Environmental Dermatology

Identifying Characteristics and Disease Transmission

Cheyletiella are nonburrowing mites characterized by hooklike anterior palps (Figure 1) that have a worldwide distribution. Human dermatitis is the result of contact with an affected animal and may present as papular or bullous lesions. Cheyletiella blakei affects cats, Cheyletiella parasitovorax is found on rabbits, and Cheyletiella yasguri is found on dogs. The mites live in the outer layer of the epidermis of the host animal and feed on surface debris and tissue fluids.¹ They complete an entire 35-day life cycle on a single animal host. The larval, nymph, and adult male mites die within 48 hours of separation from a host. The female mite and possibly the eggs can live up to 10 days off the host, which makes environmental decontamination a critical part of pest control.² In animals, the mite often produces a subtle dermatitis sometimes called walking dandruff (Figure 2).³ Affected animals also can be asymptomatic, and up to 50% of rabbits in commercial colonies may harbor Cheyletiella or other mites.⁴

The typical human patient with Cheyletiella-associated dermatitis is a female 40 years or younger who presents with grouped pruritic papules.⁵ Although papules usually are grouped on exposed areas, they also may be widespread.^6,7 Bullous eruptions caused by Cheyletiella mites may mimic those found in immunobullous diseases (Figure 3).⁸ Children may experience widespread dermatitis after taking a nap where a dog has slept.⁹ Pet owners, farmers, and veterinarians frequently present with zoonotic mite-induced dermatitis.¹⁰ Arthralgia and peripheral eosinophilia caused by Cheyletiella infestation also has been reported.¹¹

Management of Affected Pets

In a case of human infestation resulting from an affected pet, the implicated pet should be evaluated by a qualified veterinarian. Various diagnostic techniques for animals have been used, including adhesive tape preparations.¹² A rapid knockdown insecticidal spray marketed for use on animals has been used to facilitate collection of mites, but some pets may be susceptible to toxicity from insecticides. The scaly area should be carefully brushed with a toothbrush or fine-tooth comb, and all scales, crust, and hair collected should be placed in a resealable plastic storage bag. When alcohol is added to the bag, most contents will sink, but the mites tend to float. Vacuum cleaners fitted with in-line filters also have been used to collect mites. The filter samples can be treated with hot potassium hydroxide, then floated in a concentrated sugar solution to collect the ectoparasites.¹³ Often, a straightforward approach using a #10 blade to provide a skin scraping from the animal in question is effective.¹⁴

Various treatment modalities may be employed by the veterinarian, including dips or shampoos, as well as fipronil.^15,16 A single application of fipronil 10% has been shown to be highly effective in the elimination of mites after a single application in cats.¹⁷ Oral ivermectin and topical amitraz also have been used.^18,19 A veterinarian should treat the animals, as some are more susceptible to toxicity from topical or systemic agents.

Treatment in Humans

Cheyletiella infestations in humans usually are self-limited and resolve within a few weeks after treatment of the source animal. Symptomatic treatment with antipruritic medications and topical steroids may be of use while awaiting resolution. Identification and treatment of the vector is key to eliminating the infestation and preventing recurrence.

Identifying Characteristics and Disease Transmission

Cheyletiella are nonburrowing mites characterized by hooklike anterior palps (Figure 1) that have a worldwide distribution. Human dermatitis is the result of contact with an affected animal and may present as papular or bullous lesions. Cheyletiella blakei affects cats, Cheyletiella parasitovorax is found on rabbits, and Cheyletiella yasguri is found on dogs. The mites live in the outer layer of the epidermis of the host animal and feed on surface debris and tissue fluids.¹ They complete an entire 35-day life cycle on a single animal host. The larval, nymph, and adult male mites die within 48 hours of separation from a host. The female mite and possibly the eggs can live up to 10 days off the host, which makes environmental decontamination a critical part of pest control.² In animals, the mite often produces a subtle dermatitis sometimes called walking dandruff (Figure 2).³ Affected animals also can be asymptomatic, and up to 50% of rabbits in commercial colonies may harbor Cheyletiella or other mites.⁴

The typical human patient with Cheyletiella-associated dermatitis is a female 40 years or younger who presents with grouped pruritic papules.⁵ Although papules usually are grouped on exposed areas, they also may be widespread.^6,7 Bullous eruptions caused by Cheyletiella mites may mimic those found in immunobullous diseases (Figure 3).⁸ Children may experience widespread dermatitis after taking a nap where a dog has slept.⁹ Pet owners, farmers, and veterinarians frequently present with zoonotic mite-induced dermatitis.¹⁰ Arthralgia and peripheral eosinophilia caused by Cheyletiella infestation also has been reported.¹¹

Management of Affected Pets

In a case of human infestation resulting from an affected pet, the implicated pet should be evaluated by a qualified veterinarian. Various diagnostic techniques for animals have been used, including adhesive tape preparations.¹² A rapid knockdown insecticidal spray marketed for use on animals has been used to facilitate collection of mites, but some pets may be susceptible to toxicity from insecticides. The scaly area should be carefully brushed with a toothbrush or fine-tooth comb, and all scales, crust, and hair collected should be placed in a resealable plastic storage bag. When alcohol is added to the bag, most contents will sink, but the mites tend to float. Vacuum cleaners fitted with in-line filters also have been used to collect mites. The filter samples can be treated with hot potassium hydroxide, then floated in a concentrated sugar solution to collect the ectoparasites.¹³ Often, a straightforward approach using a #10 blade to provide a skin scraping from the animal in question is effective.¹⁴

Various treatment modalities may be employed by the veterinarian, including dips or shampoos, as well as fipronil.^15,16 A single application of fipronil 10% has been shown to be highly effective in the elimination of mites after a single application in cats.¹⁷ Oral ivermectin and topical amitraz also have been used.^18,19 A veterinarian should treat the animals, as some are more susceptible to toxicity from topical or systemic agents.

Treatment in Humans

Cheyletiella infestations in humans usually are self-limited and resolve within a few weeks after treatment of the source animal. Symptomatic treatment with antipruritic medications and topical steroids may be of use while awaiting resolution. Identification and treatment of the vector is key to eliminating the infestation and preventing recurrence.

Identifying Characteristics and Disease Transmission

Cheyletiella are nonburrowing mites characterized by hooklike anterior palps (Figure 1) that have a worldwide distribution. Human dermatitis is the result of contact with an affected animal and may present as papular or bullous lesions. Cheyletiella blakei affects cats, Cheyletiella parasitovorax is found on rabbits, and Cheyletiella yasguri is found on dogs. The mites live in the outer layer of the epidermis of the host animal and feed on surface debris and tissue fluids.¹ They complete an entire 35-day life cycle on a single animal host. The larval, nymph, and adult male mites die within 48 hours of separation from a host. The female mite and possibly the eggs can live up to 10 days off the host, which makes environmental decontamination a critical part of pest control.² In animals, the mite often produces a subtle dermatitis sometimes called walking dandruff (Figure 2).³ Affected animals also can be asymptomatic, and up to 50% of rabbits in commercial colonies may harbor Cheyletiella or other mites.⁴

The typical human patient with Cheyletiella-associated dermatitis is a female 40 years or younger who presents with grouped pruritic papules.⁵ Although papules usually are grouped on exposed areas, they also may be widespread.^6,7 Bullous eruptions caused by Cheyletiella mites may mimic those found in immunobullous diseases (Figure 3).⁸ Children may experience widespread dermatitis after taking a nap where a dog has slept.⁹ Pet owners, farmers, and veterinarians frequently present with zoonotic mite-induced dermatitis.¹⁰ Arthralgia and peripheral eosinophilia caused by Cheyletiella infestation also has been reported.¹¹

Management of Affected Pets

In a case of human infestation resulting from an affected pet, the implicated pet should be evaluated by a qualified veterinarian. Various diagnostic techniques for animals have been used, including adhesive tape preparations.¹² A rapid knockdown insecticidal spray marketed for use on animals has been used to facilitate collection of mites, but some pets may be susceptible to toxicity from insecticides. The scaly area should be carefully brushed with a toothbrush or fine-tooth comb, and all scales, crust, and hair collected should be placed in a resealable plastic storage bag. When alcohol is added to the bag, most contents will sink, but the mites tend to float. Vacuum cleaners fitted with in-line filters also have been used to collect mites. The filter samples can be treated with hot potassium hydroxide, then floated in a concentrated sugar solution to collect the ectoparasites.¹³ Often, a straightforward approach using a #10 blade to provide a skin scraping from the animal in question is effective.¹⁴

Various treatment modalities may be employed by the veterinarian, including dips or shampoos, as well as fipronil.^15,16 A single application of fipronil 10% has been shown to be highly effective in the elimination of mites after a single application in cats.¹⁷ Oral ivermectin and topical amitraz also have been used.^18,19 A veterinarian should treat the animals, as some are more susceptible to toxicity from topical or systemic agents.

Treatment in Humans

Cheyletiella infestations in humans usually are self-limited and resolve within a few weeks after treatment of the source animal. Symptomatic treatment with antipruritic medications and topical steroids may be of use while awaiting resolution. Identification and treatment of the vector is key to eliminating the infestation and preventing recurrence.

The lone star tick (Amblyomma americanum) is distributed throughout much of the eastern United States. It serves as a vector for species of Rickettsia, Ehrlichia, and Borrelia that are an important cause of tick-borne illness (Table). In addition, the bite of the lone star tick can cause impressive local and systemic reactions. Delayed anaphylaxis to ingestion of red meat has been attributed to the bite of A americanum.¹ Herein, we discuss human disease associated with the lone star tick as well as potential tick-control measures.

Tick Characteristics

Lone star ticks are characterized by long anterior mouthparts and an ornate scutum (hard dorsal plate). Widely spaced eyes and posterior festoons also are present. In contrast to some other ticks, adanal plates are absent on the ventral surface in male lone star ticks. Amblyomma americanum demonstrates a single white spot on the female’s scutum (Figure 1). The male has inverted horseshoe markings on the posterior scutum. The female’s scutum often covers only a portion of the body to allow room for engorgement.

Patients usually become aware of tick bites while the tick is still attached to the skin, which provides the physician with an opportunity to identify the tick and discuss tick-control measures as well as symptoms of tick-borne disease. Once the tick has been removed, delayed-type hypersensitivity to the tick antigens continues at the attachment site. Erythema and pruritus can be dramatic. Nodules with a pseudolymphomatous histology can occur. Milder reactions respond to application of topical corticosteroids. More intense reactions may require intralesional corticosteroid injection or even surgical excision.

Most hard ticks have a 3-host life cycle, meaning they attach for one long blood meal during each phase of the life cycle. Because they search for a new host for each blood meal, they are efficient disease vectors. The larval ticks, so-called seed ticks, have 6 legs and feed on small animals. Nymphs and adults feed on larger animals. Nymphs resemble small adult ticks with 8 legs but are sexually immature.

Distribution

Amblyomma americanum has a wide distribution in the United States from Texas to Iowa and as far north as Maine (Figure 2).² Tick attachments often are seen in individuals who work outdoors, especially in areas where new commercial or residential development disrupts the environment and the tick’s usual hosts move out of the area. Hungry ticks are left behind in search of a host.

Disease Transmission

Lone star ticks have been implicated as vectors of Ehrlichia chaffeensis, the agent of human monocytic ehrlichiosis (HME),³ which has been documented from the mid-Atlantic to south-central United States. It may present as a somewhat milder Rocky Mountain spotted fever–like illness with fever and headache or as a life-threatening systemic illness with organ failure. Prompt diagnosis and treatment with a tetracycline has been correlated with a better prognosis.⁴ Immunofluorescent antibody testing and polymerase chain reaction can be used to establish the diagnosis.⁵ Two tick species—A americanum and Dermacentor variabilis—have been implicated as vectors, but A americanum appears to be the major vector.^6,7

The lone star tick also is a vector for Erlichia ewingii, the cause of human ehrlichiosis ewingii. Human ehrlichiosis ewingii is a rare disease that presents similar to HME, with most reported cases occurring in immunocompromised hosts.⁸

A novel member of the Phlebovirus genus, the Heartland virus, was first described in 2 Missouri farmers who presented with symptoms similar to HME but did not respond to doxycycline treatment.⁹ The virus has since been isolated from A americanum adult ticks, implicating them as the major vectors of the disease.¹⁰

Rickettsia parkeri, a cause of spotted fever rickettsiosis, is responsible for an eschar-associated illness in affected individuals.¹¹ The organism has been detected in A americanum ticks collected from the wild. Experiments show the tick is capable of transmitting R parkeri to animals in the laboratory. It is unclear, however, what role A americanum plays in the natural transmission of the disease.¹²

In Missouri, strains of Borrelia have been isolated from A americanum ticks that feed on cottontail rabbits, but it seems unlikely that the tick plays any role in transmission of true Lyme disease^13,14; Borrelia has been shown to have poor survival in the saliva of A americanum beyond 24 hours.¹⁵ Southern tick–associated rash illness is a Lyme disease–like illness with several reported cases due to A americanum.¹⁶ Patients generally present with an erythema migrans–like rash and may have headache, fever, arthralgia, or myalgia.¹⁶ The causative organism remains unclear, though Borrelia lonestari has been implicated.¹⁷ Lone star ticks also transmit tularemia and may transmit Rocky Mountain spotted fever and Q fever.¹³

Bullis fever (first reported at Camp Bullis near San Antonio, Texas) affected huge numbers of military personnel from 1942 to 1943.¹⁸ The causative organism appears to be rickettsial. During one outbreak of Bullis fever, it was noted that A americanum was so numerous that more than 4000 adult ticks were collected under a single juniper tree and more than 1000 ticks were removed from a single soldier who sat in a thicket for 2 hours.¹² No cases of Bullis fever have been reported in recent years,¹² which probably relates to the introduction of fire ants.

Disease Hosts

At Little Rock Air Force Base in Arkansas, A americanum has been a source of Ehrlichia infection. During one outbreak, deer in the area were found to have as many as 2550 ticks per ear,¹⁹ which demonstrates the magnitude of tick infestation in some areas of the United States. Tick infestation is not merely of concern to the US military. Ticks are ubiquitous and can be found on neatly trimmed suburban lawns as well as in rough thickets.

More recently, bites from A americanum have been found to induce allergies to red meat in some patients.¹ IgE antibodies directed against galactose-alpha-1,3-galactose (alpha gal) have been implicated as the cause of this reaction. These antibodies cause delayed-onset anaphylaxis occurring 3 to 6 hours after ingestion of red meat. Tick bites appear to be the most important and perhaps the only cause of IgE antibodies to alpha gal in the United States.¹

Wild white-tailed deer serve as reservoir hosts for several diseases transmitted by A americanum, including HME, human ehrlichiosis ewingii, and Southern tick–associated rash illness.^12,20 Communities located close to wildlife reserves may have higher rates of infection.²¹ Application of acaricides to corn contained in deer feeders has been shown to be an effective method of decreasing local tick populations, which is a potential method for disease control in at-risk areas, though it is costly and time consuming.²²

Tick-Control Measures

Hard ticks produce little urine. Instead, excess water is eliminated via salivation back into the host. Loss of water also occurs through spiracles. Absorption of water from the atmosphere is important for the tick to maintain hydration. The tick produces intensely hygroscopic saliva that absorbs water from surrounding moist air. The humidified saliva is then reingested by the tick. In hot climates, ticks are prone to dehydration unless they can find a source of moist air, usually within a layer of leaf debris.²³ When the leaf debris is stirred by a human walking through the area, the tick can make contact with the human. Therefore, removal of leaf debris is a critical part of tick-control efforts, as it reduces tick numbers by means of dehydration. Tick eggs also require sufficient humidity to hatch. Leaf removal increases the effectiveness of insecticide applications, which would otherwise do little harm to the ticks below if sprayed on top of leaf debris.

Some lone star ticks attach to birds and disseminate widely. Attachments to animal hosts with long-range migration patterns complicate tick-control efforts.²⁴ Animal migration may contribute to the spread of disease from one geographic region to another.

Imported fire ants are voracious eaters that gather and consume ticks eggs. Fire ants provide an excellent natural means of tick control. Tick numbers in places such as Camp Bullis have declined dramatically since the introduction of imported fire ants.²⁵

The lone star tick (Amblyomma americanum) is distributed throughout much of the eastern United States. It serves as a vector for species of Rickettsia, Ehrlichia, and Borrelia that are an important cause of tick-borne illness (Table). In addition, the bite of the lone star tick can cause impressive local and systemic reactions. Delayed anaphylaxis to ingestion of red meat has been attributed to the bite of A americanum.¹ Herein, we discuss human disease associated with the lone star tick as well as potential tick-control measures.

Tick Characteristics

Lone star ticks are characterized by long anterior mouthparts and an ornate scutum (hard dorsal plate). Widely spaced eyes and posterior festoons also are present. In contrast to some other ticks, adanal plates are absent on the ventral surface in male lone star ticks. Amblyomma americanum demonstrates a single white spot on the female’s scutum (Figure 1). The male has inverted horseshoe markings on the posterior scutum. The female’s scutum often covers only a portion of the body to allow room for engorgement.

Patients usually become aware of tick bites while the tick is still attached to the skin, which provides the physician with an opportunity to identify the tick and discuss tick-control measures as well as symptoms of tick-borne disease. Once the tick has been removed, delayed-type hypersensitivity to the tick antigens continues at the attachment site. Erythema and pruritus can be dramatic. Nodules with a pseudolymphomatous histology can occur. Milder reactions respond to application of topical corticosteroids. More intense reactions may require intralesional corticosteroid injection or even surgical excision.

Most hard ticks have a 3-host life cycle, meaning they attach for one long blood meal during each phase of the life cycle. Because they search for a new host for each blood meal, they are efficient disease vectors. The larval ticks, so-called seed ticks, have 6 legs and feed on small animals. Nymphs and adults feed on larger animals. Nymphs resemble small adult ticks with 8 legs but are sexually immature.

Distribution

Amblyomma americanum has a wide distribution in the United States from Texas to Iowa and as far north as Maine (Figure 2).² Tick attachments often are seen in individuals who work outdoors, especially in areas where new commercial or residential development disrupts the environment and the tick’s usual hosts move out of the area. Hungry ticks are left behind in search of a host.

Disease Transmission

Lone star ticks have been implicated as vectors of Ehrlichia chaffeensis, the agent of human monocytic ehrlichiosis (HME),³ which has been documented from the mid-Atlantic to south-central United States. It may present as a somewhat milder Rocky Mountain spotted fever–like illness with fever and headache or as a life-threatening systemic illness with organ failure. Prompt diagnosis and treatment with a tetracycline has been correlated with a better prognosis.⁴ Immunofluorescent antibody testing and polymerase chain reaction can be used to establish the diagnosis.⁵ Two tick species—A americanum and Dermacentor variabilis—have been implicated as vectors, but A americanum appears to be the major vector.^6,7

The lone star tick also is a vector for Erlichia ewingii, the cause of human ehrlichiosis ewingii. Human ehrlichiosis ewingii is a rare disease that presents similar to HME, with most reported cases occurring in immunocompromised hosts.⁸

A novel member of the Phlebovirus genus, the Heartland virus, was first described in 2 Missouri farmers who presented with symptoms similar to HME but did not respond to doxycycline treatment.⁹ The virus has since been isolated from A americanum adult ticks, implicating them as the major vectors of the disease.¹⁰

Rickettsia parkeri, a cause of spotted fever rickettsiosis, is responsible for an eschar-associated illness in affected individuals.¹¹ The organism has been detected in A americanum ticks collected from the wild. Experiments show the tick is capable of transmitting R parkeri to animals in the laboratory. It is unclear, however, what role A americanum plays in the natural transmission of the disease.¹²

In Missouri, strains of Borrelia have been isolated from A americanum ticks that feed on cottontail rabbits, but it seems unlikely that the tick plays any role in transmission of true Lyme disease^13,14; Borrelia has been shown to have poor survival in the saliva of A americanum beyond 24 hours.¹⁵ Southern tick–associated rash illness is a Lyme disease–like illness with several reported cases due to A americanum.¹⁶ Patients generally present with an erythema migrans–like rash and may have headache, fever, arthralgia, or myalgia.¹⁶ The causative organism remains unclear, though Borrelia lonestari has been implicated.¹⁷ Lone star ticks also transmit tularemia and may transmit Rocky Mountain spotted fever and Q fever.¹³

Bullis fever (first reported at Camp Bullis near San Antonio, Texas) affected huge numbers of military personnel from 1942 to 1943.¹⁸ The causative organism appears to be rickettsial. During one outbreak of Bullis fever, it was noted that A americanum was so numerous that more than 4000 adult ticks were collected under a single juniper tree and more than 1000 ticks were removed from a single soldier who sat in a thicket for 2 hours.¹² No cases of Bullis fever have been reported in recent years,¹² which probably relates to the introduction of fire ants.

Disease Hosts

At Little Rock Air Force Base in Arkansas, A americanum has been a source of Ehrlichia infection. During one outbreak, deer in the area were found to have as many as 2550 ticks per ear,¹⁹ which demonstrates the magnitude of tick infestation in some areas of the United States. Tick infestation is not merely of concern to the US military. Ticks are ubiquitous and can be found on neatly trimmed suburban lawns as well as in rough thickets.

More recently, bites from A americanum have been found to induce allergies to red meat in some patients.¹ IgE antibodies directed against galactose-alpha-1,3-galactose (alpha gal) have been implicated as the cause of this reaction. These antibodies cause delayed-onset anaphylaxis occurring 3 to 6 hours after ingestion of red meat. Tick bites appear to be the most important and perhaps the only cause of IgE antibodies to alpha gal in the United States.¹

Wild white-tailed deer serve as reservoir hosts for several diseases transmitted by A americanum, including HME, human ehrlichiosis ewingii, and Southern tick–associated rash illness.^12,20 Communities located close to wildlife reserves may have higher rates of infection.²¹ Application of acaricides to corn contained in deer feeders has been shown to be an effective method of decreasing local tick populations, which is a potential method for disease control in at-risk areas, though it is costly and time consuming.²²

Tick-Control Measures

Hard ticks produce little urine. Instead, excess water is eliminated via salivation back into the host. Loss of water also occurs through spiracles. Absorption of water from the atmosphere is important for the tick to maintain hydration. The tick produces intensely hygroscopic saliva that absorbs water from surrounding moist air. The humidified saliva is then reingested by the tick. In hot climates, ticks are prone to dehydration unless they can find a source of moist air, usually within a layer of leaf debris.²³ When the leaf debris is stirred by a human walking through the area, the tick can make contact with the human. Therefore, removal of leaf debris is a critical part of tick-control efforts, as it reduces tick numbers by means of dehydration. Tick eggs also require sufficient humidity to hatch. Leaf removal increases the effectiveness of insecticide applications, which would otherwise do little harm to the ticks below if sprayed on top of leaf debris.

Some lone star ticks attach to birds and disseminate widely. Attachments to animal hosts with long-range migration patterns complicate tick-control efforts.²⁴ Animal migration may contribute to the spread of disease from one geographic region to another.

Imported fire ants are voracious eaters that gather and consume ticks eggs. Fire ants provide an excellent natural means of tick control. Tick numbers in places such as Camp Bullis have declined dramatically since the introduction of imported fire ants.²⁵

The lone star tick (Amblyomma americanum) is distributed throughout much of the eastern United States. It serves as a vector for species of Rickettsia, Ehrlichia, and Borrelia that are an important cause of tick-borne illness (Table). In addition, the bite of the lone star tick can cause impressive local and systemic reactions. Delayed anaphylaxis to ingestion of red meat has been attributed to the bite of A americanum.¹ Herein, we discuss human disease associated with the lone star tick as well as potential tick-control measures.

Tick Characteristics

Lone star ticks are characterized by long anterior mouthparts and an ornate scutum (hard dorsal plate). Widely spaced eyes and posterior festoons also are present. In contrast to some other ticks, adanal plates are absent on the ventral surface in male lone star ticks. Amblyomma americanum demonstrates a single white spot on the female’s scutum (Figure 1). The male has inverted horseshoe markings on the posterior scutum. The female’s scutum often covers only a portion of the body to allow room for engorgement.

Patients usually become aware of tick bites while the tick is still attached to the skin, which provides the physician with an opportunity to identify the tick and discuss tick-control measures as well as symptoms of tick-borne disease. Once the tick has been removed, delayed-type hypersensitivity to the tick antigens continues at the attachment site. Erythema and pruritus can be dramatic. Nodules with a pseudolymphomatous histology can occur. Milder reactions respond to application of topical corticosteroids. More intense reactions may require intralesional corticosteroid injection or even surgical excision.

Most hard ticks have a 3-host life cycle, meaning they attach for one long blood meal during each phase of the life cycle. Because they search for a new host for each blood meal, they are efficient disease vectors. The larval ticks, so-called seed ticks, have 6 legs and feed on small animals. Nymphs and adults feed on larger animals. Nymphs resemble small adult ticks with 8 legs but are sexually immature.

Distribution

Amblyomma americanum has a wide distribution in the United States from Texas to Iowa and as far north as Maine (Figure 2).² Tick attachments often are seen in individuals who work outdoors, especially in areas where new commercial or residential development disrupts the environment and the tick’s usual hosts move out of the area. Hungry ticks are left behind in search of a host.

Disease Transmission

Lone star ticks have been implicated as vectors of Ehrlichia chaffeensis, the agent of human monocytic ehrlichiosis (HME),³ which has been documented from the mid-Atlantic to south-central United States. It may present as a somewhat milder Rocky Mountain spotted fever–like illness with fever and headache or as a life-threatening systemic illness with organ failure. Prompt diagnosis and treatment with a tetracycline has been correlated with a better prognosis.⁴ Immunofluorescent antibody testing and polymerase chain reaction can be used to establish the diagnosis.⁵ Two tick species—A americanum and Dermacentor variabilis—have been implicated as vectors, but A americanum appears to be the major vector.^6,7

The lone star tick also is a vector for Erlichia ewingii, the cause of human ehrlichiosis ewingii. Human ehrlichiosis ewingii is a rare disease that presents similar to HME, with most reported cases occurring in immunocompromised hosts.⁸

A novel member of the Phlebovirus genus, the Heartland virus, was first described in 2 Missouri farmers who presented with symptoms similar to HME but did not respond to doxycycline treatment.⁹ The virus has since been isolated from A americanum adult ticks, implicating them as the major vectors of the disease.¹⁰

Rickettsia parkeri, a cause of spotted fever rickettsiosis, is responsible for an eschar-associated illness in affected individuals.¹¹ The organism has been detected in A americanum ticks collected from the wild. Experiments show the tick is capable of transmitting R parkeri to animals in the laboratory. It is unclear, however, what role A americanum plays in the natural transmission of the disease.¹²

In Missouri, strains of Borrelia have been isolated from A americanum ticks that feed on cottontail rabbits, but it seems unlikely that the tick plays any role in transmission of true Lyme disease^13,14; Borrelia has been shown to have poor survival in the saliva of A americanum beyond 24 hours.¹⁵ Southern tick–associated rash illness is a Lyme disease–like illness with several reported cases due to A americanum.¹⁶ Patients generally present with an erythema migrans–like rash and may have headache, fever, arthralgia, or myalgia.¹⁶ The causative organism remains unclear, though Borrelia lonestari has been implicated.¹⁷ Lone star ticks also transmit tularemia and may transmit Rocky Mountain spotted fever and Q fever.¹³

Bullis fever (first reported at Camp Bullis near San Antonio, Texas) affected huge numbers of military personnel from 1942 to 1943.¹⁸ The causative organism appears to be rickettsial. During one outbreak of Bullis fever, it was noted that A americanum was so numerous that more than 4000 adult ticks were collected under a single juniper tree and more than 1000 ticks were removed from a single soldier who sat in a thicket for 2 hours.¹² No cases of Bullis fever have been reported in recent years,¹² which probably relates to the introduction of fire ants.

Disease Hosts

At Little Rock Air Force Base in Arkansas, A americanum has been a source of Ehrlichia infection. During one outbreak, deer in the area were found to have as many as 2550 ticks per ear,¹⁹ which demonstrates the magnitude of tick infestation in some areas of the United States. Tick infestation is not merely of concern to the US military. Ticks are ubiquitous and can be found on neatly trimmed suburban lawns as well as in rough thickets.

More recently, bites from A americanum have been found to induce allergies to red meat in some patients.¹ IgE antibodies directed against galactose-alpha-1,3-galactose (alpha gal) have been implicated as the cause of this reaction. These antibodies cause delayed-onset anaphylaxis occurring 3 to 6 hours after ingestion of red meat. Tick bites appear to be the most important and perhaps the only cause of IgE antibodies to alpha gal in the United States.¹

Wild white-tailed deer serve as reservoir hosts for several diseases transmitted by A americanum, including HME, human ehrlichiosis ewingii, and Southern tick–associated rash illness.^12,20 Communities located close to wildlife reserves may have higher rates of infection.²¹ Application of acaricides to corn contained in deer feeders has been shown to be an effective method of decreasing local tick populations, which is a potential method for disease control in at-risk areas, though it is costly and time consuming.²²

Tick-Control Measures

Hard ticks produce little urine. Instead, excess water is eliminated via salivation back into the host. Loss of water also occurs through spiracles. Absorption of water from the atmosphere is important for the tick to maintain hydration. The tick produces intensely hygroscopic saliva that absorbs water from surrounding moist air. The humidified saliva is then reingested by the tick. In hot climates, ticks are prone to dehydration unless they can find a source of moist air, usually within a layer of leaf debris.²³ When the leaf debris is stirred by a human walking through the area, the tick can make contact with the human. Therefore, removal of leaf debris is a critical part of tick-control efforts, as it reduces tick numbers by means of dehydration. Tick eggs also require sufficient humidity to hatch. Leaf removal increases the effectiveness of insecticide applications, which would otherwise do little harm to the ticks below if sprayed on top of leaf debris.

Some lone star ticks attach to birds and disseminate widely. Attachments to animal hosts with long-range migration patterns complicate tick-control efforts.²⁴ Animal migration may contribute to the spread of disease from one geographic region to another.

Imported fire ants are voracious eaters that gather and consume ticks eggs. Fire ants provide an excellent natural means of tick control. Tick numbers in places such as Camp Bullis have declined dramatically since the introduction of imported fire ants.²⁵

Sea urchin injuries are commonly seen in coastal regions near both warm and cold salt water with frequent recreational water activities or fishing. Sea urchins belong to the class Echinoidea with approximately 600 species, of which roughly 80 are poisonous to humans.^1,2 When a human comes in contact with a sea urchin, the spines of the sea urchin (made of calcium carbonate) can penetrate the skin and break off from the sea urchin, becoming embedded in the skin. Injuries from sea urchin spines are most commonly seen on the hands and feet, as the likelihood of contact with a sea urchin is greater on these sites. The severity of sea urchin spine injuries can vary widely, from minimal local trauma and pain to arthritis, synovitis, and occasionally systemic illness.^1,3 It is important to recognize the wide variety of responses to sea urchin spine injuries and the impact of prompt treatment. Many published reports on injuries from sea urchin spines describe arthritis and synovitis from spines in the joints.^1,2,4-6 Fewer reports discuss nonjoint injuries and the dermatologic aspects of sea urchin spine injuries.^3,7,8 We pre-sent a case of a patient with a puncture injury from sea urchin spines that resulted in painful granulomas.

Case Report

A 29-year-old otherwise healthy man was referred to our dermatology clinic by the university student health center due to continued pain in the right thigh. Five weeks prior to presentation to the student health center, the patient had fallen on a sea urchin while snorkeling in Hawaii. Sea urchin spines became lodged in the right thigh, some of which were removed in a local medical clinic in Hawaii. He was given oral antibiotics prior to his return home. A plain film radiograph of the affected area ordered by the student health center showed several punctate and linear densities in the lateral aspect of the right mid thigh (Figure 1). These findings were consistent with sea urchin spines within the superficial soft tissues of the lateral thigh.

At the time of presentation to our dermatology clinic, the patient reported sharp intermittent pain localized to the right thigh. The patient denied any fever, chills, or pain in the joints. On physical examination, there were several firm nodules on the right thigh, ranging from 4 to 20 mm in diameter (Figure 2). The nodules were tender to palpation with some surrounding edema. Drainage was not noted. Several scars were visible at sites of the original puncture injuries and removal of the spines.

Two 6-mm punch biopsies were performed on representative nodules on the right thigh for histopathologic examination. Along with the biopsy tissue, firm, brown-black, linear foreign bodies consistent with sea urchin spines were extracted with forceps (Figure 3). Histopathologic examination revealed a dense, diffuse, mixed inflammatory cell infiltrate in the dermis predominantly composed of lymphocytes, histiocytes, and numerous eosinophils. Proliferation of small vessels was noted. In one of the biopsies, small fragments of necrotic tissue were present. These findings were consistent with granulomatous inflammation and granulation tissue due to a foreign body.

At the time of suture removal 2 weeks later, the biopsied areas were well healed with minimal erythema. The patient reported decreased pain in the involved areas. He was not seen in clinic again due to resolution of the nodules and associated pain.

Comment

Sea urchin spine injuries are commonly seen in coastal regions with frequent participation in recreational and occupational water activities. A wide variety of responses can be seen in sea urchin spine injuries. There generally are 2 types of cutaneous reaction patterns to sea urchin spines: a primary initial reaction and a secondary delayed/granulomatous reaction. When the spines initially penetrate the skin, the primary initial reaction consists of sharp localized pain that worsens with applied pressure. In addition to pain, bleeding, erythema, edema, and myalgia can occur.³ These symptoms typically subside a few hours after complete removal of the spines from the skin.⁶ If some spines remain in the skin, a secondary delayed/granulomatous reaction can occur, which can lead to the formation of granulomas that can manifest as nodules or papules and can be diffuse.

Many patients may think their painful encounter with a sea urchin was just an unfortunate event, but depending on the location of the injury, more serious extracutaneous reactions and chronic symptoms may occur. Some cases have described the development of arthritis and synovitis from the implantation of spines into joints.^1,2,4-6 Other extracutaneous complications include neuropathy and paresthesia, local bone destruction, radiating pain, muscular weakness, and hypotension.³

The severity of the injury also can depend on the sea urchin species and the number of spines implanted. There are approximately 80 poisonous sea urchin species possessing toxins in venomous spines, resulting in edema and change in the leukocyte-endothelial interaction.⁹ Substances identified in the spines include proteins, steroids, serotonin, histamine, and glycosides.^3,9 The number of spines implanted, particularly the number of venomous spines, can lead to more severe complications. Penetration of 15 or more venomous spines can commonly lead to extracutaneous symptoms.³ Another concern, irrespective of species type, is the potential for secondary infection associated with the spine penetration or implantation into the skin. Mycobacterium marinum infections have been reported in some sea urchin granulomas,¹⁰ as well as fungal infection, bacterial infection, and tetanus.³

The diagnosis of sea urchin spine injuries starts with a thorough history and physical examination. A positive history of sea urchin contact suggests the diagnosis, and radiographs can be useful to find the location of the spine(s), especially if there are no visible nodules on the skin. However, small fragments of spine may not be completely observed on plain radiographs. Any signs or symptoms of infection should prompt a culture for confirmation and guidance for management. Cutaneous biopsies can be helpful for both diagnosis confirmation and symptomatic relief. Reported cases have described granulomatous reactions in the vast majority of the histologic specimens, with necrosis an additional common finding.^7,8 Sea urchin granulomas can be of varying types, the majority being foreign-body and sarcoid types.^3,6,7

Treatment of sea urchin spine injuries primarily involves removal of the spines by a physician. Patients may soak the affected areas in warm water prior to the removal of the spines to aid in pain relief. Surgical removal with local anesthesia and cutaneous extraction is a common treatment method, and more extensive surgical removal of the spines is another option, especially in areas around the joints.² The use of liquid nitrogen or skin punch biopsy also have been described as possible methods to remove the spines.^11,12

Conclusion

Sea urchin spine injuries can result in a wide range of cutaneous and systemic complications. Prompt diagnosis and treatment to remove the sea urchin spines can lessen the associated pain and is important in the prevention of more serious complications.

Sea urchin injuries are commonly seen in coastal regions near both warm and cold salt water with frequent recreational water activities or fishing. Sea urchins belong to the class Echinoidea with approximately 600 species, of which roughly 80 are poisonous to humans.^1,2 When a human comes in contact with a sea urchin, the spines of the sea urchin (made of calcium carbonate) can penetrate the skin and break off from the sea urchin, becoming embedded in the skin. Injuries from sea urchin spines are most commonly seen on the hands and feet, as the likelihood of contact with a sea urchin is greater on these sites. The severity of sea urchin spine injuries can vary widely, from minimal local trauma and pain to arthritis, synovitis, and occasionally systemic illness.^1,3 It is important to recognize the wide variety of responses to sea urchin spine injuries and the impact of prompt treatment. Many published reports on injuries from sea urchin spines describe arthritis and synovitis from spines in the joints.^1,2,4-6 Fewer reports discuss nonjoint injuries and the dermatologic aspects of sea urchin spine injuries.^3,7,8 We pre-sent a case of a patient with a puncture injury from sea urchin spines that resulted in painful granulomas.

Case Report

A 29-year-old otherwise healthy man was referred to our dermatology clinic by the university student health center due to continued pain in the right thigh. Five weeks prior to presentation to the student health center, the patient had fallen on a sea urchin while snorkeling in Hawaii. Sea urchin spines became lodged in the right thigh, some of which were removed in a local medical clinic in Hawaii. He was given oral antibiotics prior to his return home. A plain film radiograph of the affected area ordered by the student health center showed several punctate and linear densities in the lateral aspect of the right mid thigh (Figure 1). These findings were consistent with sea urchin spines within the superficial soft tissues of the lateral thigh.

At the time of presentation to our dermatology clinic, the patient reported sharp intermittent pain localized to the right thigh. The patient denied any fever, chills, or pain in the joints. On physical examination, there were several firm nodules on the right thigh, ranging from 4 to 20 mm in diameter (Figure 2). The nodules were tender to palpation with some surrounding edema. Drainage was not noted. Several scars were visible at sites of the original puncture injuries and removal of the spines.

Two 6-mm punch biopsies were performed on representative nodules on the right thigh for histopathologic examination. Along with the biopsy tissue, firm, brown-black, linear foreign bodies consistent with sea urchin spines were extracted with forceps (Figure 3). Histopathologic examination revealed a dense, diffuse, mixed inflammatory cell infiltrate in the dermis predominantly composed of lymphocytes, histiocytes, and numerous eosinophils. Proliferation of small vessels was noted. In one of the biopsies, small fragments of necrotic tissue were present. These findings were consistent with granulomatous inflammation and granulation tissue due to a foreign body.

At the time of suture removal 2 weeks later, the biopsied areas were well healed with minimal erythema. The patient reported decreased pain in the involved areas. He was not seen in clinic again due to resolution of the nodules and associated pain.

Comment

Sea urchin spine injuries are commonly seen in coastal regions with frequent participation in recreational and occupational water activities. A wide variety of responses can be seen in sea urchin spine injuries. There generally are 2 types of cutaneous reaction patterns to sea urchin spines: a primary initial reaction and a secondary delayed/granulomatous reaction. When the spines initially penetrate the skin, the primary initial reaction consists of sharp localized pain that worsens with applied pressure. In addition to pain, bleeding, erythema, edema, and myalgia can occur.³ These symptoms typically subside a few hours after complete removal of the spines from the skin.⁶ If some spines remain in the skin, a secondary delayed/granulomatous reaction can occur, which can lead to the formation of granulomas that can manifest as nodules or papules and can be diffuse.

Many patients may think their painful encounter with a sea urchin was just an unfortunate event, but depending on the location of the injury, more serious extracutaneous reactions and chronic symptoms may occur. Some cases have described the development of arthritis and synovitis from the implantation of spines into joints.^1,2,4-6 Other extracutaneous complications include neuropathy and paresthesia, local bone destruction, radiating pain, muscular weakness, and hypotension.³

The severity of the injury also can depend on the sea urchin species and the number of spines implanted. There are approximately 80 poisonous sea urchin species possessing toxins in venomous spines, resulting in edema and change in the leukocyte-endothelial interaction.⁹ Substances identified in the spines include proteins, steroids, serotonin, histamine, and glycosides.^3,9 The number of spines implanted, particularly the number of venomous spines, can lead to more severe complications. Penetration of 15 or more venomous spines can commonly lead to extracutaneous symptoms.³ Another concern, irrespective of species type, is the potential for secondary infection associated with the spine penetration or implantation into the skin. Mycobacterium marinum infections have been reported in some sea urchin granulomas,¹⁰ as well as fungal infection, bacterial infection, and tetanus.³

The diagnosis of sea urchin spine injuries starts with a thorough history and physical examination. A positive history of sea urchin contact suggests the diagnosis, and radiographs can be useful to find the location of the spine(s), especially if there are no visible nodules on the skin. However, small fragments of spine may not be completely observed on plain radiographs. Any signs or symptoms of infection should prompt a culture for confirmation and guidance for management. Cutaneous biopsies can be helpful for both diagnosis confirmation and symptomatic relief. Reported cases have described granulomatous reactions in the vast majority of the histologic specimens, with necrosis an additional common finding.^7,8 Sea urchin granulomas can be of varying types, the majority being foreign-body and sarcoid types.^3,6,7

Treatment of sea urchin spine injuries primarily involves removal of the spines by a physician. Patients may soak the affected areas in warm water prior to the removal of the spines to aid in pain relief. Surgical removal with local anesthesia and cutaneous extraction is a common treatment method, and more extensive surgical removal of the spines is another option, especially in areas around the joints.² The use of liquid nitrogen or skin punch biopsy also have been described as possible methods to remove the spines.^11,12

Conclusion

Sea urchin spine injuries can result in a wide range of cutaneous and systemic complications. Prompt diagnosis and treatment to remove the sea urchin spines can lessen the associated pain and is important in the prevention of more serious complications.

Sea urchin injuries are commonly seen in coastal regions near both warm and cold salt water with frequent recreational water activities or fishing. Sea urchins belong to the class Echinoidea with approximately 600 species, of which roughly 80 are poisonous to humans.^1,2 When a human comes in contact with a sea urchin, the spines of the sea urchin (made of calcium carbonate) can penetrate the skin and break off from the sea urchin, becoming embedded in the skin. Injuries from sea urchin spines are most commonly seen on the hands and feet, as the likelihood of contact with a sea urchin is greater on these sites. The severity of sea urchin spine injuries can vary widely, from minimal local trauma and pain to arthritis, synovitis, and occasionally systemic illness.^1,3 It is important to recognize the wide variety of responses to sea urchin spine injuries and the impact of prompt treatment. Many published reports on injuries from sea urchin spines describe arthritis and synovitis from spines in the joints.^1,2,4-6 Fewer reports discuss nonjoint injuries and the dermatologic aspects of sea urchin spine injuries.^3,7,8 We pre-sent a case of a patient with a puncture injury from sea urchin spines that resulted in painful granulomas.

Case Report

A 29-year-old otherwise healthy man was referred to our dermatology clinic by the university student health center due to continued pain in the right thigh. Five weeks prior to presentation to the student health center, the patient had fallen on a sea urchin while snorkeling in Hawaii. Sea urchin spines became lodged in the right thigh, some of which were removed in a local medical clinic in Hawaii. He was given oral antibiotics prior to his return home. A plain film radiograph of the affected area ordered by the student health center showed several punctate and linear densities in the lateral aspect of the right mid thigh (Figure 1). These findings were consistent with sea urchin spines within the superficial soft tissues of the lateral thigh.

At the time of presentation to our dermatology clinic, the patient reported sharp intermittent pain localized to the right thigh. The patient denied any fever, chills, or pain in the joints. On physical examination, there were several firm nodules on the right thigh, ranging from 4 to 20 mm in diameter (Figure 2). The nodules were tender to palpation with some surrounding edema. Drainage was not noted. Several scars were visible at sites of the original puncture injuries and removal of the spines.

Two 6-mm punch biopsies were performed on representative nodules on the right thigh for histopathologic examination. Along with the biopsy tissue, firm, brown-black, linear foreign bodies consistent with sea urchin spines were extracted with forceps (Figure 3). Histopathologic examination revealed a dense, diffuse, mixed inflammatory cell infiltrate in the dermis predominantly composed of lymphocytes, histiocytes, and numerous eosinophils. Proliferation of small vessels was noted. In one of the biopsies, small fragments of necrotic tissue were present. These findings were consistent with granulomatous inflammation and granulation tissue due to a foreign body.

At the time of suture removal 2 weeks later, the biopsied areas were well healed with minimal erythema. The patient reported decreased pain in the involved areas. He was not seen in clinic again due to resolution of the nodules and associated pain.

Comment

Sea urchin spine injuries are commonly seen in coastal regions with frequent participation in recreational and occupational water activities. A wide variety of responses can be seen in sea urchin spine injuries. There generally are 2 types of cutaneous reaction patterns to sea urchin spines: a primary initial reaction and a secondary delayed/granulomatous reaction. When the spines initially penetrate the skin, the primary initial reaction consists of sharp localized pain that worsens with applied pressure. In addition to pain, bleeding, erythema, edema, and myalgia can occur.³ These symptoms typically subside a few hours after complete removal of the spines from the skin.⁶ If some spines remain in the skin, a secondary delayed/granulomatous reaction can occur, which can lead to the formation of granulomas that can manifest as nodules or papules and can be diffuse.

Many patients may think their painful encounter with a sea urchin was just an unfortunate event, but depending on the location of the injury, more serious extracutaneous reactions and chronic symptoms may occur. Some cases have described the development of arthritis and synovitis from the implantation of spines into joints.^1,2,4-6 Other extracutaneous complications include neuropathy and paresthesia, local bone destruction, radiating pain, muscular weakness, and hypotension.³

The severity of the injury also can depend on the sea urchin species and the number of spines implanted. There are approximately 80 poisonous sea urchin species possessing toxins in venomous spines, resulting in edema and change in the leukocyte-endothelial interaction.⁹ Substances identified in the spines include proteins, steroids, serotonin, histamine, and glycosides.^3,9 The number of spines implanted, particularly the number of venomous spines, can lead to more severe complications. Penetration of 15 or more venomous spines can commonly lead to extracutaneous symptoms.³ Another concern, irrespective of species type, is the potential for secondary infection associated with the spine penetration or implantation into the skin. Mycobacterium marinum infections have been reported in some sea urchin granulomas,¹⁰ as well as fungal infection, bacterial infection, and tetanus.³

The diagnosis of sea urchin spine injuries starts with a thorough history and physical examination. A positive history of sea urchin contact suggests the diagnosis, and radiographs can be useful to find the location of the spine(s), especially if there are no visible nodules on the skin. However, small fragments of spine may not be completely observed on plain radiographs. Any signs or symptoms of infection should prompt a culture for confirmation and guidance for management. Cutaneous biopsies can be helpful for both diagnosis confirmation and symptomatic relief. Reported cases have described granulomatous reactions in the vast majority of the histologic specimens, with necrosis an additional common finding.^7,8 Sea urchin granulomas can be of varying types, the majority being foreign-body and sarcoid types.^3,6,7

Treatment of sea urchin spine injuries primarily involves removal of the spines by a physician. Patients may soak the affected areas in warm water prior to the removal of the spines to aid in pain relief. Surgical removal with local anesthesia and cutaneous extraction is a common treatment method, and more extensive surgical removal of the spines is another option, especially in areas around the joints.² The use of liquid nitrogen or skin punch biopsy also have been described as possible methods to remove the spines.^11,12

Conclusion

Sea urchin spine injuries can result in a wide range of cutaneous and systemic complications. Prompt diagnosis and treatment to remove the sea urchin spines can lessen the associated pain and is important in the prevention of more serious complications.

Case Report

A 44-year-old woman presented with a localized patch of hair loss on the frontal scalp of several month’s duration. She had been bitten by a tick at this site during the summer. Two months later a primary care provider prescribed triamcinolone cream because of intense itching at the bite site. The patient returned to her primary care provider 2 weeks later due to persistent itching, hyperpigmentation, and hair loss. At that time, the clinician probed the central portion of the lesion because of a concern for retained tick parts. A few weeks later, a dermatologist evaluated the patient and found a roughly circular zone of alopecia measuring approximately 5 cm in diameter that was just posterior to the left frontal hairline (Figure 1). In the center of the plaque there was a small eschar surrounded by a zone of hyperpigmentation, mild induration, and almost complete loss of terminal hairs. At the periphery of the lesion, hair density gradually increased and skin pigmentation normalized.

A punch biopsy was obtained from an indurated area of hyperpigmentation adjacent to the eschar. Both vertical and horizontal sections were obtained, revealing a relatively normal epidermis, a marked decrease in follicular structures with loss of sebaceous glands, and dense perifollicular lymphocytic inflammation with a few scattered eosinophils (Figures 2 and 3).

Historical Perspective

Tick bite alopecia was first described in the French literature in 1921¹ and in the English-language literature in 1955.² A few additional cases were subsequently reported.^3-5 In 2008, Castelli et al⁶ described the histologic and immunohistochemical features of 25 tick bite cases, a few of which resulted in alopecia. Other than these reports, little original information has been written about tick bite alopecia.

Clinical and Histologic Presentation

Tick bite alopecia is well described in the veterinary literature.^7-9 It is possible that the condition is underreported in humans because the cause is often obvious or the alopecia is never discovered. The typical presentation is a roughly oval zone of alopecia that develops 1 to 2 weeks after the removal of a tick from the scalp. Often there is a small central eschar representing the site of tick attachment and the surrounding scalp may appear scaly. In one report of 2 siblings, multiple oval zones of alopecia resembling the moth-eaten alopecia of syphilis were noted in both patients, but only a single attached tick was found.² In some reported cases, hair loss was only temporary, and at least partial if not complete regrowth of hair occurred.^3,4 Follow-up on most cases is not provided, but to our knowledge permanent alopecia has not been described.

Information about the histologic findings of tick bite alopecia is particularly limited. In a report by Heyl,³ biopsies were conducted in 2 patients, but the areas selected for biopsy were the sites of tick attachment. Centrally dense, acute, and chronic inflammation was seen, as well as marked tissue necrosis of the connective tissue and hair follicles. Peripheral to the attachment zone, tissue necrosis was not found, but telogen hairs with “crumpled up hair shafts” were present.³ The histologic findings presented by Castelli et al⁶ were based on a single case of tick bite alopecia; however, the specimen was a generous excisional biopsy, allowing for a panoramic histologic view of the lesion. In the center of the specimen, hair follicles were absent, but residual follicular streamers and follicular remnants were surrounded by lymphocytic inflammation. Sebaceous glands were conspicuously absent, but foci with naked hairs, fibrosis, and granulomatous inflammation were seen. Peripherally, the hair follicles were thinned and miniaturized with an increased number of catagen/telogen hairs. Some follicles showed lamellar fibroplasia and perifollicular chronic inflammation. The inflammatory infiltrate consisted predominantly of helper T cells with a smaller population of B lymphocytes and a few plasma cells.⁶ In 2016, Lynch et al⁵ described a single case of tick bite alopecia and noted pseudolymphomatous inflammation with germinal center formation associated with hair miniaturization and an elevated catagen/telogen count; focal follicular mucinosis also was noted.Our histologic findings are similar to those of Castelli et al,⁶ except that the inflammatory infiltrate was clearly B-cell dominant, with a suggestion of germinal center formation, as noted by Lynch et al.⁵ This inflammatory pattern often can be encountered in a chronic tick bite lesion. Destruction of follicles and associated sebaceous glands and their replacement by follicular scars indicate that at least in the central portion of the lesion some permanent hair loss occurs. The presence of catagen/telogen hairs and miniaturized follicles indicates the potential for at least partial regrowth.

Similar to other investigators who have described tick bite alopecia, we can only speculate as to the mechanism by which clinical alopecia occurs. Given the density of the inflammatory infiltrate and perifollicular inflammation, it seems reasonable to assume that inflammation either destroys hair follicles or precipitates the catagen/telogen phase, resulting in temporary hair loss. The inflammation itself may be due to the presence of tick parts or the antigens in their saliva (or both). The delay between tick attachment and the onset of alopecia can be attributed to the time it takes follicles to cycle into the catagen/telogen phase and shed the hair shaft.

Case Report

A 44-year-old woman presented with a localized patch of hair loss on the frontal scalp of several month’s duration. She had been bitten by a tick at this site during the summer. Two months later a primary care provider prescribed triamcinolone cream because of intense itching at the bite site. The patient returned to her primary care provider 2 weeks later due to persistent itching, hyperpigmentation, and hair loss. At that time, the clinician probed the central portion of the lesion because of a concern for retained tick parts. A few weeks later, a dermatologist evaluated the patient and found a roughly circular zone of alopecia measuring approximately 5 cm in diameter that was just posterior to the left frontal hairline (Figure 1). In the center of the plaque there was a small eschar surrounded by a zone of hyperpigmentation, mild induration, and almost complete loss of terminal hairs. At the periphery of the lesion, hair density gradually increased and skin pigmentation normalized.

A punch biopsy was obtained from an indurated area of hyperpigmentation adjacent to the eschar. Both vertical and horizontal sections were obtained, revealing a relatively normal epidermis, a marked decrease in follicular structures with loss of sebaceous glands, and dense perifollicular lymphocytic inflammation with a few scattered eosinophils (Figures 2 and 3).

Historical Perspective

Tick bite alopecia was first described in the French literature in 1921¹ and in the English-language literature in 1955.² A few additional cases were subsequently reported.^3-5 In 2008, Castelli et al⁶ described the histologic and immunohistochemical features of 25 tick bite cases, a few of which resulted in alopecia. Other than these reports, little original information has been written about tick bite alopecia.

Clinical and Histologic Presentation

Tick bite alopecia is well described in the veterinary literature.^7-9 It is possible that the condition is underreported in humans because the cause is often obvious or the alopecia is never discovered. The typical presentation is a roughly oval zone of alopecia that develops 1 to 2 weeks after the removal of a tick from the scalp. Often there is a small central eschar representing the site of tick attachment and the surrounding scalp may appear scaly. In one report of 2 siblings, multiple oval zones of alopecia resembling the moth-eaten alopecia of syphilis were noted in both patients, but only a single attached tick was found.² In some reported cases, hair loss was only temporary, and at least partial if not complete regrowth of hair occurred.^3,4 Follow-up on most cases is not provided, but to our knowledge permanent alopecia has not been described.

Information about the histologic findings of tick bite alopecia is particularly limited. In a report by Heyl,³ biopsies were conducted in 2 patients, but the areas selected for biopsy were the sites of tick attachment. Centrally dense, acute, and chronic inflammation was seen, as well as marked tissue necrosis of the connective tissue and hair follicles. Peripheral to the attachment zone, tissue necrosis was not found, but telogen hairs with “crumpled up hair shafts” were present.³ The histologic findings presented by Castelli et al⁶ were based on a single case of tick bite alopecia; however, the specimen was a generous excisional biopsy, allowing for a panoramic histologic view of the lesion. In the center of the specimen, hair follicles were absent, but residual follicular streamers and follicular remnants were surrounded by lymphocytic inflammation. Sebaceous glands were conspicuously absent, but foci with naked hairs, fibrosis, and granulomatous inflammation were seen. Peripherally, the hair follicles were thinned and miniaturized with an increased number of catagen/telogen hairs. Some follicles showed lamellar fibroplasia and perifollicular chronic inflammation. The inflammatory infiltrate consisted predominantly of helper T cells with a smaller population of B lymphocytes and a few plasma cells.⁶ In 2016, Lynch et al⁵ described a single case of tick bite alopecia and noted pseudolymphomatous inflammation with germinal center formation associated with hair miniaturization and an elevated catagen/telogen count; focal follicular mucinosis also was noted.Our histologic findings are similar to those of Castelli et al,⁶ except that the inflammatory infiltrate was clearly B-cell dominant, with a suggestion of germinal center formation, as noted by Lynch et al.⁵ This inflammatory pattern often can be encountered in a chronic tick bite lesion. Destruction of follicles and associated sebaceous glands and their replacement by follicular scars indicate that at least in the central portion of the lesion some permanent hair loss occurs. The presence of catagen/telogen hairs and miniaturized follicles indicates the potential for at least partial regrowth.

Similar to other investigators who have described tick bite alopecia, we can only speculate as to the mechanism by which clinical alopecia occurs. Given the density of the inflammatory infiltrate and perifollicular inflammation, it seems reasonable to assume that inflammation either destroys hair follicles or precipitates the catagen/telogen phase, resulting in temporary hair loss. The inflammation itself may be due to the presence of tick parts or the antigens in their saliva (or both). The delay between tick attachment and the onset of alopecia can be attributed to the time it takes follicles to cycle into the catagen/telogen phase and shed the hair shaft.

Case Report

A 44-year-old woman presented with a localized patch of hair loss on the frontal scalp of several month’s duration. She had been bitten by a tick at this site during the summer. Two months later a primary care provider prescribed triamcinolone cream because of intense itching at the bite site. The patient returned to her primary care provider 2 weeks later due to persistent itching, hyperpigmentation, and hair loss. At that time, the clinician probed the central portion of the lesion because of a concern for retained tick parts. A few weeks later, a dermatologist evaluated the patient and found a roughly circular zone of alopecia measuring approximately 5 cm in diameter that was just posterior to the left frontal hairline (Figure 1). In the center of the plaque there was a small eschar surrounded by a zone of hyperpigmentation, mild induration, and almost complete loss of terminal hairs. At the periphery of the lesion, hair density gradually increased and skin pigmentation normalized.

A punch biopsy was obtained from an indurated area of hyperpigmentation adjacent to the eschar. Both vertical and horizontal sections were obtained, revealing a relatively normal epidermis, a marked decrease in follicular structures with loss of sebaceous glands, and dense perifollicular lymphocytic inflammation with a few scattered eosinophils (Figures 2 and 3).

Historical Perspective

Tick bite alopecia was first described in the French literature in 1921¹ and in the English-language literature in 1955.² A few additional cases were subsequently reported.^3-5 In 2008, Castelli et al⁶ described the histologic and immunohistochemical features of 25 tick bite cases, a few of which resulted in alopecia. Other than these reports, little original information has been written about tick bite alopecia.

Clinical and Histologic Presentation

Tick bite alopecia is well described in the veterinary literature.^7-9 It is possible that the condition is underreported in humans because the cause is often obvious or the alopecia is never discovered. The typical presentation is a roughly oval zone of alopecia that develops 1 to 2 weeks after the removal of a tick from the scalp. Often there is a small central eschar representing the site of tick attachment and the surrounding scalp may appear scaly. In one report of 2 siblings, multiple oval zones of alopecia resembling the moth-eaten alopecia of syphilis were noted in both patients, but only a single attached tick was found.² In some reported cases, hair loss was only temporary, and at least partial if not complete regrowth of hair occurred.^3,4 Follow-up on most cases is not provided, but to our knowledge permanent alopecia has not been described.

Information about the histologic findings of tick bite alopecia is particularly limited. In a report by Heyl,³ biopsies were conducted in 2 patients, but the areas selected for biopsy were the sites of tick attachment. Centrally dense, acute, and chronic inflammation was seen, as well as marked tissue necrosis of the connective tissue and hair follicles. Peripheral to the attachment zone, tissue necrosis was not found, but telogen hairs with “crumpled up hair shafts” were present.³ The histologic findings presented by Castelli et al⁶ were based on a single case of tick bite alopecia; however, the specimen was a generous excisional biopsy, allowing for a panoramic histologic view of the lesion. In the center of the specimen, hair follicles were absent, but residual follicular streamers and follicular remnants were surrounded by lymphocytic inflammation. Sebaceous glands were conspicuously absent, but foci with naked hairs, fibrosis, and granulomatous inflammation were seen. Peripherally, the hair follicles were thinned and miniaturized with an increased number of catagen/telogen hairs. Some follicles showed lamellar fibroplasia and perifollicular chronic inflammation. The inflammatory infiltrate consisted predominantly of helper T cells with a smaller population of B lymphocytes and a few plasma cells.⁶ In 2016, Lynch et al⁵ described a single case of tick bite alopecia and noted pseudolymphomatous inflammation with germinal center formation associated with hair miniaturization and an elevated catagen/telogen count; focal follicular mucinosis also was noted.Our histologic findings are similar to those of Castelli et al,⁶ except that the inflammatory infiltrate was clearly B-cell dominant, with a suggestion of germinal center formation, as noted by Lynch et al.⁵ This inflammatory pattern often can be encountered in a chronic tick bite lesion. Destruction of follicles and associated sebaceous glands and their replacement by follicular scars indicate that at least in the central portion of the lesion some permanent hair loss occurs. The presence of catagen/telogen hairs and miniaturized follicles indicates the potential for at least partial regrowth.

Similar to other investigators who have described tick bite alopecia, we can only speculate as to the mechanism by which clinical alopecia occurs. Given the density of the inflammatory infiltrate and perifollicular inflammation, it seems reasonable to assume that inflammation either destroys hair follicles or precipitates the catagen/telogen phase, resulting in temporary hair loss. The inflammation itself may be due to the presence of tick parts or the antigens in their saliva (or both). The delay between tick attachment and the onset of alopecia can be attributed to the time it takes follicles to cycle into the catagen/telogen phase and shed the hair shaft.

Case Report

An 18-year-old Iranian man presented to the dermatology clinic with hair loss of 1 night’s duration. He denied pruritus, pain, discharge, or flaking. The patient had no notable personal, family, or surgical history and was not currently taking any medications. He denied recent travel. The patient reported that he found hair on his pillow upon waking up in the morning prior to coming to the clinic. On physical examination, 2 ants 
(Figure 1) were found on the scalp and alopecia with a vertical linear distribution was noted (Figure 2). Hairs of various lengths were found on the scalp within the distribution of the alopecia. No excoriations, crusting, seborrhea, or other areas of hair loss were detected. Wood lamp examination was negative. Based on these findings, which were concordant with similar findings from prior reports,^1-4 a diagnosis of ant-induced alopecia was made. Hair regrowth was noted within 1 week with full appearance of normal-length hair within 2.5 weeks.

Comment

Ant-induced alopecia is a form of localized hair loss caused by the Pheidole genus, the second largest genus of ants in the world.⁵ These ants can be found worldwide, but most cases of ant-induced alopecia have been from Iran, with at least 1 reported case from Turkey.^1-4,6 An early case series of ant-induced alopecia was reported in 1999,⁶ but the causative species was not described at that time.

The majority of reported cases of ant-induced alopecia are attributed to the barber ant (Pheidole pallidula). This type of alopecia is caused by worker ants within the species hierarchy.^1,4,6 The P pallidula worker ants are dimorphic and are classified as major and minor workers.⁷ Major workers have body lengths ranging up to 6 mm, whereas minor workers have body lengths ranging up to 4 mm. Major workers have larger heads and mandibles than minor workers and also have up to 2 pairs of denticles on the cranium.⁵ The minor workers are foragers and mainly collect food, whereas the major workers defend the nest and store food.⁸ These ants have widespread habitats with the ability to live in indoor and outdoor environments.

The presentation of hair loss caused by these ants is acute. Hair loss usually is confined to one specific area. Some patients may report pruritus or may present with erythematous lesions from ant stings or manual scratching.⁵ None of these signs or symptoms were seen in our patient. Some investigators have suggested that the barber ant is attracted to the hair of individuals with seborrheic dermatitis,¹ but our patient had no medical history of seborrheic dermatitis. Most likely, ants are attracted to excess sebum on the scalp in select individuals in their search for food and cause localized hair destruction.

Localized hair loss, as depicted in our case, should warrant a thorough evaluation for alopecia areata, trichotillomania, and tinea capitis.⁹ Alopecia areata should be considered in individuals with multiple focal patches of hair loss that have a positive hair pull test from peripheral sites of active lesions. Tinea capitis usually has localized sites of hair loss with underlying scaling, crusting, pruritus, erythema, and discharge from lesions, with positive potassium hydroxide preparations or fungal cultures. Trichotillomania typically presents with a spared peripheral fringe of hair. Remaining hairs may be thick and hyperpigmented as a response to repeated pulling, and biopsy often demonstrates fracture or degeneration of the hair shaft. A psychiatric evaluation may be warranted in cases of trichotillomania. Other cases of arthropod-induced hair loss include tick bite alopecia^10,11 and hair loss induced by numerous honeybee stings,¹² and these diagnoses should be suspected in patients with a history of ants on their pillow or in those from endemic areas.

No specific treatment is indicated in cases of 
ant-induced alopecia because hair usually regrows to its normal length without intervention.

Case Report

An 18-year-old Iranian man presented to the dermatology clinic with hair loss of 1 night’s duration. He denied pruritus, pain, discharge, or flaking. The patient had no notable personal, family, or surgical history and was not currently taking any medications. He denied recent travel. The patient reported that he found hair on his pillow upon waking up in the morning prior to coming to the clinic. On physical examination, 2 ants 
(Figure 1) were found on the scalp and alopecia with a vertical linear distribution was noted (Figure 2). Hairs of various lengths were found on the scalp within the distribution of the alopecia. No excoriations, crusting, seborrhea, or other areas of hair loss were detected. Wood lamp examination was negative. Based on these findings, which were concordant with similar findings from prior reports,^1-4 a diagnosis of ant-induced alopecia was made. Hair regrowth was noted within 1 week with full appearance of normal-length hair within 2.5 weeks.

Comment

Ant-induced alopecia is a form of localized hair loss caused by the Pheidole genus, the second largest genus of ants in the world.⁵ These ants can be found worldwide, but most cases of ant-induced alopecia have been from Iran, with at least 1 reported case from Turkey.^1-4,6 An early case series of ant-induced alopecia was reported in 1999,⁶ but the causative species was not described at that time.

The majority of reported cases of ant-induced alopecia are attributed to the barber ant (Pheidole pallidula). This type of alopecia is caused by worker ants within the species hierarchy.^1,4,6 The P pallidula worker ants are dimorphic and are classified as major and minor workers.⁷ Major workers have body lengths ranging up to 6 mm, whereas minor workers have body lengths ranging up to 4 mm. Major workers have larger heads and mandibles than minor workers and also have up to 2 pairs of denticles on the cranium.⁵ The minor workers are foragers and mainly collect food, whereas the major workers defend the nest and store food.⁸ These ants have widespread habitats with the ability to live in indoor and outdoor environments.

The presentation of hair loss caused by these ants is acute. Hair loss usually is confined to one specific area. Some patients may report pruritus or may present with erythematous lesions from ant stings or manual scratching.⁵ None of these signs or symptoms were seen in our patient. Some investigators have suggested that the barber ant is attracted to the hair of individuals with seborrheic dermatitis,¹ but our patient had no medical history of seborrheic dermatitis. Most likely, ants are attracted to excess sebum on the scalp in select individuals in their search for food and cause localized hair destruction.

Localized hair loss, as depicted in our case, should warrant a thorough evaluation for alopecia areata, trichotillomania, and tinea capitis.⁹ Alopecia areata should be considered in individuals with multiple focal patches of hair loss that have a positive hair pull test from peripheral sites of active lesions. Tinea capitis usually has localized sites of hair loss with underlying scaling, crusting, pruritus, erythema, and discharge from lesions, with positive potassium hydroxide preparations or fungal cultures. Trichotillomania typically presents with a spared peripheral fringe of hair. Remaining hairs may be thick and hyperpigmented as a response to repeated pulling, and biopsy often demonstrates fracture or degeneration of the hair shaft. A psychiatric evaluation may be warranted in cases of trichotillomania. Other cases of arthropod-induced hair loss include tick bite alopecia^10,11 and hair loss induced by numerous honeybee stings,¹² and these diagnoses should be suspected in patients with a history of ants on their pillow or in those from endemic areas.

No specific treatment is indicated in cases of 
ant-induced alopecia because hair usually regrows to its normal length without intervention.

Case Report

An 18-year-old Iranian man presented to the dermatology clinic with hair loss of 1 night’s duration. He denied pruritus, pain, discharge, or flaking. The patient had no notable personal, family, or surgical history and was not currently taking any medications. He denied recent travel. The patient reported that he found hair on his pillow upon waking up in the morning prior to coming to the clinic. On physical examination, 2 ants 
(Figure 1) were found on the scalp and alopecia with a vertical linear distribution was noted (Figure 2). Hairs of various lengths were found on the scalp within the distribution of the alopecia. No excoriations, crusting, seborrhea, or other areas of hair loss were detected. Wood lamp examination was negative. Based on these findings, which were concordant with similar findings from prior reports,^1-4 a diagnosis of ant-induced alopecia was made. Hair regrowth was noted within 1 week with full appearance of normal-length hair within 2.5 weeks.

Comment

Ant-induced alopecia is a form of localized hair loss caused by the Pheidole genus, the second largest genus of ants in the world.⁵ These ants can be found worldwide, but most cases of ant-induced alopecia have been from Iran, with at least 1 reported case from Turkey.^1-4,6 An early case series of ant-induced alopecia was reported in 1999,⁶ but the causative species was not described at that time.

The majority of reported cases of ant-induced alopecia are attributed to the barber ant (Pheidole pallidula). This type of alopecia is caused by worker ants within the species hierarchy.^1,4,6 The P pallidula worker ants are dimorphic and are classified as major and minor workers.⁷ Major workers have body lengths ranging up to 6 mm, whereas minor workers have body lengths ranging up to 4 mm. Major workers have larger heads and mandibles than minor workers and also have up to 2 pairs of denticles on the cranium.⁵ The minor workers are foragers and mainly collect food, whereas the major workers defend the nest and store food.⁸ These ants have widespread habitats with the ability to live in indoor and outdoor environments.

The presentation of hair loss caused by these ants is acute. Hair loss usually is confined to one specific area. Some patients may report pruritus or may present with erythematous lesions from ant stings or manual scratching.⁵ None of these signs or symptoms were seen in our patient. Some investigators have suggested that the barber ant is attracted to the hair of individuals with seborrheic dermatitis,¹ but our patient had no medical history of seborrheic dermatitis. Most likely, ants are attracted to excess sebum on the scalp in select individuals in their search for food and cause localized hair destruction.

Localized hair loss, as depicted in our case, should warrant a thorough evaluation for alopecia areata, trichotillomania, and tinea capitis.⁹ Alopecia areata should be considered in individuals with multiple focal patches of hair loss that have a positive hair pull test from peripheral sites of active lesions. Tinea capitis usually has localized sites of hair loss with underlying scaling, crusting, pruritus, erythema, and discharge from lesions, with positive potassium hydroxide preparations or fungal cultures. Trichotillomania typically presents with a spared peripheral fringe of hair. Remaining hairs may be thick and hyperpigmented as a response to repeated pulling, and biopsy often demonstrates fracture or degeneration of the hair shaft. A psychiatric evaluation may be warranted in cases of trichotillomania. Other cases of arthropod-induced hair loss include tick bite alopecia^10,11 and hair loss induced by numerous honeybee stings,¹² and these diagnoses should be suspected in patients with a history of ants on their pillow or in those from endemic areas.

No specific treatment is indicated in cases of 
ant-induced alopecia because hair usually regrows to its normal length without intervention.

Cutaneous larva migrans (CLM), also known as creeping eruption, is a pruritic serpiginous eruption caused by the migration of animal hookworm larvae through the epidermis.^1,2 The most common parasites are Ancylostoma braziliense (common in dogs and cats) and Ancylostoma caninum (common in dogs).¹

Disease Transmission

The infection is typically acquired in warm climates and tropical areas after coming in direct contact with sand or soil that is contaminated with animal feces. Therefore, the eruption most commonly occurs as a single or unilateral erythematous, pruritic, serpiginous tract on the feet, hands, or buttocks (Figure).² The larval tract typically migrates at a rate of 1 to 2 cm per day,³ which is in contrast to the serpiginous urticarial rash of larva currens of strongyloidiasis that can travel up to 10 cm per hour.⁴

Serpiginous tract of cutaneous larva migrans on the palm (A) and dorsal aspect of the foot (B).

Clinical Presentation

Rarely, CLM can present with bilateral lesions⁵; in severe cases a single patient can have hundreds of lesions. It also may present as folliculitis and urticarial papules.⁶ Shih et al⁷ reported a patient with CLM that presented as a diffuse papular urticarialike eruption following a trip to Thailand. This case may represent an underdiagnosed presentation of CLM. Patients with a history of exposure to contaminated sand or soil diffusely on the body may exhibit lesions in less classic locations, such as the trunk and upper proximal extremities.³

Cutaneous larva migrans is a self-limited eruption, as the larvae cannot complete their lifecycles in the human body and typically die within 2 to 8 weeks.² However, rare cases lasting up to a year have been reported.³ Sarasombath and Young² reported a case of CLM that persisted for 4 months with intermittent symptoms characterized by several weeklong intervals with no symptoms or visible rash.

Cutaneous larva migrans typically presents with isolated dermatologic symptoms. Rare cases associated with Löffler syndrome characterized by migratory pulmonary infiltrates and peripheral eosinophilia have been reported.⁸ Two proposed mechanisms for pulmonary involvement include direct invasion of the lungs by the helminths and a systemic immunologic process triggered by the helminths, resulting in eosinophilic pulmonary infiltration.⁹

Diagnosis

Cutaneous larva migrans is a clinical diagnosis and skin biopsy usually is not obtained because the larvae often are located 1 to 2 cm beyond the visible erythematous border.^3,5 Rarely, the parasites are found on biopsy, revealing larvae that are 0.5-mm thick and up to 10-mm long.¹⁰ The larvae typically are confined to the deep epidermis because the parasite lacks the collagenase required to penetrate the basement membrane.²

Langley et al¹¹ showed that confocal scanning laser microscopy can be an effective method for identifying the highly refractile oval larva that disrupt the normal honeycomb pattern of the epidermis. Performing a 4-mm punch biopsy over the identified site can allow for precise excision and treatment of the intact hookworm larvae of CLM. There also are limited reports of dermoscopy being used to facilitate diagnosis of CLM.¹² Dermoscopic features of CLM include translucent, brown, structureless areas in a segmental arrangement corresponding to the larval bodies and red-dotted vessels corresponding to an empty burrow.¹³ However, Zalaudek et al¹³ concluded that the efficacy of dermoscopy in aiding in the diagnosis of CLM has not been fully established.

Treatment

Cutaneous larva migrans is a self-limited condition that often resolves within 2 to 8 weeks; however, pruritus can be intense and patients therefore are seldom willing to forego treatment. Treatment options include a single oral dose of albendazole 400 mg in adults, with increased efficacy if administered daily for 3 to 5 days (or 10–15 mg/kg, with a maximum dose of 800 mg daily in children), a single oral dose of ivermectin 12 mg in adults (or 150 µg/kg in children), or topical application of thiabendazole 10% to 15% three times daily for at least 15 days.¹⁴ Cases of CLM complicated by Löffler syndrome may require a longer treatment course, such as a 7-day course of albendazole 400 mg daily. Tan and Liu⁹ reported a case of CLM complicated by Löffler syndrome that was successfully treated with albendazole. In this patient, initial treatment with 2 courses of mebendazole (3 days each for a total of 6 days) resulted in improvement of cutaneous lesions but not the pulmonary infiltrate. A subsequent prolonged course of albendazole and intravenous hydrocortisone for 5 days resulted in complete resolution of the pulmonary infiltrate and peripheral eosinophilia. The authors concluded that inadequacy of treatment with mebendazole may be related to differences in the rate of absorption and efficacy when compared to albendazole.⁹

Conclusion

Cutaneous larva migrans is a self-limited and pruritic skin eruption that is acquired after direct inoculation with sand or soil that is contaminated with feces containing A braziliense or A caninum. Although the classic presentation is readily identifiable, there are a variety of atypical presentations that may go undiagnosed. Symptomatic relief usually can be achieved with short courses of oral or topical antihelminth medications.

Cutaneous larva migrans (CLM), also known as creeping eruption, is a pruritic serpiginous eruption caused by the migration of animal hookworm larvae through the epidermis.^1,2 The most common parasites are Ancylostoma braziliense (common in dogs and cats) and Ancylostoma caninum (common in dogs).¹

Disease Transmission

The infection is typically acquired in warm climates and tropical areas after coming in direct contact with sand or soil that is contaminated with animal feces. Therefore, the eruption most commonly occurs as a single or unilateral erythematous, pruritic, serpiginous tract on the feet, hands, or buttocks (Figure).² The larval tract typically migrates at a rate of 1 to 2 cm per day,³ which is in contrast to the serpiginous urticarial rash of larva currens of strongyloidiasis that can travel up to 10 cm per hour.⁴

Serpiginous tract of cutaneous larva migrans on the palm (A) and dorsal aspect of the foot (B).

Clinical Presentation

Rarely, CLM can present with bilateral lesions⁵; in severe cases a single patient can have hundreds of lesions. It also may present as folliculitis and urticarial papules.⁶ Shih et al⁷ reported a patient with CLM that presented as a diffuse papular urticarialike eruption following a trip to Thailand. This case may represent an underdiagnosed presentation of CLM. Patients with a history of exposure to contaminated sand or soil diffusely on the body may exhibit lesions in less classic locations, such as the trunk and upper proximal extremities.³

Cutaneous larva migrans is a self-limited eruption, as the larvae cannot complete their lifecycles in the human body and typically die within 2 to 8 weeks.² However, rare cases lasting up to a year have been reported.³ Sarasombath and Young² reported a case of CLM that persisted for 4 months with intermittent symptoms characterized by several weeklong intervals with no symptoms or visible rash.

Cutaneous larva migrans typically presents with isolated dermatologic symptoms. Rare cases associated with Löffler syndrome characterized by migratory pulmonary infiltrates and peripheral eosinophilia have been reported.⁸ Two proposed mechanisms for pulmonary involvement include direct invasion of the lungs by the helminths and a systemic immunologic process triggered by the helminths, resulting in eosinophilic pulmonary infiltration.⁹

Diagnosis

Cutaneous larva migrans is a clinical diagnosis and skin biopsy usually is not obtained because the larvae often are located 1 to 2 cm beyond the visible erythematous border.^3,5 Rarely, the parasites are found on biopsy, revealing larvae that are 0.5-mm thick and up to 10-mm long.¹⁰ The larvae typically are confined to the deep epidermis because the parasite lacks the collagenase required to penetrate the basement membrane.²

Langley et al¹¹ showed that confocal scanning laser microscopy can be an effective method for identifying the highly refractile oval larva that disrupt the normal honeycomb pattern of the epidermis. Performing a 4-mm punch biopsy over the identified site can allow for precise excision and treatment of the intact hookworm larvae of CLM. There also are limited reports of dermoscopy being used to facilitate diagnosis of CLM.¹² Dermoscopic features of CLM include translucent, brown, structureless areas in a segmental arrangement corresponding to the larval bodies and red-dotted vessels corresponding to an empty burrow.¹³ However, Zalaudek et al¹³ concluded that the efficacy of dermoscopy in aiding in the diagnosis of CLM has not been fully established.

Treatment

Cutaneous larva migrans is a self-limited condition that often resolves within 2 to 8 weeks; however, pruritus can be intense and patients therefore are seldom willing to forego treatment. Treatment options include a single oral dose of albendazole 400 mg in adults, with increased efficacy if administered daily for 3 to 5 days (or 10–15 mg/kg, with a maximum dose of 800 mg daily in children), a single oral dose of ivermectin 12 mg in adults (or 150 µg/kg in children), or topical application of thiabendazole 10% to 15% three times daily for at least 15 days.¹⁴ Cases of CLM complicated by Löffler syndrome may require a longer treatment course, such as a 7-day course of albendazole 400 mg daily. Tan and Liu⁹ reported a case of CLM complicated by Löffler syndrome that was successfully treated with albendazole. In this patient, initial treatment with 2 courses of mebendazole (3 days each for a total of 6 days) resulted in improvement of cutaneous lesions but not the pulmonary infiltrate. A subsequent prolonged course of albendazole and intravenous hydrocortisone for 5 days resulted in complete resolution of the pulmonary infiltrate and peripheral eosinophilia. The authors concluded that inadequacy of treatment with mebendazole may be related to differences in the rate of absorption and efficacy when compared to albendazole.⁹

Conclusion

Cutaneous larva migrans is a self-limited and pruritic skin eruption that is acquired after direct inoculation with sand or soil that is contaminated with feces containing A braziliense or A caninum. Although the classic presentation is readily identifiable, there are a variety of atypical presentations that may go undiagnosed. Symptomatic relief usually can be achieved with short courses of oral or topical antihelminth medications.

Cutaneous larva migrans (CLM), also known as creeping eruption, is a pruritic serpiginous eruption caused by the migration of animal hookworm larvae through the epidermis.^1,2 The most common parasites are Ancylostoma braziliense (common in dogs and cats) and Ancylostoma caninum (common in dogs).¹

Disease Transmission

The infection is typically acquired in warm climates and tropical areas after coming in direct contact with sand or soil that is contaminated with animal feces. Therefore, the eruption most commonly occurs as a single or unilateral erythematous, pruritic, serpiginous tract on the feet, hands, or buttocks (Figure).² The larval tract typically migrates at a rate of 1 to 2 cm per day,³ which is in contrast to the serpiginous urticarial rash of larva currens of strongyloidiasis that can travel up to 10 cm per hour.⁴

Serpiginous tract of cutaneous larva migrans on the palm (A) and dorsal aspect of the foot (B).

Clinical Presentation

Rarely, CLM can present with bilateral lesions⁵; in severe cases a single patient can have hundreds of lesions. It also may present as folliculitis and urticarial papules.⁶ Shih et al⁷ reported a patient with CLM that presented as a diffuse papular urticarialike eruption following a trip to Thailand. This case may represent an underdiagnosed presentation of CLM. Patients with a history of exposure to contaminated sand or soil diffusely on the body may exhibit lesions in less classic locations, such as the trunk and upper proximal extremities.³

Cutaneous larva migrans is a self-limited eruption, as the larvae cannot complete their lifecycles in the human body and typically die within 2 to 8 weeks.² However, rare cases lasting up to a year have been reported.³ Sarasombath and Young² reported a case of CLM that persisted for 4 months with intermittent symptoms characterized by several weeklong intervals with no symptoms or visible rash.

Cutaneous larva migrans typically presents with isolated dermatologic symptoms. Rare cases associated with Löffler syndrome characterized by migratory pulmonary infiltrates and peripheral eosinophilia have been reported.⁸ Two proposed mechanisms for pulmonary involvement include direct invasion of the lungs by the helminths and a systemic immunologic process triggered by the helminths, resulting in eosinophilic pulmonary infiltration.⁹

Diagnosis

Cutaneous larva migrans is a clinical diagnosis and skin biopsy usually is not obtained because the larvae often are located 1 to 2 cm beyond the visible erythematous border.^3,5 Rarely, the parasites are found on biopsy, revealing larvae that are 0.5-mm thick and up to 10-mm long.¹⁰ The larvae typically are confined to the deep epidermis because the parasite lacks the collagenase required to penetrate the basement membrane.²

Langley et al¹¹ showed that confocal scanning laser microscopy can be an effective method for identifying the highly refractile oval larva that disrupt the normal honeycomb pattern of the epidermis. Performing a 4-mm punch biopsy over the identified site can allow for precise excision and treatment of the intact hookworm larvae of CLM. There also are limited reports of dermoscopy being used to facilitate diagnosis of CLM.¹² Dermoscopic features of CLM include translucent, brown, structureless areas in a segmental arrangement corresponding to the larval bodies and red-dotted vessels corresponding to an empty burrow.¹³ However, Zalaudek et al¹³ concluded that the efficacy of dermoscopy in aiding in the diagnosis of CLM has not been fully established.

Treatment

Cutaneous larva migrans is a self-limited condition that often resolves within 2 to 8 weeks; however, pruritus can be intense and patients therefore are seldom willing to forego treatment. Treatment options include a single oral dose of albendazole 400 mg in adults, with increased efficacy if administered daily for 3 to 5 days (or 10–15 mg/kg, with a maximum dose of 800 mg daily in children), a single oral dose of ivermectin 12 mg in adults (or 150 µg/kg in children), or topical application of thiabendazole 10% to 15% three times daily for at least 15 days.¹⁴ Cases of CLM complicated by Löffler syndrome may require a longer treatment course, such as a 7-day course of albendazole 400 mg daily. Tan and Liu⁹ reported a case of CLM complicated by Löffler syndrome that was successfully treated with albendazole. In this patient, initial treatment with 2 courses of mebendazole (3 days each for a total of 6 days) resulted in improvement of cutaneous lesions but not the pulmonary infiltrate. A subsequent prolonged course of albendazole and intravenous hydrocortisone for 5 days resulted in complete resolution of the pulmonary infiltrate and peripheral eosinophilia. The authors concluded that inadequacy of treatment with mebendazole may be related to differences in the rate of absorption and efficacy when compared to albendazole.⁹

Conclusion

Cutaneous larva migrans is a self-limited and pruritic skin eruption that is acquired after direct inoculation with sand or soil that is contaminated with feces containing A braziliense or A caninum. Although the classic presentation is readily identifiable, there are a variety of atypical presentations that may go undiagnosed. Symptomatic relief usually can be achieved with short courses of oral or topical antihelminth medications.