Environmental Dermatology

Identification

The Hymenoptera order of insects includes Apidae (bees), Vespidae (wasps, yellow jackets, hornets), and Formicidae (fire ants). All 3 of these families of insects inject venom into their prey or as a defense mechanism via ovipositors in their abdomen. Vespids are the most aggressive and are found in each of the United States.¹ They have membranous wings, broad antennae, and a nonbarbed stinger (Figure 1).² The nonbarbed stinger of Vespidae differentiates them from Apidae and allows these insects to sting their prey multiple times. Vespids can build nests in the ground (yellow jackets), trees (hornets), or areas of cover such as window shutters (mud wasps). Because only the queens survive winter, larger populations do not develop until late summer when the most stings take place. Stings most often take place near the nest of the vespid or while the victim is eating outdoors.³

Envenomation

When vespids sting their prey they inject venom via their ovipositors.¹ The venom is composed of a mixture of low-molecular-weight proteins, kinins, proteolytic enzymes, lipids, carbohydrates, and high-molecular-weight proteins that act as allergens.^1,4,5 The proteolytic enzymes degrade the surrounding tissue, basophils become activated, and histamine is released secondary to mast cell degranulation, which results in vasodilation and an inflammatory response characterized by edema, erythema, warmth, and pain.¹ The pain of the sting is immediate and can be intense; almost all victims are acutely aware of the discomforting sensation.⁴

Management of Reactions

Three types of reactions can be seen after a vespid sting: uncomplicated local reactions, large local reactions, and systemic reactions (SRs). The most common reaction is the self-limiting uncomplicated local reaction that includes a focal area of warmth, edema, erythema, induration, and tenderness.¹ Treatment of this kind of reaction is supportive, with ice, nonsteroidal anti-inflammatory drugs, and H₁ and H₂ blockers being commonly used methods. Large local reactions (Figure 2) are similar to uncomplicated local reactions but are greater than 10 cm in diameter and last longer. The same symptomatic treatment may be used along with possible short (3–5 days) oral glucocorticoid (40–60 mg prednisone) or potent topical steroid administration if symptoms persist. Systemic reactions involve IgE-mediated generalized urticaria, angioedema, face swelling, stridor, bronchospasm, nausea, vomiting, flushing, and respiratory distress.¹ Emergency management includes maintenance of airway, breathing, and circulation. Epinephrine injection commonly is employed and should be given via intramuscular injection into the anterolateral thigh; a dose of 0.3 to 0.5 mg can be repeatedly injected every 5 to 15 minutes, as needed.¹

If an individual has an SR, it is recommended to go to an emergency department after stabilization for monitoring. Referral to an allergist for desensitization is appropriate. A radioallergosorbent test to measure allergen-specific IgE can be helpful to confirm an allergy.⁴ This test also should be done weeks after the incident because during the first few days IgE may be too low to measure. Once the allergy is confirmed, the desensitization with venom immunotherapy (VIT) can begin. Venom immunotherapy is effective and reduces a patient’s risk for recurrent SRs to less than 5% to 20%.⁶ A 2015 study recommended longer duration of VIT therapy due to risk for repeat SRs after discontinuing therapy. This study concluded that VIT is to be administered for 5 years, unless the patient is at high risk for SRs after VIT therapy—risk factors include older age, cardiopulmonary disease, SR during VIT treatment, mast cell disorders, and elevated serum tryptase—in which case VIT may have to be continued indefinitely. It is recommended that all patients with history of SR carry an epinephrine autoinjector in case of emergency.⁶

Epidemiologic data show a prevalence of 0.3% to 7.5% for self-reported SRs due to stings, with lower prevalence in children (0.15%–0.3%).^4,7 An additional study looking at data from an allergy practice determined 24% of all cases of anaphylaxis were due to insect stings.⁵

Conclusion

Although many vespid stings can be managed symptomatically, it is imperative for patients and providers to be aware of the possible severe reactions that can take place. It is essential for providers to be aware of how to care for and treat large local reactions and SRs, as symptom recognition and timely treatment can improve patient safety and result in better outcomes.

Identification

The Hymenoptera order of insects includes Apidae (bees), Vespidae (wasps, yellow jackets, hornets), and Formicidae (fire ants). All 3 of these families of insects inject venom into their prey or as a defense mechanism via ovipositors in their abdomen. Vespids are the most aggressive and are found in each of the United States.¹ They have membranous wings, broad antennae, and a nonbarbed stinger (Figure 1).² The nonbarbed stinger of Vespidae differentiates them from Apidae and allows these insects to sting their prey multiple times. Vespids can build nests in the ground (yellow jackets), trees (hornets), or areas of cover such as window shutters (mud wasps). Because only the queens survive winter, larger populations do not develop until late summer when the most stings take place. Stings most often take place near the nest of the vespid or while the victim is eating outdoors.³

Envenomation

When vespids sting their prey they inject venom via their ovipositors.¹ The venom is composed of a mixture of low-molecular-weight proteins, kinins, proteolytic enzymes, lipids, carbohydrates, and high-molecular-weight proteins that act as allergens.^1,4,5 The proteolytic enzymes degrade the surrounding tissue, basophils become activated, and histamine is released secondary to mast cell degranulation, which results in vasodilation and an inflammatory response characterized by edema, erythema, warmth, and pain.¹ The pain of the sting is immediate and can be intense; almost all victims are acutely aware of the discomforting sensation.⁴

Management of Reactions

Three types of reactions can be seen after a vespid sting: uncomplicated local reactions, large local reactions, and systemic reactions (SRs). The most common reaction is the self-limiting uncomplicated local reaction that includes a focal area of warmth, edema, erythema, induration, and tenderness.¹ Treatment of this kind of reaction is supportive, with ice, nonsteroidal anti-inflammatory drugs, and H₁ and H₂ blockers being commonly used methods. Large local reactions (Figure 2) are similar to uncomplicated local reactions but are greater than 10 cm in diameter and last longer. The same symptomatic treatment may be used along with possible short (3–5 days) oral glucocorticoid (40–60 mg prednisone) or potent topical steroid administration if symptoms persist. Systemic reactions involve IgE-mediated generalized urticaria, angioedema, face swelling, stridor, bronchospasm, nausea, vomiting, flushing, and respiratory distress.¹ Emergency management includes maintenance of airway, breathing, and circulation. Epinephrine injection commonly is employed and should be given via intramuscular injection into the anterolateral thigh; a dose of 0.3 to 0.5 mg can be repeatedly injected every 5 to 15 minutes, as needed.¹

If an individual has an SR, it is recommended to go to an emergency department after stabilization for monitoring. Referral to an allergist for desensitization is appropriate. A radioallergosorbent test to measure allergen-specific IgE can be helpful to confirm an allergy.⁴ This test also should be done weeks after the incident because during the first few days IgE may be too low to measure. Once the allergy is confirmed, the desensitization with venom immunotherapy (VIT) can begin. Venom immunotherapy is effective and reduces a patient’s risk for recurrent SRs to less than 5% to 20%.⁶ A 2015 study recommended longer duration of VIT therapy due to risk for repeat SRs after discontinuing therapy. This study concluded that VIT is to be administered for 5 years, unless the patient is at high risk for SRs after VIT therapy—risk factors include older age, cardiopulmonary disease, SR during VIT treatment, mast cell disorders, and elevated serum tryptase—in which case VIT may have to be continued indefinitely. It is recommended that all patients with history of SR carry an epinephrine autoinjector in case of emergency.⁶

Epidemiologic data show a prevalence of 0.3% to 7.5% for self-reported SRs due to stings, with lower prevalence in children (0.15%–0.3%).^4,7 An additional study looking at data from an allergy practice determined 24% of all cases of anaphylaxis were due to insect stings.⁵

Conclusion

Although many vespid stings can be managed symptomatically, it is imperative for patients and providers to be aware of the possible severe reactions that can take place. It is essential for providers to be aware of how to care for and treat large local reactions and SRs, as symptom recognition and timely treatment can improve patient safety and result in better outcomes.

Identification

The Hymenoptera order of insects includes Apidae (bees), Vespidae (wasps, yellow jackets, hornets), and Formicidae (fire ants). All 3 of these families of insects inject venom into their prey or as a defense mechanism via ovipositors in their abdomen. Vespids are the most aggressive and are found in each of the United States.¹ They have membranous wings, broad antennae, and a nonbarbed stinger (Figure 1).² The nonbarbed stinger of Vespidae differentiates them from Apidae and allows these insects to sting their prey multiple times. Vespids can build nests in the ground (yellow jackets), trees (hornets), or areas of cover such as window shutters (mud wasps). Because only the queens survive winter, larger populations do not develop until late summer when the most stings take place. Stings most often take place near the nest of the vespid or while the victim is eating outdoors.³

Envenomation

When vespids sting their prey they inject venom via their ovipositors.¹ The venom is composed of a mixture of low-molecular-weight proteins, kinins, proteolytic enzymes, lipids, carbohydrates, and high-molecular-weight proteins that act as allergens.^1,4,5 The proteolytic enzymes degrade the surrounding tissue, basophils become activated, and histamine is released secondary to mast cell degranulation, which results in vasodilation and an inflammatory response characterized by edema, erythema, warmth, and pain.¹ The pain of the sting is immediate and can be intense; almost all victims are acutely aware of the discomforting sensation.⁴

Management of Reactions

Three types of reactions can be seen after a vespid sting: uncomplicated local reactions, large local reactions, and systemic reactions (SRs). The most common reaction is the self-limiting uncomplicated local reaction that includes a focal area of warmth, edema, erythema, induration, and tenderness.¹ Treatment of this kind of reaction is supportive, with ice, nonsteroidal anti-inflammatory drugs, and H₁ and H₂ blockers being commonly used methods. Large local reactions (Figure 2) are similar to uncomplicated local reactions but are greater than 10 cm in diameter and last longer. The same symptomatic treatment may be used along with possible short (3–5 days) oral glucocorticoid (40–60 mg prednisone) or potent topical steroid administration if symptoms persist. Systemic reactions involve IgE-mediated generalized urticaria, angioedema, face swelling, stridor, bronchospasm, nausea, vomiting, flushing, and respiratory distress.¹ Emergency management includes maintenance of airway, breathing, and circulation. Epinephrine injection commonly is employed and should be given via intramuscular injection into the anterolateral thigh; a dose of 0.3 to 0.5 mg can be repeatedly injected every 5 to 15 minutes, as needed.¹

If an individual has an SR, it is recommended to go to an emergency department after stabilization for monitoring. Referral to an allergist for desensitization is appropriate. A radioallergosorbent test to measure allergen-specific IgE can be helpful to confirm an allergy.⁴ This test also should be done weeks after the incident because during the first few days IgE may be too low to measure. Once the allergy is confirmed, the desensitization with venom immunotherapy (VIT) can begin. Venom immunotherapy is effective and reduces a patient’s risk for recurrent SRs to less than 5% to 20%.⁶ A 2015 study recommended longer duration of VIT therapy due to risk for repeat SRs after discontinuing therapy. This study concluded that VIT is to be administered for 5 years, unless the patient is at high risk for SRs after VIT therapy—risk factors include older age, cardiopulmonary disease, SR during VIT treatment, mast cell disorders, and elevated serum tryptase—in which case VIT may have to be continued indefinitely. It is recommended that all patients with history of SR carry an epinephrine autoinjector in case of emergency.⁶

Epidemiologic data show a prevalence of 0.3% to 7.5% for self-reported SRs due to stings, with lower prevalence in children (0.15%–0.3%).^4,7 An additional study looking at data from an allergy practice determined 24% of all cases of anaphylaxis were due to insect stings.⁵

Conclusion

Although many vespid stings can be managed symptomatically, it is imperative for patients and providers to be aware of the possible severe reactions that can take place. It is essential for providers to be aware of how to care for and treat large local reactions and SRs, as symptom recognition and timely treatment can improve patient safety and result in better outcomes.

Classification

Blister beetles are both a scourge and the source of medical cantharidin (Figure 1). The term blister beetle refers to 3 families of the order Coleoptera: Meloidae, Oedemeridae, and Staphylinidae (Figure 2).

Meloidae is the most well-known family of blister beetles, with more than 200 species worldwide identified as a cause of blistering dermatitis.¹ The most notorious is Lytta vesicatoria, also known as the Spanish fly. Although some blister beetles are inconspicuous in appearance, most are brightly colored and easily spotted, making them attractive to small children.² They may be attracted to fluorescent lighting and commonly enter through open windows.³ Blister beetles do not bite or sting; rather, they release cantharidin via hemolymph, an oily yellow substance that is copiously expressed from the leg joints when disturbed by rubbing or pressing.^1,3-5 Blistering also is associated with exposure to the contents of crushed beetles, which is the source of pharmacologic cantharidin.^2,4,6

Oedemeridae are the smallest and least known beetles within the Coleoptera family. They often are called false blister beetles, which is a misnomer. Oedemeridae beetles also produce cantharidin, similar to Meloidae beetles; however, because Oedemeridae beetles are smaller, the vesiculobullous eruptions also are less pronounced.¹

A third well-known family of blister beetles is the Staphylinidae family. Rove beetles (genus Paederus) differ from the Meloidae and Oedemeridae families in that they produce the vesicant pederin rather than cantharidin. Pederin causes a more violent eruption called dermatitis linearis, which often is associated with intense urticaria prior to blistering.¹ Rove beetles are found in moist environments and tend to favor tropical and subtropical climates. They may emerge in large numbers after heavy rainfall.

Clinical Presentation

Blistering dermatitis—caused by exposure to cantharidin (families Meloidae and Oedemeridae) or pederin (genus Paederus)—begins as burning and tingling within minutes of exposure. Bullae later develop, often in a linear fashion, with subsequent bursting and crust formation.^1,3 Secondary infection can occur.⁵ Exposure occurring on the elbows, knees, or mirroring skin folds results in lesions on opposing surfaces that come into contact, otherwise known as kissing lesions.^1,3 Acantholysis of suprabasal keratinocytes can be seen on histologic sections of blisters (Figure 3)^1,7 due to cantharidin activation of the serine/threonine protein phosphatases that cause detachment of tonofilaments from desmosomes.^1,8 Washing of exposed sites with soap or alcohol can potentially prevent development of blistering dermatitis; however, lesions usually heal without complication when treated with topical antibiotics.³

If blister beetles are ingested, they can cause poisoning characterized by abdominal pain and hematuria.^1,3,9,10 In fact, blister beetle ingestion by animals consuming baled hay is an important agricultural and economical implication. Several cases of fatal farm animal ingestion resulting in gastrointestinal erosion have been reported.^4,6

Medicinal Properties

Medicinal use of cantharidin has been recorded as early as the 19th century and is believed to have been part of ancient medicinal practices in China, Spain, South Africa, and pre-Columbian America for its vesicant, abortifacient, and supposed aphrodisiac properties.^2,4,8

Toxicity from internal ingestion has been well documented.^1,3,9,10 The Mylabris and Epicauta genera of the family Meloidae, most commonly the Spanish fly, are used for modern extraction of cantharidin. Up to 5% of the dry weight of a blister beetle can be constituted by cantharidin.⁴

Although its use has diminished due to limited availability, cantharidin is still used for treatment of common warts, periungual warts, and molluscum contagiosum. It is a favorable choice for treating pediatric patients because of the tolerability and painlessness of application. Due to its acantholytic properties, warts generally slough with the cantharidin-induced blister.¹¹

In recent years, cantharidin has been studied for its anticancer properties. It has been shown to weaken cancer cell antioxidant properties by interfering with glutathione-related enzymes, thus inducing oxidative damage. Additionally, cantharidin is associated with decreased mitochondrial cytochrome C and increased cytosolic cytochrome C, an important signal for apoptosis.¹² Furthermore, cantharidin recently was shown to increase expression of proapoptotic proteins and decrease expression of antiapoptotic proteins causing cell death in nasopharyngeal carcinoma, making it a potential anticancer treatment.¹³

Conclusion

Blister beetles, long known for their production of vesicant agents, are both a cause of as well as a potential treatment of dermatologic disease. The blistering associated with exposure to a disturbed beetle generally is mild and heals without scarring if vital areas such as the eyelids are not affected.

Classification

Blister beetles are both a scourge and the source of medical cantharidin (Figure 1). The term blister beetle refers to 3 families of the order Coleoptera: Meloidae, Oedemeridae, and Staphylinidae (Figure 2).

Meloidae is the most well-known family of blister beetles, with more than 200 species worldwide identified as a cause of blistering dermatitis.¹ The most notorious is Lytta vesicatoria, also known as the Spanish fly. Although some blister beetles are inconspicuous in appearance, most are brightly colored and easily spotted, making them attractive to small children.² They may be attracted to fluorescent lighting and commonly enter through open windows.³ Blister beetles do not bite or sting; rather, they release cantharidin via hemolymph, an oily yellow substance that is copiously expressed from the leg joints when disturbed by rubbing or pressing.^1,3-5 Blistering also is associated with exposure to the contents of crushed beetles, which is the source of pharmacologic cantharidin.^2,4,6

Oedemeridae are the smallest and least known beetles within the Coleoptera family. They often are called false blister beetles, which is a misnomer. Oedemeridae beetles also produce cantharidin, similar to Meloidae beetles; however, because Oedemeridae beetles are smaller, the vesiculobullous eruptions also are less pronounced.¹

A third well-known family of blister beetles is the Staphylinidae family. Rove beetles (genus Paederus) differ from the Meloidae and Oedemeridae families in that they produce the vesicant pederin rather than cantharidin. Pederin causes a more violent eruption called dermatitis linearis, which often is associated with intense urticaria prior to blistering.¹ Rove beetles are found in moist environments and tend to favor tropical and subtropical climates. They may emerge in large numbers after heavy rainfall.

Clinical Presentation

Blistering dermatitis—caused by exposure to cantharidin (families Meloidae and Oedemeridae) or pederin (genus Paederus)—begins as burning and tingling within minutes of exposure. Bullae later develop, often in a linear fashion, with subsequent bursting and crust formation.^1,3 Secondary infection can occur.⁵ Exposure occurring on the elbows, knees, or mirroring skin folds results in lesions on opposing surfaces that come into contact, otherwise known as kissing lesions.^1,3 Acantholysis of suprabasal keratinocytes can be seen on histologic sections of blisters (Figure 3)^1,7 due to cantharidin activation of the serine/threonine protein phosphatases that cause detachment of tonofilaments from desmosomes.^1,8 Washing of exposed sites with soap or alcohol can potentially prevent development of blistering dermatitis; however, lesions usually heal without complication when treated with topical antibiotics.³

If blister beetles are ingested, they can cause poisoning characterized by abdominal pain and hematuria.^1,3,9,10 In fact, blister beetle ingestion by animals consuming baled hay is an important agricultural and economical implication. Several cases of fatal farm animal ingestion resulting in gastrointestinal erosion have been reported.^4,6

Medicinal Properties

Medicinal use of cantharidin has been recorded as early as the 19th century and is believed to have been part of ancient medicinal practices in China, Spain, South Africa, and pre-Columbian America for its vesicant, abortifacient, and supposed aphrodisiac properties.^2,4,8

Toxicity from internal ingestion has been well documented.^1,3,9,10 The Mylabris and Epicauta genera of the family Meloidae, most commonly the Spanish fly, are used for modern extraction of cantharidin. Up to 5% of the dry weight of a blister beetle can be constituted by cantharidin.⁴

Although its use has diminished due to limited availability, cantharidin is still used for treatment of common warts, periungual warts, and molluscum contagiosum. It is a favorable choice for treating pediatric patients because of the tolerability and painlessness of application. Due to its acantholytic properties, warts generally slough with the cantharidin-induced blister.¹¹

In recent years, cantharidin has been studied for its anticancer properties. It has been shown to weaken cancer cell antioxidant properties by interfering with glutathione-related enzymes, thus inducing oxidative damage. Additionally, cantharidin is associated with decreased mitochondrial cytochrome C and increased cytosolic cytochrome C, an important signal for apoptosis.¹² Furthermore, cantharidin recently was shown to increase expression of proapoptotic proteins and decrease expression of antiapoptotic proteins causing cell death in nasopharyngeal carcinoma, making it a potential anticancer treatment.¹³

Conclusion

Blister beetles, long known for their production of vesicant agents, are both a cause of as well as a potential treatment of dermatologic disease. The blistering associated with exposure to a disturbed beetle generally is mild and heals without scarring if vital areas such as the eyelids are not affected.

Classification

Blister beetles are both a scourge and the source of medical cantharidin (Figure 1). The term blister beetle refers to 3 families of the order Coleoptera: Meloidae, Oedemeridae, and Staphylinidae (Figure 2).

Meloidae is the most well-known family of blister beetles, with more than 200 species worldwide identified as a cause of blistering dermatitis.¹ The most notorious is Lytta vesicatoria, also known as the Spanish fly. Although some blister beetles are inconspicuous in appearance, most are brightly colored and easily spotted, making them attractive to small children.² They may be attracted to fluorescent lighting and commonly enter through open windows.³ Blister beetles do not bite or sting; rather, they release cantharidin via hemolymph, an oily yellow substance that is copiously expressed from the leg joints when disturbed by rubbing or pressing.^1,3-5 Blistering also is associated with exposure to the contents of crushed beetles, which is the source of pharmacologic cantharidin.^2,4,6

Oedemeridae are the smallest and least known beetles within the Coleoptera family. They often are called false blister beetles, which is a misnomer. Oedemeridae beetles also produce cantharidin, similar to Meloidae beetles; however, because Oedemeridae beetles are smaller, the vesiculobullous eruptions also are less pronounced.¹

A third well-known family of blister beetles is the Staphylinidae family. Rove beetles (genus Paederus) differ from the Meloidae and Oedemeridae families in that they produce the vesicant pederin rather than cantharidin. Pederin causes a more violent eruption called dermatitis linearis, which often is associated with intense urticaria prior to blistering.¹ Rove beetles are found in moist environments and tend to favor tropical and subtropical climates. They may emerge in large numbers after heavy rainfall.

Clinical Presentation

Blistering dermatitis—caused by exposure to cantharidin (families Meloidae and Oedemeridae) or pederin (genus Paederus)—begins as burning and tingling within minutes of exposure. Bullae later develop, often in a linear fashion, with subsequent bursting and crust formation.^1,3 Secondary infection can occur.⁵ Exposure occurring on the elbows, knees, or mirroring skin folds results in lesions on opposing surfaces that come into contact, otherwise known as kissing lesions.^1,3 Acantholysis of suprabasal keratinocytes can be seen on histologic sections of blisters (Figure 3)^1,7 due to cantharidin activation of the serine/threonine protein phosphatases that cause detachment of tonofilaments from desmosomes.^1,8 Washing of exposed sites with soap or alcohol can potentially prevent development of blistering dermatitis; however, lesions usually heal without complication when treated with topical antibiotics.³

If blister beetles are ingested, they can cause poisoning characterized by abdominal pain and hematuria.^1,3,9,10 In fact, blister beetle ingestion by animals consuming baled hay is an important agricultural and economical implication. Several cases of fatal farm animal ingestion resulting in gastrointestinal erosion have been reported.^4,6

Medicinal Properties

Medicinal use of cantharidin has been recorded as early as the 19th century and is believed to have been part of ancient medicinal practices in China, Spain, South Africa, and pre-Columbian America for its vesicant, abortifacient, and supposed aphrodisiac properties.^2,4,8

Toxicity from internal ingestion has been well documented.^1,3,9,10 The Mylabris and Epicauta genera of the family Meloidae, most commonly the Spanish fly, are used for modern extraction of cantharidin. Up to 5% of the dry weight of a blister beetle can be constituted by cantharidin.⁴

Although its use has diminished due to limited availability, cantharidin is still used for treatment of common warts, periungual warts, and molluscum contagiosum. It is a favorable choice for treating pediatric patients because of the tolerability and painlessness of application. Due to its acantholytic properties, warts generally slough with the cantharidin-induced blister.¹¹

In recent years, cantharidin has been studied for its anticancer properties. It has been shown to weaken cancer cell antioxidant properties by interfering with glutathione-related enzymes, thus inducing oxidative damage. Additionally, cantharidin is associated with decreased mitochondrial cytochrome C and increased cytosolic cytochrome C, an important signal for apoptosis.¹² Furthermore, cantharidin recently was shown to increase expression of proapoptotic proteins and decrease expression of antiapoptotic proteins causing cell death in nasopharyngeal carcinoma, making it a potential anticancer treatment.¹³

Conclusion

Blister beetles, long known for their production of vesicant agents, are both a cause of as well as a potential treatment of dermatologic disease. The blistering associated with exposure to a disturbed beetle generally is mild and heals without scarring if vital areas such as the eyelids are not affected.

Rattlesnakes are pit vipers with a rattle attached to the tip of the tail and facial pits located between the eyes and nose with a special organ that detects heat energy (infrared light) and is used for hunting prey. There are 2 genera of rattlesnakes, Sistrurus (3 species) and Crotalus (23 species). ¹ The pigmy rattlesnake belongs to the Sistrurus miliarius species that is subdivided into 3 subspecies: the Carolina pigmy rattlesnake (Sistrurus miliarius miliarius), the Western pigmy rattlesnake (Sistrurus miliarius streckeri ), and the dusky pigmy rattlesnake (Sistrurus miliarius barbouri ). ¹ The dusky pigmy rattlesnake is found in South Carolina, southern Georgia, southern Alabama, southeastern Mississippi, and Florida. ² It is the most abundant venomous snake in Florida. ³ Its rattle is barely audible, and it is an aggressive small snake ranging in length from 38 to 56 cm. ⁴ Its venom is hemorrhagic, causing tissue damage but not containing neurotoxins. ⁴ Although bites can be painful, resulting in localized necrosis and rare loss of digits, it is unlikely for bites to be fatal given the snake’s small fangs, small size, and amount of envenomation. However, bites on children may require hospitalization. The venom contains proteins, polypeptides, and enzymes. ⁵ One such peptide, barbourin, inhibits a transmembrane receptor that plays a role in platelet aggregation. ⁶

We report a case of a 54-year-old man who was bitten on the left index finger by a dusky pigmy rattlesnake. We describe the clinical course and successful treatment with crotalidae polyvalent immune fab (CPIF) antivenom.

Case Report

A 54-year-old man presented to the emergency department with a rapidly swelling and erythematous left hand following a snakebite to the left index fingertip while weeding in his yard (Figure 1). The patient was able to kill the snake with a shovel and photograph it, which helped identify it as a dusky pigmy rattlesnake (Figure 2). Vitals on presentation included a blood pressure of 161/98, pulse oximeter of 99%, temperature of 36.4°C, pulse of 84 beats per minute, and respiratory rate of 16 breaths per minute.

Given the poisonous snakebite, the patient was admitted to the intensive care unit. Laboratory test results at admission revealed the following values: platelet count, 235,000/µL (reference range, 150,000–450,000/µL); fibrinogen, 226.1 mg/dL (reference range, 185–410 mg/dL); fibrin degradation products, less than 10 µg/mL (reference range, <10 µg/mL); glucose, 145 mg/dL (reference range, 74–106 mg/dL). The remainder of the complete blood cell count and metabolic panel was unremarkable. His blood type was O Rh+. Radiography of the left second digit did not show any fractures, dislocations, or foreign object.

After consulting with the Tampa General Hospital Florida Poison Information Center, 6 vials of CPIF antivenom in 250 mL of sodium chloride initially were infused intravenously, followed by 2 additional vials each at 6, 12, and 18 hours. Serial laboratory test results revealed white blood cell counts of 13,600, 10,000, 6800, 6100, and 6800/µL at 4, 15, 43, 65, and 88 hours postadmission, respectively. Platelet counts were 222,000, 159,000, 116,000, 99,000, and 129,000/µL at 4, 15, 43, 65, and 88 hours postadmission, respectively. The hemoglobin level was 14.8, 13.1, 13.8, 13.7, and 14.3 g/dL at 4, 15, 43, 65, and 88 hours postadmission, respectively. Other laboratory test results including prothrombin time (10.0 s), fibrinogen (226.1 mg/dL), and fibrin degradation products (<10 µg/mL) at 4 hours postadmission remained within reference range during serial monitoring.

Comment

Envenomation
Snakebites and envenomation are a complex and broad subject beyond the scope of this article and further reading on this subject is highly encouraged. The clinical findings from snakebites range from mild local tissue reactions to severe systemic symptoms depending on the volume of venom injected, snake species, age and health of victim, and location of bite. Severe systemic symptoms include disseminated intravascular coagulation, acute renal failure, hypovolemic shock, and death.⁵ Venom can be hemotoxic and/or neurotoxic. Hemotoxic symptoms include pain, edema, swelling, ecchymoses, necrosis, and hemolysis. Neurotoxic symptoms may encompass diplopia, dysphagia, sweating, salivation, diaphoresis, respiratory depression, and paralysis.⁵ The pigmy rattlesnake venom is only hemotoxic, not neurotoxic.⁴ Eastern and western variety rattlesnakes account for most snake deaths due to their potent venom. Water moccasins (cottonmouths) have intermediate-potency venom, and copperhead snakes have the least-potent venom.⁵ Coral snakes are not pit vipers and require a different antivenom.

Management of Snakebites
Venomous snakes may bite a person without injecting venom. In fact, as many as 20% to 25% of all pit viper bites are dry.⁷ No attempts should be made to capture or kill the biting snake, but identifying it safely is helpful. Dead snakes should not be handled carelessly, as reflex biting after death has been reported.⁸ Cutting or suctioning the bite wound, nonsteroidal anti-inflammatory drugs, prophylactic antibiotics, tourniquets, prophylactic fasciotomy, and ice have not proven to be beneficial in the management of viper envenomation.^5,9-11 The best management involves immobilizing the affected extremity, seeking immediate medical attention, and initiating antivenom therapy as soon as possible.

Antivenom Therapy
Crotalidae polyvalent immune fab is an antivenom comprised of purified, sheep-derived fab IgG fragments and was approved by the US Food and Drug Administration in 2000 for the treatment of North American crotalid envenomation.^12,13 Its venom-specific fab fragments of IgG bind to and neutralize venom toxins and facilitate their elimination. Crotalidae polyvalent immune fab does not contain the Fc fragment of the IgG antibody, resulting in a low incidence of hypersensitivity reactions (8%) and serum sickness (13%).¹³ It is produced using 4 North American venoms: Crotalus atrox (western diamondback rattlesnake), Crotalus adamanteus (eastern diamondback rattlesnake), Crotalus scutulatus (Mojave rattlesnake), and Agkistrodon piscivorus (water moccasin).¹² It has become the standard-of-care antivenom for pit viper bites and has replaced its equine-derived predecessor antivenin crotalidae polyvalent, which is known for high rates of acute allergic reactions (23%–56%) including anaphylaxis and delayed serum sickness.^13,14 In postmarketing studies, CPIF has demonstrated control of envenomation regardless of severity. The most common adverse reactions reported include urticaria, rash, nausea, pruritus, and back pain.¹³ Anaphylaxis and anaphylactoid reactions may occur, and patients should be carefully observed during antivenom infusion. Appropriate management should be readily available including epinephrine, intravenous antihistamines, and/or albuterol. Contraindications include known hypersensitivity to papaya or papain, which is used to cleave the antibodies into fragments during the processing of CPIF. Patients also may react to it if allergic to other papaya extracts, chymopapain, or bromelain (pineapple enzyme), as well as some dust mite allergens and latex allergens that share antigenic structures with papain.¹⁵ Each vial of CPIF is reconstituted with 18 mL of 0.9% sodium chloride, as described in the package insert.¹³ The total dose (minimum of 4 to maximum of 12 vials initial dose) is then diluted in 250 mL of normal saline and infused over 1 hour starting for the first 10 minutes at a rate of 25 to 50 mL/h, and if tolerated, then increased to 250 mL/h until completion.

Treatment Algorithm
According to the envenomation consensus treatment algorithm, assess the site of the snakebite and mark leading edge of swelling every 15 to 30 minutes,¹⁶ as shown in our patient in Figure 6.Immobilize and elevate the affected extremity. Update tetanus vaccine and order initial laboratory tests to include prothrombin time, hemoglobin, platelets, and fibrinogen. If the patient does not exhibit local signs of envenomation such as redness, swelling, or ecchymosis, and the patient has no coagulation laboratory abnormalities and exhibits no systemic signs such as diarrhea, vomiting or angioedema, withhold CPIF and observe the patient for a minimum of 8 hours. Repeat laboratory tests prior to discharge. This clinical scenario most likely occurs in the setting of a dry bite or no bite at all. For minor envenomation, it also is possible to withhold CPIF and observe the patient for 12 to 24 hours if he/she remains stable and laboratory tests remain within reference range. If the patient has local or systemic signs of envenomation, start CPIF (4–6 vials and up to a maximum of 12 vials). The first dose of CPIF should be administered in the emergency department or intensive care unit. If after the first hour envenomation is worsening, an additional 4 to 6 vials may be infused. If after the first hour of observation the envenomation is controlled based on decreased swelling or lack of progression and there is improvement in laboratory values, then a maintenance regimen can be initiated. The maintenance dose consists of 2 vials every 6 hours for up to 18 hours (3 separate 2-vial doses). Patients can be discharged if stable and with no negative laboratory trends during the observation period.¹⁶ If CPIF was administered, follow-up laboratory tests results are dependent on prior findings of coagulation abnormalities, degree of envenomation, and signs and symptoms of coagulopathy postdischarge. Recurrent coagulopathy can occur in patients with coagulation abnormalities during initial envenomation, and patients should be monitored for possible re-treatment for at least 1 week or longer.¹⁷ Coagulopathy can present with decreased fibrinogen, decreased platelets, and elevated prothrombin time. Our patient experienced a drop in platelet count and hemoglobin level in addition to localized tissue effects, but he responded to the antivenom therapy. Lastly and importantly, no pediatric adjustments are necessary, and although mercury has been removed from the product’s manufacturing process, certain easily identifiable antivenom lots that have not expired contain ethyl mercury from thimerosal.^13,18,19 Some side effects of thimerosal include redness and swelling of the injection site, but scientific research does not show a connection with autism.²⁰

Conclusion

Dusky pigmy rattlesnake envenomations are clinically responsive to CPIF antivenom treatment.²¹ Although no clearly documented fatalities have been reported from dusky pigmy rattlesnake bites, coagulopathy and local tissue necrosis—as described in our patient—can result from such snakebites, requiring hospitalization. These snakes are common in the southeastern United States, and the treatment algorithm presented can be extrapolated to other more serious and deadly pit viper bites.

Rattlesnakes are pit vipers with a rattle attached to the tip of the tail and facial pits located between the eyes and nose with a special organ that detects heat energy (infrared light) and is used for hunting prey. There are 2 genera of rattlesnakes, Sistrurus (3 species) and Crotalus (23 species). ¹ The pigmy rattlesnake belongs to the Sistrurus miliarius species that is subdivided into 3 subspecies: the Carolina pigmy rattlesnake (Sistrurus miliarius miliarius), the Western pigmy rattlesnake (Sistrurus miliarius streckeri ), and the dusky pigmy rattlesnake (Sistrurus miliarius barbouri ). ¹ The dusky pigmy rattlesnake is found in South Carolina, southern Georgia, southern Alabama, southeastern Mississippi, and Florida. ² It is the most abundant venomous snake in Florida. ³ Its rattle is barely audible, and it is an aggressive small snake ranging in length from 38 to 56 cm. ⁴ Its venom is hemorrhagic, causing tissue damage but not containing neurotoxins. ⁴ Although bites can be painful, resulting in localized necrosis and rare loss of digits, it is unlikely for bites to be fatal given the snake’s small fangs, small size, and amount of envenomation. However, bites on children may require hospitalization. The venom contains proteins, polypeptides, and enzymes. ⁵ One such peptide, barbourin, inhibits a transmembrane receptor that plays a role in platelet aggregation. ⁶

We report a case of a 54-year-old man who was bitten on the left index finger by a dusky pigmy rattlesnake. We describe the clinical course and successful treatment with crotalidae polyvalent immune fab (CPIF) antivenom.

Case Report

A 54-year-old man presented to the emergency department with a rapidly swelling and erythematous left hand following a snakebite to the left index fingertip while weeding in his yard (Figure 1). The patient was able to kill the snake with a shovel and photograph it, which helped identify it as a dusky pigmy rattlesnake (Figure 2). Vitals on presentation included a blood pressure of 161/98, pulse oximeter of 99%, temperature of 36.4°C, pulse of 84 beats per minute, and respiratory rate of 16 breaths per minute.

Given the poisonous snakebite, the patient was admitted to the intensive care unit. Laboratory test results at admission revealed the following values: platelet count, 235,000/µL (reference range, 150,000–450,000/µL); fibrinogen, 226.1 mg/dL (reference range, 185–410 mg/dL); fibrin degradation products, less than 10 µg/mL (reference range, <10 µg/mL); glucose, 145 mg/dL (reference range, 74–106 mg/dL). The remainder of the complete blood cell count and metabolic panel was unremarkable. His blood type was O Rh+. Radiography of the left second digit did not show any fractures, dislocations, or foreign object.

After consulting with the Tampa General Hospital Florida Poison Information Center, 6 vials of CPIF antivenom in 250 mL of sodium chloride initially were infused intravenously, followed by 2 additional vials each at 6, 12, and 18 hours. Serial laboratory test results revealed white blood cell counts of 13,600, 10,000, 6800, 6100, and 6800/µL at 4, 15, 43, 65, and 88 hours postadmission, respectively. Platelet counts were 222,000, 159,000, 116,000, 99,000, and 129,000/µL at 4, 15, 43, 65, and 88 hours postadmission, respectively. The hemoglobin level was 14.8, 13.1, 13.8, 13.7, and 14.3 g/dL at 4, 15, 43, 65, and 88 hours postadmission, respectively. Other laboratory test results including prothrombin time (10.0 s), fibrinogen (226.1 mg/dL), and fibrin degradation products (<10 µg/mL) at 4 hours postadmission remained within reference range during serial monitoring.

Comment

Envenomation
Snakebites and envenomation are a complex and broad subject beyond the scope of this article and further reading on this subject is highly encouraged. The clinical findings from snakebites range from mild local tissue reactions to severe systemic symptoms depending on the volume of venom injected, snake species, age and health of victim, and location of bite. Severe systemic symptoms include disseminated intravascular coagulation, acute renal failure, hypovolemic shock, and death.⁵ Venom can be hemotoxic and/or neurotoxic. Hemotoxic symptoms include pain, edema, swelling, ecchymoses, necrosis, and hemolysis. Neurotoxic symptoms may encompass diplopia, dysphagia, sweating, salivation, diaphoresis, respiratory depression, and paralysis.⁵ The pigmy rattlesnake venom is only hemotoxic, not neurotoxic.⁴ Eastern and western variety rattlesnakes account for most snake deaths due to their potent venom. Water moccasins (cottonmouths) have intermediate-potency venom, and copperhead snakes have the least-potent venom.⁵ Coral snakes are not pit vipers and require a different antivenom.

Management of Snakebites
Venomous snakes may bite a person without injecting venom. In fact, as many as 20% to 25% of all pit viper bites are dry.⁷ No attempts should be made to capture or kill the biting snake, but identifying it safely is helpful. Dead snakes should not be handled carelessly, as reflex biting after death has been reported.⁸ Cutting or suctioning the bite wound, nonsteroidal anti-inflammatory drugs, prophylactic antibiotics, tourniquets, prophylactic fasciotomy, and ice have not proven to be beneficial in the management of viper envenomation.^5,9-11 The best management involves immobilizing the affected extremity, seeking immediate medical attention, and initiating antivenom therapy as soon as possible.

Antivenom Therapy
Crotalidae polyvalent immune fab is an antivenom comprised of purified, sheep-derived fab IgG fragments and was approved by the US Food and Drug Administration in 2000 for the treatment of North American crotalid envenomation.^12,13 Its venom-specific fab fragments of IgG bind to and neutralize venom toxins and facilitate their elimination. Crotalidae polyvalent immune fab does not contain the Fc fragment of the IgG antibody, resulting in a low incidence of hypersensitivity reactions (8%) and serum sickness (13%).¹³ It is produced using 4 North American venoms: Crotalus atrox (western diamondback rattlesnake), Crotalus adamanteus (eastern diamondback rattlesnake), Crotalus scutulatus (Mojave rattlesnake), and Agkistrodon piscivorus (water moccasin).¹² It has become the standard-of-care antivenom for pit viper bites and has replaced its equine-derived predecessor antivenin crotalidae polyvalent, which is known for high rates of acute allergic reactions (23%–56%) including anaphylaxis and delayed serum sickness.^13,14 In postmarketing studies, CPIF has demonstrated control of envenomation regardless of severity. The most common adverse reactions reported include urticaria, rash, nausea, pruritus, and back pain.¹³ Anaphylaxis and anaphylactoid reactions may occur, and patients should be carefully observed during antivenom infusion. Appropriate management should be readily available including epinephrine, intravenous antihistamines, and/or albuterol. Contraindications include known hypersensitivity to papaya or papain, which is used to cleave the antibodies into fragments during the processing of CPIF. Patients also may react to it if allergic to other papaya extracts, chymopapain, or bromelain (pineapple enzyme), as well as some dust mite allergens and latex allergens that share antigenic structures with papain.¹⁵ Each vial of CPIF is reconstituted with 18 mL of 0.9% sodium chloride, as described in the package insert.¹³ The total dose (minimum of 4 to maximum of 12 vials initial dose) is then diluted in 250 mL of normal saline and infused over 1 hour starting for the first 10 minutes at a rate of 25 to 50 mL/h, and if tolerated, then increased to 250 mL/h until completion.

Treatment Algorithm
According to the envenomation consensus treatment algorithm, assess the site of the snakebite and mark leading edge of swelling every 15 to 30 minutes,¹⁶ as shown in our patient in Figure 6.Immobilize and elevate the affected extremity. Update tetanus vaccine and order initial laboratory tests to include prothrombin time, hemoglobin, platelets, and fibrinogen. If the patient does not exhibit local signs of envenomation such as redness, swelling, or ecchymosis, and the patient has no coagulation laboratory abnormalities and exhibits no systemic signs such as diarrhea, vomiting or angioedema, withhold CPIF and observe the patient for a minimum of 8 hours. Repeat laboratory tests prior to discharge. This clinical scenario most likely occurs in the setting of a dry bite or no bite at all. For minor envenomation, it also is possible to withhold CPIF and observe the patient for 12 to 24 hours if he/she remains stable and laboratory tests remain within reference range. If the patient has local or systemic signs of envenomation, start CPIF (4–6 vials and up to a maximum of 12 vials). The first dose of CPIF should be administered in the emergency department or intensive care unit. If after the first hour envenomation is worsening, an additional 4 to 6 vials may be infused. If after the first hour of observation the envenomation is controlled based on decreased swelling or lack of progression and there is improvement in laboratory values, then a maintenance regimen can be initiated. The maintenance dose consists of 2 vials every 6 hours for up to 18 hours (3 separate 2-vial doses). Patients can be discharged if stable and with no negative laboratory trends during the observation period.¹⁶ If CPIF was administered, follow-up laboratory tests results are dependent on prior findings of coagulation abnormalities, degree of envenomation, and signs and symptoms of coagulopathy postdischarge. Recurrent coagulopathy can occur in patients with coagulation abnormalities during initial envenomation, and patients should be monitored for possible re-treatment for at least 1 week or longer.¹⁷ Coagulopathy can present with decreased fibrinogen, decreased platelets, and elevated prothrombin time. Our patient experienced a drop in platelet count and hemoglobin level in addition to localized tissue effects, but he responded to the antivenom therapy. Lastly and importantly, no pediatric adjustments are necessary, and although mercury has been removed from the product’s manufacturing process, certain easily identifiable antivenom lots that have not expired contain ethyl mercury from thimerosal.^13,18,19 Some side effects of thimerosal include redness and swelling of the injection site, but scientific research does not show a connection with autism.²⁰

Conclusion

Dusky pigmy rattlesnake envenomations are clinically responsive to CPIF antivenom treatment.²¹ Although no clearly documented fatalities have been reported from dusky pigmy rattlesnake bites, coagulopathy and local tissue necrosis—as described in our patient—can result from such snakebites, requiring hospitalization. These snakes are common in the southeastern United States, and the treatment algorithm presented can be extrapolated to other more serious and deadly pit viper bites.

Rattlesnakes are pit vipers with a rattle attached to the tip of the tail and facial pits located between the eyes and nose with a special organ that detects heat energy (infrared light) and is used for hunting prey. There are 2 genera of rattlesnakes, Sistrurus (3 species) and Crotalus (23 species). ¹ The pigmy rattlesnake belongs to the Sistrurus miliarius species that is subdivided into 3 subspecies: the Carolina pigmy rattlesnake (Sistrurus miliarius miliarius), the Western pigmy rattlesnake (Sistrurus miliarius streckeri ), and the dusky pigmy rattlesnake (Sistrurus miliarius barbouri ). ¹ The dusky pigmy rattlesnake is found in South Carolina, southern Georgia, southern Alabama, southeastern Mississippi, and Florida. ² It is the most abundant venomous snake in Florida. ³ Its rattle is barely audible, and it is an aggressive small snake ranging in length from 38 to 56 cm. ⁴ Its venom is hemorrhagic, causing tissue damage but not containing neurotoxins. ⁴ Although bites can be painful, resulting in localized necrosis and rare loss of digits, it is unlikely for bites to be fatal given the snake’s small fangs, small size, and amount of envenomation. However, bites on children may require hospitalization. The venom contains proteins, polypeptides, and enzymes. ⁵ One such peptide, barbourin, inhibits a transmembrane receptor that plays a role in platelet aggregation. ⁶

We report a case of a 54-year-old man who was bitten on the left index finger by a dusky pigmy rattlesnake. We describe the clinical course and successful treatment with crotalidae polyvalent immune fab (CPIF) antivenom.

Case Report

A 54-year-old man presented to the emergency department with a rapidly swelling and erythematous left hand following a snakebite to the left index fingertip while weeding in his yard (Figure 1). The patient was able to kill the snake with a shovel and photograph it, which helped identify it as a dusky pigmy rattlesnake (Figure 2). Vitals on presentation included a blood pressure of 161/98, pulse oximeter of 99%, temperature of 36.4°C, pulse of 84 beats per minute, and respiratory rate of 16 breaths per minute.

Given the poisonous snakebite, the patient was admitted to the intensive care unit. Laboratory test results at admission revealed the following values: platelet count, 235,000/µL (reference range, 150,000–450,000/µL); fibrinogen, 226.1 mg/dL (reference range, 185–410 mg/dL); fibrin degradation products, less than 10 µg/mL (reference range, <10 µg/mL); glucose, 145 mg/dL (reference range, 74–106 mg/dL). The remainder of the complete blood cell count and metabolic panel was unremarkable. His blood type was O Rh+. Radiography of the left second digit did not show any fractures, dislocations, or foreign object.

After consulting with the Tampa General Hospital Florida Poison Information Center, 6 vials of CPIF antivenom in 250 mL of sodium chloride initially were infused intravenously, followed by 2 additional vials each at 6, 12, and 18 hours. Serial laboratory test results revealed white blood cell counts of 13,600, 10,000, 6800, 6100, and 6800/µL at 4, 15, 43, 65, and 88 hours postadmission, respectively. Platelet counts were 222,000, 159,000, 116,000, 99,000, and 129,000/µL at 4, 15, 43, 65, and 88 hours postadmission, respectively. The hemoglobin level was 14.8, 13.1, 13.8, 13.7, and 14.3 g/dL at 4, 15, 43, 65, and 88 hours postadmission, respectively. Other laboratory test results including prothrombin time (10.0 s), fibrinogen (226.1 mg/dL), and fibrin degradation products (<10 µg/mL) at 4 hours postadmission remained within reference range during serial monitoring.

Comment

Envenomation
Snakebites and envenomation are a complex and broad subject beyond the scope of this article and further reading on this subject is highly encouraged. The clinical findings from snakebites range from mild local tissue reactions to severe systemic symptoms depending on the volume of venom injected, snake species, age and health of victim, and location of bite. Severe systemic symptoms include disseminated intravascular coagulation, acute renal failure, hypovolemic shock, and death.⁵ Venom can be hemotoxic and/or neurotoxic. Hemotoxic symptoms include pain, edema, swelling, ecchymoses, necrosis, and hemolysis. Neurotoxic symptoms may encompass diplopia, dysphagia, sweating, salivation, diaphoresis, respiratory depression, and paralysis.⁵ The pigmy rattlesnake venom is only hemotoxic, not neurotoxic.⁴ Eastern and western variety rattlesnakes account for most snake deaths due to their potent venom. Water moccasins (cottonmouths) have intermediate-potency venom, and copperhead snakes have the least-potent venom.⁵ Coral snakes are not pit vipers and require a different antivenom.

Management of Snakebites
Venomous snakes may bite a person without injecting venom. In fact, as many as 20% to 25% of all pit viper bites are dry.⁷ No attempts should be made to capture or kill the biting snake, but identifying it safely is helpful. Dead snakes should not be handled carelessly, as reflex biting after death has been reported.⁸ Cutting or suctioning the bite wound, nonsteroidal anti-inflammatory drugs, prophylactic antibiotics, tourniquets, prophylactic fasciotomy, and ice have not proven to be beneficial in the management of viper envenomation.^5,9-11 The best management involves immobilizing the affected extremity, seeking immediate medical attention, and initiating antivenom therapy as soon as possible.

Antivenom Therapy
Crotalidae polyvalent immune fab is an antivenom comprised of purified, sheep-derived fab IgG fragments and was approved by the US Food and Drug Administration in 2000 for the treatment of North American crotalid envenomation.^12,13 Its venom-specific fab fragments of IgG bind to and neutralize venom toxins and facilitate their elimination. Crotalidae polyvalent immune fab does not contain the Fc fragment of the IgG antibody, resulting in a low incidence of hypersensitivity reactions (8%) and serum sickness (13%).¹³ It is produced using 4 North American venoms: Crotalus atrox (western diamondback rattlesnake), Crotalus adamanteus (eastern diamondback rattlesnake), Crotalus scutulatus (Mojave rattlesnake), and Agkistrodon piscivorus (water moccasin).¹² It has become the standard-of-care antivenom for pit viper bites and has replaced its equine-derived predecessor antivenin crotalidae polyvalent, which is known for high rates of acute allergic reactions (23%–56%) including anaphylaxis and delayed serum sickness.^13,14 In postmarketing studies, CPIF has demonstrated control of envenomation regardless of severity. The most common adverse reactions reported include urticaria, rash, nausea, pruritus, and back pain.¹³ Anaphylaxis and anaphylactoid reactions may occur, and patients should be carefully observed during antivenom infusion. Appropriate management should be readily available including epinephrine, intravenous antihistamines, and/or albuterol. Contraindications include known hypersensitivity to papaya or papain, which is used to cleave the antibodies into fragments during the processing of CPIF. Patients also may react to it if allergic to other papaya extracts, chymopapain, or bromelain (pineapple enzyme), as well as some dust mite allergens and latex allergens that share antigenic structures with papain.¹⁵ Each vial of CPIF is reconstituted with 18 mL of 0.9% sodium chloride, as described in the package insert.¹³ The total dose (minimum of 4 to maximum of 12 vials initial dose) is then diluted in 250 mL of normal saline and infused over 1 hour starting for the first 10 minutes at a rate of 25 to 50 mL/h, and if tolerated, then increased to 250 mL/h until completion.

Treatment Algorithm
According to the envenomation consensus treatment algorithm, assess the site of the snakebite and mark leading edge of swelling every 15 to 30 minutes,¹⁶ as shown in our patient in Figure 6.Immobilize and elevate the affected extremity. Update tetanus vaccine and order initial laboratory tests to include prothrombin time, hemoglobin, platelets, and fibrinogen. If the patient does not exhibit local signs of envenomation such as redness, swelling, or ecchymosis, and the patient has no coagulation laboratory abnormalities and exhibits no systemic signs such as diarrhea, vomiting or angioedema, withhold CPIF and observe the patient for a minimum of 8 hours. Repeat laboratory tests prior to discharge. This clinical scenario most likely occurs in the setting of a dry bite or no bite at all. For minor envenomation, it also is possible to withhold CPIF and observe the patient for 12 to 24 hours if he/she remains stable and laboratory tests remain within reference range. If the patient has local or systemic signs of envenomation, start CPIF (4–6 vials and up to a maximum of 12 vials). The first dose of CPIF should be administered in the emergency department or intensive care unit. If after the first hour envenomation is worsening, an additional 4 to 6 vials may be infused. If after the first hour of observation the envenomation is controlled based on decreased swelling or lack of progression and there is improvement in laboratory values, then a maintenance regimen can be initiated. The maintenance dose consists of 2 vials every 6 hours for up to 18 hours (3 separate 2-vial doses). Patients can be discharged if stable and with no negative laboratory trends during the observation period.¹⁶ If CPIF was administered, follow-up laboratory tests results are dependent on prior findings of coagulation abnormalities, degree of envenomation, and signs and symptoms of coagulopathy postdischarge. Recurrent coagulopathy can occur in patients with coagulation abnormalities during initial envenomation, and patients should be monitored for possible re-treatment for at least 1 week or longer.¹⁷ Coagulopathy can present with decreased fibrinogen, decreased platelets, and elevated prothrombin time. Our patient experienced a drop in platelet count and hemoglobin level in addition to localized tissue effects, but he responded to the antivenom therapy. Lastly and importantly, no pediatric adjustments are necessary, and although mercury has been removed from the product’s manufacturing process, certain easily identifiable antivenom lots that have not expired contain ethyl mercury from thimerosal.^13,18,19 Some side effects of thimerosal include redness and swelling of the injection site, but scientific research does not show a connection with autism.²⁰

Conclusion

Dusky pigmy rattlesnake envenomations are clinically responsive to CPIF antivenom treatment.²¹ Although no clearly documented fatalities have been reported from dusky pigmy rattlesnake bites, coagulopathy and local tissue necrosis—as described in our patient—can result from such snakebites, requiring hospitalization. These snakes are common in the southeastern United States, and the treatment algorithm presented can be extrapolated to other more serious and deadly pit viper bites.

Identification

The South African fattail scorpion (Parabuthus transvaalicus)(Figure) is one of the most poisonous scorpions in southern Africa.¹ A member of the Buthidae scorpion family, it can grow as long as 15 cm and is dark brown-black with lighter red-brown pincers. Similar to other fattail scorpions, it has slender pincers (pedipalps) and a thick square tail (the telson). Parabuthus transvaalicus inhabits hot dry deserts, scrublands, and semiarid regions.^1,2 It also is popular in exotic pet collections, the most common source of stings in the United States.

Stings and Envenomation

Scorpions with thicker tails generally have more potent venom than those with slender tails and thick pincers. Venom is injected by a stinger at the tip of the telson¹; P transvaalicus also can spray venom as far as 3 m.^1,2 Venom is not known to cause toxicity through skin contact but could represent a hazard if sprayed in the eye.

Scorpion toxins are a group of complex neurotoxins that act on sodium channels, either retarding inactivation (α toxin) or enhancing activation (β toxin), causing massive depolarization of excitable cells.^1,3 The toxin causes neurons to fire repetitively.⁴ Neurotransmitters—noradrenaline, adrenaline, and acetylcholine—cause the observed sympathetic, parasympathetic, and skeletal muscle effects.¹

Incidence
Worldwide, more than 1.2 million individuals are stung by a scorpion annually, causing more than 3250 deaths a year.⁵ Adults are stung more often, but children experience more severe envenomation, are more likely to develop severe illness requiring intensive supportive care, and have a higher mortality.⁴

As many as one-third of patients stung by a Parabuthus scorpion develop neuromuscular toxicity, which can be life-threatening.⁶ In a study of 277 envenomations by P transvaalicus, 10% of patients developed severe symptoms and 5 died. Children younger than 10 years and adults older than 50 years are at greatest risk for adverse outcomes.⁶ Children have a case fatality rate as high as 10 times the adult fatality rate.⁷

Clinical Presentation
The clinical presentation of scorpion envenomation varies with the species involved, the amount of venom injected, and the victim’s weight and baseline health.¹ Scorpion envenomation is divided into 4 grades based on the severity of a sting:

• Grade I: pain and paresthesia at the envenomation site; usually, no local inflammation

• Grade II: local symptoms as well as more remote pain and paresthesia; pain can radiate up the affected limb

• Grade III: cranial nerve or somatic skeletal neuromuscular dysfunction; either presentation can have associated autonomic dysfunction

• Grade IV: both cranial nerve and somatic skeletal neuromuscular dysfunction, with associated auto-nomic dysfunction

 

 

The initial symptom of a scorpion sting is intense burning pain. The sting site might be unimpressive, with only a mild local reaction. Symptoms usually progress to maximum severity within 5 hours.¹ Muscle pain, cramps, and weakness are prominent. The patient might have difficulty walking and swallowing, with increased salivation and drooling, and visual disturbance with abnormal eye movements. Pulse, blood pressure, and temperature often are elevated. The patient might be hyperreflexic with clonus.^1,6

Symptoms of increased sympathetic activity are hypertension, tachycardia, cardiac dysrhythmia, perspiration, hyperglycemia, and restlessness.^1,2 Parasympathetic effects are increased salivation, hypotension, bradycardia, and gastric distension. Skeletal muscle effects include tremors and involuntary muscle movement, which can be severe. Cranial nerve dysfunction may manifest as dysphagia, drooling, abnormal eye movements, blurred vision, slurred speech, and tongue fasciculations. Subsequent development of muscle weakness, bulbar paralysis, and difficulty breathing may be caused by depletion of neurotransmitters after prolonged excessive neuronal activity.¹

Distinctive Signs in Younger Patients
A child who is stung by a scorpion might have symptoms similar to those seen in an adult victim but can also experience an extreme form of restlessness that indicates severe envenomation characterized by inability to lay still, violent muscle twitching, and uncontrollable flailing of extremities. The child might have facial grimacing, with lip-smacking and chewing motions. In addition, bulbar paralysis and respiratory distress are more likely in children who have been stung than in adults.^1,2

Management

Treatment of a P transvaalicus sting is directed at “scorpionism,” envenomation that is associated with systemic symptoms that can be life-threatening. Treatment comprises support of vital functions, symptomatic measures, and injection of antivenin.⁸

Support of Vital Functions
In adults, systemic symptoms can be delayed as long as 8 hours after the sting. However, most severe cases usually are evident within 60 minutes; infants can reach grade IV as quickly as 15 to 30 minutes.^9,10 Loss of pharyngeal reflexes and development of respiratory distress are ominous warning signs requiring immediate respiratory support. Respiratory failure is the most common cause of death.¹ An asymptomatic child should be admitted to a hospital for observation for a minimum of 12 hours if the species of scorpion was not identified.²

Pain Relief
Most patients cannot tolerate an ice pack because of severe hyperesthesia. Infiltration of the local sting site with an anesthetic generally is safe and can provide some local pain relief. Intravenous fentanyl has been used in closely monitored patients because the drug is not associated with histamine release. Medications that cause release of histamine, such as morphine, can exacerbate or confuse the clinical picture.

Antivenin
Scorpion antivenin contains purified IgG fragments; allergic reactions are now rare. The sooner antivenin is administered, the greater the benefit. When administered early, it can prevent many of the most serious complications.⁷ In a randomized, double-blind study of critically ill children with clinically significant signs of scorpion envenomation, intravenous administration of scorpion-specific fragment antigen-binding 2 (F[(ab’]₂) antivenin resulted in resolution of clinical symptoms within 4 hours.¹¹

When managing grade III or IV scorpion envenomation, all patients should be admitted to a medical facility equipped to provide intensive supportive care; consider consultation with a regional poison control center. The World Health Organization maintains an international poison control center (at https://www.who.int/ipcs/poisons/centre/en/) with regional telephone numbers; alternatively, in the United States, call the nationwide telephone number of the Poison Control Center (800-222-1222).

The World Health Organization has identified declining production of antivenin as a crisis.¹²

Resolution
Symptoms of envenomation typically resolve 9 to 30 hours after a sting in a patient with grade III or IV envenomation not treated with antivenin.⁴ However, pain and paresthesia occasionally last as long as 2 weeks. In rare cases, more long-term sequelae of burning paresthesia persist for months.⁴

Conclusion

It is important for dermatologists to be aware of the potential for life-threatening envenomation by certain scorpion species native to southern Africa. In the United States, stings of these species most often are seen in patients with a pet collection, but late sequelae also can be seen in travelers returning from an endemic region. The site of a sting often appears unimpressive initially, but severe hyperesthesia is common. Patients with cardiac, neurologic, or respiratory symptoms require intensive supportive care. Proper care can be lifesaving.

Identification

The South African fattail scorpion (Parabuthus transvaalicus)(Figure) is one of the most poisonous scorpions in southern Africa.¹ A member of the Buthidae scorpion family, it can grow as long as 15 cm and is dark brown-black with lighter red-brown pincers. Similar to other fattail scorpions, it has slender pincers (pedipalps) and a thick square tail (the telson). Parabuthus transvaalicus inhabits hot dry deserts, scrublands, and semiarid regions.^1,2 It also is popular in exotic pet collections, the most common source of stings in the United States.

Stings and Envenomation

Scorpions with thicker tails generally have more potent venom than those with slender tails and thick pincers. Venom is injected by a stinger at the tip of the telson¹; P transvaalicus also can spray venom as far as 3 m.^1,2 Venom is not known to cause toxicity through skin contact but could represent a hazard if sprayed in the eye.

Scorpion toxins are a group of complex neurotoxins that act on sodium channels, either retarding inactivation (α toxin) or enhancing activation (β toxin), causing massive depolarization of excitable cells.^1,3 The toxin causes neurons to fire repetitively.⁴ Neurotransmitters—noradrenaline, adrenaline, and acetylcholine—cause the observed sympathetic, parasympathetic, and skeletal muscle effects.¹

Incidence
Worldwide, more than 1.2 million individuals are stung by a scorpion annually, causing more than 3250 deaths a year.⁵ Adults are stung more often, but children experience more severe envenomation, are more likely to develop severe illness requiring intensive supportive care, and have a higher mortality.⁴

As many as one-third of patients stung by a Parabuthus scorpion develop neuromuscular toxicity, which can be life-threatening.⁶ In a study of 277 envenomations by P transvaalicus, 10% of patients developed severe symptoms and 5 died. Children younger than 10 years and adults older than 50 years are at greatest risk for adverse outcomes.⁶ Children have a case fatality rate as high as 10 times the adult fatality rate.⁷

Clinical Presentation
The clinical presentation of scorpion envenomation varies with the species involved, the amount of venom injected, and the victim’s weight and baseline health.¹ Scorpion envenomation is divided into 4 grades based on the severity of a sting:

• Grade I: pain and paresthesia at the envenomation site; usually, no local inflammation

• Grade II: local symptoms as well as more remote pain and paresthesia; pain can radiate up the affected limb

• Grade III: cranial nerve or somatic skeletal neuromuscular dysfunction; either presentation can have associated autonomic dysfunction

• Grade IV: both cranial nerve and somatic skeletal neuromuscular dysfunction, with associated auto-nomic dysfunction

 

 

The initial symptom of a scorpion sting is intense burning pain. The sting site might be unimpressive, with only a mild local reaction. Symptoms usually progress to maximum severity within 5 hours.¹ Muscle pain, cramps, and weakness are prominent. The patient might have difficulty walking and swallowing, with increased salivation and drooling, and visual disturbance with abnormal eye movements. Pulse, blood pressure, and temperature often are elevated. The patient might be hyperreflexic with clonus.^1,6

Symptoms of increased sympathetic activity are hypertension, tachycardia, cardiac dysrhythmia, perspiration, hyperglycemia, and restlessness.^1,2 Parasympathetic effects are increased salivation, hypotension, bradycardia, and gastric distension. Skeletal muscle effects include tremors and involuntary muscle movement, which can be severe. Cranial nerve dysfunction may manifest as dysphagia, drooling, abnormal eye movements, blurred vision, slurred speech, and tongue fasciculations. Subsequent development of muscle weakness, bulbar paralysis, and difficulty breathing may be caused by depletion of neurotransmitters after prolonged excessive neuronal activity.¹

Distinctive Signs in Younger Patients
A child who is stung by a scorpion might have symptoms similar to those seen in an adult victim but can also experience an extreme form of restlessness that indicates severe envenomation characterized by inability to lay still, violent muscle twitching, and uncontrollable flailing of extremities. The child might have facial grimacing, with lip-smacking and chewing motions. In addition, bulbar paralysis and respiratory distress are more likely in children who have been stung than in adults.^1,2

Management

Treatment of a P transvaalicus sting is directed at “scorpionism,” envenomation that is associated with systemic symptoms that can be life-threatening. Treatment comprises support of vital functions, symptomatic measures, and injection of antivenin.⁸

Support of Vital Functions
In adults, systemic symptoms can be delayed as long as 8 hours after the sting. However, most severe cases usually are evident within 60 minutes; infants can reach grade IV as quickly as 15 to 30 minutes.^9,10 Loss of pharyngeal reflexes and development of respiratory distress are ominous warning signs requiring immediate respiratory support. Respiratory failure is the most common cause of death.¹ An asymptomatic child should be admitted to a hospital for observation for a minimum of 12 hours if the species of scorpion was not identified.²

Pain Relief
Most patients cannot tolerate an ice pack because of severe hyperesthesia. Infiltration of the local sting site with an anesthetic generally is safe and can provide some local pain relief. Intravenous fentanyl has been used in closely monitored patients because the drug is not associated with histamine release. Medications that cause release of histamine, such as morphine, can exacerbate or confuse the clinical picture.

Antivenin
Scorpion antivenin contains purified IgG fragments; allergic reactions are now rare. The sooner antivenin is administered, the greater the benefit. When administered early, it can prevent many of the most serious complications.⁷ In a randomized, double-blind study of critically ill children with clinically significant signs of scorpion envenomation, intravenous administration of scorpion-specific fragment antigen-binding 2 (F[(ab’]₂) antivenin resulted in resolution of clinical symptoms within 4 hours.¹¹

When managing grade III or IV scorpion envenomation, all patients should be admitted to a medical facility equipped to provide intensive supportive care; consider consultation with a regional poison control center. The World Health Organization maintains an international poison control center (at https://www.who.int/ipcs/poisons/centre/en/) with regional telephone numbers; alternatively, in the United States, call the nationwide telephone number of the Poison Control Center (800-222-1222).

The World Health Organization has identified declining production of antivenin as a crisis.¹²

Resolution
Symptoms of envenomation typically resolve 9 to 30 hours after a sting in a patient with grade III or IV envenomation not treated with antivenin.⁴ However, pain and paresthesia occasionally last as long as 2 weeks. In rare cases, more long-term sequelae of burning paresthesia persist for months.⁴

Conclusion

It is important for dermatologists to be aware of the potential for life-threatening envenomation by certain scorpion species native to southern Africa. In the United States, stings of these species most often are seen in patients with a pet collection, but late sequelae also can be seen in travelers returning from an endemic region. The site of a sting often appears unimpressive initially, but severe hyperesthesia is common. Patients with cardiac, neurologic, or respiratory symptoms require intensive supportive care. Proper care can be lifesaving.

Identification

The South African fattail scorpion (Parabuthus transvaalicus)(Figure) is one of the most poisonous scorpions in southern Africa.¹ A member of the Buthidae scorpion family, it can grow as long as 15 cm and is dark brown-black with lighter red-brown pincers. Similar to other fattail scorpions, it has slender pincers (pedipalps) and a thick square tail (the telson). Parabuthus transvaalicus inhabits hot dry deserts, scrublands, and semiarid regions.^1,2 It also is popular in exotic pet collections, the most common source of stings in the United States.

Stings and Envenomation

Scorpions with thicker tails generally have more potent venom than those with slender tails and thick pincers. Venom is injected by a stinger at the tip of the telson¹; P transvaalicus also can spray venom as far as 3 m.^1,2 Venom is not known to cause toxicity through skin contact but could represent a hazard if sprayed in the eye.

Scorpion toxins are a group of complex neurotoxins that act on sodium channels, either retarding inactivation (α toxin) or enhancing activation (β toxin), causing massive depolarization of excitable cells.^1,3 The toxin causes neurons to fire repetitively.⁴ Neurotransmitters—noradrenaline, adrenaline, and acetylcholine—cause the observed sympathetic, parasympathetic, and skeletal muscle effects.¹

Incidence
Worldwide, more than 1.2 million individuals are stung by a scorpion annually, causing more than 3250 deaths a year.⁵ Adults are stung more often, but children experience more severe envenomation, are more likely to develop severe illness requiring intensive supportive care, and have a higher mortality.⁴

As many as one-third of patients stung by a Parabuthus scorpion develop neuromuscular toxicity, which can be life-threatening.⁶ In a study of 277 envenomations by P transvaalicus, 10% of patients developed severe symptoms and 5 died. Children younger than 10 years and adults older than 50 years are at greatest risk for adverse outcomes.⁶ Children have a case fatality rate as high as 10 times the adult fatality rate.⁷

Clinical Presentation
The clinical presentation of scorpion envenomation varies with the species involved, the amount of venom injected, and the victim’s weight and baseline health.¹ Scorpion envenomation is divided into 4 grades based on the severity of a sting:

• Grade I: pain and paresthesia at the envenomation site; usually, no local inflammation

• Grade II: local symptoms as well as more remote pain and paresthesia; pain can radiate up the affected limb

• Grade III: cranial nerve or somatic skeletal neuromuscular dysfunction; either presentation can have associated autonomic dysfunction

• Grade IV: both cranial nerve and somatic skeletal neuromuscular dysfunction, with associated auto-nomic dysfunction

 

 

The initial symptom of a scorpion sting is intense burning pain. The sting site might be unimpressive, with only a mild local reaction. Symptoms usually progress to maximum severity within 5 hours.¹ Muscle pain, cramps, and weakness are prominent. The patient might have difficulty walking and swallowing, with increased salivation and drooling, and visual disturbance with abnormal eye movements. Pulse, blood pressure, and temperature often are elevated. The patient might be hyperreflexic with clonus.^1,6

Symptoms of increased sympathetic activity are hypertension, tachycardia, cardiac dysrhythmia, perspiration, hyperglycemia, and restlessness.^1,2 Parasympathetic effects are increased salivation, hypotension, bradycardia, and gastric distension. Skeletal muscle effects include tremors and involuntary muscle movement, which can be severe. Cranial nerve dysfunction may manifest as dysphagia, drooling, abnormal eye movements, blurred vision, slurred speech, and tongue fasciculations. Subsequent development of muscle weakness, bulbar paralysis, and difficulty breathing may be caused by depletion of neurotransmitters after prolonged excessive neuronal activity.¹

Distinctive Signs in Younger Patients
A child who is stung by a scorpion might have symptoms similar to those seen in an adult victim but can also experience an extreme form of restlessness that indicates severe envenomation characterized by inability to lay still, violent muscle twitching, and uncontrollable flailing of extremities. The child might have facial grimacing, with lip-smacking and chewing motions. In addition, bulbar paralysis and respiratory distress are more likely in children who have been stung than in adults.^1,2

Management

Treatment of a P transvaalicus sting is directed at “scorpionism,” envenomation that is associated with systemic symptoms that can be life-threatening. Treatment comprises support of vital functions, symptomatic measures, and injection of antivenin.⁸

Support of Vital Functions
In adults, systemic symptoms can be delayed as long as 8 hours after the sting. However, most severe cases usually are evident within 60 minutes; infants can reach grade IV as quickly as 15 to 30 minutes.^9,10 Loss of pharyngeal reflexes and development of respiratory distress are ominous warning signs requiring immediate respiratory support. Respiratory failure is the most common cause of death.¹ An asymptomatic child should be admitted to a hospital for observation for a minimum of 12 hours if the species of scorpion was not identified.²

Pain Relief
Most patients cannot tolerate an ice pack because of severe hyperesthesia. Infiltration of the local sting site with an anesthetic generally is safe and can provide some local pain relief. Intravenous fentanyl has been used in closely monitored patients because the drug is not associated with histamine release. Medications that cause release of histamine, such as morphine, can exacerbate or confuse the clinical picture.

Antivenin
Scorpion antivenin contains purified IgG fragments; allergic reactions are now rare. The sooner antivenin is administered, the greater the benefit. When administered early, it can prevent many of the most serious complications.⁷ In a randomized, double-blind study of critically ill children with clinically significant signs of scorpion envenomation, intravenous administration of scorpion-specific fragment antigen-binding 2 (F[(ab’]₂) antivenin resulted in resolution of clinical symptoms within 4 hours.¹¹

When managing grade III or IV scorpion envenomation, all patients should be admitted to a medical facility equipped to provide intensive supportive care; consider consultation with a regional poison control center. The World Health Organization maintains an international poison control center (at https://www.who.int/ipcs/poisons/centre/en/) with regional telephone numbers; alternatively, in the United States, call the nationwide telephone number of the Poison Control Center (800-222-1222).

The World Health Organization has identified declining production of antivenin as a crisis.¹²

Resolution
Symptoms of envenomation typically resolve 9 to 30 hours after a sting in a patient with grade III or IV envenomation not treated with antivenin.⁴ However, pain and paresthesia occasionally last as long as 2 weeks. In rare cases, more long-term sequelae of burning paresthesia persist for months.⁴

Conclusion

It is important for dermatologists to be aware of the potential for life-threatening envenomation by certain scorpion species native to southern Africa. In the United States, stings of these species most often are seen in patients with a pet collection, but late sequelae also can be seen in travelers returning from an endemic region. The site of a sting often appears unimpressive initially, but severe hyperesthesia is common. Patients with cardiac, neurologic, or respiratory symptoms require intensive supportive care. Proper care can be lifesaving.

Fleas of the order Siphonaptera are insects that feed on the blood of a mammalian host. They have no wings but jump to near 150 times their body lengths to reach potential hosts.¹ An epidemiologic survey performed in 2016 demonstrated that 96% of fleas in the United States are cat fleas (Ctenocephalides felis).² The bites often present as pruritic, nonfollicular-based, excoriated papules; papular urticaria; or vesiculobullous lesions distributed across the lower legs. Antihistamines and topical steroids may be helpful for symptomatic relief, but flea eradication is key.

Identification

Ctenocephalides fleas, including the common cat flea and the dog flea, have a characteristic pronotal comb that resembles a mane of hair (Figure 1) and genal comb that resembles a mustache. Compared to the dog flea (Ctenocephalides canis), cat fleas have a flatter head and fewer hair-bearing notches on the dorsal hind tibia (the dog flea has 8 notches and the cat flea has 6 notches)(Figure 2).

Flea Prevention and Eradication

Effective management of flea bites requires avoidance of infested areas and eradication of fleas from the home and pets. Home treatment should be performed by a qualified specialist and a veterinarian should treat the pet, but the dermatologist must be knowledgeable about treatment options. Flea pupae can lie dormant between floorboards for extended periods of time and hatch rapidly when new tenants enter a house or apartment. Insecticidal dusts and spray formulations frequently are used to treat infested homes. It also is important to reduce flea egg numbers by vacuuming carpets and areas where pets sleep.³ Rodents often introduce fleas to households and pets, so eliminating them from the area may play an important role in flea control. Consulting with a veterinarian is important, as treatment directed at pets is critical to control flea populations. Oral agents, including fluralaner, afoxolaner, sarolaner, and spinosad, can reduce flea populations on animals by as much as 99.3% after 7 days.^4,5 Fast-acting pulicidal agents, such as the combination of dinotefuran and fipronil, demonstrate curative activity as soon as 3 hours after treatment, which also may prevent reinfestation for as long as 6 weeks after treatment.⁶

Vector-Borne Disease

Fleas living on animals in close contact with humans, such as cats and dogs, can transmit zoonotic pathogens. Around 12,000 outpatients and 500 inpatients are diagnosed with cat scratch disease, a form of bartonellosis, annually. Ctenocephalides felis transmits Bartonella henselae from cat-to-cat and often cat-to-human through infected flea feces, causing a primary inoculation lesion and lymphadenitis. Of 3011 primary care providers surveyed from 2014 to 2015, 37.2% had treated at least 1 patient with cat scratch disease, yet knowledge gaps remain regarding the proper treatment and preventative measures for the disease.⁷ Current recommendations for the treatment of lymphadenitis caused by B henselae include a 5-day course of oral azithromycin.⁸ The preferred dosing regimen in adults is 500 mg on day 1 and 250 mg on days 2 through 5. Pediatric patients weighing less than 45.5 kg should receive 10 mg/kg on day 1 and 5 mg/kg on days 2 through 5.⁸ Additionally, less than one-third of the primary care providers surveyed from 2014 to 2015 said they would discuss the importance of pet flea control with immunocompromised patients who own cats, despite evidence implicating fleas in disease transmission.⁷ Pet-directed topical therapy with agents such as selamectin prescribed by a qualified veterinarian can prevent transmission of B henselae in cats exposed to fleas infected with the bacteria,⁹ which supports the importance of patient education and flea control, especially in pets owned by immunocompromised patients. Patients who are immunocompromised are at increased risk for persistent or disseminated bartonellosis, including endocarditis, in addition to cat scratch disease. Although arriving at a diagnosis may be difficult, one study found that bartonellosis in 13 renal transplant recipients was best diagnosed using both serology and polymerase chain reaction via DNA extraction of tissue specimens.¹⁰ These findings may enhance diagnostic yield for similar patients when bartonellosis is suspected.

Flea-borne typhus is endemic to Texas and Southern California.^11,12 Evidence suggests that the pathogenic bacteria, Rickettsia typhi and Rickettsia felis, also commonly infect fleas in the Great Plains area.¹³ Opossums carry R felis, and the fleas transmit murine or endemic typhus. A retrospective case series in Texas identified 11 cases of fatal flea-borne typhus from 1985 to 2015.¹¹ More than half of the patients reported contact with animals or fleas prior to the illness. Patients with typhus may present with fever, nausea, vomiting, rash (macular, maculopapular, papular, petechial, or morbilliform), respiratory or neurologic symptoms, thrombocytopenia, and elevated hepatic liver enzymes. Unfortunately, there often is a notable delay in initiation of treatment with the appropriate class of antibiotics—tetracyclines—and such delays can prove fatal.¹¹ The current recommendation for nonpregnant adults is oral doxycycline 100 mg twice daily continued 48 hours after the patient becomes afebrile or for 7 days, whichever therapy duration is longer.¹⁴ Because of the consequences of delayed treatment, it is important for clinicians to consider a diagnosis of vector-borne illness in a febrile patient with other associated gastrointestinal, cutaneous, respiratory, or neurologic symptoms, especially if they have animal or flea exposures. Flea control and exposure awareness remains paramount in preventing and treating this illness.

Yersinia pestis causes the plague, an important re-emerging disease that causes infection through flea bites, inhalation, or ingestion.¹⁵ From 2000 to 2009, 56 cases and 7 deaths in the United States—New Mexico, Arizona, Colorado, California, and Texas—and 21,725 cases and 1612 deaths worldwide were attributed to Y pestis. Most patients present with the bubonic form of the disease, with fever and an enlarging painful femoral or inguinal lymph node due to leg flea bites.¹⁶ Other forms of disease, including septicemic and pneumonic plague, are less common but relevant, as one-third of cases in the United States present with septicemia.^15,17,18 Although molecular diagnosis and immunohistochemistry play important roles, the diagnosis of Y pestis infection often is still accomplished with culture. A 2012 survey of 392 strains from 17 countries demonstrated that Y pestis remained susceptible to the antibiotics currently used to treat the disease, including doxycycline, streptomycin, gentamicin, tetracycline, trimethoprim-sulfamethoxazole, and ciprofloxacin.¹⁹

Human infection with Dipylidium caninum, a dog tapeworm, has been reported after suspected accidental ingestion of cat fleas carrying the parasite.²⁰ Children, who may present with diarrhea or white worms in their feces, are more susceptible to the infection, perhaps due to accidental flea consumption while being licked by the pet.^20,21

Conclusion

Cat fleas may act as a pruritic nuisance for pet owners and even deliver deadly pathogens to immunocompromised patients. Providers can minimize their impact by educating patients on flea prevention and eradication as well as astutely recognizing and treating flea-borne diseases.

Fleas of the order Siphonaptera are insects that feed on the blood of a mammalian host. They have no wings but jump to near 150 times their body lengths to reach potential hosts.¹ An epidemiologic survey performed in 2016 demonstrated that 96% of fleas in the United States are cat fleas (Ctenocephalides felis).² The bites often present as pruritic, nonfollicular-based, excoriated papules; papular urticaria; or vesiculobullous lesions distributed across the lower legs. Antihistamines and topical steroids may be helpful for symptomatic relief, but flea eradication is key.

Identification

Ctenocephalides fleas, including the common cat flea and the dog flea, have a characteristic pronotal comb that resembles a mane of hair (Figure 1) and genal comb that resembles a mustache. Compared to the dog flea (Ctenocephalides canis), cat fleas have a flatter head and fewer hair-bearing notches on the dorsal hind tibia (the dog flea has 8 notches and the cat flea has 6 notches)(Figure 2).

Flea Prevention and Eradication

Effective management of flea bites requires avoidance of infested areas and eradication of fleas from the home and pets. Home treatment should be performed by a qualified specialist and a veterinarian should treat the pet, but the dermatologist must be knowledgeable about treatment options. Flea pupae can lie dormant between floorboards for extended periods of time and hatch rapidly when new tenants enter a house or apartment. Insecticidal dusts and spray formulations frequently are used to treat infested homes. It also is important to reduce flea egg numbers by vacuuming carpets and areas where pets sleep.³ Rodents often introduce fleas to households and pets, so eliminating them from the area may play an important role in flea control. Consulting with a veterinarian is important, as treatment directed at pets is critical to control flea populations. Oral agents, including fluralaner, afoxolaner, sarolaner, and spinosad, can reduce flea populations on animals by as much as 99.3% after 7 days.^4,5 Fast-acting pulicidal agents, such as the combination of dinotefuran and fipronil, demonstrate curative activity as soon as 3 hours after treatment, which also may prevent reinfestation for as long as 6 weeks after treatment.⁶

Vector-Borne Disease

Fleas living on animals in close contact with humans, such as cats and dogs, can transmit zoonotic pathogens. Around 12,000 outpatients and 500 inpatients are diagnosed with cat scratch disease, a form of bartonellosis, annually. Ctenocephalides felis transmits Bartonella henselae from cat-to-cat and often cat-to-human through infected flea feces, causing a primary inoculation lesion and lymphadenitis. Of 3011 primary care providers surveyed from 2014 to 2015, 37.2% had treated at least 1 patient with cat scratch disease, yet knowledge gaps remain regarding the proper treatment and preventative measures for the disease.⁷ Current recommendations for the treatment of lymphadenitis caused by B henselae include a 5-day course of oral azithromycin.⁸ The preferred dosing regimen in adults is 500 mg on day 1 and 250 mg on days 2 through 5. Pediatric patients weighing less than 45.5 kg should receive 10 mg/kg on day 1 and 5 mg/kg on days 2 through 5.⁸ Additionally, less than one-third of the primary care providers surveyed from 2014 to 2015 said they would discuss the importance of pet flea control with immunocompromised patients who own cats, despite evidence implicating fleas in disease transmission.⁷ Pet-directed topical therapy with agents such as selamectin prescribed by a qualified veterinarian can prevent transmission of B henselae in cats exposed to fleas infected with the bacteria,⁹ which supports the importance of patient education and flea control, especially in pets owned by immunocompromised patients. Patients who are immunocompromised are at increased risk for persistent or disseminated bartonellosis, including endocarditis, in addition to cat scratch disease. Although arriving at a diagnosis may be difficult, one study found that bartonellosis in 13 renal transplant recipients was best diagnosed using both serology and polymerase chain reaction via DNA extraction of tissue specimens.¹⁰ These findings may enhance diagnostic yield for similar patients when bartonellosis is suspected.

Flea-borne typhus is endemic to Texas and Southern California.^11,12 Evidence suggests that the pathogenic bacteria, Rickettsia typhi and Rickettsia felis, also commonly infect fleas in the Great Plains area.¹³ Opossums carry R felis, and the fleas transmit murine or endemic typhus. A retrospective case series in Texas identified 11 cases of fatal flea-borne typhus from 1985 to 2015.¹¹ More than half of the patients reported contact with animals or fleas prior to the illness. Patients with typhus may present with fever, nausea, vomiting, rash (macular, maculopapular, papular, petechial, or morbilliform), respiratory or neurologic symptoms, thrombocytopenia, and elevated hepatic liver enzymes. Unfortunately, there often is a notable delay in initiation of treatment with the appropriate class of antibiotics—tetracyclines—and such delays can prove fatal.¹¹ The current recommendation for nonpregnant adults is oral doxycycline 100 mg twice daily continued 48 hours after the patient becomes afebrile or for 7 days, whichever therapy duration is longer.¹⁴ Because of the consequences of delayed treatment, it is important for clinicians to consider a diagnosis of vector-borne illness in a febrile patient with other associated gastrointestinal, cutaneous, respiratory, or neurologic symptoms, especially if they have animal or flea exposures. Flea control and exposure awareness remains paramount in preventing and treating this illness.

Yersinia pestis causes the plague, an important re-emerging disease that causes infection through flea bites, inhalation, or ingestion.¹⁵ From 2000 to 2009, 56 cases and 7 deaths in the United States—New Mexico, Arizona, Colorado, California, and Texas—and 21,725 cases and 1612 deaths worldwide were attributed to Y pestis. Most patients present with the bubonic form of the disease, with fever and an enlarging painful femoral or inguinal lymph node due to leg flea bites.¹⁶ Other forms of disease, including septicemic and pneumonic plague, are less common but relevant, as one-third of cases in the United States present with septicemia.^15,17,18 Although molecular diagnosis and immunohistochemistry play important roles, the diagnosis of Y pestis infection often is still accomplished with culture. A 2012 survey of 392 strains from 17 countries demonstrated that Y pestis remained susceptible to the antibiotics currently used to treat the disease, including doxycycline, streptomycin, gentamicin, tetracycline, trimethoprim-sulfamethoxazole, and ciprofloxacin.¹⁹

Human infection with Dipylidium caninum, a dog tapeworm, has been reported after suspected accidental ingestion of cat fleas carrying the parasite.²⁰ Children, who may present with diarrhea or white worms in their feces, are more susceptible to the infection, perhaps due to accidental flea consumption while being licked by the pet.^20,21

Conclusion

Cat fleas may act as a pruritic nuisance for pet owners and even deliver deadly pathogens to immunocompromised patients. Providers can minimize their impact by educating patients on flea prevention and eradication as well as astutely recognizing and treating flea-borne diseases.

Fleas of the order Siphonaptera are insects that feed on the blood of a mammalian host. They have no wings but jump to near 150 times their body lengths to reach potential hosts.¹ An epidemiologic survey performed in 2016 demonstrated that 96% of fleas in the United States are cat fleas (Ctenocephalides felis).² The bites often present as pruritic, nonfollicular-based, excoriated papules; papular urticaria; or vesiculobullous lesions distributed across the lower legs. Antihistamines and topical steroids may be helpful for symptomatic relief, but flea eradication is key.

Identification

Ctenocephalides fleas, including the common cat flea and the dog flea, have a characteristic pronotal comb that resembles a mane of hair (Figure 1) and genal comb that resembles a mustache. Compared to the dog flea (Ctenocephalides canis), cat fleas have a flatter head and fewer hair-bearing notches on the dorsal hind tibia (the dog flea has 8 notches and the cat flea has 6 notches)(Figure 2).

Flea Prevention and Eradication

Effective management of flea bites requires avoidance of infested areas and eradication of fleas from the home and pets. Home treatment should be performed by a qualified specialist and a veterinarian should treat the pet, but the dermatologist must be knowledgeable about treatment options. Flea pupae can lie dormant between floorboards for extended periods of time and hatch rapidly when new tenants enter a house or apartment. Insecticidal dusts and spray formulations frequently are used to treat infested homes. It also is important to reduce flea egg numbers by vacuuming carpets and areas where pets sleep.³ Rodents often introduce fleas to households and pets, so eliminating them from the area may play an important role in flea control. Consulting with a veterinarian is important, as treatment directed at pets is critical to control flea populations. Oral agents, including fluralaner, afoxolaner, sarolaner, and spinosad, can reduce flea populations on animals by as much as 99.3% after 7 days.^4,5 Fast-acting pulicidal agents, such as the combination of dinotefuran and fipronil, demonstrate curative activity as soon as 3 hours after treatment, which also may prevent reinfestation for as long as 6 weeks after treatment.⁶

Vector-Borne Disease

Fleas living on animals in close contact with humans, such as cats and dogs, can transmit zoonotic pathogens. Around 12,000 outpatients and 500 inpatients are diagnosed with cat scratch disease, a form of bartonellosis, annually. Ctenocephalides felis transmits Bartonella henselae from cat-to-cat and often cat-to-human through infected flea feces, causing a primary inoculation lesion and lymphadenitis. Of 3011 primary care providers surveyed from 2014 to 2015, 37.2% had treated at least 1 patient with cat scratch disease, yet knowledge gaps remain regarding the proper treatment and preventative measures for the disease.⁷ Current recommendations for the treatment of lymphadenitis caused by B henselae include a 5-day course of oral azithromycin.⁸ The preferred dosing regimen in adults is 500 mg on day 1 and 250 mg on days 2 through 5. Pediatric patients weighing less than 45.5 kg should receive 10 mg/kg on day 1 and 5 mg/kg on days 2 through 5.⁸ Additionally, less than one-third of the primary care providers surveyed from 2014 to 2015 said they would discuss the importance of pet flea control with immunocompromised patients who own cats, despite evidence implicating fleas in disease transmission.⁷ Pet-directed topical therapy with agents such as selamectin prescribed by a qualified veterinarian can prevent transmission of B henselae in cats exposed to fleas infected with the bacteria,⁹ which supports the importance of patient education and flea control, especially in pets owned by immunocompromised patients. Patients who are immunocompromised are at increased risk for persistent or disseminated bartonellosis, including endocarditis, in addition to cat scratch disease. Although arriving at a diagnosis may be difficult, one study found that bartonellosis in 13 renal transplant recipients was best diagnosed using both serology and polymerase chain reaction via DNA extraction of tissue specimens.¹⁰ These findings may enhance diagnostic yield for similar patients when bartonellosis is suspected.

Flea-borne typhus is endemic to Texas and Southern California.^11,12 Evidence suggests that the pathogenic bacteria, Rickettsia typhi and Rickettsia felis, also commonly infect fleas in the Great Plains area.¹³ Opossums carry R felis, and the fleas transmit murine or endemic typhus. A retrospective case series in Texas identified 11 cases of fatal flea-borne typhus from 1985 to 2015.¹¹ More than half of the patients reported contact with animals or fleas prior to the illness. Patients with typhus may present with fever, nausea, vomiting, rash (macular, maculopapular, papular, petechial, or morbilliform), respiratory or neurologic symptoms, thrombocytopenia, and elevated hepatic liver enzymes. Unfortunately, there often is a notable delay in initiation of treatment with the appropriate class of antibiotics—tetracyclines—and such delays can prove fatal.¹¹ The current recommendation for nonpregnant adults is oral doxycycline 100 mg twice daily continued 48 hours after the patient becomes afebrile or for 7 days, whichever therapy duration is longer.¹⁴ Because of the consequences of delayed treatment, it is important for clinicians to consider a diagnosis of vector-borne illness in a febrile patient with other associated gastrointestinal, cutaneous, respiratory, or neurologic symptoms, especially if they have animal or flea exposures. Flea control and exposure awareness remains paramount in preventing and treating this illness.

Yersinia pestis causes the plague, an important re-emerging disease that causes infection through flea bites, inhalation, or ingestion.¹⁵ From 2000 to 2009, 56 cases and 7 deaths in the United States—New Mexico, Arizona, Colorado, California, and Texas—and 21,725 cases and 1612 deaths worldwide were attributed to Y pestis. Most patients present with the bubonic form of the disease, with fever and an enlarging painful femoral or inguinal lymph node due to leg flea bites.¹⁶ Other forms of disease, including septicemic and pneumonic plague, are less common but relevant, as one-third of cases in the United States present with septicemia.^15,17,18 Although molecular diagnosis and immunohistochemistry play important roles, the diagnosis of Y pestis infection often is still accomplished with culture. A 2012 survey of 392 strains from 17 countries demonstrated that Y pestis remained susceptible to the antibiotics currently used to treat the disease, including doxycycline, streptomycin, gentamicin, tetracycline, trimethoprim-sulfamethoxazole, and ciprofloxacin.¹⁹

Human infection with Dipylidium caninum, a dog tapeworm, has been reported after suspected accidental ingestion of cat fleas carrying the parasite.²⁰ Children, who may present with diarrhea or white worms in their feces, are more susceptible to the infection, perhaps due to accidental flea consumption while being licked by the pet.^20,21

Conclusion

Cat fleas may act as a pruritic nuisance for pet owners and even deliver deadly pathogens to immunocompromised patients. Providers can minimize their impact by educating patients on flea prevention and eradication as well as astutely recognizing and treating flea-borne diseases.

Clinical Presentation

Millipedes secrete a noxious toxin implicated in millipede burns. The toxic substance is benzoquinone, a strong irritant secreted from the repugnatorial glands contained in each segment of the arthropod (Figure 1). This compound serves as a natural insect repellant, acting as the millipede’s defense mechanism from potential predators.¹ On human skin, benzoquinone causes localized pigmentary changes most commonly presenting on the feet and toes. Local lesions may be associated with pain or burning, but there are no known reports of adverse systemic effects.² Affected patients experience cutaneous pigmentary changes, which may be dark red, blue, or black, and spontaneously resolve over time.² The degree of pigment change may be associated with duration of skin contact with the toxin. The affected areas may resemble burns, dermatitis, or skin necrosis. More distal lesions may present similarly to blue toe syndrome or acute arterial occlusion but can be differentiated by the presence of intact peripheral pulses and lack of temperature discrepancy between the feet.^3,4 Histologic evaluation of the lesions generally reveals nonspecific full-thickness epidermal necrosis, making clinical suspicion and physical examination paramount to the diagnosis of millipede burns.⁵

Diagnostic Difficulties

Accurate diagnosis of millipede burns is more difficult when the burn involves an unusual site. The most common site of involvement is the foot (Figure 2), followed by other commonly exposed areas such as the arms, face, and eyes.^2,3,6,7 Covered parts of the body are much less commonly affected, requiring the arthropod to gain access via infiltration of clothing, often when hanging on a clothesline. In these cases, burns may be mistaken for child abuse, especially if certain areas of the body are involved, such as the groin and genitals.² The well-defined arcuate lesions of the burns may resemble injuries from a wire or belt to the unsuspecting observer.

Conclusion

Although millipedes often are regarded as harmless, they are capable of causing adverse reactions through the secretion of toxic chemicals. Millipede burns cause localized pigmentary changes that may be associated with pain or burning in some patients. Because these burns may resemble child abuse in pediatric patients, physicians should be aware of this diagnosis when unusual parts of the body are involved.

Clinical Presentation

Millipedes secrete a noxious toxin implicated in millipede burns. The toxic substance is benzoquinone, a strong irritant secreted from the repugnatorial glands contained in each segment of the arthropod (Figure 1). This compound serves as a natural insect repellant, acting as the millipede’s defense mechanism from potential predators.¹ On human skin, benzoquinone causes localized pigmentary changes most commonly presenting on the feet and toes. Local lesions may be associated with pain or burning, but there are no known reports of adverse systemic effects.² Affected patients experience cutaneous pigmentary changes, which may be dark red, blue, or black, and spontaneously resolve over time.² The degree of pigment change may be associated with duration of skin contact with the toxin. The affected areas may resemble burns, dermatitis, or skin necrosis. More distal lesions may present similarly to blue toe syndrome or acute arterial occlusion but can be differentiated by the presence of intact peripheral pulses and lack of temperature discrepancy between the feet.^3,4 Histologic evaluation of the lesions generally reveals nonspecific full-thickness epidermal necrosis, making clinical suspicion and physical examination paramount to the diagnosis of millipede burns.⁵

Diagnostic Difficulties

Accurate diagnosis of millipede burns is more difficult when the burn involves an unusual site. The most common site of involvement is the foot (Figure 2), followed by other commonly exposed areas such as the arms, face, and eyes.^2,3,6,7 Covered parts of the body are much less commonly affected, requiring the arthropod to gain access via infiltration of clothing, often when hanging on a clothesline. In these cases, burns may be mistaken for child abuse, especially if certain areas of the body are involved, such as the groin and genitals.² The well-defined arcuate lesions of the burns may resemble injuries from a wire or belt to the unsuspecting observer.

Conclusion

Although millipedes often are regarded as harmless, they are capable of causing adverse reactions through the secretion of toxic chemicals. Millipede burns cause localized pigmentary changes that may be associated with pain or burning in some patients. Because these burns may resemble child abuse in pediatric patients, physicians should be aware of this diagnosis when unusual parts of the body are involved.

Clinical Presentation

Millipedes secrete a noxious toxin implicated in millipede burns. The toxic substance is benzoquinone, a strong irritant secreted from the repugnatorial glands contained in each segment of the arthropod (Figure 1). This compound serves as a natural insect repellant, acting as the millipede’s defense mechanism from potential predators.¹ On human skin, benzoquinone causes localized pigmentary changes most commonly presenting on the feet and toes. Local lesions may be associated with pain or burning, but there are no known reports of adverse systemic effects.² Affected patients experience cutaneous pigmentary changes, which may be dark red, blue, or black, and spontaneously resolve over time.² The degree of pigment change may be associated with duration of skin contact with the toxin. The affected areas may resemble burns, dermatitis, or skin necrosis. More distal lesions may present similarly to blue toe syndrome or acute arterial occlusion but can be differentiated by the presence of intact peripheral pulses and lack of temperature discrepancy between the feet.^3,4 Histologic evaluation of the lesions generally reveals nonspecific full-thickness epidermal necrosis, making clinical suspicion and physical examination paramount to the diagnosis of millipede burns.⁵

Diagnostic Difficulties

Accurate diagnosis of millipede burns is more difficult when the burn involves an unusual site. The most common site of involvement is the foot (Figure 2), followed by other commonly exposed areas such as the arms, face, and eyes.^2,3,6,7 Covered parts of the body are much less commonly affected, requiring the arthropod to gain access via infiltration of clothing, often when hanging on a clothesline. In these cases, burns may be mistaken for child abuse, especially if certain areas of the body are involved, such as the groin and genitals.² The well-defined arcuate lesions of the burns may resemble injuries from a wire or belt to the unsuspecting observer.

Conclusion

Although millipedes often are regarded as harmless, they are capable of causing adverse reactions through the secretion of toxic chemicals. Millipede burns cause localized pigmentary changes that may be associated with pain or burning in some patients. Because these burns may resemble child abuse in pediatric patients, physicians should be aware of this diagnosis when unusual parts of the body are involved.

Incidence and Characteristics

Stingrays are the most common cause of fish-related stings worldwide.¹ The Urolophidae and Dasyatidae stingray families are responsible for most marine stingray injuries, including approximately 1500 reported injuries in the United States annually.^1,2 Saltwater stingrays from these families commonly are encountered in shallow temperate and tropical coastal waters across the globe and possess dorsally and distally located spines capable of injuring humans that step on them (Figure 1).^1,3 Freshwater stingrays (Potamotrygonidae family)(Figure 2) are not present in North America but rather inhabit lakes and river systems in South America, Africa, Laos, and Vietnam.⁴ Although recent incidence is unknown, Marinkelle⁵ estimated that thousands of stingray injuries occurred annually in the freshwater of Columbia during the 1960s. Unfortunately, the annual worldwide incidence of stingray injuries is generally unknown and is difficult to estimate, in part because injuries often go unreported.

Stingrays are dorsoventrally flattened, diamond-shaped fish with light-colored ventral and dark-colored dorsal surfaces. They have strong pectoral wings that allow them to swim forward and backward and even launch off waves.³ Stingrays range in size from the palm of a human hand to 6.5 ft in width. They possess 1 or more spines (2.5 to >30 cm in length) that are disguised by much longer tails.^6,7 They often are encountered accidentally because they bury themselves in the sand or mud of shallow coastal waters or rivers with only their eyes and tails exposed to fool prey and avoid predators.

Injury Clinical Presentation

Stingray injuries typically involve the lower legs, ankles, or feet after stepping on a stingray.⁸ Fishermen can present with injuries of the upper extremities after handling fish with their hands.⁹ Other rarer injuries occur when individuals are swimming alongside stingrays or when stingrays catapult off waves into moving boats.^10,11 Stingrays impale victims by using their tails to direct a retroserrate barb composed of a strong cartilaginous material called vasodentin. The barb releases venom by breaking through the venom-containing integumentary sheath that encapsulates it. Stingray venom contains phosphodiesterase, serotonin, and 5′-nucleotidase. It causes severe pain, vasoconstriction, ischemia, and poor wound healing, along with systemic effects such as disorientation, syncope, seizures, salivation, nausea, vomiting, abdominal pain, diarrhea, muscle cramps or fasciculations, pruritus, allergic reaction, hypotension, cardiac arrhythmias, dyspnea, paralysis, and possibly death.^1,8,12,13

Management

Pain Relief
As with many marine envenomations, immersion in hot but not scalding water can inactivate venom and reduce symptoms.^8,9 In one retrospective review, 52 of 75 (69%) patients reporting to a California poison center with stingray injuries had improvement in pain within 1 hour of hot water immersion before any analgesics were instituted.⁸ In another review, 65 of 74 (88%) patients presenting to a California emergency department within 24 hours of sustaining a stingray injury had complete relief of pain within 30 minutes of hot water immersion. Patients who received analgesics in addition to hot water immersion did not require a second dose.⁹ In concordance with these studies, we suggest immersing areas affected by stingray injuries in hot water (temperature, 43.3°C to 46.1°C [110°F–115°F]; or as close to this range as tolerated) until pain subsides.^8,9,14 Ice packs are an alternative to hot water immersion that may be more readily available to patients. If pain does not resolve following hot water immersion or application of an ice pack, additional analgesics and xylocaine without epinephrine may be helpful.^9,15

Infection
One major complication of stingray injuries is infection.^8,9 Many bacterial species reside in stingray mucus, the marine environment, or on human skin that may be introduced during a single injury. Marine envenomations can involve organisms such as Vibrio, Aeromonas, and Mycobacterium species, which often are resistant to antibiotic prophylaxis covering common causes of soft-tissue infection such as Staphylococcus and Streptococcus species.^8,9,16,17 Additionally, physicians should cover for Clostridium species and ensure patients are up-to-date on vaccinations because severe cases of tetanus following stingray injuries have been reported.¹⁸ Lastly, fungal infections including fusariosis have been reported following stingray injuries and should be considered if a patient develops an infection.¹⁹

Several authors support the use of prophylactic broad-spectrum antibiotics in all but mild stingray injuries.^8,9,20,21 Although no standardized definition exists, mild injuries generally represent patients with superficial lacerations or less, while deeper lacerations and puncture wounds require prophylaxis. Several authors agree on the use of fluoroquinolone antibiotics (eg, ciprofloxacin 500 mg twice daily) for 5 to 7 days following severe stingray injuries.^1,9,13,22 Other proposed antibiotic regimens include trimethoprim-sulfamethoxazole (160/800 mg twice daily) or tetracycline (500 mg 4 times daily) for 7 days.¹³ Failure of ciprofloxacin therapy after 7 days has been reported, with resolution of infection after treatment with an intravenous cephalosporin for 7 days.²⁰ Failure of trimethoprim-sulfamethoxazole therapy also has been reported, with one case requiring levofloxacin for a much longer course.²¹ Clinical follow-up remains essential after prescribing prophylactic antibiotics, as resistance is common.

Foreign Bodies
Stingray injuries also are often complicated by foreign bodies or retained spines.^3,8 Although these complications are less severe than infection, all wounds should be explored for material under local anesthesia. Furthermore, there has been support for thorough debridement of necrotic tissue with referral to a hand specialist for deeper injuries to the hands as well as referral to a foot and ankle specialist for deeper injuries of the lower extremities.^23,24 More serious injuries with penetration of vital structures, such as through the chest or abdomen, require immediate exploration in an operating room.^1,24

Imaging
Routine imaging of stingray injuries remains controversial. In a case series of 119 patients presenting to a California emergency department with stingray injuries, Clark et al⁹ found that radiographs were not helpful. This finding likely is due in part to an inability to detect hypodense material such as integumentary or glandular tissue via radiography.³ However, radiographs have been used to identify retained stingray barbs in select cases in which retained barbs are suspected.^2,25 Lastly, ultrasonography potentially may offer a better first choice when a barb is not readily apparent; magnetic resonance imaging may be indicated for more involved areas and for further visualization of suspected hypodense material, though at a higher expense.^2,9

Biopsy
Biopsies of stingray injuries are rarely performed, and the findings are not well characterized. One case biopsied 2 months after injury showed a large zone of paucicellular necrosis with superficial ulceration and granulomatous inflammation. The stingray venom was most likely responsible for the pattern of necrosis noted in the biopsy.²¹

Avoidance and Prevention

Patients traveling to areas of the world inhabited by stingrays should receive counseling on how to avoid injury. Prior to entry, individuals can throw stones or use a long stick to clear their walking or swimming areas of venomous fish.²⁶ Polarized sunglasses may help spot stingrays in shallow water. Furthermore, wading through water with a shuffling gait can help individuals avoid stepping directly on a stingray and also warns stingrays that someone is in the area. Individuals who spend more time in coastal waters or river systems inhabited by stingrays may invest in protective stingray gear such as leg guards or specialized wading boots.²⁶ Lastly, fishermen should be advised to avoid handling stingrays with their hands and instead cut their fishing line to release the fish.

Incidence and Characteristics

Stingrays are the most common cause of fish-related stings worldwide.¹ The Urolophidae and Dasyatidae stingray families are responsible for most marine stingray injuries, including approximately 1500 reported injuries in the United States annually.^1,2 Saltwater stingrays from these families commonly are encountered in shallow temperate and tropical coastal waters across the globe and possess dorsally and distally located spines capable of injuring humans that step on them (Figure 1).^1,3 Freshwater stingrays (Potamotrygonidae family)(Figure 2) are not present in North America but rather inhabit lakes and river systems in South America, Africa, Laos, and Vietnam.⁴ Although recent incidence is unknown, Marinkelle⁵ estimated that thousands of stingray injuries occurred annually in the freshwater of Columbia during the 1960s. Unfortunately, the annual worldwide incidence of stingray injuries is generally unknown and is difficult to estimate, in part because injuries often go unreported.

Stingrays are dorsoventrally flattened, diamond-shaped fish with light-colored ventral and dark-colored dorsal surfaces. They have strong pectoral wings that allow them to swim forward and backward and even launch off waves.³ Stingrays range in size from the palm of a human hand to 6.5 ft in width. They possess 1 or more spines (2.5 to >30 cm in length) that are disguised by much longer tails.^6,7 They often are encountered accidentally because they bury themselves in the sand or mud of shallow coastal waters or rivers with only their eyes and tails exposed to fool prey and avoid predators.

Injury Clinical Presentation

Stingray injuries typically involve the lower legs, ankles, or feet after stepping on a stingray.⁸ Fishermen can present with injuries of the upper extremities after handling fish with their hands.⁹ Other rarer injuries occur when individuals are swimming alongside stingrays or when stingrays catapult off waves into moving boats.^10,11 Stingrays impale victims by using their tails to direct a retroserrate barb composed of a strong cartilaginous material called vasodentin. The barb releases venom by breaking through the venom-containing integumentary sheath that encapsulates it. Stingray venom contains phosphodiesterase, serotonin, and 5′-nucleotidase. It causes severe pain, vasoconstriction, ischemia, and poor wound healing, along with systemic effects such as disorientation, syncope, seizures, salivation, nausea, vomiting, abdominal pain, diarrhea, muscle cramps or fasciculations, pruritus, allergic reaction, hypotension, cardiac arrhythmias, dyspnea, paralysis, and possibly death.^1,8,12,13

Management

Pain Relief
As with many marine envenomations, immersion in hot but not scalding water can inactivate venom and reduce symptoms.^8,9 In one retrospective review, 52 of 75 (69%) patients reporting to a California poison center with stingray injuries had improvement in pain within 1 hour of hot water immersion before any analgesics were instituted.⁸ In another review, 65 of 74 (88%) patients presenting to a California emergency department within 24 hours of sustaining a stingray injury had complete relief of pain within 30 minutes of hot water immersion. Patients who received analgesics in addition to hot water immersion did not require a second dose.⁹ In concordance with these studies, we suggest immersing areas affected by stingray injuries in hot water (temperature, 43.3°C to 46.1°C [110°F–115°F]; or as close to this range as tolerated) until pain subsides.^8,9,14 Ice packs are an alternative to hot water immersion that may be more readily available to patients. If pain does not resolve following hot water immersion or application of an ice pack, additional analgesics and xylocaine without epinephrine may be helpful.^9,15

Infection
One major complication of stingray injuries is infection.^8,9 Many bacterial species reside in stingray mucus, the marine environment, or on human skin that may be introduced during a single injury. Marine envenomations can involve organisms such as Vibrio, Aeromonas, and Mycobacterium species, which often are resistant to antibiotic prophylaxis covering common causes of soft-tissue infection such as Staphylococcus and Streptococcus species.^8,9,16,17 Additionally, physicians should cover for Clostridium species and ensure patients are up-to-date on vaccinations because severe cases of tetanus following stingray injuries have been reported.¹⁸ Lastly, fungal infections including fusariosis have been reported following stingray injuries and should be considered if a patient develops an infection.¹⁹

Several authors support the use of prophylactic broad-spectrum antibiotics in all but mild stingray injuries.^8,9,20,21 Although no standardized definition exists, mild injuries generally represent patients with superficial lacerations or less, while deeper lacerations and puncture wounds require prophylaxis. Several authors agree on the use of fluoroquinolone antibiotics (eg, ciprofloxacin 500 mg twice daily) for 5 to 7 days following severe stingray injuries.^1,9,13,22 Other proposed antibiotic regimens include trimethoprim-sulfamethoxazole (160/800 mg twice daily) or tetracycline (500 mg 4 times daily) for 7 days.¹³ Failure of ciprofloxacin therapy after 7 days has been reported, with resolution of infection after treatment with an intravenous cephalosporin for 7 days.²⁰ Failure of trimethoprim-sulfamethoxazole therapy also has been reported, with one case requiring levofloxacin for a much longer course.²¹ Clinical follow-up remains essential after prescribing prophylactic antibiotics, as resistance is common.

Foreign Bodies
Stingray injuries also are often complicated by foreign bodies or retained spines.^3,8 Although these complications are less severe than infection, all wounds should be explored for material under local anesthesia. Furthermore, there has been support for thorough debridement of necrotic tissue with referral to a hand specialist for deeper injuries to the hands as well as referral to a foot and ankle specialist for deeper injuries of the lower extremities.^23,24 More serious injuries with penetration of vital structures, such as through the chest or abdomen, require immediate exploration in an operating room.^1,24

Imaging
Routine imaging of stingray injuries remains controversial. In a case series of 119 patients presenting to a California emergency department with stingray injuries, Clark et al⁹ found that radiographs were not helpful. This finding likely is due in part to an inability to detect hypodense material such as integumentary or glandular tissue via radiography.³ However, radiographs have been used to identify retained stingray barbs in select cases in which retained barbs are suspected.^2,25 Lastly, ultrasonography potentially may offer a better first choice when a barb is not readily apparent; magnetic resonance imaging may be indicated for more involved areas and for further visualization of suspected hypodense material, though at a higher expense.^2,9

Biopsy
Biopsies of stingray injuries are rarely performed, and the findings are not well characterized. One case biopsied 2 months after injury showed a large zone of paucicellular necrosis with superficial ulceration and granulomatous inflammation. The stingray venom was most likely responsible for the pattern of necrosis noted in the biopsy.²¹

Avoidance and Prevention

Patients traveling to areas of the world inhabited by stingrays should receive counseling on how to avoid injury. Prior to entry, individuals can throw stones or use a long stick to clear their walking or swimming areas of venomous fish.²⁶ Polarized sunglasses may help spot stingrays in shallow water. Furthermore, wading through water with a shuffling gait can help individuals avoid stepping directly on a stingray and also warns stingrays that someone is in the area. Individuals who spend more time in coastal waters or river systems inhabited by stingrays may invest in protective stingray gear such as leg guards or specialized wading boots.²⁶ Lastly, fishermen should be advised to avoid handling stingrays with their hands and instead cut their fishing line to release the fish.

Incidence and Characteristics

Stingrays are the most common cause of fish-related stings worldwide.¹ The Urolophidae and Dasyatidae stingray families are responsible for most marine stingray injuries, including approximately 1500 reported injuries in the United States annually.^1,2 Saltwater stingrays from these families commonly are encountered in shallow temperate and tropical coastal waters across the globe and possess dorsally and distally located spines capable of injuring humans that step on them (Figure 1).^1,3 Freshwater stingrays (Potamotrygonidae family)(Figure 2) are not present in North America but rather inhabit lakes and river systems in South America, Africa, Laos, and Vietnam.⁴ Although recent incidence is unknown, Marinkelle⁵ estimated that thousands of stingray injuries occurred annually in the freshwater of Columbia during the 1960s. Unfortunately, the annual worldwide incidence of stingray injuries is generally unknown and is difficult to estimate, in part because injuries often go unreported.

Stingrays are dorsoventrally flattened, diamond-shaped fish with light-colored ventral and dark-colored dorsal surfaces. They have strong pectoral wings that allow them to swim forward and backward and even launch off waves.³ Stingrays range in size from the palm of a human hand to 6.5 ft in width. They possess 1 or more spines (2.5 to >30 cm in length) that are disguised by much longer tails.^6,7 They often are encountered accidentally because they bury themselves in the sand or mud of shallow coastal waters or rivers with only their eyes and tails exposed to fool prey and avoid predators.

Injury Clinical Presentation

Stingray injuries typically involve the lower legs, ankles, or feet after stepping on a stingray.⁸ Fishermen can present with injuries of the upper extremities after handling fish with their hands.⁹ Other rarer injuries occur when individuals are swimming alongside stingrays or when stingrays catapult off waves into moving boats.^10,11 Stingrays impale victims by using their tails to direct a retroserrate barb composed of a strong cartilaginous material called vasodentin. The barb releases venom by breaking through the venom-containing integumentary sheath that encapsulates it. Stingray venom contains phosphodiesterase, serotonin, and 5′-nucleotidase. It causes severe pain, vasoconstriction, ischemia, and poor wound healing, along with systemic effects such as disorientation, syncope, seizures, salivation, nausea, vomiting, abdominal pain, diarrhea, muscle cramps or fasciculations, pruritus, allergic reaction, hypotension, cardiac arrhythmias, dyspnea, paralysis, and possibly death.^1,8,12,13

Management

Pain Relief
As with many marine envenomations, immersion in hot but not scalding water can inactivate venom and reduce symptoms.^8,9 In one retrospective review, 52 of 75 (69%) patients reporting to a California poison center with stingray injuries had improvement in pain within 1 hour of hot water immersion before any analgesics were instituted.⁸ In another review, 65 of 74 (88%) patients presenting to a California emergency department within 24 hours of sustaining a stingray injury had complete relief of pain within 30 minutes of hot water immersion. Patients who received analgesics in addition to hot water immersion did not require a second dose.⁹ In concordance with these studies, we suggest immersing areas affected by stingray injuries in hot water (temperature, 43.3°C to 46.1°C [110°F–115°F]; or as close to this range as tolerated) until pain subsides.^8,9,14 Ice packs are an alternative to hot water immersion that may be more readily available to patients. If pain does not resolve following hot water immersion or application of an ice pack, additional analgesics and xylocaine without epinephrine may be helpful.^9,15

Infection
One major complication of stingray injuries is infection.^8,9 Many bacterial species reside in stingray mucus, the marine environment, or on human skin that may be introduced during a single injury. Marine envenomations can involve organisms such as Vibrio, Aeromonas, and Mycobacterium species, which often are resistant to antibiotic prophylaxis covering common causes of soft-tissue infection such as Staphylococcus and Streptococcus species.^8,9,16,17 Additionally, physicians should cover for Clostridium species and ensure patients are up-to-date on vaccinations because severe cases of tetanus following stingray injuries have been reported.¹⁸ Lastly, fungal infections including fusariosis have been reported following stingray injuries and should be considered if a patient develops an infection.¹⁹

Several authors support the use of prophylactic broad-spectrum antibiotics in all but mild stingray injuries.^8,9,20,21 Although no standardized definition exists, mild injuries generally represent patients with superficial lacerations or less, while deeper lacerations and puncture wounds require prophylaxis. Several authors agree on the use of fluoroquinolone antibiotics (eg, ciprofloxacin 500 mg twice daily) for 5 to 7 days following severe stingray injuries.^1,9,13,22 Other proposed antibiotic regimens include trimethoprim-sulfamethoxazole (160/800 mg twice daily) or tetracycline (500 mg 4 times daily) for 7 days.¹³ Failure of ciprofloxacin therapy after 7 days has been reported, with resolution of infection after treatment with an intravenous cephalosporin for 7 days.²⁰ Failure of trimethoprim-sulfamethoxazole therapy also has been reported, with one case requiring levofloxacin for a much longer course.²¹ Clinical follow-up remains essential after prescribing prophylactic antibiotics, as resistance is common.

Foreign Bodies
Stingray injuries also are often complicated by foreign bodies or retained spines.^3,8 Although these complications are less severe than infection, all wounds should be explored for material under local anesthesia. Furthermore, there has been support for thorough debridement of necrotic tissue with referral to a hand specialist for deeper injuries to the hands as well as referral to a foot and ankle specialist for deeper injuries of the lower extremities.^23,24 More serious injuries with penetration of vital structures, such as through the chest or abdomen, require immediate exploration in an operating room.^1,24

Imaging
Routine imaging of stingray injuries remains controversial. In a case series of 119 patients presenting to a California emergency department with stingray injuries, Clark et al⁹ found that radiographs were not helpful. This finding likely is due in part to an inability to detect hypodense material such as integumentary or glandular tissue via radiography.³ However, radiographs have been used to identify retained stingray barbs in select cases in which retained barbs are suspected.^2,25 Lastly, ultrasonography potentially may offer a better first choice when a barb is not readily apparent; magnetic resonance imaging may be indicated for more involved areas and for further visualization of suspected hypodense material, though at a higher expense.^2,9

Biopsy
Biopsies of stingray injuries are rarely performed, and the findings are not well characterized. One case biopsied 2 months after injury showed a large zone of paucicellular necrosis with superficial ulceration and granulomatous inflammation. The stingray venom was most likely responsible for the pattern of necrosis noted in the biopsy.²¹

Avoidance and Prevention

Patients traveling to areas of the world inhabited by stingrays should receive counseling on how to avoid injury. Prior to entry, individuals can throw stones or use a long stick to clear their walking or swimming areas of venomous fish.²⁶ Polarized sunglasses may help spot stingrays in shallow water. Furthermore, wading through water with a shuffling gait can help individuals avoid stepping directly on a stingray and also warns stingrays that someone is in the area. Individuals who spend more time in coastal waters or river systems inhabited by stingrays may invest in protective stingray gear such as leg guards or specialized wading boots.²⁶ Lastly, fishermen should be advised to avoid handling stingrays with their hands and instead cut their fishing line to release the fish.

Bedbugs are common pests causing several health and economic consequences. With increased travel, pesticide resistance, and a lack of awareness about prevention, bedbugs have become even more difficult to control, especially within large population centers.¹ The US Environmental Protection Agency considers bedbugs to be a considerable public health issue.² Typically, they are found in private residences; however, there have been more reports of bedbugs discovered in the workplace within the last 20 years.^3-5 Herein, we present a case of bedbugs presenting in this unusual environment.

Case Report

A 42-year-old man presented to our dermatology clinic with intensely itchy bumps over the bilateral posterior arms of 3 months’ duration. He had no other skin, hair, or nail concerns. Over the last 3 months prior to dermatologic evaluation, he was treated by an outside physician with topical steroids, systemic antibiotics, topical antifungals, and even systemic steroids with no improvement of the lesions or symptoms. On clinical examination at the current presentation, 8 to 10 pink dermal papules coalescing into 10-cm round patches were noted on the bilateral posterior arms (Figure 1). A punch biopsy of the posterior right arm was performed, and histologic analysis showed a dense superficial and deep infiltrate and a perivascular infiltrate of lymphocytes and eosinophils (Figure 2). No notable epidermal changes were observed.

At this time, the patient was counseled that the most likely cause was some unknown arthropod exposure. Given the chronicity of the patient’s disease course, bedbugs were favored; however, an extensive search of the patient’s home failed to uncover any arthropods, let alone bedbugs. A few weeks later, the patient discovered insects emanating from the mesh backing of his office chair while at work (Figure 3). The location of the intruders corresponded exactly with the lesions on the posterior arms. The occupational health office at his workplace collected samples of the arthropods and confirmed they were bedbugs. The patient’s lesions resolved with topical clobetasol once eradication of the workplace was complete.

Morphology and Epidemiology
Bedbugs are wingless arthropods that have flat, oval-shaped, reddish brown bodies. They are approximately 4.5-mm long and 2.5-mm wide (Figure 4). The 2 most common species of bedbugs that infect humans are Cimex lectularius and Cimex hemipterus. Bedbugs are most commonly found in hotels, apartments, and residential households near sleep locations. They reside in crevices, cracks, mattresses, cushions, dressers, and other structures proximal to the bed. During the day they remain hidden, but at night they emerge for a blood meal. The average lifespan of a bedbug is 6 to 12 months.⁶ Females lay more than 200 eggs that hatch in approximately 6 to 10 days.⁷ Bedbugs progress through 5 nymph stages before becoming adults; several blood meals are required to advance each stage.⁶

Although commonly attributed to the home, bedbugs are being increasingly seen in the office setting.^3-5 In a survey given to pest management professionals in 2015, more than 45% reported that they were contracted by corporations for bedbug infestations in office settings, an increase from 18% in 2010 and 36% in 2013.³ Bedbugs are brought into offices through clothing, luggage, books, and other personal items. Unable to find hosts at night, bedbugs adapt to daytime hours and spread to more unpredictable locations, including chairs, office equipment, desks, and computers.⁴ Additionally, they frequently move around to find a suitable host.⁵ As a result, the growth rate of bedbugs in an office setting is much slower than in the home, with fewer insects. Our patient did not have bedbugs at home, but it is possible that other employees transported them to the office over time.

Clinical Manifestations
Bedbugs cause pruritic and nonpruritic skin rashes, often of the arms, legs, neck, and face. A common reaction is an erythematous papule with a hemorrhagic punctum caused by one bite.⁸ Other presentations include purpuric macules, bullae, and papular urticaria.^8-10 Although bedbugs are suspected to transmit infectious diseases, no reports have substantiated that claim.¹¹

Our patient had several coalescing dermal papules on the arms indicating multiple bites around the same area. Due to the stationary aspect of his job—with the arms resting on his chair while typing at his desk—our patient was an easy target for consistent blood meals.

Detection
Due to an overall smaller population of insects in an office setting, detection of bedbugs in the workplace can be difficult. Infestations can be primarily identified on visual inspection by pest control.¹² The mesh backing on our patient’s chair was one site where bedbugs resided. It is important to check areas where employees congregate, such as lounges, lunch areas, conference rooms, and printers.⁴ It also is essential to examine coatracks and locker rooms, as employees may leave personal items that can serve as a source of transmission of the bugs from home. Additional detection tools provided by pest management professionals include canines, as well as devices that emit pheromones, carbon dioxide, or heat to ensnare the insects.¹²

Treatment
Treatment of bedbug bites is quite variable. For some patients, lesions may resolve on their own. Pruritic maculopapular eruptions can be treated with topical pramoxine or doxepin.⁸ Patients who develop allergic urticaria can use oral antihistamines. Systemic reactions such as anaphylaxis can be treated with a combination of intramuscular epinephrine, antihistamines, and corticosteroids.⁸ The etiology of our patient’s condition initially was unknown, and thus he was given unnecessary systemic steroids and antifungals until the source of the rash was identified and eradicated. Topical clobetasol was subsequently administered and was sufficient to resolve his symptoms.

Final Thoughts

Bedbugs continue to remain a nuisance in the home. This case provides an example of bedbugs in the office, a location that is not commonly associated with bedbug infestations. Bedbugs pose numerous psychological, economic, and health consequences.² Productivity can be reduced, as patients with symptomatic lesions will be unable to work effectively, and those who are unaffected may be unwilling to work knowing their office environment poses a health risk. In addition, employees may worry about bringing the bedbugs home. It is important that employees be educated on the signs of a bedbug infestation and take preventive measures to stop spreading or introducing them to the office space. Due to the scattered habitation of bedbugs in offices, pest control managers need to be vigilant to identify sources of infestation and eradicate accordingly. Clinical manifestations can be nonspecific, resembling autoimmune disorders, fungal infections, or bites from other various arthropods; thus, treatment is highly dependent on the patient’s history and occupational exposure.

Bedbugs have successfully adapted to a new environment in the office space. Dermatologists and other health care professionals can no longer exclusively associate bedbugs with the home. When the clinical and histological presentation suggests an arthropod assault, we must counsel our patients to surveil their homes and work settings alike. If necessary, they should seek the assistance of occupational health professionals.

Bedbugs are common pests causing several health and economic consequences. With increased travel, pesticide resistance, and a lack of awareness about prevention, bedbugs have become even more difficult to control, especially within large population centers.¹ The US Environmental Protection Agency considers bedbugs to be a considerable public health issue.² Typically, they are found in private residences; however, there have been more reports of bedbugs discovered in the workplace within the last 20 years.^3-5 Herein, we present a case of bedbugs presenting in this unusual environment.

Case Report

A 42-year-old man presented to our dermatology clinic with intensely itchy bumps over the bilateral posterior arms of 3 months’ duration. He had no other skin, hair, or nail concerns. Over the last 3 months prior to dermatologic evaluation, he was treated by an outside physician with topical steroids, systemic antibiotics, topical antifungals, and even systemic steroids with no improvement of the lesions or symptoms. On clinical examination at the current presentation, 8 to 10 pink dermal papules coalescing into 10-cm round patches were noted on the bilateral posterior arms (Figure 1). A punch biopsy of the posterior right arm was performed, and histologic analysis showed a dense superficial and deep infiltrate and a perivascular infiltrate of lymphocytes and eosinophils (Figure 2). No notable epidermal changes were observed.

At this time, the patient was counseled that the most likely cause was some unknown arthropod exposure. Given the chronicity of the patient’s disease course, bedbugs were favored; however, an extensive search of the patient’s home failed to uncover any arthropods, let alone bedbugs. A few weeks later, the patient discovered insects emanating from the mesh backing of his office chair while at work (Figure 3). The location of the intruders corresponded exactly with the lesions on the posterior arms. The occupational health office at his workplace collected samples of the arthropods and confirmed they were bedbugs. The patient’s lesions resolved with topical clobetasol once eradication of the workplace was complete.

Morphology and Epidemiology
Bedbugs are wingless arthropods that have flat, oval-shaped, reddish brown bodies. They are approximately 4.5-mm long and 2.5-mm wide (Figure 4). The 2 most common species of bedbugs that infect humans are Cimex lectularius and Cimex hemipterus. Bedbugs are most commonly found in hotels, apartments, and residential households near sleep locations. They reside in crevices, cracks, mattresses, cushions, dressers, and other structures proximal to the bed. During the day they remain hidden, but at night they emerge for a blood meal. The average lifespan of a bedbug is 6 to 12 months.⁶ Females lay more than 200 eggs that hatch in approximately 6 to 10 days.⁷ Bedbugs progress through 5 nymph stages before becoming adults; several blood meals are required to advance each stage.⁶

Although commonly attributed to the home, bedbugs are being increasingly seen in the office setting.^3-5 In a survey given to pest management professionals in 2015, more than 45% reported that they were contracted by corporations for bedbug infestations in office settings, an increase from 18% in 2010 and 36% in 2013.³ Bedbugs are brought into offices through clothing, luggage, books, and other personal items. Unable to find hosts at night, bedbugs adapt to daytime hours and spread to more unpredictable locations, including chairs, office equipment, desks, and computers.⁴ Additionally, they frequently move around to find a suitable host.⁵ As a result, the growth rate of bedbugs in an office setting is much slower than in the home, with fewer insects. Our patient did not have bedbugs at home, but it is possible that other employees transported them to the office over time.

Clinical Manifestations
Bedbugs cause pruritic and nonpruritic skin rashes, often of the arms, legs, neck, and face. A common reaction is an erythematous papule with a hemorrhagic punctum caused by one bite.⁸ Other presentations include purpuric macules, bullae, and papular urticaria.^8-10 Although bedbugs are suspected to transmit infectious diseases, no reports have substantiated that claim.¹¹

Our patient had several coalescing dermal papules on the arms indicating multiple bites around the same area. Due to the stationary aspect of his job—with the arms resting on his chair while typing at his desk—our patient was an easy target for consistent blood meals.

Detection
Due to an overall smaller population of insects in an office setting, detection of bedbugs in the workplace can be difficult. Infestations can be primarily identified on visual inspection by pest control.¹² The mesh backing on our patient’s chair was one site where bedbugs resided. It is important to check areas where employees congregate, such as lounges, lunch areas, conference rooms, and printers.⁴ It also is essential to examine coatracks and locker rooms, as employees may leave personal items that can serve as a source of transmission of the bugs from home. Additional detection tools provided by pest management professionals include canines, as well as devices that emit pheromones, carbon dioxide, or heat to ensnare the insects.¹²

Treatment
Treatment of bedbug bites is quite variable. For some patients, lesions may resolve on their own. Pruritic maculopapular eruptions can be treated with topical pramoxine or doxepin.⁸ Patients who develop allergic urticaria can use oral antihistamines. Systemic reactions such as anaphylaxis can be treated with a combination of intramuscular epinephrine, antihistamines, and corticosteroids.⁸ The etiology of our patient’s condition initially was unknown, and thus he was given unnecessary systemic steroids and antifungals until the source of the rash was identified and eradicated. Topical clobetasol was subsequently administered and was sufficient to resolve his symptoms.

Final Thoughts

Bedbugs continue to remain a nuisance in the home. This case provides an example of bedbugs in the office, a location that is not commonly associated with bedbug infestations. Bedbugs pose numerous psychological, economic, and health consequences.² Productivity can be reduced, as patients with symptomatic lesions will be unable to work effectively, and those who are unaffected may be unwilling to work knowing their office environment poses a health risk. In addition, employees may worry about bringing the bedbugs home. It is important that employees be educated on the signs of a bedbug infestation and take preventive measures to stop spreading or introducing them to the office space. Due to the scattered habitation of bedbugs in offices, pest control managers need to be vigilant to identify sources of infestation and eradicate accordingly. Clinical manifestations can be nonspecific, resembling autoimmune disorders, fungal infections, or bites from other various arthropods; thus, treatment is highly dependent on the patient’s history and occupational exposure.

Bedbugs have successfully adapted to a new environment in the office space. Dermatologists and other health care professionals can no longer exclusively associate bedbugs with the home. When the clinical and histological presentation suggests an arthropod assault, we must counsel our patients to surveil their homes and work settings alike. If necessary, they should seek the assistance of occupational health professionals.

Bedbugs are common pests causing several health and economic consequences. With increased travel, pesticide resistance, and a lack of awareness about prevention, bedbugs have become even more difficult to control, especially within large population centers.¹ The US Environmental Protection Agency considers bedbugs to be a considerable public health issue.² Typically, they are found in private residences; however, there have been more reports of bedbugs discovered in the workplace within the last 20 years.^3-5 Herein, we present a case of bedbugs presenting in this unusual environment.

Case Report

A 42-year-old man presented to our dermatology clinic with intensely itchy bumps over the bilateral posterior arms of 3 months’ duration. He had no other skin, hair, or nail concerns. Over the last 3 months prior to dermatologic evaluation, he was treated by an outside physician with topical steroids, systemic antibiotics, topical antifungals, and even systemic steroids with no improvement of the lesions or symptoms. On clinical examination at the current presentation, 8 to 10 pink dermal papules coalescing into 10-cm round patches were noted on the bilateral posterior arms (Figure 1). A punch biopsy of the posterior right arm was performed, and histologic analysis showed a dense superficial and deep infiltrate and a perivascular infiltrate of lymphocytes and eosinophils (Figure 2). No notable epidermal changes were observed.

At this time, the patient was counseled that the most likely cause was some unknown arthropod exposure. Given the chronicity of the patient’s disease course, bedbugs were favored; however, an extensive search of the patient’s home failed to uncover any arthropods, let alone bedbugs. A few weeks later, the patient discovered insects emanating from the mesh backing of his office chair while at work (Figure 3). The location of the intruders corresponded exactly with the lesions on the posterior arms. The occupational health office at his workplace collected samples of the arthropods and confirmed they were bedbugs. The patient’s lesions resolved with topical clobetasol once eradication of the workplace was complete.

Morphology and Epidemiology
Bedbugs are wingless arthropods that have flat, oval-shaped, reddish brown bodies. They are approximately 4.5-mm long and 2.5-mm wide (Figure 4). The 2 most common species of bedbugs that infect humans are Cimex lectularius and Cimex hemipterus. Bedbugs are most commonly found in hotels, apartments, and residential households near sleep locations. They reside in crevices, cracks, mattresses, cushions, dressers, and other structures proximal to the bed. During the day they remain hidden, but at night they emerge for a blood meal. The average lifespan of a bedbug is 6 to 12 months.⁶ Females lay more than 200 eggs that hatch in approximately 6 to 10 days.⁷ Bedbugs progress through 5 nymph stages before becoming adults; several blood meals are required to advance each stage.⁶

Although commonly attributed to the home, bedbugs are being increasingly seen in the office setting.^3-5 In a survey given to pest management professionals in 2015, more than 45% reported that they were contracted by corporations for bedbug infestations in office settings, an increase from 18% in 2010 and 36% in 2013.³ Bedbugs are brought into offices through clothing, luggage, books, and other personal items. Unable to find hosts at night, bedbugs adapt to daytime hours and spread to more unpredictable locations, including chairs, office equipment, desks, and computers.⁴ Additionally, they frequently move around to find a suitable host.⁵ As a result, the growth rate of bedbugs in an office setting is much slower than in the home, with fewer insects. Our patient did not have bedbugs at home, but it is possible that other employees transported them to the office over time.

Clinical Manifestations
Bedbugs cause pruritic and nonpruritic skin rashes, often of the arms, legs, neck, and face. A common reaction is an erythematous papule with a hemorrhagic punctum caused by one bite.⁸ Other presentations include purpuric macules, bullae, and papular urticaria.^8-10 Although bedbugs are suspected to transmit infectious diseases, no reports have substantiated that claim.¹¹

Our patient had several coalescing dermal papules on the arms indicating multiple bites around the same area. Due to the stationary aspect of his job—with the arms resting on his chair while typing at his desk—our patient was an easy target for consistent blood meals.

Detection
Due to an overall smaller population of insects in an office setting, detection of bedbugs in the workplace can be difficult. Infestations can be primarily identified on visual inspection by pest control.¹² The mesh backing on our patient’s chair was one site where bedbugs resided. It is important to check areas where employees congregate, such as lounges, lunch areas, conference rooms, and printers.⁴ It also is essential to examine coatracks and locker rooms, as employees may leave personal items that can serve as a source of transmission of the bugs from home. Additional detection tools provided by pest management professionals include canines, as well as devices that emit pheromones, carbon dioxide, or heat to ensnare the insects.¹²

Treatment
Treatment of bedbug bites is quite variable. For some patients, lesions may resolve on their own. Pruritic maculopapular eruptions can be treated with topical pramoxine or doxepin.⁸ Patients who develop allergic urticaria can use oral antihistamines. Systemic reactions such as anaphylaxis can be treated with a combination of intramuscular epinephrine, antihistamines, and corticosteroids.⁸ The etiology of our patient’s condition initially was unknown, and thus he was given unnecessary systemic steroids and antifungals until the source of the rash was identified and eradicated. Topical clobetasol was subsequently administered and was sufficient to resolve his symptoms.

Final Thoughts

Bedbugs continue to remain a nuisance in the home. This case provides an example of bedbugs in the office, a location that is not commonly associated with bedbug infestations. Bedbugs pose numerous psychological, economic, and health consequences.² Productivity can be reduced, as patients with symptomatic lesions will be unable to work effectively, and those who are unaffected may be unwilling to work knowing their office environment poses a health risk. In addition, employees may worry about bringing the bedbugs home. It is important that employees be educated on the signs of a bedbug infestation and take preventive measures to stop spreading or introducing them to the office space. Due to the scattered habitation of bedbugs in offices, pest control managers need to be vigilant to identify sources of infestation and eradicate accordingly. Clinical manifestations can be nonspecific, resembling autoimmune disorders, fungal infections, or bites from other various arthropods; thus, treatment is highly dependent on the patient’s history and occupational exposure.

Bedbugs have successfully adapted to a new environment in the office space. Dermatologists and other health care professionals can no longer exclusively associate bedbugs with the home. When the clinical and histological presentation suggests an arthropod assault, we must counsel our patients to surveil their homes and work settings alike. If necessary, they should seek the assistance of occupational health professionals.

The lionfish (Pterois volitans) is a member of the Scorpaenidae family of venomous fish.^1-3 Lionfish are an invasive species originally from the Indian and Pacific oceans and the Red Sea that now are widely found throughout tropical and temperate oceans in both hemispheres. They are a popular aquarium fish and were inadvertently introduced in the Atlantic Ocean in South Florida during the late 1980s to early 1990s.^2,4 Since then, lionfish have spread into reef systems throughout the Atlantic Ocean, Caribbean Sea, and Gulf of Mexico in rapidly growing numbers, and they are now fo und all along the southeastern coast of the United States.⁵

Characteristics

Lionfish are brightly colored with red or maroon and white stripes, tentacles above the eyes and mouth, fan-shaped pectoral fins, and spines that deliver an especially painful venomous sting that often results in edema (Figure 1). They have 12 dorsal spines, 2 pelvic spines, and 3 anal spines.

Symptoms of Envenomation

As lionfish continue to spread to popular areas of the southeast Atlantic Ocean and Caribbean Sea, the chances of human contact with lionfish have increased. Lionfish stings are now the second most common marine envenomation injury after those caused by stingrays.⁴ Lionfish stings usually occur on the hands, fingers, or forearms during handling of the fish in ocean waters or in maintenance of aquariums. The mechanism of the venom apparatus is similar for all venomous fish. The spines have surrounding integumentary sheaths containing venom that rupture and inject venom when they penetrate the skin.⁶ The venom is a heat-labile neuromuscular toxin that causes edema (Figure 2), plasma extravasation, and thrombotic skin lesions.⁷

Wounds are classified into 3 categories: grade I consists of local erythema/ecchymosis, grade II involves vesicle or blister formation, and grade III denotes wounds that develop local necrosis.⁸ The sting causes immediate and severe throbbing pain, often described as excruciating or rated 10/10 on a basic pain scale, typically radiating up the affected limb. Puncture sites may bleed and often have associated redness and swelling. Pain may last up to 24 hours. Occasionally, foreign material may be left in the wound requiring removal. There also is a chance of secondary infection at the wound site, and severe envenomation can lead to local tissue necrosis.⁸ Systemic effects can occur in some cases, including nausea, vomiting, sweating, headache, dizziness, disorientation, palpitations, and even syncope.⁹ However, to our knowledge there are no documented cases of human death from a lionfish sting. Anaphylactic reactions are possible and require immediate treatment.⁶

A study conducted in the French West Indies evaluated 117 patients with lionfish envenomation and found that victims experienced severe pain and local edema (100%), paresthesia (90%), abdominal cramps (62%), extensive edema (53%), tachycardia (34%), skin rash (32%), gastrointestinal tract symptoms (28%), syncope (27%), transient weakness (24%), hypertension (21%), hypotension (18%), and hyperthermia (9%).⁹ Complications included local infection (18%) such as skin abscess (5%), skin necrosis (3%), and septic arthritis (2%). Twenty-two percent of patients were hospitalized and 8% required surgery. Local infectious complications were more frequent in those with multiple stings (19%). The study concluded that lionfish now represent a major health threat in the West Indies.⁹ As lionfish numbers have grown, health care providers are seeing increasing numbers of envenomation cases in areas of the coastal southeastern United States and Caribbean associated with considerable morbidity. Providers in nonendemic areas also may see envenomation injuries due to the lionfish popularity in home aquariums.⁹

Management

Individuals with lionfish stings should immerse the affected area in hot but not scalding water. Those with more serious injuries should seek medical attention. Home remedies that are generally contraindicated include application of topical papain or meat tenderizer.¹⁰ Data on ice packs are mixed, but because the toxin is heat labile, the most effective initial step in treatment is immersion of the affected area in water (temperature, 40°C to 45°C) for 30 to 90 minutes.⁶ The hot water inactivates the heat-labile toxin, leading to near-complete symptomatic relief in 80% of cases and moderate relief in an additional 14%. Immersion time more than 90 minutes considerably increases the risk for burns. Children should always be monitored to prevent burns. If a patient has received a nerve block for analgesia, the wound should not be immersed in hot water to avoid burns to the skin. The wound should be meticulously cleaned with saline irrigation, and radiography or ultrasonography should be performed as deemed necessary to look for any retained foreign bodies.⁸ Patients may require parenteral or oral analgesia as well as careful follow-up to ensure proper healing.⁹ Systemic symptoms require supportive care. Venomous fish wounds typically are small and superficial. Empiric antibiotic therapy is not advised for superficial wounds but may be required for clinically infected wounds.⁸ Tetanus prophylaxis should be given as appropriate to all affected patients. It has been noted that blister fluid contains high concentrations of lionfish venom, and when present, it increases the likelihood of converting the injury from a grade II to grade III wound with tissue necrosis; therefore, blisters should be drained or excised to decrease the chances of subsequent tissue necrosis.^11,12 If secondary infection such as cellulitis develops, antibiotics should be chosen to cover likely pathogens including common skin flora such as staphylococci and marine organisms such as Vibrio species. Wounds showing signs of infection should be cultured, with antibiotics adjusted according to sensitivities.⁵ Deeper wounds should be left open (unsutured) with a proper dressing to heal. Any wounds that involve vascular or joint structures require specialty management. Wounds involving joints may on occasion require surgical exploration and debridement.

Public Health Concerns

In an attempt to slow the growth of their population, human consumption of the fish has been encouraged. The lionfish toxin is inactivated by cooking, and the fish is considered a delicacy; however, a study in the Virgin Islands found that in areas with endemic ciguatera poisoning, 12% of lionfish carried amounts of the toxin above the level considered safe for consumption. This toxin is not inactivated by cooking or freezing and can lead to ciguatera fish poisoning for which there is no antidote and can be associated with prolonged neurotoxicity.¹³

Conclusion

As lionfish numbers continue to increase, physicians across multiple specialties and regions may see an increase in envenomation injuries. It is important that physicians are aware of how to recognize and treat lionfish stings, as prompt and comprehensive treatment provides benefit to the patient.

The lionfish (Pterois volitans) is a member of the Scorpaenidae family of venomous fish.^1-3 Lionfish are an invasive species originally from the Indian and Pacific oceans and the Red Sea that now are widely found throughout tropical and temperate oceans in both hemispheres. They are a popular aquarium fish and were inadvertently introduced in the Atlantic Ocean in South Florida during the late 1980s to early 1990s.^2,4 Since then, lionfish have spread into reef systems throughout the Atlantic Ocean, Caribbean Sea, and Gulf of Mexico in rapidly growing numbers, and they are now fo und all along the southeastern coast of the United States.⁵

Characteristics

Lionfish are brightly colored with red or maroon and white stripes, tentacles above the eyes and mouth, fan-shaped pectoral fins, and spines that deliver an especially painful venomous sting that often results in edema (Figure 1). They have 12 dorsal spines, 2 pelvic spines, and 3 anal spines.

Symptoms of Envenomation

As lionfish continue to spread to popular areas of the southeast Atlantic Ocean and Caribbean Sea, the chances of human contact with lionfish have increased. Lionfish stings are now the second most common marine envenomation injury after those caused by stingrays.⁴ Lionfish stings usually occur on the hands, fingers, or forearms during handling of the fish in ocean waters or in maintenance of aquariums. The mechanism of the venom apparatus is similar for all venomous fish. The spines have surrounding integumentary sheaths containing venom that rupture and inject venom when they penetrate the skin.⁶ The venom is a heat-labile neuromuscular toxin that causes edema (Figure 2), plasma extravasation, and thrombotic skin lesions.⁷

Wounds are classified into 3 categories: grade I consists of local erythema/ecchymosis, grade II involves vesicle or blister formation, and grade III denotes wounds that develop local necrosis.⁸ The sting causes immediate and severe throbbing pain, often described as excruciating or rated 10/10 on a basic pain scale, typically radiating up the affected limb. Puncture sites may bleed and often have associated redness and swelling. Pain may last up to 24 hours. Occasionally, foreign material may be left in the wound requiring removal. There also is a chance of secondary infection at the wound site, and severe envenomation can lead to local tissue necrosis.⁸ Systemic effects can occur in some cases, including nausea, vomiting, sweating, headache, dizziness, disorientation, palpitations, and even syncope.⁹ However, to our knowledge there are no documented cases of human death from a lionfish sting. Anaphylactic reactions are possible and require immediate treatment.⁶

A study conducted in the French West Indies evaluated 117 patients with lionfish envenomation and found that victims experienced severe pain and local edema (100%), paresthesia (90%), abdominal cramps (62%), extensive edema (53%), tachycardia (34%), skin rash (32%), gastrointestinal tract symptoms (28%), syncope (27%), transient weakness (24%), hypertension (21%), hypotension (18%), and hyperthermia (9%).⁹ Complications included local infection (18%) such as skin abscess (5%), skin necrosis (3%), and septic arthritis (2%). Twenty-two percent of patients were hospitalized and 8% required surgery. Local infectious complications were more frequent in those with multiple stings (19%). The study concluded that lionfish now represent a major health threat in the West Indies.⁹ As lionfish numbers have grown, health care providers are seeing increasing numbers of envenomation cases in areas of the coastal southeastern United States and Caribbean associated with considerable morbidity. Providers in nonendemic areas also may see envenomation injuries due to the lionfish popularity in home aquariums.⁹

Management

Individuals with lionfish stings should immerse the affected area in hot but not scalding water. Those with more serious injuries should seek medical attention. Home remedies that are generally contraindicated include application of topical papain or meat tenderizer.¹⁰ Data on ice packs are mixed, but because the toxin is heat labile, the most effective initial step in treatment is immersion of the affected area in water (temperature, 40°C to 45°C) for 30 to 90 minutes.⁶ The hot water inactivates the heat-labile toxin, leading to near-complete symptomatic relief in 80% of cases and moderate relief in an additional 14%. Immersion time more than 90 minutes considerably increases the risk for burns. Children should always be monitored to prevent burns. If a patient has received a nerve block for analgesia, the wound should not be immersed in hot water to avoid burns to the skin. The wound should be meticulously cleaned with saline irrigation, and radiography or ultrasonography should be performed as deemed necessary to look for any retained foreign bodies.⁸ Patients may require parenteral or oral analgesia as well as careful follow-up to ensure proper healing.⁹ Systemic symptoms require supportive care. Venomous fish wounds typically are small and superficial. Empiric antibiotic therapy is not advised for superficial wounds but may be required for clinically infected wounds.⁸ Tetanus prophylaxis should be given as appropriate to all affected patients. It has been noted that blister fluid contains high concentrations of lionfish venom, and when present, it increases the likelihood of converting the injury from a grade II to grade III wound with tissue necrosis; therefore, blisters should be drained or excised to decrease the chances of subsequent tissue necrosis.^11,12 If secondary infection such as cellulitis develops, antibiotics should be chosen to cover likely pathogens including common skin flora such as staphylococci and marine organisms such as Vibrio species. Wounds showing signs of infection should be cultured, with antibiotics adjusted according to sensitivities.⁵ Deeper wounds should be left open (unsutured) with a proper dressing to heal. Any wounds that involve vascular or joint structures require specialty management. Wounds involving joints may on occasion require surgical exploration and debridement.

Public Health Concerns

In an attempt to slow the growth of their population, human consumption of the fish has been encouraged. The lionfish toxin is inactivated by cooking, and the fish is considered a delicacy; however, a study in the Virgin Islands found that in areas with endemic ciguatera poisoning, 12% of lionfish carried amounts of the toxin above the level considered safe for consumption. This toxin is not inactivated by cooking or freezing and can lead to ciguatera fish poisoning for which there is no antidote and can be associated with prolonged neurotoxicity.¹³

Conclusion

As lionfish numbers continue to increase, physicians across multiple specialties and regions may see an increase in envenomation injuries. It is important that physicians are aware of how to recognize and treat lionfish stings, as prompt and comprehensive treatment provides benefit to the patient.

The lionfish (Pterois volitans) is a member of the Scorpaenidae family of venomous fish.^1-3 Lionfish are an invasive species originally from the Indian and Pacific oceans and the Red Sea that now are widely found throughout tropical and temperate oceans in both hemispheres. They are a popular aquarium fish and were inadvertently introduced in the Atlantic Ocean in South Florida during the late 1980s to early 1990s.^2,4 Since then, lionfish have spread into reef systems throughout the Atlantic Ocean, Caribbean Sea, and Gulf of Mexico in rapidly growing numbers, and they are now fo und all along the southeastern coast of the United States.⁵

Characteristics

Lionfish are brightly colored with red or maroon and white stripes, tentacles above the eyes and mouth, fan-shaped pectoral fins, and spines that deliver an especially painful venomous sting that often results in edema (Figure 1). They have 12 dorsal spines, 2 pelvic spines, and 3 anal spines.

Symptoms of Envenomation

As lionfish continue to spread to popular areas of the southeast Atlantic Ocean and Caribbean Sea, the chances of human contact with lionfish have increased. Lionfish stings are now the second most common marine envenomation injury after those caused by stingrays.⁴ Lionfish stings usually occur on the hands, fingers, or forearms during handling of the fish in ocean waters or in maintenance of aquariums. The mechanism of the venom apparatus is similar for all venomous fish. The spines have surrounding integumentary sheaths containing venom that rupture and inject venom when they penetrate the skin.⁶ The venom is a heat-labile neuromuscular toxin that causes edema (Figure 2), plasma extravasation, and thrombotic skin lesions.⁷

Wounds are classified into 3 categories: grade I consists of local erythema/ecchymosis, grade II involves vesicle or blister formation, and grade III denotes wounds that develop local necrosis.⁸ The sting causes immediate and severe throbbing pain, often described as excruciating or rated 10/10 on a basic pain scale, typically radiating up the affected limb. Puncture sites may bleed and often have associated redness and swelling. Pain may last up to 24 hours. Occasionally, foreign material may be left in the wound requiring removal. There also is a chance of secondary infection at the wound site, and severe envenomation can lead to local tissue necrosis.⁸ Systemic effects can occur in some cases, including nausea, vomiting, sweating, headache, dizziness, disorientation, palpitations, and even syncope.⁹ However, to our knowledge there are no documented cases of human death from a lionfish sting. Anaphylactic reactions are possible and require immediate treatment.⁶

A study conducted in the French West Indies evaluated 117 patients with lionfish envenomation and found that victims experienced severe pain and local edema (100%), paresthesia (90%), abdominal cramps (62%), extensive edema (53%), tachycardia (34%), skin rash (32%), gastrointestinal tract symptoms (28%), syncope (27%), transient weakness (24%), hypertension (21%), hypotension (18%), and hyperthermia (9%).⁹ Complications included local infection (18%) such as skin abscess (5%), skin necrosis (3%), and septic arthritis (2%). Twenty-two percent of patients were hospitalized and 8% required surgery. Local infectious complications were more frequent in those with multiple stings (19%). The study concluded that lionfish now represent a major health threat in the West Indies.⁹ As lionfish numbers have grown, health care providers are seeing increasing numbers of envenomation cases in areas of the coastal southeastern United States and Caribbean associated with considerable morbidity. Providers in nonendemic areas also may see envenomation injuries due to the lionfish popularity in home aquariums.⁹

Management

Individuals with lionfish stings should immerse the affected area in hot but not scalding water. Those with more serious injuries should seek medical attention. Home remedies that are generally contraindicated include application of topical papain or meat tenderizer.¹⁰ Data on ice packs are mixed, but because the toxin is heat labile, the most effective initial step in treatment is immersion of the affected area in water (temperature, 40°C to 45°C) for 30 to 90 minutes.⁶ The hot water inactivates the heat-labile toxin, leading to near-complete symptomatic relief in 80% of cases and moderate relief in an additional 14%. Immersion time more than 90 minutes considerably increases the risk for burns. Children should always be monitored to prevent burns. If a patient has received a nerve block for analgesia, the wound should not be immersed in hot water to avoid burns to the skin. The wound should be meticulously cleaned with saline irrigation, and radiography or ultrasonography should be performed as deemed necessary to look for any retained foreign bodies.⁸ Patients may require parenteral or oral analgesia as well as careful follow-up to ensure proper healing.⁹ Systemic symptoms require supportive care. Venomous fish wounds typically are small and superficial. Empiric antibiotic therapy is not advised for superficial wounds but may be required for clinically infected wounds.⁸ Tetanus prophylaxis should be given as appropriate to all affected patients. It has been noted that blister fluid contains high concentrations of lionfish venom, and when present, it increases the likelihood of converting the injury from a grade II to grade III wound with tissue necrosis; therefore, blisters should be drained or excised to decrease the chances of subsequent tissue necrosis.^11,12 If secondary infection such as cellulitis develops, antibiotics should be chosen to cover likely pathogens including common skin flora such as staphylococci and marine organisms such as Vibrio species. Wounds showing signs of infection should be cultured, with antibiotics adjusted according to sensitivities.⁵ Deeper wounds should be left open (unsutured) with a proper dressing to heal. Any wounds that involve vascular or joint structures require specialty management. Wounds involving joints may on occasion require surgical exploration and debridement.

Public Health Concerns

In an attempt to slow the growth of their population, human consumption of the fish has been encouraged. The lionfish toxin is inactivated by cooking, and the fish is considered a delicacy; however, a study in the Virgin Islands found that in areas with endemic ciguatera poisoning, 12% of lionfish carried amounts of the toxin above the level considered safe for consumption. This toxin is not inactivated by cooking or freezing and can lead to ciguatera fish poisoning for which there is no antidote and can be associated with prolonged neurotoxicity.¹³

Conclusion

As lionfish numbers continue to increase, physicians across multiple specialties and regions may see an increase in envenomation injuries. It is important that physicians are aware of how to recognize and treat lionfish stings, as prompt and comprehensive treatment provides benefit to the patient.

Clothes moths are common pests found inside buildings such as homes, stores, and museums. The most common species of importance include the webbing clothes moth (Tineola bisselliella)(Figure) and the casemaking clothes moth (Tineola pellionella). Both species target textiles such as wool, rugs, feathers, felts, hair, furs, and even grains.^1,2 They avoid synthetics and plant materials such as cottons.¹

Characteristics

Adult clothes moths extend 7 to 8 mm and are a golden (T bisselliella) to brown (T pellionella) color with fringed wings and a tuft on their heads.^1,3 Adults do not eat; females die within a few days of laying eggs, while males live approximately 1 month. Once laid, eggs hatch within 4 to 10 days.^1,3 The larvae (caterpillars) incur damage to clothes and other household goods. Fully mature larvae are 12- to 13-mm long, and the Tineola species have white- to cream-colored bodies with brown heads. The webbing clothes moth larva lacks ocelli (eyes), while the casemaking moth larva has a singular ocellus.¹

Transmission

An infestation is evidenced by woolen items that have furrows or holes in them. Pheromone traps also can expose an active infestation.³ The webbing moth larvae can be found beneath a self-spun silken mat on the food source that offers the insect protection and camouflage while it eats; the mat collects frass (feces) and clothes particles.^1,3,4 The casemaking moth larvae drag around a portable silken bag that takes on the color of the fabric being eaten and serves as a refuge when disturbed.^1,3,4 Both adult and larval stages prefer low light conditions. The total time of development from caterpillar to adult varies depending on the temperature and humidity of the environment, but most clothes moths complete their life cycle within 1 to 3 months.¹

Management of an Infestation

Multiple infestation treatment options exist should a patient present with a clothes moth infestation. Infested clothing articles or small blankets and rugs can be dry-cleaned or laundered. Any items not in use should be laundered before being sealed in airtight storage containers. Mothball vapor at appropriate concentrations is lethal to the moths, and when possible, clothing should be stored with mothballs or flakes at the concentration recommended by the manufacturer.⁴ Individuals should avoid application of household insecticides to clothing or bedding, which may be poisonous to people.^1,4 Freezing, heating, and dry ice fumigation techniques also can be used to treat infested products.³ Cedarwood usually is insufficient to deter an infestation, as the oil vapor rarely reaches an effective concentration to repel or harm the insects.^3,4 Strict housekeeping with attention to vacuuming carpets, baseboards, closets, and laundering all linens and furniture covers can further reduce an infestation.⁴ Clothes items can be set in the sunlight and brushed to help loosen the pests, as they dislike direct light and may fall from the garments.³ Dust insecticides also can be used per the manufacturer label to treat crevices and baseboards in an active area of infestation that may otherwise be difficult to clean.³ If an extensive infestation exists or larger items are infested, then a professional pest control agency should be employed for proper eradication.

Conclusion

Understanding the life cycle and basic biology of clothes moths and other common household pests will help the clinician identify an infestation and counsel patients if an insect is a true ectoparasite. Clothes moth larvae are not parasites but can be found on clothing and can be confused with myiasis or true parasites.

Clothes moths are common pests found inside buildings such as homes, stores, and museums. The most common species of importance include the webbing clothes moth (Tineola bisselliella)(Figure) and the casemaking clothes moth (Tineola pellionella). Both species target textiles such as wool, rugs, feathers, felts, hair, furs, and even grains.^1,2 They avoid synthetics and plant materials such as cottons.¹

Characteristics

Adult clothes moths extend 7 to 8 mm and are a golden (T bisselliella) to brown (T pellionella) color with fringed wings and a tuft on their heads.^1,3 Adults do not eat; females die within a few days of laying eggs, while males live approximately 1 month. Once laid, eggs hatch within 4 to 10 days.^1,3 The larvae (caterpillars) incur damage to clothes and other household goods. Fully mature larvae are 12- to 13-mm long, and the Tineola species have white- to cream-colored bodies with brown heads. The webbing clothes moth larva lacks ocelli (eyes), while the casemaking moth larva has a singular ocellus.¹

Transmission

An infestation is evidenced by woolen items that have furrows or holes in them. Pheromone traps also can expose an active infestation.³ The webbing moth larvae can be found beneath a self-spun silken mat on the food source that offers the insect protection and camouflage while it eats; the mat collects frass (feces) and clothes particles.^1,3,4 The casemaking moth larvae drag around a portable silken bag that takes on the color of the fabric being eaten and serves as a refuge when disturbed.^1,3,4 Both adult and larval stages prefer low light conditions. The total time of development from caterpillar to adult varies depending on the temperature and humidity of the environment, but most clothes moths complete their life cycle within 1 to 3 months.¹

Management of an Infestation

Multiple infestation treatment options exist should a patient present with a clothes moth infestation. Infested clothing articles or small blankets and rugs can be dry-cleaned or laundered. Any items not in use should be laundered before being sealed in airtight storage containers. Mothball vapor at appropriate concentrations is lethal to the moths, and when possible, clothing should be stored with mothballs or flakes at the concentration recommended by the manufacturer.⁴ Individuals should avoid application of household insecticides to clothing or bedding, which may be poisonous to people.^1,4 Freezing, heating, and dry ice fumigation techniques also can be used to treat infested products.³ Cedarwood usually is insufficient to deter an infestation, as the oil vapor rarely reaches an effective concentration to repel or harm the insects.^3,4 Strict housekeeping with attention to vacuuming carpets, baseboards, closets, and laundering all linens and furniture covers can further reduce an infestation.⁴ Clothes items can be set in the sunlight and brushed to help loosen the pests, as they dislike direct light and may fall from the garments.³ Dust insecticides also can be used per the manufacturer label to treat crevices and baseboards in an active area of infestation that may otherwise be difficult to clean.³ If an extensive infestation exists or larger items are infested, then a professional pest control agency should be employed for proper eradication.

Conclusion

Understanding the life cycle and basic biology of clothes moths and other common household pests will help the clinician identify an infestation and counsel patients if an insect is a true ectoparasite. Clothes moth larvae are not parasites but can be found on clothing and can be confused with myiasis or true parasites.

Clothes moths are common pests found inside buildings such as homes, stores, and museums. The most common species of importance include the webbing clothes moth (Tineola bisselliella)(Figure) and the casemaking clothes moth (Tineola pellionella). Both species target textiles such as wool, rugs, feathers, felts, hair, furs, and even grains.^1,2 They avoid synthetics and plant materials such as cottons.¹

Characteristics

Adult clothes moths extend 7 to 8 mm and are a golden (T bisselliella) to brown (T pellionella) color with fringed wings and a tuft on their heads.^1,3 Adults do not eat; females die within a few days of laying eggs, while males live approximately 1 month. Once laid, eggs hatch within 4 to 10 days.^1,3 The larvae (caterpillars) incur damage to clothes and other household goods. Fully mature larvae are 12- to 13-mm long, and the Tineola species have white- to cream-colored bodies with brown heads. The webbing clothes moth larva lacks ocelli (eyes), while the casemaking moth larva has a singular ocellus.¹

Transmission

An infestation is evidenced by woolen items that have furrows or holes in them. Pheromone traps also can expose an active infestation.³ The webbing moth larvae can be found beneath a self-spun silken mat on the food source that offers the insect protection and camouflage while it eats; the mat collects frass (feces) and clothes particles.^1,3,4 The casemaking moth larvae drag around a portable silken bag that takes on the color of the fabric being eaten and serves as a refuge when disturbed.^1,3,4 Both adult and larval stages prefer low light conditions. The total time of development from caterpillar to adult varies depending on the temperature and humidity of the environment, but most clothes moths complete their life cycle within 1 to 3 months.¹

Management of an Infestation

Multiple infestation treatment options exist should a patient present with a clothes moth infestation. Infested clothing articles or small blankets and rugs can be dry-cleaned or laundered. Any items not in use should be laundered before being sealed in airtight storage containers. Mothball vapor at appropriate concentrations is lethal to the moths, and when possible, clothing should be stored with mothballs or flakes at the concentration recommended by the manufacturer.⁴ Individuals should avoid application of household insecticides to clothing or bedding, which may be poisonous to people.^1,4 Freezing, heating, and dry ice fumigation techniques also can be used to treat infested products.³ Cedarwood usually is insufficient to deter an infestation, as the oil vapor rarely reaches an effective concentration to repel or harm the insects.^3,4 Strict housekeeping with attention to vacuuming carpets, baseboards, closets, and laundering all linens and furniture covers can further reduce an infestation.⁴ Clothes items can be set in the sunlight and brushed to help loosen the pests, as they dislike direct light and may fall from the garments.³ Dust insecticides also can be used per the manufacturer label to treat crevices and baseboards in an active area of infestation that may otherwise be difficult to clean.³ If an extensive infestation exists or larger items are infested, then a professional pest control agency should be employed for proper eradication.

Conclusion

Understanding the life cycle and basic biology of clothes moths and other common household pests will help the clinician identify an infestation and counsel patients if an insect is a true ectoparasite. Clothes moth larvae are not parasites but can be found on clothing and can be confused with myiasis or true parasites.