Posts Tagged ‘bracket fungus’

Moulds and Other Fungi

The air around us is full of bits and pieces that are mostly too small to be seen without a microscope - pollen grains, mould spores, fragments from plants, fibres from clothing, specks of ash from smoke, skin flakes and diesel particles. Of these, mould spores are by far the most abundant.
Except in very dry climates, there are more mould spores in the air than anything else. In Britain the record count is over 160,000 spores per cubic metre of air, compared to a record pollen count of only 2800 grains per cubic metre. Luckily, mould spores are not particularly allergenic or even more people would be suffering as a result of inhaling such huge quantities of them.
Spores are produced by moulds and other fungi, and they are to the fungus what seeds are to a plant – they can grow into new fungi. Doctors generally speak just of ‘mould allergy’ because moulds are the most common offenders, but larger fungi – mushrooms and toadstools – also produce allergenic spores. For example, a bracket fungus called Ganoderma, that infests dead trees and produces spores prolifically in mid-June, has been found to affect 16% of asthmatics in one part of New Zealand. Bracket fungi occur all over the world, but until recently no one had suspected them of causing allergic reactions, so the extent to which they cause allergies has not been investigated. The same is true of other large fungi.
Yeasts (single-celled fungi) are also found in the air, and it is possible –though this has not been investigated – that people with an allergy to yeast in food would also react to inhaled yeasts.
Indoors and out
Mould spores are a particular nuisance because they can be produced both indoors and out. There are different species of mould in different places, and you may be lucky and only react to one or two uncommon species. But many moulds grow in a very wide range of situations, both indoors and outdoors. There are also cross-reactions (see p. 14) between some of the moulds, unfortunately, which means that people generally react to a great number of different moulds. You will probably need to reduce mould growth inside your home as well as avoiding mould-rich places outside. Changes to your garden that eliminate havens for moulds, such as leaf piles, may also be helpful.
Moulds may only be growing in one part of a house – the cellar perhaps – but can be carried all around the house on air currents.
The size of the allergen particles
Most mould spores are between 2 and 10 microns in size. A few species have spores that are smaller than 2 microns.
(A micron is one thousandth of a millimetre.) Some people with mould allergy may be protected by an ordinary dust mask (see p. 109), but most will probably need a better-quality mask.
Avoiding outdoor moulds
Moulds live in the soil, and grow on any decaying plant matter, such as dead leaves, dying plants, fallen trees, hay and straw. Spore counts are highest in the autumn. A thick covering of snow reduces the numbers of mould spores in the air dramatically. Once the snow melts in spring, moulds flourish on the plants killed by the cold, so spore counts soon rise again.
The effect of the weather on spore release is very complex. Some moulds like to release their spores when it is dry and windy, but others favour fog, mist or dew. Rainfall washes a lot of spores out of the air, but it stimulates the release of some small spores.
A few pollen information services also give current mould-spore counts, but predicting spore counts for the following day is well-nigh impossible.
Drastic avoidance measures, for those who are severely sensitive, include moving to a desert or semi-arid area where there are far fewer mould spores in the air.
Listed below are the mould-rich situations and activities which could provoke your allergy symptoms. If they do, you should avoid them, or wear a mask that will prevent the spores being inhaled (see box on p. 120).
Places
• Near fields of cereal crops in late summer, because of moulds growing on the cereal leaves. Symptoms are likely at harvest time, when combine harvesters disperse the spores.
• In forests and old orchards, in gardens with compost heaps or piles of dead leaves, and in greenhouses.
• Near springs, waterfalls, and other damp, shady places.
Times
• During late summer and autumn, when moulds flourish outdoors on fallen leaves and fruit.
• Following the first frost of autumn, which triggers spore release by fungi in the soil.
Activities
• Disturbing compost heaps, damp straw or hay, piles of grass clippings or heaps of fallen leaves, all of which are absolutely full of moulds.
• Collecting up fallen leaves or fruit.
• Watering the garden because mould spores are released when water hits the dry soil.
• Mowing grass, if the clippings were not cleared up after the last mowing. Unless the weather is very dry, the clippings tend to go mouldy.
• Removing dead leaves or flowers from plants.
A dangerous mould allergy
Anyone with asthma who also has allergy to the mould Alternaria should –with their doctor’s agreement – increase their dose of preventer inhaler (e.g. steroid or cromoglycate) during the spore-producing season. Research shows that severe near-fatal asthma attacks often occur during the Alternaria spore season among those allergic to this mould.
Spore release by Alternaria usually occurs in the summer or autumn, but the timing varies from one part of the world to another, so check with your doctor or a local pollen/spore monitoring service. Alternaria can live outdoors in soil, and on seeds and plants. Indoors, it is a denizen of window frames, carpets and textiles.
Indoor moulds
These are the indoor situations that can be difficult for mould-sensitive people. You should either avoid these, wear a mask, or tackle the problem at source – for example, by reducing dampness (see p. 119).
Places
• Buildings that are damp, because moisture encourages mould growth. Never sleep in a room which has mould growing on the walls or window-panes. In addition to damp houses – now very common – you may encounter moulds in old churches and church halls.
• Buildings that are near lakes, rivers or the sea, because of the dampness of the air. Rooms with humidifiers.
• Bathrooms and shower rooms, unless well ventilated, owing to the steam and condensation.
• Rooms that are generally left unheated, and are therefore colder than the rest of the house, as these tend to suffer from condensation.
• Buildings with dry rot or wet rot. Not all mould-sensitive people react to the spores of these dreaded timber-rotting fungi, but some do.
• Buildings where old timbers are being removed, as this stirs up huge numbers of spores.
• Buildings where central heating has recently been installed, as the warmer temperatures in the building stimulates the existing moulds to release their spores.
• Buildings with lots of indoor plants. There are moulds you cannot see growing on the surface of the soil around a potted plant.
• Cellars and basements. Conservatories can also be full of moulds if not well maintained.
• Antique shops, farms, mills, holiday cottages.
On the first day of Christmas…
Christmas trees usually have moulds (which you can’t see) growing on the needles. When the tree is brought indoors, the warmth encourages these moulds to shed their spores.
Times
• During the winter, when there are usually more moulds growing indoors due to condensation.
Activities
• Handling clothes, curtains or furnishings that smell mildewy: they may be dry now but they will still be full of mould spores.
• Handling vegetables or fruit that have been stored a long
time, or in damp conditions (e.g. in plastic wrapping). Note
that this can include mushrooms – they often have white
moulds growing on them, which can be quite inconspicuous. If looking around your house for moulds, bear in mind that they vary a great deal in colour. Bread, vegetables, cheese and other foods that are past their best grow green, grey or white moulds, often furry, and these are the ones most people are familiar with. But the black stuff on the walls of bathrooms and in the door seals of refrigerators is also mould. In some situations it takes a practised eye to spot this type of mould – around window frames for example, or in the patterns of bathroom-window glass, it can easily be mistaken for ordinary dirt. On shower curtains and cubicles you may find pinkish-red moulds as well as these black kinds. Garden plants and crops can have bright orange moulds (called ‘rusts’) on their leaves, as well as the more familiar grey or black kinds.
Combating indoor moulds
The crucial task here is to reduce dampness and condensation in the house – see p. 119 for the details – as this encourages mould growth on all kinds of surfaces, including walls, ceilings, windows, bathroom tiles, shower curtains, and even carpets. Once you have reduced the humidity, then you can have a big clean-up and remove the spores that have been left by moulds.
If your allergy symptoms are very bad, and you need some immediate relief, then you could get someone to clean away the mould growth and spores first, then tackle the damp problem, then repeat the cleaning operation. Obviously, this is less efficient, but it may be the best approach if you are severely affected.
Note that the cleaning will, in itself, stir up a massive but unseen cloud of spores, so the allergy sufferer should not be at home during this work (see p. 109).
Cleaning away moulds and stopping regrowth
There are two aspects to this task:
• a one-off effort to clear the accumulation of mould growth and old mould spores – trillions of them are probably lying around your house – since these spores are the cause of the allergic reaction
• an ongoing effort to prevent the regrowth of moulds in problem areas such as the bathroom.
Get rid of any furniture that smells ‘mildewy’: it is packed with old mould spores. Fabric items that have this smell should be washed thoroughly. Old clothing, books and newspapers may also be a source of mould spores.
Any carpets or other porous materials (e.g. ceiling tiles, wall panels) that have ever been soaked by flood or storm waters should be disposed of now – and, unless everything can be dried within 24 hours, this should be always be done if there is water penetration in the future. Research shows that such materials quickly become infested with moulds. Check above the flood line, as water can seep upwards through the walls or panelling.
On fridges and freezers, clean out the rubber seals around the doors, going into all the crevices to get out the black mould that lives there. Also clean out the drip-pans of fridges, freezers and dehumidifiers. Keep shower heads and air conditioning equipment (including the filters) very clean. This all needs to be done regularly from now on.
Clean off all the mould growing around windows, or on walls and ceilings, tiles or other surfaces. Alcohol (e.g, white spirit or surgical spirit) kills it very effectively, without the use of water, and it takes a long time to grow back again. You could, alternatively, wash down the walls with a mix of one part bleach to two parts water. (But note that chlorine fumes may be irritating to the airways of those with rhinitis or asthma.) Special anti-mould sprays are also available, but try them out cautiously as they too may be irritants. Do not brush mould growth off with a dry cloth, as this simply disperses the spores. In the future, keep an eye out for new mould growth, and remove it promptly.
Buy a new shower curtain and replace it regularly, or clean it thoroughly with an anti-mould spray.
Can foods and mould spores cross-react?
Some people with mould allergy appear to be affected by eating mushrooms, or foods that contain yeasts or other fungi, e.g. certain well-ripened cheeses, dried fruit, soy sauce and vinegar. There has been little scientific investigation of these claims.
No cause for concern
The drug penicillin – which can cause severe allergic reactions – comes from the Penicillium mould. Fortunately, there appears to be no cross-reaction between the drug and the spores of Penicillium.
Cut down on the number of houseplants, and find a new home for any that need constant moisture. With the remaining plants, take off dying leaves and flowers promptly, and remove the top layer of soil occasionally, replacing it with fresh soil or – even better – sand or grit. Pot-pourri should also be evicted, as it can be full of mould spores.
Use vegetables and fruit promptly, and do not allow bread to go stale, or jam to go mouldy.
What to do if these measures fail
Where there is an invincible damp problem, a really powerful dehumidifier used during the day in bedrooms, and at night in the sitting room, will kill off most moulds and defeat their efforts to regrow. Close all the doors and windows in the room where the dehumidifier is operating, and shut off air vents. Note that air conditioning will also reduce the humidity of the air, but not as much.
Keeping mould spores out of the airways
Ordinary house dust can contain a lot of mould spores. The allergic individual should not dust, vacuum clean, sweep floors or make beds until the anti-mould measures have begun to bite. Ideally the allergic person should go out while housework is done, and the house should be thoroughly aired before their return. If this is impossible, then wearing a good mask all the time is essential. A special vacuum cleaner that retains allergens, or vents them outside. may be helpful in addition to the mask.
Even though you have cut down on moisture and condensation, and tackled mould growth, there could still be a lot of mould spores around, especially in an old house, one that has been very damp in the past, or one that is close to water. If symptoms persist, then think about hiring or buying a high-quality HEPA air filter (see p. 108) to take mould spores out of the air.
Do not use fans or fan heaters, as these churn up mould spores from the floor and other surfaces.
Beating athlete’s foot
Allergenic fungi can grow on your body, as well as in your house (see pp. 16-17). If athlete’s foot is playing a part in your allergies, it is vital to treat the infection thoroughly with drugs, because the fungus grows deep into the skin and can quickly stage a come-back if not completely destroyed. You should also be careful not to reinfect yourself:
• always dry your feet very thoroughly, especially between the toes; kitchen roll does a better job than towels, and can be discarded, reducing the risk of re-infection
• wear cotton socks and shoes made of leather or canvas, which allow sweat to evaporate; only wear trainers or gumboots, or any other footwear that makes your feet feel sweaty, when you really need to
• when your feet get wet, change your socks and shoes promptly
• launder all towels and bath mats at high temperatures when you start the course of anti-fungal drugs, and again when you complete it
• never share towels, bath mats, socks, sandals or shoes
• wear flip-flops at the swimming pool or sauna, and in changing rooms; if any other member of the household has athlete’s foot, take the same precautions in the bathroom at home – and make sure they seek treatment.
Occasionally athlete’s foot is a misdiagnosis for atopic eczema of the feet, which is a common problem among allergy-prone children (see box on p. 45). If the skin between the toes is not affected, it’s unlikely to be athlete’s foot and more likely to be eczema.

`When I first arrived in Charlottesville in 1982, the senior allergist said “I’ve got to warn you that here in Virginia we have patients who have very severe fungal infection of their feet, and they also have urticaria. If you treat their feet, their urticaria gets better.”‘ Professor Tom Platts-Mills of the University of Virginia in Charlottesville is recalling how his innovative studies of fungal infections and allergy began. That surprising observation about athlete’s foot (a fungal infection) and urticaria (nettle rash) was made by his predecessor, Professor John Guerrant,
‘I followed his advice,’ Platts-Mills continues, ‘and found he was right. Then I started noticing asthmatics in our allergy clinic who also had fungal infections of their feet. They were mostly men with severe adult-onset asthma. We gave them skin-prick tests with the fungus Trichophyton and these were positive – showing they had an allergic reaction to it. So we tried treating them with anti-fungal drugs and the asthma got much better.’
This discovery is not an isolated instance. Research over the last decade or so has revealed that allergic reactions to long-standing infections (chronic infection is the medical term) are far more common than anyone expected. Infections by fungi are frequent offenders.
An infection becomes chronic because, although the immune system tries to rout the infectious agent, it never succeeds. Making IgE may be part of that futile defensive effort. Once the immune system starts making IgE against the allergens produced by the infectious microbe, new symptoms may begin, or existing allergic symptoms may get much worse. The link between the infection and the allergy is far from obvious, however. Both the allergens and the IgE can be carried in the
Fungal infections
‘Fungus’ means everything from an edible mushroom or a huge bracket fungus to the specks of mould on stale bread or a shower curtain. Fungal infections are caused, not by mushroom-like fungi, but by inconspicuous mould-like forms, or by yeasts (which are single-celled fungi).
Once they are flourishing, some fungal infections may be seen as whitish or creamy-coloured patches. But at an earlier stage, the fungi are so small that they cannot be seen without a microscope. They spread as invisibly as bacteria or viruses.
Some infectious fungi can exist in two different forms – a mycelial form (long thin strands, as in a mould) or a yeast form (single cells).
bloodstream, so the symptoms may be somewhere else in the body, far away from the site of infection.
If the symptoms of the infection itself are relatively mild, they may not receive medical attention. Infection-plus-allergy often explains severe long-term allergic problems for which no cause could previously be found. This is the kind of case that gets labelled as ‘intrinsic’ or ‘endogenous’, because all the allergy tests have proved negative. Most patients in this category have had years of simply being treated with steroids (often at high doses) to suppress the symptoms.
Sometimes the infection-plus-allergy is part of a larger picture, with other allergens or irritants also contributing to the symptoms, but with no stunning improvements when they are avoided because the allergic stimulus from the infection remains.
The links between allergy and fungal infections – all those that have been discovered so far – are described below. In such cases, anti-fungal drugs, taken by mouth, usually in capsule form, could be of value. However, they must be taken for an adequate length of time, normally several months.
Bear in mind that, with the possible exception of chronic sinusitis, an allergic reaction to fungal infection is a relatively uncommon cause of symptoms. It is important that, with the help of your doctor, you start with the more likely suspects such as airborne or contact allergens. These are described in detail, for each allergic disease, in the relevant sections of Chapter 2.
Asthma
the common causes and usual treatment of asthma.
Trichophyton – the fungus that causes athlete’s foot – can provoke allergic reactions that contribute to asthma, as already described. This fungus may also infect other parts of the body. Trichophyton diseases have names that begin with tinea (athlete’s foot, for example, is tinea pedis). Other terms you may come across are intertrigo (an itchy rash which develops in skin folds) and onychomycosis (also called `ringworm of the nails’ or tinea unguinum). The research on the link with asthma was published in a respected medical journal, The Lancet, but has been widely ignored, so if you think you have this problem, you may have to be quite persistent with your doctor. Very thorough treatment with anti-fungal drugs (swallowed in capsule form) is required.
Chronic urticaria
many possible causes of chronic urticaria.
Trichophyton infections in any part of the body (see above) can provoke allergies, producing chronic urticarla. A great variety of other infections, including fungal, viral and chronic bacterial
infections, can be the root of the problem in chronic urticaria . However, this may not be an allergic reaction. It could be a direct effect of the infection, provoking the immune system in such a way that it triggers mast cells by itself, without IgE.
Chronic sinusitis
 the causes and treatment of chronic sinusitis.
Long-standing (chronic) sinusitis may be due to a fungal infection with a subsequent allergy. This is now called allergic fungal sinusitis. Some doctors believe that a sensitivity reaction to fungal infection (not necessarily an allergic reaction) could account for 96% of chronic sinusitis. However this is widely disputed .
Atopic eczema (atopic dermatitis)
the causes and treatment of atopic eczema.
The Trichophyton fungus can infect eczematous skin, though this is far less common than infection by Staphylococcus aureus (see below). Among patients infected by it, there can be an allergic reaction to Trichophyton which then makes the eczema worse.
There can also be an IgE reaction to a yeast, Pityrosporum ovale (also called Malassezia ovalis), in atopic eczema. This yeast is a commensal – i.e. a natural, and normally harmless, inhabitant of healthy skin. The inflammation of eczema makes the immune system far more tetchy so that it reacts allergically to this yeast, an innocent bystander which it normally disregards.
Candida  can also provoke an allergic reaction in eczematous skin. This is a more complex story, because while Candida is a commensal in the gut, it does not normally live on the skin. However, it may flourish in the disturbed skin of eczema patients.
Those with atopic eczema may also develop an allergic reaction to toxins from Staphylococcus aureus, a bacterium that often infects skin which is inflamed by eczema and damaged by scratching. Antibiotics are needed to treat the infection .
Seborrheic dermatitis
Not so long ago, this disease – which causes a red, scaly rash on the forehead, nose and cheeks, and sometimes on the chest –was labelled ’cause unknown’. Now most doctors believe that the yeast Pityrosporum ovale could well have a role in causing it. This yeast is part of the normal skin flora (see above), but it is found in greater numbers on the skin of seborrheic dermatitis patients. As well as overgrowth of the yeast, there is an immune reaction against it, usually involving the antibody known as IgG, rather than Fungi in the lungs
One form of infection-plus-allergy has been well recognised for many years - allergic bronchopulmonary aspergillosis, often shortened to aspergillosis.
The problem starts with the fungus Aspergillus fumigates, a ubiquitous mould that is found in special abundance in damp straw, compost heaps, bird cages and any decomposing material. Its spores are everywhere, and most immune systems quickly defeat them, but in some people, especially those with asthma, the spores begin to grow in the lungs. The fungus is found in the lung mucus, but does not actually invade the lungs. However, an allergic reation then occurs to the fungus.
This disease often goes together with asthma, or can be mistaken for asthma. There are three clues that point to aspergillosis:
• rubbery plugs of phlegm, either golden-
brown or green in colour
• fever whenever the asthma is severe
• worsening symptoms despite treatment.
Allergic bronchopulmonary aspergillosis is treated with steroids to control the allergic reaction, and physiotherapy to clear the mucus from the lungs.
Anti-fungal drugs have not proved very effective in the past. There are some newer anti-fungal drugs that may well be more useful, such as itraconazole and terbinafine. These are not widely used for aspergillosis at present, except in patients who also have cystic fibrosis or an immune deficiency. Because there has been no large-scale trial of these drugs, they are not usually given to people who simply have aspergillosis. However, they are sometimes prescribed for people who are unable to take steroids, or are not responding to steroid treatment. Anti-fungal drugs may become more widely used in the next few years, so it is worth discussing the possibility of this treatment with your doctor.
the allergy antibody IgE. Only about 12% of people who suffer from seborrheic dermatitis make IgE against the yeast.
One problem with seborrheic dermatitis is that, while it may improve with anti-fungal treatment, it usually comes back when the treatment stops. Doctors have therefore been looking for ways of keeping seborrheic dermatitis at bay after a successful course of anti-fungal treatment. One method that seems to work is to use a good anti-dandruff shampoo, in place of soap, to wash your skin once a week.
A medical earthquake
The recent discoveries about infection-plus-allergy have not posed any serious challenge to conventional thinking about allergy, because a disease of just this kind - aspergillosis (see box at left) - was already well known. A far more fundamental shake-up of traditional ideas about allergy and sensitivity has been necessitated by new research into atopic eczema. It is little short of an earthquake in the basic concepts of allergy and sensitivity.
To understand the extent of this earthquake, you need to know about the time-honoured system for classifying hypersensitivity reactions, which recognises four distinct types:
• Type I hypersensitivity — the IgE-mediated allergies  such as hayfever.
• Type II hypersensitivity - irrelevant to allergy, these antibody reactions mainly occur after transplant surgery, if the transplanted organ is rejected.
• Type III hypersensitivity - caused by a massive overload of antibodies and antigen in the blood. It is a feature of certain infections and autoimmune diseases, and can also occur in allergic reactions, though this is rare (13).
• Type IV hypersensitivity - the odd man out, because antibodies are not involved, or are not of central importance. Immune cells that can launch a direct attack are the movers and shakers here. These attacking-cells are sensitised for a particular antigen, such as dust mite or lanolin. Type IV hypersensitivity is a very slow reaction. Generally speaking, 48 hours pass, after an encounter with the offending substance, before the symptoms appear. The most common form of Type IV hypersensitivity is contact dermatitis (54).
Mystery has always surrounded atopic eczema. Although it crops up in the same atopic families that suffer from hayfever and asthma, and high levels of IgE in the bloodstream are typical of the disease, the actual role played by allergies in causing the symptoms is far from obvious.
The results of skin-prick tests - the standard test for an IgEmediated reaction - are puzzling. Patients tend to give a lot of positive results, many of which don’t mean much - the substances concerned do not provoke actual symptoms. On the other hand, skin-prick tests are often negative for substances that clearly do cause symptoms in challenge tests. Many children who regularly get eczema when they drink cow’s milk, for example, give a negative skin-prick test to milk. This conundrum has puzzled allergists for decades.
New discoveries about eczema do not entirely solve the puzzle, but they do go some way towards an answer, by revealing an immune response that cuts across the traditional categories. The most surprising fact is that even where skin-prick tests are positive and milk-specific IgE is involved in milk-induced eczema, this is not necessarily a standard IgE-mediated allergy.
While IgE antibodies may be involved, they are not necessarily teamed up with mast cells, their usual partners in crime (see box on p. 12). Instead, the IgE molecules are attached to special skin cells called Langerhans cells and dendritic cells. These have the role of picking up the antigen and showing or ‘presenting’ it to attacking-cells in the skin (a task called antigen presentation which is the ‘go’ signal that starts off all immune reactions).
The involvement of these attacking-cells, which are sensitised for a particular antigen, was a big surprise when first discovered. It makes this resemble a Type IV hypersensitivity reaction rather than a Type I.
IgE is not essential here, it seems — some patients do not have IgE for the substance that triggers their atopic eczema — but when Langerhans cells and dendritic cells are associated with IgE they do become far more zealous. This excitement is communicated to the attacking-cells, which mount a more powerful attack.
It looks as if what really matters in atopic eczema is the presence of antigen-specific attacking-cells in the skin, plus the heightened activity of the Langerhans cells and dendritic cells. If the individual has IgE for the antigen, it can play a part, but it is not essential.
In other words, this reaction cuts across two different categories of immune response — Type I and Type IV. (However, the kind of antigens that provoke the reaction are typical of IgEmediated allergy, rather than the kind of antigens that provoke contact dermatitis.) This has been exploited in a new and more sensitive set of diagnostic tests for food-induced atopic eczema (69).
Why atopic eczema is a feature of atopic families is the crucial question that remains unanswered. One factor may be that high levels of IgE in the bloodstream (not IgE for a particular allergen, but total IgE) make the whole immune system more excitable and prone to over-react. The next few years will no doubt solve this part of the puzzle too.
Peace-keepers or aggressors?
`It is bad enough having a child on an ultra-strict diet — Tim can’t have even a trace of cow’s milk or else he becomes violently ill. What makes it worse is when people — teachers, for example —ask what’s wrong. I take a deep breath and say “eosinophilic oesophagitis” then watch their eyes roll in disbelief.’
Tim’s disease is caused by a particular type of immune cell called an eosinophil. In the right circumstances, eosinophils can be valuable — like IgE and mast cells, they are geared to destroying parasitic worms . They produce some very toxic substances to kill these invaders, and it is the toxins that cause serious symptoms for Tim and others like him.
Any disease with ‘eosinophilic’ in the name involves vast numbers of eosinophils converging on some unfortunate part of the body. The stimulus that attracts them often remains unknown but once there, the toxins they generate cause inflammation (140) of a particularly violent kind.
It is only in recent years that doctors have begun to distinguish between patients such as Tim and children with classical food allergy, and to understand the cause of Tim’s symptoms. Several different forms of eosinophilic food sensitivity are now recognised (72). The exact relationship with IgE-mediated allergy remains a puzzle, because some sufferers make IgE to the culprit food but others do not.
That is not all — the eosinophil is finally coming out of the shadows and being recognised as an important agent in classical allergic diseases as well.
The fact that eosinophils appeared during the aftermath of an allergic reaction had long been known, but their role was misunderstood. What confused researchers was that eosinophils can break down histamine, the substance that kick-starts allergic symptoms. This ability gave eosinophils the appearance of peacekeeping troops, coming in at the close of battle to restore order. In fact, eosinophils are major aggressors — they do a whole lot of other things besides breaking down histamine, most of them pro-inflammatory. They can release toxins, just as they do in eosinophilic diseases, and they attract other inflammatory cells into the area. In short, eosinophils play a big part in keeping allergic reactions going once the initial burst of activity is over. This `Late Phase Reaction’ is enormously important .