Transcriptome profiling reveals Th2 bias and identifies endogenous itch mediators in poison ivy contact dermatitis.

In the United States, poison ivy exposure is the most common naturally occurring allergen to cause allergic contact dermatitis (ACD). The immune and pruritic mechanisms associated with poison ivy ACD remain largely unexplored. Here, we compared skin whole transcriptomes and itch mediator levels in mouse ACD models induced by the poison ivy allergen, urushiol, and the synthetic allergen, oxazolone. The urushiol model produced a Th2-biased immune response and scratching behavior, resembling findings in poison ivy patients. Urushiol-challenged skin contained elevated levels of the cytokine thymic stromal lymphopoietin (TSLP), a T-cell regulator and itch mediator, and pruritogenic serotonin (5-HT) and endothelin (ET-1), but not substance P (SP) or histamine. The oxazolone model generated a mixed Th1/Th2 response associated with increased levels of substance P, 5-HT, ET-1, but not TSLP or histamine. Injections of a TSLP monoclonal neutralizing antibody, serotonergic or endothelin inhibitors, but not SP inhibitors or antihistamines, reduced scratching behaviors in urushiol-challenged mice. Our findings suggest that the mouse urushiol model may serve as a translational model of human poison ivy ACD study. Inhibiting signaling by TSLP and other cytokines may represent alternatives to the standard steroid/antihistamine regimen for steroid-resistant or -intolerant patients and in exaggerated systemic responses to poison ivy.

Dermoscopy of black-spot poison ivy.

Black-spot poison ivy is an uncommon presentation of poison ivy (Toxicodendron) allergic contact dermatitis. A 78-year-old sought evaluation of a black spot present on her right hand amid pruritic vesicles. The presentation of a black spot on the skin in a clinical context suggesting poison ivy is indicative of black-spot poison ivy. Dermoscopy revealed a jagged, centrally homogeneous, dark brown lesion with a red rim. A skin sample was obtained and compared against a poison ivy standard using ultra-fast liquid chromatography-tandem mass spectrometry (UFLC-MS/MS). This finding confirmed the presence of multiple urushiol congeners in the skin sample. Black-spot poison ivy may be added to the list of diagnoses that show a specific dermoscopic pattern.

Milia after allergic contact dermatitis from poison ivy: two cases.

Milia have rarely been reported as a complication of severe allergic contact dermatitis. To our knowledge, milia have not previously been associated with poison ivy dermatitis. We present two cases of milia after allergic contact dermatitis to poison ivy.

Poison ivy: an underreported cause of erythema multiforme.

The relationship between herpes simplex virus (HSV) and erythema multiforme (EM) has been well described. Many authors contend that EM (excluding Stevens-Johnson syndrome and toxic epidermal necrolysis) occurs almost exclusively as a response to HSV infection. During the past year, however, we have observed several cases of EM complicating severe Rhus allergic contact dermatitis. Although this association has been previously documented, the paucity of cases in the literature, along with our experience, suggests that this is an underreported phenomenon. We describe 4 of our cases.

Secondary bacterial infections complicating skin lesions.

Secondary bacterial infection in skin lesions is a common problem. This review summarises a series of studies of the microbiology of several of these infections: scabies, psoriasis, poison ivy, atopic dermatitis, eczema herpeticum and kerion. Staphylococcus aureus and group A beta-haemolytic streptococci were the most prevalent aerobes and were isolated from all body sites. In contrast, organisms that reside in the mucous membranes close to the lesions predominated in infections next to these membranes. In this fashion, enteric gram-negative bacilli and Bacteroides spp. were found most often in buttock and leg lesions. The probable sources of these organisms are the rectum and vagina, where they normally reside. Group A beta-haemolytic streptococci, pigmented Prevotella and Porphyromonas spp. and Fusobacterium spp. were most commonly found in lesions of the head, face, neck and fingers. These organisms probably reached these sites from the oral cavity, where they are part of the normal flora. This review highlights the polymicrobial aerobic-anaerobic microbiology of secondarily infected skin lesions.

Erythema multiforme associated with Rhus contact dermatitis.

A case of erythema multiforme and Rhus contact dermatitis is presented herein. Due to the association of nephritis and other complications with Rhus poison oak, we recommend that patients with contact dermatitis due to poison ivy who incur secondary erythema multiforme be hospitalized and closely monitored.

Microhyphema.

A case of microscopic hemorrhage into the anterior chamber is described. Slit-lamp examination disclosed a steady fine stream of blood issuing from a tiny grayish bulblike microhemangioma at the pupillary border. Fluorescein biomicroscopy revealed several similar microhemangiomas on the borders of each pupil. It is presumed that minor ocular irritation, due either to poison ivy or to a menthol (0.70%) cream which the patient applied to her face, precipitated the microhyphema.

Renal lesions accompanying poison oak dermatitis.

Renal damage associated with poison oak dermatitis is extremely rare in humans after exposure to urushiol antigen. Three renal lesions have been described: proliferative glomerulonephritis, arteritis, and membranous nephropathy. The present study reports on three patients who developed nephropathy after exposure to poison oak. One patient was studied by renal biopsy (including electron microscopy and immunofluorescence techniques) and another by autopsy findings. One of these patients had a typical membranous nephropathy, the other, proliferative glomerulonephritis with necrotizing arteritis and glomerulitis. In the patient with membranous nephropathy antibody to urushiol was discovered by passive cutaneous anaphylaxis in the guinea pig.