Morphine causes itching and hives if you have an allergic reaction to it.
Allergic conjunctivitis is inflammation of the conjunctiva (the membrane covering the white part of the eye) due to allergy. Although allergens differ between patients, the most common cause is hay fever. Symptoms consist of redness (mainly due to vasodilation of the peripheral small blood vessels), oedema (swelling) of the conjunctiva, itching and increased lacrimation (production of tears). If this is combined with rhinitis, the condition is termed allergic rhinoconjunctivitis.
The symptoms are due to release of histamine and other active substances by mast cells, which stimulate dilation of blood vessels, irritate nerve endings and increase secretion of tears.
Treatment of allergic conjunctivitis is by avoiding the allergen (e.g. avoiding grass in bloom during the "hay fever season") and treatment with antihistamines, either topical (in the form of eye drops), or systemic (in the form of tablets). Antihistamines, medication that stabilizes mast cells, and non-steroidal anti-inflammatory drugs (NSAIDs) are safe and usually effective.
The conjunctiva is a thin membrane that covers the eye. When an allergen irritates the conjunctiva, common symptoms that occur in the eye include: ocular itching, eyelid swelling, tearing, photophobia, watery discharge, and foreign body sensation (with pain).
Itching is the most typical symptom of ocular allergy and more than 75% of patients report this symptom when seeking treatment.
Symptoms are usually worse for patients when the weather is warm and dry, whereas cooler temperatures and rain tend to assuage symptoms.
A study by Klein et al. showed that in addition to the physical discomfort allergic conjunctivitis causes, it also alters patients' routines, with patients limiting certain activities such as going outdoors, reading, sleeping, and driving. Therefore, treating patients with allergic conjunctivitis may improve their everyday "quality of life."
Signs in phlyctenular keratoconjunctivitis include small yellow nodules that develop over the cornea, which ulcerate after a few days.
The cause of allergic conjunctivitis is an allergic reaction of the body's immune system to an allergen. Allergic conjunctivitis is common in people who have other signs of allergic disease such as hay fever, asthma and eczema.
Among the most common allergens that cause conjunctivitis are:
Most cases of seasonal conjunctivitis are due to pollen and occur in the hay fever season, grass pollens in early summer and various other pollens and moulds may cause symptoms later in the summer.
Perennial conjunctivitis is commonly due to an allergy to house dust mite (a tiny insect-like creature that lives in every home).
Giant papillary conjunctivitis is a very rare condition that is mainly caused by an allergic reaction to "debris". Surgery may also cause this type of allergic conjunctivitis.
Contact dermatoconjunctivitis is caused by the rest of the allergens that conjunctiva may come into contact with: cosmetics, medications and so on.
The ocular allergic response is a cascade of events that is coordinated by mast cells. Beta chemokines such as eotaxin and MIP-1 alpha have been implicated in the priming and activation of mast cells in the ocular surface. When a particular allergen is present, sensitization takes place and prepares the system to launch an antigen specific response. TH2 differentiated T cells release cytokines, which promote the production of antigen specific immunoglobulin E (IgE). IgE then binds to IgE receptors on the surface of mast cells. Then, mast cells release histamine, which then leads to the release of cytokines, prostaglandins, and platelet-activating factor. Mast cell intermediaries cause an allergic inflammation and symptoms through the activation of inflammatory cells.
When histamine is released from mast cells, it binds to H1 receptors on nerve endings and causes the ocular symptom of itching. Histamine also binds to H1 and H2 receptors of the conjunctival vasculature and causes vasodilatation. Mast cell-derived cytokines such as chemokine interleukin IL-8 are involved in recruitment of neutrophils. TH2 cytokines such as IL-5 recruit eosinophils and IL-4, IL-6, and IL-13, which promote increased sensitivity. Immediate symptoms are due to the molecular cascade. Encountering the allergen a patient is sensitive to leads to increased sensitation of the system and more powerful reactions. Advanced cases can progress to a state of chronic allergic inflammation.
Both seasonal allergic conjunctivitis and perennial allergic conjunctivitis are two acute allergic conjunctival disorders. SAC is the most common ocular allergy. Symptoms of the aforementioned ocular diseases include itching and pink to reddish eye(s). These two eye conditions are mediated by mast cells. Nonspecific measures to ameliorate symptoms include cold compresses, eyewashes with tear substitutes, and avoidance of allergens. Treatment consists of antihistamine, mast cell stabilizers, dual mechanism anti-allergen agents, or topical antihistamines. Corticosteroids are another option, but, considering the side-effects of cataracts and increased intraocular pressure, corticosteroids are reserved for more severe forms of allergic conjunctivitis such as vernal keratoconjunctivitis (VKC) and atopic keratoconjunctivitis (AKC).
Both vernal keratoconjunctivitis and atopic keratoconjunctivitis are chronic allergic diseases wherein eosinophils, conjunctival fibroblasts, epithelial cells, mast cells, and TH2 lymphocytes aggravate the biochemistry and histology of the conjunctiva. VKC is a disease of childhood and is prevalent in males living in warm climates. AKC is frequently observed in males between the ages of 30 and 50. VKC and AKC can be treated by medications used to combat allergic conjunctivitis or the use of steroids.
Giant papillary conjunctivitis is not a true ocular allergic reaction and is caused by repeated mechanical irritation of the conjunctiva. Repeated contact with the conjunctival surface caused by the use of contact lenses is associated with GPC.
PKC results from a hypersensitivity/inflammatory reaction to bacteria. Common pathogens include Staph. aureus, Mycobacterium tuberculosis, Chlamydia and Candida.
A detailed history allows physicians to determine whether the presenting symptoms are due to an allergen or another source. Diagnostic tests such as conjunctival scrapings to look for eosinophils are helpful in determining the cause of the allergic response. Antihistamines, medication that stabilizes mast cells, and non-steroidal anti-inflammatory drugs (NSAIDs) are safe and usually effective. Corticosteroids are reserved for more severe cases of ocular allergy disease, and their use should be monitored by an eye care physician due to possible side-effects. When an allergen is identified, the patient should avoid the allergen as much as possible.
If the allergen is encountered and the symptoms are mild, a cold compress can be used to provide relief. It is a quick and easy solution without using any medications. The cold temperature of the water will help to bring down swelling, as it would in a bruise or burn. In addition, there are many antihistamine medications available for purchase.
Mast cell stabilizers can help curing patients with allergic conjunctivitis when cold compress are no longer effective. They tend to have delayed results, but they have fewer side-effects than the other treatments and last much longer than those of antihistamines. Some patients are given an antihistamine at the same time so that there is some relief of symptoms before the mast cell stabilizers becomes effective. Doctors commonly prescribe lodoxamide and nedocromil as mast cell stabilizers, which come as eye drops.
A mast cell stabilizer is a class of non-steroid controller medicine that reduces the release of inflammation-causing chemicals from mast cells. They block a calcium channel essential for mast cell degranulation, stabilizing the cell, thus preventing the release of histamine. Decongestants may also be prescribed. Another common mast cell stabilizer that is used for treating allergic conjunctivitis is sodium cromoglicate.
Antihistamines such as diphenhydramine and chlorpheniramine are commonly used as treatment. Patients treated with H1 antihistamines exhibit reduced production of histamine and leukotrienes as well as downregulation of adhesion molecule expression on the vasculature which in turn attenuates allergic symptoms by 40–50%.
Dual-action medications are also prescribed frequently. Olopatadine (Patanol) and Ketotifen Fumarate (Alaway or Zaditor) both provide protection by acting as an antihistamine and a mast cell stabilizer together. Patanol is a prescription medication, whereas Ketotifen Fumarate is not.
Many of the eye drops can cause burning and stinging, and have side-effects. Proper eye hygiene can improve symptoms, especially with contact lenses. Avoiding precipitants, such as pollen or mold can be preventative.][ Desensitization allergen immunotherapy with subcutaneous introduction of allergens can be performed in atopic individuals as well. Sublingual administration has also shown effect, although multiple allergens are more difficult to combine with this approach.
Experimental research has targeted adhesion molecules known as selectins on epithelial cells. These molecules initiate the early capturing and margination of leukocytes from circulation. Selectin antagonists have been examined in preclinical studies, including cutaneous inflammation, allergy and ischemia-reperfusion injury. There are four classes of selectin blocking agents: (i) carbohydrate based inhibitors targeting all P-, E-, and L-selectins, (ii) antihuman selectin antibodies, (iii) a recombinant truncated form of PSGL-1 immunoglobulin fusion protein, and (iv) small-molecule inhibitors of selectins. Most selectin blockers have failed phase II/III clinical trials, or the studies were ceased due to their unfavorable pharmacokinetics or prohibitive cost. Sphingolipids, present in yeast like Saccharomyces cerevisiae and plants, have also shown mitigative effects in animal models of gene knockout mice.
Allergic conjunctivitis occurs more frequently among those with allergic conditions, with the symptoms having a seasonal correlation.
Allergic conjunctivitis is a frequent condition as it is estimated to affect 20 percent of the population on an annual basis and approximately one-half of these people have a personal or family history of atopy.
Giant papillary conjunctivitis accounts for 0.5–1.0% of eye disease in most countries.
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Itch (Latin: pruritus) is a sensation that causes the desire or reflex to scratch. Itch has resisted many attempts to classify it as any one type of sensory experience. Modern science has shown that itch has many similarities to pain, and while both are unpleasant sensory experiences, their behavioral response patterns are different. Pain creates a withdrawal reflex while itch leads to a scratch reflex.
Unmyelinated nerve fibers for itch and pain both originate in the skin; however, information for them is conveyed centrally in two distinct systems that both use the same nerve bundle and spinothalamic tract.
Pain and itch have very different behavioral response patterns. Pain evokes a withdrawal reflex which leads to retraction and therefore a reaction trying to protect an endangered part of the body. Itch creates a scratch reflex which draws one to the affected skin site. For example, responding to a local itch sensation is an effective way to remove insects on the skin. Scratching has traditionally been regarded as a way to relieve oneself by reducing the annoying itch sensation. However there are hedonic aspects of scratching as one would find noxious scratching highly pleasurable. This can be problematic with chronic itch patients, such as ones with atopic dermatitis, who may scratch affected spots until it no longer produces a pleasant or painful sensation instead of when the itch sensation disappears.It has been hypothesized that motivational aspects of scratching include the frontal brain areas of reward and decision making. These aspects might therefore contribute to the compulsive nature of itch and scratching.
Events of "contagious itch" are very common occurrences. Even a discussion on the topic of itch can give one the desire to scratch. Itch is likely to be more than a localized phenomenon in the place we scratch. Results from a recent study showed that itching and scratching were induced purely by visual stimuli in a public lecture on itching. There is currently little detailed data on central activation for contagious itching but it is hypothesized that a human mirror neuron system exists in which we imitate certain motor actions when we view others performing the same action. A similar phenomenon in which mirror neurons are used to explain the cause is contagious yawning.
Infections and infestations:
Environmental and allergic:
Related to pregnancy:
Itch can originate in the peripheral nervous system (dermal or neuropathic) or in the central nervous system (neuropathic, neurogenic, or psychogenic).
Itch originating in the skin is known as pruritoceptive, and can be induced by a variety of stimuli, including mechanical, chemical, thermal and electrical stimulation. The primary afferent neurons responsible for histamine-induced itch are unmyelinated C-fibres. Two major classes of human C-fibre nociceptors exist: mechano-responsive nociceptors and mechano-insensitive nociceptors. Mechano-responsive nociceptors have been shown in studies to respond to mostly pain and mechano-insensitive receptors respond mostly to itch induced by histamine. However it does not explain mechanically induced itch or when itch is produced without a flare reaction which involves no histamine. Therefore it is possible that pruritoceptive nerve fibres have different classes of fibres, which is unclear in current research.
Studies have been done to show that itch receptors are found only on the top two skin layers, the epidermis and the epidermal/dermal transition layers.][ Shelley and Arthur had verified the depth by injecting individual itch powder spicules (Mucuna pruriens) and found that maximal sensitivity was found at the basal cell layer or the innermost layer of the epidermis. Surgical removal of those skin layers removed the ability for a patient to perceive itch.][ Itch is never felt in muscle or joints, which strongly suggests that deep tissue probably does not contain itch signaling apparatuses.
Sensitivity to pruritic stimuli is evenly distributed across the skin and has a clear spot distribution with similar density to that of pain. The different substances that elicit itch upon intracutaneous injection (injection within the skin) elicit only pain when injected subcutaneously (beneath the skin). Itch is readily abolished in skin areas treated with nociceptor excitotoxin capsaicin but remains unchanged in skin areas which were rendered touch-insensitive by pretreatment with saponins, an anti-inflammatory agent. Although experimentally induced itch can still be perceived under a complete A-fiber conduction block, it is significantly diminished. Overall, itch sensation is mediated by A-delta and C nociceptors located in the uppermost layer of the skin.
Neuropathic itch can originate at any point along the afferent pathway as a result of damage of the nervous system. They could include diseases or disorders in the central nervous system or peripheral nervous system. Examples of neuropathic itch in origin are notalgia paresthetica, brachioradial pruritis, brain tumors, multiple sclerosis, peripheral neuropathy, and nerve irritation.
Neurogenic itch, which is itch induced centrally but with no neural damage, is mostly associated with increased accumulation of exogenous opioids and possibly synthetic opioids.
Itch is also associated with some symptoms of psychiatric disorders such as tactile hallucinations, delusions of parasitosis, or obsessive-compulsive disorders (as in OCD-related neurotic scratching).
The sensation of itch can be reduced by many painful sensations. Numerous studies done in the last decade have shown that itch can be inhibited by many other forms of painful stimuli, such as noxious heat, physical rubbing/scratching, noxious chemicals, and electric shock.][
The inhibition of itch by painful stimuli, including heat, physical stimulus, and chemical stimulus, has been shown experimentally. In an article written by Louise Ward and others, the effects of noxious and non-noxious counterstimuli, such as heat, physical vibration, or chemical stimulation on skin, were studied in healthy adults after they had experimentally induced itch (transdermal iontophoresis of histamine) and pain (with topical mustard oil) in their skin. They found that when they induced non-noxious counterstimuli, the reduction of pain and itch only lasted for up to 20 seconds. However when they induced noxious counterstimuli, there was a significant inhibition of itch for an extended period of time but no inhibition of pain. In addition, it was found that brief noxious stimuli created an anti-itch state for more than 30 minutes. These findings show that itch is not a subliminal form of pain and that noxious counterstimulus is likely to act through a central mechanism, instead of a peripheral one.
Chloroquine has been used in animal studies and in humans as a tool to study the itch mechanisms. In studies in rats, an inverted U-shaped dose response curve to chloroquine pruritogenicity was first described by Onigbogi et al., and has been subsequently confirmed by others. This may suggest the involvement of several receptor types centrally. Indeed, naltrexone and Mu opiate down-regulation with chronic morphine attenuated the frequency of chloroquine pruritus in rats and in mice. Further, a kappa-opioid antagonist, nalfurafine further attenuated the chloroquine-induced itching frequency in mice. These results further suggested that multiple opiate receptors (mu and kappa) interact to modulate itching behavior to chloroquine. Chloroquine exhibits a pharmacogenetic variation in its itch sensitivity, being common in Africans but rare in other races. It also shows an age-related difference in prevalence. Chloroquine itching is uncommon in children but increases in age with a peak in the fourth decade of life and with increased familial concurrence in families and concordance among twins. Whether the pain sensation exhibits such distribution in Africans is yet to be studied.
Painful electrical stimulation reduced histamine-induced itch for several hours at a maximum distance of 10 cm from the stimulated site, which suggests a central mode of action.][ A new method has been recently found, by Hans-Jorgen Nilsson and others,][ that is able to relieve itch without damaging the skin: cutaneous field stimulation (CFS). CFS consists of a flexible rubber plate with 16 needle-like electrodes placed regularly at 2-centimeter intervals in a 4 by 4 matrix used to electrically stimulate nerve fibers in the surface of the skin. The electrodes were stimulated continuously at 4 hertz per electrode, with a pulse duration of 1 millisecond, and an intensity of 0.4–0.8 milliampere lasting for 25 minutes. CFS resulted in a pricking and burning sensation that usually faded away very quickly. The burning sensation was still present during a selective block of impulse conduction of A-fibres in myelinated fibers, which indicates that nociceptive C-fibres are activated by CFS. In addition, a flare reaction was noted to develop around the CFS electrodes, suggesting activation of axon reflexes in nociceptive C-fibres. Itch, which was induced by transdermal iontophoresis of histamine, was inhibited within the skin area treated with CFS and was also significantly reduced at 10 cm from the treatment area. CFS proves to offer a new method of combating itch by using painful electrical stimulation as it creates a long-lasting inhibitory effect, does not create any significant skin injuries, and is simple to apply. It is able to activate powerful itch-inhibitory mechanisms possibly routed through central mechanisms, which could normally be activated by scratching the skin.
A study done by Gil Yosipovitch, Katharine Fast, and Jeffrey Bernhard showed that noxious heat and scratching were able to inhibit or decrease itch induced by transdermal iontophoresis of histamine and, most interestingly, decrease skin blood flow. Twenty-one healthy volunteers participated in the study. Baseline measurements of skin blood flow were obtained on the flexor part of the forearm and then compared with skin blood flow after various stimuli. Then transdermal iontophoresis of histamine was performed and tested with various stimuli. It is well known that skin blood flow is significantly increased during mechanical scratching, warming, and noxious heat. This study is the first to examine the changes of blood flow by stimuli during iontophoresis of histamine and how itch is perceived in those conditions. Its examination provided an unexpected result that noxious heat and scratching have an inhibitory effect.
A negative correlation was found between pain sensitivity and itch sensitivity. In a study done by Amanda Green and others, they aimed to determine itch-related genetic factors and establish a more useful animal model for itch. They looked at 11 inbred mouse strains and compared their scratching behavior in response to two itch-inducing agents, histamine and chloroquine. Every strain revealed an inverted-U-shaped dose response relationship from chloroquine, indicating that moderate dosages produced more scratching than at higher dosages. An explanation is that higher dosage produces more pain and the presence of pain inhibits itch thereby lowering the amount of overall scratching. Another notable result was that histamine-induced scratching occurred in female mice on average 23% more than in males. Finally, it was found that mice having strains sensitive to pain were resistant to itch and vice versa.
Inflammatory mediators—such as bradykinin, serotonin (5-HT) and prostaglandins—released during a painful or pruritic inflammatory condition not only activate pruriceptors but also cause acute sensitization of the nociceptors. In addition, expression of neuro growth factors (NGF) can cause structural changes in nociceptors, such as sprouting. NGF is high in injured or inflamed tissue. Increased NGF is also found in atopic dermatitis, a hereditary and non-contagious skin disease with chronic inflammation. NGF is known to up-regulate neuropeptides, especially substance P. Substance P has been found to have an important role in inducing pain; however, there is no confirmation that substance P directly causes acute sensitization. Instead, substance P may contribute to itch by increasing neuronal sensitization and may affect release of mast cells, which contain many granules rich in histamine, during long-term interaction.
Noxious input to the spinal cord is known to produce central sensitization, which consists of allodynia, exaggeration of pain, and punctuate hyperalgesia, extreme sensitivity to pain. Two types of mechanical hyperalgesia can occur: 1) touch that is normally painless in the uninjured surroundings of a cut or tear can trigger painful sensations (touch-evoked hyperalgesia), and 2) a slightly painful pin prick stimulation is perceived as more painful around a focused area of inflammation (punctuate hyperalgesia). Touch-evoked hyperalgesia requires continuous firing of primary afferent nociceptors, and punctuate hyperalgesia does not require continuous firing which means it can persist for hours after a trauma and can be stronger than normally experienced. In addition, it was found that patients with neuropathic pain, histamine ionophoresis resulted in a sensation of burning pain rather than itch, which would be induced in normal healthy patients. This shows that there is spinal hypersensitivity to C-fiber input in chronic pain.
A variety of over-the-counter and prescription anti-itch drugs are available. Some plant products have been found to be effective anti-pruritics, others not. Non-chemical remedies include cooling, warming, soft stimulation.
Topical antipruritics in the form of creams and sprays are often available over-the-counter. Oral anti-itch drugs also exist and are usually prescription drugs. The active ingredients usually belong to the following classes:
Phototherapy is helpful for severe itching, especially if caused by renal failure. The common type of light used is UVB.
Sometimes scratching relieves isolated itches, hence the existence of devices such as the back scratcher. Often, however, scratching can intensify itching and even cause further damage to the skin, dubbed the "itch-scratch-itch cycle"][.
The mainstay of therapy for dry skin is maintaining adequate skin moisture and topical emollients.
Approximately 280 million people globally (4% of the population) have difficulty with itchyness.
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Itch is the second extended play (EP) by English alternative rock group Radiohead, released exclusively to Japan on 1 June 1994.
Although the EP presented no new material, it does contain the US version of "Stop Whispering", which was remixed by Chris Sheldon. It features strings and has a slower tempo. This version of the song had previously been available on the "Stop Whispering" single released in 1993. The EP's second track, "Thinking About You", a faster and more punk-driven version than the one on the band's first album Pablo Honey, also appeared on the Drill EP.
"Faithless, the Wonderboy" was first released as a B-side on the 1993 single "Anyone Can Play Guitar". The version of "Banana Co." present on this EP is acoustic, which could also be found on the 1993 single "Pop Is Dead", and is not to be confused with the studio version of the song which was released on the "Street Spirit (Fade Out)" CD2 single two years later in 1996. This recording was made at Signal One radio station (formerly 'Signal Radio').
The live versions of "Killer Cars," "You," and "Vegetable" had been previously released only on the extremely rare "Creep" reissue 12" vinyl. The three songs were recorded at the Metro in Chicago on 30 June 1993. The final track, "Creep (Acoustic)", is also present on the My Iron Lung EP, and was recorded at KROQ-FM studios, Los Angeles, on 13 July 1993.
in U.S. English) is an opiate derivative, the 3,6-dipropanoyl ester of morphine. It was developed in 1972 as an analgesic. It is rarely used in some countries for the relief of severe pain such as that caused by terminal cancer, as an alternative to diamorphine (heroin) and morphine.
Dipropanoylmorphine, though rarely used, is considered to be a safer and less addictive alternative to morphine. Studies and clinical trials comparing dipropanoylmorphine to morphine have produced results that indicate the incidence of side-effects are far more common with morphine. Respiratory depression, euphoria, excessive sedation and somnolence (so-called 'nodding' by recreational opioid users), constipation, miosis (pinpoint pupils), nausea, bradycardia, behavioral disturbances, and severe physical and psychological dependence on morphine is more likely with the use of morphine versus dipropanoylmorphine.
Dipropanoylmorphine is slightly slower acting than diamorphine and morphine, but longer lasting, and is slightly more potent by weight due to its higher lipophilicity. Side effects are generally relatively mild for an opioid with a similar profile to morphine/heroin and typical of other opioids. The most common side effects associated with dipropanoylmorphine are itching, nausea and respiratory depression.
Dipropanoylmorphine is prepared by reacting morphine with propionic anhydride, in an analogous manner to how heroin is produced by reacting morphine with acetic anhydride.
While acetic anhydride is a restricted chemical around the world due to its potential uses in making heroin from morphine for the illicit market, it is used in vast amounts by the chemical industry for the manufacture of drugs such as aspirin. Propanoic anhydride however is much less widely used. Although it is used in the manufacture of a range of pharmaceuticals, none of these are produced in nearly as large quantities, and sales of propanoic anhydride in quantities larger than one gram must be reported in many countries because of its potential use in making fentanyl type synthetic opiates.
Also known as Queensland Itch, Seasonal Recurrent Dermatitis (SSRD) , Summer Itch or more technically, Culicoides Hypersensitivity.
Sweet Itch is a medical condition in equines caused by an allergic response to the bites of Culicoides midges. It may be found in any horses and ponies, especially in the warmer regions. It may also occur, too, in other equines. It is also found in Canada, Australia, the US and many other parts of the world.
A hypersensitivity reaction to specific allergens (protein molecules causing an extreme immune response in sensitised individuals) in the saliva of Culicoides midges. There are multiple allergens involved, although some workers claim that the larger proteins (of molecular weight 65kDa) are the most important. These allergens appear to be cross-reactive across many species of Culicoides - i.e. many different varieties of midges produce similar allergens, giving the same effects upon horses.
The hypersensitivity response is mediated by IgE, an antibody produced by the horse's immune system which binds the allergens, causing a cascade production of histamine and cytokines which make the horse's skin inflamed and itchy. Of these, histamine appears the most important in the initial phase of reaction.
Few treatments are fully efficacious once lesions have appeared. The only effective form of treatment is preventitive - i.e. prevent further insect bites - so these techniques will also be discussed here. Treatments generally fall into one of the following categories:
1) Insecticides and Repellents: These may be applied to the horse or its environment. The most commonly used and effective are permethrins. and benzyl benzoate Citronella has been used, with variable effect. Some sources advocate draining of any stagnant water or pools, to reduce the local breeding potential of the insects. Midge numbers are often larger near water sources, for example ponds, bogs, and slow moving water. Moving the horse away from these areas may help to prevent further problems.
2) Barrier Techniques: Rugs etc., that prevent flies and midges settling on the animal's skin to bite. These include "Boett Rugs" and fly masks. In addition, thin screens may be placed over stable doors and windows to exclude biting insects. Stabling the horse at times of day when the midges are most prevalent is also quite effective.
3) Immunotherapy: A wide variety immunotherapy and desensitisation protocols have been trialled in attempts to reduce or modify the immune response, with variable success rates. So far, there appear to be none that show a benefit in more than a very small, statistically insignificant, number of cases. The most recent trial results have not yet been published, however, BioEos is confident that the results will be positive and has said that the 2007 series will be the "final" trials for the product. The BioEos vaccination protocol is designed to shift the immune system from a Th2 (theoretically allergy-producing) to Th1 (non-allergy producing) mode.
4) Nutritional supplements: Various supplements may be effective in individuals, including fatty acid supplemantation and linseed oil. However, although owners perceived an improvement, this was not bourne out by objective statistical analysis.
5) Symptomatic Control: Control of symptoms to some degree can be achieved with antihistamines (especially hydroxyzine, and with corticosteroids, although the potential side effects (e.g. laminitis, immune suppression) make this a less preferred option. In addition, antibiotics may be required to manage any secondary infection.
6) Alternative Medicines: A wide variety of herbal, homeopathic and other alternative remedies have been suggested. Among the natural remedies suggested are sulfur, wild geranium (as the base for a shampoo), Lavender oil, Aloe vera (to reduce the itching).
Overall, the wide variety of treatments proposed leads to the conclusion that no one method is universally effective.
Ceratopogonidae (The family of which Culicoides is a member)
Culicoides imicola (species of midge)
Culicoides Impunctatus (species of midge)
PonyGalaxy Detailed Information On SSRD
Darier's sign is a change observed after stroking the skin of a person with systemic mastocytosis or urticaria pigmentosa.
In general, the skin becomes swollen, itchy and red. This is a result of compression of mast cells, which are hyperactive in these diseases. These mast cells release inflammatory granules which contain histamine. It is the histamine which is responsible for the response seen after rubbing the skin.
Darier's sign is named after the French dermatologist Ferdinand-Jean Darier who first described it.
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Type 1 hypersensitivity
Bristleworm stings are a cutaneous condition caused by contact with bristleworms, in which an allergic or irritant reaction may result.:431
Type I hypersensitivity (or immediate hypersensitivity) is an allergic reaction provoked by reexposure to a specific type of antigen referred to as an allergen. Type I is not to be confused with Type II, Type III, or Type IV hypersensitivities.
Exposure may be by ingestion, inhalation, injection, or direct contact.
The immune system is a system of biological structures and processes within an organism that protects against disease. To function properly, an immune system must detect a wide variety of agents, from viruses to parasitic worms, and distinguish them from the organism's own healthy tissue.
Pathogens can rapidly evolve and adapt, and thereby avoid detection and neutralization by the immune system, however, multiple defense mechanisms have also evolved to recognize and neutralize pathogens. Even simple unicellular organisms such as bacteria possess a rudimentary immune system, in the form of enzymes that protect against bacteriophage infections. Other basic immune mechanisms evolved in ancient eukaryotes and remain in their modern descendants, such as plants and insects. These mechanisms include phagocytosis, antimicrobial peptides called defensins, and the complement system. Jawed vertebrates, including humans, have even more sophisticated defense mechanisms, including the ability to adapt over time to recognize specific pathogens more efficiently. Adaptive (or acquired) immunity creates immunological memory after an initial response to a specific pathogen, leading to an enhanced response to subsequent encounters with that same pathogen. This process of acquired immunity is the basis of vaccination.