Environmental Dermatology

The order Lepidoptera (phylum Arthropoda, class Hexapoda) is comprised of moths and butterflies.¹ Lepidopterism refers to a range of adverse medical conditions resulting from contact with these insects, typically during the caterpillar (larval) stage. It involves multiple pathologic mechanisms, including direct toxicity of venom and mechanical irritant effects.² Erucism has been defined as any reaction caused by contact with caterpillars or any reaction limited to the skin caused by contact with caterpillars, butterflies, or moths. Lepidopterism can mean any reaction to caterpillars or moths, referring only to reactions from contact with scales or hairs from adult moths or butterflies, or referring only to cases with systemic signs and symptoms (eg, rhinoconjunctival or asthmatic symptoms, angioedema and anaphylaxis, hemorrhagic diathesis) with or without cutaneous findings, resulting from contact with any lepidopteran source.¹ Strictly speaking, erucism should refer to any reaction from caterpillars and lepidopterism to reactions from moths or butterflies. Because reactions to both larval and adult lepidoptera can cause a variety of either cutaneous and/or systemic symptoms, classifying reactions into erucism or lepidopterism is only of academic interest.¹

We report a documented case of lepidopterism in a patient with acute cutaneous lesions following exposure to an adult-stage black butterfly (Hylesia nigricans).

Case Report

A 21-year-old oil well worker presented with pruritic skin lesions on the right arm and flank of 3 hours’ duration. He reported that a black butterfly had perched on his arm while he was working and left a considerable number of small yellowish hairs on the skin, after which an intense pruritus and skin lesions began to develop. He denied other associated symptoms. Physical examination revealed numerous 1- to 2-mm, nonconfluent, erythematous and edematous papules on the right forearm, arm (Figure 1A), and flank. Some abrasions of the skin due to scratching and crusting were noted (Figure 1B). A skin biopsy from the right arm showed a superficial perivascular dermatitis with a mixed infiltrate of polymorphonuclear predominance with eosinophils (Figure 2A). Importantly, a structure resembling an urticating spicule was identified in the stratum corneum (Figure 2B); spicules are located on the abdomen of arthropods and are associated with an inflammatory response in human skin.

Based on the patient’s history of butterfly exposure, clinical presentation of the lesions, and histopathologic findings demonstrating the presence of the spicules, the diagnosis of lepidopterism was confirmed. The patient was treated with oral antihistamines and topical steroids for 1 week with complete resolution of the lesions.

Comment

Epidemiology of Envenomation
Although many tropical insects carry infectious diseases, cutaneous injury can occur by other mechanisms, such as dermatitis caused by contact with the skin (erucism or lepidopterism). Caterpillar envenomation is common, but this phenomenon rarely has been studied due to few reported cases, which hinders a complete understanding of the problem.³

The order Lepidoptera comprises 2 suborders: Rhopalocera, with adult specimens that fly during the daytime (butterflies), and Heterocera, which are largely nocturnal (moths). The stages of development include egg, larva (caterpillar), pupa (chrysalis), and adult (imago), constituting a holometabolic life cycle.⁴ Adult butterflies and moths represent the reproductive stage of lepidoptera.

The pathology of lepidopterism is attributed to contact with fluids such as hemolymph and secretions from the spicules, with histamine being identified as the main causative component.³ During the reproductive stage, female insects approach light sources and release clouds of bristles from their abdomens that can penetrate human skin and cause an irritating dermatitis.⁵ Lepidopterism can occur following contact with bristles from insects of the Hylesia genus (Saturniidae family), such as in our patient.^3,6 Epidemic outbreaks have been reported in several countries, mainly Argentina, Brazil, and Venezuela.⁵ The patient was located in Colombia, a country without any reported cases of lepidopterism from the black butterfly (H nigricans). Cutaneous reactions to lepidoptera insects come in many forms, most commonly presenting as a mild stinging reaction with a papular eruption, pruritic urticarial papules and plaques, or scaly erythematous papules and plaques in exposed areas.⁷

Histopathologic Findings
The histology of lepidoptera exposure is nonspecific, typically demonstrating epidermal edema, superficial perivascular lymphocytic infiltrate, and eosinophils. Epidermal necrosis and vasculitis rarely are seen. Embedded spines from Hylesia insects have been described.⁷ The histopathologic examination generally reveals a foreign body reaction in addition to granulomas.³

Therapy
The use of oral antihistamines is indicated for the control of pruritus, and topical treatment with cold compresses, baths, and corticosteroid creams is recommended.^3,8,9

Conclusion

We report the case of a patient with lepidopterism, a rare entity confirmed histologically with documentation of a spicule in the stratum corneum in the patient’s biopsy. Changes due to urbanization and industrialization have a closer relationship with various animal species that are pathogenic to humans; therefore, we encourage dermatologists to be aware of these diseases.

The order Lepidoptera (phylum Arthropoda, class Hexapoda) is comprised of moths and butterflies.¹ Lepidopterism refers to a range of adverse medical conditions resulting from contact with these insects, typically during the caterpillar (larval) stage. It involves multiple pathologic mechanisms, including direct toxicity of venom and mechanical irritant effects.² Erucism has been defined as any reaction caused by contact with caterpillars or any reaction limited to the skin caused by contact with caterpillars, butterflies, or moths. Lepidopterism can mean any reaction to caterpillars or moths, referring only to reactions from contact with scales or hairs from adult moths or butterflies, or referring only to cases with systemic signs and symptoms (eg, rhinoconjunctival or asthmatic symptoms, angioedema and anaphylaxis, hemorrhagic diathesis) with or without cutaneous findings, resulting from contact with any lepidopteran source.¹ Strictly speaking, erucism should refer to any reaction from caterpillars and lepidopterism to reactions from moths or butterflies. Because reactions to both larval and adult lepidoptera can cause a variety of either cutaneous and/or systemic symptoms, classifying reactions into erucism or lepidopterism is only of academic interest.¹

We report a documented case of lepidopterism in a patient with acute cutaneous lesions following exposure to an adult-stage black butterfly (Hylesia nigricans).

Case Report

A 21-year-old oil well worker presented with pruritic skin lesions on the right arm and flank of 3 hours’ duration. He reported that a black butterfly had perched on his arm while he was working and left a considerable number of small yellowish hairs on the skin, after which an intense pruritus and skin lesions began to develop. He denied other associated symptoms. Physical examination revealed numerous 1- to 2-mm, nonconfluent, erythematous and edematous papules on the right forearm, arm (Figure 1A), and flank. Some abrasions of the skin due to scratching and crusting were noted (Figure 1B). A skin biopsy from the right arm showed a superficial perivascular dermatitis with a mixed infiltrate of polymorphonuclear predominance with eosinophils (Figure 2A). Importantly, a structure resembling an urticating spicule was identified in the stratum corneum (Figure 2B); spicules are located on the abdomen of arthropods and are associated with an inflammatory response in human skin.

Based on the patient’s history of butterfly exposure, clinical presentation of the lesions, and histopathologic findings demonstrating the presence of the spicules, the diagnosis of lepidopterism was confirmed. The patient was treated with oral antihistamines and topical steroids for 1 week with complete resolution of the lesions.

Comment

Epidemiology of Envenomation
Although many tropical insects carry infectious diseases, cutaneous injury can occur by other mechanisms, such as dermatitis caused by contact with the skin (erucism or lepidopterism). Caterpillar envenomation is common, but this phenomenon rarely has been studied due to few reported cases, which hinders a complete understanding of the problem.³

The order Lepidoptera comprises 2 suborders: Rhopalocera, with adult specimens that fly during the daytime (butterflies), and Heterocera, which are largely nocturnal (moths). The stages of development include egg, larva (caterpillar), pupa (chrysalis), and adult (imago), constituting a holometabolic life cycle.⁴ Adult butterflies and moths represent the reproductive stage of lepidoptera.

The pathology of lepidopterism is attributed to contact with fluids such as hemolymph and secretions from the spicules, with histamine being identified as the main causative component.³ During the reproductive stage, female insects approach light sources and release clouds of bristles from their abdomens that can penetrate human skin and cause an irritating dermatitis.⁵ Lepidopterism can occur following contact with bristles from insects of the Hylesia genus (Saturniidae family), such as in our patient.^3,6 Epidemic outbreaks have been reported in several countries, mainly Argentina, Brazil, and Venezuela.⁵ The patient was located in Colombia, a country without any reported cases of lepidopterism from the black butterfly (H nigricans). Cutaneous reactions to lepidoptera insects come in many forms, most commonly presenting as a mild stinging reaction with a papular eruption, pruritic urticarial papules and plaques, or scaly erythematous papules and plaques in exposed areas.⁷

Histopathologic Findings
The histology of lepidoptera exposure is nonspecific, typically demonstrating epidermal edema, superficial perivascular lymphocytic infiltrate, and eosinophils. Epidermal necrosis and vasculitis rarely are seen. Embedded spines from Hylesia insects have been described.⁷ The histopathologic examination generally reveals a foreign body reaction in addition to granulomas.³

Therapy
The use of oral antihistamines is indicated for the control of pruritus, and topical treatment with cold compresses, baths, and corticosteroid creams is recommended.^3,8,9

Conclusion

We report the case of a patient with lepidopterism, a rare entity confirmed histologically with documentation of a spicule in the stratum corneum in the patient’s biopsy. Changes due to urbanization and industrialization have a closer relationship with various animal species that are pathogenic to humans; therefore, we encourage dermatologists to be aware of these diseases.

The order Lepidoptera (phylum Arthropoda, class Hexapoda) is comprised of moths and butterflies.¹ Lepidopterism refers to a range of adverse medical conditions resulting from contact with these insects, typically during the caterpillar (larval) stage. It involves multiple pathologic mechanisms, including direct toxicity of venom and mechanical irritant effects.² Erucism has been defined as any reaction caused by contact with caterpillars or any reaction limited to the skin caused by contact with caterpillars, butterflies, or moths. Lepidopterism can mean any reaction to caterpillars or moths, referring only to reactions from contact with scales or hairs from adult moths or butterflies, or referring only to cases with systemic signs and symptoms (eg, rhinoconjunctival or asthmatic symptoms, angioedema and anaphylaxis, hemorrhagic diathesis) with or without cutaneous findings, resulting from contact with any lepidopteran source.¹ Strictly speaking, erucism should refer to any reaction from caterpillars and lepidopterism to reactions from moths or butterflies. Because reactions to both larval and adult lepidoptera can cause a variety of either cutaneous and/or systemic symptoms, classifying reactions into erucism or lepidopterism is only of academic interest.¹

We report a documented case of lepidopterism in a patient with acute cutaneous lesions following exposure to an adult-stage black butterfly (Hylesia nigricans).

Case Report

A 21-year-old oil well worker presented with pruritic skin lesions on the right arm and flank of 3 hours’ duration. He reported that a black butterfly had perched on his arm while he was working and left a considerable number of small yellowish hairs on the skin, after which an intense pruritus and skin lesions began to develop. He denied other associated symptoms. Physical examination revealed numerous 1- to 2-mm, nonconfluent, erythematous and edematous papules on the right forearm, arm (Figure 1A), and flank. Some abrasions of the skin due to scratching and crusting were noted (Figure 1B). A skin biopsy from the right arm showed a superficial perivascular dermatitis with a mixed infiltrate of polymorphonuclear predominance with eosinophils (Figure 2A). Importantly, a structure resembling an urticating spicule was identified in the stratum corneum (Figure 2B); spicules are located on the abdomen of arthropods and are associated with an inflammatory response in human skin.

Based on the patient’s history of butterfly exposure, clinical presentation of the lesions, and histopathologic findings demonstrating the presence of the spicules, the diagnosis of lepidopterism was confirmed. The patient was treated with oral antihistamines and topical steroids for 1 week with complete resolution of the lesions.

Comment

Epidemiology of Envenomation
Although many tropical insects carry infectious diseases, cutaneous injury can occur by other mechanisms, such as dermatitis caused by contact with the skin (erucism or lepidopterism). Caterpillar envenomation is common, but this phenomenon rarely has been studied due to few reported cases, which hinders a complete understanding of the problem.³

The order Lepidoptera comprises 2 suborders: Rhopalocera, with adult specimens that fly during the daytime (butterflies), and Heterocera, which are largely nocturnal (moths). The stages of development include egg, larva (caterpillar), pupa (chrysalis), and adult (imago), constituting a holometabolic life cycle.⁴ Adult butterflies and moths represent the reproductive stage of lepidoptera.

The pathology of lepidopterism is attributed to contact with fluids such as hemolymph and secretions from the spicules, with histamine being identified as the main causative component.³ During the reproductive stage, female insects approach light sources and release clouds of bristles from their abdomens that can penetrate human skin and cause an irritating dermatitis.⁵ Lepidopterism can occur following contact with bristles from insects of the Hylesia genus (Saturniidae family), such as in our patient.^3,6 Epidemic outbreaks have been reported in several countries, mainly Argentina, Brazil, and Venezuela.⁵ The patient was located in Colombia, a country without any reported cases of lepidopterism from the black butterfly (H nigricans). Cutaneous reactions to lepidoptera insects come in many forms, most commonly presenting as a mild stinging reaction with a papular eruption, pruritic urticarial papules and plaques, or scaly erythematous papules and plaques in exposed areas.⁷

Histopathologic Findings
The histology of lepidoptera exposure is nonspecific, typically demonstrating epidermal edema, superficial perivascular lymphocytic infiltrate, and eosinophils. Epidermal necrosis and vasculitis rarely are seen. Embedded spines from Hylesia insects have been described.⁷ The histopathologic examination generally reveals a foreign body reaction in addition to granulomas.³

Therapy
The use of oral antihistamines is indicated for the control of pruritus, and topical treatment with cold compresses, baths, and corticosteroid creams is recommended.^3,8,9

Conclusion

We report the case of a patient with lepidopterism, a rare entity confirmed histologically with documentation of a spicule in the stratum corneum in the patient’s biopsy. Changes due to urbanization and industrialization have a closer relationship with various animal species that are pathogenic to humans; therefore, we encourage dermatologists to be aware of these diseases.

Sponges are among the oldest animals on earth, appearing more than 640 million years ago before the Cambrian explosion, a period when most major animal phyla appeared in the fossil records.¹ More than 10,000 species of sponges have been identified worldwide and are distributed from polar to tropical regions in both marine (Figure 1) and freshwater (Figure 2) environments. They inhabit both shallow waters as well as depths of more than 2800 m, with shallower sponges tending to be more vibrantly colored than their deeper counterparts. The wide-ranging habitats of sponges have led to size variations from as small as 0.05 mm to more than 3 m in height.² Their taxonomic phylum, Porifera (meaning pore bearers), is derived from the millions of pores lining the surface of the sponge that are used to filter planktonic organisms.³ Flagellated epithelioid cells called choanocytes line the internal chambers of sponges, creating a water current that promotes filter feeding as well as nutrient absorption across their microvilli.⁴ The body walls of many sponges consist of a collagenous skeleton made up of spongin and spicules of silicon dioxide (silica) or calcium carbonate embedded in the spongin connective tissue matrix.⁵ Bath sponges lack silica spicules.

Sponges have been used in medicine for centuries. The first use in Western culture was recorded in 405 bce in The Frogs, a comedy by Aristophanes in which a sponge was placed on a character’s heart following a syncopal episode. Additionally, in many Hippocratic writings, the use of sponges is outlined in the treatment of a variety of ailments. Similarly, the ancient Chinese and Greeks used burnt sponge and seaweed as a source of iodine to treat goiters.^6,7 Modern research focuses on the use of sponge metabolites for their antineoplastic, antimicrobial, and anti-inflammatory effects.⁸ Identification of spongouridine and spongothymidine from the sponge Tectitethya crypta led to the development of cytarabine and gemcitabine⁸ as well as the discovery of the antiviral agent vidarabine.⁹ The monoclonal antibody assay for the detection of shellfish poisoning was prepared using the sponge Halichondria okadai.¹⁰

Mechanisms and Symptoms of Injury

Bathing sponges (silk sponges) derived from Spongia officinalis are harmless. Other sponges can exert their damaging effects through a variety of mechanisms that lead to dermatologic manifestations (eTable). Some species of sponges produce and secrete toxic metabolites (eg, crinotoxins) onto the body surface or into the surrounding water. They also are capable of synthesizing a mucous slime that can be irritating to human skin. Direct trauma also can be caused by fragments of the silica or calcium carbonate sponge skeleton penetrating the skin. Stinging members of the phylum Cnidaria can colonize the sponge, leading to injury when a human handles the sponge.^25-27

Sponge dermatitis can be divided into 2 major categories: an initial pruritic dermatitis (Figure 3) that occurs within 20 minutes to a few hours after contact and a delayed irritant dermatitis caused by penetration of the spicules and chemical agents into skin.²⁸ Importantly, different species can lead to varying manifestations.

The initial pruritic dermatitis is characterized by itching and burning that progresses to local edema, vesiculation, joint swelling, and stiffness. Because most contact with sponges occurs with handling, joint immobility may ensue within 24 hours of the encounter. Rarely, larger areas of the skin are affected, and fever, chills, malaise, dizziness, nausea, purulent bullae, muscle cramps, and formication may occur.²⁸ Anaphylactic reactions have been described in a small subset of patients. There have even been reports of delayed (ie, 1–2 weeks following exposure) erythema multiforme, livedo reticularis, purpura, and dyshidrotic eczema.^16,20,29 The irritant dermatitis caused by spicule trauma is due to a foreign body reaction that can be exacerbated by toxins entering the skin. In severe cases, desquamation, recurrent eczema, and arthralgia can occur.³⁰ In general, more mild cases should self-resolve within 3 to 7 days. Dermatologic conditions also can be caused by organisms that inhabit sponges and as a result produce a dermatitis when the sponge is handled, including sponge divers disease (maladie des plongeurs), a necrotic dermatitis caused by stinging Cnidaria species.³¹ Dogger Bank itch, first described as a dermatitis caused by sensitization to (2-hydroxyethyl) dimethylsulfoxonium chloride, initially was isolated from the sea chervil (a type of Bryozoan); however, that same chemical also was later found in sponges, producing the same dermatitis after handling the sponge.³² Freshwater sponges also have been reported to be injurious and exist worldwide. In contrast to marine sponges, lesions from freshwater sponges are disseminated pruritic erythematous papules with ulcerations, crusts, and secondary infections.²² The disseminated nature of the dermatitis caused by freshwater sponges is due to contact with the spicules of dead sponges that are dispersed throughout the water rather than from direct handling. Sponge dermatitis occurs mostly in sponge collectors, divers, trawlers, and biology students and has been reported extensively in the United States, Caribbean Islands, Australia, New Zealand, and Brazil.^18,27,33,34

Management

Treatment should consist of an initial decontamination; the skin should be dried, and adhesive tape or rubber cement should be utilized to remove any spicules embedded in the skin. Diluted vinegar soaks should be initiated for 10 to 30 minutes on the affected area(s) 3 or 4 times daily.¹⁹ The initial decontamination should occur immediately, as delay may lead to persistent purulent bullae that may take months to heal. Topical steroids may be used following the initial decontamination to help relieve inflammation. Antihistamines and nonsteroidal anti-inflammatory drugs may be used to alleviate pruritus and pain, respectively. Severe cases may require systemic glucocorticoids. Additionally, immunization status against tetanus toxoid should be assessed.³⁵ In the event of an anaphylactic reaction, it is important to maintain a patent airway and normalized blood pressure through the use of intramuscular epinephrine.³⁶ Frequent follow-up is warranted, as serious secondary infections can develop.³⁷ Patients also should be counseled on the potential for delayed dermatologic reactions, including erythema multiforme. Contact between humans and coastal environments has been increasing in the last few decades; therefore, an increase in contact with sponges is to be expected.²²

Sponges are among the oldest animals on earth, appearing more than 640 million years ago before the Cambrian explosion, a period when most major animal phyla appeared in the fossil records.¹ More than 10,000 species of sponges have been identified worldwide and are distributed from polar to tropical regions in both marine (Figure 1) and freshwater (Figure 2) environments. They inhabit both shallow waters as well as depths of more than 2800 m, with shallower sponges tending to be more vibrantly colored than their deeper counterparts. The wide-ranging habitats of sponges have led to size variations from as small as 0.05 mm to more than 3 m in height.² Their taxonomic phylum, Porifera (meaning pore bearers), is derived from the millions of pores lining the surface of the sponge that are used to filter planktonic organisms.³ Flagellated epithelioid cells called choanocytes line the internal chambers of sponges, creating a water current that promotes filter feeding as well as nutrient absorption across their microvilli.⁴ The body walls of many sponges consist of a collagenous skeleton made up of spongin and spicules of silicon dioxide (silica) or calcium carbonate embedded in the spongin connective tissue matrix.⁵ Bath sponges lack silica spicules.

Sponges have been used in medicine for centuries. The first use in Western culture was recorded in 405 bce in The Frogs, a comedy by Aristophanes in which a sponge was placed on a character’s heart following a syncopal episode. Additionally, in many Hippocratic writings, the use of sponges is outlined in the treatment of a variety of ailments. Similarly, the ancient Chinese and Greeks used burnt sponge and seaweed as a source of iodine to treat goiters.^6,7 Modern research focuses on the use of sponge metabolites for their antineoplastic, antimicrobial, and anti-inflammatory effects.⁸ Identification of spongouridine and spongothymidine from the sponge Tectitethya crypta led to the development of cytarabine and gemcitabine⁸ as well as the discovery of the antiviral agent vidarabine.⁹ The monoclonal antibody assay for the detection of shellfish poisoning was prepared using the sponge Halichondria okadai.¹⁰

Mechanisms and Symptoms of Injury

Bathing sponges (silk sponges) derived from Spongia officinalis are harmless. Other sponges can exert their damaging effects through a variety of mechanisms that lead to dermatologic manifestations (eTable). Some species of sponges produce and secrete toxic metabolites (eg, crinotoxins) onto the body surface or into the surrounding water. They also are capable of synthesizing a mucous slime that can be irritating to human skin. Direct trauma also can be caused by fragments of the silica or calcium carbonate sponge skeleton penetrating the skin. Stinging members of the phylum Cnidaria can colonize the sponge, leading to injury when a human handles the sponge.^25-27

Sponge dermatitis can be divided into 2 major categories: an initial pruritic dermatitis (Figure 3) that occurs within 20 minutes to a few hours after contact and a delayed irritant dermatitis caused by penetration of the spicules and chemical agents into skin.²⁸ Importantly, different species can lead to varying manifestations.

The initial pruritic dermatitis is characterized by itching and burning that progresses to local edema, vesiculation, joint swelling, and stiffness. Because most contact with sponges occurs with handling, joint immobility may ensue within 24 hours of the encounter. Rarely, larger areas of the skin are affected, and fever, chills, malaise, dizziness, nausea, purulent bullae, muscle cramps, and formication may occur.²⁸ Anaphylactic reactions have been described in a small subset of patients. There have even been reports of delayed (ie, 1–2 weeks following exposure) erythema multiforme, livedo reticularis, purpura, and dyshidrotic eczema.^16,20,29 The irritant dermatitis caused by spicule trauma is due to a foreign body reaction that can be exacerbated by toxins entering the skin. In severe cases, desquamation, recurrent eczema, and arthralgia can occur.³⁰ In general, more mild cases should self-resolve within 3 to 7 days. Dermatologic conditions also can be caused by organisms that inhabit sponges and as a result produce a dermatitis when the sponge is handled, including sponge divers disease (maladie des plongeurs), a necrotic dermatitis caused by stinging Cnidaria species.³¹ Dogger Bank itch, first described as a dermatitis caused by sensitization to (2-hydroxyethyl) dimethylsulfoxonium chloride, initially was isolated from the sea chervil (a type of Bryozoan); however, that same chemical also was later found in sponges, producing the same dermatitis after handling the sponge.³² Freshwater sponges also have been reported to be injurious and exist worldwide. In contrast to marine sponges, lesions from freshwater sponges are disseminated pruritic erythematous papules with ulcerations, crusts, and secondary infections.²² The disseminated nature of the dermatitis caused by freshwater sponges is due to contact with the spicules of dead sponges that are dispersed throughout the water rather than from direct handling. Sponge dermatitis occurs mostly in sponge collectors, divers, trawlers, and biology students and has been reported extensively in the United States, Caribbean Islands, Australia, New Zealand, and Brazil.^18,27,33,34

Management

Treatment should consist of an initial decontamination; the skin should be dried, and adhesive tape or rubber cement should be utilized to remove any spicules embedded in the skin. Diluted vinegar soaks should be initiated for 10 to 30 minutes on the affected area(s) 3 or 4 times daily.¹⁹ The initial decontamination should occur immediately, as delay may lead to persistent purulent bullae that may take months to heal. Topical steroids may be used following the initial decontamination to help relieve inflammation. Antihistamines and nonsteroidal anti-inflammatory drugs may be used to alleviate pruritus and pain, respectively. Severe cases may require systemic glucocorticoids. Additionally, immunization status against tetanus toxoid should be assessed.³⁵ In the event of an anaphylactic reaction, it is important to maintain a patent airway and normalized blood pressure through the use of intramuscular epinephrine.³⁶ Frequent follow-up is warranted, as serious secondary infections can develop.³⁷ Patients also should be counseled on the potential for delayed dermatologic reactions, including erythema multiforme. Contact between humans and coastal environments has been increasing in the last few decades; therefore, an increase in contact with sponges is to be expected.²²

Sponges are among the oldest animals on earth, appearing more than 640 million years ago before the Cambrian explosion, a period when most major animal phyla appeared in the fossil records.¹ More than 10,000 species of sponges have been identified worldwide and are distributed from polar to tropical regions in both marine (Figure 1) and freshwater (Figure 2) environments. They inhabit both shallow waters as well as depths of more than 2800 m, with shallower sponges tending to be more vibrantly colored than their deeper counterparts. The wide-ranging habitats of sponges have led to size variations from as small as 0.05 mm to more than 3 m in height.² Their taxonomic phylum, Porifera (meaning pore bearers), is derived from the millions of pores lining the surface of the sponge that are used to filter planktonic organisms.³ Flagellated epithelioid cells called choanocytes line the internal chambers of sponges, creating a water current that promotes filter feeding as well as nutrient absorption across their microvilli.⁴ The body walls of many sponges consist of a collagenous skeleton made up of spongin and spicules of silicon dioxide (silica) or calcium carbonate embedded in the spongin connective tissue matrix.⁵ Bath sponges lack silica spicules.

Sponges have been used in medicine for centuries. The first use in Western culture was recorded in 405 bce in The Frogs, a comedy by Aristophanes in which a sponge was placed on a character’s heart following a syncopal episode. Additionally, in many Hippocratic writings, the use of sponges is outlined in the treatment of a variety of ailments. Similarly, the ancient Chinese and Greeks used burnt sponge and seaweed as a source of iodine to treat goiters.^6,7 Modern research focuses on the use of sponge metabolites for their antineoplastic, antimicrobial, and anti-inflammatory effects.⁸ Identification of spongouridine and spongothymidine from the sponge Tectitethya crypta led to the development of cytarabine and gemcitabine⁸ as well as the discovery of the antiviral agent vidarabine.⁹ The monoclonal antibody assay for the detection of shellfish poisoning was prepared using the sponge Halichondria okadai.¹⁰

Mechanisms and Symptoms of Injury

Bathing sponges (silk sponges) derived from Spongia officinalis are harmless. Other sponges can exert their damaging effects through a variety of mechanisms that lead to dermatologic manifestations (eTable). Some species of sponges produce and secrete toxic metabolites (eg, crinotoxins) onto the body surface or into the surrounding water. They also are capable of synthesizing a mucous slime that can be irritating to human skin. Direct trauma also can be caused by fragments of the silica or calcium carbonate sponge skeleton penetrating the skin. Stinging members of the phylum Cnidaria can colonize the sponge, leading to injury when a human handles the sponge.^25-27

Sponge dermatitis can be divided into 2 major categories: an initial pruritic dermatitis (Figure 3) that occurs within 20 minutes to a few hours after contact and a delayed irritant dermatitis caused by penetration of the spicules and chemical agents into skin.²⁸ Importantly, different species can lead to varying manifestations.

The initial pruritic dermatitis is characterized by itching and burning that progresses to local edema, vesiculation, joint swelling, and stiffness. Because most contact with sponges occurs with handling, joint immobility may ensue within 24 hours of the encounter. Rarely, larger areas of the skin are affected, and fever, chills, malaise, dizziness, nausea, purulent bullae, muscle cramps, and formication may occur.²⁸ Anaphylactic reactions have been described in a small subset of patients. There have even been reports of delayed (ie, 1–2 weeks following exposure) erythema multiforme, livedo reticularis, purpura, and dyshidrotic eczema.^16,20,29 The irritant dermatitis caused by spicule trauma is due to a foreign body reaction that can be exacerbated by toxins entering the skin. In severe cases, desquamation, recurrent eczema, and arthralgia can occur.³⁰ In general, more mild cases should self-resolve within 3 to 7 days. Dermatologic conditions also can be caused by organisms that inhabit sponges and as a result produce a dermatitis when the sponge is handled, including sponge divers disease (maladie des plongeurs), a necrotic dermatitis caused by stinging Cnidaria species.³¹ Dogger Bank itch, first described as a dermatitis caused by sensitization to (2-hydroxyethyl) dimethylsulfoxonium chloride, initially was isolated from the sea chervil (a type of Bryozoan); however, that same chemical also was later found in sponges, producing the same dermatitis after handling the sponge.³² Freshwater sponges also have been reported to be injurious and exist worldwide. In contrast to marine sponges, lesions from freshwater sponges are disseminated pruritic erythematous papules with ulcerations, crusts, and secondary infections.²² The disseminated nature of the dermatitis caused by freshwater sponges is due to contact with the spicules of dead sponges that are dispersed throughout the water rather than from direct handling. Sponge dermatitis occurs mostly in sponge collectors, divers, trawlers, and biology students and has been reported extensively in the United States, Caribbean Islands, Australia, New Zealand, and Brazil.^18,27,33,34

Management

Treatment should consist of an initial decontamination; the skin should be dried, and adhesive tape or rubber cement should be utilized to remove any spicules embedded in the skin. Diluted vinegar soaks should be initiated for 10 to 30 minutes on the affected area(s) 3 or 4 times daily.¹⁹ The initial decontamination should occur immediately, as delay may lead to persistent purulent bullae that may take months to heal. Topical steroids may be used following the initial decontamination to help relieve inflammation. Antihistamines and nonsteroidal anti-inflammatory drugs may be used to alleviate pruritus and pain, respectively. Severe cases may require systemic glucocorticoids. Additionally, immunization status against tetanus toxoid should be assessed.³⁵ In the event of an anaphylactic reaction, it is important to maintain a patent airway and normalized blood pressure through the use of intramuscular epinephrine.³⁶ Frequent follow-up is warranted, as serious secondary infections can develop.³⁷ Patients also should be counseled on the potential for delayed dermatologic reactions, including erythema multiforme. Contact between humans and coastal environments has been increasing in the last few decades; therefore, an increase in contact with sponges is to be expected.²²

 

Characteristics

The ubiquitous human flea, Pulex irritans, is a hematophagous wingless ectoparasite in the order Siphonaptera (wingless siphon) that survives by consuming the blood of its mammalian and avian hosts. Due to diseases such as the bubonic plague, fleas have claimed more victims than all the wars ever fought; in the 14th century, the Black Death caused more than 200 million deaths. Fleas fossilized in amber have been found to be 200 million years old and closely resemble the modern human flea, demonstrating the resilience of the species.

The adult human flea is a small, reddish brown, laterally compressed, wingless insect that is approximately 2- to 3.5-mm long (females, 2.5–3.5 mm; males, 2–2.5 mm) and enclosed by a tough cuticle. Compared to the dog flea (Ctenocephalides canis) and cat flea (Ctenocephalides felis), P irritans has no combs or ctenidia (Figure 1). Fleas have large powerful hind legs enabling them to jump horizontally or vertically 200 times their body length (equivalent to a 6-foot human jumping 1200 feet) using stored muscle energy in a pad on the hind legs composed of the elastic protein resilin.¹ They feed off a wide variety of hosts, including humans, pigs, cats, dogs, goats, sheep, cattle, chickens, owls, foxes, rabbits, mice, and feral cats. The flea’s mouthparts are highly specialized for piercing the skin and sucking its blood meal via direct capillary cannulation.

Life Cycle

There are 4 stages of the flea life cycle: egg, larva, pupa, and adult. Most adult flea species mate on the host; the female will lay an average of 4 to 8 small white eggs on the host after each blood meal, laying more than 400 eggs during her lifetime. The eggs then drop from the host and hatch in approximately 4 to 6 days to become larvae. The active larvae feed on available organic matter in their environment, such as their parents’ feces and detritus, while undergoing 3 molts within 1 week to several months.² The larva then spins a silken cocoon from modified salivary glands to form the pupa. In favorable conditions, the pupa lasts only a few weeks; however, it can last for a year or more in unfavorable conditions. Triggers for emergence of the adult flea from the pupa include high humidity, warm temperatures, increased levels of carbon dioxide, and vibrations including sound. An adult P irritans flea can live for a few weeks to more than 1.5 years in favorable conditions of lower air temperature, high relative humidity, and access to a host.³

Related Diseases

Pulex irritans can be a vector for several human diseases. Yersinia pestis is a gram-negative bacteria that causes plague, a highly virulent disease that killed millions of people during its 3 largest human pandemics. The black rat (Rattus rattus) and the oriental rat flea (Xenopsylla cheopis) have been implicated as initial vectors; however, transmission may be human-to-human with pneumonic plague, and septicemic plague may be spread via Pulex fleas or body lice.^4,5 In 1971, Y pestis was isolated from P irritans on a dog in the home of a plague patient in Kayenta, Arizona.⁶Yersinia pestis bacterial DNA also was extracted from P irritans during a plague outbreak in Madagascar in 2014⁷ and was implicated in epidemiologic studies of plague in Tanzania from 1986 to 2004, suggesting it also plays a role in endemic disease.⁸

Bartonellosis is an emerging disease caused by different species of the gram-negative intracellular bacteria of the genus Bartonella transmitted by lice, ticks, and fleas. Bartonella quintana causes trench fever primarily transmitted by the human body louse, Pediculus humanus corporis, and resulted in more than 1 million cases during World War I. Trench fever is characterized by headache, fever, dizziness, and shin pain that lasts 1 to 3 days and recurs in cycles every 4 to 6 days. Other clinical manifestations of B quintana include chronic bacteremia, endocarditis, lymphadenopathy, and bacillary angiomatosis.⁹Bartonella henselae causes cat scratch fever, characterized by lymphadenopathy, fever, headache, joint pain, and lethargy from infected cat scratches or the bite of an infected flea. Bartonella rochalimae also has been found to cause a trench fever–like bacteremia.¹⁰Bartonella species have been found in P irritans, and the flea is implicated as a vector of bartonellosis in humans.^11-15

Rickettsioses are worldwide diseases caused by the gram-negative intracellular bacteria of the genus Rickettsia transmitted to humans via hematophagous arthropods. The rickettsiae traditionally have been classified into the spotted fever or typhus groups. The spotted fever group (ie, Rocky Mountain spotted fever, Mediterranean spotted fever) is transmitted via ticks. The typhus group is transmitted via lice (epidemic typhus) and fleas (endemic or murine typhus). Murine typhus can be caused by Rickettsia typhi in warm coastal areas around the world where the main mammal reservoir is the rat and the rat flea vector X cheopis. Clinical signs of infection are abrupt onset of fever, headaches, myalgia, malaise, and chills, with a truncal maculopapular rash progressing peripherally several days after the initial clinical signs. Rash is present in up to 50% of cases.¹⁶Rickettsia felis is an emerging flea-borne pathogen causing an acute febrile illness usually transmitted via the cat flea C felis.¹⁷Rickettsia species DNA have been found to be present in P irritans from dogs¹⁸ and livestock¹⁹ and pose a risk for causing rickettsioses in humans.

Environmental Treatment and Prevention

Flea bites present as intense, pruritic, urticarial to vesicular papules that usually are located on the lower extremities but also can be present on exposed areas of the upper extremities and hands (Figure 2). Human fleas infest clothing, and bites can be widespread. Topical antipruritics and corticosteroids can be used for controlling itch and the intense cutaneous inflammatory response. The flea host should be identified in areas of the home, school, farm, work, or local environment. House pets should be examined and treated by a veterinarian. The pet’s bedding should be washed and dried at high temperatures, and carpets and floors should be routinely vacuumed or cleaned to remove eggs, larvae, flea feces, and/or pupae. The killing of adult fleas with insecticidal products (eg, imidacloprid, fipronil, spinosad, selamectin, lufenuron, ivermectin) is the primary method of flea control. Use of insect growth regulators such as pyriproxyfen inhibits adult reproduction and blocks the organogenesis of immature larval stages via hormonal or enzymatic actions.²⁰ The combination of an insecticide and an insect growth regulator appears to be most effective in their synergistic actions against adult fleas and larvae. There have been reports of insecticidal resistance in the flea population, especially with pyrethroids.^21,22 A professional exterminator and veterinarian should be consulted. In recalcitrant cases, evaluation for other wild mammals or birds should be performed in unoccupied areas of the home such as the attic, crawl spaces, and basements, as well as inside walls.

 

Conclusion

The human flea, P irritans, is an important vector in the transmission of human diseases such as the bubonic plague, bartonellosis, and rickettsioses. Flea bites present as intensely pruritic, urticarial to vesicular papules that most commonly present on the lower extremities. Flea bites can be treated with topical steroids, and fleas can be controlled by a combination of insecticidal products and insect growth regulators.

 

Characteristics

The ubiquitous human flea, Pulex irritans, is a hematophagous wingless ectoparasite in the order Siphonaptera (wingless siphon) that survives by consuming the blood of its mammalian and avian hosts. Due to diseases such as the bubonic plague, fleas have claimed more victims than all the wars ever fought; in the 14th century, the Black Death caused more than 200 million deaths. Fleas fossilized in amber have been found to be 200 million years old and closely resemble the modern human flea, demonstrating the resilience of the species.

The adult human flea is a small, reddish brown, laterally compressed, wingless insect that is approximately 2- to 3.5-mm long (females, 2.5–3.5 mm; males, 2–2.5 mm) and enclosed by a tough cuticle. Compared to the dog flea (Ctenocephalides canis) and cat flea (Ctenocephalides felis), P irritans has no combs or ctenidia (Figure 1). Fleas have large powerful hind legs enabling them to jump horizontally or vertically 200 times their body length (equivalent to a 6-foot human jumping 1200 feet) using stored muscle energy in a pad on the hind legs composed of the elastic protein resilin.¹ They feed off a wide variety of hosts, including humans, pigs, cats, dogs, goats, sheep, cattle, chickens, owls, foxes, rabbits, mice, and feral cats. The flea’s mouthparts are highly specialized for piercing the skin and sucking its blood meal via direct capillary cannulation.

Life Cycle

There are 4 stages of the flea life cycle: egg, larva, pupa, and adult. Most adult flea species mate on the host; the female will lay an average of 4 to 8 small white eggs on the host after each blood meal, laying more than 400 eggs during her lifetime. The eggs then drop from the host and hatch in approximately 4 to 6 days to become larvae. The active larvae feed on available organic matter in their environment, such as their parents’ feces and detritus, while undergoing 3 molts within 1 week to several months.² The larva then spins a silken cocoon from modified salivary glands to form the pupa. In favorable conditions, the pupa lasts only a few weeks; however, it can last for a year or more in unfavorable conditions. Triggers for emergence of the adult flea from the pupa include high humidity, warm temperatures, increased levels of carbon dioxide, and vibrations including sound. An adult P irritans flea can live for a few weeks to more than 1.5 years in favorable conditions of lower air temperature, high relative humidity, and access to a host.³

Related Diseases

Pulex irritans can be a vector for several human diseases. Yersinia pestis is a gram-negative bacteria that causes plague, a highly virulent disease that killed millions of people during its 3 largest human pandemics. The black rat (Rattus rattus) and the oriental rat flea (Xenopsylla cheopis) have been implicated as initial vectors; however, transmission may be human-to-human with pneumonic plague, and septicemic plague may be spread via Pulex fleas or body lice.^4,5 In 1971, Y pestis was isolated from P irritans on a dog in the home of a plague patient in Kayenta, Arizona.⁶Yersinia pestis bacterial DNA also was extracted from P irritans during a plague outbreak in Madagascar in 2014⁷ and was implicated in epidemiologic studies of plague in Tanzania from 1986 to 2004, suggesting it also plays a role in endemic disease.⁸

Bartonellosis is an emerging disease caused by different species of the gram-negative intracellular bacteria of the genus Bartonella transmitted by lice, ticks, and fleas. Bartonella quintana causes trench fever primarily transmitted by the human body louse, Pediculus humanus corporis, and resulted in more than 1 million cases during World War I. Trench fever is characterized by headache, fever, dizziness, and shin pain that lasts 1 to 3 days and recurs in cycles every 4 to 6 days. Other clinical manifestations of B quintana include chronic bacteremia, endocarditis, lymphadenopathy, and bacillary angiomatosis.⁹Bartonella henselae causes cat scratch fever, characterized by lymphadenopathy, fever, headache, joint pain, and lethargy from infected cat scratches or the bite of an infected flea. Bartonella rochalimae also has been found to cause a trench fever–like bacteremia.¹⁰Bartonella species have been found in P irritans, and the flea is implicated as a vector of bartonellosis in humans.^11-15

Rickettsioses are worldwide diseases caused by the gram-negative intracellular bacteria of the genus Rickettsia transmitted to humans via hematophagous arthropods. The rickettsiae traditionally have been classified into the spotted fever or typhus groups. The spotted fever group (ie, Rocky Mountain spotted fever, Mediterranean spotted fever) is transmitted via ticks. The typhus group is transmitted via lice (epidemic typhus) and fleas (endemic or murine typhus). Murine typhus can be caused by Rickettsia typhi in warm coastal areas around the world where the main mammal reservoir is the rat and the rat flea vector X cheopis. Clinical signs of infection are abrupt onset of fever, headaches, myalgia, malaise, and chills, with a truncal maculopapular rash progressing peripherally several days after the initial clinical signs. Rash is present in up to 50% of cases.¹⁶Rickettsia felis is an emerging flea-borne pathogen causing an acute febrile illness usually transmitted via the cat flea C felis.¹⁷Rickettsia species DNA have been found to be present in P irritans from dogs¹⁸ and livestock¹⁹ and pose a risk for causing rickettsioses in humans.

Environmental Treatment and Prevention

Flea bites present as intense, pruritic, urticarial to vesicular papules that usually are located on the lower extremities but also can be present on exposed areas of the upper extremities and hands (Figure 2). Human fleas infest clothing, and bites can be widespread. Topical antipruritics and corticosteroids can be used for controlling itch and the intense cutaneous inflammatory response. The flea host should be identified in areas of the home, school, farm, work, or local environment. House pets should be examined and treated by a veterinarian. The pet’s bedding should be washed and dried at high temperatures, and carpets and floors should be routinely vacuumed or cleaned to remove eggs, larvae, flea feces, and/or pupae. The killing of adult fleas with insecticidal products (eg, imidacloprid, fipronil, spinosad, selamectin, lufenuron, ivermectin) is the primary method of flea control. Use of insect growth regulators such as pyriproxyfen inhibits adult reproduction and blocks the organogenesis of immature larval stages via hormonal or enzymatic actions.²⁰ The combination of an insecticide and an insect growth regulator appears to be most effective in their synergistic actions against adult fleas and larvae. There have been reports of insecticidal resistance in the flea population, especially with pyrethroids.^21,22 A professional exterminator and veterinarian should be consulted. In recalcitrant cases, evaluation for other wild mammals or birds should be performed in unoccupied areas of the home such as the attic, crawl spaces, and basements, as well as inside walls.

 

Conclusion

The human flea, P irritans, is an important vector in the transmission of human diseases such as the bubonic plague, bartonellosis, and rickettsioses. Flea bites present as intensely pruritic, urticarial to vesicular papules that most commonly present on the lower extremities. Flea bites can be treated with topical steroids, and fleas can be controlled by a combination of insecticidal products and insect growth regulators.

 

Characteristics

The ubiquitous human flea, Pulex irritans, is a hematophagous wingless ectoparasite in the order Siphonaptera (wingless siphon) that survives by consuming the blood of its mammalian and avian hosts. Due to diseases such as the bubonic plague, fleas have claimed more victims than all the wars ever fought; in the 14th century, the Black Death caused more than 200 million deaths. Fleas fossilized in amber have been found to be 200 million years old and closely resemble the modern human flea, demonstrating the resilience of the species.

The adult human flea is a small, reddish brown, laterally compressed, wingless insect that is approximately 2- to 3.5-mm long (females, 2.5–3.5 mm; males, 2–2.5 mm) and enclosed by a tough cuticle. Compared to the dog flea (Ctenocephalides canis) and cat flea (Ctenocephalides felis), P irritans has no combs or ctenidia (Figure 1). Fleas have large powerful hind legs enabling them to jump horizontally or vertically 200 times their body length (equivalent to a 6-foot human jumping 1200 feet) using stored muscle energy in a pad on the hind legs composed of the elastic protein resilin.¹ They feed off a wide variety of hosts, including humans, pigs, cats, dogs, goats, sheep, cattle, chickens, owls, foxes, rabbits, mice, and feral cats. The flea’s mouthparts are highly specialized for piercing the skin and sucking its blood meal via direct capillary cannulation.

Life Cycle

There are 4 stages of the flea life cycle: egg, larva, pupa, and adult. Most adult flea species mate on the host; the female will lay an average of 4 to 8 small white eggs on the host after each blood meal, laying more than 400 eggs during her lifetime. The eggs then drop from the host and hatch in approximately 4 to 6 days to become larvae. The active larvae feed on available organic matter in their environment, such as their parents’ feces and detritus, while undergoing 3 molts within 1 week to several months.² The larva then spins a silken cocoon from modified salivary glands to form the pupa. In favorable conditions, the pupa lasts only a few weeks; however, it can last for a year or more in unfavorable conditions. Triggers for emergence of the adult flea from the pupa include high humidity, warm temperatures, increased levels of carbon dioxide, and vibrations including sound. An adult P irritans flea can live for a few weeks to more than 1.5 years in favorable conditions of lower air temperature, high relative humidity, and access to a host.³

Related Diseases

Pulex irritans can be a vector for several human diseases. Yersinia pestis is a gram-negative bacteria that causes plague, a highly virulent disease that killed millions of people during its 3 largest human pandemics. The black rat (Rattus rattus) and the oriental rat flea (Xenopsylla cheopis) have been implicated as initial vectors; however, transmission may be human-to-human with pneumonic plague, and septicemic plague may be spread via Pulex fleas or body lice.^4,5 In 1971, Y pestis was isolated from P irritans on a dog in the home of a plague patient in Kayenta, Arizona.⁶Yersinia pestis bacterial DNA also was extracted from P irritans during a plague outbreak in Madagascar in 2014⁷ and was implicated in epidemiologic studies of plague in Tanzania from 1986 to 2004, suggesting it also plays a role in endemic disease.⁸

Bartonellosis is an emerging disease caused by different species of the gram-negative intracellular bacteria of the genus Bartonella transmitted by lice, ticks, and fleas. Bartonella quintana causes trench fever primarily transmitted by the human body louse, Pediculus humanus corporis, and resulted in more than 1 million cases during World War I. Trench fever is characterized by headache, fever, dizziness, and shin pain that lasts 1 to 3 days and recurs in cycles every 4 to 6 days. Other clinical manifestations of B quintana include chronic bacteremia, endocarditis, lymphadenopathy, and bacillary angiomatosis.⁹Bartonella henselae causes cat scratch fever, characterized by lymphadenopathy, fever, headache, joint pain, and lethargy from infected cat scratches or the bite of an infected flea. Bartonella rochalimae also has been found to cause a trench fever–like bacteremia.¹⁰Bartonella species have been found in P irritans, and the flea is implicated as a vector of bartonellosis in humans.^11-15

Rickettsioses are worldwide diseases caused by the gram-negative intracellular bacteria of the genus Rickettsia transmitted to humans via hematophagous arthropods. The rickettsiae traditionally have been classified into the spotted fever or typhus groups. The spotted fever group (ie, Rocky Mountain spotted fever, Mediterranean spotted fever) is transmitted via ticks. The typhus group is transmitted via lice (epidemic typhus) and fleas (endemic or murine typhus). Murine typhus can be caused by Rickettsia typhi in warm coastal areas around the world where the main mammal reservoir is the rat and the rat flea vector X cheopis. Clinical signs of infection are abrupt onset of fever, headaches, myalgia, malaise, and chills, with a truncal maculopapular rash progressing peripherally several days after the initial clinical signs. Rash is present in up to 50% of cases.¹⁶Rickettsia felis is an emerging flea-borne pathogen causing an acute febrile illness usually transmitted via the cat flea C felis.¹⁷Rickettsia species DNA have been found to be present in P irritans from dogs¹⁸ and livestock¹⁹ and pose a risk for causing rickettsioses in humans.

Environmental Treatment and Prevention

Flea bites present as intense, pruritic, urticarial to vesicular papules that usually are located on the lower extremities but also can be present on exposed areas of the upper extremities and hands (Figure 2). Human fleas infest clothing, and bites can be widespread. Topical antipruritics and corticosteroids can be used for controlling itch and the intense cutaneous inflammatory response. The flea host should be identified in areas of the home, school, farm, work, or local environment. House pets should be examined and treated by a veterinarian. The pet’s bedding should be washed and dried at high temperatures, and carpets and floors should be routinely vacuumed or cleaned to remove eggs, larvae, flea feces, and/or pupae. The killing of adult fleas with insecticidal products (eg, imidacloprid, fipronil, spinosad, selamectin, lufenuron, ivermectin) is the primary method of flea control. Use of insect growth regulators such as pyriproxyfen inhibits adult reproduction and blocks the organogenesis of immature larval stages via hormonal or enzymatic actions.²⁰ The combination of an insecticide and an insect growth regulator appears to be most effective in their synergistic actions against adult fleas and larvae. There have been reports of insecticidal resistance in the flea population, especially with pyrethroids.^21,22 A professional exterminator and veterinarian should be consulted. In recalcitrant cases, evaluation for other wild mammals or birds should be performed in unoccupied areas of the home such as the attic, crawl spaces, and basements, as well as inside walls.

 

Conclusion

The human flea, P irritans, is an important vector in the transmission of human diseases such as the bubonic plague, bartonellosis, and rickettsioses. Flea bites present as intensely pruritic, urticarial to vesicular papules that most commonly present on the lower extremities. Flea bites can be treated with topical steroids, and fleas can be controlled by a combination of insecticidal products and insect growth regulators.

A dult Siphonaptera (fleas) are highly adapted to life on the surface of their hosts. Their small 2- to 10-mm bodies are laterally flattened and wingless. They utilize particularly strong hind legs for jumping up to 150 times their body length and backward-directed spines on their legs and bodies for moving forward through fur, hair, and feathers. Xenopsylla cheopis , the oriental rat flea, lacks pronotal and genal combs and has a mesopleuron divided by internal scleritinization (Figure). These features differentiate the species from its close relatives, Ctenocephalides (cat and dog fleas), which have both sets of combs, as well as Pulex irritans (human flea), which do not have a divided mesopleuron. ^1,2

Flea-borne infections are extremely important to public health and are present throughout the world. Further, humidity and warmth are essential for the life cycle of many species of fleas. Predicted global warming likely will increase their distribution, allowing the spread of diseases they carry into previously untouched areas.¹ Therefore, it is important to continue to examine species that carry particularly dangerous pathogens, such as X cheopis.

Disease Vector

Xenopsylla cheopis primarily is known for being a vector in the transmission of Yersinia pestis, the etiologic agent of the plague. Plague occurs in 3 forms: bubonic, pneumonic, and septicemic. It has caused major epidemics throughout history, the most widely known being the Black Death, which lasted for 130 years, beginning in the 1330s in China and spreading into Europe where it wiped out one-third of the population. However, bubonic plague is thought to have caused documented outbreaks as early as 320 bce, and it still remains endemic today.^3,4

Between January 2010 and December 2015, 3248 cases of plague in humans were reported, resulting in 584 deaths worldwide.⁵ It is thought that the plague originated in Central Asia, and this area still is a focus of disease. However, the at-risk population is reduced to breeders and hunters of gerbils and marmots, the main reservoirs in the area. In Africa, 4 countries still regularly report cases, with Madagascar being the most severely affected country in the world.⁵ The Democratic Republic of the Congo, Uganda, and Tanzania also are affected. The Americas also experience the plague. There are sporadic cases of bubonic plague in the northwest corner of Peru, mostly in rural areas. In the western United States, plague circulates among wild rodents, resulting in several reported cases each year, with the most recent confirmed case noted in California in August 2020.^5,6 Further adding to its relevance, Y pestis is one of several organisms most likely to be used as a biologic weapon.^3,4

Due to the historical and continued significance of Y pestis, many studies have been performed over the decades regarding its association with X cheopis. It has been discovered that fleas transmit the bacteria to the host in 2 ways. The most well-defined form of transmission occurs after an incubation period of Y pestis in the flea for 7 to 31 days. During this time, the bacteria form a dense biofilm on a valve in the flea foregut—the proventriculus—interfering with its function, which allows regurgitation of the blood and the bacteria it contains into the bite site and consequently disease transmission. The proventriculus can become completely blocked in some fleas, preventing any blood from reaching the midgut and causing starvation. In these scenarios, the flea will make continuous attempts to feed, increasing transmission.⁷ The hemin storage gene, hms, encoding the second messenger molecule cyclic di-GMP plays a critical role in biofilm formation and proventricular blockage.⁸ The phosphoheptose isomerase gene, GmhA, also has been elucidated as crucial in late transmission due to its role in biofilm formation.⁹ Early-phase transmission, or biofilm-independent transmission, has been documented to occur as early as 3 hours after infection of the flea but can occur for up to 4 days.¹⁰ Historically, the importance of early-phase transmission has been overlooked. Research has shown that it likely is crucial to the epizootic transmission of the plague.¹⁰ As a result, the search has begun for genes that contribute to the maintenance of Y pestis in the flea vector during the first 4 days of colonization. It is thought that a key evolutionary development was the selective loss-of-function mutation in a gene essential for the activity of urease, an enzyme that causes acute oral toxicity and mortality in fleas.^11,12 The Yersinia murine toxin gene, Ymt, also allows for early survival of Y pestis in the flea midgut by producing a phospholipase D that protects the bacteria from toxic by-products produced during digestion of blood.^11,13 In addition, gene products that function in lipid A modification are crucial for the ability of Y pestis to resist the action of cationic antimicrobial peptides it produces, such as cecropin A and polymyxin B.¹³

Murine typhus, an acute febrile illness caused by Rickettsia typhi, is another disease that can be spread by oriental rat fleas. It has a worldwide distribution. In the United States, R typhi–induced rickettsia mainly is concentrated in suburban areas of Texas and California where it is thought to be mainly spread by Ctenocephalides, but it also is found in Hawaii where spread by X cheopis has been documented.^14,15 The most common symptoms of rickettsia include fever, headache, arthralgia, and a characteristic rash that is pruritic and maculopapular, starting on the trunk and spreading peripherally but sparing the palms and soles. This rash occurs about a week after the onset of fever.¹⁴Rickettsia felis also has been isolated in the oriental rat flea. However, only a handful of cases of human disease caused by this bacterium have been reported throughout the world, with clinical similarity to murine typhus likely leading to underestimation of disease prevalence.¹⁵Bartonella and other species of bacteria also have been documented to be spread by X cheopis.¹⁶ Unfortunately, the interactions of X cheopis with these other bacteria are not as well studied as its relationship with Y pestis.

Adverse Reactions

A flea bite itself can cause discomfort. It begins as a punctate hemorrhagic area that develops a surrounding wheal within 30 minutes. Over the course of 1 to 2 days, a delayed reaction occurs and there is a transition to an extremely pruritic, papular lesion. Bites often occur in clusters and can persist for weeks.¹

Prevention and Treatment

Control of host animals via extermination and proper sanitation can secondarily reduce the population of X cheopis. Direct pesticide control of the flea population also has been suggested to reduce flea-borne disease. However, insecticides cause a selective pressure on the flea population, leading to populations that are resistant to them. For example, the flea population in Madagascar developed resistance to DDT (dichlorodiphenyltrichloroethane), dieldrin, deltamethrin, and cyfluthrin after their widespread use.¹⁷ Further, a recent study revealed resistance of X cheopis populations to alphacypermethrin, lambda-cyhalothrin, and etofenprox, none of which were used in mass vector control, indicating that some cross-resistance mechanism between these and the extensively used insecticides may exist. With the development of widespread resistance to most pesticides, flea control in endemic areas is difficult. Insecticide targeting to fleas on rodents (eg, rodent bait containing insecticide) can allow for more targeted insecticide treatment, limiting the development of resistance.¹⁷ Recent development of a maceration protocol used to detect zoonotic pathogens in fleas in the field also will allow management with pesticides to be targeted geographically and temporally where infected vectors are located.¹⁸ Research of the interaction between vector, pathogen, and insect microbiome also should continue, as it may allow for development of biopesticides, limiting the use of chemical pesticides all together. The strategy is based on the introduction of microorganisms that can reduce vector lifespan or their ability to transmit pathogens.¹⁷

When flea-transmitted diseases do occur, treatment with antibiotics is advised. Early treatment of the plague with effective antibiotics such as streptomycin, gentamicin, tetracycline, or chloramphenicol for a minimum of 10 days is critical for survival. Additionally, patients with bubonic plague should be isolated for at least 2 days after administration of antibiotics, while patients with the pneumonic form should be isolated for 4 days into therapy to prevent the spread of disease. Prophylactic therapy for individuals who come into contact with infected individuals also is advised.⁴ Patients with murine typhus typically respond to doxycycline, tetracycline, or fluoroquinolones. The few cases of R felis–induced disease have responded to doxycycline. Of note, short courses of treatment of doxycycline are appropriate and safe in young children. The short (3–7 day) nature of the course limits the chances of teeth staining.¹⁴

A dult Siphonaptera (fleas) are highly adapted to life on the surface of their hosts. Their small 2- to 10-mm bodies are laterally flattened and wingless. They utilize particularly strong hind legs for jumping up to 150 times their body length and backward-directed spines on their legs and bodies for moving forward through fur, hair, and feathers. Xenopsylla cheopis , the oriental rat flea, lacks pronotal and genal combs and has a mesopleuron divided by internal scleritinization (Figure). These features differentiate the species from its close relatives, Ctenocephalides (cat and dog fleas), which have both sets of combs, as well as Pulex irritans (human flea), which do not have a divided mesopleuron. ^1,2

Flea-borne infections are extremely important to public health and are present throughout the world. Further, humidity and warmth are essential for the life cycle of many species of fleas. Predicted global warming likely will increase their distribution, allowing the spread of diseases they carry into previously untouched areas.¹ Therefore, it is important to continue to examine species that carry particularly dangerous pathogens, such as X cheopis.

Disease Vector

Xenopsylla cheopis primarily is known for being a vector in the transmission of Yersinia pestis, the etiologic agent of the plague. Plague occurs in 3 forms: bubonic, pneumonic, and septicemic. It has caused major epidemics throughout history, the most widely known being the Black Death, which lasted for 130 years, beginning in the 1330s in China and spreading into Europe where it wiped out one-third of the population. However, bubonic plague is thought to have caused documented outbreaks as early as 320 bce, and it still remains endemic today.^3,4

Between January 2010 and December 2015, 3248 cases of plague in humans were reported, resulting in 584 deaths worldwide.⁵ It is thought that the plague originated in Central Asia, and this area still is a focus of disease. However, the at-risk population is reduced to breeders and hunters of gerbils and marmots, the main reservoirs in the area. In Africa, 4 countries still regularly report cases, with Madagascar being the most severely affected country in the world.⁵ The Democratic Republic of the Congo, Uganda, and Tanzania also are affected. The Americas also experience the plague. There are sporadic cases of bubonic plague in the northwest corner of Peru, mostly in rural areas. In the western United States, plague circulates among wild rodents, resulting in several reported cases each year, with the most recent confirmed case noted in California in August 2020.^5,6 Further adding to its relevance, Y pestis is one of several organisms most likely to be used as a biologic weapon.^3,4

Due to the historical and continued significance of Y pestis, many studies have been performed over the decades regarding its association with X cheopis. It has been discovered that fleas transmit the bacteria to the host in 2 ways. The most well-defined form of transmission occurs after an incubation period of Y pestis in the flea for 7 to 31 days. During this time, the bacteria form a dense biofilm on a valve in the flea foregut—the proventriculus—interfering with its function, which allows regurgitation of the blood and the bacteria it contains into the bite site and consequently disease transmission. The proventriculus can become completely blocked in some fleas, preventing any blood from reaching the midgut and causing starvation. In these scenarios, the flea will make continuous attempts to feed, increasing transmission.⁷ The hemin storage gene, hms, encoding the second messenger molecule cyclic di-GMP plays a critical role in biofilm formation and proventricular blockage.⁸ The phosphoheptose isomerase gene, GmhA, also has been elucidated as crucial in late transmission due to its role in biofilm formation.⁹ Early-phase transmission, or biofilm-independent transmission, has been documented to occur as early as 3 hours after infection of the flea but can occur for up to 4 days.¹⁰ Historically, the importance of early-phase transmission has been overlooked. Research has shown that it likely is crucial to the epizootic transmission of the plague.¹⁰ As a result, the search has begun for genes that contribute to the maintenance of Y pestis in the flea vector during the first 4 days of colonization. It is thought that a key evolutionary development was the selective loss-of-function mutation in a gene essential for the activity of urease, an enzyme that causes acute oral toxicity and mortality in fleas.^11,12 The Yersinia murine toxin gene, Ymt, also allows for early survival of Y pestis in the flea midgut by producing a phospholipase D that protects the bacteria from toxic by-products produced during digestion of blood.^11,13 In addition, gene products that function in lipid A modification are crucial for the ability of Y pestis to resist the action of cationic antimicrobial peptides it produces, such as cecropin A and polymyxin B.¹³

Murine typhus, an acute febrile illness caused by Rickettsia typhi, is another disease that can be spread by oriental rat fleas. It has a worldwide distribution. In the United States, R typhi–induced rickettsia mainly is concentrated in suburban areas of Texas and California where it is thought to be mainly spread by Ctenocephalides, but it also is found in Hawaii where spread by X cheopis has been documented.^14,15 The most common symptoms of rickettsia include fever, headache, arthralgia, and a characteristic rash that is pruritic and maculopapular, starting on the trunk and spreading peripherally but sparing the palms and soles. This rash occurs about a week after the onset of fever.¹⁴Rickettsia felis also has been isolated in the oriental rat flea. However, only a handful of cases of human disease caused by this bacterium have been reported throughout the world, with clinical similarity to murine typhus likely leading to underestimation of disease prevalence.¹⁵Bartonella and other species of bacteria also have been documented to be spread by X cheopis.¹⁶ Unfortunately, the interactions of X cheopis with these other bacteria are not as well studied as its relationship with Y pestis.

Adverse Reactions

A flea bite itself can cause discomfort. It begins as a punctate hemorrhagic area that develops a surrounding wheal within 30 minutes. Over the course of 1 to 2 days, a delayed reaction occurs and there is a transition to an extremely pruritic, papular lesion. Bites often occur in clusters and can persist for weeks.¹

Prevention and Treatment

Control of host animals via extermination and proper sanitation can secondarily reduce the population of X cheopis. Direct pesticide control of the flea population also has been suggested to reduce flea-borne disease. However, insecticides cause a selective pressure on the flea population, leading to populations that are resistant to them. For example, the flea population in Madagascar developed resistance to DDT (dichlorodiphenyltrichloroethane), dieldrin, deltamethrin, and cyfluthrin after their widespread use.¹⁷ Further, a recent study revealed resistance of X cheopis populations to alphacypermethrin, lambda-cyhalothrin, and etofenprox, none of which were used in mass vector control, indicating that some cross-resistance mechanism between these and the extensively used insecticides may exist. With the development of widespread resistance to most pesticides, flea control in endemic areas is difficult. Insecticide targeting to fleas on rodents (eg, rodent bait containing insecticide) can allow for more targeted insecticide treatment, limiting the development of resistance.¹⁷ Recent development of a maceration protocol used to detect zoonotic pathogens in fleas in the field also will allow management with pesticides to be targeted geographically and temporally where infected vectors are located.¹⁸ Research of the interaction between vector, pathogen, and insect microbiome also should continue, as it may allow for development of biopesticides, limiting the use of chemical pesticides all together. The strategy is based on the introduction of microorganisms that can reduce vector lifespan or their ability to transmit pathogens.¹⁷

When flea-transmitted diseases do occur, treatment with antibiotics is advised. Early treatment of the plague with effective antibiotics such as streptomycin, gentamicin, tetracycline, or chloramphenicol for a minimum of 10 days is critical for survival. Additionally, patients with bubonic plague should be isolated for at least 2 days after administration of antibiotics, while patients with the pneumonic form should be isolated for 4 days into therapy to prevent the spread of disease. Prophylactic therapy for individuals who come into contact with infected individuals also is advised.⁴ Patients with murine typhus typically respond to doxycycline, tetracycline, or fluoroquinolones. The few cases of R felis–induced disease have responded to doxycycline. Of note, short courses of treatment of doxycycline are appropriate and safe in young children. The short (3–7 day) nature of the course limits the chances of teeth staining.¹⁴

A dult Siphonaptera (fleas) are highly adapted to life on the surface of their hosts. Their small 2- to 10-mm bodies are laterally flattened and wingless. They utilize particularly strong hind legs for jumping up to 150 times their body length and backward-directed spines on their legs and bodies for moving forward through fur, hair, and feathers. Xenopsylla cheopis , the oriental rat flea, lacks pronotal and genal combs and has a mesopleuron divided by internal scleritinization (Figure). These features differentiate the species from its close relatives, Ctenocephalides (cat and dog fleas), which have both sets of combs, as well as Pulex irritans (human flea), which do not have a divided mesopleuron. ^1,2

Flea-borne infections are extremely important to public health and are present throughout the world. Further, humidity and warmth are essential for the life cycle of many species of fleas. Predicted global warming likely will increase their distribution, allowing the spread of diseases they carry into previously untouched areas.¹ Therefore, it is important to continue to examine species that carry particularly dangerous pathogens, such as X cheopis.

Disease Vector

Xenopsylla cheopis primarily is known for being a vector in the transmission of Yersinia pestis, the etiologic agent of the plague. Plague occurs in 3 forms: bubonic, pneumonic, and septicemic. It has caused major epidemics throughout history, the most widely known being the Black Death, which lasted for 130 years, beginning in the 1330s in China and spreading into Europe where it wiped out one-third of the population. However, bubonic plague is thought to have caused documented outbreaks as early as 320 bce, and it still remains endemic today.^3,4

Between January 2010 and December 2015, 3248 cases of plague in humans were reported, resulting in 584 deaths worldwide.⁵ It is thought that the plague originated in Central Asia, and this area still is a focus of disease. However, the at-risk population is reduced to breeders and hunters of gerbils and marmots, the main reservoirs in the area. In Africa, 4 countries still regularly report cases, with Madagascar being the most severely affected country in the world.⁵ The Democratic Republic of the Congo, Uganda, and Tanzania also are affected. The Americas also experience the plague. There are sporadic cases of bubonic plague in the northwest corner of Peru, mostly in rural areas. In the western United States, plague circulates among wild rodents, resulting in several reported cases each year, with the most recent confirmed case noted in California in August 2020.^5,6 Further adding to its relevance, Y pestis is one of several organisms most likely to be used as a biologic weapon.^3,4

Due to the historical and continued significance of Y pestis, many studies have been performed over the decades regarding its association with X cheopis. It has been discovered that fleas transmit the bacteria to the host in 2 ways. The most well-defined form of transmission occurs after an incubation period of Y pestis in the flea for 7 to 31 days. During this time, the bacteria form a dense biofilm on a valve in the flea foregut—the proventriculus—interfering with its function, which allows regurgitation of the blood and the bacteria it contains into the bite site and consequently disease transmission. The proventriculus can become completely blocked in some fleas, preventing any blood from reaching the midgut and causing starvation. In these scenarios, the flea will make continuous attempts to feed, increasing transmission.⁷ The hemin storage gene, hms, encoding the second messenger molecule cyclic di-GMP plays a critical role in biofilm formation and proventricular blockage.⁸ The phosphoheptose isomerase gene, GmhA, also has been elucidated as crucial in late transmission due to its role in biofilm formation.⁹ Early-phase transmission, or biofilm-independent transmission, has been documented to occur as early as 3 hours after infection of the flea but can occur for up to 4 days.¹⁰ Historically, the importance of early-phase transmission has been overlooked. Research has shown that it likely is crucial to the epizootic transmission of the plague.¹⁰ As a result, the search has begun for genes that contribute to the maintenance of Y pestis in the flea vector during the first 4 days of colonization. It is thought that a key evolutionary development was the selective loss-of-function mutation in a gene essential for the activity of urease, an enzyme that causes acute oral toxicity and mortality in fleas.^11,12 The Yersinia murine toxin gene, Ymt, also allows for early survival of Y pestis in the flea midgut by producing a phospholipase D that protects the bacteria from toxic by-products produced during digestion of blood.^11,13 In addition, gene products that function in lipid A modification are crucial for the ability of Y pestis to resist the action of cationic antimicrobial peptides it produces, such as cecropin A and polymyxin B.¹³

Murine typhus, an acute febrile illness caused by Rickettsia typhi, is another disease that can be spread by oriental rat fleas. It has a worldwide distribution. In the United States, R typhi–induced rickettsia mainly is concentrated in suburban areas of Texas and California where it is thought to be mainly spread by Ctenocephalides, but it also is found in Hawaii where spread by X cheopis has been documented.^14,15 The most common symptoms of rickettsia include fever, headache, arthralgia, and a characteristic rash that is pruritic and maculopapular, starting on the trunk and spreading peripherally but sparing the palms and soles. This rash occurs about a week after the onset of fever.¹⁴Rickettsia felis also has been isolated in the oriental rat flea. However, only a handful of cases of human disease caused by this bacterium have been reported throughout the world, with clinical similarity to murine typhus likely leading to underestimation of disease prevalence.¹⁵Bartonella and other species of bacteria also have been documented to be spread by X cheopis.¹⁶ Unfortunately, the interactions of X cheopis with these other bacteria are not as well studied as its relationship with Y pestis.

Adverse Reactions

A flea bite itself can cause discomfort. It begins as a punctate hemorrhagic area that develops a surrounding wheal within 30 minutes. Over the course of 1 to 2 days, a delayed reaction occurs and there is a transition to an extremely pruritic, papular lesion. Bites often occur in clusters and can persist for weeks.¹

Prevention and Treatment

Control of host animals via extermination and proper sanitation can secondarily reduce the population of X cheopis. Direct pesticide control of the flea population also has been suggested to reduce flea-borne disease. However, insecticides cause a selective pressure on the flea population, leading to populations that are resistant to them. For example, the flea population in Madagascar developed resistance to DDT (dichlorodiphenyltrichloroethane), dieldrin, deltamethrin, and cyfluthrin after their widespread use.¹⁷ Further, a recent study revealed resistance of X cheopis populations to alphacypermethrin, lambda-cyhalothrin, and etofenprox, none of which were used in mass vector control, indicating that some cross-resistance mechanism between these and the extensively used insecticides may exist. With the development of widespread resistance to most pesticides, flea control in endemic areas is difficult. Insecticide targeting to fleas on rodents (eg, rodent bait containing insecticide) can allow for more targeted insecticide treatment, limiting the development of resistance.¹⁷ Recent development of a maceration protocol used to detect zoonotic pathogens in fleas in the field also will allow management with pesticides to be targeted geographically and temporally where infected vectors are located.¹⁸ Research of the interaction between vector, pathogen, and insect microbiome also should continue, as it may allow for development of biopesticides, limiting the use of chemical pesticides all together. The strategy is based on the introduction of microorganisms that can reduce vector lifespan or their ability to transmit pathogens.¹⁷

When flea-transmitted diseases do occur, treatment with antibiotics is advised. Early treatment of the plague with effective antibiotics such as streptomycin, gentamicin, tetracycline, or chloramphenicol for a minimum of 10 days is critical for survival. Additionally, patients with bubonic plague should be isolated for at least 2 days after administration of antibiotics, while patients with the pneumonic form should be isolated for 4 days into therapy to prevent the spread of disease. Prophylactic therapy for individuals who come into contact with infected individuals also is advised.⁴ Patients with murine typhus typically respond to doxycycline, tetracycline, or fluoroquinolones. The few cases of R felis–induced disease have responded to doxycycline. Of note, short courses of treatment of doxycycline are appropriate and safe in young children. The short (3–7 day) nature of the course limits the chances of teeth staining.¹⁴

Lepidoptera is the second largest order of the class Insecta and comprises approximately 160,000 species of butterflies and moths classified among approximately 124 families and subfamilies. Venomous properties have been identified in 12 of these families, posing a serious threat to human health. ¹

The clinical manifestations from Lepidoptera envenomation can range from general systemic symptoms such as fever and abdominal distress; to more complex focal affections including hemorrhage, ophthalmologic lesions, and irritation of the respiratory tracts; to less severe reactions of the skin, which are the most common presentation.¹

Terminology

Lepidopterism is the term used to address a clinical spectrum of systemic manifestations from direct contact with venomous butterflies or moths and/or their products.² Conversely, erucism is a term used to describe localized cutaneous reactions after direct contact with toxins from caterpillars.

Lepidopterism is derived from the Greek roots lepis, meaning scale, and pteron, meaning wing. The term erucism stems from the Latin word eruca, which means larva.²

Ideally, lepidopterism should refer solely to reactions from butterflies and moths—adult forms of insects with scaly wings—while erucism should refer to reactions from contact with caterpillars—the larval form of butterflies and moths.

In common use, lepidopterism can describe any reaction from caterpillars, moths, or adult butterflies, as well as any case of Lepidoptera exposure with only systemic manifestations, regardless of cutaneous findings. Concurrently, erucism has been defined as either any reaction from caterpillars or any skin reaction from contact with caterpillars or moths.²

Because caterpillars are the larval form of butterflies and moths, caterpillar-associated skin reactions also have been conveniently denominated caterpillar dermatitis.¹ Henceforth in this article, both terms erucism and caterpillar dermatitis are used interchangeably.

Caterpillar Envenomation

Caterpillars cause the vast majority of adverse events from lepidopteran exposures.² Envenomation by caterpillars might stand as the world’s most common envenomation given the larvae proximity to humans.³ Although involvement of internal organs (eg, renal failure), cerebral hemorrhage, and joint lesions can occur, skin manifestations are more predominant with the majority of species. Initial localized pain, edema, and erythema usually are present at the site of direct contact and subsequently progress toward maculopapular to bullous lesions, erosions, petechiae, necrosis, and ulceration depending on the offending species.^1,4

Megalopyge opercularis

In the United States, more than 50 species of caterpillars have been identified as poisonous or venomous.⁵ Megalopyge opercularis (Figure 1), the larval form of the flannel moth, is an important cause of caterpillar-associated dermatitis in the southern United States.^6,7 Megalopyge opercularis also is commonly known as the puss caterpillar, opossum bug, wooly slug, el perrito, tree asp, or Italian asp.⁶ This lepidopteran insect is mainly found in the southeastern and southcentral United States, with noted particular abundance in Texas, Louisiana, and Florida.^6,8 The puss caterpillar has 2 generations per year; the first develops during the months of June to July, and the second develops from September to October, carrying seasonal health hazards.^6,8

 

Megalopyge opercularis is tapered at the ends and can measure 2.5 to 3.5×1 cm at maturity. It is covered by silky, long-streaked, wavy hairs that may appear single colored or as a mix of colors—from white to gray to brown—forming a mid-dorsal crest.⁶ Beneath this furry coat, rows of short sharp spines are hidden. Upon contact with the human skin, these spines will break and discharge venom.^1,6,8 Toxins contained within the hollow spines are thought to be produced by specialized basal cells, but there still is little knowledge about the dynamics and composition of the venom.¹

Clinical Manifestations

The severity of the reaction depends on the caterpillar’s size and the extent of contact.^1,4 Contact with M opercularis instantly presents with a throbbing or burning pain that may be followed by localized erythema and rash.^1,6 A characteristic gridlike pattern of erythematous macules develops, reflecting each site of puncture from the insect’s spines (Figure 2).^8,9 Skin lesions can progress from erythematous macules to hemorrhagic vesicles or pustules, usually self-resolving after a few days. The reaction also can present with radiating pain to regional lymph nodes and numbness of the affected area.^1,6,8 Moreover, some patients may report urticaria and pruritus.⁹

Envenomation by a puss caterpillar also can present with systemic manifestations including fever, headache, nausea, vomiting, shocklike symptoms, and seizures.^1,6,7 Anaphylactic reaction is rare but also can present.⁷ Uncommon cases have been reported with severe abdominal pain and muscle spasm mimicking acute appendicitis and latrodectism, respectively.^7,9

Diagnosis

The diagnosis of M opercularis envenomation is made clinically based on the morphology of the skin lesions and a history of probable exposure. Coexistent leukocytosis is likely, but laboratory testing is not warranted, as it is both nonspecific and insensitive.⁹

Management/Treatment

The most commonly reported immediate approaches to treatment involve attempts to remove the spines from the skin with tape (stripping), application of ice packs over the affected area, oral antihistamines, topical and intralesional anesthetics, regional nerve block, and oral analgesics.^6,9 There have been several cases detailing the successful use of parenteral calcium gluconate,^5,7 and diazepam has been used to treat severe muscle spasms. Anaphylactic reactions should be managed in a controlled monitored setting with subcutaneous epinephrine.⁷ Despite their common use, some data suggest that ice packs and mid- to high-potency topical steroids are ineffective.⁹

Incidence

From 2001 to 2005, a mean average of 94,552 annual cases of animal bites and stings were reported to poison control centers in the United States, of which 2094 were linked to caterpillars in this 5-year period.¹⁰ There were 3484 M opercularis caterpillar stings reported to the Texas Poison Center Network from 2000 to 2016.^5,6 Given their ability to sting throughout their life cycle, thousands of M opercularis caterpillar stings can occur each year.^1,6 Existing literature on M opercularis caterpillar stings mainly involves case reports with affections of the skin and oral mucosa, self-reported envenomation, and case studies.^5,6,8

Although multiple health concerns associated with caterpillar envenomation have been reported worldwide, the lack of official epidemiologic reports highly suggests that this problem remains underestimated. There also may be many unreported cases because certain reactions are mild or self-limited and can even go unnoticed.¹¹ Nonetheless, there is an evident rise of cases reported in the United States. According to the 2018 annual report of the American Association of Poison Control Centers, there were 2815 case mentions from caterpillar envenomation.¹²

In 1921 and 1952, some public schools in Texas were temporarily closed due to outbreaks of puss caterpillar–associated dermatitis.⁸ Similar outbreaks also have been reported in South Carolina, Virginia, and Oklahoma.⁹ Emerging data suggest that plant oil products and the pesticide cypermethrin may be helpful in controlling local infestations of the puss caterpillar.⁸

Lepidoptera is the second largest order of the class Insecta and comprises approximately 160,000 species of butterflies and moths classified among approximately 124 families and subfamilies. Venomous properties have been identified in 12 of these families, posing a serious threat to human health. ¹

The clinical manifestations from Lepidoptera envenomation can range from general systemic symptoms such as fever and abdominal distress; to more complex focal affections including hemorrhage, ophthalmologic lesions, and irritation of the respiratory tracts; to less severe reactions of the skin, which are the most common presentation.¹

Terminology

Lepidopterism is the term used to address a clinical spectrum of systemic manifestations from direct contact with venomous butterflies or moths and/or their products.² Conversely, erucism is a term used to describe localized cutaneous reactions after direct contact with toxins from caterpillars.

Lepidopterism is derived from the Greek roots lepis, meaning scale, and pteron, meaning wing. The term erucism stems from the Latin word eruca, which means larva.²

Ideally, lepidopterism should refer solely to reactions from butterflies and moths—adult forms of insects with scaly wings—while erucism should refer to reactions from contact with caterpillars—the larval form of butterflies and moths.

In common use, lepidopterism can describe any reaction from caterpillars, moths, or adult butterflies, as well as any case of Lepidoptera exposure with only systemic manifestations, regardless of cutaneous findings. Concurrently, erucism has been defined as either any reaction from caterpillars or any skin reaction from contact with caterpillars or moths.²

Because caterpillars are the larval form of butterflies and moths, caterpillar-associated skin reactions also have been conveniently denominated caterpillar dermatitis.¹ Henceforth in this article, both terms erucism and caterpillar dermatitis are used interchangeably.

Caterpillar Envenomation

Caterpillars cause the vast majority of adverse events from lepidopteran exposures.² Envenomation by caterpillars might stand as the world’s most common envenomation given the larvae proximity to humans.³ Although involvement of internal organs (eg, renal failure), cerebral hemorrhage, and joint lesions can occur, skin manifestations are more predominant with the majority of species. Initial localized pain, edema, and erythema usually are present at the site of direct contact and subsequently progress toward maculopapular to bullous lesions, erosions, petechiae, necrosis, and ulceration depending on the offending species.^1,4

Megalopyge opercularis

In the United States, more than 50 species of caterpillars have been identified as poisonous or venomous.⁵ Megalopyge opercularis (Figure 1), the larval form of the flannel moth, is an important cause of caterpillar-associated dermatitis in the southern United States.^6,7 Megalopyge opercularis also is commonly known as the puss caterpillar, opossum bug, wooly slug, el perrito, tree asp, or Italian asp.⁶ This lepidopteran insect is mainly found in the southeastern and southcentral United States, with noted particular abundance in Texas, Louisiana, and Florida.^6,8 The puss caterpillar has 2 generations per year; the first develops during the months of June to July, and the second develops from September to October, carrying seasonal health hazards.^6,8

 

Megalopyge opercularis is tapered at the ends and can measure 2.5 to 3.5×1 cm at maturity. It is covered by silky, long-streaked, wavy hairs that may appear single colored or as a mix of colors—from white to gray to brown—forming a mid-dorsal crest.⁶ Beneath this furry coat, rows of short sharp spines are hidden. Upon contact with the human skin, these spines will break and discharge venom.^1,6,8 Toxins contained within the hollow spines are thought to be produced by specialized basal cells, but there still is little knowledge about the dynamics and composition of the venom.¹

Clinical Manifestations

The severity of the reaction depends on the caterpillar’s size and the extent of contact.^1,4 Contact with M opercularis instantly presents with a throbbing or burning pain that may be followed by localized erythema and rash.^1,6 A characteristic gridlike pattern of erythematous macules develops, reflecting each site of puncture from the insect’s spines (Figure 2).^8,9 Skin lesions can progress from erythematous macules to hemorrhagic vesicles or pustules, usually self-resolving after a few days. The reaction also can present with radiating pain to regional lymph nodes and numbness of the affected area.^1,6,8 Moreover, some patients may report urticaria and pruritus.⁹

Envenomation by a puss caterpillar also can present with systemic manifestations including fever, headache, nausea, vomiting, shocklike symptoms, and seizures.^1,6,7 Anaphylactic reaction is rare but also can present.⁷ Uncommon cases have been reported with severe abdominal pain and muscle spasm mimicking acute appendicitis and latrodectism, respectively.^7,9

Diagnosis

The diagnosis of M opercularis envenomation is made clinically based on the morphology of the skin lesions and a history of probable exposure. Coexistent leukocytosis is likely, but laboratory testing is not warranted, as it is both nonspecific and insensitive.⁹

Management/Treatment

The most commonly reported immediate approaches to treatment involve attempts to remove the spines from the skin with tape (stripping), application of ice packs over the affected area, oral antihistamines, topical and intralesional anesthetics, regional nerve block, and oral analgesics.^6,9 There have been several cases detailing the successful use of parenteral calcium gluconate,^5,7 and diazepam has been used to treat severe muscle spasms. Anaphylactic reactions should be managed in a controlled monitored setting with subcutaneous epinephrine.⁷ Despite their common use, some data suggest that ice packs and mid- to high-potency topical steroids are ineffective.⁹

Incidence

From 2001 to 2005, a mean average of 94,552 annual cases of animal bites and stings were reported to poison control centers in the United States, of which 2094 were linked to caterpillars in this 5-year period.¹⁰ There were 3484 M opercularis caterpillar stings reported to the Texas Poison Center Network from 2000 to 2016.^5,6 Given their ability to sting throughout their life cycle, thousands of M opercularis caterpillar stings can occur each year.^1,6 Existing literature on M opercularis caterpillar stings mainly involves case reports with affections of the skin and oral mucosa, self-reported envenomation, and case studies.^5,6,8

Although multiple health concerns associated with caterpillar envenomation have been reported worldwide, the lack of official epidemiologic reports highly suggests that this problem remains underestimated. There also may be many unreported cases because certain reactions are mild or self-limited and can even go unnoticed.¹¹ Nonetheless, there is an evident rise of cases reported in the United States. According to the 2018 annual report of the American Association of Poison Control Centers, there were 2815 case mentions from caterpillar envenomation.¹²

In 1921 and 1952, some public schools in Texas were temporarily closed due to outbreaks of puss caterpillar–associated dermatitis.⁸ Similar outbreaks also have been reported in South Carolina, Virginia, and Oklahoma.⁹ Emerging data suggest that plant oil products and the pesticide cypermethrin may be helpful in controlling local infestations of the puss caterpillar.⁸

Lepidoptera is the second largest order of the class Insecta and comprises approximately 160,000 species of butterflies and moths classified among approximately 124 families and subfamilies. Venomous properties have been identified in 12 of these families, posing a serious threat to human health. ¹

The clinical manifestations from Lepidoptera envenomation can range from general systemic symptoms such as fever and abdominal distress; to more complex focal affections including hemorrhage, ophthalmologic lesions, and irritation of the respiratory tracts; to less severe reactions of the skin, which are the most common presentation.¹

Terminology

Lepidopterism is the term used to address a clinical spectrum of systemic manifestations from direct contact with venomous butterflies or moths and/or their products.² Conversely, erucism is a term used to describe localized cutaneous reactions after direct contact with toxins from caterpillars.

Lepidopterism is derived from the Greek roots lepis, meaning scale, and pteron, meaning wing. The term erucism stems from the Latin word eruca, which means larva.²

Ideally, lepidopterism should refer solely to reactions from butterflies and moths—adult forms of insects with scaly wings—while erucism should refer to reactions from contact with caterpillars—the larval form of butterflies and moths.

In common use, lepidopterism can describe any reaction from caterpillars, moths, or adult butterflies, as well as any case of Lepidoptera exposure with only systemic manifestations, regardless of cutaneous findings. Concurrently, erucism has been defined as either any reaction from caterpillars or any skin reaction from contact with caterpillars or moths.²

Because caterpillars are the larval form of butterflies and moths, caterpillar-associated skin reactions also have been conveniently denominated caterpillar dermatitis.¹ Henceforth in this article, both terms erucism and caterpillar dermatitis are used interchangeably.

Caterpillar Envenomation

Caterpillars cause the vast majority of adverse events from lepidopteran exposures.² Envenomation by caterpillars might stand as the world’s most common envenomation given the larvae proximity to humans.³ Although involvement of internal organs (eg, renal failure), cerebral hemorrhage, and joint lesions can occur, skin manifestations are more predominant with the majority of species. Initial localized pain, edema, and erythema usually are present at the site of direct contact and subsequently progress toward maculopapular to bullous lesions, erosions, petechiae, necrosis, and ulceration depending on the offending species.^1,4

Megalopyge opercularis

In the United States, more than 50 species of caterpillars have been identified as poisonous or venomous.⁵ Megalopyge opercularis (Figure 1), the larval form of the flannel moth, is an important cause of caterpillar-associated dermatitis in the southern United States.^6,7 Megalopyge opercularis also is commonly known as the puss caterpillar, opossum bug, wooly slug, el perrito, tree asp, or Italian asp.⁶ This lepidopteran insect is mainly found in the southeastern and southcentral United States, with noted particular abundance in Texas, Louisiana, and Florida.^6,8 The puss caterpillar has 2 generations per year; the first develops during the months of June to July, and the second develops from September to October, carrying seasonal health hazards.^6,8

 

Megalopyge opercularis is tapered at the ends and can measure 2.5 to 3.5×1 cm at maturity. It is covered by silky, long-streaked, wavy hairs that may appear single colored or as a mix of colors—from white to gray to brown—forming a mid-dorsal crest.⁶ Beneath this furry coat, rows of short sharp spines are hidden. Upon contact with the human skin, these spines will break and discharge venom.^1,6,8 Toxins contained within the hollow spines are thought to be produced by specialized basal cells, but there still is little knowledge about the dynamics and composition of the venom.¹

Clinical Manifestations

The severity of the reaction depends on the caterpillar’s size and the extent of contact.^1,4 Contact with M opercularis instantly presents with a throbbing or burning pain that may be followed by localized erythema and rash.^1,6 A characteristic gridlike pattern of erythematous macules develops, reflecting each site of puncture from the insect’s spines (Figure 2).^8,9 Skin lesions can progress from erythematous macules to hemorrhagic vesicles or pustules, usually self-resolving after a few days. The reaction also can present with radiating pain to regional lymph nodes and numbness of the affected area.^1,6,8 Moreover, some patients may report urticaria and pruritus.⁹

Envenomation by a puss caterpillar also can present with systemic manifestations including fever, headache, nausea, vomiting, shocklike symptoms, and seizures.^1,6,7 Anaphylactic reaction is rare but also can present.⁷ Uncommon cases have been reported with severe abdominal pain and muscle spasm mimicking acute appendicitis and latrodectism, respectively.^7,9

Diagnosis

The diagnosis of M opercularis envenomation is made clinically based on the morphology of the skin lesions and a history of probable exposure. Coexistent leukocytosis is likely, but laboratory testing is not warranted, as it is both nonspecific and insensitive.⁹

Management/Treatment

The most commonly reported immediate approaches to treatment involve attempts to remove the spines from the skin with tape (stripping), application of ice packs over the affected area, oral antihistamines, topical and intralesional anesthetics, regional nerve block, and oral analgesics.^6,9 There have been several cases detailing the successful use of parenteral calcium gluconate,^5,7 and diazepam has been used to treat severe muscle spasms. Anaphylactic reactions should be managed in a controlled monitored setting with subcutaneous epinephrine.⁷ Despite their common use, some data suggest that ice packs and mid- to high-potency topical steroids are ineffective.⁹

Incidence

From 2001 to 2005, a mean average of 94,552 annual cases of animal bites and stings were reported to poison control centers in the United States, of which 2094 were linked to caterpillars in this 5-year period.¹⁰ There were 3484 M opercularis caterpillar stings reported to the Texas Poison Center Network from 2000 to 2016.^5,6 Given their ability to sting throughout their life cycle, thousands of M opercularis caterpillar stings can occur each year.^1,6 Existing literature on M opercularis caterpillar stings mainly involves case reports with affections of the skin and oral mucosa, self-reported envenomation, and case studies.^5,6,8

Although multiple health concerns associated with caterpillar envenomation have been reported worldwide, the lack of official epidemiologic reports highly suggests that this problem remains underestimated. There also may be many unreported cases because certain reactions are mild or self-limited and can even go unnoticed.¹¹ Nonetheless, there is an evident rise of cases reported in the United States. According to the 2018 annual report of the American Association of Poison Control Centers, there were 2815 case mentions from caterpillar envenomation.¹²

In 1921 and 1952, some public schools in Texas were temporarily closed due to outbreaks of puss caterpillar–associated dermatitis.⁸ Similar outbreaks also have been reported in South Carolina, Virginia, and Oklahoma.⁹ Emerging data suggest that plant oil products and the pesticide cypermethrin may be helpful in controlling local infestations of the puss caterpillar.⁸

Epidemiology and Identification

Centruroides is a common genus of bark scorpions in the United States with at least 21 species considered to be medically important, including the closely related Centruroides exilicauda and Centruroides sculpturatus.¹ Scorpions can be recognized by a bulbous sac and pointed stinger at the end of a tail-like abdomen. They also have long lobsterlike pedipalps (pincers) for grasping their prey. Identifying characteristics for C exilicauda and C sculpturatus include a small, slender, yellow to light brown or tan body typically measuring 1.3 to 7.6 cm in length with a subaculear tooth or tubercle at the base of the stinger, a characteristic that is common to all Centruroides species (Figure).² Some variability in size has been shown, with smaller scorpions found in increased elevations and cooler temperatures.^1,3 Both C exilicauda and C sculpturatus are found in northern Mexico as well as the southwestern United States (eg, Arizona, New Mexico, Texas, California, Nevada).¹ They have a preference for residing in or around trees and often are found on the underside of bark, stones, or tables as well as inside shoes or small cracks and crevices. Scorpions typically sting in self-defense, and stings commonly occur when humans attempt to move tables, put on shoes, or walk barefoot in scorpion-infested areas. Most stings occur from the end of spring through the end summer, but many may go unreported.^1,4

The venom of the Centruroides genus includes peptides and proteins that play a fundamental role in toxic activity by impairing potassium, sodium, and calcium ion channels.^1,3 Toxins have been shown to be species specific, functioning either in capturing prey or deterring predators. Intraspecies variability in toxins has been demonstrated, which may complicate the production of adequate antivenin.³ Many have thought that C exilicauda Wood and C sculpturatus Ewing are the same species, and the names have been used synonymously in the past; however, genetic and biochemical studies of their venom components have shown that they are distinct species and that C sculpturatus is the more dangerous of the two.⁵ The median lethal dose 50% of C sculpturatus was found to be 22.7 μg in CD1 mice.⁶

Envenomation and Clinical Manifestations

Stings from C exilicauda and C sculpturatus have been shown to cause fatality in children more often than in adults.⁷ In the United States, Arizona has the highest frequency of serious symptoms of envenomation as well as the highest hospital and intensive care unit admission rates.⁶ Envenomation results in an immediate sharp burning pain followed by numbness.⁴ Wounds can produce some regional lymph node swelling, ecchymosis, paresthesia, and lymphangitis. More often than not, however, wounds have little to no inflammation and are characterized only by pain.⁴ The puncture wound is too small to be seen, and C exilicauda and C sculpturatus venom do not cause local tissue destruction, an important factor in distinguishing it from other scorpion envenomations.

More severe complications that may follow are caused by the neurotoxin released by Centruroides stings. The toxin components can increase the duration and amplitude of the neuronal action potential and enhance the release of neurotransmitters such as acetylcholine and norepinephrine.⁸ Stings can lead to cranial nerve dysfunction and somatic skeletal neuromuscular dysfunction as well as autonomic dysfunction, specifically salivation, fever, tongue and muscle fasciculations, opsoclonus, vomiting, bronchoconstriction, diaphoresis, nystagmus, blurred vision, slurred speech, hypertension, rhabdomyolysis, stridor, wheezing, aspiration, anaphylaxis, and tachycardia, leading to cardiac and respiratory compromise.^4,8 Some patients have experienced a decreased sense of smell or hearing and decreased fine motor movements.⁷ Although pancreatitis may occur with scorpion stings, it is not common for C exilicauda.⁹ Comorbidities such as cardiac disease and substance use disorders contribute to prolonged length of hospital stay and poor outcome.⁸

Treatment

Most Centruroides stings can be managed at home, but patients with more serious symptoms and children younger than 2 years should be taken to a hospital for treatment.⁷ If a patient reports only pain but shows no other signs of neurotoxicity, observation and pain relief with rest, ice, and elevation is appropriate management. Patients with severe manifestations have been treated with various combinations of lorazepam, glycopyrrolate, ipratropium bromide, and ondansetron, but the only treatment definitively shown to decrease time to symptom abatement is antivenin.⁷ It has been demonstrated that C exilicauda and C sculpturatus antivenin is relatively safe.⁷ Most patients, especially adults, do not die from C exilicauda and C sculpturatus stings; therefore, antivenin more commonly is symptom abating than it is lifesaving.¹⁰ In children, time to symptom resolution was decreased to fewer than 4 hours with antivenin, and there is a lower rate of inpatient admission when antivenin is administered.^4,10,11 There is a low incidence of anaphylactic reaction after antivenin, but there have been reported cases of self-limited serum sickness after antivenin use that generally can be managed with antihistamines and corticosteroids.^4,7

Epidemiology and Identification

Centruroides is a common genus of bark scorpions in the United States with at least 21 species considered to be medically important, including the closely related Centruroides exilicauda and Centruroides sculpturatus.¹ Scorpions can be recognized by a bulbous sac and pointed stinger at the end of a tail-like abdomen. They also have long lobsterlike pedipalps (pincers) for grasping their prey. Identifying characteristics for C exilicauda and C sculpturatus include a small, slender, yellow to light brown or tan body typically measuring 1.3 to 7.6 cm in length with a subaculear tooth or tubercle at the base of the stinger, a characteristic that is common to all Centruroides species (Figure).² Some variability in size has been shown, with smaller scorpions found in increased elevations and cooler temperatures.^1,3 Both C exilicauda and C sculpturatus are found in northern Mexico as well as the southwestern United States (eg, Arizona, New Mexico, Texas, California, Nevada).¹ They have a preference for residing in or around trees and often are found on the underside of bark, stones, or tables as well as inside shoes or small cracks and crevices. Scorpions typically sting in self-defense, and stings commonly occur when humans attempt to move tables, put on shoes, or walk barefoot in scorpion-infested areas. Most stings occur from the end of spring through the end summer, but many may go unreported.^1,4

The venom of the Centruroides genus includes peptides and proteins that play a fundamental role in toxic activity by impairing potassium, sodium, and calcium ion channels.^1,3 Toxins have been shown to be species specific, functioning either in capturing prey or deterring predators. Intraspecies variability in toxins has been demonstrated, which may complicate the production of adequate antivenin.³ Many have thought that C exilicauda Wood and C sculpturatus Ewing are the same species, and the names have been used synonymously in the past; however, genetic and biochemical studies of their venom components have shown that they are distinct species and that C sculpturatus is the more dangerous of the two.⁵ The median lethal dose 50% of C sculpturatus was found to be 22.7 μg in CD1 mice.⁶

Envenomation and Clinical Manifestations

Stings from C exilicauda and C sculpturatus have been shown to cause fatality in children more often than in adults.⁷ In the United States, Arizona has the highest frequency of serious symptoms of envenomation as well as the highest hospital and intensive care unit admission rates.⁶ Envenomation results in an immediate sharp burning pain followed by numbness.⁴ Wounds can produce some regional lymph node swelling, ecchymosis, paresthesia, and lymphangitis. More often than not, however, wounds have little to no inflammation and are characterized only by pain.⁴ The puncture wound is too small to be seen, and C exilicauda and C sculpturatus venom do not cause local tissue destruction, an important factor in distinguishing it from other scorpion envenomations.

More severe complications that may follow are caused by the neurotoxin released by Centruroides stings. The toxin components can increase the duration and amplitude of the neuronal action potential and enhance the release of neurotransmitters such as acetylcholine and norepinephrine.⁸ Stings can lead to cranial nerve dysfunction and somatic skeletal neuromuscular dysfunction as well as autonomic dysfunction, specifically salivation, fever, tongue and muscle fasciculations, opsoclonus, vomiting, bronchoconstriction, diaphoresis, nystagmus, blurred vision, slurred speech, hypertension, rhabdomyolysis, stridor, wheezing, aspiration, anaphylaxis, and tachycardia, leading to cardiac and respiratory compromise.^4,8 Some patients have experienced a decreased sense of smell or hearing and decreased fine motor movements.⁷ Although pancreatitis may occur with scorpion stings, it is not common for C exilicauda.⁹ Comorbidities such as cardiac disease and substance use disorders contribute to prolonged length of hospital stay and poor outcome.⁸

Treatment

Most Centruroides stings can be managed at home, but patients with more serious symptoms and children younger than 2 years should be taken to a hospital for treatment.⁷ If a patient reports only pain but shows no other signs of neurotoxicity, observation and pain relief with rest, ice, and elevation is appropriate management. Patients with severe manifestations have been treated with various combinations of lorazepam, glycopyrrolate, ipratropium bromide, and ondansetron, but the only treatment definitively shown to decrease time to symptom abatement is antivenin.⁷ It has been demonstrated that C exilicauda and C sculpturatus antivenin is relatively safe.⁷ Most patients, especially adults, do not die from C exilicauda and C sculpturatus stings; therefore, antivenin more commonly is symptom abating than it is lifesaving.¹⁰ In children, time to symptom resolution was decreased to fewer than 4 hours with antivenin, and there is a lower rate of inpatient admission when antivenin is administered.^4,10,11 There is a low incidence of anaphylactic reaction after antivenin, but there have been reported cases of self-limited serum sickness after antivenin use that generally can be managed with antihistamines and corticosteroids.^4,7

Epidemiology and Identification

Centruroides is a common genus of bark scorpions in the United States with at least 21 species considered to be medically important, including the closely related Centruroides exilicauda and Centruroides sculpturatus.¹ Scorpions can be recognized by a bulbous sac and pointed stinger at the end of a tail-like abdomen. They also have long lobsterlike pedipalps (pincers) for grasping their prey. Identifying characteristics for C exilicauda and C sculpturatus include a small, slender, yellow to light brown or tan body typically measuring 1.3 to 7.6 cm in length with a subaculear tooth or tubercle at the base of the stinger, a characteristic that is common to all Centruroides species (Figure).² Some variability in size has been shown, with smaller scorpions found in increased elevations and cooler temperatures.^1,3 Both C exilicauda and C sculpturatus are found in northern Mexico as well as the southwestern United States (eg, Arizona, New Mexico, Texas, California, Nevada).¹ They have a preference for residing in or around trees and often are found on the underside of bark, stones, or tables as well as inside shoes or small cracks and crevices. Scorpions typically sting in self-defense, and stings commonly occur when humans attempt to move tables, put on shoes, or walk barefoot in scorpion-infested areas. Most stings occur from the end of spring through the end summer, but many may go unreported.^1,4

The venom of the Centruroides genus includes peptides and proteins that play a fundamental role in toxic activity by impairing potassium, sodium, and calcium ion channels.^1,3 Toxins have been shown to be species specific, functioning either in capturing prey or deterring predators. Intraspecies variability in toxins has been demonstrated, which may complicate the production of adequate antivenin.³ Many have thought that C exilicauda Wood and C sculpturatus Ewing are the same species, and the names have been used synonymously in the past; however, genetic and biochemical studies of their venom components have shown that they are distinct species and that C sculpturatus is the more dangerous of the two.⁵ The median lethal dose 50% of C sculpturatus was found to be 22.7 μg in CD1 mice.⁶

Envenomation and Clinical Manifestations

Stings from C exilicauda and C sculpturatus have been shown to cause fatality in children more often than in adults.⁷ In the United States, Arizona has the highest frequency of serious symptoms of envenomation as well as the highest hospital and intensive care unit admission rates.⁶ Envenomation results in an immediate sharp burning pain followed by numbness.⁴ Wounds can produce some regional lymph node swelling, ecchymosis, paresthesia, and lymphangitis. More often than not, however, wounds have little to no inflammation and are characterized only by pain.⁴ The puncture wound is too small to be seen, and C exilicauda and C sculpturatus venom do not cause local tissue destruction, an important factor in distinguishing it from other scorpion envenomations.

More severe complications that may follow are caused by the neurotoxin released by Centruroides stings. The toxin components can increase the duration and amplitude of the neuronal action potential and enhance the release of neurotransmitters such as acetylcholine and norepinephrine.⁸ Stings can lead to cranial nerve dysfunction and somatic skeletal neuromuscular dysfunction as well as autonomic dysfunction, specifically salivation, fever, tongue and muscle fasciculations, opsoclonus, vomiting, bronchoconstriction, diaphoresis, nystagmus, blurred vision, slurred speech, hypertension, rhabdomyolysis, stridor, wheezing, aspiration, anaphylaxis, and tachycardia, leading to cardiac and respiratory compromise.^4,8 Some patients have experienced a decreased sense of smell or hearing and decreased fine motor movements.⁷ Although pancreatitis may occur with scorpion stings, it is not common for C exilicauda.⁹ Comorbidities such as cardiac disease and substance use disorders contribute to prolonged length of hospital stay and poor outcome.⁸

Treatment

Most Centruroides stings can be managed at home, but patients with more serious symptoms and children younger than 2 years should be taken to a hospital for treatment.⁷ If a patient reports only pain but shows no other signs of neurotoxicity, observation and pain relief with rest, ice, and elevation is appropriate management. Patients with severe manifestations have been treated with various combinations of lorazepam, glycopyrrolate, ipratropium bromide, and ondansetron, but the only treatment definitively shown to decrease time to symptom abatement is antivenin.⁷ It has been demonstrated that C exilicauda and C sculpturatus antivenin is relatively safe.⁷ Most patients, especially adults, do not die from C exilicauda and C sculpturatus stings; therefore, antivenin more commonly is symptom abating than it is lifesaving.¹⁰ In children, time to symptom resolution was decreased to fewer than 4 hours with antivenin, and there is a lower rate of inpatient admission when antivenin is administered.^4,10,11 There is a low incidence of anaphylactic reaction after antivenin, but there have been reported cases of self-limited serum sickness after antivenin use that generally can be managed with antihistamines and corticosteroids.^4,7

Epidemiology and Transmission

Pediculus humanus corporis, commonly known as the human body louse, is one in a family of 3 ectoparasites of the same suborder that also encompasses pubic lice (Phthirus pubis) and head lice (Pediculus humanus capitis). Adults are approximately 2 mm in size, with the same life cycle as head lice (Figure 1). They require blood meals roughly 5 times per day and cannot survive longer than 2 days without feeding.¹ Although similar in structure to head lice, body lice differ behaviorally in that they do not reside on their human host’s body; instead, they infest the host’s clothing, localizing to seams (Figure 2), and migrate to the host for blood meals. In fact, based on this behavior, genetic analysis of early human body lice has been used to postulate when clothing was first used by humans as well as to determine early human migration patterns.^2,3

Although clinicians in developed countries may be less familiar with body lice compared to their counterparts, body lice nevertheless remain a global health concern in impoverished, densely populated areas, as well as in homeless populations due to poor hygiene. Transmission frequently occurs via physical contact with an affected individual and his/her personal items (eg, linens) via fomites.^4,5 Body louse infestation is more prevalent in homeless individuals who sleep outside vs in shelters; a history of pubic lice and lack of regular bathing have been reported as additional risk factors.⁶ Outbreaks have been noted in the wake of natural disasters, in the setting of political upheavals, and in refugee camps, as well as in individuals seeking political asylum.⁷ Unlike head and pubic lice, body lice can serve as vectors for infectious diseases including Rickettsia prowazekii (epidemic typhus), Borrelia recurrentis (louse-borne relapsing fever), Bartonella quintana (trench fever), and Yersinia pestis (plague).^5,8,9 Several Acinetobacter species were isolated from nearly one-third of collected body louse specimens in a French study.¹⁰ Additionally, serology for B quintana was found to be positive in up to 30% of cases in one United States urban homeless population.⁴

Clinical Manifestations

Patients often present with generalized pruritus, usually considerably more severe than with P humanus capitis, with lesions concentrated on the trunk.¹¹ In addition to often impetiginized, self-inflicted excoriations, feeding sites may present as erythematous macules (Figure 3), papules, or papular urticaria with a central hemorrhagic punctum. Extensive infestation also can manifest as the colloquial vagabond disease, characterized by postinflammatory hyperpigmentation and thickening of the involved skin. Remarkably, patients also may present with considerable iron-deficiency anemia secondary to high parasite load and large volume blood feeding. Multiple case reports have demonstrated associated morbidity.^12-14 The differential diagnosis for pediculosis may include scabies, lichen simplex chronicus, and eczematous dermatitis, though the clinician should prudently consider whether both scabies and pediculosis may be present, as coexistence is possible.^4,15

 

Diagnosis

Diagnosis can be reached by visualizing adult lice, nymphs, or viable nits on the body or more commonly within inner clothing seams; nits also fluoresce under Wood light.¹⁵ Although dermoscopy has proven useful for increased sensitivity and differentiation between viable and hatched nits, the insects also can be viewed with the unaided eye.¹⁶

Treatment: New Concerns and Strategies

The mainstay of treatment for body lice has long consisted of thorough washing and drying of all clothing and linens in a hot dryer. Treatment can be augmented with the addition of pharmacotherapy, plus antibiotics as warranted for louse-borne disease. Pharmacologic intervention often is used in cases of mass infestation and is similar to head lice.

Options for head lice include topical permethrin, malathion, lindane, spinosad, benzyl alcohol, and ivermectin. Pyrethroids, derived from the chrysanthemum, generally are considered safe for human use with a side-effect profile limited to irritation and allergy¹⁷; however, neurotoxicity and leukemia are clinical concerns, with an association more recently shown between large-volume use of pyrethroids and acute lymphoblastic leukemia.^18,19 Use of lindane is not recommended due to a greater potential for central nervous system neurotoxicity, manifested by seizures, with repeated large surface application. Malathion is problematic due to the risk for mucosal irritation, flammability of some formulations, and theoretical organophosphate poisoning, as its mechanism of action involves inhibition of acetylcholinesterase.¹⁵ However, in the context of head lice treatment, a randomized controlled trial reported no incidence of acetylcholinesterase inhibition.²⁰ Spinosad, manufactured from the soil bacterium Saccharopolyspora spinosa, functions similarly by interfering with the nicotinic acetylcholine receptor and also carries a risk for skin irritation.²¹ Among all the treatment options, we prefer benzyl alcohol, particularly in the context of resistance, as it is effective via a physical mechanism of action and lacks notable neurotoxic effects to the host. Use of benzyl alcohol is approved for patients as young as 6 months; it functions by asphyxiating the lice via paralysis of the respiratory spiracle with occlusion by inert ingredients. Itching, episodic numbness, and scalp or mucosal irritation are possible complications of treatment.²²

Treatment resistance of body lice has increased in recent years, warranting exploration of additional management strategies. Moreover, developing resistance to lindane and malathion has been reported.²³ Resistance to pyrethroids has been attributed to mutations in a voltage-gated sodium channel, one of which was universally present in the sampling of a single population.²⁴ A randomized controlled trial showed that off-label oral ivermectin 400 μg/kg was superior to malathion lotion 0.5% in difficult-to-treat cases of head lice²⁵; utility of oral ivermectin also has been reported in body lice.²⁶ In vitro studies also have shown promise for pursuing synergistic treatment of body lice with both ivermectin and antibiotics.²⁷

A novel primary prophylaxis approach for at-risk homeless individuals recently utilized permethrin-impregnated underwear. Although the intervention provided short-term infestation improvement, longer-term use did not show improvement from placebo and also increased prevalence of permethrin-resistant haplotypes.²

Epidemiology and Transmission

Pediculus humanus corporis, commonly known as the human body louse, is one in a family of 3 ectoparasites of the same suborder that also encompasses pubic lice (Phthirus pubis) and head lice (Pediculus humanus capitis). Adults are approximately 2 mm in size, with the same life cycle as head lice (Figure 1). They require blood meals roughly 5 times per day and cannot survive longer than 2 days without feeding.¹ Although similar in structure to head lice, body lice differ behaviorally in that they do not reside on their human host’s body; instead, they infest the host’s clothing, localizing to seams (Figure 2), and migrate to the host for blood meals. In fact, based on this behavior, genetic analysis of early human body lice has been used to postulate when clothing was first used by humans as well as to determine early human migration patterns.^2,3

Although clinicians in developed countries may be less familiar with body lice compared to their counterparts, body lice nevertheless remain a global health concern in impoverished, densely populated areas, as well as in homeless populations due to poor hygiene. Transmission frequently occurs via physical contact with an affected individual and his/her personal items (eg, linens) via fomites.^4,5 Body louse infestation is more prevalent in homeless individuals who sleep outside vs in shelters; a history of pubic lice and lack of regular bathing have been reported as additional risk factors.⁶ Outbreaks have been noted in the wake of natural disasters, in the setting of political upheavals, and in refugee camps, as well as in individuals seeking political asylum.⁷ Unlike head and pubic lice, body lice can serve as vectors for infectious diseases including Rickettsia prowazekii (epidemic typhus), Borrelia recurrentis (louse-borne relapsing fever), Bartonella quintana (trench fever), and Yersinia pestis (plague).^5,8,9 Several Acinetobacter species were isolated from nearly one-third of collected body louse specimens in a French study.¹⁰ Additionally, serology for B quintana was found to be positive in up to 30% of cases in one United States urban homeless population.⁴

Clinical Manifestations

Patients often present with generalized pruritus, usually considerably more severe than with P humanus capitis, with lesions concentrated on the trunk.¹¹ In addition to often impetiginized, self-inflicted excoriations, feeding sites may present as erythematous macules (Figure 3), papules, or papular urticaria with a central hemorrhagic punctum. Extensive infestation also can manifest as the colloquial vagabond disease, characterized by postinflammatory hyperpigmentation and thickening of the involved skin. Remarkably, patients also may present with considerable iron-deficiency anemia secondary to high parasite load and large volume blood feeding. Multiple case reports have demonstrated associated morbidity.^12-14 The differential diagnosis for pediculosis may include scabies, lichen simplex chronicus, and eczematous dermatitis, though the clinician should prudently consider whether both scabies and pediculosis may be present, as coexistence is possible.^4,15

 

Diagnosis

Diagnosis can be reached by visualizing adult lice, nymphs, or viable nits on the body or more commonly within inner clothing seams; nits also fluoresce under Wood light.¹⁵ Although dermoscopy has proven useful for increased sensitivity and differentiation between viable and hatched nits, the insects also can be viewed with the unaided eye.¹⁶

Treatment: New Concerns and Strategies

The mainstay of treatment for body lice has long consisted of thorough washing and drying of all clothing and linens in a hot dryer. Treatment can be augmented with the addition of pharmacotherapy, plus antibiotics as warranted for louse-borne disease. Pharmacologic intervention often is used in cases of mass infestation and is similar to head lice.

Options for head lice include topical permethrin, malathion, lindane, spinosad, benzyl alcohol, and ivermectin. Pyrethroids, derived from the chrysanthemum, generally are considered safe for human use with a side-effect profile limited to irritation and allergy¹⁷; however, neurotoxicity and leukemia are clinical concerns, with an association more recently shown between large-volume use of pyrethroids and acute lymphoblastic leukemia.^18,19 Use of lindane is not recommended due to a greater potential for central nervous system neurotoxicity, manifested by seizures, with repeated large surface application. Malathion is problematic due to the risk for mucosal irritation, flammability of some formulations, and theoretical organophosphate poisoning, as its mechanism of action involves inhibition of acetylcholinesterase.¹⁵ However, in the context of head lice treatment, a randomized controlled trial reported no incidence of acetylcholinesterase inhibition.²⁰ Spinosad, manufactured from the soil bacterium Saccharopolyspora spinosa, functions similarly by interfering with the nicotinic acetylcholine receptor and also carries a risk for skin irritation.²¹ Among all the treatment options, we prefer benzyl alcohol, particularly in the context of resistance, as it is effective via a physical mechanism of action and lacks notable neurotoxic effects to the host. Use of benzyl alcohol is approved for patients as young as 6 months; it functions by asphyxiating the lice via paralysis of the respiratory spiracle with occlusion by inert ingredients. Itching, episodic numbness, and scalp or mucosal irritation are possible complications of treatment.²²

Treatment resistance of body lice has increased in recent years, warranting exploration of additional management strategies. Moreover, developing resistance to lindane and malathion has been reported.²³ Resistance to pyrethroids has been attributed to mutations in a voltage-gated sodium channel, one of which was universally present in the sampling of a single population.²⁴ A randomized controlled trial showed that off-label oral ivermectin 400 μg/kg was superior to malathion lotion 0.5% in difficult-to-treat cases of head lice²⁵; utility of oral ivermectin also has been reported in body lice.²⁶ In vitro studies also have shown promise for pursuing synergistic treatment of body lice with both ivermectin and antibiotics.²⁷

A novel primary prophylaxis approach for at-risk homeless individuals recently utilized permethrin-impregnated underwear. Although the intervention provided short-term infestation improvement, longer-term use did not show improvement from placebo and also increased prevalence of permethrin-resistant haplotypes.²

Epidemiology and Transmission

Pediculus humanus corporis, commonly known as the human body louse, is one in a family of 3 ectoparasites of the same suborder that also encompasses pubic lice (Phthirus pubis) and head lice (Pediculus humanus capitis). Adults are approximately 2 mm in size, with the same life cycle as head lice (Figure 1). They require blood meals roughly 5 times per day and cannot survive longer than 2 days without feeding.¹ Although similar in structure to head lice, body lice differ behaviorally in that they do not reside on their human host’s body; instead, they infest the host’s clothing, localizing to seams (Figure 2), and migrate to the host for blood meals. In fact, based on this behavior, genetic analysis of early human body lice has been used to postulate when clothing was first used by humans as well as to determine early human migration patterns.^2,3

Although clinicians in developed countries may be less familiar with body lice compared to their counterparts, body lice nevertheless remain a global health concern in impoverished, densely populated areas, as well as in homeless populations due to poor hygiene. Transmission frequently occurs via physical contact with an affected individual and his/her personal items (eg, linens) via fomites.^4,5 Body louse infestation is more prevalent in homeless individuals who sleep outside vs in shelters; a history of pubic lice and lack of regular bathing have been reported as additional risk factors.⁶ Outbreaks have been noted in the wake of natural disasters, in the setting of political upheavals, and in refugee camps, as well as in individuals seeking political asylum.⁷ Unlike head and pubic lice, body lice can serve as vectors for infectious diseases including Rickettsia prowazekii (epidemic typhus), Borrelia recurrentis (louse-borne relapsing fever), Bartonella quintana (trench fever), and Yersinia pestis (plague).^5,8,9 Several Acinetobacter species were isolated from nearly one-third of collected body louse specimens in a French study.¹⁰ Additionally, serology for B quintana was found to be positive in up to 30% of cases in one United States urban homeless population.⁴

Clinical Manifestations

Patients often present with generalized pruritus, usually considerably more severe than with P humanus capitis, with lesions concentrated on the trunk.¹¹ In addition to often impetiginized, self-inflicted excoriations, feeding sites may present as erythematous macules (Figure 3), papules, or papular urticaria with a central hemorrhagic punctum. Extensive infestation also can manifest as the colloquial vagabond disease, characterized by postinflammatory hyperpigmentation and thickening of the involved skin. Remarkably, patients also may present with considerable iron-deficiency anemia secondary to high parasite load and large volume blood feeding. Multiple case reports have demonstrated associated morbidity.^12-14 The differential diagnosis for pediculosis may include scabies, lichen simplex chronicus, and eczematous dermatitis, though the clinician should prudently consider whether both scabies and pediculosis may be present, as coexistence is possible.^4,15

 

Diagnosis

Diagnosis can be reached by visualizing adult lice, nymphs, or viable nits on the body or more commonly within inner clothing seams; nits also fluoresce under Wood light.¹⁵ Although dermoscopy has proven useful for increased sensitivity and differentiation between viable and hatched nits, the insects also can be viewed with the unaided eye.¹⁶

Treatment: New Concerns and Strategies

The mainstay of treatment for body lice has long consisted of thorough washing and drying of all clothing and linens in a hot dryer. Treatment can be augmented with the addition of pharmacotherapy, plus antibiotics as warranted for louse-borne disease. Pharmacologic intervention often is used in cases of mass infestation and is similar to head lice.

Options for head lice include topical permethrin, malathion, lindane, spinosad, benzyl alcohol, and ivermectin. Pyrethroids, derived from the chrysanthemum, generally are considered safe for human use with a side-effect profile limited to irritation and allergy¹⁷; however, neurotoxicity and leukemia are clinical concerns, with an association more recently shown between large-volume use of pyrethroids and acute lymphoblastic leukemia.^18,19 Use of lindane is not recommended due to a greater potential for central nervous system neurotoxicity, manifested by seizures, with repeated large surface application. Malathion is problematic due to the risk for mucosal irritation, flammability of some formulations, and theoretical organophosphate poisoning, as its mechanism of action involves inhibition of acetylcholinesterase.¹⁵ However, in the context of head lice treatment, a randomized controlled trial reported no incidence of acetylcholinesterase inhibition.²⁰ Spinosad, manufactured from the soil bacterium Saccharopolyspora spinosa, functions similarly by interfering with the nicotinic acetylcholine receptor and also carries a risk for skin irritation.²¹ Among all the treatment options, we prefer benzyl alcohol, particularly in the context of resistance, as it is effective via a physical mechanism of action and lacks notable neurotoxic effects to the host. Use of benzyl alcohol is approved for patients as young as 6 months; it functions by asphyxiating the lice via paralysis of the respiratory spiracle with occlusion by inert ingredients. Itching, episodic numbness, and scalp or mucosal irritation are possible complications of treatment.²²

Treatment resistance of body lice has increased in recent years, warranting exploration of additional management strategies. Moreover, developing resistance to lindane and malathion has been reported.²³ Resistance to pyrethroids has been attributed to mutations in a voltage-gated sodium channel, one of which was universally present in the sampling of a single population.²⁴ A randomized controlled trial showed that off-label oral ivermectin 400 μg/kg was superior to malathion lotion 0.5% in difficult-to-treat cases of head lice²⁵; utility of oral ivermectin also has been reported in body lice.²⁶ In vitro studies also have shown promise for pursuing synergistic treatment of body lice with both ivermectin and antibiotics.²⁷

A novel primary prophylaxis approach for at-risk homeless individuals recently utilized permethrin-impregnated underwear. Although the intervention provided short-term infestation improvement, longer-term use did not show improvement from placebo and also increased prevalence of permethrin-resistant haplotypes.²

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.

 

The patient was hospitalized for 4 days until the erythema of the left arm receded and only involved the left second phalanx where he eventually experienced localized skin necrosis (Figures 3 and 4). His thrombocytopenia trended upward from a low of 99,000/µL to 121,000/µL at the time of discharge. During his hospital stay, the patient developed hypertension from which he remained asymptomatic and was treated with lisinopril. The patient was treated with intravenous cefazolin and discharged on oral cephalexin due to an elevation in his white blood cell count on admission (13,600/µL). His cultures remained negative, and on discharge his white blood cell count had normalized (6800/µL) and he was transitioned to oral antibiotics to complete his treatment course. Following a surgical consultation, it was decided that skin debridement of the localized area of necrosis of the index fingertip was not necessary. The area of skin necrosis sloughed uneventfully with no residual functional impairment; however, the patient was left with residual numbness of the left second digit (Figure 5). He did not experience recurrent coagulopathy.

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.

 

The patient was hospitalized for 4 days until the erythema of the left arm receded and only involved the left second phalanx where he eventually experienced localized skin necrosis (Figures 3 and 4). His thrombocytopenia trended upward from a low of 99,000/µL to 121,000/µL at the time of discharge. During his hospital stay, the patient developed hypertension from which he remained asymptomatic and was treated with lisinopril. The patient was treated with intravenous cefazolin and discharged on oral cephalexin due to an elevation in his white blood cell count on admission (13,600/µL). His cultures remained negative, and on discharge his white blood cell count had normalized (6800/µL) and he was transitioned to oral antibiotics to complete his treatment course. Following a surgical consultation, it was decided that skin debridement of the localized area of necrosis of the index fingertip was not necessary. The area of skin necrosis sloughed uneventfully with no residual functional impairment; however, the patient was left with residual numbness of the left second digit (Figure 5). He did not experience recurrent coagulopathy.

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.

 

The patient was hospitalized for 4 days until the erythema of the left arm receded and only involved the left second phalanx where he eventually experienced localized skin necrosis (Figures 3 and 4). His thrombocytopenia trended upward from a low of 99,000/µL to 121,000/µL at the time of discharge. During his hospital stay, the patient developed hypertension from which he remained asymptomatic and was treated with lisinopril. The patient was treated with intravenous cefazolin and discharged on oral cephalexin due to an elevation in his white blood cell count on admission (13,600/µL). His cultures remained negative, and on discharge his white blood cell count had normalized (6800/µL) and he was transitioned to oral antibiotics to complete his treatment course. Following a surgical consultation, it was decided that skin debridement of the localized area of necrosis of the index fingertip was not necessary. The area of skin necrosis sloughed uneventfully with no residual functional impairment; however, the patient was left with residual numbness of the left second digit (Figure 5). He did not experience recurrent coagulopathy.

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.