Report
Red Sea Corai Contact Dermatitis Jonathan H. Addy, M.D.
Abstract: Six of nine adults who developed Red Sea coral contact dermatitis had seafood allergies. Contact with the "fire" coral was followed by a series of skin eruptions starting with an immediate pruritic urticaria-like lesion which forced the victims out of the water. Within minutes the affected area became erythematous and edematous with eventual blister formation approximately 6 hours after the initial contact. The blisters resolved, leaving violaceous papules and plaques in a streaky fashion corresponding to where the coral brushed the skin. The iesions became shiny and lichenoid in 3 weeks while pruritus persisted. Treatment with topical corticosteroids and oral antihistamines reduced the severity of the disease but did not stop its evolution to the lichenoid stage. Complete resolution usually occurred after 15 weeks, leaving residual hyperpigmented macules.
The earliest ofthe very few records found in the literature on dermatitis due to contact with corals is that of Levin and Behrman (1941).' Seville in 1957^ and Neuhanse (1966)^ described the clinical features of a skin disease they called Dogger Bank itch, and attributed the cause to contact with coral. Both authors concluded that Dogger Bank itch was an allergic dermatitis due to contact with live animals in the form of the coralline Alcyonidium hirsutum, found in the shallow waters of the North Sea. A similar disease in the Persian Gulf area was documented in 1950 by Preston,'' who described acute, painful lesions produced by contact with corals not specified or named. This article documents the results of an investigation conducted on several cases of contact dermatitis caused by corals in the shallow, warm waters of the eastern coastline of the Red Sea. Materials and Methods • The study was conducted on nine adult men and women who presented at the dermatoiogy clinic in a general hospital over a period of 2 years, suffering from From Korle Bu Teaching Hospital, University of Ghana Medical School, Accra, Ghana. Address correspondence to; Jonathan H. Addy, M.D., Korle Bu Teaching Hospital, University of Ghana Medical School, P.O. Box 4236, Accra, Ghana. April 1991, Vol. 30, No. 4
dermatitis which had started suddenly while they pursued their various hobbies in the Red Sea. Full clinical history and physical examination were done in all of them. Relevant laboratory investigations in all patients and histologic investigation of punch skin biopsies on three patients were also done.
Results The pertinent clinical data on the nine patients are shown in Table 1. Their ages ranged from 14 to 55 years with a mean of 35 years. There were six men and three women. There were no obvious racial or national predilections. What was common to all nine patients was that they all acquired their disease while pursuing recreational activities, which included snorkling, skin diving, coral collecting, swimming, or surfing in the Red Sea at Yanbu in Saudi Arabia. Four out of the nine patients gave history of seafood allergy. One of the four specified allergy to oysters. Ofthe two who had history of atopic eczema, one also had seafood allergy. There was remarkable uniformity in the physical signs and their evolution in all of the patients. Variation was limited to distribution of the skin lesions (see Table 1). The disease went through four stages, as follows: stage 1, acute urticaria; stage 2, acute vesiculo-bullous dermatitis (Fig. 1); stage 3, subacute fieshy granulomatous dermatitis; and stage 4, chronic lichenoid dermatitis (Fig. 2). Brief contact with the oflFending material (identified by the victims and local people as "fire" or yellow coral) while in the water was followed immediately by an intense itching and sometimes burning sensation, necessitating exit from the sea. Itching continued on leaving the water, and within 10 minutes the area involved becarne erythematous and edematous with an orange-peel texture. Blisters began to appear after a few hours followed by oozing and rupture ofthe larger blisters and bullae. The acute dermatitis stage remained for several days. Drying up produced crusts that were followed by pruritic, fleshy, red granulomatous lesions. The soft lesions gradually hardened, becoming smaller and shiny, assuming a lichenoid tex271
272
International Journal of Dermatology • April 1991
Figure 1. Coral contact dermatitis, acute stage.
ture that remained static and pruritic for several weeks despite topical corticosteroids. Healing was usually a slow process taking up to 15 weeks and accompanied by fine desquamation and flattening of the papules, leaving residual postinflammatory hyperpigmentation. Results of laboratory investigations showed no systemic features. Patch tests using animal material were not done. Histologic study of the acute stage showed spongiosis with microvesicles, intracellular edema of the epidermis, and edema of papillary dermis. Histologic study of the second stage showed all the above plus superficial mononuclear perivascular dermatitis with extravasation of red blood cells. In the epidermis there were blisters and bullae with exocytosis of mononuclear cells with more acanthosis. Histologic study of the chronic lichenoid stage showed acanthosis, parakeratosis, and an increased granular layer, in addition to a diffuse dense mononuclear cell infiltration in upper dermis and around dermal papillae.
Vol. 30
Figure 2. Coral contact dermatitis, chronic lichenoid stage.
Oral antihistamines relieved itching and burning sensations to tolerable states in the acute stages in all except two patients, who had widespread lesions, and needed systemic corticosteroids (oral prednisolone), 30 mg daily for the first 3 days. The acute urticarial and eczematous lesions responded satisfactorily to topical corticosteroid lotions and creams, which reduced the intensity ofthe inflammatory reaction. Despite daily application of corticosteroid with salicylic acid ointments, the chronic hchenoid lesion ran a prolonged course. Discussion The disease was first noted to occur in the shallow waters of the North Sea and was proven by patch tests to be an allergic dermatitis caused by animal tissue of the coralline Alcyonidium hirsutum.^-^ The coral collectors among the patients described in this paper pro-
Table 1. Patient Data
Patient
Age
No.
(yr)
Sex
1 2 3
14 20 35
4
Nationality
Sea Hobby
History ofAllergy
M M M
Saudi Saudi Jordanian
+vi Seafood +ve Oysters
25
F
White American
Skin diver Skin diver Coral reef collector Swimming
5 6 7
49 35 30
F M M
Swedish Filipino Filipino
8
54
F
9
55
M
Nil
Distribution of Lesion All over All over Wrists
+ve Atopic eczema
All over
Nil
Wrists Thighs Legs
German
Snorkling Snorkling Fishing with spear-gun Snorkling
British
Snorkling
+ve Hand eczema. and seafood allergy
+ve Seafood Nil
+ve Nickel allergy
Forearms and wrists Arms
No. 4
Red Sea Coral Contact Dermatitis • Addy
duced specimens of limestone skeletons that turned out to be inert and produced no dermatitis when used for patch testing. It is presumed that contact with the organism before it had had time to secrete an exoskeleton was the cause of the skin lesions. There are accounts in the literature that attribute the skin lesions to stings and subsequent retention of stinging parts, like silicon-tipped nematocytes, under the skin." No such evidence was found in the cases of this study. Yanbu is situated on the Red Sea coast, Saudi Arabia, in the desert belt. Large numbers of adults and children spend their entire weekends on the beaches of the Red Sea. The relatively small number of patients with coral contact dermatitis described in this paper implies that not all who come into contact with coral develop the dermatitis. By inference. Red Sea coral dermatitis is an allergic contact dermatitis—this was also the impression of the earlier workers who were able to prove it by patch testing. Red Sea coral dermatitis is a distressing disease
273
that, in the acute stages, rnimics sequentially acute urticaria and eczematous dermatitis. In the chronic stage it was indistinguishable clinically and histologically from lichen planus. Coral contact dermatitis may therefore be considered as one of the causes of lichenoid eruptions. The risk groups are those with seafood allergy and atopic eczema. It is suggested that patch tests using coralline animal material on those in the high-risk groups should be done before allowing them to venture into the waters of the seas around the Arabian peninsula.
References 1. Levin OL, Behrman HT. Corai dermatitis. Arch Dermatol Syphilis. I94I;44:6OO-6O2. 2. Seville RH. Dogger Bank itch; Report of a case. Br J Dermatol. 1957;69;92-95. 3. Newhouse ML. Dogger bank itch; Survey of trawlermen. Br Med J. 1966;l;l 142-1145. 4. Preston FS. Coral ulcer. Br Med J. 1950;! l;687-690.
Plaster model of a woman who died of Cushing's syndrome. The sculptor's name was Nobas and the date was 1880; the diagnosis is retrospective. From the Fundacio-Museu d'Historia de la Medicina (Barcelona). Submitted by Felipe Cid, M.D., Barcelona, Spain.
Red Sea Corai Contact Dermatitis Jonathan H. Addy, M.D.
Abstract: Six of nine adults who developed Red Sea coral contact dermatitis had seafood allergies. Contact with the "fire" coral was followed by a series of skin eruptions starting with an immediate pruritic urticaria-like lesion which forced the victims out of the water. Within minutes the affected area became erythematous and edematous with eventual blister formation approximately 6 hours after the initial contact. The blisters resolved, leaving violaceous papules and plaques in a streaky fashion corresponding to where the coral brushed the skin. The iesions became shiny and lichenoid in 3 weeks while pruritus persisted. Treatment with topical corticosteroids and oral antihistamines reduced the severity of the disease but did not stop its evolution to the lichenoid stage. Complete resolution usually occurred after 15 weeks, leaving residual hyperpigmented macules.
The earliest ofthe very few records found in the literature on dermatitis due to contact with corals is that of Levin and Behrman (1941).' Seville in 1957^ and Neuhanse (1966)^ described the clinical features of a skin disease they called Dogger Bank itch, and attributed the cause to contact with coral. Both authors concluded that Dogger Bank itch was an allergic dermatitis due to contact with live animals in the form of the coralline Alcyonidium hirsutum, found in the shallow waters of the North Sea. A similar disease in the Persian Gulf area was documented in 1950 by Preston,'' who described acute, painful lesions produced by contact with corals not specified or named. This article documents the results of an investigation conducted on several cases of contact dermatitis caused by corals in the shallow, warm waters of the eastern coastline of the Red Sea. Materials and Methods • The study was conducted on nine adult men and women who presented at the dermatoiogy clinic in a general hospital over a period of 2 years, suffering from From Korle Bu Teaching Hospital, University of Ghana Medical School, Accra, Ghana. Address correspondence to; Jonathan H. Addy, M.D., Korle Bu Teaching Hospital, University of Ghana Medical School, P.O. Box 4236, Accra, Ghana. April 1991, Vol. 30, No. 4
dermatitis which had started suddenly while they pursued their various hobbies in the Red Sea. Full clinical history and physical examination were done in all of them. Relevant laboratory investigations in all patients and histologic investigation of punch skin biopsies on three patients were also done.
Results The pertinent clinical data on the nine patients are shown in Table 1. Their ages ranged from 14 to 55 years with a mean of 35 years. There were six men and three women. There were no obvious racial or national predilections. What was common to all nine patients was that they all acquired their disease while pursuing recreational activities, which included snorkling, skin diving, coral collecting, swimming, or surfing in the Red Sea at Yanbu in Saudi Arabia. Four out of the nine patients gave history of seafood allergy. One of the four specified allergy to oysters. Ofthe two who had history of atopic eczema, one also had seafood allergy. There was remarkable uniformity in the physical signs and their evolution in all of the patients. Variation was limited to distribution of the skin lesions (see Table 1). The disease went through four stages, as follows: stage 1, acute urticaria; stage 2, acute vesiculo-bullous dermatitis (Fig. 1); stage 3, subacute fieshy granulomatous dermatitis; and stage 4, chronic lichenoid dermatitis (Fig. 2). Brief contact with the oflFending material (identified by the victims and local people as "fire" or yellow coral) while in the water was followed immediately by an intense itching and sometimes burning sensation, necessitating exit from the sea. Itching continued on leaving the water, and within 10 minutes the area involved becarne erythematous and edematous with an orange-peel texture. Blisters began to appear after a few hours followed by oozing and rupture ofthe larger blisters and bullae. The acute dermatitis stage remained for several days. Drying up produced crusts that were followed by pruritic, fleshy, red granulomatous lesions. The soft lesions gradually hardened, becoming smaller and shiny, assuming a lichenoid tex271
272
International Journal of Dermatology • April 1991
Figure 1. Coral contact dermatitis, acute stage.
ture that remained static and pruritic for several weeks despite topical corticosteroids. Healing was usually a slow process taking up to 15 weeks and accompanied by fine desquamation and flattening of the papules, leaving residual postinflammatory hyperpigmentation. Results of laboratory investigations showed no systemic features. Patch tests using animal material were not done. Histologic study of the acute stage showed spongiosis with microvesicles, intracellular edema of the epidermis, and edema of papillary dermis. Histologic study of the second stage showed all the above plus superficial mononuclear perivascular dermatitis with extravasation of red blood cells. In the epidermis there were blisters and bullae with exocytosis of mononuclear cells with more acanthosis. Histologic study of the chronic lichenoid stage showed acanthosis, parakeratosis, and an increased granular layer, in addition to a diffuse dense mononuclear cell infiltration in upper dermis and around dermal papillae.
Vol. 30
Figure 2. Coral contact dermatitis, chronic lichenoid stage.
Oral antihistamines relieved itching and burning sensations to tolerable states in the acute stages in all except two patients, who had widespread lesions, and needed systemic corticosteroids (oral prednisolone), 30 mg daily for the first 3 days. The acute urticarial and eczematous lesions responded satisfactorily to topical corticosteroid lotions and creams, which reduced the intensity ofthe inflammatory reaction. Despite daily application of corticosteroid with salicylic acid ointments, the chronic hchenoid lesion ran a prolonged course. Discussion The disease was first noted to occur in the shallow waters of the North Sea and was proven by patch tests to be an allergic dermatitis caused by animal tissue of the coralline Alcyonidium hirsutum.^-^ The coral collectors among the patients described in this paper pro-
Table 1. Patient Data
Patient
Age
No.
(yr)
Sex
1 2 3
14 20 35
4
Nationality
Sea Hobby
History ofAllergy
M M M
Saudi Saudi Jordanian
+vi Seafood +ve Oysters
25
F
White American
Skin diver Skin diver Coral reef collector Swimming
5 6 7
49 35 30
F M M
Swedish Filipino Filipino
8
54
F
9
55
M
Nil
Distribution of Lesion All over All over Wrists
+ve Atopic eczema
All over
Nil
Wrists Thighs Legs
German
Snorkling Snorkling Fishing with spear-gun Snorkling
British
Snorkling
+ve Hand eczema. and seafood allergy
+ve Seafood Nil
+ve Nickel allergy
Forearms and wrists Arms
No. 4
Red Sea Coral Contact Dermatitis • Addy
duced specimens of limestone skeletons that turned out to be inert and produced no dermatitis when used for patch testing. It is presumed that contact with the organism before it had had time to secrete an exoskeleton was the cause of the skin lesions. There are accounts in the literature that attribute the skin lesions to stings and subsequent retention of stinging parts, like silicon-tipped nematocytes, under the skin." No such evidence was found in the cases of this study. Yanbu is situated on the Red Sea coast, Saudi Arabia, in the desert belt. Large numbers of adults and children spend their entire weekends on the beaches of the Red Sea. The relatively small number of patients with coral contact dermatitis described in this paper implies that not all who come into contact with coral develop the dermatitis. By inference. Red Sea coral dermatitis is an allergic contact dermatitis—this was also the impression of the earlier workers who were able to prove it by patch testing. Red Sea coral dermatitis is a distressing disease
273
that, in the acute stages, rnimics sequentially acute urticaria and eczematous dermatitis. In the chronic stage it was indistinguishable clinically and histologically from lichen planus. Coral contact dermatitis may therefore be considered as one of the causes of lichenoid eruptions. The risk groups are those with seafood allergy and atopic eczema. It is suggested that patch tests using coralline animal material on those in the high-risk groups should be done before allowing them to venture into the waters of the seas around the Arabian peninsula.
References 1. Levin OL, Behrman HT. Corai dermatitis. Arch Dermatol Syphilis. I94I;44:6OO-6O2. 2. Seville RH. Dogger Bank itch; Report of a case. Br J Dermatol. 1957;69;92-95. 3. Newhouse ML. Dogger bank itch; Survey of trawlermen. Br Med J. 1966;l;l 142-1145. 4. Preston FS. Coral ulcer. Br Med J. 1950;! l;687-690.
Plaster model of a woman who died of Cushing's syndrome. The sculptor's name was Nobas and the date was 1880; the diagnosis is retrospective. From the Fundacio-Museu d'Historia de la Medicina (Barcelona). Submitted by Felipe Cid, M.D., Barcelona, Spain.
