Dirk M. Elston, MD

The head louse (Pediculus humanus capitis) is a blood-sucking arthropod of the suborder Anoplura. Lice are obligate human parasites that have infested humans since antiquity. Pediculosis capitis is an infestation of the scalp by head lice. It is estimated that 6 to 12 million individuals in the United States are affected with head lice per year.¹ Resistance to topical chemical pediculicides is widespread, and new agents have been developed to address this gap in care.

Characteristics of Head Lice

The head louse is a tan-gray–colored, wingless insect measuring approximately 2- to 3-mm long with 3 body segments. It has 6 legs with claws used to grasp individual hairs, and it moves by crawling; it does not fly or jump.^2,3 The head louse has an elongated abdomen and a small head with short antennae and anterior piercing mouthparts (Figure 1).⁴ Nits are transparent, flask-shaped, 0.5- to 0.8-mm egg cases found firmly cemented to the hair shafts approximately 1 to 4 mm above the level of the scalp (Figure 2).⁵ The head louse resides on scalp hair and feeds off the scalp itself. Both lice and nits can be present throughout the scalp but are most commonly found in the postauricular and occipital scalp.^3,4

Female lice live approximately 30 days and lay 5 to 10 eggs per day. Eggs incubate individually in nits laid close to the scalp for 8 to 10 days before hatching.^1,6 The newly hatched nymphs (also called instars) have multiple exoskeletons that are shed as they grow.⁷ Nymphs mature into adults in approximately 2 weeks, and the life cycle begins again.⁸ Head lice are obligate human parasites, feeding approximately every 4 to 6 hours on the blood of the host; however, they can survive up to 4 days without a blood meal on fomites if the climate and conditions are favorable.^5,9

Epidemiology and Transmission

Head lice infestations commonly occur in children aged 3 to 11 years and are more prevalent in girls and women.^1,10 Infestation rates are not reliably recorded, and few population-based studies have been performed; however, it is estimated that 6 to 12 million individuals are infested annually in the United States.¹ Prevalence in some European populations has been estimated to range from 1% to 20%.¹¹ A 2008 literature review found that worldwide prevalence varied across populations from 0.7% to 59%.¹⁰

Transmission occurs most frequently from direct head-to-head contact. One study found that transmission is most likely to occur when hairs are arranged in a parallel alignment and move slowly in relation to one another.¹² Although controversial and probably less notable, transmission also may occur indirectly via fomites or the sharing of hairbrushes, hats, or other headgear.^13,14 Classrooms are a common place for transmission.¹ A 2009 study in Germany found an increase in health department consultations for head lice when schools reopened after vacations. The investigators also found that pediculicide sales peaked from mid-September through October, subsequent to schools reopening after the summer holiday.¹⁵ There is some evidence that overcrowded housing also can lead to increased incidence and transmission.^16,17 There is no consistent correlation of infestation with socioeconomic status.^1,17,18

Clinical Manifestations and Diagnosis

Clinically, patients with head lice present with scalp pruritus and sometimes posterior cervical or occipital lymphadenopathy. Pediculosis also can be asymptomatic. With the first exposure, symptoms may not develop for up to 4 to 6 weeks as the immune system develops sensitivity to the louse saliva.⁶ Bite reactions consisting of papules or wheals are related to immune sensitization.⁵ Louse feces and excoriations from scratching to relieve itch also may be present on examination. Secondary infection of excoriations also is possible.¹

Diagnosis of an active infestation is made by identifying living lice. Because lice move quickly and can be difficult to detect, tightly attached nits on the hair shaft within 4 mm of the scalp are at least indicative of a historic infestation and can be suggestive of active infestation.^1,19 Dermoscopy is a helpful tool in differentiating eggs containing nymphs from the empty cases of hatched lice and also from amorphous pseudonits (hair casts)(Figure 3).^19,20 Wet combing improves the accuracy of diagnosing an active infection.²¹

Treatment

Effective treatment of head lice requires eradication of all living lice as well as louse eggs. Topically applied pyrethroids, including pyrethrin shampoos and mousses and permethrin lotion 1%, are considered the first-line therapy.⁸ Pyrethroids are over-the-counter treatments that act by interfering with sodium transport in the louse, causing depolarization of the neuromembranes and respiratory paralysis.²² Pyrethrins are natural compounds derived from the chrysanthemum plant; permethrin is a synthetic compound. Pyrethrins often are combined with piperonyl butoxide, an insecticide synergist that improves efficacy by inhibiting pyrethrin catabolism.²³ Resistance to pyrethroids has become an increasingly important problem in the United States and worldwide.

Malathion lotion 0.5% is another therapeutic option for head lice. Malathion is a prescription organophosphate cholinesterase inhibitor that also causes respiratory paralysis of the louse and is one of the few treatments that is ovicidal.²² It was withdrawn from the market in 1995 due to its flammability and a theoretical risk of respiratory depression if ingested; however, it was reintroduced in 1999 and remains an effective treatment option with little resistance in the United States.²⁴

Lindane 1% (shampoo and lotion), an organochloride compound that acts by causing neuronal hyperstimulation and eventual paralysis of lice, is no longer recommended due to its serious side effects, including central nervous system toxicity and increased risk of seizure.^8,24

New US Food and Drug Administration–Approved Therapies
Newer topical treatments include benzyl alcohol lotion 5%, spinosad topical suspension 0.9%, ivermectin lotion 0.5%, and dimethicone-based products. Benzyl alcohol was approved by the US Food and Drug Administration (FDA) in 2009 and is available in the United States by prescription.²⁵ Benzyl alcohol kills lice by asphyxiation. Phase 2 and 3 clinical trials showed significant treatment success 1 day posttreatment (fewer live lice than the vehicle alone; P=.004) and 2 weeks posttreatment (absence of live lice compared to the vehicle alone; P=.001).²⁶

Spinosad was approved by the FDA in 2011 and is available in the United States by prescription.²⁵ It contains the compounds spinosyn A and spinosyn D, which are naturally derived through fermentation by the soil bacterium Saccharopolyspora spinosa. It also contains benzyl alcohol. Spinosad paralyzes lice by disrupting neuronal activity and is at least partially ovicidal.²⁷ Phase 3 clinical trials published in 2009 showed that spinosad was significantly more effective than permethrin in eradicating head lice (P<.001).²⁸

Topical ivermectin was approved by the FDA in 2012 for prescription use.²⁵ It acts on chloride ion channels, causing hyperpolarization of the muscle cells of lice and resulting in paralysis and death. Oral ivermectin (200 μg/kg) given once and repeated in 10 days is not FDA approved for the treatment of head lice but has shown some effectiveness and is sometimes used.⁸ A comparison study of topical versus oral ivermectin published in 2014 found that eradication was achieved in 88% (n=27) of topical ivermectin users after 1 treatment and 100% (n=31) after 2 treatments. Oral ivermectin produced cure rates of 45% (n=14) after 1 treatment and 97% (n=30) after 2 treatments. Both topical and oral ivermectin treatments are well tolerated.²⁹

Physically Acting Preparations
Products with a physical mode of action are a new attractive option for treatment of pediculosis because the development of resistance is less likely. Studies of silicone-based fluids that physically occlude the respiratory system of the louse, such as dimethicone liquid gel 4%, have shown superiority over treatment with pyrethroids.^30,31 Although the safety of dimethicone has been demonstrated, silicone-based treatments have not yet been widely adopted in the United States and are not currently used as a first-line treatment.³² However, use of such physically acting pediculicides may in time surpass traditional neurotoxic treatments due to their low susceptibility to resistance and good safety profile.^33,34

Alternative Therapies
Nonchemical treatments for head lice that have shown variable success include wet combing, hot air treatments, and varying occlusive treatments. Physical removal via wet combing requires persistent repeated treatments over several weeks; for example, wet combing may be performed every 3 days for at least 2 weeks or until no head lice are detected on 4 consecutive occasions.³⁵ Cure rates range from 38% to 75% with wet combing as a sole treatment of head lice.³⁶ Because this treatment has minimal risks and no adverse side effects, it can be considered as an alternative treatment for some patients.

Hot air treatments also have been studied. A 2006 study showed that a hot air treatment device had the potential to eradicate head lice, most likely by desiccation. Specifically, 30 minutes of exposure to hot air (at 58.9°F, slightly cooler than a standard hair dryer) using the custom-built device resulted in 98% mortality of eggs and 80% mortality of hatched lice.³⁷ Large randomized controlled trials of hot air treatments have not been performed.

Other alternative treatments include plant-derived oils. A laboratory study of essential oils found that spearmint, cassia, and clove showed pediculicidal activity similar to malathion with improved ovicidal activity.³⁸ However, there is a potential for development of contact dermatitis from essential oils.

Complete Eradication of Head Lice
Removal of nits is an important component of effective lice eradication. Biochemical analysis has revealed that the nit sheath of the head louse is similar in composition to amyloid, rendering it difficult to design products that will unravel the nit sheath while leaving human hair undamaged.³⁹ Because pediculicides are not necessarily ovicidal and complete physical nit removal is difficult to achieve, re-treatment in 7 to 10 days often is advisable to ensure that lice in all stages of the life cycle have been killed.⁴ Treatment of any secondary bacterial infection also is important. Although transmission of lice via fomites is less likely than from head-to-head contact, the cleaning of hats, hairbrushes, and linens is prudent. Diagnosing and treating infested close contacts also is essential to achieving eradication.⁴ Coordinated surveillance, education, and treatment efforts in high-risk communities can help detect asymptomatic cases and control local epidemics in a cost-effective manner.⁴⁰ However, “no nit” policies at schools likely cause a net harm, as nit removal is difficult and children with nonviable nits are then excluded from the classroom.⁵

Treatment Resistance
Resistance to topical neurotoxic treatments is becoming increasingly common.^41-43 Therefore, it is important to identify local patterns of resistance, if possible, when selecting a therapy for head lice. Improper usage, changes in pediculicide formulations and packaging, decreased product efficacy, and natural selection have all contributed to this rise in resistance.⁷ Additionally, due to protection from multiple exoskeletons and the natural molting process as they mature into adults, nymphs may only receive a sublethal dose when exposed to pediculicides, contributing further to resistance.⁷ Resistance to synthetic pyrethroids is most predominant, likely due to selection pressure because permethrin historically has been the most widely used insecticide for pediculosis. A 2014 study found that the frequency of sodium-channel insensitivity to pyrethroids, also known as knockdown resistance (or kdr), in US head louse populations collected over a 10-year period was 84.4% and approached 100% in some communities in recent years.⁴⁴ This evidence strongly supports the use of alternative therapeutic categories to effectively eradicate head lice infestations.

Conclusion

Head lice infestation is common in children, and although it is not harmful to the host, it can be an irritating and symptomatic problem and can lead to notable distress, missed days of school, and secondary infections. Identifying active adult lice is the gold standard for diagnosis. Current recommended treatments include pyrethroids as the first-line therapy; however, resistance to these neurotoxic agents is becoming increasingly common. Alternative therapies such as newer neurotoxic agents or pediculicides with physical mechanisms of action (eg, dimethicone-based products) should be considered, particularly in regions where resistance is known to be high. Education about head lice, proper use of treatment, and coordinated diagnosis are necessary for effective management of this problem.

The head louse (Pediculus humanus capitis) is a blood-sucking arthropod of the suborder Anoplura. Lice are obligate human parasites that have infested humans since antiquity. Pediculosis capitis is an infestation of the scalp by head lice. It is estimated that 6 to 12 million individuals in the United States are affected with head lice per year.¹ Resistance to topical chemical pediculicides is widespread, and new agents have been developed to address this gap in care.

Characteristics of Head Lice

The head louse is a tan-gray–colored, wingless insect measuring approximately 2- to 3-mm long with 3 body segments. It has 6 legs with claws used to grasp individual hairs, and it moves by crawling; it does not fly or jump.^2,3 The head louse has an elongated abdomen and a small head with short antennae and anterior piercing mouthparts (Figure 1).⁴ Nits are transparent, flask-shaped, 0.5- to 0.8-mm egg cases found firmly cemented to the hair shafts approximately 1 to 4 mm above the level of the scalp (Figure 2).⁵ The head louse resides on scalp hair and feeds off the scalp itself. Both lice and nits can be present throughout the scalp but are most commonly found in the postauricular and occipital scalp.^3,4

Female lice live approximately 30 days and lay 5 to 10 eggs per day. Eggs incubate individually in nits laid close to the scalp for 8 to 10 days before hatching.^1,6 The newly hatched nymphs (also called instars) have multiple exoskeletons that are shed as they grow.⁷ Nymphs mature into adults in approximately 2 weeks, and the life cycle begins again.⁸ Head lice are obligate human parasites, feeding approximately every 4 to 6 hours on the blood of the host; however, they can survive up to 4 days without a blood meal on fomites if the climate and conditions are favorable.^5,9

Epidemiology and Transmission

Head lice infestations commonly occur in children aged 3 to 11 years and are more prevalent in girls and women.^1,10 Infestation rates are not reliably recorded, and few population-based studies have been performed; however, it is estimated that 6 to 12 million individuals are infested annually in the United States.¹ Prevalence in some European populations has been estimated to range from 1% to 20%.¹¹ A 2008 literature review found that worldwide prevalence varied across populations from 0.7% to 59%.¹⁰

Transmission occurs most frequently from direct head-to-head contact. One study found that transmission is most likely to occur when hairs are arranged in a parallel alignment and move slowly in relation to one another.¹² Although controversial and probably less notable, transmission also may occur indirectly via fomites or the sharing of hairbrushes, hats, or other headgear.^13,14 Classrooms are a common place for transmission.¹ A 2009 study in Germany found an increase in health department consultations for head lice when schools reopened after vacations. The investigators also found that pediculicide sales peaked from mid-September through October, subsequent to schools reopening after the summer holiday.¹⁵ There is some evidence that overcrowded housing also can lead to increased incidence and transmission.^16,17 There is no consistent correlation of infestation with socioeconomic status.^1,17,18

Clinical Manifestations and Diagnosis

Clinically, patients with head lice present with scalp pruritus and sometimes posterior cervical or occipital lymphadenopathy. Pediculosis also can be asymptomatic. With the first exposure, symptoms may not develop for up to 4 to 6 weeks as the immune system develops sensitivity to the louse saliva.⁶ Bite reactions consisting of papules or wheals are related to immune sensitization.⁵ Louse feces and excoriations from scratching to relieve itch also may be present on examination. Secondary infection of excoriations also is possible.¹

Diagnosis of an active infestation is made by identifying living lice. Because lice move quickly and can be difficult to detect, tightly attached nits on the hair shaft within 4 mm of the scalp are at least indicative of a historic infestation and can be suggestive of active infestation.^1,19 Dermoscopy is a helpful tool in differentiating eggs containing nymphs from the empty cases of hatched lice and also from amorphous pseudonits (hair casts)(Figure 3).^19,20 Wet combing improves the accuracy of diagnosing an active infection.²¹

Treatment

Effective treatment of head lice requires eradication of all living lice as well as louse eggs. Topically applied pyrethroids, including pyrethrin shampoos and mousses and permethrin lotion 1%, are considered the first-line therapy.⁸ Pyrethroids are over-the-counter treatments that act by interfering with sodium transport in the louse, causing depolarization of the neuromembranes and respiratory paralysis.²² Pyrethrins are natural compounds derived from the chrysanthemum plant; permethrin is a synthetic compound. Pyrethrins often are combined with piperonyl butoxide, an insecticide synergist that improves efficacy by inhibiting pyrethrin catabolism.²³ Resistance to pyrethroids has become an increasingly important problem in the United States and worldwide.

Malathion lotion 0.5% is another therapeutic option for head lice. Malathion is a prescription organophosphate cholinesterase inhibitor that also causes respiratory paralysis of the louse and is one of the few treatments that is ovicidal.²² It was withdrawn from the market in 1995 due to its flammability and a theoretical risk of respiratory depression if ingested; however, it was reintroduced in 1999 and remains an effective treatment option with little resistance in the United States.²⁴

Lindane 1% (shampoo and lotion), an organochloride compound that acts by causing neuronal hyperstimulation and eventual paralysis of lice, is no longer recommended due to its serious side effects, including central nervous system toxicity and increased risk of seizure.^8,24

New US Food and Drug Administration–Approved Therapies
Newer topical treatments include benzyl alcohol lotion 5%, spinosad topical suspension 0.9%, ivermectin lotion 0.5%, and dimethicone-based products. Benzyl alcohol was approved by the US Food and Drug Administration (FDA) in 2009 and is available in the United States by prescription.²⁵ Benzyl alcohol kills lice by asphyxiation. Phase 2 and 3 clinical trials showed significant treatment success 1 day posttreatment (fewer live lice than the vehicle alone; P=.004) and 2 weeks posttreatment (absence of live lice compared to the vehicle alone; P=.001).²⁶

Spinosad was approved by the FDA in 2011 and is available in the United States by prescription.²⁵ It contains the compounds spinosyn A and spinosyn D, which are naturally derived through fermentation by the soil bacterium Saccharopolyspora spinosa. It also contains benzyl alcohol. Spinosad paralyzes lice by disrupting neuronal activity and is at least partially ovicidal.²⁷ Phase 3 clinical trials published in 2009 showed that spinosad was significantly more effective than permethrin in eradicating head lice (P<.001).²⁸

Topical ivermectin was approved by the FDA in 2012 for prescription use.²⁵ It acts on chloride ion channels, causing hyperpolarization of the muscle cells of lice and resulting in paralysis and death. Oral ivermectin (200 μg/kg) given once and repeated in 10 days is not FDA approved for the treatment of head lice but has shown some effectiveness and is sometimes used.⁸ A comparison study of topical versus oral ivermectin published in 2014 found that eradication was achieved in 88% (n=27) of topical ivermectin users after 1 treatment and 100% (n=31) after 2 treatments. Oral ivermectin produced cure rates of 45% (n=14) after 1 treatment and 97% (n=30) after 2 treatments. Both topical and oral ivermectin treatments are well tolerated.²⁹

Physically Acting Preparations
Products with a physical mode of action are a new attractive option for treatment of pediculosis because the development of resistance is less likely. Studies of silicone-based fluids that physically occlude the respiratory system of the louse, such as dimethicone liquid gel 4%, have shown superiority over treatment with pyrethroids.^30,31 Although the safety of dimethicone has been demonstrated, silicone-based treatments have not yet been widely adopted in the United States and are not currently used as a first-line treatment.³² However, use of such physically acting pediculicides may in time surpass traditional neurotoxic treatments due to their low susceptibility to resistance and good safety profile.^33,34

Alternative Therapies
Nonchemical treatments for head lice that have shown variable success include wet combing, hot air treatments, and varying occlusive treatments. Physical removal via wet combing requires persistent repeated treatments over several weeks; for example, wet combing may be performed every 3 days for at least 2 weeks or until no head lice are detected on 4 consecutive occasions.³⁵ Cure rates range from 38% to 75% with wet combing as a sole treatment of head lice.³⁶ Because this treatment has minimal risks and no adverse side effects, it can be considered as an alternative treatment for some patients.

Hot air treatments also have been studied. A 2006 study showed that a hot air treatment device had the potential to eradicate head lice, most likely by desiccation. Specifically, 30 minutes of exposure to hot air (at 58.9°F, slightly cooler than a standard hair dryer) using the custom-built device resulted in 98% mortality of eggs and 80% mortality of hatched lice.³⁷ Large randomized controlled trials of hot air treatments have not been performed.

Other alternative treatments include plant-derived oils. A laboratory study of essential oils found that spearmint, cassia, and clove showed pediculicidal activity similar to malathion with improved ovicidal activity.³⁸ However, there is a potential for development of contact dermatitis from essential oils.

Complete Eradication of Head Lice
Removal of nits is an important component of effective lice eradication. Biochemical analysis has revealed that the nit sheath of the head louse is similar in composition to amyloid, rendering it difficult to design products that will unravel the nit sheath while leaving human hair undamaged.³⁹ Because pediculicides are not necessarily ovicidal and complete physical nit removal is difficult to achieve, re-treatment in 7 to 10 days often is advisable to ensure that lice in all stages of the life cycle have been killed.⁴ Treatment of any secondary bacterial infection also is important. Although transmission of lice via fomites is less likely than from head-to-head contact, the cleaning of hats, hairbrushes, and linens is prudent. Diagnosing and treating infested close contacts also is essential to achieving eradication.⁴ Coordinated surveillance, education, and treatment efforts in high-risk communities can help detect asymptomatic cases and control local epidemics in a cost-effective manner.⁴⁰ However, “no nit” policies at schools likely cause a net harm, as nit removal is difficult and children with nonviable nits are then excluded from the classroom.⁵

Treatment Resistance
Resistance to topical neurotoxic treatments is becoming increasingly common.^41-43 Therefore, it is important to identify local patterns of resistance, if possible, when selecting a therapy for head lice. Improper usage, changes in pediculicide formulations and packaging, decreased product efficacy, and natural selection have all contributed to this rise in resistance.⁷ Additionally, due to protection from multiple exoskeletons and the natural molting process as they mature into adults, nymphs may only receive a sublethal dose when exposed to pediculicides, contributing further to resistance.⁷ Resistance to synthetic pyrethroids is most predominant, likely due to selection pressure because permethrin historically has been the most widely used insecticide for pediculosis. A 2014 study found that the frequency of sodium-channel insensitivity to pyrethroids, also known as knockdown resistance (or kdr), in US head louse populations collected over a 10-year period was 84.4% and approached 100% in some communities in recent years.⁴⁴ This evidence strongly supports the use of alternative therapeutic categories to effectively eradicate head lice infestations.

Conclusion

Head lice infestation is common in children, and although it is not harmful to the host, it can be an irritating and symptomatic problem and can lead to notable distress, missed days of school, and secondary infections. Identifying active adult lice is the gold standard for diagnosis. Current recommended treatments include pyrethroids as the first-line therapy; however, resistance to these neurotoxic agents is becoming increasingly common. Alternative therapies such as newer neurotoxic agents or pediculicides with physical mechanisms of action (eg, dimethicone-based products) should be considered, particularly in regions where resistance is known to be high. Education about head lice, proper use of treatment, and coordinated diagnosis are necessary for effective management of this problem.

The head louse (Pediculus humanus capitis) is a blood-sucking arthropod of the suborder Anoplura. Lice are obligate human parasites that have infested humans since antiquity. Pediculosis capitis is an infestation of the scalp by head lice. It is estimated that 6 to 12 million individuals in the United States are affected with head lice per year.¹ Resistance to topical chemical pediculicides is widespread, and new agents have been developed to address this gap in care.

Characteristics of Head Lice

The head louse is a tan-gray–colored, wingless insect measuring approximately 2- to 3-mm long with 3 body segments. It has 6 legs with claws used to grasp individual hairs, and it moves by crawling; it does not fly or jump.^2,3 The head louse has an elongated abdomen and a small head with short antennae and anterior piercing mouthparts (Figure 1).⁴ Nits are transparent, flask-shaped, 0.5- to 0.8-mm egg cases found firmly cemented to the hair shafts approximately 1 to 4 mm above the level of the scalp (Figure 2).⁵ The head louse resides on scalp hair and feeds off the scalp itself. Both lice and nits can be present throughout the scalp but are most commonly found in the postauricular and occipital scalp.^3,4

Female lice live approximately 30 days and lay 5 to 10 eggs per day. Eggs incubate individually in nits laid close to the scalp for 8 to 10 days before hatching.^1,6 The newly hatched nymphs (also called instars) have multiple exoskeletons that are shed as they grow.⁷ Nymphs mature into adults in approximately 2 weeks, and the life cycle begins again.⁸ Head lice are obligate human parasites, feeding approximately every 4 to 6 hours on the blood of the host; however, they can survive up to 4 days without a blood meal on fomites if the climate and conditions are favorable.^5,9

Epidemiology and Transmission

Head lice infestations commonly occur in children aged 3 to 11 years and are more prevalent in girls and women.^1,10 Infestation rates are not reliably recorded, and few population-based studies have been performed; however, it is estimated that 6 to 12 million individuals are infested annually in the United States.¹ Prevalence in some European populations has been estimated to range from 1% to 20%.¹¹ A 2008 literature review found that worldwide prevalence varied across populations from 0.7% to 59%.¹⁰

Transmission occurs most frequently from direct head-to-head contact. One study found that transmission is most likely to occur when hairs are arranged in a parallel alignment and move slowly in relation to one another.¹² Although controversial and probably less notable, transmission also may occur indirectly via fomites or the sharing of hairbrushes, hats, or other headgear.^13,14 Classrooms are a common place for transmission.¹ A 2009 study in Germany found an increase in health department consultations for head lice when schools reopened after vacations. The investigators also found that pediculicide sales peaked from mid-September through October, subsequent to schools reopening after the summer holiday.¹⁵ There is some evidence that overcrowded housing also can lead to increased incidence and transmission.^16,17 There is no consistent correlation of infestation with socioeconomic status.^1,17,18

Clinical Manifestations and Diagnosis

Clinically, patients with head lice present with scalp pruritus and sometimes posterior cervical or occipital lymphadenopathy. Pediculosis also can be asymptomatic. With the first exposure, symptoms may not develop for up to 4 to 6 weeks as the immune system develops sensitivity to the louse saliva.⁶ Bite reactions consisting of papules or wheals are related to immune sensitization.⁵ Louse feces and excoriations from scratching to relieve itch also may be present on examination. Secondary infection of excoriations also is possible.¹

Diagnosis of an active infestation is made by identifying living lice. Because lice move quickly and can be difficult to detect, tightly attached nits on the hair shaft within 4 mm of the scalp are at least indicative of a historic infestation and can be suggestive of active infestation.^1,19 Dermoscopy is a helpful tool in differentiating eggs containing nymphs from the empty cases of hatched lice and also from amorphous pseudonits (hair casts)(Figure 3).^19,20 Wet combing improves the accuracy of diagnosing an active infection.²¹

Treatment

Effective treatment of head lice requires eradication of all living lice as well as louse eggs. Topically applied pyrethroids, including pyrethrin shampoos and mousses and permethrin lotion 1%, are considered the first-line therapy.⁸ Pyrethroids are over-the-counter treatments that act by interfering with sodium transport in the louse, causing depolarization of the neuromembranes and respiratory paralysis.²² Pyrethrins are natural compounds derived from the chrysanthemum plant; permethrin is a synthetic compound. Pyrethrins often are combined with piperonyl butoxide, an insecticide synergist that improves efficacy by inhibiting pyrethrin catabolism.²³ Resistance to pyrethroids has become an increasingly important problem in the United States and worldwide.

Malathion lotion 0.5% is another therapeutic option for head lice. Malathion is a prescription organophosphate cholinesterase inhibitor that also causes respiratory paralysis of the louse and is one of the few treatments that is ovicidal.²² It was withdrawn from the market in 1995 due to its flammability and a theoretical risk of respiratory depression if ingested; however, it was reintroduced in 1999 and remains an effective treatment option with little resistance in the United States.²⁴

Lindane 1% (shampoo and lotion), an organochloride compound that acts by causing neuronal hyperstimulation and eventual paralysis of lice, is no longer recommended due to its serious side effects, including central nervous system toxicity and increased risk of seizure.^8,24

New US Food and Drug Administration–Approved Therapies
Newer topical treatments include benzyl alcohol lotion 5%, spinosad topical suspension 0.9%, ivermectin lotion 0.5%, and dimethicone-based products. Benzyl alcohol was approved by the US Food and Drug Administration (FDA) in 2009 and is available in the United States by prescription.²⁵ Benzyl alcohol kills lice by asphyxiation. Phase 2 and 3 clinical trials showed significant treatment success 1 day posttreatment (fewer live lice than the vehicle alone; P=.004) and 2 weeks posttreatment (absence of live lice compared to the vehicle alone; P=.001).²⁶

Spinosad was approved by the FDA in 2011 and is available in the United States by prescription.²⁵ It contains the compounds spinosyn A and spinosyn D, which are naturally derived through fermentation by the soil bacterium Saccharopolyspora spinosa. It also contains benzyl alcohol. Spinosad paralyzes lice by disrupting neuronal activity and is at least partially ovicidal.²⁷ Phase 3 clinical trials published in 2009 showed that spinosad was significantly more effective than permethrin in eradicating head lice (P<.001).²⁸

Topical ivermectin was approved by the FDA in 2012 for prescription use.²⁵ It acts on chloride ion channels, causing hyperpolarization of the muscle cells of lice and resulting in paralysis and death. Oral ivermectin (200 μg/kg) given once and repeated in 10 days is not FDA approved for the treatment of head lice but has shown some effectiveness and is sometimes used.⁸ A comparison study of topical versus oral ivermectin published in 2014 found that eradication was achieved in 88% (n=27) of topical ivermectin users after 1 treatment and 100% (n=31) after 2 treatments. Oral ivermectin produced cure rates of 45% (n=14) after 1 treatment and 97% (n=30) after 2 treatments. Both topical and oral ivermectin treatments are well tolerated.²⁹

Physically Acting Preparations
Products with a physical mode of action are a new attractive option for treatment of pediculosis because the development of resistance is less likely. Studies of silicone-based fluids that physically occlude the respiratory system of the louse, such as dimethicone liquid gel 4%, have shown superiority over treatment with pyrethroids.^30,31 Although the safety of dimethicone has been demonstrated, silicone-based treatments have not yet been widely adopted in the United States and are not currently used as a first-line treatment.³² However, use of such physically acting pediculicides may in time surpass traditional neurotoxic treatments due to their low susceptibility to resistance and good safety profile.^33,34

Alternative Therapies
Nonchemical treatments for head lice that have shown variable success include wet combing, hot air treatments, and varying occlusive treatments. Physical removal via wet combing requires persistent repeated treatments over several weeks; for example, wet combing may be performed every 3 days for at least 2 weeks or until no head lice are detected on 4 consecutive occasions.³⁵ Cure rates range from 38% to 75% with wet combing as a sole treatment of head lice.³⁶ Because this treatment has minimal risks and no adverse side effects, it can be considered as an alternative treatment for some patients.

Hot air treatments also have been studied. A 2006 study showed that a hot air treatment device had the potential to eradicate head lice, most likely by desiccation. Specifically, 30 minutes of exposure to hot air (at 58.9°F, slightly cooler than a standard hair dryer) using the custom-built device resulted in 98% mortality of eggs and 80% mortality of hatched lice.³⁷ Large randomized controlled trials of hot air treatments have not been performed.

Other alternative treatments include plant-derived oils. A laboratory study of essential oils found that spearmint, cassia, and clove showed pediculicidal activity similar to malathion with improved ovicidal activity.³⁸ However, there is a potential for development of contact dermatitis from essential oils.

Complete Eradication of Head Lice
Removal of nits is an important component of effective lice eradication. Biochemical analysis has revealed that the nit sheath of the head louse is similar in composition to amyloid, rendering it difficult to design products that will unravel the nit sheath while leaving human hair undamaged.³⁹ Because pediculicides are not necessarily ovicidal and complete physical nit removal is difficult to achieve, re-treatment in 7 to 10 days often is advisable to ensure that lice in all stages of the life cycle have been killed.⁴ Treatment of any secondary bacterial infection also is important. Although transmission of lice via fomites is less likely than from head-to-head contact, the cleaning of hats, hairbrushes, and linens is prudent. Diagnosing and treating infested close contacts also is essential to achieving eradication.⁴ Coordinated surveillance, education, and treatment efforts in high-risk communities can help detect asymptomatic cases and control local epidemics in a cost-effective manner.⁴⁰ However, “no nit” policies at schools likely cause a net harm, as nit removal is difficult and children with nonviable nits are then excluded from the classroom.⁵

Treatment Resistance
Resistance to topical neurotoxic treatments is becoming increasingly common.^41-43 Therefore, it is important to identify local patterns of resistance, if possible, when selecting a therapy for head lice. Improper usage, changes in pediculicide formulations and packaging, decreased product efficacy, and natural selection have all contributed to this rise in resistance.⁷ Additionally, due to protection from multiple exoskeletons and the natural molting process as they mature into adults, nymphs may only receive a sublethal dose when exposed to pediculicides, contributing further to resistance.⁷ Resistance to synthetic pyrethroids is most predominant, likely due to selection pressure because permethrin historically has been the most widely used insecticide for pediculosis. A 2014 study found that the frequency of sodium-channel insensitivity to pyrethroids, also known as knockdown resistance (or kdr), in US head louse populations collected over a 10-year period was 84.4% and approached 100% in some communities in recent years.⁴⁴ This evidence strongly supports the use of alternative therapeutic categories to effectively eradicate head lice infestations.

Conclusion

Head lice infestation is common in children, and although it is not harmful to the host, it can be an irritating and symptomatic problem and can lead to notable distress, missed days of school, and secondary infections. Identifying active adult lice is the gold standard for diagnosis. Current recommended treatments include pyrethroids as the first-line therapy; however, resistance to these neurotoxic agents is becoming increasingly common. Alternative therapies such as newer neurotoxic agents or pediculicides with physical mechanisms of action (eg, dimethicone-based products) should be considered, particularly in regions where resistance is known to be high. Education about head lice, proper use of treatment, and coordinated diagnosis are necessary for effective management of this problem.

Scabies is caused by the mite Sarcoptes scabiei var hominis.¹ It is in the arthropod class Arachnida, subclass Acari, and family Sarcoptidae.² Historically, scabies was first described in the Old Testament and by Aristotle,² but the causative organism was not identified until 1687 using a light microscope.³ Scabies affects all age groups, races, and social classes and is globally widespread. It is most prevalent in developing tropical countries.¹ It is estimated that 300 million individuals worldwide are infested with scabies mites annually, with the highest burden in young children.^4-7 In industrialized societies, infections often are seen in young adults and in institutional settings such as nursing homes.⁸ Scabies disproportionately impacts impoverished communities with crowded living conditions, poor hygiene and nutrition, and substandard housing^.5,9 Controlling the spread of the disease in these communities presents challenges but is important because of the connection between scabies and chronic kidney disease.¹⁰ As such, scabies represents a major health problem in the developing world and has been the focus of major health initiatives.^1,11

Identifying Characteristics

Adult females are 0.4-mm long and 0.3-mm wide, with males being smaller. Adult nymphs have 8 legs and larvae have 6 legs. Scabies mites are distinguishable from other arachnids by the position of a distinct gnathosoma and the lack of a division between the abdomen and cephalothorax.¹² They are ovoid with a small anterior cephalic and caudal thoracoabdominal portion with hairlike projections coming off from the rudimentary legs. They can crawl as fast as 2.5 cm per minute on warm skin.² The life cycle of the mite begins after mating: the male mite dies, and the female lays up to 3 eggs per day, which hatch in 3 to 4 days,² in skin burrows within the stratum granulosum.¹² Maturation from larva to adult takes 10 to 14 days.¹² A female mite can live for 4 to 6 weeks and can produce up to 40 ova (Figure 1).

Disease Transmission

Without a host, mites are able to survive and remain capable of infestation for 24 to 36 hours at 21°C and 40% to 80% relative humidity. Lower temperatures and higher humidity prolong survival, but infectivity decreases the longer they are without a host.¹³

An adult human with ordinary scabies will have an average of 12 adult female mites on the body surface at a given time.¹⁴ However, hundreds of mites can be found in neglected children in underprivileged communities and millions in patients with crusted scabies.¹³ Transmission of typical scabies requires close direct skin-to-skin contact for 15 to 20 minutes.^2,8 Transmission from clothing or fomites are an unlikely source of infestation with the exception of patients who are heavily infested such as in crusted scabies.¹² In adults, sexual contact is an important method of transmission,¹² and patients with scabies should be screened for other sexually transmitted diseases.⁸

Clinical Manifestations

Signs of scabies on the skin include burrows, erythematous papules, and generalized pruritus (Figure 2).¹² The scalp, face, and neck frequently are involved in infants and children,² and the hands, wrists, elbows, genitalia, axillae, umbilicus, belt line, nipples, and buttocks commonly are involved in adults.¹² Itching is characteristically worse at night.⁸ In tropical climates, patients with scabies are predisposed to secondary bacterial skin infections, particularly Streptococcus pyogenes (group A streptococci). The association between scabies and pyoderma caused by group A streptococci has been well established.^15,16 Mika et al¹⁰ suggested that local complement inhibition plays an important role in the development of pyoderma in scabies-infested skin. A relationship between scabies and poststreptococcal glomerulonephritis (PSGN) has been established.^11,17 An outbreak of PSGN in Brazil following an epidemic of Streptococcus zooepidemicus resulted in a high prevalence of renal abnormalities (mean follow-up, 5.4 years).¹⁸ In an aboriginal population with high rates of end-stage renal disease, follow-up in children 6 to 18 years after an epidemic of PSGN (mean follow-up, 14.6 years) showed that risk for overt proteinuria was more than 6 times greater than in healthy controls (95% confidence interval, 2.2-16.9).¹⁹ Scabies skin infestations and infections are endemic in many remote aboriginal communities²⁰ where 70% of children younger than 2 years have chronic scabies and skin sores.²¹ In Dhaka, an urban slum in Bangladesh, the incidence of at least one scabies infection in children younger than 6 years was 952 per 1000 per year. In urban settlements in Dhaka, 49% (288/589) of infested children were not treated for up to 44 weeks after the characteristic signs and symptoms had developed due to restricted access to health care.²² In Brazil, scabies is hyperendemic in many poor communities and slums and is commonly associated with considerable morbidity.²³ Edison et al²⁴ reported that scabies and bacterial superinfections cause substantial morbidity among American Samoan children, with superinfections present in 53% (604/1139) of children diagnosed with scabies. Steer et al²⁵ found that impetigo and scabies had been underestimated in Fiji where 25.6% and 18.5% of primary school children and 12.2% and 14.0% of infants had impetigo and scabies, respectively. In a systematic review of scabies and impetigo prevalence, Romani et al²⁶ concluded that scabies and associated impetigo are common problems in the developing world that disproportionately affect children and communities in underprivileged areas and tropical countries, with the Pacific and Latin American regions having the highest prevalence of scabies. Scabies represents a major health concern worldwide due to the strong relationship between scabies and secondary infection.²⁷

Prevention and Control in the Developing World

Low-cost diagnostic equipment can play a key role in the definitive diagnosis and management of scabies outbreaks in the developing world. Micali et al²⁸ found that a $30 videomicroscope was as effective in scabies diagnosis as a $20,000 videodermatoscope. Because of the low cost of benzyl benzoate, it is commonly used as a first-line drug in many parts of the world,¹³ whereas permethrin cream 5% is the standard treatment in the developed world.²⁹ Recognition of the role of scabies in patients with pyoderma is key, and one study indicated clinically apparent scabies went unnoticed by physicians in 52% of patients presenting with skin lesions.³⁰ Drug shortages also can contribute to a high prevalence of scabies infestation in the community.³¹ Mass treatment with ivermectin has proven to be an effective means of reducing the prevalence of many parasitic diseases,^1,32,33 and it shows great promise for crusted scabies, institutional outbreaks, and mass administration in highly endemic communites.⁸ However, there is evidence of ivermectin tolerance among mites, which could undermine the success of mass drug administration.³⁴ Another important consideration is population mobility and the risk for rapid reintroduction of scabies infection across regions.³⁵

Complicating disease control are the socioeconomic factors associated with scabies in the developing world. Families with scabies infestation typically do not own their homes, are less likely to have constant electricity, have a lower monthly income, and live in substandard housing.²⁰ Families can spend a substantial part of their household income on treatment, impacting what they can spend on food.^8,11 In addition to medication, control of scabies requires community education and involvement, along with access to primary care and attention to living conditions and environmental factors.^34,36

Scabies is caused by the mite Sarcoptes scabiei var hominis.¹ It is in the arthropod class Arachnida, subclass Acari, and family Sarcoptidae.² Historically, scabies was first described in the Old Testament and by Aristotle,² but the causative organism was not identified until 1687 using a light microscope.³ Scabies affects all age groups, races, and social classes and is globally widespread. It is most prevalent in developing tropical countries.¹ It is estimated that 300 million individuals worldwide are infested with scabies mites annually, with the highest burden in young children.^4-7 In industrialized societies, infections often are seen in young adults and in institutional settings such as nursing homes.⁸ Scabies disproportionately impacts impoverished communities with crowded living conditions, poor hygiene and nutrition, and substandard housing^.5,9 Controlling the spread of the disease in these communities presents challenges but is important because of the connection between scabies and chronic kidney disease.¹⁰ As such, scabies represents a major health problem in the developing world and has been the focus of major health initiatives.^1,11

Identifying Characteristics

Adult females are 0.4-mm long and 0.3-mm wide, with males being smaller. Adult nymphs have 8 legs and larvae have 6 legs. Scabies mites are distinguishable from other arachnids by the position of a distinct gnathosoma and the lack of a division between the abdomen and cephalothorax.¹² They are ovoid with a small anterior cephalic and caudal thoracoabdominal portion with hairlike projections coming off from the rudimentary legs. They can crawl as fast as 2.5 cm per minute on warm skin.² The life cycle of the mite begins after mating: the male mite dies, and the female lays up to 3 eggs per day, which hatch in 3 to 4 days,² in skin burrows within the stratum granulosum.¹² Maturation from larva to adult takes 10 to 14 days.¹² A female mite can live for 4 to 6 weeks and can produce up to 40 ova (Figure 1).

Disease Transmission

Without a host, mites are able to survive and remain capable of infestation for 24 to 36 hours at 21°C and 40% to 80% relative humidity. Lower temperatures and higher humidity prolong survival, but infectivity decreases the longer they are without a host.¹³

An adult human with ordinary scabies will have an average of 12 adult female mites on the body surface at a given time.¹⁴ However, hundreds of mites can be found in neglected children in underprivileged communities and millions in patients with crusted scabies.¹³ Transmission of typical scabies requires close direct skin-to-skin contact for 15 to 20 minutes.^2,8 Transmission from clothing or fomites are an unlikely source of infestation with the exception of patients who are heavily infested such as in crusted scabies.¹² In adults, sexual contact is an important method of transmission,¹² and patients with scabies should be screened for other sexually transmitted diseases.⁸

Clinical Manifestations

Signs of scabies on the skin include burrows, erythematous papules, and generalized pruritus (Figure 2).¹² The scalp, face, and neck frequently are involved in infants and children,² and the hands, wrists, elbows, genitalia, axillae, umbilicus, belt line, nipples, and buttocks commonly are involved in adults.¹² Itching is characteristically worse at night.⁸ In tropical climates, patients with scabies are predisposed to secondary bacterial skin infections, particularly Streptococcus pyogenes (group A streptococci). The association between scabies and pyoderma caused by group A streptococci has been well established.^15,16 Mika et al¹⁰ suggested that local complement inhibition plays an important role in the development of pyoderma in scabies-infested skin. A relationship between scabies and poststreptococcal glomerulonephritis (PSGN) has been established.^11,17 An outbreak of PSGN in Brazil following an epidemic of Streptococcus zooepidemicus resulted in a high prevalence of renal abnormalities (mean follow-up, 5.4 years).¹⁸ In an aboriginal population with high rates of end-stage renal disease, follow-up in children 6 to 18 years after an epidemic of PSGN (mean follow-up, 14.6 years) showed that risk for overt proteinuria was more than 6 times greater than in healthy controls (95% confidence interval, 2.2-16.9).¹⁹ Scabies skin infestations and infections are endemic in many remote aboriginal communities²⁰ where 70% of children younger than 2 years have chronic scabies and skin sores.²¹ In Dhaka, an urban slum in Bangladesh, the incidence of at least one scabies infection in children younger than 6 years was 952 per 1000 per year. In urban settlements in Dhaka, 49% (288/589) of infested children were not treated for up to 44 weeks after the characteristic signs and symptoms had developed due to restricted access to health care.²² In Brazil, scabies is hyperendemic in many poor communities and slums and is commonly associated with considerable morbidity.²³ Edison et al²⁴ reported that scabies and bacterial superinfections cause substantial morbidity among American Samoan children, with superinfections present in 53% (604/1139) of children diagnosed with scabies. Steer et al²⁵ found that impetigo and scabies had been underestimated in Fiji where 25.6% and 18.5% of primary school children and 12.2% and 14.0% of infants had impetigo and scabies, respectively. In a systematic review of scabies and impetigo prevalence, Romani et al²⁶ concluded that scabies and associated impetigo are common problems in the developing world that disproportionately affect children and communities in underprivileged areas and tropical countries, with the Pacific and Latin American regions having the highest prevalence of scabies. Scabies represents a major health concern worldwide due to the strong relationship between scabies and secondary infection.²⁷

Prevention and Control in the Developing World

Low-cost diagnostic equipment can play a key role in the definitive diagnosis and management of scabies outbreaks in the developing world. Micali et al²⁸ found that a $30 videomicroscope was as effective in scabies diagnosis as a $20,000 videodermatoscope. Because of the low cost of benzyl benzoate, it is commonly used as a first-line drug in many parts of the world,¹³ whereas permethrin cream 5% is the standard treatment in the developed world.²⁹ Recognition of the role of scabies in patients with pyoderma is key, and one study indicated clinically apparent scabies went unnoticed by physicians in 52% of patients presenting with skin lesions.³⁰ Drug shortages also can contribute to a high prevalence of scabies infestation in the community.³¹ Mass treatment with ivermectin has proven to be an effective means of reducing the prevalence of many parasitic diseases,^1,32,33 and it shows great promise for crusted scabies, institutional outbreaks, and mass administration in highly endemic communites.⁸ However, there is evidence of ivermectin tolerance among mites, which could undermine the success of mass drug administration.³⁴ Another important consideration is population mobility and the risk for rapid reintroduction of scabies infection across regions.³⁵

Complicating disease control are the socioeconomic factors associated with scabies in the developing world. Families with scabies infestation typically do not own their homes, are less likely to have constant electricity, have a lower monthly income, and live in substandard housing.²⁰ Families can spend a substantial part of their household income on treatment, impacting what they can spend on food.^8,11 In addition to medication, control of scabies requires community education and involvement, along with access to primary care and attention to living conditions and environmental factors.^34,36

Scabies is caused by the mite Sarcoptes scabiei var hominis.¹ It is in the arthropod class Arachnida, subclass Acari, and family Sarcoptidae.² Historically, scabies was first described in the Old Testament and by Aristotle,² but the causative organism was not identified until 1687 using a light microscope.³ Scabies affects all age groups, races, and social classes and is globally widespread. It is most prevalent in developing tropical countries.¹ It is estimated that 300 million individuals worldwide are infested with scabies mites annually, with the highest burden in young children.^4-7 In industrialized societies, infections often are seen in young adults and in institutional settings such as nursing homes.⁸ Scabies disproportionately impacts impoverished communities with crowded living conditions, poor hygiene and nutrition, and substandard housing^.5,9 Controlling the spread of the disease in these communities presents challenges but is important because of the connection between scabies and chronic kidney disease.¹⁰ As such, scabies represents a major health problem in the developing world and has been the focus of major health initiatives.^1,11

Identifying Characteristics

Adult females are 0.4-mm long and 0.3-mm wide, with males being smaller. Adult nymphs have 8 legs and larvae have 6 legs. Scabies mites are distinguishable from other arachnids by the position of a distinct gnathosoma and the lack of a division between the abdomen and cephalothorax.¹² They are ovoid with a small anterior cephalic and caudal thoracoabdominal portion with hairlike projections coming off from the rudimentary legs. They can crawl as fast as 2.5 cm per minute on warm skin.² The life cycle of the mite begins after mating: the male mite dies, and the female lays up to 3 eggs per day, which hatch in 3 to 4 days,² in skin burrows within the stratum granulosum.¹² Maturation from larva to adult takes 10 to 14 days.¹² A female mite can live for 4 to 6 weeks and can produce up to 40 ova (Figure 1).

Disease Transmission

Without a host, mites are able to survive and remain capable of infestation for 24 to 36 hours at 21°C and 40% to 80% relative humidity. Lower temperatures and higher humidity prolong survival, but infectivity decreases the longer they are without a host.¹³

An adult human with ordinary scabies will have an average of 12 adult female mites on the body surface at a given time.¹⁴ However, hundreds of mites can be found in neglected children in underprivileged communities and millions in patients with crusted scabies.¹³ Transmission of typical scabies requires close direct skin-to-skin contact for 15 to 20 minutes.^2,8 Transmission from clothing or fomites are an unlikely source of infestation with the exception of patients who are heavily infested such as in crusted scabies.¹² In adults, sexual contact is an important method of transmission,¹² and patients with scabies should be screened for other sexually transmitted diseases.⁸

Clinical Manifestations

Signs of scabies on the skin include burrows, erythematous papules, and generalized pruritus (Figure 2).¹² The scalp, face, and neck frequently are involved in infants and children,² and the hands, wrists, elbows, genitalia, axillae, umbilicus, belt line, nipples, and buttocks commonly are involved in adults.¹² Itching is characteristically worse at night.⁸ In tropical climates, patients with scabies are predisposed to secondary bacterial skin infections, particularly Streptococcus pyogenes (group A streptococci). The association between scabies and pyoderma caused by group A streptococci has been well established.^15,16 Mika et al¹⁰ suggested that local complement inhibition plays an important role in the development of pyoderma in scabies-infested skin. A relationship between scabies and poststreptococcal glomerulonephritis (PSGN) has been established.^11,17 An outbreak of PSGN in Brazil following an epidemic of Streptococcus zooepidemicus resulted in a high prevalence of renal abnormalities (mean follow-up, 5.4 years).¹⁸ In an aboriginal population with high rates of end-stage renal disease, follow-up in children 6 to 18 years after an epidemic of PSGN (mean follow-up, 14.6 years) showed that risk for overt proteinuria was more than 6 times greater than in healthy controls (95% confidence interval, 2.2-16.9).¹⁹ Scabies skin infestations and infections are endemic in many remote aboriginal communities²⁰ where 70% of children younger than 2 years have chronic scabies and skin sores.²¹ In Dhaka, an urban slum in Bangladesh, the incidence of at least one scabies infection in children younger than 6 years was 952 per 1000 per year. In urban settlements in Dhaka, 49% (288/589) of infested children were not treated for up to 44 weeks after the characteristic signs and symptoms had developed due to restricted access to health care.²² In Brazil, scabies is hyperendemic in many poor communities and slums and is commonly associated with considerable morbidity.²³ Edison et al²⁴ reported that scabies and bacterial superinfections cause substantial morbidity among American Samoan children, with superinfections present in 53% (604/1139) of children diagnosed with scabies. Steer et al²⁵ found that impetigo and scabies had been underestimated in Fiji where 25.6% and 18.5% of primary school children and 12.2% and 14.0% of infants had impetigo and scabies, respectively. In a systematic review of scabies and impetigo prevalence, Romani et al²⁶ concluded that scabies and associated impetigo are common problems in the developing world that disproportionately affect children and communities in underprivileged areas and tropical countries, with the Pacific and Latin American regions having the highest prevalence of scabies. Scabies represents a major health concern worldwide due to the strong relationship between scabies and secondary infection.²⁷

Prevention and Control in the Developing World

Low-cost diagnostic equipment can play a key role in the definitive diagnosis and management of scabies outbreaks in the developing world. Micali et al²⁸ found that a $30 videomicroscope was as effective in scabies diagnosis as a $20,000 videodermatoscope. Because of the low cost of benzyl benzoate, it is commonly used as a first-line drug in many parts of the world,¹³ whereas permethrin cream 5% is the standard treatment in the developed world.²⁹ Recognition of the role of scabies in patients with pyoderma is key, and one study indicated clinically apparent scabies went unnoticed by physicians in 52% of patients presenting with skin lesions.³⁰ Drug shortages also can contribute to a high prevalence of scabies infestation in the community.³¹ Mass treatment with ivermectin has proven to be an effective means of reducing the prevalence of many parasitic diseases,^1,32,33 and it shows great promise for crusted scabies, institutional outbreaks, and mass administration in highly endemic communites.⁸ However, there is evidence of ivermectin tolerance among mites, which could undermine the success of mass drug administration.³⁴ Another important consideration is population mobility and the risk for rapid reintroduction of scabies infection across regions.³⁵

Complicating disease control are the socioeconomic factors associated with scabies in the developing world. Families with scabies infestation typically do not own their homes, are less likely to have constant electricity, have a lower monthly income, and live in substandard housing.²⁰ Families can spend a substantial part of their household income on treatment, impacting what they can spend on food.^8,11 In addition to medication, control of scabies requires community education and involvement, along with access to primary care and attention to living conditions and environmental factors.^34,36

The Diagnosis: Lichen Aureus

The clinicopathological findings were diagnostic of lichen aureus (LA). Microscopic examination revealed a relatively sparse, superficial, perivascular and interstitial lymphohistiocytic infiltrate with scattered siderophages in the upper dermis. Extravasation of red blood cells also was noted (Figure 1). An immunohistochemical stain for Melan-A highlighted a normal number and distribution of single melanocytes at the dermoepidermal junction with no evidence of pagetoid scatter. A Perls Prussian blue stain for iron demonstrated abundant hemosiderin in the dermis (Figure 2).

Pigmented purpuric dermatosis (PPD) describes a group of cutaneous lesions that are characterized by petechiae and pigmentary changes. These lesions most commonly present on the lower limbs; however, other sites have been reported.1 This group includes several major clinical forms such as Schamberg disease, LA, purpura annularis telangiectodes of Majocchi, eczematidlike purpura of Doucas and Kapetanakis, and lichenoid PPD of Gougerot and Blum. Lesions typically demonstrate a striking golden brown color clinically and by definition occur in the absence of platelet defects or vasculitis.¹

Factors implicated in the pathogenesis of pigmented purpura include gravitational dependency, venous stasis, infection, and drugs.² It is suggested that cellular immunity may play a role in the development of the disease based on the presence of CD4⁺ T lymphocytes in the infiltrate and the expression of HLA-DR by these lymphocytes and the keratinocytes.³ Lichen aureus differs in that it relates to increased intravascular pressure from an incompetent valve in an underlying perforating vein.⁴

Lichen aureus, also referred to as lichen purpuricus, is one major variant of PPD. The name reflects both the characteristic golden brown color and the histopathologic pattern of inflammation.¹ Lichen aureus usually presents as a unilateral, asymptomatic, confined single lesion located mainly on the leg,¹ though it can develop at other sites or as a localized group of lesions. Extensive lesions have been reported⁵ and cases with a segmental distribution have been described.⁶ In contrast, Schamberg disease demonstrates pinhead-sized reddish lesions giving the characteristic cayenne pepper pigmentation. These lesions coalesce to form thumbprint patches that progress proximally.¹ Majocchi purpura is annular and telangiectatic, while lichenoid purpura of Gougerot and Blum presents with flat-topped, polygonal, violaceous papules that turn brown over time.

Some authors have championed a role for dermoscopy in diagnosis of LA.⁷ By dermoscopy, LA demonstrates a diffuse copper background reflecting the lymphohistiocytic dermal infiltrate, red dots and globules representing the extravasated red blood cells and the dilated swollen vessels, and grey dots that reflect the hemosiderin present in the dermis.⁸

Histologically, LA demonstrates a superficial perivascular infiltrate composed mainly of CD4⁺ lymphocytes surrounding the superficial capillaries. Over time, red cell extravasation leads to the formation of hemosiderin-laden macrophages, which can be highlighted with Perls Prussian blue stain. A bandlike infiltrate with thin strands of collagen separating it from the epidermis also may be noted.⁹

An important consideration in the differential diagnosis of PPD is mycosis fungoides (MF). Mycosis fungoides is a cutaneous T-cell lymphoma that clinically presents as a single or multiple hypopigmented or hyperpigmented patches or as erythematous scaly lesions in the patch or plaque stage. These lesions eventually may evolve into tumor stage.¹⁰ Mycosis fungoides may mimic PPD clinically and/or histopathologically, and rarely PPD also may precede MF.¹¹ Involvement of the trunk, especially the lower abdomen and buttock region, favors a diagnosis of MF. Typically, histopathologic examination of MF demonstrates an epidermotropic lymphocytic infiltrate composed of atypical cerebriform lymphocytes overlying papillary dermal fibrosis. Although classic MF would be difficult to confuse with PPD, the atrophic lichenoid pattern of MF may show remarkable overlap with PPD.¹² Such cases require clinicopathologic correlation, immunophenotyping of the epidermotropic lymphocytes, and occasionally T-cell clonality studies.

Lichen aureus is a chronic persistent disease unless the underlying incompetent perforator vessel is ligated. Various treatments have been used for other forms of pigmented purpura including topical corticosteroids, topical tacrolimus, systemic vasodilators such as prostacyclin and pentoxifylline, and phototherapy.¹ Clinical follow-up is recommended for lesions that show some clinical or histopathological overlap with MF. Additional biopsies also may prove useful in establishing a definitive diagnosis in ambiguous cases.

The Diagnosis: Lichen Aureus

The clinicopathological findings were diagnostic of lichen aureus (LA). Microscopic examination revealed a relatively sparse, superficial, perivascular and interstitial lymphohistiocytic infiltrate with scattered siderophages in the upper dermis. Extravasation of red blood cells also was noted (Figure 1). An immunohistochemical stain for Melan-A highlighted a normal number and distribution of single melanocytes at the dermoepidermal junction with no evidence of pagetoid scatter. A Perls Prussian blue stain for iron demonstrated abundant hemosiderin in the dermis (Figure 2).

Pigmented purpuric dermatosis (PPD) describes a group of cutaneous lesions that are characterized by petechiae and pigmentary changes. These lesions most commonly present on the lower limbs; however, other sites have been reported.1 This group includes several major clinical forms such as Schamberg disease, LA, purpura annularis telangiectodes of Majocchi, eczematidlike purpura of Doucas and Kapetanakis, and lichenoid PPD of Gougerot and Blum. Lesions typically demonstrate a striking golden brown color clinically and by definition occur in the absence of platelet defects or vasculitis.¹

Factors implicated in the pathogenesis of pigmented purpura include gravitational dependency, venous stasis, infection, and drugs.² It is suggested that cellular immunity may play a role in the development of the disease based on the presence of CD4⁺ T lymphocytes in the infiltrate and the expression of HLA-DR by these lymphocytes and the keratinocytes.³ Lichen aureus differs in that it relates to increased intravascular pressure from an incompetent valve in an underlying perforating vein.⁴

Lichen aureus, also referred to as lichen purpuricus, is one major variant of PPD. The name reflects both the characteristic golden brown color and the histopathologic pattern of inflammation.¹ Lichen aureus usually presents as a unilateral, asymptomatic, confined single lesion located mainly on the leg,¹ though it can develop at other sites or as a localized group of lesions. Extensive lesions have been reported⁵ and cases with a segmental distribution have been described.⁶ In contrast, Schamberg disease demonstrates pinhead-sized reddish lesions giving the characteristic cayenne pepper pigmentation. These lesions coalesce to form thumbprint patches that progress proximally.¹ Majocchi purpura is annular and telangiectatic, while lichenoid purpura of Gougerot and Blum presents with flat-topped, polygonal, violaceous papules that turn brown over time.

Some authors have championed a role for dermoscopy in diagnosis of LA.⁷ By dermoscopy, LA demonstrates a diffuse copper background reflecting the lymphohistiocytic dermal infiltrate, red dots and globules representing the extravasated red blood cells and the dilated swollen vessels, and grey dots that reflect the hemosiderin present in the dermis.⁸

Histologically, LA demonstrates a superficial perivascular infiltrate composed mainly of CD4⁺ lymphocytes surrounding the superficial capillaries. Over time, red cell extravasation leads to the formation of hemosiderin-laden macrophages, which can be highlighted with Perls Prussian blue stain. A bandlike infiltrate with thin strands of collagen separating it from the epidermis also may be noted.⁹

An important consideration in the differential diagnosis of PPD is mycosis fungoides (MF). Mycosis fungoides is a cutaneous T-cell lymphoma that clinically presents as a single or multiple hypopigmented or hyperpigmented patches or as erythematous scaly lesions in the patch or plaque stage. These lesions eventually may evolve into tumor stage.¹⁰ Mycosis fungoides may mimic PPD clinically and/or histopathologically, and rarely PPD also may precede MF.¹¹ Involvement of the trunk, especially the lower abdomen and buttock region, favors a diagnosis of MF. Typically, histopathologic examination of MF demonstrates an epidermotropic lymphocytic infiltrate composed of atypical cerebriform lymphocytes overlying papillary dermal fibrosis. Although classic MF would be difficult to confuse with PPD, the atrophic lichenoid pattern of MF may show remarkable overlap with PPD.¹² Such cases require clinicopathologic correlation, immunophenotyping of the epidermotropic lymphocytes, and occasionally T-cell clonality studies.

Lichen aureus is a chronic persistent disease unless the underlying incompetent perforator vessel is ligated. Various treatments have been used for other forms of pigmented purpura including topical corticosteroids, topical tacrolimus, systemic vasodilators such as prostacyclin and pentoxifylline, and phototherapy.¹ Clinical follow-up is recommended for lesions that show some clinical or histopathological overlap with MF. Additional biopsies also may prove useful in establishing a definitive diagnosis in ambiguous cases.

The Diagnosis: Lichen Aureus

The clinicopathological findings were diagnostic of lichen aureus (LA). Microscopic examination revealed a relatively sparse, superficial, perivascular and interstitial lymphohistiocytic infiltrate with scattered siderophages in the upper dermis. Extravasation of red blood cells also was noted (Figure 1). An immunohistochemical stain for Melan-A highlighted a normal number and distribution of single melanocytes at the dermoepidermal junction with no evidence of pagetoid scatter. A Perls Prussian blue stain for iron demonstrated abundant hemosiderin in the dermis (Figure 2).

Pigmented purpuric dermatosis (PPD) describes a group of cutaneous lesions that are characterized by petechiae and pigmentary changes. These lesions most commonly present on the lower limbs; however, other sites have been reported.1 This group includes several major clinical forms such as Schamberg disease, LA, purpura annularis telangiectodes of Majocchi, eczematidlike purpura of Doucas and Kapetanakis, and lichenoid PPD of Gougerot and Blum. Lesions typically demonstrate a striking golden brown color clinically and by definition occur in the absence of platelet defects or vasculitis.¹

Factors implicated in the pathogenesis of pigmented purpura include gravitational dependency, venous stasis, infection, and drugs.² It is suggested that cellular immunity may play a role in the development of the disease based on the presence of CD4⁺ T lymphocytes in the infiltrate and the expression of HLA-DR by these lymphocytes and the keratinocytes.³ Lichen aureus differs in that it relates to increased intravascular pressure from an incompetent valve in an underlying perforating vein.⁴

Lichen aureus, also referred to as lichen purpuricus, is one major variant of PPD. The name reflects both the characteristic golden brown color and the histopathologic pattern of inflammation.¹ Lichen aureus usually presents as a unilateral, asymptomatic, confined single lesion located mainly on the leg,¹ though it can develop at other sites or as a localized group of lesions. Extensive lesions have been reported⁵ and cases with a segmental distribution have been described.⁶ In contrast, Schamberg disease demonstrates pinhead-sized reddish lesions giving the characteristic cayenne pepper pigmentation. These lesions coalesce to form thumbprint patches that progress proximally.¹ Majocchi purpura is annular and telangiectatic, while lichenoid purpura of Gougerot and Blum presents with flat-topped, polygonal, violaceous papules that turn brown over time.

Some authors have championed a role for dermoscopy in diagnosis of LA.⁷ By dermoscopy, LA demonstrates a diffuse copper background reflecting the lymphohistiocytic dermal infiltrate, red dots and globules representing the extravasated red blood cells and the dilated swollen vessels, and grey dots that reflect the hemosiderin present in the dermis.⁸

Histologically, LA demonstrates a superficial perivascular infiltrate composed mainly of CD4⁺ lymphocytes surrounding the superficial capillaries. Over time, red cell extravasation leads to the formation of hemosiderin-laden macrophages, which can be highlighted with Perls Prussian blue stain. A bandlike infiltrate with thin strands of collagen separating it from the epidermis also may be noted.⁹

An important consideration in the differential diagnosis of PPD is mycosis fungoides (MF). Mycosis fungoides is a cutaneous T-cell lymphoma that clinically presents as a single or multiple hypopigmented or hyperpigmented patches or as erythematous scaly lesions in the patch or plaque stage. These lesions eventually may evolve into tumor stage.¹⁰ Mycosis fungoides may mimic PPD clinically and/or histopathologically, and rarely PPD also may precede MF.¹¹ Involvement of the trunk, especially the lower abdomen and buttock region, favors a diagnosis of MF. Typically, histopathologic examination of MF demonstrates an epidermotropic lymphocytic infiltrate composed of atypical cerebriform lymphocytes overlying papillary dermal fibrosis. Although classic MF would be difficult to confuse with PPD, the atrophic lichenoid pattern of MF may show remarkable overlap with PPD.¹² Such cases require clinicopathologic correlation, immunophenotyping of the epidermotropic lymphocytes, and occasionally T-cell clonality studies.

Lichen aureus is a chronic persistent disease unless the underlying incompetent perforator vessel is ligated. Various treatments have been used for other forms of pigmented purpura including topical corticosteroids, topical tacrolimus, systemic vasodilators such as prostacyclin and pentoxifylline, and phototherapy.¹ Clinical follow-up is recommended for lesions that show some clinical or histopathological overlap with MF. Additional biopsies also may prove useful in establishing a definitive diagnosis in ambiguous cases.

Identifying Characteristics

The sticktight flea (Echidnophaga gallinacea) earns its name by embedding its head in the host's skin using broad and serrated laciniae and can feed at one site for up to 19 days.¹ It differs in morphology from dog (Ctenocephalides canis) and cat (Ctenocephalides felis) fleas, lacking genal (mustache area) and promotal (back of the head) ctenidia (combs), and is half the size of the cat flea. It has 2 pairs of setae (hairs) behind the antennae with an anteriorly flattened head (Figure). 

Disease Transmission

Although its primary host is poultry and it also is known as the stickfast or chicken flea, the sticktight flea has been found in many species of birds and mammals, including humans. It is becoming more common in dogs in many parts of the world, including the United States,^2-5 and has been found to be the most common flea on dogs in areas of South Africa.⁶ Other noted hosts of E gallinacea are rodents, cottontail rabbits, cats, ground squirrels, and pigs.^7-14 Human infestation occurs from exposure to affected animals.¹⁵ As blood feeders, fleas have long been known to serve as vectors for many diseases, including bubonic plague, typhus, and tularemia, as well as an intermediate host of the dog tapeworm (Dipylidium caninum).⁵Rickettsia felis, belonging to the spotted fever group, is an emerging infectious disease in humans commonly found in the cat flea (C felis) but also has been detected in E gallinacea.⁷Echidnophaga gallinacea is found worldwide in the tropics, subtropics, and temperate zones, and it is the only representative of the genus found in the United States.¹ Given the wide range of wild and domestic animal hosts and wide geographic distribution for E gallinacea, it represents an increasing risk for humans.

Echidnophaga gallinacea favors feeding from fleshy areas without thick fur or plumage. In birds, the area around the eyes, comb, and wattles is included; in dogs, it can be the eyes, in between the toes, and in the genital area.¹ Flea bites cause irritation and itching for hosts including humans, typically resulting in clusters of firm, pruritic, erythematous papules with a central punctum.¹⁵ Severe bites also may lead to bullous lesions. In birds, symptoms can be extreme, with infestation around the eyes leading to swelling and blindness, a decline in egg production, weight loss, and death in young birds.¹ Similar to other fleas, E gallinacea is wingless and depends on jumping onto a host for transmission, which can be from the ground, carpeting and flooring, furniture, or another host. Fleas are champion jumpers (relative to body size) and can jump 100 times their length.¹⁶

Management

Treating sticktight fleas can be tricky, as they embed tightly into the host's skin. Animals should be treated by a qualified veterinarian. Removal of attached fleas in humans requires grasping the flea firmly with tweezers and pulling from the skin. If the infestation is considerable, malathion 5% liquid or gel can be applied. Patients can treat itching with topical steroids and antipruritic creams, and oral antihistamines can be used to relieve symptoms and reduce the likelihood of damaged skin as well as the potential for secondary infection. The flea-infested environment should be treated with insecticides. For treatment of hard surfaces, dichlorvos and propetamphos are effective. Organophosphates work well on fabric and carpeting. Domestic pets and livestock may be treated by a veterinarian with agents such as fipronil, selamectin, imidacloprid, metaflumizone, nitenpyram, lufenuron, methoprene, and pyriproxyfen.
 

Identifying Characteristics

The sticktight flea (Echidnophaga gallinacea) earns its name by embedding its head in the host's skin using broad and serrated laciniae and can feed at one site for up to 19 days.¹ It differs in morphology from dog (Ctenocephalides canis) and cat (Ctenocephalides felis) fleas, lacking genal (mustache area) and promotal (back of the head) ctenidia (combs), and is half the size of the cat flea. It has 2 pairs of setae (hairs) behind the antennae with an anteriorly flattened head (Figure). 

Disease Transmission

Although its primary host is poultry and it also is known as the stickfast or chicken flea, the sticktight flea has been found in many species of birds and mammals, including humans. It is becoming more common in dogs in many parts of the world, including the United States,^2-5 and has been found to be the most common flea on dogs in areas of South Africa.⁶ Other noted hosts of E gallinacea are rodents, cottontail rabbits, cats, ground squirrels, and pigs.^7-14 Human infestation occurs from exposure to affected animals.¹⁵ As blood feeders, fleas have long been known to serve as vectors for many diseases, including bubonic plague, typhus, and tularemia, as well as an intermediate host of the dog tapeworm (Dipylidium caninum).⁵Rickettsia felis, belonging to the spotted fever group, is an emerging infectious disease in humans commonly found in the cat flea (C felis) but also has been detected in E gallinacea.⁷Echidnophaga gallinacea is found worldwide in the tropics, subtropics, and temperate zones, and it is the only representative of the genus found in the United States.¹ Given the wide range of wild and domestic animal hosts and wide geographic distribution for E gallinacea, it represents an increasing risk for humans.

Echidnophaga gallinacea favors feeding from fleshy areas without thick fur or plumage. In birds, the area around the eyes, comb, and wattles is included; in dogs, it can be the eyes, in between the toes, and in the genital area.¹ Flea bites cause irritation and itching for hosts including humans, typically resulting in clusters of firm, pruritic, erythematous papules with a central punctum.¹⁵ Severe bites also may lead to bullous lesions. In birds, symptoms can be extreme, with infestation around the eyes leading to swelling and blindness, a decline in egg production, weight loss, and death in young birds.¹ Similar to other fleas, E gallinacea is wingless and depends on jumping onto a host for transmission, which can be from the ground, carpeting and flooring, furniture, or another host. Fleas are champion jumpers (relative to body size) and can jump 100 times their length.¹⁶

Management

Treating sticktight fleas can be tricky, as they embed tightly into the host's skin. Animals should be treated by a qualified veterinarian. Removal of attached fleas in humans requires grasping the flea firmly with tweezers and pulling from the skin. If the infestation is considerable, malathion 5% liquid or gel can be applied. Patients can treat itching with topical steroids and antipruritic creams, and oral antihistamines can be used to relieve symptoms and reduce the likelihood of damaged skin as well as the potential for secondary infection. The flea-infested environment should be treated with insecticides. For treatment of hard surfaces, dichlorvos and propetamphos are effective. Organophosphates work well on fabric and carpeting. Domestic pets and livestock may be treated by a veterinarian with agents such as fipronil, selamectin, imidacloprid, metaflumizone, nitenpyram, lufenuron, methoprene, and pyriproxyfen.
 

Identifying Characteristics

The sticktight flea (Echidnophaga gallinacea) earns its name by embedding its head in the host's skin using broad and serrated laciniae and can feed at one site for up to 19 days.¹ It differs in morphology from dog (Ctenocephalides canis) and cat (Ctenocephalides felis) fleas, lacking genal (mustache area) and promotal (back of the head) ctenidia (combs), and is half the size of the cat flea. It has 2 pairs of setae (hairs) behind the antennae with an anteriorly flattened head (Figure). 

Disease Transmission

Although its primary host is poultry and it also is known as the stickfast or chicken flea, the sticktight flea has been found in many species of birds and mammals, including humans. It is becoming more common in dogs in many parts of the world, including the United States,^2-5 and has been found to be the most common flea on dogs in areas of South Africa.⁶ Other noted hosts of E gallinacea are rodents, cottontail rabbits, cats, ground squirrels, and pigs.^7-14 Human infestation occurs from exposure to affected animals.¹⁵ As blood feeders, fleas have long been known to serve as vectors for many diseases, including bubonic plague, typhus, and tularemia, as well as an intermediate host of the dog tapeworm (Dipylidium caninum).⁵Rickettsia felis, belonging to the spotted fever group, is an emerging infectious disease in humans commonly found in the cat flea (C felis) but also has been detected in E gallinacea.⁷Echidnophaga gallinacea is found worldwide in the tropics, subtropics, and temperate zones, and it is the only representative of the genus found in the United States.¹ Given the wide range of wild and domestic animal hosts and wide geographic distribution for E gallinacea, it represents an increasing risk for humans.

Echidnophaga gallinacea favors feeding from fleshy areas without thick fur or plumage. In birds, the area around the eyes, comb, and wattles is included; in dogs, it can be the eyes, in between the toes, and in the genital area.¹ Flea bites cause irritation and itching for hosts including humans, typically resulting in clusters of firm, pruritic, erythematous papules with a central punctum.¹⁵ Severe bites also may lead to bullous lesions. In birds, symptoms can be extreme, with infestation around the eyes leading to swelling and blindness, a decline in egg production, weight loss, and death in young birds.¹ Similar to other fleas, E gallinacea is wingless and depends on jumping onto a host for transmission, which can be from the ground, carpeting and flooring, furniture, or another host. Fleas are champion jumpers (relative to body size) and can jump 100 times their length.¹⁶

Management

Treating sticktight fleas can be tricky, as they embed tightly into the host's skin. Animals should be treated by a qualified veterinarian. Removal of attached fleas in humans requires grasping the flea firmly with tweezers and pulling from the skin. If the infestation is considerable, malathion 5% liquid or gel can be applied. Patients can treat itching with topical steroids and antipruritic creams, and oral antihistamines can be used to relieve symptoms and reduce the likelihood of damaged skin as well as the potential for secondary infection. The flea-infested environment should be treated with insecticides. For treatment of hard surfaces, dichlorvos and propetamphos are effective. Organophosphates work well on fabric and carpeting. Domestic pets and livestock may be treated by a veterinarian with agents such as fipronil, selamectin, imidacloprid, metaflumizone, nitenpyram, lufenuron, methoprene, and pyriproxyfen.
 

Identifying Characteristics and Disease Transmission

Chiggers belong to the Trombiculidae family of mites and also are referred to as harvest mites, harvest bugs, harvest lice, mower’s mites, and redbugs.¹ The term chigger specifically describes the larval stage of this mite’s life cycle, as it is the only stage responsible for chigger bites. The nymph and adult phases feed on vegetable matter. Trombiculid mites are most often found in forests, grassy areas, gardens, and moist areas of soil near bodies of water. Trombicula alfreddugesi is the most common species in the United States, and these mites mainly live in the southeastern and south central regions of the country. Conversely, Trombicula autumnalis is most predominant in Western Europe and East Asia.¹

The life cycle of the mite includes the egg, larval, nymphal, and adult stages.² Due to their need for air humidity greater than 80%, mites lay their eggs on low leaves, blades of grass, or on the ground. They spend most of their lives on vegetation no more than 30 cm above ground level.³ Eggs remain dormant for approximately 6 days until the hatching of the prelarvae, which have 6 legs and are nonfeeding. It takes another 6 days for the prelarvae to mature into larvae. Measuring 0.15 to 0.3 mm in length, mite larvae are a mere fraction of the size of adult mites, which generally are 1 to 2 mm in length, and are bright red or brown-red in color (Figure 1).

The biting larvae have many acceptable hosts including turtles, toads, birds, small mammals, and humans, which act as accidental hosts. Larvae remain on vegetation waiting for a suitable host to pass by so they may attach to its skin and remain there for several days. In the exploration for an ideal area to begin feeding (eg, thin epidermis,⁴ localized increased air humidity⁵), larvae can travel extensively on the skin; however, they often are stopped by tight-fitting sections of clothing (eg, waistbands), so bites are mostly found in clusters. To feed, mite larvae latch onto the skin using chelicerae, jawlike appendages found in the front of the mouth in arachnids.⁶ They then inject digestive enzymes that liquefy epidermal cells on direct contact, which results in the formation of a stylostome from which the mites may suck up lymph fluid and broken down tissue.⁷ Although the actual initial bite is painless, this feeding process leads to the localized inflammation and irritation noticed by infested patients.⁸

The classic clinical presentation includes severe pruritus and cutaneous swelling as well as erythema caused by the combination of several factors, such as enzyme-induced cellular mechanical damage, human immune response, and sometimes a superimposed bacterial infection. Papules and papulovesicles appear in groups, most commonly affecting the legs and waistline (Figure 2).⁹ Itching generally occurs within hours of larval latching and subsides within 72 hours. Cutaneous lesions typically take 1 to 2 weeks to heal. In some rare cases, patients may react with urticarial, bullous, or morbilliform eruptions, and the inflammation and pruritus can last for weeks.⁶ Summer penile syndrome has been noted in boys who display a local hypersensitivity to chigger bites.¹⁰ This syndrome represents a triad of penile swelling, dysuria, and pruritus, which lasts for a few days to a few weeks.

Disease Management

Because the lesions are self-healing, treatment is focused on symptomatic relief of itching by means of topical antipruritics (eg, camphor and menthol, pramoxine lotion) or oral antihistamines (eg, diphenhydramine, hydroxyzine). Potent topical corticosteroids may be used to alleviate inflammation and pruritus, especially when occluded under plastic wrap to increase absorption. In severe cases, an intralesional triamcinolone acetonide (2.5–5 mg/mL) injection may be required.⁹ The best practice, however, is to take preventative measures to avoid becoming a host for the mites. Patients should take special care when traveling in infested areas by completely covering their skin, tucking pant cuffs into their socks, and applying products containing DEET (N,N-diethyl-meta-toluamide or N,N-diethyl-3-methylbenzamide) to the skin and clothing. The odds of prevention are increased even further when clothing also is treated with permethrin.¹¹

In parts of Asia and Australia, these mites may transmit Orientia tsutsugamushi, the organism responsible for scrub typhus, through their saliva during a bite.¹² Scrub typhus is associated with an eschar, as well as fever, intense headache, and diffuse myalgia. It responds well to treatment with doxycycline 100 mg twice daily.¹³ Studies investigating genetic material found in trombiculid mites across the globe have detected Ehrlichia-specific DNA in Spain,¹⁴Borrelia-specific DNA in the Czech Republic,^15,16 and Hantavirus-specific RNA in Texas.¹⁷ There is evidence that the mites play a role in maintenance of zoonotic reservoirs, while humans are infected via ingestion or inhalation of infectious rodent extreta.¹⁸

Identifying Characteristics and Disease Transmission

Chiggers belong to the Trombiculidae family of mites and also are referred to as harvest mites, harvest bugs, harvest lice, mower’s mites, and redbugs.¹ The term chigger specifically describes the larval stage of this mite’s life cycle, as it is the only stage responsible for chigger bites. The nymph and adult phases feed on vegetable matter. Trombiculid mites are most often found in forests, grassy areas, gardens, and moist areas of soil near bodies of water. Trombicula alfreddugesi is the most common species in the United States, and these mites mainly live in the southeastern and south central regions of the country. Conversely, Trombicula autumnalis is most predominant in Western Europe and East Asia.¹

The life cycle of the mite includes the egg, larval, nymphal, and adult stages.² Due to their need for air humidity greater than 80%, mites lay their eggs on low leaves, blades of grass, or on the ground. They spend most of their lives on vegetation no more than 30 cm above ground level.³ Eggs remain dormant for approximately 6 days until the hatching of the prelarvae, which have 6 legs and are nonfeeding. It takes another 6 days for the prelarvae to mature into larvae. Measuring 0.15 to 0.3 mm in length, mite larvae are a mere fraction of the size of adult mites, which generally are 1 to 2 mm in length, and are bright red or brown-red in color (Figure 1).

The biting larvae have many acceptable hosts including turtles, toads, birds, small mammals, and humans, which act as accidental hosts. Larvae remain on vegetation waiting for a suitable host to pass by so they may attach to its skin and remain there for several days. In the exploration for an ideal area to begin feeding (eg, thin epidermis,⁴ localized increased air humidity⁵), larvae can travel extensively on the skin; however, they often are stopped by tight-fitting sections of clothing (eg, waistbands), so bites are mostly found in clusters. To feed, mite larvae latch onto the skin using chelicerae, jawlike appendages found in the front of the mouth in arachnids.⁶ They then inject digestive enzymes that liquefy epidermal cells on direct contact, which results in the formation of a stylostome from which the mites may suck up lymph fluid and broken down tissue.⁷ Although the actual initial bite is painless, this feeding process leads to the localized inflammation and irritation noticed by infested patients.⁸

The classic clinical presentation includes severe pruritus and cutaneous swelling as well as erythema caused by the combination of several factors, such as enzyme-induced cellular mechanical damage, human immune response, and sometimes a superimposed bacterial infection. Papules and papulovesicles appear in groups, most commonly affecting the legs and waistline (Figure 2).⁹ Itching generally occurs within hours of larval latching and subsides within 72 hours. Cutaneous lesions typically take 1 to 2 weeks to heal. In some rare cases, patients may react with urticarial, bullous, or morbilliform eruptions, and the inflammation and pruritus can last for weeks.⁶ Summer penile syndrome has been noted in boys who display a local hypersensitivity to chigger bites.¹⁰ This syndrome represents a triad of penile swelling, dysuria, and pruritus, which lasts for a few days to a few weeks.

Disease Management

Because the lesions are self-healing, treatment is focused on symptomatic relief of itching by means of topical antipruritics (eg, camphor and menthol, pramoxine lotion) or oral antihistamines (eg, diphenhydramine, hydroxyzine). Potent topical corticosteroids may be used to alleviate inflammation and pruritus, especially when occluded under plastic wrap to increase absorption. In severe cases, an intralesional triamcinolone acetonide (2.5–5 mg/mL) injection may be required.⁹ The best practice, however, is to take preventative measures to avoid becoming a host for the mites. Patients should take special care when traveling in infested areas by completely covering their skin, tucking pant cuffs into their socks, and applying products containing DEET (N,N-diethyl-meta-toluamide or N,N-diethyl-3-methylbenzamide) to the skin and clothing. The odds of prevention are increased even further when clothing also is treated with permethrin.¹¹

In parts of Asia and Australia, these mites may transmit Orientia tsutsugamushi, the organism responsible for scrub typhus, through their saliva during a bite.¹² Scrub typhus is associated with an eschar, as well as fever, intense headache, and diffuse myalgia. It responds well to treatment with doxycycline 100 mg twice daily.¹³ Studies investigating genetic material found in trombiculid mites across the globe have detected Ehrlichia-specific DNA in Spain,¹⁴Borrelia-specific DNA in the Czech Republic,^15,16 and Hantavirus-specific RNA in Texas.¹⁷ There is evidence that the mites play a role in maintenance of zoonotic reservoirs, while humans are infected via ingestion or inhalation of infectious rodent extreta.¹⁸

Identifying Characteristics and Disease Transmission

Chiggers belong to the Trombiculidae family of mites and also are referred to as harvest mites, harvest bugs, harvest lice, mower’s mites, and redbugs.¹ The term chigger specifically describes the larval stage of this mite’s life cycle, as it is the only stage responsible for chigger bites. The nymph and adult phases feed on vegetable matter. Trombiculid mites are most often found in forests, grassy areas, gardens, and moist areas of soil near bodies of water. Trombicula alfreddugesi is the most common species in the United States, and these mites mainly live in the southeastern and south central regions of the country. Conversely, Trombicula autumnalis is most predominant in Western Europe and East Asia.¹

The life cycle of the mite includes the egg, larval, nymphal, and adult stages.² Due to their need for air humidity greater than 80%, mites lay their eggs on low leaves, blades of grass, or on the ground. They spend most of their lives on vegetation no more than 30 cm above ground level.³ Eggs remain dormant for approximately 6 days until the hatching of the prelarvae, which have 6 legs and are nonfeeding. It takes another 6 days for the prelarvae to mature into larvae. Measuring 0.15 to 0.3 mm in length, mite larvae are a mere fraction of the size of adult mites, which generally are 1 to 2 mm in length, and are bright red or brown-red in color (Figure 1).

The biting larvae have many acceptable hosts including turtles, toads, birds, small mammals, and humans, which act as accidental hosts. Larvae remain on vegetation waiting for a suitable host to pass by so they may attach to its skin and remain there for several days. In the exploration for an ideal area to begin feeding (eg, thin epidermis,⁴ localized increased air humidity⁵), larvae can travel extensively on the skin; however, they often are stopped by tight-fitting sections of clothing (eg, waistbands), so bites are mostly found in clusters. To feed, mite larvae latch onto the skin using chelicerae, jawlike appendages found in the front of the mouth in arachnids.⁶ They then inject digestive enzymes that liquefy epidermal cells on direct contact, which results in the formation of a stylostome from which the mites may suck up lymph fluid and broken down tissue.⁷ Although the actual initial bite is painless, this feeding process leads to the localized inflammation and irritation noticed by infested patients.⁸

The classic clinical presentation includes severe pruritus and cutaneous swelling as well as erythema caused by the combination of several factors, such as enzyme-induced cellular mechanical damage, human immune response, and sometimes a superimposed bacterial infection. Papules and papulovesicles appear in groups, most commonly affecting the legs and waistline (Figure 2).⁹ Itching generally occurs within hours of larval latching and subsides within 72 hours. Cutaneous lesions typically take 1 to 2 weeks to heal. In some rare cases, patients may react with urticarial, bullous, or morbilliform eruptions, and the inflammation and pruritus can last for weeks.⁶ Summer penile syndrome has been noted in boys who display a local hypersensitivity to chigger bites.¹⁰ This syndrome represents a triad of penile swelling, dysuria, and pruritus, which lasts for a few days to a few weeks.

Disease Management

Because the lesions are self-healing, treatment is focused on symptomatic relief of itching by means of topical antipruritics (eg, camphor and menthol, pramoxine lotion) or oral antihistamines (eg, diphenhydramine, hydroxyzine). Potent topical corticosteroids may be used to alleviate inflammation and pruritus, especially when occluded under plastic wrap to increase absorption. In severe cases, an intralesional triamcinolone acetonide (2.5–5 mg/mL) injection may be required.⁹ The best practice, however, is to take preventative measures to avoid becoming a host for the mites. Patients should take special care when traveling in infested areas by completely covering their skin, tucking pant cuffs into their socks, and applying products containing DEET (N,N-diethyl-meta-toluamide or N,N-diethyl-3-methylbenzamide) to the skin and clothing. The odds of prevention are increased even further when clothing also is treated with permethrin.¹¹

In parts of Asia and Australia, these mites may transmit Orientia tsutsugamushi, the organism responsible for scrub typhus, through their saliva during a bite.¹² Scrub typhus is associated with an eschar, as well as fever, intense headache, and diffuse myalgia. It responds well to treatment with doxycycline 100 mg twice daily.¹³ Studies investigating genetic material found in trombiculid mites across the globe have detected Ehrlichia-specific DNA in Spain,¹⁴Borrelia-specific DNA in the Czech Republic,^15,16 and Hantavirus-specific RNA in Texas.¹⁷ There is evidence that the mites play a role in maintenance of zoonotic reservoirs, while humans are infected via ingestion or inhalation of infectious rodent extreta.¹⁸

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 Diagnosis: Collision Tumor

Excisional biopsy and histopathological examination demonstrated a collision tumor composed of a benign intradermal melanocytic nevus, tumor of follicular infundibulum, and an underlying sclerosing epithelial neoplasm, with a differential diagnosis of desmoplastic trichoepithelioma, morpheaform basal cell carcinoma, and microcystic adnexal carcinoma (Figure).

Common acquired melanocytic nevus presents clinically as a macule, papule, or nodule with smooth regular borders. The pigmented variant displays an evenly distributed pigment on the lesion. Intradermal melanocytic nevus often presents as a flesh-colored nodule, as in our case. Histopathologically, benign intradermal nevus typically is composed of a proliferation of melanocytes that exhibit dispersion as they go deeper in the dermis and maturation that manifests as melanocytes becoming smaller and more spindled in the deeper portions of the lesion.¹ These 2 characteristics plus the bland cytology seen in the present case confirm the benign characteristic of this lesion (Figure, B).

In addition to the benign intradermal melanocytic nevus, an adjacent tumor of follicular infundibulum was noted. Tumor of follicular infundibulum is a rare adnexal tumor. It occurs frequently on the head and neck and shows some female predominance.^2,3 Multiple lesions and eruptive lesions are rare forms that also have been reported.⁴ Histopathologically, the tumor demonstrates an epithelial plate that is present in the papillary dermis and is connected to the epidermis at multiple points with attachment to the follicular outer root sheath. Peripheral palisading is characteristically present above an eosinophilic basement membrane (Figure, A). Rare reports have documented sebaceous and eccrine differentiation.^5,6

Tumor of follicular infundibulum has been reported to be associated with other tumors. Organoid nevus (nevus sebaceous), trichilemmal tumor, and fibroma have been reported to occur as a collision tumor with tumor of follicular infundibulum. An association with Cowden disease also has been described.⁷ Biopsies that represent partial samples should be interpreted cautiously, as step sections can reveal basal cell carcinoma.

The term sclerosing epithelial neoplasm describes tumors that share a paisley tielike epithelial pattern and sclerotic stroma. Small specimens often require clinicopathologic correlation (Figure, C). The differential diagnosis includes morpheaform basal cell carcinoma, desmoplastic trichoepithelioma, and microcystic adnexal carcinoma. A panel of stains using Ber-EP4, PHLDA1, cytokeratin 15, and cytokeratin 19 has been proposed to help differentiate these entities.⁸ CD34 and cytokeratin 20 also have been used with varying success in small specimens.^9,10

The Diagnosis: Collision Tumor

Excisional biopsy and histopathological examination demonstrated a collision tumor composed of a benign intradermal melanocytic nevus, tumor of follicular infundibulum, and an underlying sclerosing epithelial neoplasm, with a differential diagnosis of desmoplastic trichoepithelioma, morpheaform basal cell carcinoma, and microcystic adnexal carcinoma (Figure).

Common acquired melanocytic nevus presents clinically as a macule, papule, or nodule with smooth regular borders. The pigmented variant displays an evenly distributed pigment on the lesion. Intradermal melanocytic nevus often presents as a flesh-colored nodule, as in our case. Histopathologically, benign intradermal nevus typically is composed of a proliferation of melanocytes that exhibit dispersion as they go deeper in the dermis and maturation that manifests as melanocytes becoming smaller and more spindled in the deeper portions of the lesion.¹ These 2 characteristics plus the bland cytology seen in the present case confirm the benign characteristic of this lesion (Figure, B).

In addition to the benign intradermal melanocytic nevus, an adjacent tumor of follicular infundibulum was noted. Tumor of follicular infundibulum is a rare adnexal tumor. It occurs frequently on the head and neck and shows some female predominance.^2,3 Multiple lesions and eruptive lesions are rare forms that also have been reported.⁴ Histopathologically, the tumor demonstrates an epithelial plate that is present in the papillary dermis and is connected to the epidermis at multiple points with attachment to the follicular outer root sheath. Peripheral palisading is characteristically present above an eosinophilic basement membrane (Figure, A). Rare reports have documented sebaceous and eccrine differentiation.^5,6

Tumor of follicular infundibulum has been reported to be associated with other tumors. Organoid nevus (nevus sebaceous), trichilemmal tumor, and fibroma have been reported to occur as a collision tumor with tumor of follicular infundibulum. An association with Cowden disease also has been described.⁷ Biopsies that represent partial samples should be interpreted cautiously, as step sections can reveal basal cell carcinoma.

The term sclerosing epithelial neoplasm describes tumors that share a paisley tielike epithelial pattern and sclerotic stroma. Small specimens often require clinicopathologic correlation (Figure, C). The differential diagnosis includes morpheaform basal cell carcinoma, desmoplastic trichoepithelioma, and microcystic adnexal carcinoma. A panel of stains using Ber-EP4, PHLDA1, cytokeratin 15, and cytokeratin 19 has been proposed to help differentiate these entities.⁸ CD34 and cytokeratin 20 also have been used with varying success in small specimens.^9,10

The Diagnosis: Collision Tumor

Excisional biopsy and histopathological examination demonstrated a collision tumor composed of a benign intradermal melanocytic nevus, tumor of follicular infundibulum, and an underlying sclerosing epithelial neoplasm, with a differential diagnosis of desmoplastic trichoepithelioma, morpheaform basal cell carcinoma, and microcystic adnexal carcinoma (Figure).

Common acquired melanocytic nevus presents clinically as a macule, papule, or nodule with smooth regular borders. The pigmented variant displays an evenly distributed pigment on the lesion. Intradermal melanocytic nevus often presents as a flesh-colored nodule, as in our case. Histopathologically, benign intradermal nevus typically is composed of a proliferation of melanocytes that exhibit dispersion as they go deeper in the dermis and maturation that manifests as melanocytes becoming smaller and more spindled in the deeper portions of the lesion.¹ These 2 characteristics plus the bland cytology seen in the present case confirm the benign characteristic of this lesion (Figure, B).

In addition to the benign intradermal melanocytic nevus, an adjacent tumor of follicular infundibulum was noted. Tumor of follicular infundibulum is a rare adnexal tumor. It occurs frequently on the head and neck and shows some female predominance.^2,3 Multiple lesions and eruptive lesions are rare forms that also have been reported.⁴ Histopathologically, the tumor demonstrates an epithelial plate that is present in the papillary dermis and is connected to the epidermis at multiple points with attachment to the follicular outer root sheath. Peripheral palisading is characteristically present above an eosinophilic basement membrane (Figure, A). Rare reports have documented sebaceous and eccrine differentiation.^5,6

Tumor of follicular infundibulum has been reported to be associated with other tumors. Organoid nevus (nevus sebaceous), trichilemmal tumor, and fibroma have been reported to occur as a collision tumor with tumor of follicular infundibulum. An association with Cowden disease also has been described.⁷ Biopsies that represent partial samples should be interpreted cautiously, as step sections can reveal basal cell carcinoma.

The term sclerosing epithelial neoplasm describes tumors that share a paisley tielike epithelial pattern and sclerotic stroma. Small specimens often require clinicopathologic correlation (Figure, C). The differential diagnosis includes morpheaform basal cell carcinoma, desmoplastic trichoepithelioma, and microcystic adnexal carcinoma. A panel of stains using Ber-EP4, PHLDA1, cytokeratin 15, and cytokeratin 19 has been proposed to help differentiate these entities.⁸ CD34 and cytokeratin 20 also have been used with varying success in small specimens.^9,10

The Diagnosis: Erythema Dyschromicum Perstans

Erythema dyschromicum perstans (EDP), also referred to as ashy dermatosis, was first described by Ramirez¹ in 1957 who labeled the patients los cenicientos (the ashen ones). It preferentially affects women in the second decade of life; however, patients of all ages can be affected, with reported cases occurring in children as young as 2 years of age.² Most patients have Fitzpatrick skin type IV, mainly Amerindian, Hispanic South Asian, and Southwest Asian; however, there are cases reported worldwide.³ A genetic predisposition is proposed, as major histocompatibility complex genes associated with HLA-DR4⁎0407 are frequent in Mexican patients with ashy dermatosis and in the Amerindian population.⁴

The etiology of EDP is unknown. Various contributing factors have been reported including alimentary, occupational, and climatic factors,^5,6 yet none have been conclusively demonstrated. High expression of CD36 (thrombospondin receptor not found in normal skin) in spinous and granular layers, CD94 (cytotoxic cell marker) in the basal cell layer and in the inflammatory dermal infiltrate,⁷ and focal keratinocytic expression of intercellular adhesion molecule I (CD54) in the active lesions of EDP, as well as the absence of these findings in normal skin, suggests an immunologic role in the development of the disease.⁸

Erythema dyschromicum perstans presents clinically with blue-gray hyperpigmented macules varying in size and shape and developing symmetrically in both sun-exposed and sun-protected areas of the face, neck, trunk, arms, and sometimes the dorsal hands (Figures 1 and 2). Notable sparing of the palms, soles, scalp, and mucous membranes occurs.

Occasionally, in the early active stage of the disease, elevated erythematous borders are noted surrounding the hyperpigmented macules. Eventually a hypopigmented halo develops after a prolonged duration of disease.⁹ The eruption typically is chronic and asymptomatic, though some cases may be pruritic.¹⁰

Histopathologically, the early lesions of EDP with an erythematous active border reveal lichenoid dermatitis with basal vacuolar change and occasional Civatte bodies. A mild to moderate perivascular lymphohistiocytic infiltrate admixed with melanophages can be seen in the papillary dermis (Figure 3). In older lesions, the inflammatory infiltrate is sparse, and pigment incontinence consistent with postinflammatory pigmentation is prominent, though melanophages extending deep into the reticular dermis may aid in distinguishing EDP from other causes of postinflammatory pigment alteration.^7,11

Erythema dyschromicum perstans and lichen planus pigmentosus (LPP) may be indistinguishable histopathologically and may both be variants of lichen planus actinicus. Lichen planus pigmentosus often differs from EDP in that it presents with brown-black macules and patches often on the face and flexural areas. A subset of cases of LPP also may have mucous membrane involvement. The erythematous border that characterizes the active lesion of EDP is characteristically absent in LPP. In addition, pruritus often is reported with LPP. Direct immunofluorescence is not a beneficial tool in distinguishing the entities.¹²

Other differential diagnoses of predominantly facial hyperpigmentation include a lichenoid drug eruption; drug-induced hyperpigmentation (deposition disorder); postinflammatory hyperpigmentation following atopic dermatitis; contact dermatitis or photosensitivity reaction; early pinta; and cutaneous findings of systemic diseases manifesting with diffuse hyperpigmentation such as lupus erythematosus, dermatomyositis, hemochromatosis, and Addison disease. A detailed history including medication use, thorough clinical examination, and careful histopathologic evaluation will help distinguish these conditions.

Chrysiasis is a rare bluish to slate gray discoloration of the skin that predominantly occurs in sun-exposed areas. It is caused by chronic use of gold salts, which have been used to treat rheumatoid arthritis. UV light may contribute to induce the uptake of gold and subsequently stimulate tyrosinase activity.¹³ Histologic features of chrysiasis include dermal and perivascular gold deposition within the macrophages and endothelial cells as well as extracellular granules. It demonstrates an orange-red birefringence on fluorescent microscopy.^14,15

Minocycline-induced hyperpigmentation is a well-recognized side effect of this drug. It is dose dependent and appears as a blue-black pigmentation that most frequently affects the shins, ankles, and arms.¹⁶ Three distinct types were documented: abnormal discoloration of the skin that has been linked to deposition of pigmented metabolites of minocycline producing blue-black pigmentation at the site of scarring or prior inflammation (type 1); blue-gray pigmentation affecting normal skin, mainly the legs (type 2); and elevated levels of melanin on the sun-exposed areas producing dirty skin syndrome (type 3).^17,18

Topical and systemic corticosteroids, UV light therapy, oral dapsone, griseofulvin, retinoids, and clofazimine are reported as treatment options for ashy dermatosis, though results typically are disappointing.⁷

The Diagnosis: Erythema Dyschromicum Perstans

Erythema dyschromicum perstans (EDP), also referred to as ashy dermatosis, was first described by Ramirez¹ in 1957 who labeled the patients los cenicientos (the ashen ones). It preferentially affects women in the second decade of life; however, patients of all ages can be affected, with reported cases occurring in children as young as 2 years of age.² Most patients have Fitzpatrick skin type IV, mainly Amerindian, Hispanic South Asian, and Southwest Asian; however, there are cases reported worldwide.³ A genetic predisposition is proposed, as major histocompatibility complex genes associated with HLA-DR4⁎0407 are frequent in Mexican patients with ashy dermatosis and in the Amerindian population.⁴

The etiology of EDP is unknown. Various contributing factors have been reported including alimentary, occupational, and climatic factors,^5,6 yet none have been conclusively demonstrated. High expression of CD36 (thrombospondin receptor not found in normal skin) in spinous and granular layers, CD94 (cytotoxic cell marker) in the basal cell layer and in the inflammatory dermal infiltrate,⁷ and focal keratinocytic expression of intercellular adhesion molecule I (CD54) in the active lesions of EDP, as well as the absence of these findings in normal skin, suggests an immunologic role in the development of the disease.⁸

Erythema dyschromicum perstans presents clinically with blue-gray hyperpigmented macules varying in size and shape and developing symmetrically in both sun-exposed and sun-protected areas of the face, neck, trunk, arms, and sometimes the dorsal hands (Figures 1 and 2). Notable sparing of the palms, soles, scalp, and mucous membranes occurs.

Occasionally, in the early active stage of the disease, elevated erythematous borders are noted surrounding the hyperpigmented macules. Eventually a hypopigmented halo develops after a prolonged duration of disease.⁹ The eruption typically is chronic and asymptomatic, though some cases may be pruritic.¹⁰

Histopathologically, the early lesions of EDP with an erythematous active border reveal lichenoid dermatitis with basal vacuolar change and occasional Civatte bodies. A mild to moderate perivascular lymphohistiocytic infiltrate admixed with melanophages can be seen in the papillary dermis (Figure 3). In older lesions, the inflammatory infiltrate is sparse, and pigment incontinence consistent with postinflammatory pigmentation is prominent, though melanophages extending deep into the reticular dermis may aid in distinguishing EDP from other causes of postinflammatory pigment alteration.^7,11

Erythema dyschromicum perstans and lichen planus pigmentosus (LPP) may be indistinguishable histopathologically and may both be variants of lichen planus actinicus. Lichen planus pigmentosus often differs from EDP in that it presents with brown-black macules and patches often on the face and flexural areas. A subset of cases of LPP also may have mucous membrane involvement. The erythematous border that characterizes the active lesion of EDP is characteristically absent in LPP. In addition, pruritus often is reported with LPP. Direct immunofluorescence is not a beneficial tool in distinguishing the entities.¹²

Other differential diagnoses of predominantly facial hyperpigmentation include a lichenoid drug eruption; drug-induced hyperpigmentation (deposition disorder); postinflammatory hyperpigmentation following atopic dermatitis; contact dermatitis or photosensitivity reaction; early pinta; and cutaneous findings of systemic diseases manifesting with diffuse hyperpigmentation such as lupus erythematosus, dermatomyositis, hemochromatosis, and Addison disease. A detailed history including medication use, thorough clinical examination, and careful histopathologic evaluation will help distinguish these conditions.

Chrysiasis is a rare bluish to slate gray discoloration of the skin that predominantly occurs in sun-exposed areas. It is caused by chronic use of gold salts, which have been used to treat rheumatoid arthritis. UV light may contribute to induce the uptake of gold and subsequently stimulate tyrosinase activity.¹³ Histologic features of chrysiasis include dermal and perivascular gold deposition within the macrophages and endothelial cells as well as extracellular granules. It demonstrates an orange-red birefringence on fluorescent microscopy.^14,15

Minocycline-induced hyperpigmentation is a well-recognized side effect of this drug. It is dose dependent and appears as a blue-black pigmentation that most frequently affects the shins, ankles, and arms.¹⁶ Three distinct types were documented: abnormal discoloration of the skin that has been linked to deposition of pigmented metabolites of minocycline producing blue-black pigmentation at the site of scarring or prior inflammation (type 1); blue-gray pigmentation affecting normal skin, mainly the legs (type 2); and elevated levels of melanin on the sun-exposed areas producing dirty skin syndrome (type 3).^17,18

Topical and systemic corticosteroids, UV light therapy, oral dapsone, griseofulvin, retinoids, and clofazimine are reported as treatment options for ashy dermatosis, though results typically are disappointing.⁷

The Diagnosis: Erythema Dyschromicum Perstans

Erythema dyschromicum perstans (EDP), also referred to as ashy dermatosis, was first described by Ramirez¹ in 1957 who labeled the patients los cenicientos (the ashen ones). It preferentially affects women in the second decade of life; however, patients of all ages can be affected, with reported cases occurring in children as young as 2 years of age.² Most patients have Fitzpatrick skin type IV, mainly Amerindian, Hispanic South Asian, and Southwest Asian; however, there are cases reported worldwide.³ A genetic predisposition is proposed, as major histocompatibility complex genes associated with HLA-DR4⁎0407 are frequent in Mexican patients with ashy dermatosis and in the Amerindian population.⁴

The etiology of EDP is unknown. Various contributing factors have been reported including alimentary, occupational, and climatic factors,^5,6 yet none have been conclusively demonstrated. High expression of CD36 (thrombospondin receptor not found in normal skin) in spinous and granular layers, CD94 (cytotoxic cell marker) in the basal cell layer and in the inflammatory dermal infiltrate,⁷ and focal keratinocytic expression of intercellular adhesion molecule I (CD54) in the active lesions of EDP, as well as the absence of these findings in normal skin, suggests an immunologic role in the development of the disease.⁸

Erythema dyschromicum perstans presents clinically with blue-gray hyperpigmented macules varying in size and shape and developing symmetrically in both sun-exposed and sun-protected areas of the face, neck, trunk, arms, and sometimes the dorsal hands (Figures 1 and 2). Notable sparing of the palms, soles, scalp, and mucous membranes occurs.

Occasionally, in the early active stage of the disease, elevated erythematous borders are noted surrounding the hyperpigmented macules. Eventually a hypopigmented halo develops after a prolonged duration of disease.⁹ The eruption typically is chronic and asymptomatic, though some cases may be pruritic.¹⁰

Histopathologically, the early lesions of EDP with an erythematous active border reveal lichenoid dermatitis with basal vacuolar change and occasional Civatte bodies. A mild to moderate perivascular lymphohistiocytic infiltrate admixed with melanophages can be seen in the papillary dermis (Figure 3). In older lesions, the inflammatory infiltrate is sparse, and pigment incontinence consistent with postinflammatory pigmentation is prominent, though melanophages extending deep into the reticular dermis may aid in distinguishing EDP from other causes of postinflammatory pigment alteration.^7,11

Erythema dyschromicum perstans and lichen planus pigmentosus (LPP) may be indistinguishable histopathologically and may both be variants of lichen planus actinicus. Lichen planus pigmentosus often differs from EDP in that it presents with brown-black macules and patches often on the face and flexural areas. A subset of cases of LPP also may have mucous membrane involvement. The erythematous border that characterizes the active lesion of EDP is characteristically absent in LPP. In addition, pruritus often is reported with LPP. Direct immunofluorescence is not a beneficial tool in distinguishing the entities.¹²

Other differential diagnoses of predominantly facial hyperpigmentation include a lichenoid drug eruption; drug-induced hyperpigmentation (deposition disorder); postinflammatory hyperpigmentation following atopic dermatitis; contact dermatitis or photosensitivity reaction; early pinta; and cutaneous findings of systemic diseases manifesting with diffuse hyperpigmentation such as lupus erythematosus, dermatomyositis, hemochromatosis, and Addison disease. A detailed history including medication use, thorough clinical examination, and careful histopathologic evaluation will help distinguish these conditions.

Chrysiasis is a rare bluish to slate gray discoloration of the skin that predominantly occurs in sun-exposed areas. It is caused by chronic use of gold salts, which have been used to treat rheumatoid arthritis. UV light may contribute to induce the uptake of gold and subsequently stimulate tyrosinase activity.¹³ Histologic features of chrysiasis include dermal and perivascular gold deposition within the macrophages and endothelial cells as well as extracellular granules. It demonstrates an orange-red birefringence on fluorescent microscopy.^14,15

Minocycline-induced hyperpigmentation is a well-recognized side effect of this drug. It is dose dependent and appears as a blue-black pigmentation that most frequently affects the shins, ankles, and arms.¹⁶ Three distinct types were documented: abnormal discoloration of the skin that has been linked to deposition of pigmented metabolites of minocycline producing blue-black pigmentation at the site of scarring or prior inflammation (type 1); blue-gray pigmentation affecting normal skin, mainly the legs (type 2); and elevated levels of melanin on the sun-exposed areas producing dirty skin syndrome (type 3).^17,18

Topical and systemic corticosteroids, UV light therapy, oral dapsone, griseofulvin, retinoids, and clofazimine are reported as treatment options for ashy dermatosis, though results typically are disappointing.⁷

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

As employers search for ways to reduce the cost of providing health care to their employees, there is a growing trend toward narrowed provider networks and exclusive laboratory contracts. In the case of clinical pathology, some of these choices make sense from the employer’s perspective. A complete blood cell count or comprehensive metabolic panel is done on a machine and the result is much the same regardless of the laboratory. So why not have all laboratory tests performed by the lowest bidder?

Laboratories vary in quality and anatomic pathology services are different from blood tests. Each slide must be interpreted by a physician and skill in the interpretation of skin specimens varies widely. Dermatopathology was one of the first subspecialties to be recognized within pathology, as it requires a high level of expertise. Clinicopathological correlation often is key to the accurate interpretation of a specimen. The stakes are high, and a delay in diagnosis of melanoma remains one of the most serious errors in medicine and one of the most common causes for litigation in dermatology.

The accurate interpretation of skin biopsy specimens becomes especially difficult when inadequate or misleading clinical information accompanies the specimen. A study of 589 biopsies submitted by primary care physicians and reported by general pathologists demonstrated a 6.5% error rate. False-negative errors were the most common, but false-positives also were observed.¹ A study of pigmented lesions referred to the University of California, San Francisco, demonstrated a discordance rate of 14.3%.² The degree of discordance would be expected to vary based on the range of diagnoses included in each study.

Board-certified dermatopathologists have varying areas of expertise and there is notable subjectivity in the interpretation of biopsy specimens. In the case of problematic pigmented lesions such as atypical Spitz nevi, there can be low interobserver agreement even among the experts in categorizing lesions as malignant versus nonmalignant (κ=0.30).³ The low concordance among expert dermatopathologists demonstrates that light microscopic features alone often are inadequate for diagnosis. Advanced studies, including immunohistochemical stains, can help to clarify the diagnosis. In the case of atypical Spitz tumors, the contribution of special stains to the final diagnosis is statistically similar to that of hematoxylin and eosin sections and age, suggesting that nothing alone is sufficiently reliable to establish a definitive diagnosis in every case.⁴ Although helpful, these studies are costly, and savings obtained by sending cases to the lowest bidder can evaporate quickly. Costs are higher when factoring in molecular studies, which can run upwards of $3000 per slide; the cost of litigation related to incorrect diagnoses; or the human costs of an incorrect diagnosis.

As a group, dermatopathologists are highly skilled in the interpretation of skin specimens, but challenging lesions are common in the routine practice of dermatopathology. A study of 1249 pigmented melanocytic lesions demonstrated substantial agreement among expert dermatopathologists for less problematic lesions, though agreement was greater for patients 40 years and older (κ=0.67) than for younger patients (κ=0.49). Agreement was lower for patients with atypical mole syndrome (κ=0.31).⁵ These discrepancies occur despite the fact that there is good interobserver reproducibility for grading of individual histological features such as asymmetry, circumscription, irregular confluent nests, single melanocytes predominating, absence of maturation, suprabasal melanocytes, symmetrical melanin, deep melanin, cytological atypia, mitoses, dermal lymphocytic infiltrate, and necrosis.⁶ These results indicate that accurate diagnoses cannot be reliably established simply by grading a list of histological features. Accurate diagnosis requires complex pattern recognition and integration of findings. Conflicting criteria often are present and an accurate interpretation requires considerable judgment as to which features are significant and which are not.

Separation of sebaceous adenoma, sebaceoma, and well-differentiated sebaceous carcinoma is another challenging area, and interobserver consensus can be as low as 11%,⁷ which suggests notable subjectivity in the criteria for diagnosis of nonmelanocytic tumors and emphasizes the importance of communication between the dermatopathologist and clinician when determining how to manage an ambiguous lesion. The interpretation of inflammatory skin diseases, alopecia, and lymphoid proliferations also can be problematic, and expert consultation often is required.

All dermatologists receive substantial training in dermatopathology, which puts them in an excellent position to interpret ambiguous findings in the context of the clinical presentation. Sometimes the dermatologist who has seen the clinical presentation can be in the best position to make the diagnosis. All clinicians must be wary of bias and an objective set of eyes often can be helpful. Communication is crucial to ensure appropriate care for each patient, and policies that restrict the choice of pathologist can be damaging.

As employers search for ways to reduce the cost of providing health care to their employees, there is a growing trend toward narrowed provider networks and exclusive laboratory contracts. In the case of clinical pathology, some of these choices make sense from the employer’s perspective. A complete blood cell count or comprehensive metabolic panel is done on a machine and the result is much the same regardless of the laboratory. So why not have all laboratory tests performed by the lowest bidder?

Laboratories vary in quality and anatomic pathology services are different from blood tests. Each slide must be interpreted by a physician and skill in the interpretation of skin specimens varies widely. Dermatopathology was one of the first subspecialties to be recognized within pathology, as it requires a high level of expertise. Clinicopathological correlation often is key to the accurate interpretation of a specimen. The stakes are high, and a delay in diagnosis of melanoma remains one of the most serious errors in medicine and one of the most common causes for litigation in dermatology.

The accurate interpretation of skin biopsy specimens becomes especially difficult when inadequate or misleading clinical information accompanies the specimen. A study of 589 biopsies submitted by primary care physicians and reported by general pathologists demonstrated a 6.5% error rate. False-negative errors were the most common, but false-positives also were observed.¹ A study of pigmented lesions referred to the University of California, San Francisco, demonstrated a discordance rate of 14.3%.² The degree of discordance would be expected to vary based on the range of diagnoses included in each study.

Board-certified dermatopathologists have varying areas of expertise and there is notable subjectivity in the interpretation of biopsy specimens. In the case of problematic pigmented lesions such as atypical Spitz nevi, there can be low interobserver agreement even among the experts in categorizing lesions as malignant versus nonmalignant (κ=0.30).³ The low concordance among expert dermatopathologists demonstrates that light microscopic features alone often are inadequate for diagnosis. Advanced studies, including immunohistochemical stains, can help to clarify the diagnosis. In the case of atypical Spitz tumors, the contribution of special stains to the final diagnosis is statistically similar to that of hematoxylin and eosin sections and age, suggesting that nothing alone is sufficiently reliable to establish a definitive diagnosis in every case.⁴ Although helpful, these studies are costly, and savings obtained by sending cases to the lowest bidder can evaporate quickly. Costs are higher when factoring in molecular studies, which can run upwards of $3000 per slide; the cost of litigation related to incorrect diagnoses; or the human costs of an incorrect diagnosis.

As a group, dermatopathologists are highly skilled in the interpretation of skin specimens, but challenging lesions are common in the routine practice of dermatopathology. A study of 1249 pigmented melanocytic lesions demonstrated substantial agreement among expert dermatopathologists for less problematic lesions, though agreement was greater for patients 40 years and older (κ=0.67) than for younger patients (κ=0.49). Agreement was lower for patients with atypical mole syndrome (κ=0.31).⁵ These discrepancies occur despite the fact that there is good interobserver reproducibility for grading of individual histological features such as asymmetry, circumscription, irregular confluent nests, single melanocytes predominating, absence of maturation, suprabasal melanocytes, symmetrical melanin, deep melanin, cytological atypia, mitoses, dermal lymphocytic infiltrate, and necrosis.⁶ These results indicate that accurate diagnoses cannot be reliably established simply by grading a list of histological features. Accurate diagnosis requires complex pattern recognition and integration of findings. Conflicting criteria often are present and an accurate interpretation requires considerable judgment as to which features are significant and which are not.

Separation of sebaceous adenoma, sebaceoma, and well-differentiated sebaceous carcinoma is another challenging area, and interobserver consensus can be as low as 11%,⁷ which suggests notable subjectivity in the criteria for diagnosis of nonmelanocytic tumors and emphasizes the importance of communication between the dermatopathologist and clinician when determining how to manage an ambiguous lesion. The interpretation of inflammatory skin diseases, alopecia, and lymphoid proliferations also can be problematic, and expert consultation often is required.

All dermatologists receive substantial training in dermatopathology, which puts them in an excellent position to interpret ambiguous findings in the context of the clinical presentation. Sometimes the dermatologist who has seen the clinical presentation can be in the best position to make the diagnosis. All clinicians must be wary of bias and an objective set of eyes often can be helpful. Communication is crucial to ensure appropriate care for each patient, and policies that restrict the choice of pathologist can be damaging.

As employers search for ways to reduce the cost of providing health care to their employees, there is a growing trend toward narrowed provider networks and exclusive laboratory contracts. In the case of clinical pathology, some of these choices make sense from the employer’s perspective. A complete blood cell count or comprehensive metabolic panel is done on a machine and the result is much the same regardless of the laboratory. So why not have all laboratory tests performed by the lowest bidder?

Laboratories vary in quality and anatomic pathology services are different from blood tests. Each slide must be interpreted by a physician and skill in the interpretation of skin specimens varies widely. Dermatopathology was one of the first subspecialties to be recognized within pathology, as it requires a high level of expertise. Clinicopathological correlation often is key to the accurate interpretation of a specimen. The stakes are high, and a delay in diagnosis of melanoma remains one of the most serious errors in medicine and one of the most common causes for litigation in dermatology.

The accurate interpretation of skin biopsy specimens becomes especially difficult when inadequate or misleading clinical information accompanies the specimen. A study of 589 biopsies submitted by primary care physicians and reported by general pathologists demonstrated a 6.5% error rate. False-negative errors were the most common, but false-positives also were observed.¹ A study of pigmented lesions referred to the University of California, San Francisco, demonstrated a discordance rate of 14.3%.² The degree of discordance would be expected to vary based on the range of diagnoses included in each study.

Board-certified dermatopathologists have varying areas of expertise and there is notable subjectivity in the interpretation of biopsy specimens. In the case of problematic pigmented lesions such as atypical Spitz nevi, there can be low interobserver agreement even among the experts in categorizing lesions as malignant versus nonmalignant (κ=0.30).³ The low concordance among expert dermatopathologists demonstrates that light microscopic features alone often are inadequate for diagnosis. Advanced studies, including immunohistochemical stains, can help to clarify the diagnosis. In the case of atypical Spitz tumors, the contribution of special stains to the final diagnosis is statistically similar to that of hematoxylin and eosin sections and age, suggesting that nothing alone is sufficiently reliable to establish a definitive diagnosis in every case.⁴ Although helpful, these studies are costly, and savings obtained by sending cases to the lowest bidder can evaporate quickly. Costs are higher when factoring in molecular studies, which can run upwards of $3000 per slide; the cost of litigation related to incorrect diagnoses; or the human costs of an incorrect diagnosis.

As a group, dermatopathologists are highly skilled in the interpretation of skin specimens, but challenging lesions are common in the routine practice of dermatopathology. A study of 1249 pigmented melanocytic lesions demonstrated substantial agreement among expert dermatopathologists for less problematic lesions, though agreement was greater for patients 40 years and older (κ=0.67) than for younger patients (κ=0.49). Agreement was lower for patients with atypical mole syndrome (κ=0.31).⁵ These discrepancies occur despite the fact that there is good interobserver reproducibility for grading of individual histological features such as asymmetry, circumscription, irregular confluent nests, single melanocytes predominating, absence of maturation, suprabasal melanocytes, symmetrical melanin, deep melanin, cytological atypia, mitoses, dermal lymphocytic infiltrate, and necrosis.⁶ These results indicate that accurate diagnoses cannot be reliably established simply by grading a list of histological features. Accurate diagnosis requires complex pattern recognition and integration of findings. Conflicting criteria often are present and an accurate interpretation requires considerable judgment as to which features are significant and which are not.

Separation of sebaceous adenoma, sebaceoma, and well-differentiated sebaceous carcinoma is another challenging area, and interobserver consensus can be as low as 11%,⁷ which suggests notable subjectivity in the criteria for diagnosis of nonmelanocytic tumors and emphasizes the importance of communication between the dermatopathologist and clinician when determining how to manage an ambiguous lesion. The interpretation of inflammatory skin diseases, alopecia, and lymphoid proliferations also can be problematic, and expert consultation often is required.

All dermatologists receive substantial training in dermatopathology, which puts them in an excellent position to interpret ambiguous findings in the context of the clinical presentation. Sometimes the dermatologist who has seen the clinical presentation can be in the best position to make the diagnosis. All clinicians must be wary of bias and an objective set of eyes often can be helpful. Communication is crucial to ensure appropriate care for each patient, and policies that restrict the choice of pathologist can be damaging.