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PubMedDate not supplied

Identification and treatment of poison ivy dermatitis.

Poison ivy dermatitis is an acute self-limiting problem of two or three weeks' duration that can cause significant discomfort. Poison ivy, poison oak and poison sumac cause more cases of allergic contact dermatitis than all the other contact allergens combined. Treatment of poison ivy dermatitis depends on the severity of the reaction. The nurse practitioner can manage the majority of poison ivy cases. However, if there is systemic involvement, a physician consultation is necessary. The patient can best be assisted by assessing the severity of the dermatitis, prescribing an appropriate supportive therapy and teaching preventive measures.

Adolescent↗
PubMed2000

Cost-effective post-exposure prevention of poison ivy dermatitis.

BACKGROUND: Poison ivy (toxicodendron) dermatitis is the most common allergic contact dermatitis in the USA. No studies have shown an effect of washing after a short period of time for the prevention of binding of urushiol to the skin. Objective To evaluate the efficacy of three different modes of postcontact prevention using a surfactant (Dial ultra dishwashing soap), an oil-removing compound (Goop), and chemical inactivation (a commercial product Tecnu). METHODS: A consented, unsponsored, volunteer experimental study on medical students from the University of Missouri School of Medicine, Kansas City. Each subject served as his/her own control, comparing four 2.5-cm exposed squares on the inner aspect of the forearm, three of which were treated and one untreated. RESULTS: Comparisons between the different agents were nonsignificant with P > 0.05. Each treatment, however, was significantly improved over the untreated control. CONCLUSIONS: Our study showed 70%, 61.8%, and 56. 4% protection with Tecnu, Goop, and Dial, respectively, when compared to the positive control, or to the possible maximum response, with a cost per ounce (in a local drug and automotive store) of $1.25, $0.07, and $0.07, respectively, for a decrease in protection that is nonsignificant.

Adult↗
PubMed1990

Poison ivy dermatitis.

Eruptions caused by poison ivy and related plants are almost always a form of allergic contact dermatitis. Usually they can be readily recognized because of their characteristic streak-or-line-like appearance. They usually clear within one to three weeks unless there is continued exposure to the allergen. Local treatment suffices in mild to moderate cases, but in more severe cases systemic corticosteroids can be added.

Adrenal Cortex Hormones↗
PubMed1986

Poison ivy dermatitis.

Eruptions caused by poison ivy (see Cover) and related plants are almost always a form of allergic contact dermatitis. Usually they can be readily recognized because of their characteristic streak- or line-like appearance. They usually clear within one to three weeks unless there is continued exposure to the allergen. Local treatment suffices in mild to moderate cases, but in more severe cases systemic corticosteroids can be added.

Acute Disease↗
PubMed1994

Poison ivy dermatitis. Nuances in treatment.

Acute allergic contact dermatitis due to poison ivy or poison oak is a common presenting complaint in the practices of many primary care physicians. While the clinical features are well described, reported treatment regimens vary in both topical and systemic therapies. We review herein the variability of presenting morphologic features of the disease and common treatment regimens, with attention given to complications of therapy. We also comment on the correct botanical designation, incidence, and immune mechanisms of the disease state and review measures to avoid allergic contact dermatitis due to poison ivy and poison oak.

Adrenal Cortex Hormones↗
PubMed2000

Microbiology of infected poison ivy dermatitis.

We report the aerobic and anaerobic microbiology of secondarily infected poison ivy dermatitis. The study involved retrospective review of clinical and microbiology laboratory records of patients with secondarily infected poison ivy lesions. Bacterial growth was noted in 33 specimens. Aerobic or facultative anaerobic bacteria only were present in 18 (55%) patients, anaerobic bacteria only in seven (21%), and mixed anaerobic-aerobic bacteria in eight (24%). Forty-five isolates were recovered (1.4 per specimen): 27 aerobic or facultative anaerobic bacteria, and 18 strict anaerobes. The predominant aerobic and facultative anaerobic bacteria were Staphylococcus aureus (13 isolates) and group A beta-haemolytic streptococci (six). The predominant anaerobes were Peptostreptococcus spp. (seven isolates), pigmented Prevotella and Porphyromonas spp. (four) and Fusobacterium spp. (two). Single bacterial isolates were recovered in 18 (55%) patients, eight of which were S. aureus. Nineteen of the organisms isolated from 16 (48%) patients produced the enzyme beta-lactamase. Organisms that resided in the mucous membranes close to the lesions predominated in those infections. Enteric gram-negative rods and Bacteroides fragilis group predominated in leg and buttock lesions. Group A beta-haemolytic streptococci, pigmented Prevotella and Porphyromonas and Fusobacterium spp. were most frequently recovered from lesions of the finger, face and neck. The polymicrobial aetiology of secondarily infected poison ivy lesions, and the association of bacterial flora with the anatomical site of the lesions, are demonstrated.

Bacterial Infections↗
PubMed1984

Black-spot poison ivy dermatitis. An acute irritant contact dermatitis superimposed upon an allergic contact dermatitis.

A black spot in the epidermis over a blister of poison ivy dermatitis is an uncommon finding. Four patients with the phenomenon are described. Histologic and histochemical studies were made on biopsy material and the blackish deposit on the skin surface was compared with black deposits in and on leaves of the species of poison ivy. This examination revealed a yellow, amorphous substance on the stratum corneum of the lesions and a similar substance in and on leaves of the poison ivy plant, Toxicodendron radicans ssp. negundo. Associated with the pigmentary deposits there were distinct changes of acute irritant contact dermatitis superimposed upon allergic contact dermatitis. Our findings support the view that the black material is the oleoresin of the plant, and that this substance behaves both as an irritant and an allergen.

Adolescent↗
PubMed2001

Treatment of toxicodendron dermatitis (poison ivy and poison oak).

Toxicodendron dermatitis results from a reaction to an oil soluble oleoresin that is present in many parts of the poison ivy and poison oak plants. Prophylactic measures include avoidance, protective clothing, barrier creams and hyposensitization. Treatments include washing the area immediately with a solvent suitable for lipids and the use of anti-inflammatory agents, especially corticosteroids.

Bentonite↗
PubMed2006

Toxicodendron dermatitis: poison ivy, oak, and sumac.

Allergic contact dermatitis caused by the Toxicodendron (formerly Rhus) species-poison ivy, poison oak, and poison sumac-affects millions of North Americans every year. In certain outdoor occupations, for example, agriculture and forestry, as well as among many outdoor enthusiasts, Toxicodendron dermatitis presents a significant hazard. This review considers the epidemiology, identification, immunochemistry, pathophysiology, clinical features, treatment, and prevention of this common dermatologic problem. Recent research in prevention is emphasized, and resources to help in the identification of plants are provided in the bibliography. The literature was searched using a MEDLINE query for "Toxicodendron dermatitis", and the identified article bibliographies were searched as well.

Dermatitis, Toxicodendron↗
PubMed1994

Keratinocyte interleukin-10 expression is upregulated in tape-stripped skin, poison ivy dermatitis, and Sezary syndrome, but not in psoriatic plaques.

Despite the highly diverse reaction patterns of benign and malignant skin diseases involving T lymphocytes, polymerase chain reaction analysis of cytokine mRNAs present in biopsy samples has revealed that many cutaneous responses can be categorized into essentially two discrete groups. One group exemplified by psoriasis is characterized by consistently detectable mRNAs for IL-2, IFN-gamma, and TNF-alpha, but not IL-4, IL-5, IL-10, thereby closely resembling the murine Th1-type cell-mediated response. The second group exemplified by tape-stripped skin, poison ivy dermatitis, and Sezary syndrome contains predominantly IL-4, IL-5, and IL-10 mRNAs resembling the Th2-type cytokine profile. Because of the growing interest in the immunoregulatory role of IL-10, which can suppress IFN-gamma production and inhibit cell-mediated reactions, we produced a rabbit antiserum that was used to immunohistochemically localize IL-10 in a total of 27 biopsies. The results revealed that in Th2-type skin diseases, IL-10 was predominantly identified throughout all levels of epidermis in the cytoplasm of keratinocytes (KCs), with accentuation of their membranes in upper level cells. In Sezary syndrome, T cells were also immunoreactive for IL-10, which was confirmed using the HUT 78 T cell line derived from a Sezary syndrome patient. While normal skin was devoid of IL-10 expression, KCs began expressing it as early as 6 hr following tape stripping or application of poison ivy antigen and became strongly and diffusely positive by 18-24 hr. In contrast, psoriatic plaques contained no IL-10 immunoreactivity in either the parakeratotic scale or the epidermal KCs. These results confirm the earlier IL-10 mRNA analysis using whole skin samples and immunolocalize IL-10 to epidermal KCs in the Th2 diseases.

Biopsy↗