Cpt Naomi B. Creel, MC, USA

Case Report

A healthy 12-year-old African American boy presented with a 3-month history of an asymptomatic, papular, perioral eruption. He had been previously treated by a primary care provider, who had prescribed a low-potency and then a medium-potency topical corticosteroid, without improvement. The patient's parents denied that he had used topical corticosteroids or other topical preparations prior to the eruption. He took no oral medications, and the findings of the review of systems were within reference range. Results of a physical examination revealed numerous, discrete and coalescing, firm, pink, hyperpigmented papules ranging from 2 to 4 mm in diameter, primarily located in the perioral area (Figure). A few papules were noted around the nose and eyes. Results of a shave biopsy of a perioral papule revealed dermal granulomatous inflammation. The infiltrate consisted of histiocytes and lymphocytes and also included several focal collections of neutrophils. There was overlying parakeratosis. Results of a periodic acid–Schiff, Gomori methenamine-silver, Brown-Brenn, and Fite-Farraco stains were negative for organisms.

The patient was diagnosed with granulomatous periorificial dermatitis (GPD), and treatment with oral tetracycline 500 mg twice a day was initiated. Six days later, a tapering course of oral prednisone was added (consisting of 40 mg for 3 days, 30 mg for 3 days, 20 mg for 3 days, and 10 mg for 3 days) because of the severe extent of the eruption and the social distress it was causing the patient. Within 3 weeks, a dramatic decrease in the eruption was noted, with only a few small papules remaining. The patient was then switched from oral tetracycline to topical clindamycin twice a day for maintenance, but he did not return for follow-up. 

Comment

GPD is characterized by a monomorphic papular eruption occurring in the perinasal, perioral, and periocular areas. Gianotti et al1 first described the condition in 5 children, ranging in age from 2 to 7 years, who had asymptomatic, distinctive, flesh-colored, "micronodular," periorificial eruptions. In the literature, the condition has been variably called Gianotti-type perioral dermatitis, sarcoidlike granulomatous dermatitis, facial Afro-Caribbean childhood eruption, and childhood granulomatous perioral dermatitis. It has been proposed that GPD is a form of perioral dermatitis with granulomatous histologic features.^2,3 GPD typically affects prepubertal children, predominantly African Americans and others with dark skin. Several cases involving fair-skinned children have been reported.² Both genders are equally affected. Typical lesions have been described as flesh-colored, yellow-brown, or red papules or micronodules.^2,3 Slight scaling of lesions or surrounding erythema may occur.² Scarring is absent in most cases; however, pinpoint atrophy or scarring occasionally occurs.² In addition to the characteristic facial distribution, extrafacial and generalized lesions on the trunk, extremities, and labia majora have been described.² In all reported cases, the lesions, including extrafacial lesions, were histologically similar and self-limited and were not accompanied by associated systemic symptoms. The presence of extrafacial lesions did not affect the duration of disease or the response to treatment.

The etiology of GPD is unknown. It may represent an unusual inflammatory granulomatous response to allergens.³ The initial allergen may cause inflammation and a focal disruption of the follicular wall, inciting a granulomatous reaction.³ In 1978, Georgouras and Kocsard4 described a case of Gianotti-type perioral dermatitis as an unusual reaction to bubble gum. Other reports have implicated reactions to formaldehyde, cosmetic preparations, and antiseptic solutions.⁵ Topical corticosteroids may induce or exacerbate both perioral dermatitis and GPD.^3,6

Histologic findings consist of upper dermal and perifollicular granulomas admixed with lymphocytes. The inflammation surrounding a focally disrupted hair follicle may range from a primarily lymphocytic inflammation with focal granuloma formation to a denser dermal granulomatous infiltrate. The presence of lymphocytic inflammation can help distinguish GPD from the "naked" granulomas in cutaneous sarcoidosis that typically lack inflammatory cells. GPD also may show epidermal change with mild to moderate spongiosis.^3,7

The clinical differential diagnosis of granulomatous papules on the face of a child includes GPD, granulomatous rosacea, lupus miliaris disseminatus faciei, and cutaneous sarcoidosis. Other cutaneous diseases that may occur in a periorificial distribution include perioral dermatitis, telangiectatic fibromas, and trichoepitheliomas. Although similar in distribution to GPD, the primary lesions in these latter 3 conditions are not granulomatous and can often be distinguished clinically. Deep fungal infection, atypical mycobacterial infection, and leishmaniasis can be considered in the histologic differential diagnosis of granulomatous dermatitis, but these conditions usually present as nodules, plaques, or ulcers and not necessarily in a perioral distribution.

Granulomatous rosacea and GPD have a similar clinical and histopathologic presentation. Both conditions can present as red or yellow-brown, dome-shaped facial papules with histologic findings of a perifollicular lymphohistiocytic or granulomatous infiltrate. The major distinguishing features of granulomatous rosacea are erythema, telangiectasias, pustules, and edema.8 Granulomatous rosacea is not characterized by a concentration of lesions in the perioral area, and it is most common in 30- to 50-year-old women.⁹ Rosacea also involves the eyes in about 17% of patients seen by dermatologists.¹⁰ Ocular rosacea can manifest as blepharitis, conjunctival injection, and chalazion.

Lupus miliaris disseminatus faciei is another chronic facial papular eruption with a high predilection for the eyelids. The lesions are usually red or yellow-brown dome-shaped papules. Histologic examination demonstrates well-formed granulomas with central caseation necrosis. Lesions resolve spontaneously in 12 to 24 months with scarring. To our knowledge, lupus miliaris disseminatus faciei has not been reported in children. It has been hypothesized that most patients with this eruption actually have a form of granulomatous rosacea.⁷

Sarcoidosis is a systemic granulomatous disease with cutaneous manifestations. Cutaneous involvement occurs in up to one third of patients and can present as macules, papules, nodules, plaques, subcutaneous nodules, infiltrative scars, and ichthyosis. Maculopapular lesions are the most common cutaneous manifestation of sarcoidosis and can occur anywhere on the skin.¹¹ Lupus pernio is a variant of sarcoidosis characterized by violaceous papules and plaques on the nasal alar rims, ears, and cheeks. This variant of sarcoidosis occurs most frequently in middle-aged women and is associated with chronic fibrotic respiratory tract involvement. Patients with cutaneous sarcoidosis may have systemic symptoms including weight loss, shortness of breath, cough, fatigue, and bone and joint pain.

Perioral dermatitis most commonly occurs in young women between 16 and 45 years of age. The characteristic eruption consists of pustular or papulovesicular lesions on an erythematous background.¹² The lesions are usually confined to the chin and nasolabial folds, with sparing around the vermilion border. GPD may be distinguished from perioral dermatitis by the presence of discrete yellow-brown papules rather than erythematous papules, the lack of pustules, and the presence of a perifollicular granulomatous infiltrate seen on examination of biopsy material.⁵

Treatment of GPD is based on anecdotal reports. Tetracycline has been recommended for GPD in children older than 8 years.^3,13 Recent studies have demonstrated that tetracyclines inhibit granuloma formation in vitro.¹⁴ Tetracyclines are also effective treatment for rosacea and perioral dermatitis because of their anti-inflammatory properties.¹⁵ According to anecdotal reports, topical tetracycline and topical clindamycin are sometimes effective therapy for perioral dermatitis and may be helpful in GPD when oral agents are undesirable. GPD also has responded to topical treatment with metronidazole gel in some reports.^3,16 Mild GPD may resolve spontaneously over several months without therapy. The use of oral steroids in this condition has not been reported, but in our patient, a tapering course of prednisone seemed justified because of the distressing nature of the eruption to the patient. Oral prednisone may produce anti-inflammatory effects more quickly than tetracycline, but it is not necessary in most patients.

GPD represents a benign cutaneous inflammatory process that resolves without serious sequelae. The granulomatous inflammation is most likely a nonspecific reaction to a variety of insults. Topical corticosteroids may initiate or exacerbate the granulomatous reaction and should be strictly avoided. Practitioners should recognize and distinguish this condition from other granulomatous eruptions so that patients are appropriately managed.

Case Report

A healthy 12-year-old African American boy presented with a 3-month history of an asymptomatic, papular, perioral eruption. He had been previously treated by a primary care provider, who had prescribed a low-potency and then a medium-potency topical corticosteroid, without improvement. The patient's parents denied that he had used topical corticosteroids or other topical preparations prior to the eruption. He took no oral medications, and the findings of the review of systems were within reference range. Results of a physical examination revealed numerous, discrete and coalescing, firm, pink, hyperpigmented papules ranging from 2 to 4 mm in diameter, primarily located in the perioral area (Figure). A few papules were noted around the nose and eyes. Results of a shave biopsy of a perioral papule revealed dermal granulomatous inflammation. The infiltrate consisted of histiocytes and lymphocytes and also included several focal collections of neutrophils. There was overlying parakeratosis. Results of a periodic acid–Schiff, Gomori methenamine-silver, Brown-Brenn, and Fite-Farraco stains were negative for organisms.

The patient was diagnosed with granulomatous periorificial dermatitis (GPD), and treatment with oral tetracycline 500 mg twice a day was initiated. Six days later, a tapering course of oral prednisone was added (consisting of 40 mg for 3 days, 30 mg for 3 days, 20 mg for 3 days, and 10 mg for 3 days) because of the severe extent of the eruption and the social distress it was causing the patient. Within 3 weeks, a dramatic decrease in the eruption was noted, with only a few small papules remaining. The patient was then switched from oral tetracycline to topical clindamycin twice a day for maintenance, but he did not return for follow-up. 

Comment

GPD is characterized by a monomorphic papular eruption occurring in the perinasal, perioral, and periocular areas. Gianotti et al1 first described the condition in 5 children, ranging in age from 2 to 7 years, who had asymptomatic, distinctive, flesh-colored, "micronodular," periorificial eruptions. In the literature, the condition has been variably called Gianotti-type perioral dermatitis, sarcoidlike granulomatous dermatitis, facial Afro-Caribbean childhood eruption, and childhood granulomatous perioral dermatitis. It has been proposed that GPD is a form of perioral dermatitis with granulomatous histologic features.^2,3 GPD typically affects prepubertal children, predominantly African Americans and others with dark skin. Several cases involving fair-skinned children have been reported.² Both genders are equally affected. Typical lesions have been described as flesh-colored, yellow-brown, or red papules or micronodules.^2,3 Slight scaling of lesions or surrounding erythema may occur.² Scarring is absent in most cases; however, pinpoint atrophy or scarring occasionally occurs.² In addition to the characteristic facial distribution, extrafacial and generalized lesions on the trunk, extremities, and labia majora have been described.² In all reported cases, the lesions, including extrafacial lesions, were histologically similar and self-limited and were not accompanied by associated systemic symptoms. The presence of extrafacial lesions did not affect the duration of disease or the response to treatment.

The etiology of GPD is unknown. It may represent an unusual inflammatory granulomatous response to allergens.³ The initial allergen may cause inflammation and a focal disruption of the follicular wall, inciting a granulomatous reaction.³ In 1978, Georgouras and Kocsard4 described a case of Gianotti-type perioral dermatitis as an unusual reaction to bubble gum. Other reports have implicated reactions to formaldehyde, cosmetic preparations, and antiseptic solutions.⁵ Topical corticosteroids may induce or exacerbate both perioral dermatitis and GPD.^3,6

Histologic findings consist of upper dermal and perifollicular granulomas admixed with lymphocytes. The inflammation surrounding a focally disrupted hair follicle may range from a primarily lymphocytic inflammation with focal granuloma formation to a denser dermal granulomatous infiltrate. The presence of lymphocytic inflammation can help distinguish GPD from the "naked" granulomas in cutaneous sarcoidosis that typically lack inflammatory cells. GPD also may show epidermal change with mild to moderate spongiosis.^3,7

The clinical differential diagnosis of granulomatous papules on the face of a child includes GPD, granulomatous rosacea, lupus miliaris disseminatus faciei, and cutaneous sarcoidosis. Other cutaneous diseases that may occur in a periorificial distribution include perioral dermatitis, telangiectatic fibromas, and trichoepitheliomas. Although similar in distribution to GPD, the primary lesions in these latter 3 conditions are not granulomatous and can often be distinguished clinically. Deep fungal infection, atypical mycobacterial infection, and leishmaniasis can be considered in the histologic differential diagnosis of granulomatous dermatitis, but these conditions usually present as nodules, plaques, or ulcers and not necessarily in a perioral distribution.

Granulomatous rosacea and GPD have a similar clinical and histopathologic presentation. Both conditions can present as red or yellow-brown, dome-shaped facial papules with histologic findings of a perifollicular lymphohistiocytic or granulomatous infiltrate. The major distinguishing features of granulomatous rosacea are erythema, telangiectasias, pustules, and edema.8 Granulomatous rosacea is not characterized by a concentration of lesions in the perioral area, and it is most common in 30- to 50-year-old women.⁹ Rosacea also involves the eyes in about 17% of patients seen by dermatologists.¹⁰ Ocular rosacea can manifest as blepharitis, conjunctival injection, and chalazion.

Lupus miliaris disseminatus faciei is another chronic facial papular eruption with a high predilection for the eyelids. The lesions are usually red or yellow-brown dome-shaped papules. Histologic examination demonstrates well-formed granulomas with central caseation necrosis. Lesions resolve spontaneously in 12 to 24 months with scarring. To our knowledge, lupus miliaris disseminatus faciei has not been reported in children. It has been hypothesized that most patients with this eruption actually have a form of granulomatous rosacea.⁷

Sarcoidosis is a systemic granulomatous disease with cutaneous manifestations. Cutaneous involvement occurs in up to one third of patients and can present as macules, papules, nodules, plaques, subcutaneous nodules, infiltrative scars, and ichthyosis. Maculopapular lesions are the most common cutaneous manifestation of sarcoidosis and can occur anywhere on the skin.¹¹ Lupus pernio is a variant of sarcoidosis characterized by violaceous papules and plaques on the nasal alar rims, ears, and cheeks. This variant of sarcoidosis occurs most frequently in middle-aged women and is associated with chronic fibrotic respiratory tract involvement. Patients with cutaneous sarcoidosis may have systemic symptoms including weight loss, shortness of breath, cough, fatigue, and bone and joint pain.

Perioral dermatitis most commonly occurs in young women between 16 and 45 years of age. The characteristic eruption consists of pustular or papulovesicular lesions on an erythematous background.¹² The lesions are usually confined to the chin and nasolabial folds, with sparing around the vermilion border. GPD may be distinguished from perioral dermatitis by the presence of discrete yellow-brown papules rather than erythematous papules, the lack of pustules, and the presence of a perifollicular granulomatous infiltrate seen on examination of biopsy material.⁵

Treatment of GPD is based on anecdotal reports. Tetracycline has been recommended for GPD in children older than 8 years.^3,13 Recent studies have demonstrated that tetracyclines inhibit granuloma formation in vitro.¹⁴ Tetracyclines are also effective treatment for rosacea and perioral dermatitis because of their anti-inflammatory properties.¹⁵ According to anecdotal reports, topical tetracycline and topical clindamycin are sometimes effective therapy for perioral dermatitis and may be helpful in GPD when oral agents are undesirable. GPD also has responded to topical treatment with metronidazole gel in some reports.^3,16 Mild GPD may resolve spontaneously over several months without therapy. The use of oral steroids in this condition has not been reported, but in our patient, a tapering course of prednisone seemed justified because of the distressing nature of the eruption to the patient. Oral prednisone may produce anti-inflammatory effects more quickly than tetracycline, but it is not necessary in most patients.

GPD represents a benign cutaneous inflammatory process that resolves without serious sequelae. The granulomatous inflammation is most likely a nonspecific reaction to a variety of insults. Topical corticosteroids may initiate or exacerbate the granulomatous reaction and should be strictly avoided. Practitioners should recognize and distinguish this condition from other granulomatous eruptions so that patients are appropriately managed.

Case Report

A healthy 12-year-old African American boy presented with a 3-month history of an asymptomatic, papular, perioral eruption. He had been previously treated by a primary care provider, who had prescribed a low-potency and then a medium-potency topical corticosteroid, without improvement. The patient's parents denied that he had used topical corticosteroids or other topical preparations prior to the eruption. He took no oral medications, and the findings of the review of systems were within reference range. Results of a physical examination revealed numerous, discrete and coalescing, firm, pink, hyperpigmented papules ranging from 2 to 4 mm in diameter, primarily located in the perioral area (Figure). A few papules were noted around the nose and eyes. Results of a shave biopsy of a perioral papule revealed dermal granulomatous inflammation. The infiltrate consisted of histiocytes and lymphocytes and also included several focal collections of neutrophils. There was overlying parakeratosis. Results of a periodic acid–Schiff, Gomori methenamine-silver, Brown-Brenn, and Fite-Farraco stains were negative for organisms.

The patient was diagnosed with granulomatous periorificial dermatitis (GPD), and treatment with oral tetracycline 500 mg twice a day was initiated. Six days later, a tapering course of oral prednisone was added (consisting of 40 mg for 3 days, 30 mg for 3 days, 20 mg for 3 days, and 10 mg for 3 days) because of the severe extent of the eruption and the social distress it was causing the patient. Within 3 weeks, a dramatic decrease in the eruption was noted, with only a few small papules remaining. The patient was then switched from oral tetracycline to topical clindamycin twice a day for maintenance, but he did not return for follow-up. 

Comment

GPD is characterized by a monomorphic papular eruption occurring in the perinasal, perioral, and periocular areas. Gianotti et al1 first described the condition in 5 children, ranging in age from 2 to 7 years, who had asymptomatic, distinctive, flesh-colored, "micronodular," periorificial eruptions. In the literature, the condition has been variably called Gianotti-type perioral dermatitis, sarcoidlike granulomatous dermatitis, facial Afro-Caribbean childhood eruption, and childhood granulomatous perioral dermatitis. It has been proposed that GPD is a form of perioral dermatitis with granulomatous histologic features.^2,3 GPD typically affects prepubertal children, predominantly African Americans and others with dark skin. Several cases involving fair-skinned children have been reported.² Both genders are equally affected. Typical lesions have been described as flesh-colored, yellow-brown, or red papules or micronodules.^2,3 Slight scaling of lesions or surrounding erythema may occur.² Scarring is absent in most cases; however, pinpoint atrophy or scarring occasionally occurs.² In addition to the characteristic facial distribution, extrafacial and generalized lesions on the trunk, extremities, and labia majora have been described.² In all reported cases, the lesions, including extrafacial lesions, were histologically similar and self-limited and were not accompanied by associated systemic symptoms. The presence of extrafacial lesions did not affect the duration of disease or the response to treatment.

The etiology of GPD is unknown. It may represent an unusual inflammatory granulomatous response to allergens.³ The initial allergen may cause inflammation and a focal disruption of the follicular wall, inciting a granulomatous reaction.³ In 1978, Georgouras and Kocsard4 described a case of Gianotti-type perioral dermatitis as an unusual reaction to bubble gum. Other reports have implicated reactions to formaldehyde, cosmetic preparations, and antiseptic solutions.⁵ Topical corticosteroids may induce or exacerbate both perioral dermatitis and GPD.^3,6

Histologic findings consist of upper dermal and perifollicular granulomas admixed with lymphocytes. The inflammation surrounding a focally disrupted hair follicle may range from a primarily lymphocytic inflammation with focal granuloma formation to a denser dermal granulomatous infiltrate. The presence of lymphocytic inflammation can help distinguish GPD from the "naked" granulomas in cutaneous sarcoidosis that typically lack inflammatory cells. GPD also may show epidermal change with mild to moderate spongiosis.^3,7

The clinical differential diagnosis of granulomatous papules on the face of a child includes GPD, granulomatous rosacea, lupus miliaris disseminatus faciei, and cutaneous sarcoidosis. Other cutaneous diseases that may occur in a periorificial distribution include perioral dermatitis, telangiectatic fibromas, and trichoepitheliomas. Although similar in distribution to GPD, the primary lesions in these latter 3 conditions are not granulomatous and can often be distinguished clinically. Deep fungal infection, atypical mycobacterial infection, and leishmaniasis can be considered in the histologic differential diagnosis of granulomatous dermatitis, but these conditions usually present as nodules, plaques, or ulcers and not necessarily in a perioral distribution.

Granulomatous rosacea and GPD have a similar clinical and histopathologic presentation. Both conditions can present as red or yellow-brown, dome-shaped facial papules with histologic findings of a perifollicular lymphohistiocytic or granulomatous infiltrate. The major distinguishing features of granulomatous rosacea are erythema, telangiectasias, pustules, and edema.8 Granulomatous rosacea is not characterized by a concentration of lesions in the perioral area, and it is most common in 30- to 50-year-old women.⁹ Rosacea also involves the eyes in about 17% of patients seen by dermatologists.¹⁰ Ocular rosacea can manifest as blepharitis, conjunctival injection, and chalazion.

Lupus miliaris disseminatus faciei is another chronic facial papular eruption with a high predilection for the eyelids. The lesions are usually red or yellow-brown dome-shaped papules. Histologic examination demonstrates well-formed granulomas with central caseation necrosis. Lesions resolve spontaneously in 12 to 24 months with scarring. To our knowledge, lupus miliaris disseminatus faciei has not been reported in children. It has been hypothesized that most patients with this eruption actually have a form of granulomatous rosacea.⁷

Sarcoidosis is a systemic granulomatous disease with cutaneous manifestations. Cutaneous involvement occurs in up to one third of patients and can present as macules, papules, nodules, plaques, subcutaneous nodules, infiltrative scars, and ichthyosis. Maculopapular lesions are the most common cutaneous manifestation of sarcoidosis and can occur anywhere on the skin.¹¹ Lupus pernio is a variant of sarcoidosis characterized by violaceous papules and plaques on the nasal alar rims, ears, and cheeks. This variant of sarcoidosis occurs most frequently in middle-aged women and is associated with chronic fibrotic respiratory tract involvement. Patients with cutaneous sarcoidosis may have systemic symptoms including weight loss, shortness of breath, cough, fatigue, and bone and joint pain.

Perioral dermatitis most commonly occurs in young women between 16 and 45 years of age. The characteristic eruption consists of pustular or papulovesicular lesions on an erythematous background.¹² The lesions are usually confined to the chin and nasolabial folds, with sparing around the vermilion border. GPD may be distinguished from perioral dermatitis by the presence of discrete yellow-brown papules rather than erythematous papules, the lack of pustules, and the presence of a perifollicular granulomatous infiltrate seen on examination of biopsy material.⁵

Treatment of GPD is based on anecdotal reports. Tetracycline has been recommended for GPD in children older than 8 years.^3,13 Recent studies have demonstrated that tetracyclines inhibit granuloma formation in vitro.¹⁴ Tetracyclines are also effective treatment for rosacea and perioral dermatitis because of their anti-inflammatory properties.¹⁵ According to anecdotal reports, topical tetracycline and topical clindamycin are sometimes effective therapy for perioral dermatitis and may be helpful in GPD when oral agents are undesirable. GPD also has responded to topical treatment with metronidazole gel in some reports.^3,16 Mild GPD may resolve spontaneously over several months without therapy. The use of oral steroids in this condition has not been reported, but in our patient, a tapering course of prednisone seemed justified because of the distressing nature of the eruption to the patient. Oral prednisone may produce anti-inflammatory effects more quickly than tetracycline, but it is not necessary in most patients.

GPD represents a benign cutaneous inflammatory process that resolves without serious sequelae. The granulomatous inflammation is most likely a nonspecific reaction to a variety of insults. Topical corticosteroids may initiate or exacerbate the granulomatous reaction and should be strictly avoided. Practitioners should recognize and distinguish this condition from other granulomatous eruptions so that patients are appropriately managed.

Rat mite dermatitis is characterized by pruritic papules in a patient exposed to the tropical rat mite Ornithonyssus bacoti. We report a case of a woman with rat mite dermatitis who developed this eruption after exposure to her pet hamster. Mites were collected from the hamster and identified as O bacoti. Reported sources of rat mites, as well as avian mites and other mites that bite humans, are reviewed.

Rat mite dermatitis is a pruritic eruption in humans caused by bites from the tropical rat mite Ornithonyssus bacoti. Other biting mite species that have been reported to cause a similar dermatitis in humans include Dermanyssus gallinae (red mite or poultry mite), Ornithonyssus sylviarum (northern fowl mite), and Ornithonyssus bursa (tropical fowl mite).1-6 The eruptions caused by these mites are clinically indistinguishable. Initial case reports of mite dermatitis identified the sources of these mites to be rat-infested homes or bird nests around the home.1-6 Rat mite dermatitis also was reported in a patient who had contact with mite-infested laboratory mice.7 More recently, avian mite dermatitis was reported in patients who had mite-infested pet gerbils.8 This report describes a patient with rat mite dermatitis acquired from a pet hamster. Based on the variety of mites and sources of infestations, mite dermatitis may be more common than generally thought. back to top

CASE REPORT

A 48-year-old healthy woman presented with a complaint of pruritic papules on the wrists (Figure 1) and waist for several weeks. History revealed she maintained a small menagerie of animals including horses, dogs, cats, and hamsters. She was informed that her skin lesions were most likely the result of insect bites and she should evaluate her animals and their environment for evidence of infestation. She returned 2 days later and reported that her hamster had died the previous day. When she went to bury it, she noticed numerous red specks in its fur. She placed the hamster in a plastic bag in the freezer until she could bring it in for examination. Examination of the hamster (Figure 2) revealed numerous red mites (Figure 3). The patient's symptoms resolved over the following few weeks. The mites were identified as the tropical rat mite O bacoti. No necropsy was performed on the hamster, and a specific cause of death was never determined. This mite ingests blood and can cause debility, anemia, decreased reproduction, and death in small animals, suggesting that it may have contributed to the hamster's death.

Comment

Mites are arthropods in the class Arachnida, which includes ticks, spiders, and scorpions. The arachnids are characterized by 4 pairs of legs and 2 body regions, a cephalothorax and an abdomen. Mites and ticks are further classified in the subclass Acari. Mites of medical importance can be grouped by their pathology in humans.9 House dust mites (Dermatophagoides and Euroglyphus ssp) cause respiratory allergies, whereas human follicle mites (Demodex spp) infest hair follicles and associated sebaceous glands. Neither group of mites causes cutaneous lesions in the form of bites or burrows. The scabies mite (Sarcoptes scabiei) is a primary human parasitic mite in which the adult mite burrows and feeds on skin cells. Chiggers (family Trombiculidae) and common animal mites bite humans but do not reside on humans as a primary host. Many mite species are opportunistic, often feeding on various hosts they encounter.10 The common animal mites that bite humans include several avian mites, the rodent mites, and fur mites of rabbits (Cheyletiella parasitivorax), dogs (Cheyletiella yasguri), and cats (Cheyletiella blakei). Mites infesting grain, hay, and straw occasionally cause dermatitis in humans.

The usual hosts of the tropical rat mite O bacoti are the brown rat (Rattus norvegicus) and the black rat (Rattus rattus). This mite is yellow to dark red, when blood-fed, and ranges in size from 0.75 to 1.4 mm. It will feed on humans when its rodent hosts are killed or abandon their nests.11-16 O bacoti also infests mice and hamsters in research laboratories.7

The common avian mites D gallinae, O sylviarum, and O bursa occur on both domestic and wild bird species, including chickens, ducks, pigeons, sparrows, canaries, starlings, robins, tiger finches, and doves.1 D gallinae has been identified on commensal and laboratory rodents, and in one case it was found on a farm dog.17-19 The species are similar in size and appearance, but differ in their life cycle. The adult mite of these species ranges in color from brown to red and in size from 1 to 3 mm. D gallinae lives most of its life cycle off the hosts in nests, crevices, and cracks in buildings. It feeds on the host nocturnally for 1 to 2 hours at a time, and may live up to 8 months without a host. O sylviarum and O bursa spend their entire life cycle on the host. The mites will leave the host and bite humans in close proximity, especially in heavily infested quarters. The Ornithonyssus species live only 2 to 3 weeks without a host.9

Mite bites typically produce urticarial, pruritic papules on the skin. These papules result from an inflammatory cutaneous reaction to mite saliva as it takes a blood meal. Clinically, the bites are nonspecific, but pruritus is the most consistent feature. The lesions may be vesicular, urticarial, eczematous, or any combination of these. Secondary lesions such as persistent nodules, postinflammatory hyperpigmentation, excoriations, and secondary infection may be present. The bites tend to occur in asymmetric groups, most commonly on the abdomen and extremities. Often a patient presents with a combination of these clinical features, but denies a history of any "bites."

On pathologic examination, the lesions are nonspecific mild arthropod reactions with superficial and mid-dermal perivascular infiltrate. Eosinophils may be present. The epidermis may be mildly spongiotic.

The diagnosis of mite dermatitis should be considered in unexplained pruritic dermatitis. The rodent and avian mites are rarely found on the human host because the mites leave after feeding. History of exposure can include bird handling, bird nests or roosts near the home, rat infestations, pets, and occupational exposure to laboratory rodents. The mite may be discovered in abandoned bird or rodent nests, on pets, or in pet bedding. Speciation of the mite usually requires assistance of an entomologist or acarologist. To facilitate microscopic identification of mites, specimens can be temporarily slide-mounted in a drop of mineral oil under a coverglass. However, if they are to be sent to an acarologist or other specialist for identification, it is best to place them in 70% alcohol, rather than mineral oil. It is very difficult to remove mineral oil from mite specimens before clearing and slide-mounting them in other appropriate mounting media. This may be required to discern fine structural details needed for making species determinations.

Cheyletiella mite dermatitis also may present as a nonspecific pruritic dermatitis. These mites are parasitic on dogs, cats, and rabbits and may be discovered on the pet as "walking dandruff."20

Bites from chiggers, or red bugs, may be distinguished from other mites by the location of bites at sites of clothing constriction, such as the waistline, sock line, and beneath undergarments. These bites typically appear as papules with hemorrhagic puncta.

The scabies mite burrows in the skin and thus can be distinguished from other mites that cause dermatitis. In addition, scabies may be distinguished clinically by lesions in the interdigital web spaces and on the genitals. The mite, its eggs, and its feces can be visualized by a routine scabies preparation during the patient visit.

Other arthropod bites, including those from fleas, human body lice, and pubic lice, should be included in the differential diagnosis of mite dermatitis. In addition, systemic pruritus with excoriations, drug hypersensitivity reaction, and neurodermatitis should be considered.

Treatment focuses on reducing or eliminating problem mites in infested areas, often requiring involvement of veterinarians and pest control agencies. In the case of D gallinae, which does not live on the host, acaricides must penetrate into crevices and cracks in buildings.21 Both the host and the area of infestation must be treated to exterminate O sylviarum and O bursa. Elimination of rats and removal of their nests are important for controlling O bacoti.22 Patients may be treated with antihistamines and topical corticosteroids for symptomatic relief. The dermatitis is self-limited when the exposure is eliminated.

Two important mite-borne diseases of humans are tsutsugamushi disease (scrub typhus) and rickettsialpox, caused by the rickettsial organisms Orienta tsutsugamushi and Rickettsia akari, respectively. In the case of tsutsugamushi disease, chiggers are the vectors, whereas in rickettsialpox, the vector is the house-mouse mite (Liponyssoides sanguineus). These are the only 2 groups of mites that play a significant role in transmission of human pathogens.23

Mite dermatitis should be considered in any unexplained dermatitis. When considering a diagnosis of mite dermatitis, it is important to determine if there is a history of exposure to mice, hamsters, other rodents, or birds. Although the mites are rarely found on the patient, they may be discovered around the home or on pets. Demonstrating the presence of mites is important in diagnosing cases of mite-induced dermatitis. In many cases, reliable identification of the mite species is important in not only confirming the diagnosis but also identifying the sources of mite infestations so that they can be eliminated. The diagnosis should not be overlooked simply because the patient denies having rats or birds in the home. 

Rat mite dermatitis is characterized by pruritic papules in a patient exposed to the tropical rat mite Ornithonyssus bacoti. We report a case of a woman with rat mite dermatitis who developed this eruption after exposure to her pet hamster. Mites were collected from the hamster and identified as O bacoti. Reported sources of rat mites, as well as avian mites and other mites that bite humans, are reviewed.

Rat mite dermatitis is a pruritic eruption in humans caused by bites from the tropical rat mite Ornithonyssus bacoti. Other biting mite species that have been reported to cause a similar dermatitis in humans include Dermanyssus gallinae (red mite or poultry mite), Ornithonyssus sylviarum (northern fowl mite), and Ornithonyssus bursa (tropical fowl mite).1-6 The eruptions caused by these mites are clinically indistinguishable. Initial case reports of mite dermatitis identified the sources of these mites to be rat-infested homes or bird nests around the home.1-6 Rat mite dermatitis also was reported in a patient who had contact with mite-infested laboratory mice.7 More recently, avian mite dermatitis was reported in patients who had mite-infested pet gerbils.8 This report describes a patient with rat mite dermatitis acquired from a pet hamster. Based on the variety of mites and sources of infestations, mite dermatitis may be more common than generally thought. back to top

CASE REPORT

A 48-year-old healthy woman presented with a complaint of pruritic papules on the wrists (Figure 1) and waist for several weeks. History revealed she maintained a small menagerie of animals including horses, dogs, cats, and hamsters. She was informed that her skin lesions were most likely the result of insect bites and she should evaluate her animals and their environment for evidence of infestation. She returned 2 days later and reported that her hamster had died the previous day. When she went to bury it, she noticed numerous red specks in its fur. She placed the hamster in a plastic bag in the freezer until she could bring it in for examination. Examination of the hamster (Figure 2) revealed numerous red mites (Figure 3). The patient's symptoms resolved over the following few weeks. The mites were identified as the tropical rat mite O bacoti. No necropsy was performed on the hamster, and a specific cause of death was never determined. This mite ingests blood and can cause debility, anemia, decreased reproduction, and death in small animals, suggesting that it may have contributed to the hamster's death.

Comment

Mites are arthropods in the class Arachnida, which includes ticks, spiders, and scorpions. The arachnids are characterized by 4 pairs of legs and 2 body regions, a cephalothorax and an abdomen. Mites and ticks are further classified in the subclass Acari. Mites of medical importance can be grouped by their pathology in humans.9 House dust mites (Dermatophagoides and Euroglyphus ssp) cause respiratory allergies, whereas human follicle mites (Demodex spp) infest hair follicles and associated sebaceous glands. Neither group of mites causes cutaneous lesions in the form of bites or burrows. The scabies mite (Sarcoptes scabiei) is a primary human parasitic mite in which the adult mite burrows and feeds on skin cells. Chiggers (family Trombiculidae) and common animal mites bite humans but do not reside on humans as a primary host. Many mite species are opportunistic, often feeding on various hosts they encounter.10 The common animal mites that bite humans include several avian mites, the rodent mites, and fur mites of rabbits (Cheyletiella parasitivorax), dogs (Cheyletiella yasguri), and cats (Cheyletiella blakei). Mites infesting grain, hay, and straw occasionally cause dermatitis in humans.

The usual hosts of the tropical rat mite O bacoti are the brown rat (Rattus norvegicus) and the black rat (Rattus rattus). This mite is yellow to dark red, when blood-fed, and ranges in size from 0.75 to 1.4 mm. It will feed on humans when its rodent hosts are killed or abandon their nests.11-16 O bacoti also infests mice and hamsters in research laboratories.7

The common avian mites D gallinae, O sylviarum, and O bursa occur on both domestic and wild bird species, including chickens, ducks, pigeons, sparrows, canaries, starlings, robins, tiger finches, and doves.1 D gallinae has been identified on commensal and laboratory rodents, and in one case it was found on a farm dog.17-19 The species are similar in size and appearance, but differ in their life cycle. The adult mite of these species ranges in color from brown to red and in size from 1 to 3 mm. D gallinae lives most of its life cycle off the hosts in nests, crevices, and cracks in buildings. It feeds on the host nocturnally for 1 to 2 hours at a time, and may live up to 8 months without a host. O sylviarum and O bursa spend their entire life cycle on the host. The mites will leave the host and bite humans in close proximity, especially in heavily infested quarters. The Ornithonyssus species live only 2 to 3 weeks without a host.9

Mite bites typically produce urticarial, pruritic papules on the skin. These papules result from an inflammatory cutaneous reaction to mite saliva as it takes a blood meal. Clinically, the bites are nonspecific, but pruritus is the most consistent feature. The lesions may be vesicular, urticarial, eczematous, or any combination of these. Secondary lesions such as persistent nodules, postinflammatory hyperpigmentation, excoriations, and secondary infection may be present. The bites tend to occur in asymmetric groups, most commonly on the abdomen and extremities. Often a patient presents with a combination of these clinical features, but denies a history of any "bites."

On pathologic examination, the lesions are nonspecific mild arthropod reactions with superficial and mid-dermal perivascular infiltrate. Eosinophils may be present. The epidermis may be mildly spongiotic.

The diagnosis of mite dermatitis should be considered in unexplained pruritic dermatitis. The rodent and avian mites are rarely found on the human host because the mites leave after feeding. History of exposure can include bird handling, bird nests or roosts near the home, rat infestations, pets, and occupational exposure to laboratory rodents. The mite may be discovered in abandoned bird or rodent nests, on pets, or in pet bedding. Speciation of the mite usually requires assistance of an entomologist or acarologist. To facilitate microscopic identification of mites, specimens can be temporarily slide-mounted in a drop of mineral oil under a coverglass. However, if they are to be sent to an acarologist or other specialist for identification, it is best to place them in 70% alcohol, rather than mineral oil. It is very difficult to remove mineral oil from mite specimens before clearing and slide-mounting them in other appropriate mounting media. This may be required to discern fine structural details needed for making species determinations.

Cheyletiella mite dermatitis also may present as a nonspecific pruritic dermatitis. These mites are parasitic on dogs, cats, and rabbits and may be discovered on the pet as "walking dandruff."20

Bites from chiggers, or red bugs, may be distinguished from other mites by the location of bites at sites of clothing constriction, such as the waistline, sock line, and beneath undergarments. These bites typically appear as papules with hemorrhagic puncta.

The scabies mite burrows in the skin and thus can be distinguished from other mites that cause dermatitis. In addition, scabies may be distinguished clinically by lesions in the interdigital web spaces and on the genitals. The mite, its eggs, and its feces can be visualized by a routine scabies preparation during the patient visit.

Other arthropod bites, including those from fleas, human body lice, and pubic lice, should be included in the differential diagnosis of mite dermatitis. In addition, systemic pruritus with excoriations, drug hypersensitivity reaction, and neurodermatitis should be considered.

Treatment focuses on reducing or eliminating problem mites in infested areas, often requiring involvement of veterinarians and pest control agencies. In the case of D gallinae, which does not live on the host, acaricides must penetrate into crevices and cracks in buildings.21 Both the host and the area of infestation must be treated to exterminate O sylviarum and O bursa. Elimination of rats and removal of their nests are important for controlling O bacoti.22 Patients may be treated with antihistamines and topical corticosteroids for symptomatic relief. The dermatitis is self-limited when the exposure is eliminated.

Two important mite-borne diseases of humans are tsutsugamushi disease (scrub typhus) and rickettsialpox, caused by the rickettsial organisms Orienta tsutsugamushi and Rickettsia akari, respectively. In the case of tsutsugamushi disease, chiggers are the vectors, whereas in rickettsialpox, the vector is the house-mouse mite (Liponyssoides sanguineus). These are the only 2 groups of mites that play a significant role in transmission of human pathogens.23

Mite dermatitis should be considered in any unexplained dermatitis. When considering a diagnosis of mite dermatitis, it is important to determine if there is a history of exposure to mice, hamsters, other rodents, or birds. Although the mites are rarely found on the patient, they may be discovered around the home or on pets. Demonstrating the presence of mites is important in diagnosing cases of mite-induced dermatitis. In many cases, reliable identification of the mite species is important in not only confirming the diagnosis but also identifying the sources of mite infestations so that they can be eliminated. The diagnosis should not be overlooked simply because the patient denies having rats or birds in the home. 

Rat mite dermatitis is characterized by pruritic papules in a patient exposed to the tropical rat mite Ornithonyssus bacoti. We report a case of a woman with rat mite dermatitis who developed this eruption after exposure to her pet hamster. Mites were collected from the hamster and identified as O bacoti. Reported sources of rat mites, as well as avian mites and other mites that bite humans, are reviewed.

Rat mite dermatitis is a pruritic eruption in humans caused by bites from the tropical rat mite Ornithonyssus bacoti. Other biting mite species that have been reported to cause a similar dermatitis in humans include Dermanyssus gallinae (red mite or poultry mite), Ornithonyssus sylviarum (northern fowl mite), and Ornithonyssus bursa (tropical fowl mite).1-6 The eruptions caused by these mites are clinically indistinguishable. Initial case reports of mite dermatitis identified the sources of these mites to be rat-infested homes or bird nests around the home.1-6 Rat mite dermatitis also was reported in a patient who had contact with mite-infested laboratory mice.7 More recently, avian mite dermatitis was reported in patients who had mite-infested pet gerbils.8 This report describes a patient with rat mite dermatitis acquired from a pet hamster. Based on the variety of mites and sources of infestations, mite dermatitis may be more common than generally thought. back to top

CASE REPORT

A 48-year-old healthy woman presented with a complaint of pruritic papules on the wrists (Figure 1) and waist for several weeks. History revealed she maintained a small menagerie of animals including horses, dogs, cats, and hamsters. She was informed that her skin lesions were most likely the result of insect bites and she should evaluate her animals and their environment for evidence of infestation. She returned 2 days later and reported that her hamster had died the previous day. When she went to bury it, she noticed numerous red specks in its fur. She placed the hamster in a plastic bag in the freezer until she could bring it in for examination. Examination of the hamster (Figure 2) revealed numerous red mites (Figure 3). The patient's symptoms resolved over the following few weeks. The mites were identified as the tropical rat mite O bacoti. No necropsy was performed on the hamster, and a specific cause of death was never determined. This mite ingests blood and can cause debility, anemia, decreased reproduction, and death in small animals, suggesting that it may have contributed to the hamster's death.

Comment

Mites are arthropods in the class Arachnida, which includes ticks, spiders, and scorpions. The arachnids are characterized by 4 pairs of legs and 2 body regions, a cephalothorax and an abdomen. Mites and ticks are further classified in the subclass Acari. Mites of medical importance can be grouped by their pathology in humans.9 House dust mites (Dermatophagoides and Euroglyphus ssp) cause respiratory allergies, whereas human follicle mites (Demodex spp) infest hair follicles and associated sebaceous glands. Neither group of mites causes cutaneous lesions in the form of bites or burrows. The scabies mite (Sarcoptes scabiei) is a primary human parasitic mite in which the adult mite burrows and feeds on skin cells. Chiggers (family Trombiculidae) and common animal mites bite humans but do not reside on humans as a primary host. Many mite species are opportunistic, often feeding on various hosts they encounter.10 The common animal mites that bite humans include several avian mites, the rodent mites, and fur mites of rabbits (Cheyletiella parasitivorax), dogs (Cheyletiella yasguri), and cats (Cheyletiella blakei). Mites infesting grain, hay, and straw occasionally cause dermatitis in humans.

The usual hosts of the tropical rat mite O bacoti are the brown rat (Rattus norvegicus) and the black rat (Rattus rattus). This mite is yellow to dark red, when blood-fed, and ranges in size from 0.75 to 1.4 mm. It will feed on humans when its rodent hosts are killed or abandon their nests.11-16 O bacoti also infests mice and hamsters in research laboratories.7

The common avian mites D gallinae, O sylviarum, and O bursa occur on both domestic and wild bird species, including chickens, ducks, pigeons, sparrows, canaries, starlings, robins, tiger finches, and doves.1 D gallinae has been identified on commensal and laboratory rodents, and in one case it was found on a farm dog.17-19 The species are similar in size and appearance, but differ in their life cycle. The adult mite of these species ranges in color from brown to red and in size from 1 to 3 mm. D gallinae lives most of its life cycle off the hosts in nests, crevices, and cracks in buildings. It feeds on the host nocturnally for 1 to 2 hours at a time, and may live up to 8 months without a host. O sylviarum and O bursa spend their entire life cycle on the host. The mites will leave the host and bite humans in close proximity, especially in heavily infested quarters. The Ornithonyssus species live only 2 to 3 weeks without a host.9

Mite bites typically produce urticarial, pruritic papules on the skin. These papules result from an inflammatory cutaneous reaction to mite saliva as it takes a blood meal. Clinically, the bites are nonspecific, but pruritus is the most consistent feature. The lesions may be vesicular, urticarial, eczematous, or any combination of these. Secondary lesions such as persistent nodules, postinflammatory hyperpigmentation, excoriations, and secondary infection may be present. The bites tend to occur in asymmetric groups, most commonly on the abdomen and extremities. Often a patient presents with a combination of these clinical features, but denies a history of any "bites."

On pathologic examination, the lesions are nonspecific mild arthropod reactions with superficial and mid-dermal perivascular infiltrate. Eosinophils may be present. The epidermis may be mildly spongiotic.

The diagnosis of mite dermatitis should be considered in unexplained pruritic dermatitis. The rodent and avian mites are rarely found on the human host because the mites leave after feeding. History of exposure can include bird handling, bird nests or roosts near the home, rat infestations, pets, and occupational exposure to laboratory rodents. The mite may be discovered in abandoned bird or rodent nests, on pets, or in pet bedding. Speciation of the mite usually requires assistance of an entomologist or acarologist. To facilitate microscopic identification of mites, specimens can be temporarily slide-mounted in a drop of mineral oil under a coverglass. However, if they are to be sent to an acarologist or other specialist for identification, it is best to place them in 70% alcohol, rather than mineral oil. It is very difficult to remove mineral oil from mite specimens before clearing and slide-mounting them in other appropriate mounting media. This may be required to discern fine structural details needed for making species determinations.

Cheyletiella mite dermatitis also may present as a nonspecific pruritic dermatitis. These mites are parasitic on dogs, cats, and rabbits and may be discovered on the pet as "walking dandruff."20

Bites from chiggers, or red bugs, may be distinguished from other mites by the location of bites at sites of clothing constriction, such as the waistline, sock line, and beneath undergarments. These bites typically appear as papules with hemorrhagic puncta.

The scabies mite burrows in the skin and thus can be distinguished from other mites that cause dermatitis. In addition, scabies may be distinguished clinically by lesions in the interdigital web spaces and on the genitals. The mite, its eggs, and its feces can be visualized by a routine scabies preparation during the patient visit.

Other arthropod bites, including those from fleas, human body lice, and pubic lice, should be included in the differential diagnosis of mite dermatitis. In addition, systemic pruritus with excoriations, drug hypersensitivity reaction, and neurodermatitis should be considered.

Treatment focuses on reducing or eliminating problem mites in infested areas, often requiring involvement of veterinarians and pest control agencies. In the case of D gallinae, which does not live on the host, acaricides must penetrate into crevices and cracks in buildings.21 Both the host and the area of infestation must be treated to exterminate O sylviarum and O bursa. Elimination of rats and removal of their nests are important for controlling O bacoti.22 Patients may be treated with antihistamines and topical corticosteroids for symptomatic relief. The dermatitis is self-limited when the exposure is eliminated.

Two important mite-borne diseases of humans are tsutsugamushi disease (scrub typhus) and rickettsialpox, caused by the rickettsial organisms Orienta tsutsugamushi and Rickettsia akari, respectively. In the case of tsutsugamushi disease, chiggers are the vectors, whereas in rickettsialpox, the vector is the house-mouse mite (Liponyssoides sanguineus). These are the only 2 groups of mites that play a significant role in transmission of human pathogens.23

Mite dermatitis should be considered in any unexplained dermatitis. When considering a diagnosis of mite dermatitis, it is important to determine if there is a history of exposure to mice, hamsters, other rodents, or birds. Although the mites are rarely found on the patient, they may be discovered around the home or on pets. Demonstrating the presence of mites is important in diagnosing cases of mite-induced dermatitis. In many cases, reliable identification of the mite species is important in not only confirming the diagnosis but also identifying the sources of mite infestations so that they can be eliminated. The diagnosis should not be overlooked simply because the patient denies having rats or birds in the home.