Microbiology
08/29/08
Hypersensitivity
Transcriber: Sara McGowan
55:07
1: Prescott Atkinson, pediatric immunologist/allergist at Children’s. This is intended to be a superficial overview of the field. Try to know some examples and underlying mechanisms of the diseases and you’ll probably do fine.
2: Hypersensitivity disorders have been known for at least the past 100 years and people have been trying to understand them, what causes them and decide how to prevent them from occurring and the best methods of treatment. We’re going to go over some basic information about how we think about these disorders, some different examples of them and how they’re generally treated.
Immunologic hypersensitivity syndrome is an immunologic reaction, which produces tissue damage on re-exposure to antigen and that’s very important. Usually, these types of reactions don’t occur de novo on the first exposure; it’s something that requires sensitization. The immune system has memory and an over exuberant reaction is something it’s sensitized to is the problem. So, patients come in with a rash that’s associated with an antibiotic and they say “I’ve taken this antibiotic before and never had a problem,” well, that’s the basic idea, they didn’t until they became sensitized to it.
3. In the 60’s, Gell and Coombs devised the classification scheme that we still use today. By far, the most common type is the Type 1 or IgE-mediated types of hypersensitivity syndromes. We’ll spend the most time on those. Types 2 and 3 are mediated mainly through IgG and complement, with very important involvement of phagocytes and Fc receptors. The main difference is Type 2 reactions occur on surfaces and Type 3 reactions, at least initially, in the fluid phase, in the serum or the tissue fluids.
Type 4, or delayed-type hypersensitivity is cell-mediated, mainly T cell-mediated reactivity.
4. Highlights that we’re going to discuss Type 1 reactions now.
5. Type 1 hypersensitivity syndromes have been known for more than a century. In 1902, Portier and
Richet studied the properties of a type of jellyfish, the Portuguese Man of War (not a true jellyfish, but related to it) toxin by extracting it and injecting it into dogs. It was very toxic, many of the animals died.
When they reinjected dogs that had been injected previously, with a much smaller dose of toxin they developed a peculiar syndrome of difficulty breathing, GI distress and frequently death after the small dose (orders of magnitude smaller than the toxicity), so this was clearly an immunological type of process. They called this anaphylaxis meaning “the opposite of protection.” Prophylaxis means
“towards or supporting protection.”
Histamine, the immediate mediator of Type 1 reactions, was identified around the same time, first in bacteria and it was thought for a decade or two that it was not produced in eukaryotic tissues at all, but in the 20’s was found to be produced in mammalian tissues. Around that time, Prausnitz and Kustner showed that anaphylactic sensitivity could be transferred by serum. Kustner was allergic to fish and he would break out in hives. Prausnitz took some of Kustner’s serum and injected it into his own skin and when he ate fish he developed a hive at the same site, so there was some kind of serum factor that
Kustner had that could be transferred. This is called passive cutaneous anaphylaxis and it’s used a lot in

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Sara McGowan pg. 2 experimental models of IgE-mediated sensitivity. They didn’t know what this factor was at the time.
They knew about immunoglobulins (Ig), but this did not appear to be an IgG type of reaction or an immunoglobulin or antibody-mediated type of reaction.
Mast cells were first identified in the 50’s as the main tissue source of histamine. It wasn’t until the 60’s that a class of Ig in the serum, which was usually present in vanishingly small concentrations compared to the other classes, was identified and shown to be this mysterious sensitizing agent that Prausnitz and
Kustner and Portier and Richet had been setting. (This is IgE, I suppose, according to the slide) So the picture is fairly complete. We understand a lot about the basic mechanisms for these types of allergic disease.
6. There are several types of diseases in which allergies play a strong, if not a central role. Allergic rhinoconjunctivitis (hay fever) is probably the most common one. 10-15% of the population has it.
Asthma is an inflammatory airway disease, which, at least in children, usually has a strong allergic component. Many times adults with asthma don’t have a lot of allergies, but in children allergies are much more common in asthmatics than not. Eczema (atopic dermatitis) or allergic eczma is a very itchy skin disease with which the patients usually have many allergies, although it’s not clear, like in asthma, whether the allergies are a co-factor in the development of the disease but they are clearly important. If you can control the allergic exposure, many times you can improve the eczema considerably. Acute urticaria (hives) can be induced by foods, drugs, infections; many times the cause is unidentifiable, but in most cases it will resolve by itself. Presumably, it’s some kind of temporary sensitization to something in the environment. Anaphylaxis is the most serious and is highly fatal, if not treated.
7. This is the culprit in most Type 1 reactions: the mast cell. It was originally though to be a phagocytic cell that was stuffed with phagocytic granules. Mast means “well-stuffed.” In fact, they are modified lysosomes and they have glycosaminoglycan matrix inside, heparin, chondroitin sulfate that are negatively charged, complexed with histamine primarily in humans, which is positively charged and it contains other types of mediators as well that can be released very rapidly when the cell is activated.
What you can’t see is on the surface are hundreds of thousands of IgE receptors. These receptors can bind IgE with very high, essentially irreversibly affinity. Unlike many receptors, not much happens when
IgE binds it’s receptor on a mast cell, you have to cross-link it with an antigen or by some other means to actually activate the cell.
8. This is the molecular structure. It was first identified in the late 80’s in rodent mast cells, but it’s very similar in humans. There is a pair of disulfide linked gamma chains, which are also used by other Fc receptors, which contain signaling motifs. There’s a beta chain which upregulates the receptors ability to produce activation signals. There’s an alpha chain that binds IgE, but it doesn’t signal anything. It’s associated non-covalently with the other chains that form the signaling complex in the cell membrane.
9. Any way that you aggregate these receptors in the cell will cause activation. The usual way, like in ragweed sensitivity, you breathe in ragweed pollen and the way pollen works is it has many watersoluble proteins that rapidly dissolve out of the capsule of the pollen grain and diffuse into the epithelium and contact the IgE receptors. If you’re allergic to ragweed, you’ve made IgE, which is

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Sara McGowan pg. 3 specific to epitopes on this protein and these receptors become cross-linked, generating a signal. You only need to activate 1-2% of the receptors on the surface to activate the cell.
In the lab we’ll use IgE that’s been chemically cross-linked; it won’t make aggregates. You can use antibodies against IgE. You can use antibodies against the receptor. In chronic urticaria this is the mechanism. Patients that had chronic hives for years, the allergists knew from experience that they were unlikely to find anything that these patients were allergic to. Recently, it was figured out that these patients frequently have made autoantibodies either against IgE or more commonly against the receptor itself, so they are activating the cells sort of like the anti-thyroid antibodies that cause thyroiditis or like in myasthenia gravis. You can use antibodies against the idiotypes (used in lab).
Finally, mast cells can be stimulated by lots of different stimuli. Ionophores cause the cell to become permeable to different ions, like Ca, but they also have complement receptors and can activate with C3a and C5a, the anaphylatoxin type molecules.
10. Mast cells can spit out a wide array of preformed mediators, primarily histamine. We’re not entirely sure of the physiologic function of many of these others, like tryptase and chymase these are proteases.
Acid hydrolases cleave polysaccharides. There are also proteoglycans. We know exactly what histamine does; it’s an inflammatory mediator and the purpose of the mast cell. Mast cells are concentrated in the epithelium, the skin, GI tract, and respiratory tract. They’re sentinels, looking for damage to call in the inflammatory cells and one of the things that histamine does is it increases vascular permeability, so all the things in the local environment flood out into the tissues, tissue proteins like IgG, complement and cells like neutrophils.
Newly formed mediators are produced also. These take from minutes to hours. Prostaglandins and leukotrienes are lipid-derived mediators from arachadonic acid released from membrane lipids. The cells make a wide array of cytokines, particularly TNF, which is an inflammatory cytokine.
11. Tryptase is a protease that’s released by mast cells. The one reason to know about this protein is that it persists in the blood for several hours after anaphylaxis. If a patient has an episode that could be anaphylaxis, it can be very helpful diagnostically, because it is around in the serum if you’ve had massive mast cell mediator release. This protein is released in the blood and the level rises substantially and you can measure that and then measure hours later and see when it returns to normal levels. For example, a person is found collapsed and you need to figure out what happened to him, did he get stung by an insect or did he had a heart attack, this can be helpful in determining.
12. Histamine is the prime mediator in the acute process associated with Type 1 hypersensitivity. It’s produced in large quantities, measurable amounts in a single mast cell. It produces huge pharmacological amounts in a local area and it has these types of effects in that local area. Intense itching (pruritus), it’s used as a control in allergy skin tests and it’s very irritating. Place a drop of histamine solution and make a prick in the skin and 10-15 minutes later the patient is itching like crazy.
It’s exactly the same in your nose when it’s released physiologically by ragweed pollen. That is mediated mainly through interactions with H1 histamine receptors.

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Sara McGowan pg. 4
There’s also a very prominent effect on the vasculature, increased vascular permeability, which causes swelling, congestion in the nose. True urticaria is typically elevated because serum proteins are pouring into the tissue, causing swelling. Smooth muscle contractions, in the lungs that equates to bronchospasms or asthma attack. It also stimulates gastric acid secretion through H2 receptors
13. There’s a so-called triple response that you see when you inject histamine or when histamine is released. You get local erythema, an area of redness around the injection site itself, which is caused by direct interaction with H1 receptors on the vasculature but there’s a more widespread of erythema that’s caused by reflex neural response, so if a patient has damage to a cutaneous nerve and that areas’ numb, they don’t have sensation, they won’t get that secondary flare. If they have an underlying or an inherited neurological problem where people have insensitivity to pain and their cutaneous nerves are not functioning properly they won’t have flare. Sometimes we use it diagnostically. Lastly, there’s this wheal (welt) that’s produced by increased vascular permeability. A welt is an area of swelling.
14. This is the process of IgE production. This is mostly controlled by genetics. We’re still trying to figure out why some people make IgE to innocuous things like pollen. The suspicion is that in primitive society where parasites were a lot more important, IgE was more important because parasites can be deadly and IgE plays a strong role in the control of parasite infection, it targets parasites and it also goes up tremendously in people with parasite infection.
In our super hygienic society, we’ve largely eliminated parasites, the IgE system is just looking around for something to do and sometimes in some people with a tendency to make more IgE responses, it gets us into trouble with allergies. You produce isotype switching, so the B cell is now making IgE. With further stimulation you get differentiation into plasma cells and memory cells. The plasma cells begin pumping out IgE. IgE binds irreversibly to the mast cell and can persist there for weeks or months on the surface before it’s cleared. Then it’s triggered by an allergen such as ragweed pollen, releases theses mediators, particularly histamine and causes all these secondary effects.
15. We’ve divided IgE, the release, into two different areas: the early response, which occurs within minutes and the late phase response, which takes hours. The early response is almost entirely due to histamine. There’s a contribution with prostaglandins and leukotrienes, which are released pretty rapidly, but you can reproduce most of the effects with histamine.
The late response is more cellular in nature. They’re caused more by cellular infiltrate largely due to the effect of cytokines that are secreted by the mast cell. This is the effect that can cause serious nasal congestion, serious congestion in the airway and usually, if you do have ragweed sensitivity, you’re not just getting an acute challenge from today when you walked into class, you’re still dealing with the effects of the challenge you got last night when you went home. So, you’re having a delayed phase when you come in and then you get another acute phase superimposed on top of it, but we’ve been able to separate these out in the lab to study them.
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Sara McGowan pg. 5
17. This is what might happen to you if you go to an allergist. This is the skin testing. They take extracts made from different things, pollen, dust mites, etc, and use the skin as a test bed to see if you have IgE against those. This person is atopic. He’s having huge reactions to most of what he was tested for. You can see this area of erythema around it and a central wheal, which is the pale, raised area.
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19. Most of our therapy is designed to deal with the after-effects of mediator release. We do have some indication that topical steroid, which are used in the airways as well as the eyes, occasionally, for severe allergic conjunctivitis. They are anti-inflammatory and will inhibit the effects of mediator release.
They inhibit the influx of cells into the area it’s in. They may also inhibit mast cell mediator release when they’re used in high enough doses topically.
The mechanisms that are really used to prevent mediator release, most commonly, are shots or immunotherapy and when they’re done properly they have been shown to work. If you’re allergic to everything, you can’t take shots, but if you’re allergic to ragweed and nothing else, if you’re given injections of large enough amount of ragweed pollen, done in increasing concentration to a maintenance dose, you will begin making IgG, which will act as a blocking antibody to block the allergic reaction.
Most recently, we have a monoclonal IgE antibody called Xolair, which binds circulating IgE and prevents it binding to the mast cell to begin with. It doesn’t really lower the level of IgE, but it lowers the effective level. Also, strangely, the receptor numbers on mast cells and basophils drop if there’s no IgE around. This is approved for allergic asthma and it may have a role, which is not approved yet, but it may be beneficial for food allergies or maybe severe upper respiratory allergies. It’s very expensive.
The most common therapies are the medications that deal with the after-effects of mediator release.
Anti-histamines mostly act at the H1 receptor. Leukotriene receptor antagonists; there only a few of these. Topical and systemic corticosteroids can be helpful also.
20. So, Type 1 reactions are what we worry about the most, but we do see these others occasionally.
Types 2 and 3 both depend on complement and Fc receptors on phagocytes. The difference is where the immune reaction is occurring.
21. In Type 2 reactions, the reaction is occurring on surfaces, so antibody binds to a surface that it’s not supposed to and then complement is activated, phagocytes to both the antibody and the complement and cause damage. This can occur through complement and also through a mechanism called antibodydependent cell-mediated cytotoxicity. If cells have antibody on their surface there are other cells that will come in and destroy them through targeting through the Fc receptors.
22. This is what we’re talking about. This is the activation of complement through IgM and IgG on surfaces. IgG arms the non-specific cells, like NK cells, neutrophils, and macrophages particularly. Those together cause the damage.

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Sara McGowan pg. 6
23. This is a cartoon I like that shows the whole process. This is supposed to represent IgG bound to epitopes on the surface of a target cell membrane. C1 can bind to those and activate complement and deposit C3b on the surface. Phagocytes have receptors for C3b as well as the IgG, so that targets the phagocytes and then C3b can form part of the C5 convertase to continue complement activation and form the lytic pore called the membrane attack complex that causes cell damage and death.
24. This is the process that’s supposed to happen. The phagocyte is supposed to be targeted to harmful invading microbes, through complement fragment C3b and IgG. It uses those to target the organism, endocytose it and destroy it, but if those things are coating a body structure like the basement membrane, which the phagocyte can’t phagocytose anyway, it will go through a process called frustrated phagocytosis and secrete toxic oxygen radicals, proteases and other enzymes and cause tissue damage. This can be a very hot, inflammatory reaction. It can cause major damage.
25. There are several different types of diseases that are associated with these types of reactions. Some of them are things that occur normally in life like Rh incompatability produces a disease called hemolytic disease of the newborn. Often they are things we are doing, what we would call iatrogenic; things like transfusion reactions, hyperacute graft rejection and drug induced hemolytic anemia.
26. How do these things work? For transfusion reactions, in the 30’s Lanstiener got a Nobel Prize for working out the genetics of the human ABO blood group system. It turned out to be very simple
Mendelian system. Many of the sugar moieties that decorate proteins on the cells of our body have these ABO antigens complexed to them. The core antigen is called the H antigen and it has a galactosefucose moiety and if you have the A enzyme, you hang an N-acetyl-galactosamine on the end of the galactose and if you have the B enzyme you’ll hang a galactose there. If you have both enzymes, you have both antigens decorating the cells.
It turns out that bacteria in the colon also have these antigens and that’s why we make antibodies to them. If you don’t have either enzyme, you have blood group O, you have the H antigen, but you don’t have the others, your body recognizes the carbohydrates on the bacteria in the gut and you have IgM antibodies in very high titers. If somebody were to give you some blood containing red blood cells containing one of these antigens, you would have a devastating immune reaction. You would have a high fever, muscle aches and chills, blood in the urine and sometimes die and it’s because you have these naturally occurring IgM antibodies against the A and B antigens.
A patient who’s O negative is the universal donor, doesn’t have the Rh antigen, and doesn’t have the A or B antigens. Those are the people that blood banks love because in an emergency situation where someone needs blood fast, you can give them O negative without typing their blood. Someone who is
AB positive can receive blood from everybody because they do not have A or B antibodies. (He forgot to mention) Because of tolerance, if you have these antigens on cell surfaces you don’t make antibodies to them. The immune system automatically down regulates any harmful antibodies, so you can’t make the anti-B antibody if you have the B antigen on your cells. It turns out the blood antigen groups are very numerous and there are many other antigens you can develop antibodies to as well, but they’re not

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Sara McGowan pg. 7 usually present before you’ve been sensitized, so you’d have to receive blood repeatedly from someone who’s got that antigen before you develop antibodies like you do with most hypersensitivity syndromes.
27. Here’s the disease I was mentioning and is not really iatrogenic. If you have an RhD- negative mother who marries a RhD+ and they have a baby who is RhD+, some of the baby’s cells get into the mother’s circulation in the initial pregnancy, particularly during birth and the mother begins making RhD antibodies. With a subsequent pregnancy, the anti-Rh antibodies are transferred to the baby by the placenta. The placenta has an Fc receptor whose primary purpose is to move IgG into the baby’s circulation, so the baby will be protected at birth. For the first few months, the baby has the mother’s entire complement of IgG. If you have put an RhD antibody into a patient that’s Rh+ you begin to have blood breakdown and the fetus would go into high output heart failure, develop massive edema, basically die in utero many times because of severe anemia.
28. The solution is to give the mother an injection of antibody to the D antigen, which was initially gotten from pregnant women that developed the antibody, that it bound up all the baby’s blood cells in the initial pregnancy so there was no sensitization and they didn’t make the antibody. Once this was discovered, the incidence of Rh disease to the newborn plummeted to close to zero. Any woman who’s
Rh negative automatically receives this injection when the baby’s delivered.
Student Question: Why don’t baby’s with parents of different blood groups have problems (e.g. O mother, A father)? D antigen is more antigenic or more potent. Blood antibodies are IgM and do not cross the placenta.
29. Drug hypersensitivities can cause a wide array of hypersensitivity syndromes. The usual way that this is thought to happen is the drug complexes on the surface of the cell, you make antibodies to the drug, the drug binds, activates complement and you get breakdown. Also, red cells are important in clearing immune complexes; they have complement receptors on their surface. If these complexes activate complement strongly enough you can get bystander breakdown of the cells. Since this is drug-related, most of the time it’s self-limited and it goes away after a little while.
It’s thought that sometimes you can develop autoimmune hemolytic anemia that’s thought to be caused by the persistence of a cross-reactive antibody. In other words, you get sensitized to something on the cell surface that looks like one of your own proteins, there’s a breakdown of tolerance and the antibody which cross-reacts to this shape now can react and give a fully autonomous long term problem.
Sometimes this can cause life-threatening fatal anemia, if it’s bad enough.
30. This is the third type f condition called hyper acute graft rejection. This is what happens if you focus on the transplant group, the MHC complex, and ignore the ABO blood type. This is an ABO incompatibility. When you put in an organ that contains one of these antigens into a patient that has preformed circulating IgM, which activates complement very well, it basically toasts this organ. This organ was removed hours after transplant.
31. The third type is immune complex-mediated and this is very similar to the previous one, except the antigen antibody initially occurs in solution. There are some important conditions that we see with this

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Sara McGowan pg. 8 type of reactivity. It used to be thought that this one really didn’t require Fc receptors, didn’t require cellular input, but that’s probably not true. It’s hard to prove this in humans, but in animals it looks like you need cells to be involved in the process. At least the initial part has to do with the formation of immune complexes in solution, activation of complement, activation of mast cells, basophils, etc.
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33. There are several diseases that are associated with this. The arthus reaction, which we’ll talk about.
A group of strange diseases (referring to the group of hypersensitivity pneumonitis) that are not very common but are used as examples of this type of condition. Immune complex-meditaed glomerulonephritis, kidney damage caused by these immune complexes that form in the blood and lodge in the glomerular wall in the kidney and can cause major damage. That’s not rare at all; we see that in a number of different conditions. Serum sickness is related. One of the effects of serum sickenss is immune complex-mediated glomerulonephritis.
34. At the beginning of the 20 th century, Arthus was experimenting with serum as a therapeutic agent. If you got diphtheria, the diphtheria bacteria made a deadly toxin and causes damage to the respiratory tract. They used anti-toxin made in horses. They take a horse, immunize it repeatedly with inactivated toxin and inject the horse serum and inject it into the person with diphtheria and it was frequesnrly helpful. This strategy is still used with snakebites. Make anti-serum to snake toxin in a horse and give it to people.
He noticed that when they injected horse serum repeatedly into rabbits, the rabbits got this progressively more and more severe tissue reaction at the site, which eventually caused necrosis. It’s caused by activation of complement and phagocytes. The main thing is complement, it’s reduced if you deplete complement in the animal, it peaks after 3-6 hours and neutrophils come pouring in. This is seen in patients that get repeat immunizations, e.g. second tetanus after a few months, you will get an
Arthus reaction at the site of injection because your immune system has already formed a lot of complement activating antibodies. That’s why we usually don’t repeat these immunizations, especially in older people, at less than 5 years time, because you’ll have a pretty vigorous immune response. You can get a sterile abscess at the site.
35. When you inject these antigens into the body, if there’s preformed antibody, it complexes, activates complement, complement fragments cause both mast cell activation and activation of neutrophils. They increase vascular permeability and the whole inflammatory process occurs at the site. Eventually, you can get tissue liquification necrosis and form what’s called a sterile abscess from the intensity of the reaction.
36. There are a group of weird diseases, where you have preformed antibody. These are respiratory diseases. For example, the farmer walks into his silo and he’s sensitized to some spores from bacteria that grow in the silage and later that day has a cough and a low fever. He goes to his doctor and has infiltrates in his lungs. He’s getting an Arthus reaction along the airways and it causes a significant inflammatory reaction. You may have to give up your pigeons if you become allergic to the avian proteins. You may have to find a different line of work in all these instances. They are all rather rare.

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Sara McGowan pg. 9
37. Serum sickness was noticed when they were using serum therapeutically. We still see it in people who get treated for snakebites. It takes days to weeks to occur. You’re getting a very complex mixture of foreign proteins injected into your blood or tissue when you get anti-serum solution. You begin to make antibody, but it takes days to weeks for the antibody reaction to mature, but when it does occur, you get immune complexes forming and you get this syndrome of rash, joint pain, swollen glands, occasionally blood in the urine. Usually it’s self-limited, due to some exposure in the environment.
Sometimes infections, viral infections can trigger it, allogeneic serum or drugs.
38. This is the way the serum sickness reaction works. Instead of occurring in the tissue, you’re getting immune complex formation inside the blood vessels. The immune complexes are forming; they’re activating platelets and basophils, which release vasoactive amines. Platelets have serotonin and basophils have lots of histamine. That increases vascular permeability.
39. And then you get the usual cascade of inflammation occurring. You get immune complex deposition in the vessel wall. More complement activation calls in phagocytes that cause damage to the vessel wall and you can have significant inflammatory reactions in the vessel wall that can destroy it. This can cause hemorrhagic rashes.
40. These types of vessel inflammation tend to occur where there’s a lot of convolution of the blood vessels like in the glomerulus, the choroid plexus, the brain, the ciliary body in the eye and at branch points in the blood vessels. That’s where the endothelium is little ruffled and there’s a lot of turbulence.
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42. We’re just going to touch on Type 4 hypersensitivity. Poison ivy reaction is one of the Type 4 hypersensitivity syndromes. It’s very illustrative of the symptoms you can have.
43. It’s a cellular process, so it doesn’t occur immediately. It usually takes at least 24 hours to become noticeable. If you go to an ER or to a primary care doctor with poison ivy, they always prescribe antihistamines, but that doesn’t do anything for type 4 reactions other than make you sleepy because this is not a histamine-mediated process. The only thing that really helps are steroids, either topical or oral. That’s the usual treatment other than teaching someone to avoid poison ivy or whatever is causing the problem. The antigen is presented to the T cell; you get T cell activation, differentiation of specific delayed-type hypersensitivity T cells that localize to the area. They call in other T cells, which may be more non-specific. They activate macrophages in the area and they can cause lytic damage to keratinocytes and other cells in the local area.
44. When macrophages get activated by cytokines by these delayed-type hypersensitivity cell, particularly by interferon-gamma, they become activated and much more active in terms of secreting proteases, secreting toxic oxygen radicals, etc, that cause a lot of tissue damage.
45. The real reason that we have this reaction to begin with is to deal with infection. This is designed to combat infections that are really hard to get rid of, like TB. This inflammatory reaction produces eventually, if it persists long enough, something called a granuloma where you have a little knot of

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Sara McGowan pg. 10 activated macrophages sometimes multicellular giant cell, multinucleated giant cells, activated epithelioid macrophages, surrounded a palisade of T helper cells that help keep the organism walled up, if not killed, so it doesn’t spread.
Student Question: Can you spread poison ivy from the rash? You can spread the oil, so wash with soap and water after contact. Once it’s been going a while, it’s not going to spread per say, new rash that comes up was going to come up anyway, assuming that you washed the affected area.
46. These are the types of type 4 hypersensitivity reactions. We talked about contact dermatitis with poison ivy. Foreign body reaction is a similar reaction and type 4 reactions are seen with chronic infections and chronic graft rejection.
47/48. Ocular allergy, ocular contact allergy is seen a lot in medicine and can be caused by a very large list of different types of things in the environment like cosmetics or medicines. A typical history for the doctor is that the patient had something like pink eye and is given an eye drop, then gets a little better and then gets progressively worse and the key is that with ocular contact allergy, the thin skin around the eye also becomes eczematous and red in addition to the conjunctiva.
49. You get a lot of inflammation in the sclera, watery discharge, itching.
50. This lady had contact from hair dye. Many times they’re cosmetic products and the thin skin around the eyes is more sensitive and more likely to have a reaction even if the product is applied to the hair properly.
51. The treatment is get rid of the product and you can get diagnosed at a dermatologist to come up with a list of suspects. They’ll try patch testing with different things to elicit the same reaction on the skin, under the patch after exposure to the substance. Cold compress and occasionally steroids are used.
52. Watch out for poison ivy.
53. It secretes an oil called pentadecacatechol, which is metabolized and epitopes are presented to T cells by the usual type of mechanism.