Catherine Shirer Barker, MD

Plant Parts and Nomenclature

Ficus carica (common fig) is a deciduous shrub or small tree with smooth gray bark that can grow up to 10 m in height (Figure 1). It is characterized by many spreading branches, but the trunk rarely grows beyond a diameter of 7 in. Its hairy leaves are coarse on the upper side and soft underneath with 3 to 7 deep lobes that can extend up to 25 cm in length or width; the leaves grow individually, alternating along the sides of the branches. Fig trees often can be seen adorning yards, gardens, and parks, especially in tropical and subtropical climates. Ficus carica should not be confused with Ficus benjamina (weeping fig), a common ornamental tree that also is used to provide shade in hot climates, though both can cause phototoxic skin eruptions.

Barker_0424_1.jpg

The common fig tree originated in the Mediterranean and western Asia¹ and has been cultivated by humans since the second and third millennia bc for its fruit, which commonly is used to sweeten cookies, cakes, and jams.² Figs are the most commonly mentioned food plant in the Bible, with at least 56 references in the Old and New Testaments.³ The “fruit” technically is a syconium—a hollow fleshy receptacle with a small opening at the apex partly closed by small scales. It can be obovoid, turbinate, or pear shaped; can be 1 to 4 inches long; and can vary in color from yellowish green to coppery, bronze, or dark purple (Figure 2).

Barker_0424_2.jpg

Ficus carica is a member of the Moraceae family (derived from the Latin name for the mulberry tree), which includes 53 genera and approximately 1400 species, of which about 850 belong to the genus Ficus (the Latin name for a fig tree). The term carica likely comes from the Latin word carricare (to load) to describe a tree loaded with figs. Family members include trees, shrubs, lianas, and herbs that usually contain laticifers with a milky latex.

Traditional Uses

For centuries, components of the fig tree have been used in herbal teas and pastes to treat ailments ranging from sore throats to diarrhea, though there is no evidence to support their efficacy.⁴ Ancient Indians and Egyptians used plants such as the common fig tree containing furocoumarins to induce hyperpigmentation in vitiligo.⁵

Phototoxic Components

The leaves and sap of the common fig tree contain psoralens, which are members of the furocoumarin group of chemical compounds and are the source of its phototoxicity. The fruit does not contain psoralens.^6-9 The tree also produces proteolytic enzymes such as protease, amylase, ficin, triterpenoids, and lipodiastase that enhance its phototoxic effects.⁸ Exposure to UV light between 320 and 400 nm following contact with these phototoxic components triggers a reaction in the skin over the course of 1 to 3 days.⁵ The psoralens bind in epidermal cells, cross-link the DNA, and cause cell-membrane destruction, leading to edema and necrosis.¹⁰ The delay in symptoms may be attributed to the time needed to synthesize acute-phase reaction proteins such as tumor necrosis factor α and IL-1.¹¹ In spring and summer months, an increased concentration of psoralens in the leaves and sap contribute to an increased incidence of phytophotodermatitis.⁹ Humidity and sweat also increase the percutaneous absorption of psoralens.^12,13

Allergens

Fig trees produce a latex protein that can cause cross-reactive hypersensitivity reactions in those allergic to F benjamina latex and rubber latex.⁶ The latex proteins in fig trees can act as airborne respiratory allergens. Ingestion of figs can produce anaphylactic reactions in those sensitized to rubber latex and F benjamina latex.⁷ Other plant families associated with phototoxic reactions include Rutaceae (lemon, lime, bitter orange), Apiaceae (formerly Umbelliferae)(carrot, parsnip, parsley, dill, celery, hogweed), and Fabaceae (prairie turnip).

Most cases of fig phytophotodermatitis begin with burning, pain, and/or itching within hours of sunlight exposure in areas of the skin that encountered components of the fig tree, often in a linear pattern. The affected areas become erythematous and edematous with formation of bullae and unilocular vesicles over the course of 1 to 3 days.^12,14,15 Lesions may extend beyond the region of contact with the fig tree as they spread across the skin due to sweat or friction, and pain may linger even after the lesions resolve.^12,13,16 Adults who handle fig trees (eg, pruning) are susceptible to phototoxic reactions, especially those using chain saws or other mechanisms that result in spray exposure, as the photosensitizing sap permeates the wood and bark of the entire tree.¹⁷ Similarly, children who handle fig leaves or sap during outdoor play can develop bullous eruptions. Severe cases have resulted in hospital admission after prolonged exposure.¹⁶ Additionally, irritant dermatitis may arise from contact with the trichomes or “hairs” on various parts of the plant.

Barker_0424_3.jpg

Patients who use natural remedies containing components of the fig tree without the supervision of a medical provider put themselves at risk for unsafe or unwanted adverse effects, such as phytophotodermatitis.^12,15,16,18 An entire family presented with burns after they applied fig leaf extract to the skin prior to tanning outside in the sun.¹⁹ A 42-year-old woman acquired a severe burn covering 81% of the body surface after topically applying fig leaf tea to the skin as a tanning agent.²⁰ A subset of patients ingesting or applying fig tree components for conditions such as vitiligo, dermatitis, onychomycosis, and motor retardation developed similar cutaneous reactions.^13,14,21,22 Lesions resembling finger marks can raise concerns for potential abuse or neglect in children.²²

The differential diagnosis for fig phytophotodermatitis includes sunburn, chemical burns, drug-related photosensitivity, infectious lesions (eg, herpes simplex, bullous impetigo, Lyme disease, superficial lymphangitis), connective tissue disease (eg, systemic lupus erythematosus), contact dermatitis, and nonaccidental trauma.^12,15,18 Compared to sunburn, phytophotodermatitis tends to increase in severity over days following exposure and heals with dramatic hyperpigmentation, which also prompts visits to dermatology.¹²

Treatment

Treatment of fig phytophotodermatitis chiefly is symptomatic, including analgesia, appropriate wound care, and infection prophylaxis. Topical and systemic corticosteroids may aid in the resolution of moderate to severe reactions.^15,23,24 Even severe injuries over small areas or mild injuries to a high percentage of the total body surface area may require treatment in a burn unit. Patients should be encouraged to use mineral-based sunscreens on the affected areas to reduce the risk for hyperpigmentation. Individuals who regularly handle fig trees should use contact barriers including gloves and protective clothing (eg, long-sleeved shirts, long pants).

Plant Parts and Nomenclature

Ficus carica (common fig) is a deciduous shrub or small tree with smooth gray bark that can grow up to 10 m in height (Figure 1). It is characterized by many spreading branches, but the trunk rarely grows beyond a diameter of 7 in. Its hairy leaves are coarse on the upper side and soft underneath with 3 to 7 deep lobes that can extend up to 25 cm in length or width; the leaves grow individually, alternating along the sides of the branches. Fig trees often can be seen adorning yards, gardens, and parks, especially in tropical and subtropical climates. Ficus carica should not be confused with Ficus benjamina (weeping fig), a common ornamental tree that also is used to provide shade in hot climates, though both can cause phototoxic skin eruptions.

Barker_0424_1.jpg

The common fig tree originated in the Mediterranean and western Asia¹ and has been cultivated by humans since the second and third millennia bc for its fruit, which commonly is used to sweeten cookies, cakes, and jams.² Figs are the most commonly mentioned food plant in the Bible, with at least 56 references in the Old and New Testaments.³ The “fruit” technically is a syconium—a hollow fleshy receptacle with a small opening at the apex partly closed by small scales. It can be obovoid, turbinate, or pear shaped; can be 1 to 4 inches long; and can vary in color from yellowish green to coppery, bronze, or dark purple (Figure 2).

Barker_0424_2.jpg

Ficus carica is a member of the Moraceae family (derived from the Latin name for the mulberry tree), which includes 53 genera and approximately 1400 species, of which about 850 belong to the genus Ficus (the Latin name for a fig tree). The term carica likely comes from the Latin word carricare (to load) to describe a tree loaded with figs. Family members include trees, shrubs, lianas, and herbs that usually contain laticifers with a milky latex.

Traditional Uses

For centuries, components of the fig tree have been used in herbal teas and pastes to treat ailments ranging from sore throats to diarrhea, though there is no evidence to support their efficacy.⁴ Ancient Indians and Egyptians used plants such as the common fig tree containing furocoumarins to induce hyperpigmentation in vitiligo.⁵

Phototoxic Components

The leaves and sap of the common fig tree contain psoralens, which are members of the furocoumarin group of chemical compounds and are the source of its phototoxicity. The fruit does not contain psoralens.^6-9 The tree also produces proteolytic enzymes such as protease, amylase, ficin, triterpenoids, and lipodiastase that enhance its phototoxic effects.⁸ Exposure to UV light between 320 and 400 nm following contact with these phototoxic components triggers a reaction in the skin over the course of 1 to 3 days.⁵ The psoralens bind in epidermal cells, cross-link the DNA, and cause cell-membrane destruction, leading to edema and necrosis.¹⁰ The delay in symptoms may be attributed to the time needed to synthesize acute-phase reaction proteins such as tumor necrosis factor α and IL-1.¹¹ In spring and summer months, an increased concentration of psoralens in the leaves and sap contribute to an increased incidence of phytophotodermatitis.⁹ Humidity and sweat also increase the percutaneous absorption of psoralens.^12,13

Allergens

Fig trees produce a latex protein that can cause cross-reactive hypersensitivity reactions in those allergic to F benjamina latex and rubber latex.⁶ The latex proteins in fig trees can act as airborne respiratory allergens. Ingestion of figs can produce anaphylactic reactions in those sensitized to rubber latex and F benjamina latex.⁷ Other plant families associated with phototoxic reactions include Rutaceae (lemon, lime, bitter orange), Apiaceae (formerly Umbelliferae)(carrot, parsnip, parsley, dill, celery, hogweed), and Fabaceae (prairie turnip).

Most cases of fig phytophotodermatitis begin with burning, pain, and/or itching within hours of sunlight exposure in areas of the skin that encountered components of the fig tree, often in a linear pattern. The affected areas become erythematous and edematous with formation of bullae and unilocular vesicles over the course of 1 to 3 days.^12,14,15 Lesions may extend beyond the region of contact with the fig tree as they spread across the skin due to sweat or friction, and pain may linger even after the lesions resolve.^12,13,16 Adults who handle fig trees (eg, pruning) are susceptible to phototoxic reactions, especially those using chain saws or other mechanisms that result in spray exposure, as the photosensitizing sap permeates the wood and bark of the entire tree.¹⁷ Similarly, children who handle fig leaves or sap during outdoor play can develop bullous eruptions. Severe cases have resulted in hospital admission after prolonged exposure.¹⁶ Additionally, irritant dermatitis may arise from contact with the trichomes or “hairs” on various parts of the plant.

Barker_0424_3.jpg

Patients who use natural remedies containing components of the fig tree without the supervision of a medical provider put themselves at risk for unsafe or unwanted adverse effects, such as phytophotodermatitis.^12,15,16,18 An entire family presented with burns after they applied fig leaf extract to the skin prior to tanning outside in the sun.¹⁹ A 42-year-old woman acquired a severe burn covering 81% of the body surface after topically applying fig leaf tea to the skin as a tanning agent.²⁰ A subset of patients ingesting or applying fig tree components for conditions such as vitiligo, dermatitis, onychomycosis, and motor retardation developed similar cutaneous reactions.^13,14,21,22 Lesions resembling finger marks can raise concerns for potential abuse or neglect in children.²²

The differential diagnosis for fig phytophotodermatitis includes sunburn, chemical burns, drug-related photosensitivity, infectious lesions (eg, herpes simplex, bullous impetigo, Lyme disease, superficial lymphangitis), connective tissue disease (eg, systemic lupus erythematosus), contact dermatitis, and nonaccidental trauma.^12,15,18 Compared to sunburn, phytophotodermatitis tends to increase in severity over days following exposure and heals with dramatic hyperpigmentation, which also prompts visits to dermatology.¹²

Treatment

Treatment of fig phytophotodermatitis chiefly is symptomatic, including analgesia, appropriate wound care, and infection prophylaxis. Topical and systemic corticosteroids may aid in the resolution of moderate to severe reactions.^15,23,24 Even severe injuries over small areas or mild injuries to a high percentage of the total body surface area may require treatment in a burn unit. Patients should be encouraged to use mineral-based sunscreens on the affected areas to reduce the risk for hyperpigmentation. Individuals who regularly handle fig trees should use contact barriers including gloves and protective clothing (eg, long-sleeved shirts, long pants).

Plant Parts and Nomenclature

Ficus carica (common fig) is a deciduous shrub or small tree with smooth gray bark that can grow up to 10 m in height (Figure 1). It is characterized by many spreading branches, but the trunk rarely grows beyond a diameter of 7 in. Its hairy leaves are coarse on the upper side and soft underneath with 3 to 7 deep lobes that can extend up to 25 cm in length or width; the leaves grow individually, alternating along the sides of the branches. Fig trees often can be seen adorning yards, gardens, and parks, especially in tropical and subtropical climates. Ficus carica should not be confused with Ficus benjamina (weeping fig), a common ornamental tree that also is used to provide shade in hot climates, though both can cause phototoxic skin eruptions.

Barker_0424_1.jpg

The common fig tree originated in the Mediterranean and western Asia¹ and has been cultivated by humans since the second and third millennia bc for its fruit, which commonly is used to sweeten cookies, cakes, and jams.² Figs are the most commonly mentioned food plant in the Bible, with at least 56 references in the Old and New Testaments.³ The “fruit” technically is a syconium—a hollow fleshy receptacle with a small opening at the apex partly closed by small scales. It can be obovoid, turbinate, or pear shaped; can be 1 to 4 inches long; and can vary in color from yellowish green to coppery, bronze, or dark purple (Figure 2).

Barker_0424_2.jpg

Ficus carica is a member of the Moraceae family (derived from the Latin name for the mulberry tree), which includes 53 genera and approximately 1400 species, of which about 850 belong to the genus Ficus (the Latin name for a fig tree). The term carica likely comes from the Latin word carricare (to load) to describe a tree loaded with figs. Family members include trees, shrubs, lianas, and herbs that usually contain laticifers with a milky latex.

Traditional Uses

For centuries, components of the fig tree have been used in herbal teas and pastes to treat ailments ranging from sore throats to diarrhea, though there is no evidence to support their efficacy.⁴ Ancient Indians and Egyptians used plants such as the common fig tree containing furocoumarins to induce hyperpigmentation in vitiligo.⁵

Phototoxic Components

The leaves and sap of the common fig tree contain psoralens, which are members of the furocoumarin group of chemical compounds and are the source of its phototoxicity. The fruit does not contain psoralens.^6-9 The tree also produces proteolytic enzymes such as protease, amylase, ficin, triterpenoids, and lipodiastase that enhance its phototoxic effects.⁸ Exposure to UV light between 320 and 400 nm following contact with these phototoxic components triggers a reaction in the skin over the course of 1 to 3 days.⁵ The psoralens bind in epidermal cells, cross-link the DNA, and cause cell-membrane destruction, leading to edema and necrosis.¹⁰ The delay in symptoms may be attributed to the time needed to synthesize acute-phase reaction proteins such as tumor necrosis factor α and IL-1.¹¹ In spring and summer months, an increased concentration of psoralens in the leaves and sap contribute to an increased incidence of phytophotodermatitis.⁹ Humidity and sweat also increase the percutaneous absorption of psoralens.^12,13

Allergens

Fig trees produce a latex protein that can cause cross-reactive hypersensitivity reactions in those allergic to F benjamina latex and rubber latex.⁶ The latex proteins in fig trees can act as airborne respiratory allergens. Ingestion of figs can produce anaphylactic reactions in those sensitized to rubber latex and F benjamina latex.⁷ Other plant families associated with phototoxic reactions include Rutaceae (lemon, lime, bitter orange), Apiaceae (formerly Umbelliferae)(carrot, parsnip, parsley, dill, celery, hogweed), and Fabaceae (prairie turnip).

Most cases of fig phytophotodermatitis begin with burning, pain, and/or itching within hours of sunlight exposure in areas of the skin that encountered components of the fig tree, often in a linear pattern. The affected areas become erythematous and edematous with formation of bullae and unilocular vesicles over the course of 1 to 3 days.^12,14,15 Lesions may extend beyond the region of contact with the fig tree as they spread across the skin due to sweat or friction, and pain may linger even after the lesions resolve.^12,13,16 Adults who handle fig trees (eg, pruning) are susceptible to phototoxic reactions, especially those using chain saws or other mechanisms that result in spray exposure, as the photosensitizing sap permeates the wood and bark of the entire tree.¹⁷ Similarly, children who handle fig leaves or sap during outdoor play can develop bullous eruptions. Severe cases have resulted in hospital admission after prolonged exposure.¹⁶ Additionally, irritant dermatitis may arise from contact with the trichomes or “hairs” on various parts of the plant.

Barker_0424_3.jpg

Patients who use natural remedies containing components of the fig tree without the supervision of a medical provider put themselves at risk for unsafe or unwanted adverse effects, such as phytophotodermatitis.^12,15,16,18 An entire family presented with burns after they applied fig leaf extract to the skin prior to tanning outside in the sun.¹⁹ A 42-year-old woman acquired a severe burn covering 81% of the body surface after topically applying fig leaf tea to the skin as a tanning agent.²⁰ A subset of patients ingesting or applying fig tree components for conditions such as vitiligo, dermatitis, onychomycosis, and motor retardation developed similar cutaneous reactions.^13,14,21,22 Lesions resembling finger marks can raise concerns for potential abuse or neglect in children.²²

The differential diagnosis for fig phytophotodermatitis includes sunburn, chemical burns, drug-related photosensitivity, infectious lesions (eg, herpes simplex, bullous impetigo, Lyme disease, superficial lymphangitis), connective tissue disease (eg, systemic lupus erythematosus), contact dermatitis, and nonaccidental trauma.^12,15,18 Compared to sunburn, phytophotodermatitis tends to increase in severity over days following exposure and heals with dramatic hyperpigmentation, which also prompts visits to dermatology.¹²

Treatment

Treatment of fig phytophotodermatitis chiefly is symptomatic, including analgesia, appropriate wound care, and infection prophylaxis. Topical and systemic corticosteroids may aid in the resolution of moderate to severe reactions.^15,23,24 Even severe injuries over small areas or mild injuries to a high percentage of the total body surface area may require treatment in a burn unit. Patients should be encouraged to use mineral-based sunscreens on the affected areas to reduce the risk for hyperpigmentation. Individuals who regularly handle fig trees should use contact barriers including gloves and protective clothing (eg, long-sleeved shirts, long pants).

The Diagnosis: Erythema Migrans

The patient was clinically diagnosed with erythema migrans. He did not recall a tick bite but spent a lot of time outdoors. He was treated with 10 days of doxycycline 100 mg twice daily with complete resolution of the rash.

Lyme disease is a spirochete infection caused by the Borrelia burgdorferi sensu lato species complex and transmitted by the Ixodidae tick family. It is the most common tick-borne disease in the United States and mostly is reported in the northeastern and upper midwestern states during the warmer seasons, but it is prevalent worldwide. In geographic areas where Lyme disease is common, the incidence is approximately 40 cases per 100,000 individuals.¹ Our patient resided in coastal South Carolina. Lyme disease is more commonly reported in White individuals. The skin lesions may be more difficult to discern and diagnose in patients with darker skin types, leading to delayed diagnosis and treatment.^2,3

Patients may be diagnosed with early localized, early disseminated, or late Lyme disease. Erythema migrans is the early localized form of the disease and is classically described as an erythematous targetlike plaque with raised borders arising at the site of the tick bite 1 to 2 weeks later.⁴ However, many patients simply have a homogeneous erythematous plaque with raised advancing borders ranging in size from 5 to 68 cm.⁵ In a 2022 study of 69 patients with suspected Lyme disease, only 35 (50.7%) were determined to truly have acute Lyme disease.⁶ Of them, only 2 (5.7%) had the classic ringwithin- a-ring pattern. Most plaques were uniform, pink, oval-shaped lesions with well-demarcated borders.⁶

The rash may present with a burning sensation, or patients may experience no symptoms at all, which can lead to delayed diagnosis and progression to late disease. Patients may develop malaise, fever, headache, body aches, or joint pain. Early disseminated disease manifests similarly. Patients with disseminated disease also may develop more serious complications, including lymphadenopathy; cranial nerve palsies; ocular involvement; meningitis; or cardiac abnormalities such as myocarditis, pericarditis, or arrhythmia. Late disease most often causes arthritis of the large joints, though it also can have cardiac or neurologic manifestations. Some patients with chronic disease—the majority of whom were diagnosed in Europe—may develop acrodermatitis chronica atrophicans with edematous blue-red plaques that become atrophic and hyperpigmented fibrotic plaques over the course of years.

Allergic contact dermatitis to a plant more likely would cause itchy or painful, oozy, weepy, vesicular lesions arranged in a linear pattern. A dermatophyte infection likely would cause a scaly eruption. Although our patient presented with a sharply demarcated, raised, erythematous lesion, the distribution did not follow normal clothing lines and would be unusual for a photosensitive drug eruption. Cellulitis likely would be associated with tenderness or warmth to the touch. Finally, southern tick-associated rash illness, which is associated with Amblyomma americanum (lone star tick) bites, may appear with a similar rash but few systemic symptoms. It also can be treated with tetracycline antibiotics.⁷

Our case in South Carolina demonstrates the importance of keeping Lyme disease in the differential. Clinicians should remember to ask patients about their travel history. In endemic areas, patients with erythema migrans can be started on treatment without waiting for serology. Patients with early Lyme disease may or may not have positive serologies at the time of presentation.⁶ Guidelines for the treatment of Lyme disease have been revised in recent years to decrease patient antibiotic exposure by reducing the number of days of antibiotic therapy.⁸ A recent randomized controlled trial found no significant difference in recurrence for patients treated with 7 days of doxycycline compared with 14 days.⁹ We typically prescribe a 10-day course of doxycycline, which also is adequate for concurrent rickettsial disease. Patients who develop malarialike symptoms should be evaluated for babesiosis, which is treated with clindamycin.

The Diagnosis: Erythema Migrans

The patient was clinically diagnosed with erythema migrans. He did not recall a tick bite but spent a lot of time outdoors. He was treated with 10 days of doxycycline 100 mg twice daily with complete resolution of the rash.

Lyme disease is a spirochete infection caused by the Borrelia burgdorferi sensu lato species complex and transmitted by the Ixodidae tick family. It is the most common tick-borne disease in the United States and mostly is reported in the northeastern and upper midwestern states during the warmer seasons, but it is prevalent worldwide. In geographic areas where Lyme disease is common, the incidence is approximately 40 cases per 100,000 individuals.¹ Our patient resided in coastal South Carolina. Lyme disease is more commonly reported in White individuals. The skin lesions may be more difficult to discern and diagnose in patients with darker skin types, leading to delayed diagnosis and treatment.^2,3

Patients may be diagnosed with early localized, early disseminated, or late Lyme disease. Erythema migrans is the early localized form of the disease and is classically described as an erythematous targetlike plaque with raised borders arising at the site of the tick bite 1 to 2 weeks later.⁴ However, many patients simply have a homogeneous erythematous plaque with raised advancing borders ranging in size from 5 to 68 cm.⁵ In a 2022 study of 69 patients with suspected Lyme disease, only 35 (50.7%) were determined to truly have acute Lyme disease.⁶ Of them, only 2 (5.7%) had the classic ringwithin- a-ring pattern. Most plaques were uniform, pink, oval-shaped lesions with well-demarcated borders.⁶

The rash may present with a burning sensation, or patients may experience no symptoms at all, which can lead to delayed diagnosis and progression to late disease. Patients may develop malaise, fever, headache, body aches, or joint pain. Early disseminated disease manifests similarly. Patients with disseminated disease also may develop more serious complications, including lymphadenopathy; cranial nerve palsies; ocular involvement; meningitis; or cardiac abnormalities such as myocarditis, pericarditis, or arrhythmia. Late disease most often causes arthritis of the large joints, though it also can have cardiac or neurologic manifestations. Some patients with chronic disease—the majority of whom were diagnosed in Europe—may develop acrodermatitis chronica atrophicans with edematous blue-red plaques that become atrophic and hyperpigmented fibrotic plaques over the course of years.

Allergic contact dermatitis to a plant more likely would cause itchy or painful, oozy, weepy, vesicular lesions arranged in a linear pattern. A dermatophyte infection likely would cause a scaly eruption. Although our patient presented with a sharply demarcated, raised, erythematous lesion, the distribution did not follow normal clothing lines and would be unusual for a photosensitive drug eruption. Cellulitis likely would be associated with tenderness or warmth to the touch. Finally, southern tick-associated rash illness, which is associated with Amblyomma americanum (lone star tick) bites, may appear with a similar rash but few systemic symptoms. It also can be treated with tetracycline antibiotics.⁷

Our case in South Carolina demonstrates the importance of keeping Lyme disease in the differential. Clinicians should remember to ask patients about their travel history. In endemic areas, patients with erythema migrans can be started on treatment without waiting for serology. Patients with early Lyme disease may or may not have positive serologies at the time of presentation.⁶ Guidelines for the treatment of Lyme disease have been revised in recent years to decrease patient antibiotic exposure by reducing the number of days of antibiotic therapy.⁸ A recent randomized controlled trial found no significant difference in recurrence for patients treated with 7 days of doxycycline compared with 14 days.⁹ We typically prescribe a 10-day course of doxycycline, which also is adequate for concurrent rickettsial disease. Patients who develop malarialike symptoms should be evaluated for babesiosis, which is treated with clindamycin.

The Diagnosis: Erythema Migrans

The patient was clinically diagnosed with erythema migrans. He did not recall a tick bite but spent a lot of time outdoors. He was treated with 10 days of doxycycline 100 mg twice daily with complete resolution of the rash.

Lyme disease is a spirochete infection caused by the Borrelia burgdorferi sensu lato species complex and transmitted by the Ixodidae tick family. It is the most common tick-borne disease in the United States and mostly is reported in the northeastern and upper midwestern states during the warmer seasons, but it is prevalent worldwide. In geographic areas where Lyme disease is common, the incidence is approximately 40 cases per 100,000 individuals.¹ Our patient resided in coastal South Carolina. Lyme disease is more commonly reported in White individuals. The skin lesions may be more difficult to discern and diagnose in patients with darker skin types, leading to delayed diagnosis and treatment.^2,3

Patients may be diagnosed with early localized, early disseminated, or late Lyme disease. Erythema migrans is the early localized form of the disease and is classically described as an erythematous targetlike plaque with raised borders arising at the site of the tick bite 1 to 2 weeks later.⁴ However, many patients simply have a homogeneous erythematous plaque with raised advancing borders ranging in size from 5 to 68 cm.⁵ In a 2022 study of 69 patients with suspected Lyme disease, only 35 (50.7%) were determined to truly have acute Lyme disease.⁶ Of them, only 2 (5.7%) had the classic ringwithin- a-ring pattern. Most plaques were uniform, pink, oval-shaped lesions with well-demarcated borders.⁶

The rash may present with a burning sensation, or patients may experience no symptoms at all, which can lead to delayed diagnosis and progression to late disease. Patients may develop malaise, fever, headache, body aches, or joint pain. Early disseminated disease manifests similarly. Patients with disseminated disease also may develop more serious complications, including lymphadenopathy; cranial nerve palsies; ocular involvement; meningitis; or cardiac abnormalities such as myocarditis, pericarditis, or arrhythmia. Late disease most often causes arthritis of the large joints, though it also can have cardiac or neurologic manifestations. Some patients with chronic disease—the majority of whom were diagnosed in Europe—may develop acrodermatitis chronica atrophicans with edematous blue-red plaques that become atrophic and hyperpigmented fibrotic plaques over the course of years.

Allergic contact dermatitis to a plant more likely would cause itchy or painful, oozy, weepy, vesicular lesions arranged in a linear pattern. A dermatophyte infection likely would cause a scaly eruption. Although our patient presented with a sharply demarcated, raised, erythematous lesion, the distribution did not follow normal clothing lines and would be unusual for a photosensitive drug eruption. Cellulitis likely would be associated with tenderness or warmth to the touch. Finally, southern tick-associated rash illness, which is associated with Amblyomma americanum (lone star tick) bites, may appear with a similar rash but few systemic symptoms. It also can be treated with tetracycline antibiotics.⁷

Our case in South Carolina demonstrates the importance of keeping Lyme disease in the differential. Clinicians should remember to ask patients about their travel history. In endemic areas, patients with erythema migrans can be started on treatment without waiting for serology. Patients with early Lyme disease may or may not have positive serologies at the time of presentation.⁶ Guidelines for the treatment of Lyme disease have been revised in recent years to decrease patient antibiotic exposure by reducing the number of days of antibiotic therapy.⁸ A recent randomized controlled trial found no significant difference in recurrence for patients treated with 7 days of doxycycline compared with 14 days.⁹ We typically prescribe a 10-day course of doxycycline, which also is adequate for concurrent rickettsial disease. Patients who develop malarialike symptoms should be evaluated for babesiosis, which is treated with clindamycin.