless of symptoms. In the U.S., assistance in finding antivenom can be obtained 24 h a day from the University of Arizona Poison and Drug Information Center (520-626-6016).
Rapidly progressive and severe local findings or manifestations of systemic toxicity (signs and symptoms or laboratory abnormalities) are indications for the administration of IV antivenom. Most antivenoms are of equine origin and carry risks of anaphylactic, anaphylactoid, or delayed-hypersensitivity reactions; skin testing does not reliably predict the risk of allergic reaction. To limit acute reactions, pts should be premedicated with IV antihistamines (e.g., diphenhydramine, 1 mg/kg up to a maximum dose of 100 mg; plus cimetidine, 5–10 mg/kg up to a maximum dose of 300 mg) and given IV crystalloids to expand intravascular volume. Epinephrine should be immediately available. The antivenom should be administered slowly in dilute solution. Management of life-threatening envenomation in a victim apparently allergic to antivenom requires significant expertise but is often possible with intensive premedication (e.g., epinephrine, antihistamines, and steroids) and consultation from a poison specialist, an intensive care specialist, and/or an allergist.
The bite wound should be dressed with dry sterile gauze, splinted, and elevated only when antivenom is available. Tetanus immunization should be updated. Antibiotic prophylaxis is controversial, although many authorities recommend prophylactic therapy for the first few days (Table 46-1).
Whether or not antivenom is given, pts with signs of envenomation should be observed in the hospital for at least 24 h. Pts with apparently “dry” bites should be watched for at least 6–8 h. Symptoms from elapid or sea snake bites are commonly delayed for several hours, so victims should be observed in the hospital for 24 h.

MARINE ENVENOMATIONS
INVERTEBRATES   Hydroids, fire coral, jellyfish, Portuguese man-of- war, and sea anemones possess specialized stinging cells called nematocysts. The clinical consequences of envenomation by these species are similar but differ in severity. Pain (prickling, burning, and throbbing), pruritus, and paresthesia usually develop immediately. Neurologic, cardiovascular, respiratory, rheumatologic, GI, renal, and ocular symptoms have been described.

TREATMENT
The skin should be decontaminated immediately with a forceful jet of vinegar (5% acetic acid) or rubbing alcohol (40–70% isopropanol) to inactivate nematocysts. Shaving the skin may also be helpful to remove nematocysts. After decontamination, topical anesthetics, antihistamines, or steroids may be helpful. Narcotics may be necessary for persistent pain. Muscle spasms may respond to IV 10% calcium gluconate (5–10 mL) or diazepam (2–5 mg titrated upwards as necessary).

VERTEBRATESXS   A number of marine vertebrates, including stingrays, scorpionfish, catfish, surgeonfish (doctorfish, tang), weeverfish, and horned venomous sharks, are capable of envenomating humans. Clinical manifestations include immediate and intense pain at the envenomation site; systemic symptoms, such as weakness, diaphoresis, nausea, vomiting, diarrhea, dysrhythmia, syncope, hypotension, muscle cramps, muscle fasciculations, and paralysis; and (in rare cases) death. A stingray injury is both an envenomation and a traumatic wound, with intense pain at the site lasting up to 48 h as well as systemic symptoms secondary to serotonin and enzymes contained in the venom. Stings from stonefish, scorpionfish, and lionfish cause similar local reactions and systemic responses, although the sting of a stonefish is the most life-threatening.

TREATMENT
The management of most marine vertebrate stings is similar. Except for stonefish and serious scorpionfish envenomations (see below), no antivenom is available. The affected part should be immersed immediately in nonscalding hot water (113°F/45°C) for 30–90 min to inactivate venoms and relieve pain. Opiates or regional nerve block (with 1% lidocaine, 0.5% bupivacaine, and sodium bicarbonate mixed 5:5:1) may also help. After soaking and analgesia, the wound should be explored, debrided, and vigorously irrigated. Radiography of the envenomated area may help to locate foreign bodies. Wounds should be left to heal by secondary intention or by delayed primary closure. Tetanus immunization should be updated. Empirical antibiotics to cover Staphylococcus and Streptococcus spp. should be considered for serious wounds or envenomations in immunocompromised hosts. If the host is compromised or if infection develops, Vibrio spp. should also be targeted.
Sources of Antivenoms and Other Assistance
Antivenom for stonefish and severe scorpionfish envenomation is available in the U.S. through the pharmacies of Sharp Cabrillo Hospital Emergency Department, San Diego, CA (619-221-3429), and Community Hospital of Monterey Peninsula (CHOMP) Emergency Department, Monterey, CA (408- 625-4900). CHOMP also has sea snake antivenom. If sea snake antivenom is unavailable, tiger snake (N. scutatus) antivenom should be used. Divers Alert Network may be a source of helpful information (24 h a day at 919-684-8111 or at http://www.dan.ycg.org).

MARINE POISONINGS
CIGUATERA   Ciguatera poisoning is the most common nonbacterial food poisoning associated with fish in the U.S. Tropical and semitropical marine coral reef fish are usually the source; 75% of cases involve barracuda, snapper, jack, or grouper. Of the toxins (at least five) that may cause the ciguatera syndrome, not all affect the appearance or taste of the fish, and all are resistant to heat, cold, freeze-drying, and gastric acid. All oversized fish of any predacious reef species, moray eels, and the viscera of tropical marine fish should be suspected of harboring ciguatoxin and should not be eaten.
Most victims experience diarrhea, vomiting, and abdominal pain 3–6 h after ingestion of contaminated fish and develop systemic symptoms within 12 h. Symptoms are myriad and include paresthesia, pruritus, dysphagia, weakness, fasciculations, ataxia, blurred vision, seizures, maculopapular or vesicular rash, diaphoresis, and hemodynamic instability. A pathognomonic symptom—reversal of hot and cold perception—develops within 3–5 days and can last for months. Death is rare. Ciguatera poisoning is diagnosed on clinical grounds.

TREATMENT
Therapy is supportive and based on symptoms. Symptoms are more severe in persons who have previously had ciguatera poisoning. Gastric lavage, ipecac-induced emesis, and PO administration of activated charcoal (100 g) in sorbitol are not of proven efficacy but may be considered if undertaken within 3 h of ingestion. Prochlorperazine (2.5–5 mg IV) can be given for control of emesis. Crystalloid or pressors are given for hypotension as indicated. IV atropine (0.5 mg, up to 2 mg) is given for clinically significant bradycardia. Cool showers, hydroxyzine (25 mg PO q6–8h), or amitriptyline (25 mg PO bid) may ameliorate pruritus, and amitriptyline or tocainide may relieve dysesthesias. IV-administered mannitol (1 g/kg per day over 45–60 min, days 1–5) may alleviate neurologic or cardiovascular symptoms via reversal of Schwann cell edema and may act as a “hydroxyl scavenger.” During recovery, the pt should avoid ingestion of fish, shellfish, fish oils, fish or shellfish sauces, alcohol, nuts, and nut oils.

PARALYTIC SHELLFISH POISONING (PSP)   PSP is induced by ingestion of contaminated feral or aquacultured filter-feeding organisms, including clams, oysters, scallops, mussels, chitons, limpets, starfish, and sand crabs. These species concentrate chemical toxins via feeding on planktonic dinoflagellates and protozoan organisms that “bloom” in nutrient-rich coastal temperate and semitropical waters. These toxins are water-soluble, are heat- and acid- stable, and are not destroyed by ordinary cooking. The best-known is saxitoxin, which blocks neuromuscular transmission via inhibition of sodium conduction.
Within minutes to hours after ingestion of contaminated shellfish, the victim experiences oral paresthesia progressing to the rest of the neck and the extremities and changing to numbness. Disequilibrium, weakness, hyperreflexia, sialorrhea, diarrhea, nausea, vomiting, headache, and incoherence may develop. Flaccid paralysis and respiratory insufficiency may follow 2–12 h after ingestion.

TREATMENT
If medical attention is sought within the first few hours after ingestion, the pt should undergo gastric lavage and irrigation with 2 L of 2% sodium bicarbonate in 200-mL aliquots. Oral administration of activated charcoal (50– 100 g) in sorbitol has not proved effective. Magnesium-containing cathartics may further suppress nerve conduction and should be avoided. The pt should be monitored for respiratory paralysis for at least 24 h.

DOMOIC ACID INTOXICATION   Ingestion of mussels contaminated with domoic acid, a potent heat-stable neuroexcitatory toxin, causes arousal, confusion, disorientation, and memory loss within 24 h (median time of onset, 5.5 h). Treatment is supportive, with a focus on anticonvulsive measures.
SCOMBROID   Scombroid poisoning is a histamine intoxication due to inadequately preserved or refrigerated fish. Scombroid (mackerel-like) fish include some types of tuna, mackerel, saury, needlefish, wahoo, skipjack, and bonito; since nonscombroid fish can also be implicated, the syndrome may more appropriately be called pseudoallergic fish poisoning. Victims present within 15–90 min of ingestion with flushing, pruritus or urticaria, bronchospasm, GI symptoms, tachycardia, and hypotension; symptoms generally resolve within 8–12 h and may be more severe in pts concurrently taking isoniazid. Treatment consists of antihistamine (H1 or H2) administration. Bronchodilators may be indicated for bronchospasm. Steroids are of no proven benefit.
PFIESTERIA   Pfiesteria, a dinoflagellate with a complex life cycle, releases a neurotoxin that causes fish to die within minutes and a fat-soluble toxin that causes epidermal delamination in fish. Casual exposure to waters infested with Pfiesteria can cause a syndrome defined by the CDC as either of two groups of signs or symptoms: (1) memory loss, confusion, or acute skin burning on contact with infested water; or (2) at least three of the following: headache, rash, eye irritation, upper respiratory irritation, muscle cramps, and GI symptoms. Polluted environments favor growth of Pfiesteria. Treatment consists of 1 teaspoon of milk of magnesia followed by 1 scoop of cholestyramine in 8 oz of water and 70% sorbitol solution, administered daily for 2 weeks.
ARTHROPOD BITES AND STINGS
SPIDER BITES   Only a small minority of all spider species defend themselves aggressively and have fangs capable of penetrating human skin. While most spider bites are painful but not otherwise harmful, envenomation by the brown or fiddle spiders (Loxosceles spp.), the widow spiders (Latrodectus spp.), and certain other spiders may be life-threatening. Identification of the offending spider should be attempted; specific treatments exist for bites of widow and brown recluse spiders.
Recluse Spider Bites and Necrotic Arachnidism   Severe necrosis of skin and subcutaneous tissue follows envenomation by Loxosceles reclusa (the brown recluse spider). Initially the bite is painless or stings. Over the next few hours, the site becomes painful, pruritic, indurated, and surrounded by zones of ischemia and erythema. Fever, chills, headache, and other nonspecific systemic symptoms may develop within 3 days of the bite. Lesions typically resolve without treatment in 2–3 days. In severe cases, erythema spreads; the lesion becomes hemorrhagic and necrotic, with an overlying bulla; and a black eschar develops, sloughs, and leaves a depressed scar. Deaths, although rare, are due to severe hemolysis and renal failure.

TREATMENT
Initial management includes local cleansing, application of sterile dressings and cold compresses, elevation, and loose immobilization. Analgesics, antihistamines, antibiotics, and tetanus prophylaxis should be administered if indicated. Dapsone administration within 48–72 h (50–100 mg PO bid after G6PD deficiency has been ruled out) may halt progression of necrotic lesions. Local or systemic steroids have not proven efficacious. Immediate surgical excision of the wound is detrimental. Antivenom has not been approved for use in the U.S.

Widow Spider Bites   Female widow spiders are notorious for their potent neurotoxin. The black widow (Latrodectus mactans) has been found in every U.S. state except Alaska. The initial bite goes unnoticed or is perceived as a sharp pinprick. Two small red marks, mild erythema, and edema develop at the fang entrance site. Some persons experience no other symptoms. In others, painful cramps spread from the bite site to large muscles of the extremities and trunk within 30–60 min. Extreme abdominal muscular rigidity and pain may mimic peritonitis, but the abdomen is not tender to palpation. Other features include salivation, diaphoresis, vomiting, hypertension, tachycardia, labored breathing, anxiety, headache, weakness, fasciculations, rhabdomyolysis, paresthesia, hyperreflexia, urinary retention, uterine contractions, and premature labor. Death from respiratory arrest, cerebral hemorrhage, or cardiac failure may occur.

TREATMENT
Treatment consists of local cleansing, application of ice packs, and tetanus prophylaxis. Analgesics and antispasmodics (e.g., benzodiazepines and methocarbamol) may mitigate hypertension. If not, specific antihypertensives should be given. Equine antivenom is widely available; rapid IV administration of 1 or 2 vials relieves pain and can be life-saving. Given the risk of allergic reactions, however, the use of antivenom should be reserved for severe cases involving respiratory arrest, refractory hypertension, seizures, or pregnancy.

SCORPION STINGS   Scorpions are crablike arachnids that can inject venom from a stinger on the tip of the tail; they sting human beings only when disturbed. Painful but relatively harmless scorpion stings must be distinguished from the potentially lethal envenomations produced by ~30 of the ~1000 known scorpion species, which annually cause >5000 deaths worldwide. In the U.S., only the bark scorpion (Centruroides sculpturatus or C. exilicauda) is potentially lethal. C. sculpturatus is yellow-brown and ~7 cm long. Envenomations are usually associated with little swelling, but pain, paresthesia, and hyperesthesia can be accentuated by tapping on the affected area. Dysfunction of cranial nerves and hyperexcitability of skeletal muscle develop within hours. Pts present with restlessness, blurred vision, abnormal eye movements, profuse salivation, lacrimation, rhinorrhea, slurred speech, diaphoresis, nausea, vomiting, and difficulty handling secretions. Complications include tachycardia, arrhythmias, hypertension, hyperthermia, rhabdomyolysis, and acidosis. Manifestations are maximal after ~5 h and may subside within a day or two.

TREATMENT
Stings of nonlethal species require ice packs, analgesics, or antihistamines. Pressure dressings and cold packs can decrease the absorption of venom. For victims of envenomations who have cranial nerve or neuromuscular dysfunction, aggressive supportive care and judicious use of antivenom can reduce or eliminate mortality. Continuous IV midazolam infusion can decrease agitation and involuntary muscle movements; however, narcotics and sedatives should be avoided in the setting of neuromuscular dysfunction unless endotracheal intubation is planned. Hypertension, pulmonary edema, and bradyarrhythmias should be anticipated. An investigational caprine C. sculpturatus antivenom (available only in Arizona) carries a risk of anaphylaxis or serum sickness. The benefit of scorpion antivenom has not been established in controlled trials.

HYMENOPTERA AND FIRE ANT STINGS   Hymenoptera Stings   Stinging insects of the order Hymenoptera include apids (bees and bumblebees), vespids (wasps, hornets, and yellow jackets), and ants. About 50 deaths from hymenoptera stings occur annually in the U.S., nearly all from allergic reactions to venoms.
Bees can sting only once; vespids can sting many times in succession. The familiar honeybees (Apis mellifera) and bumblebees (Bombus and other genera) sting only when a colony is disturbed. The Africanized honeybees (“killer bees”), which have spread through South and Central America and the southeastern and western U.S., are extremely aggressive and respond to minimal intrusions in great numbers. Uncomplicated stings cause immediate pain, a wheal-and-flare reaction, and local edema that subside within hours. Multiple stings can lead to vomiting, diarrhea, generalized edema, dyspnea, hypotension, rhabdomyolysis, and renal failure. Victims have died after being stung by honeybees 300–500 times in succession.
Large (>10-cm) local reactions progressing over 1–2 days and resembling cellulitis are not uncommon and are caused by hypersensitivity. They are seldom accompanied by anaphylaxis. About 0.4–4% of the U.S. population exhibits immediate-type hypersensitivity to insect stings. Mild reactions manifest as nausea, abdominal cramps, urticaria, flushing, and angioedema. Serious reactions include upper airway edema, bronchospasm, hypotension, and shock and may be rapidly fatal. Onset usually comes within 10 min of the sting.

TREATMENT
Stingers embedded in the skin should be scraped or brushed off but not removed with a forceps, which may squeeze more venom out. The site should be cleansed and ice packs applied to slow venom absorption. Elevation of the bite site and administration of analgesics, oral antihistamines, and topical calamine lotion may ease symptoms. Oral steroids are indicated for large local reactions. Pts with multiple stings should be monitored for 24 h. Anaphylaxis is treated with epinephrine hydrochloride (0.3–0.5 mL of a 1:1000 solution SC q20–30min as needed). For profound shock, epinephrine (2–5 mL of a 1:10,000 solution by slow IV push) is indicated. Parenteral antihistamines, fluid resuscitation, bronchodilators, oxygen, endotracheal intubation, and vasopressors may be required. Pts should be observed for 24 h until the risk of recurrence has passed. Pts with a history of allergy to insect stings should carry a sting kit and seek medical attention immediately after the kit is used. Those with a history of anaphylaxis should undergo desensitization.

Fire Ant Stings   Stinging fire ants are an important medical problem in the southern U.S. Slight disturbances can provoke massive outpourings of ants from their tall mounds, resulting in as many as 10,000 stings. The initial wheal, burning, and itching resolve in ~30 min. A sterile pustule develops within a day, ulcerates over the next 2 days, and heals in 7–10 days. Stings are treated with ice packs, topical steroids, and oral antihistamines. Anaphylaxis occurs in 1–2% of cases and is managed with epinephrine and supportive measures. Immunotherapy appears to lower the rate of anaphylactic reactions.
TICK BITES AND TICK PARALYSIS
Hard ticks (Ixodidae) have become the most common carriers of vector-borne diseases in the U.S., and soft ticks are vectors of relapsing fever (Table 46-3). Ticks attach and feed painlessly on blood from their hosts; however, their secretions may produce local reactions.

Table 46-3 Diseases Transmitted by Ticks

Tick paralysis is an ascending flaccid paralysis that begins 5–6 days after the tick’s attachment in the lower extremities and ascends symmetrically. Deep tendon reflexes are decreased or absent, but sensory examination is normal. LP is normal. Removal of the tick results in improvement within hours. Failure to remove the tick may lead to dysarthria, dysphagia, and ultimately respiratory paralysis and death. The tick is usually found on the scalp.

TREATMENT
Ticks should be removed with a forceps close to the point of attachment and the skin disinfected. Retained mouth parts may cause ongoing inflammation or lead to secondary infection. Removal within 48 h of attachment usually prevents transmission of Lyme disease, babesiosis, and ehrlichiosis. Protective clothing and DEET application are protective measures against ticks.

Bibliography

For a more detailed discussion, see Madoff LC: Infectious Complications of Bites and Burns, Chap. 127, p. 817; Norris RL, Auerbach PS: Disorders Caused by Reptile Bites and Marine Animal Exposures, Chap. 397, p. 2616; and Maguire JH, Spielman A: Ectoparasite Infestations, Arthropod Bites and Stings, Chap. 398, p. 2622, in HPIM-15.

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