Cutis

Eccrine angiomatous hamartoma (EAH) is a benign and uncommon malformation, characterized by increased numbers of eccrine (sweat) glands and numerous capillary channels. It is usually congenital or arises during the prepubertal years; the lesion only rarely presents during adulthood. The color of EAH may be flesh colored, blue-brown, or reddish and may occur as a nodule, plaque, or, less commonly, a macule. In most cases, EAH arises as a single lesion on the extremity, though reports of multiple lesions and those occurring in more unusual sites exist. The symptoms most commonly associated with EAH are pain and hyperhidrosis; enlargement may occur and is usually in concordance with the growth of the patient. It is important to recognize the hamartoma as a benign clinical entity, for which aggressive management is not necessary. In this article, we report a case of EAH occurring in a young girl, and we review 41 well-documented cases in the literature. 

CASE REPORT

A 12-year-old previously healthy Hispanic girl presented with a lesion on the posterior aspect of her left lower leg. She reported that the lesion had been present since approximately 4 years of age. The patient denied spontaneous pain but described increased perspiration associated with the lesion, including occasions when she noted wet spots on her clothing overlying the area. Findings from the physical examination revealed a 6x5-cm, flesh-colored, palpable tumor in the left calf. Secretion of a clear fluid could be seen originating from the surface of the tumor, and hypertrichosis was present (Figures 1 and 2). A 4-mm punch biopsy of the mass was performed, and results confirmed the diagnosis of EAH (Figure 3). Results of histopathologic examination revealed an unremarkable epidermis. An increased number of sweat glands and terminal hair follicles were found in the dermis, and dilated sweat ducts were noted in the papillary dermis. In addition, large dilated blood vessels were seen in the deep dermis and subcutaneous tissue. Intercellular mucin also was present in the dermal stroma. The constellation of clinical and pathologic features was consistent with the diagnosis of EAH.

The patient declined further diagnostic radiographic evaluation and surgical treatment. She was treated symptomatically for the hypertrichosis and hyperhidrosis, using 13.9% eflornithine cream and topical aluminum chloride, respectively.

Comment

EAH is a rare, benign cutaneous hamartoma consisting of a proliferation of both eccrine glands and thin-walled vascular channels. First described by Lotzbeck in 18591 as an angiomatous-appearing lesion on the cheek of a child, the term EAH was coined by Hyman and coworkers2 in 1968. Since hyperhidrosis is a relatively common finding associated with this condition, various other terms have been used to describe this entity, including sudoriparous angioma3 and functioning sudoriparous angiomatous hamartoma.4 In addition to presenting an additional case of EAH, we review the other 41 cases of EAH reported in the literature (Table 1).

Typically, EAH presents as a solitary, flesh-colored, blue-brown, or reddish papule, plaque, or nodule. However, unusual morphologic variants exist and include hyperkeratotic5 and verrucous6 lesions. There appears to be no gender predilection, and the male-female ratio in the data analyzed was 1:1.1. EAH usually occurs as a solitary lesion, but cases with multiple lesions have been reported and account for approximately 26% of all cases in the literature.3,7-13 The hamartoma often appears at birth2,3,6,9,10,13-22,25 or during early childhood,7,8,16,22-24 as in the present case. In the cases reviewed that were not congenital, the mean age at the time of diagnosis was approximately 21 years, and the range was between 2 months and 73 years. EAH occurs most frequently on the acral areas and, in our review, approximately 74% of all reported lesions were limited to the extremities. However, lesions also have been reported in the sacral region,26 on the buttocks,5,19 face,9 chest,8,13,15,24 or diffusely over multiple anatomic sites.12 EAH is usually asymptomatic, but the most commonly associated symptoms are pain and hyperhidrosis reported in approximately 42% and 32% of all cases analyzed, respectively, including the present case. Approximately 17% of patients with EAH reported both pain and hyperhidrosis (sweating) simultaneously (Table 2). It is postulated that infiltration of small nerves may be responsible for the pain,27,28 and a local increase in the temperature within the angioma may produce the sweating seen in the eccrine component of the hamartoma.3,8,16,27

The diagnosis of EAH is confirmed by histology because the clinical features of the lesion are nonspecific and variable. Histologically, EAH is characterized by a dermal proliferation of well-differentiated eccrine secretory and ductal elements closely associated with thin-walled angiomatous channels. In addition to these defining elements, unusual histopathologic variants have been reported and include the infiltration of adipose tissue,11,16,29 the presence of pilar structures,6,9,11,21 apocrine glands,8 and, as in our case, increased dermal mucin.11 The epidermis typically is unremarkable but may exhibit hyperkeratosis, acanthosis, and papillomatosis.5,6 Immunohistochemical analyses using carcinoembryonic antigen and S-100 have demonstrated no difference between normal eccrine glands and those found in the hamartoma.8,10,16 In addition, ulex europaeus, CD34, CD44, and factor VIII–related antigens are expressed by the endothelial cells within the vascular component of the lesion.8,15,16 These findings help support a hamartomatous rather than tumoral origin for EAH. In addition, cytologic atypia and mitotic figures have not been reported.9,29

Imaging modalities, such as magnetic resonance imaging and ultrasound, are beginning to be used in the evaluation of EAH. One group of investigators reports that ultrasonography of a biopsy-proven EAH revealed varicose veins in cutaneous and subcutaneous layers but could not determine the size or shape of the lesion.30 Now, radiographic imaging may help confirm the clinical suspicion of an angiomatous lesion, but accurate diagnosis of EAH remains with histology.

The etiology of EAH has not been delineated clearly. Zeller and Goldman6 report that the hamartoma may be caused by abnormal induction of heterotypic dependency during organogenesis. According to this model, altered chemical interactions between the differentiating epithelium and mesenchyme result in the hamartomatous growth of these elements, generating an abnormal proliferation of vascular and eccrine structures.

The differential diagnosis of EAH includes eccrine nevus,32 a rare lesion composed of mature eccrine glands capable of producing localized hyperhidrosis. In addition, localized hyperhidrosis may be seen in a variety of other conditions, including neuritis, myelitis, syringomyelia, general paresis, and tabes dorsalis.32 However, these conditions do not produce cutaneous lesions or histologic abnormalities of eccrine glands. Localized hyperhidrosis also may accompany the blue rubber-bleb nevus syndrome, but histology may distinguish EAH from this disorder. Likewise, EAH clinically may resemble tufted angioma, macular telangiectatic mastocytosis, nevus flammeus, glomus tumor, and smooth muscle hamartoma.9,22,25 These conditions are readily differentiated by histologic analysis.

EAH is a benign and typically slow-growing lesion, though a rapid increase in size was noted in one pregnant woman, indicating that it may be under hormonal influence.31 In this case, partial amputation of the involved finger was necessary to relieve the patient's intractable pain. In general, however, aggressive treatment of EAH is unwarranted. Simple excision usually is curative and reserved for painful or cosmetically unacceptable lesions. One study reports no evidence of recurrent disease 15 months after excision.17 Indeed, the pain associated with EAH may remit spontaneously without treatment, even after several years.28 

Eccrine angiomatous hamartoma (EAH) is a benign and uncommon malformation, characterized by increased numbers of eccrine (sweat) glands and numerous capillary channels. It is usually congenital or arises during the prepubertal years; the lesion only rarely presents during adulthood. The color of EAH may be flesh colored, blue-brown, or reddish and may occur as a nodule, plaque, or, less commonly, a macule. In most cases, EAH arises as a single lesion on the extremity, though reports of multiple lesions and those occurring in more unusual sites exist. The symptoms most commonly associated with EAH are pain and hyperhidrosis; enlargement may occur and is usually in concordance with the growth of the patient. It is important to recognize the hamartoma as a benign clinical entity, for which aggressive management is not necessary. In this article, we report a case of EAH occurring in a young girl, and we review 41 well-documented cases in the literature. 

CASE REPORT

A 12-year-old previously healthy Hispanic girl presented with a lesion on the posterior aspect of her left lower leg. She reported that the lesion had been present since approximately 4 years of age. The patient denied spontaneous pain but described increased perspiration associated with the lesion, including occasions when she noted wet spots on her clothing overlying the area. Findings from the physical examination revealed a 6x5-cm, flesh-colored, palpable tumor in the left calf. Secretion of a clear fluid could be seen originating from the surface of the tumor, and hypertrichosis was present (Figures 1 and 2). A 4-mm punch biopsy of the mass was performed, and results confirmed the diagnosis of EAH (Figure 3). Results of histopathologic examination revealed an unremarkable epidermis. An increased number of sweat glands and terminal hair follicles were found in the dermis, and dilated sweat ducts were noted in the papillary dermis. In addition, large dilated blood vessels were seen in the deep dermis and subcutaneous tissue. Intercellular mucin also was present in the dermal stroma. The constellation of clinical and pathologic features was consistent with the diagnosis of EAH.

The patient declined further diagnostic radiographic evaluation and surgical treatment. She was treated symptomatically for the hypertrichosis and hyperhidrosis, using 13.9% eflornithine cream and topical aluminum chloride, respectively.

Comment

EAH is a rare, benign cutaneous hamartoma consisting of a proliferation of both eccrine glands and thin-walled vascular channels. First described by Lotzbeck in 18591 as an angiomatous-appearing lesion on the cheek of a child, the term EAH was coined by Hyman and coworkers2 in 1968. Since hyperhidrosis is a relatively common finding associated with this condition, various other terms have been used to describe this entity, including sudoriparous angioma3 and functioning sudoriparous angiomatous hamartoma.4 In addition to presenting an additional case of EAH, we review the other 41 cases of EAH reported in the literature (Table 1).

Typically, EAH presents as a solitary, flesh-colored, blue-brown, or reddish papule, plaque, or nodule. However, unusual morphologic variants exist and include hyperkeratotic5 and verrucous6 lesions. There appears to be no gender predilection, and the male-female ratio in the data analyzed was 1:1.1. EAH usually occurs as a solitary lesion, but cases with multiple lesions have been reported and account for approximately 26% of all cases in the literature.3,7-13 The hamartoma often appears at birth2,3,6,9,10,13-22,25 or during early childhood,7,8,16,22-24 as in the present case. In the cases reviewed that were not congenital, the mean age at the time of diagnosis was approximately 21 years, and the range was between 2 months and 73 years. EAH occurs most frequently on the acral areas and, in our review, approximately 74% of all reported lesions were limited to the extremities. However, lesions also have been reported in the sacral region,26 on the buttocks,5,19 face,9 chest,8,13,15,24 or diffusely over multiple anatomic sites.12 EAH is usually asymptomatic, but the most commonly associated symptoms are pain and hyperhidrosis reported in approximately 42% and 32% of all cases analyzed, respectively, including the present case. Approximately 17% of patients with EAH reported both pain and hyperhidrosis (sweating) simultaneously (Table 2). It is postulated that infiltration of small nerves may be responsible for the pain,27,28 and a local increase in the temperature within the angioma may produce the sweating seen in the eccrine component of the hamartoma.3,8,16,27

The diagnosis of EAH is confirmed by histology because the clinical features of the lesion are nonspecific and variable. Histologically, EAH is characterized by a dermal proliferation of well-differentiated eccrine secretory and ductal elements closely associated with thin-walled angiomatous channels. In addition to these defining elements, unusual histopathologic variants have been reported and include the infiltration of adipose tissue,11,16,29 the presence of pilar structures,6,9,11,21 apocrine glands,8 and, as in our case, increased dermal mucin.11 The epidermis typically is unremarkable but may exhibit hyperkeratosis, acanthosis, and papillomatosis.5,6 Immunohistochemical analyses using carcinoembryonic antigen and S-100 have demonstrated no difference between normal eccrine glands and those found in the hamartoma.8,10,16 In addition, ulex europaeus, CD34, CD44, and factor VIII–related antigens are expressed by the endothelial cells within the vascular component of the lesion.8,15,16 These findings help support a hamartomatous rather than tumoral origin for EAH. In addition, cytologic atypia and mitotic figures have not been reported.9,29

Imaging modalities, such as magnetic resonance imaging and ultrasound, are beginning to be used in the evaluation of EAH. One group of investigators reports that ultrasonography of a biopsy-proven EAH revealed varicose veins in cutaneous and subcutaneous layers but could not determine the size or shape of the lesion.30 Now, radiographic imaging may help confirm the clinical suspicion of an angiomatous lesion, but accurate diagnosis of EAH remains with histology.

The etiology of EAH has not been delineated clearly. Zeller and Goldman6 report that the hamartoma may be caused by abnormal induction of heterotypic dependency during organogenesis. According to this model, altered chemical interactions between the differentiating epithelium and mesenchyme result in the hamartomatous growth of these elements, generating an abnormal proliferation of vascular and eccrine structures.

The differential diagnosis of EAH includes eccrine nevus,32 a rare lesion composed of mature eccrine glands capable of producing localized hyperhidrosis. In addition, localized hyperhidrosis may be seen in a variety of other conditions, including neuritis, myelitis, syringomyelia, general paresis, and tabes dorsalis.32 However, these conditions do not produce cutaneous lesions or histologic abnormalities of eccrine glands. Localized hyperhidrosis also may accompany the blue rubber-bleb nevus syndrome, but histology may distinguish EAH from this disorder. Likewise, EAH clinically may resemble tufted angioma, macular telangiectatic mastocytosis, nevus flammeus, glomus tumor, and smooth muscle hamartoma.9,22,25 These conditions are readily differentiated by histologic analysis.

EAH is a benign and typically slow-growing lesion, though a rapid increase in size was noted in one pregnant woman, indicating that it may be under hormonal influence.31 In this case, partial amputation of the involved finger was necessary to relieve the patient's intractable pain. In general, however, aggressive treatment of EAH is unwarranted. Simple excision usually is curative and reserved for painful or cosmetically unacceptable lesions. One study reports no evidence of recurrent disease 15 months after excision.17 Indeed, the pain associated with EAH may remit spontaneously without treatment, even after several years.28 

Eccrine angiomatous hamartoma (EAH) is a benign and uncommon malformation, characterized by increased numbers of eccrine (sweat) glands and numerous capillary channels. It is usually congenital or arises during the prepubertal years; the lesion only rarely presents during adulthood. The color of EAH may be flesh colored, blue-brown, or reddish and may occur as a nodule, plaque, or, less commonly, a macule. In most cases, EAH arises as a single lesion on the extremity, though reports of multiple lesions and those occurring in more unusual sites exist. The symptoms most commonly associated with EAH are pain and hyperhidrosis; enlargement may occur and is usually in concordance with the growth of the patient. It is important to recognize the hamartoma as a benign clinical entity, for which aggressive management is not necessary. In this article, we report a case of EAH occurring in a young girl, and we review 41 well-documented cases in the literature. 

CASE REPORT

A 12-year-old previously healthy Hispanic girl presented with a lesion on the posterior aspect of her left lower leg. She reported that the lesion had been present since approximately 4 years of age. The patient denied spontaneous pain but described increased perspiration associated with the lesion, including occasions when she noted wet spots on her clothing overlying the area. Findings from the physical examination revealed a 6x5-cm, flesh-colored, palpable tumor in the left calf. Secretion of a clear fluid could be seen originating from the surface of the tumor, and hypertrichosis was present (Figures 1 and 2). A 4-mm punch biopsy of the mass was performed, and results confirmed the diagnosis of EAH (Figure 3). Results of histopathologic examination revealed an unremarkable epidermis. An increased number of sweat glands and terminal hair follicles were found in the dermis, and dilated sweat ducts were noted in the papillary dermis. In addition, large dilated blood vessels were seen in the deep dermis and subcutaneous tissue. Intercellular mucin also was present in the dermal stroma. The constellation of clinical and pathologic features was consistent with the diagnosis of EAH.

The patient declined further diagnostic radiographic evaluation and surgical treatment. She was treated symptomatically for the hypertrichosis and hyperhidrosis, using 13.9% eflornithine cream and topical aluminum chloride, respectively.

Comment

EAH is a rare, benign cutaneous hamartoma consisting of a proliferation of both eccrine glands and thin-walled vascular channels. First described by Lotzbeck in 18591 as an angiomatous-appearing lesion on the cheek of a child, the term EAH was coined by Hyman and coworkers2 in 1968. Since hyperhidrosis is a relatively common finding associated with this condition, various other terms have been used to describe this entity, including sudoriparous angioma3 and functioning sudoriparous angiomatous hamartoma.4 In addition to presenting an additional case of EAH, we review the other 41 cases of EAH reported in the literature (Table 1).

Typically, EAH presents as a solitary, flesh-colored, blue-brown, or reddish papule, plaque, or nodule. However, unusual morphologic variants exist and include hyperkeratotic5 and verrucous6 lesions. There appears to be no gender predilection, and the male-female ratio in the data analyzed was 1:1.1. EAH usually occurs as a solitary lesion, but cases with multiple lesions have been reported and account for approximately 26% of all cases in the literature.3,7-13 The hamartoma often appears at birth2,3,6,9,10,13-22,25 or during early childhood,7,8,16,22-24 as in the present case. In the cases reviewed that were not congenital, the mean age at the time of diagnosis was approximately 21 years, and the range was between 2 months and 73 years. EAH occurs most frequently on the acral areas and, in our review, approximately 74% of all reported lesions were limited to the extremities. However, lesions also have been reported in the sacral region,26 on the buttocks,5,19 face,9 chest,8,13,15,24 or diffusely over multiple anatomic sites.12 EAH is usually asymptomatic, but the most commonly associated symptoms are pain and hyperhidrosis reported in approximately 42% and 32% of all cases analyzed, respectively, including the present case. Approximately 17% of patients with EAH reported both pain and hyperhidrosis (sweating) simultaneously (Table 2). It is postulated that infiltration of small nerves may be responsible for the pain,27,28 and a local increase in the temperature within the angioma may produce the sweating seen in the eccrine component of the hamartoma.3,8,16,27

The diagnosis of EAH is confirmed by histology because the clinical features of the lesion are nonspecific and variable. Histologically, EAH is characterized by a dermal proliferation of well-differentiated eccrine secretory and ductal elements closely associated with thin-walled angiomatous channels. In addition to these defining elements, unusual histopathologic variants have been reported and include the infiltration of adipose tissue,11,16,29 the presence of pilar structures,6,9,11,21 apocrine glands,8 and, as in our case, increased dermal mucin.11 The epidermis typically is unremarkable but may exhibit hyperkeratosis, acanthosis, and papillomatosis.5,6 Immunohistochemical analyses using carcinoembryonic antigen and S-100 have demonstrated no difference between normal eccrine glands and those found in the hamartoma.8,10,16 In addition, ulex europaeus, CD34, CD44, and factor VIII–related antigens are expressed by the endothelial cells within the vascular component of the lesion.8,15,16 These findings help support a hamartomatous rather than tumoral origin for EAH. In addition, cytologic atypia and mitotic figures have not been reported.9,29

Imaging modalities, such as magnetic resonance imaging and ultrasound, are beginning to be used in the evaluation of EAH. One group of investigators reports that ultrasonography of a biopsy-proven EAH revealed varicose veins in cutaneous and subcutaneous layers but could not determine the size or shape of the lesion.30 Now, radiographic imaging may help confirm the clinical suspicion of an angiomatous lesion, but accurate diagnosis of EAH remains with histology.

The etiology of EAH has not been delineated clearly. Zeller and Goldman6 report that the hamartoma may be caused by abnormal induction of heterotypic dependency during organogenesis. According to this model, altered chemical interactions between the differentiating epithelium and mesenchyme result in the hamartomatous growth of these elements, generating an abnormal proliferation of vascular and eccrine structures.

The differential diagnosis of EAH includes eccrine nevus,32 a rare lesion composed of mature eccrine glands capable of producing localized hyperhidrosis. In addition, localized hyperhidrosis may be seen in a variety of other conditions, including neuritis, myelitis, syringomyelia, general paresis, and tabes dorsalis.32 However, these conditions do not produce cutaneous lesions or histologic abnormalities of eccrine glands. Localized hyperhidrosis also may accompany the blue rubber-bleb nevus syndrome, but histology may distinguish EAH from this disorder. Likewise, EAH clinically may resemble tufted angioma, macular telangiectatic mastocytosis, nevus flammeus, glomus tumor, and smooth muscle hamartoma.9,22,25 These conditions are readily differentiated by histologic analysis.

EAH is a benign and typically slow-growing lesion, though a rapid increase in size was noted in one pregnant woman, indicating that it may be under hormonal influence.31 In this case, partial amputation of the involved finger was necessary to relieve the patient's intractable pain. In general, however, aggressive treatment of EAH is unwarranted. Simple excision usually is curative and reserved for painful or cosmetically unacceptable lesions. One study reports no evidence of recurrent disease 15 months after excision.17 Indeed, the pain associated with EAH may remit spontaneously without treatment, even after several years.28 

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.