Contact dermatitis is a localized rash or irritation of the skin caused by contact with a foreign substance. Only the superficial regions of the skin are affected in contact dermatitis. Inflammation of the affected tissue is present in the epidermis (the outermost layer of skin) and the outer dermis (the layer beneath the epidermis).Unlike contact urticaria, in which a rash appears within minutes of exposure and fades a
way within minutes to hours, contact dermatitis takes days to fade away. Even then, contact dermatitis fades only if the skin no longer comes in contact with the allergen or irritant. Contact dermatitis results in large, burning, and itchy rashes, and these can take anywhere from several days to weeks to heal. Chronic contact dermatitis can develop when the removal of the offending agent no longer provides expected relief.
In North/South America, the most common causes of allerg
ic contact dermatitis are plants of the Toxicodendron genus: poison ivy, poison oak, and poison sumac. Specific plant species that can induce
such contact dermatitis include Western Poison Oak, a widespread plant in the western USA. Common causes of irritant contact dermatitis are harsh (highly alkaline) soaps, detergents, and cleaning products.
There are three types of contact dermatitis: irritant contact, allergic contact, and photocontact dermatitis. Photocontact dermatitis is divided into two categories: phototoxic and photoallergic.
Plants
Allergic contact dermatitisSometimes termed "photoaggravated"(Bourke et al. 2001)[17], and divided into two categories, phototoxic and photoallergic, PCD is the eczematous condition which is triggered by an interaction between an otherwise unharmful or less harmful substance on the skin and ultraviolet light (320-400 nm UVA) (ESCD 2006), therefore manifesting itself only in regions where the sufferer has been exposed to such rays. Without the presence of these rays, the photosensitiser is not harmful. For this reason, this form of contact dermatitis is usually associated only with areas of skin which are left uncovered by clothing. The mechanism of action varies from toxin to toxin, but is usually due to the production of a photoproduct. Toxins which are associated with PCD include the psoralens. Psoralens are in fact used therapeutically for the treatment of psoriasis, eczema and vitiligo.
Photocontact dermatitis is another condition where the distinction between forms of contact dermatitis is not clear cut. Immunological mechanisms can also play a part, causing a response similar to ACD.
Allergic dermatitis is usually confined to the area where the trigger actually touched the skin, whereas irritant dermatitis may be more widespread on the skin. Symptoms of both forms include the following:
While either form of contact dermatitis can affect any part of the body, irritant contact dermatitis often affects the hands, which have been exposed by resting in or dipping into a container (sink, pail, tub, Sun, Swimming Pools With High chlorine ), containing the irritant.
- Weak acid solutions [lemon juice, vinegar] can be used to counteract the effects of dermatitis contracted by exposure to basic irritants [phenol etc.].
If the rash does not improve or continues to spread after 2-3 of days of self-care, or if the itching and/or pain is severe, the patient should contact a dermatologist or other physician or physician assistant. Medical treatment usually consists of lotions, creams, or oral medications.
Since contact dermatitis relies on an irritant or an allergen to initiate the reaction, it is important for the patient to identify the responsible agent and avoid it. This can be accomplished by having patch tests, a method commonly known as allergy testing. The patient must know where the irritant or allergen is found to be able to avoid it. It is important to also note that chemicals sometimes have several different names.[18]
In an industrial setting the employer has a duty of care to the individual worker to provide the correct level of safety equipment to mitigate the exposure to harmful irritants. This can take the form of protective clothing, gloves or barrier cream depending on the working environment.
The year was 1959, location: The central African city of Leopoldville, now called Kinshasa, shortly before the waves of violent rebellion that 
followed the liberation of the Belgian Congo. A seemingly healthy man walked into a hospital clinic to give blood for a Western backed study of blood diseases. He walked away and was never heard from again. Doctors analyzed his sample, froze it in a test tube and forgot about it. A quarter-century later, in the mid-1980s, researchers studying the growing AIDS epidemic took a second look at the blood and discovered that it contained HIV, the virus that causes AIDS.
And not just any HIV. The Leopoldville sample is the oldest specimen of the AIDS virus ever isolated and may now help solve the mystery of how and when the virus made the leap from animals (monkeys or chimpanzees) to humans, according to a report published last week in Nature. Dr. David Ho, director of the Aaron Diamond AIDS Research Center in New York City and one of the study's authors, says a careful genetic analysis of the sample's DNA pushes the origin of the AIDS epidemic back at least a decade, to the early '50s or even the '40s.
Over the past 15 years, scientists have identified at least 10 subtypes of the virus. But they couldn't tell whether they were seeing variations on one changeable virus or the handiwork of several different viruses that had made the jump from primates to man. A look at the genetic mutations in the Leopoldville sample strongly suggests that all it took to launch the epidemic was one unlucky turn of events.
The findings underscore how rapidly HIV can adapt to its surroundings, making it difficult to develop effective vaccines. No one knows how many more subtypes of HIV will sprout in the next 40 years, but chances are they will be every bit as lethal as the ones we see today, if not more so.
