Toxicodendron
Dermatitis, Toxicodendron
Dermatitis, Atopic
Dermatitis, Allergic Contact
Dermatitis Herpetiformis
Dermatitis, Seborrheic
Secondary bacterial infections complicating skin lesions. (1/7)
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. (+info)CURRENT CONCEPTS IN DERMATOLOGY. III. THE USE OF RADIOTHERAPY AND CORTICOSTEROIDS. (2/7)
The use of ionizing radiation and corticosteroids is discussed, in this third and final part of a review of diseases of the skin. Radiation is being used less extensively because superior methods of treatment are available for many conditions which formerly were frequently treated by this modality. The concept of applying the radiation at the level of the basic pathologic process has been developed into clinical practice by the use of generators which can produce very soft (or superficial) ionizing radiation. Topical or systemic corticosteroids do not cure skin diseases but produce dramatic suppression of signs and symptoms. For best results consideration must be given to the diagnosis, the natural history of the disease to be treated, the method of administration and a search for possible contraindications to the use of these steroids. Basic dermatological principles (removal of offending agents, bland soothing applications, sedation, etc.) must be adhered to. The corticosteroids are not a panacea in the treatment of skin disease. (+info)Biomass and toxicity responses of poison ivy (Toxicodendron radicans) to elevated atmospheric CO2. (3/7)
Contact with poison ivy (Toxicodendron radicans) is one of the most widely reported ailments at poison centers in the United States, and this plant has been introduced throughout the world, where it occurs with other allergenic members of the cashew family (Anacardiaceae). Approximately 80% of humans develop dermatitis upon exposure to the carbon-based active compound, urushiol. It is not known how poison ivy might respond to increasing concentrations of atmospheric carbon dioxide (CO(2)), but previous work done in controlled growth chambers shows that other vines exhibit large growth enhancement from elevated CO(2). Rising CO(2) is potentially responsible for the increased vine abundance that is inhibiting forest regeneration and increasing tree mortality around the world. In this 6-year study at the Duke University Free-Air CO(2) Enrichment experiment, we show that elevated atmospheric CO(2) in an intact forest ecosystem increases photosynthesis, water use efficiency, growth, and population biomass of poison ivy. The CO(2) growth stimulation exceeds that of most other woody species. Furthermore, high-CO(2) plants produce a more allergenic form of urushiol. Our results indicate that Toxicodendron taxa will become more abundant and more "toxic" in the future, potentially affecting global forest dynamics and human health. (+info)Dermoscopy of black-spot poison ivy. (4/7)
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. (+info)Urushiol (poison ivy)-triggered suppressor T cell clone generated from peripheral blood. (5/7)
Allergic contact dermatitis to Toxicodendron radicans (poison ivy) is mediated by the hapten urushiol. An urushiol-specific, interleukin 2 (IL-2)-dependent T cell clone (RLB9-7) was generated from the peripheral blood of a patient with a history of allergic contact dermatitis to T. radicans. This clone proliferated specifically to both leaf extract and pure urushiol. Although the clone had the phenotype CD3+CD4+CD8+, proliferation to antigen was blocked by anti-CD8 and anti-HLA-A, B, C, but not by anti-CD4, suggesting that CD4 was not functionally associated with the T cell receptor. Furthermore, studies with antigen-presenting cells from MHC-typed donors indicated that the clone was MHC class 1 restricted. RLB9-7 was WT31 positive, indicating it bears the alpha beta T cell receptor. The clone lacked significant natural killer cell activity and produced only low levels of IL-2 or gamma-interferon upon antigen stimulation. Addition of RLB9-7 to autologous peripheral blood mononuclear cells in the presence of urushiol inhibited the pokeweed mitogen-driven IgG synthesis. This suppression was resistant to irradiation (2,000 rad) and was not seen when RLB9-7 was added to allogeneic cells, even in the presence of irradiated autologous antigen-presenting cells, suggesting that suppression was MHC restricted and not mediated by nonspecific soluble factors. However, RLB9-7 cells in the presence of urushiol inhibited the synthesis of tetanus toxoid-specific IgG by autologous lymphocytes, indicating that the suppression, although triggered specifically by urushiol, was nonspecific. (+info)Keratinocyte intercellular adhesion molecule-1 (ICAM-1) expression precedes dermal T lymphocytic infiltration in allergic contact dermatitis (Rhus dermatitis). (6/7)
The ability of small molecules such as urushiol, present as a wax on the poison ivy leaf surface, to cause allergic contact dermatitis (rhus dermatitis) has fascinated immunologists for decades. Current dogma suggests that these epicutaneously applied catechol-containing molecules serve as haptens to conjugate with larger proteins via reactive o-quinone intermediates. These complexes are then recognized as foreign antigens by the immune system and elicit a hypersensitivity reaction. Phorbol ester can directly induce cultured keratinocyte (KC) intercellular adhesion molecule-1 (ICAM-1) expression via a protein kinase C (PK-C)-dependent mechanism. As urushiol is also a known PK-C agonist, we asked if topical application of a poison ivy/oak mixture could directly induce epidermal KC ICAM-1 expression. During the pre-erythematous phase of this reaction (4 to 20 hours), epidermal KCs expressed ICAM-1; this "initiation phase" preceded the appearance of activated memory T lymphocytes in the papillary dermis, and thus appeared to be nonlymphokine mediated. A near-contiguous cellular-adhesion molecular network was identified by ICAM-1 staining of basal KCs, dermal dendrocytes, and endothelial cells. During the second 24-hour period with the onset of erythema and edema, there was an "amplification phase" of more intense KC ICAM-1 expression coupled with relatively weak KC HLA-DR expression that coincided with dermal and epidermal T-cell infiltration. This suggests the presence of lymphokines, such as gamma interferon, during the amplification phase because of KC HLA-DR expression. On cultured KCs, urushiol directly induced ICAM-1 expression but not HLA-DR. Thus, in addition to functioning as an antigenic hapten, urushiol directly induces KC ICAM-1 expression. The KC ICAM-1 expression may then alter the dynamic trafficking of memory T cells in the epidermis, so as to initiate cutaneous inflammation in a nonantigen specific manner. This initiation phase is followed by T-cell infiltration and consequent lymphokine production that significantly amplifies the original stimulus. Thus much can still be learned about the molecular pathophysiology of this common type of cutaneous inflammation. (+info)Gas plant (Dictamnus albus) phytophotodermatitis simulating poison ivy. (7/7)
A 48-year-old man presented with an itchy rash that resembled superficial burns or cane marks on his left forearm; similar lesions had appeared every summer for 5 years. Poison ivy dermatitis had been the initial diagnosis, but the patient knew that this plant was absent from his well tended garden. A visit to the garden revealed the gas plant Dictamnus albus, and occlusive patch testing with leaf cuttings produced a reaction after the skin was exposed to sunlight. Gas plant phytophotodermatitis was diagnosed. (+info)"Toxicodendron" is a genus of flowering plants in the family Anacardiaceae, also known as the cashew family. This genus includes several species that are well-known for causing allergic reactions in humans, particularly through contact with their sap or urushiol-containing parts of the plant. The most common and notorious species in this genus is Toxicodendron radicans, also known as poison ivy, poison oak, and poison sumac. These plants can cause an itchy, blistering rash upon contact with the skin, which is a type of allergic reaction called contact dermatitis. The severity of the reaction can vary from person to person, depending on their sensitivity to urushiol and the amount of exposure they have had to the plant.
Toxicodendron dermatitis is a type of contact dermatitis that results from exposure to plants belonging to the Toxicodendron genus, which includes poison ivy, poison oak, and poison sumac. The reaction is caused by an oily resin called urushiol found in these plants. When the oil comes into contact with the skin, it can cause an allergic reaction that leads to a red, itchy rash, often with blisters or weeping lesions.
The rash usually appears within 12-72 hours after exposure and can last for several weeks. The severity of the reaction varies from person to person, depending on their sensitivity to urushiol and the amount of contact they had with the plant. In addition to direct skin contact, urushiol can also be spread through secondary sources such as clothing, pets, or tools that have come into contact with the plant.
Prevention measures include avoiding contact with Toxicodendron plants, wearing protective clothing and gloves when working in areas where these plants may be present, and washing skin and clothing thoroughly with soap and water after exposure. In some cases, medical treatment may be necessary to manage symptoms and prevent complications.
Atopic dermatitis is a chronic, inflammatory skin condition that is commonly known as eczema. It is characterized by dry, itchy, and scaly patches on the skin that can become red, swollen, and cracked over time. The condition often affects the skin on the face, hands, feet, and behind the knees, and it can be triggered or worsened by exposure to certain allergens, irritants, stress, or changes in temperature and humidity. Atopic dermatitis is more common in people with a family history of allergies, such as asthma or hay fever, and it often begins in infancy or early childhood. The exact cause of atopic dermatitis is not fully understood, but it is thought to involve a combination of genetic and environmental factors that affect the immune system and the skin's ability to maintain a healthy barrier function.
Dermatitis is a general term that describes inflammation of the skin. It is often characterized by redness, swelling, itching, and tenderness. There are many different types of dermatitis, including atopic dermatitis (eczema), contact dermatitis, seborrheic dermatitis, and nummular dermatitis.
Atopic dermatitis is a chronic skin condition that often affects people with a family history of allergies, such as asthma or hay fever. It typically causes dry, scaly patches on the skin that can be extremely itchy.
Contact dermatitis occurs when the skin comes into contact with an irritant or allergen, such as poison ivy or certain chemicals. This type of dermatitis can cause redness, swelling, and blistering.
Seborrheic dermatitis is a common condition that causes a red, itchy rash, often on the scalp, face, or other areas of the body where oil glands are located. It is thought to be related to an overproduction of oil by the skin's sebaceous glands.
Nummular dermatitis is a type of eczema that causes round, coin-shaped patches of dry, scaly skin. It is more common in older adults and often occurs during the winter months.
Treatment for dermatitis depends on the underlying cause and severity of the condition. In some cases, over-the-counter creams or lotions may be sufficient to relieve symptoms. Prescription medications, such as corticosteroids or immunosuppressants, may be necessary in more severe cases. Avoiding triggers and irritants can also help prevent flare-ups of dermatitis.
Allergic contact dermatitis is a type of inflammatory skin reaction that occurs when the skin comes into contact with a substance (allergen) that the immune system recognizes as foreign and triggers an allergic response. This condition is characterized by redness, itching, swelling, blistering, and cracking of the skin, which usually develops within 24-48 hours after exposure to the allergen. Common allergens include metals (such as nickel), rubber, medications, fragrances, and cosmetics. It is important to note that a person must first be sensitized to the allergen before developing an allergic response upon subsequent exposures.
Dermatitis herpetiformis (DH) is a chronic, autoimmune blistering skin disorder that is characterized by the presence of symmetrical, pruritic (itchy), papulo-vesicular (papules and small fluid-filled blisters) eruptions on the extensor surfaces of the body, such as the elbows, knees, buttocks, and shoulders. It is often associated with gluten sensitivity or celiac disease, a condition that causes an abnormal immune response to gluten, a protein found in wheat, barley, and rye.
The exact cause of DH is not fully understood, but it is believed to result from the interaction between genetic, environmental, and immunological factors. The disorder is characterized by the presence of IgA antibodies in the skin, which trigger an immune response that leads to the formation of the characteristic rash.
DH is typically treated with a gluten-free diet, which can help to control the symptoms and prevent complications such as malabsorption and nutritional deficiencies. Medications such as dapsone may also be used to control the itching and blistering associated with the disorder. In some cases, topical corticosteroids or other anti-inflammatory medications may be prescribed to help manage symptoms.
It is important to note that DH is a chronic condition that requires ongoing management and monitoring. People with DH should work closely with their healthcare provider to develop an appropriate treatment plan and monitor their progress over time.
Seborrheic dermatitis is a common, inflammatory skin condition that mainly affects the scalp, face, and upper part of the body. It causes skin irritation, flaking, and redness, often in areas where the skin is oily or greasy. The exact cause of seborrheic dermatitis is not fully understood, but it appears to be related to a combination of genetic, environmental, and microbial factors.
The symptoms of seborrheic dermatitis can vary in severity and may include:
* Greasy or flaky scales on the scalp, eyebrows, eyelashes, ears, or beard
* Redness and inflammation of the skin
* Itching, burning, or stinging sensations
* Yellow or white crusty patches on the scalp or other affected areas
* Hair loss (in severe cases)
Seborrheic dermatitis is a chronic condition that tends to flare up and then subside over time. While there is no cure for seborrheic dermatitis, various treatments can help manage the symptoms and prevent complications. These may include medicated shampoos, topical creams or ointments, and lifestyle changes such as stress reduction and avoiding triggers that worsen symptoms.
It is important to note that seborrheic dermatitis should not be confused with other skin conditions, such as psoriasis or eczema, which may have similar symptoms. A healthcare professional can provide a proper diagnosis and recommend appropriate treatment options based on the individual's specific needs.
Occupational dermatitis is a specific type of contact dermatitis that results from exposure to certain substances or conditions in the workplace. It can be caused by direct contact with chemicals, irritants, or allergens present in the work environment. This condition typically affects the skin on the hands and forearms but can also involve other areas of the body, depending on the nature of the exposure.
There are two main types of occupational dermatitis:
1. Irritant contact dermatitis (ICD): This type occurs when the skin comes into direct contact with an irritating substance, leading to redness, swelling, itching, and sometimes blistering. Common irritants include solvents, detergents, oils, and other industrial chemicals.
2. Allergic contact dermatitis (ACD): This type is a result of an allergic reaction to a specific substance. The immune system identifies the allergen as harmful and mounts a response, causing skin inflammation. Common allergens include latex, metals (such as nickel), and certain plants (like poison ivy).
Prevention measures for occupational dermatitis include using appropriate personal protective equipment (PPE) like gloves, masks, and aprons, as well as practicing good hygiene, such as washing hands regularly and avoiding touching the face with contaminated hands. If you suspect you have developed occupational dermatitis, consult a healthcare professional for proper diagnosis and treatment.