Posts Tagged ‘nettle rash’

Allergens and irritants at work
Some workplaces have very high concentrations of allergens in the air, especially if proper safety procedures are not being followed. Occupational allergies can begin with symptoms in the nose, such as sneezing, blockage or constant streaming (allergic rhinitis). You may also suffer with itchy or watery eyes (conjunctivitis), a cough, sweating and a feverish feeling. Alternatively, direct contact with the allergen can produce a skin rash (dermatitis) or itchiness and swelling (contact urticaria/nettle rash and angioedema).
If you work somewhere with an allergy risk (see pp. 133-4), be vigilant for such symptoms and see your doctor immediately. These symptoms can be the forerunners of occupational asthma, which is a serious and potentially irreversible problem. Some allergens, such as latex, can even produce anaphylactic shock (a life-threatening allergic collapse).
Skin-prick tests (see p. 91) can show if you have an allergy to a substance encountered at work.
Acting promptly gives you the best possible chance of recovery and is vital if you have occupational asthma. Only if exposure to the allergen stops promptly do you have a good chance of shaking off the asthma. See your doctor as soon as possible and ask for a referral to a chest specialist, so that a definite diagnosis can be made. This is essential if you are going to make a claim for compensation.
Far too many people with occupational asthma are just sent off with an inhaler when they first see their doctor. By delaying the moment when work is identified as the source of the problem, and the exposure to the allergen is stopped, drug treatment can turn occupational asthma into a disabling lifelong problem. Although drugs can be helpful in speeding your recovery once exposure to the allergen
Latex allergy
Sensitisation to latex usually occurs at work (see pp. 133-4), or as a result of having many surgical operations. But latex allergy sometimes occurs in allergy-prone people even though they don’t work in a high-risk job and haven’t had many operations. Some doctors think that if a child with severe allergies needs surgery, this should be done in latex-free conditions, even though the child has no allergy to latex, because of the risk that the operation will sensitise.
Latex can cause either contact dermatitis (see p. 55) or a Type I allergy, whose symptoms can include urticaria, asthma and anaphylaxis. Latex allergy often goes undiagnosed. Once sensitised, you may react to balloons, elastic bands, condoms and household gloves. Latex in the air,
due to powdered latex gloves being used, can be a hazard for someone who is highly sensitive, as can latex traces in food (see box on p. 175). Medical treatment may be problematic (see p. 98 and box on p. 249). Cross-reactions to certain foods can occur (see p. 15 and p. 51).
For those avoiding latex, there are non-latex gloves (see p. 57), and non-latex condoms. Immunotherapy (see pp. 164-9) may be useful in severe cases: it can reduce sensitivity and eliminate cross-reactions to foods.
Other hazards
This article (pp. 132-5) deals mainly with allergens at work, that is, substances which provoke classical allergies (Type I reactions). In addition, there are skin irritants and antigens in workplaces which can provoke contact dermatitis (see p. 56) or contact urticaria (see p.50).
Some of the most dangerous workplace substances are those that bring on asthma but are not allergens. These are usually called low-molecular-weight asthmagens. The most notorious of these are platinum salts, isocyanates (used in cement, in the manufacture of foam, plastics and varnishes, and for spray-painting cars, aeroplanes and boats), colophony (used as a solder in electronics), glutaraldehyde (used in hospitals for sterilisation procedures), and persulphate (used in hairdressing). Powerful respiratory equipment, supplying air from outside the area (see p. 135) is needed if you work with some of these substances, e.g. isocyanates for spray-painting cars.
has ended, they should not be seen as a way of allowing you to go on working with the offending allergen or asthmagen.
If it seems plausible that your allergies or your asthma are related to your work, your doctor should be able to give you a sickness certificate, so that you can have some time away from the workplace, to see if you recover. The medical service at your workplace may be better at diagnosing occupational asthma than your own doctor, but be cautious. In some workplaces they do operate as they should and offer genuinely confidential treatment. But there have also been cases of information being passed to the management, and workers with the early signs of occupational allergies and/or asthma being dismissed on a pretext, or made redundant, to avoid a possible compensation claim. Most occupational health services claim to be independent, but they actually have to earn the trust of the workforce. Before you make any move, ask your colleagues for their views, especially those who have worked there for many years.
Choosing a job
If you have any tendency to allergies, or come from an allergy-prone family, you should be very choosy about where you work. Try to avoid workplaces where there is heavy exposure to allergens, especially airborne allergens which can provoke asthma:
• Bakeries and flour mills, where the allergens concerned may be wheat proteins in the flour, or enzymes added to the flour mix. These allergies can take years to begin.
• Other food-processing works, particularly those dealing with tea, soyabeans, other beans (e.g. gram flour), shellfish and fish (especially if automated gutting machines are used without adequate ventilation). Food preparation and sandwich-making can cause contact urticaria, if there is prolonged contact with a particular foodstuff (e.g. tomatoes).
• Farms, docks and cotton mills – or any other workplace generating dust from plant products. On farms, it is the dust from grain and hay that is often responsible, although mould spores (see p. 121) can also be the culprit. Allergies to mites (found in hay, grain and flour) sometimes occur and eczema is the most common symptom – often called simply ‘grain itch’.
• Saw mills and joineries, because of the wood dust, especially that from hardwoods and from red cedar (Thuja plicata).
• Paper recycling plants, if there is a lot of paper dust in the air.
• Detergent and pharmaceutical factories handling enzymes – these are added to ‘biological’ washing powders and are potential allergens. The risks are less these days, as the enzymes are in granule form rather than powder.
• Factories processing natural products such as psyllium or ispaghula, which are used as laxatives. Anyone who has been sensitised should avoid taking medicines containing the offending substance in the future, because these can sometimes provoke a dangerous anaphylactic reaction.
• Hospitals, clinics and dental surgeries, mainly due to latex rubber, used in gloves and equipment. Although nursing staff and surgeons are most susceptible, other staff including hospital administrative workers can occasionally be affected. Fears about the spread of the HIV virus has led to a huge increase in the use of latex gloves in medicine and dentistry, and a consequent epidemic of latex allergy. The main problem is with powdered latex gloves, which release 15,000 times as much allergen into the air as unpowdered gloves. Unpowdered, low-allergen gloves greatly reduce the risk of latex allergy developing, and non-latex gloves are even better. There are moves to ban the import of powdered latex gloves into Britain. They are already being phased out in hospitals and other medical facilities, but progress is slow in some areas.
• Other workplaces where powdered latex gloves are used, including
Making the workplace safe for everyone
Note that these choices about employment are for the individual employees to make for their own protection - an employer cannot refuse to take anyone on because they have allergies or come from an atopic (allergy-prone) family.
The reasoning behind this is that the workplace should be safe for everyone, as far as possible. As many as one in three of the population may be susceptible to allergies, and it is clearly wrong to bar all such people from major industries. Current thinking, in most countries, is that the focus should be on getting allergens and asthmagens out of the air, not keeping the more vulnerable workers out of the workplace.
hairdressers, dental surgeries, pathology laboratories and police stations. Construction workers wearing rubber gloves are also at risk. Someone who has been sensitised by powdered latex gloves may then react to other items (see box on p.132). Those severely affected can have great problems in daily life and with medical treatment, so anyone with a strong tendency to allergy should strenuously avoid becoming sensitised.
• Factories making or using rubber items may also expose workers to the risk of latex allergy. Anything made by the ‘dipping method’ (e.g. balloons, condoms, elastic bands and gloves) is highly allergenic. Moulded rubber items, such as tyres, are much less of a problem. Neoprene and other synthetic rubber items are not allergenic.
• Chiropody and podiatry clinics, where there is a risk of allergic reactions to the fungus that causes athlete’s foot. It is inhaled on skin flakes from the patients’ feet.
• Laboratories and other workplaces where animals are kept. In the case of mice, rats and other rodents, the allergen is found in the animals’ urine, and becomes airborne as the urine dries. Insects and spiders (e.g, those reared for biological pest control), are also allergenic due to small airborne particles from their bodies. Those working closely with bees (either honeybees or bumblebees, now reared for pollinating glasshouse crops) are liable to be stung frequently, and this can lead to sting allergy (see pp. 60-61).
• Hairdressing salons, where many different items are used that are potentially allergenic, including latex gloves (see above), permanent-wave solutions and henna. The risks of contact dermatitis are also high (see p. 55).
• Greenhouses, where the enclosed conditions can lead to high levels of allergens from plants, moulds and insect pests. There may also be exposure to pesticide sprays or their residues, which can greatly aggravate any underlying tendency to allergies.
If you have ever suffered from atopic eczema, work situations that can bring on contact dermatitis should also be avoided (see p. 55).
Taking a risky job
If circumstances force you to take a job with an allergy risk, observe all the safety procedures that are in place, and where you have the option of turning on extractor fans, wearing protective gear, or simply opening doors and windows, always do so. If the safety procedures seem inadequate, talk to your trade union Safety Representative, or the local Health and Safety Executive which can run a check on safety procedures in your workplace. This will be presented to the employer as a routine check, so they need never know that a member of the workforce has contacted the HSE.
Whatever you do, if you are in a risky job, don’t smoke. At a salmon processing plant in Scotland, 40% of the smokers developed allergies (resulting in asthma) to the fish allergens in the spray from the fish-gutting machine. Non-smokers - who formed the overwhelming majority of the workers - were not affected at all. In United States cotton mills, smokers are affected by levels of cotton dust in the air that are legally defined as ’safe’, while nonsmokers remain unaffected.
Passive smoking at work is also an important issue. A recent US study showed that non-smokers were more likely to develop asthma if they worked alongside a smoker. Your employer has a duty to provide you with clean air. This includes ensuring that other employees do not impose their cigarette smoke on you.
Respiratory equipment
Where respiratory equipment is needed, your employer must provide this, and it must be the right equipment for the job. It should be inspected, tested, cleaned and repaired after each use, and filters should be replaced regularly. All this is your employer’s responsibility, but check that it is being done, and always look the mask over before you put it on.
Two different types of respiratory equipment are currently in use:
• Those that give you a supply of air from outside the work area, either from a compressed-air cylinder, or via an air-hose (airline) supplied with fresh air. In Britain these are called breathing apparatus.
• Those that use the surrounding air but filter it to remove allergens and asthmagens. In Britain these are called respirators. (In some countries this term describes any kind of respiratory equipment.) Ordinary respirators may pose problems for some asthmatics because they cannot breathe in strongly enough to draw sufficient air through the filter. Powered respirators can be the answer: they have a battery-powered unit to help with pulling in the air.
There are government regulations concerning the type of equipment required for each type of allergen and asthmagen. Large companies generally follow these regulations, but small businesses, such as local sawmills, joineries and car-repainting workshops, may not even know about them.
Any respiratory equipment that has a face mask must form a tight seal with your face. Facial hair will prevent this, and so will stubble, so shave carefully. Faces vary enormously in shape, and if your face mask does not fit, ask for a different type of mask or a different type of respiratory equipment. Persist until you get one that’s right for you.
Carry out a ‘fit check’ each and every time you wear the mask. For example, with respirators, you can check the fit by covering the air intake completely with your hand and breathing in sharply: if the mask fits properly, it should collapse onto your face, and remain stuck to your face for several seconds. Look at the manufacturer’s instruction booklet as there may be a specific fit check recommended for the equipment you are using.
If there is any difficulty in breathing through the respiratory equipment, the replaceable filter cartridge or the equipment itself should be replaced. You should also take action immediately if you can smell the substance being handled – but never rely on this as a danger sign, because an extremely small amount, way beyond the detection capacity of the human nose, may be very damaging indeed to your health.
Keep your mask on throughout the work period. If you find this impossible, talk to your employer or
line manager about getting a different kind of respiratory equipment – a powered device, for example, that assists the inflow of air.
No form of respiratory equipment provides complete protection against allergens and asthmagens: there is always the chance of some small amount getting through. This is why respiratory equipment should not be used by those who have already developed occupational asthma but want to stay in their job.
Those who really cannot change jobs (e.g, farmers) are sometimes able to use a powered respirator helmet, which allows them to go on working despite the allergen. But this is not an ideal solution from a purely health point of view. Farmers can also improve matters, where moulds are the source of allergens, by keeping all harvested crops dry and thoroughly ventilated.
A lasting problem
As long as you catch the problem early, and are no longer anywhere near the allergen, your symptoms should disappear completely, but remember that you may still be highly sensitive to the allergen, even years afterwards. For a year or two at least, avoid contact with it again, even in tiny amounts. If someone else in your family works at the same place, they may bring home traces of the allergen on their clothes and hair: ask them to leave their workclothes outside the house and shower on arriving home.
With occupational allergies to airborne food particles, it is possible that the affected individual will later react to the same food when eaten. Experiment very cautiously, especially if the allergen is fish or shellfish.
The allergy may persist long after the job has ended. In one case, doctors found that a woman who had developed ‘baker’s asthma’, while working briefly in a bakery when young, was still allergic to the enzyme additive in bread 20 years later. She suffered an asthma attack whenever she ate bread.

Allergies and Pregnancy
Great care is taken in prescribing drugs during pregnancy. This is something that doctors are now exceedingly cautious about, but do tell the doctor as soon as you decide to try for a baby. The foetus is most vulnerable to damage by drugs during the first three months, and especially the first few weeks after conception.
Your prescription will be changed if the drugs you are currently taking could pose any threat to the unborn child. A drug that has not had sufficiently rigorous testing for safety during pregnancy, or lacks a long track record, will probably be withdrawn. New drugs are generally considered to be slightly more risky than the tried-and-true older drugs: rare side effects may not come to light during the testing which precedes release of a drug, but they do become apparent once the drug is in widespread use for a long time (see pp. 136-7).
If you are already pregnant as you read this, don’t worry too much. With a few notable exceptions – certain antihistamines and antibiotics – most of the drugs used for allergic diseases do not pose any major risk to the unborn child. There is probably nothing to worry about, but see your doctor as soon as you can – and talk to a pharmacist, in the meantime, if you are concerned. Don’t panic, and don’t stop taking your drugs unless you are absolutely sure that you can do without them. Do not stop taking your drugs if you have asthma.
Some non-prescription medicines are best avoided during pregnancy. Read the packet carefully, and talk to your pharmacist if you have any doubts.
From the moment you start trying for a baby, remember to tell any medical personnel who treat you, and any pharmacist you buy medicines from, that you could be pregnant.
Immunotherapy and skin testing
Immunotherapy should not begin during pregnancy, because of the risk of anaphylaxis (see below), but pregnant women who are already undergoing immunotherapy can continue.
The safety procedures described on p. 166-7 should be followed with meticulous care.
Most doctors continue immunotherapy at a steady ‘maintenance dose’ because there is always a small risk of anaphylaxis with immunotherapy when the dose is increased. Some doctors are even more cautious and reduce the maintenance dose during pregnancy, but give more frequent injections – this minimises the chance of bad reactions.
Many doctors do not give skin tests for allergy during pregnancy, as these also carry a very small risk of anaphylaxis. If you do have skin tests, there must be resuscitation equipment available. Intradermal tests (see p. 92) are best avoided.
Severe allergic reactions (anaphylaxis)
Special care should be taken to avoid anaphylaxis during pregnancy as this may increase the chance of a miscarriage.
Injecting adrenaline during the first three months of pregnancy may carry some small risk of malformation of the baby. But the evidence here is uncertain, whereas the danger to your own life, if you don’t use adrenaline when you need it, is both certain and substantial. If you have an adrenaline self-injection kit, talk to your doctor now about what you should do in an emergency. The best policy is to be ultra-careful about avoiding your allergen, so that anaphylaxis does not happen.
Women who suffer from exercise-induced anaphylaxis (see p. 59) generally play safe by exercising less strenuously while pregnant. The problem can get worse during pregnancy, but it does not usually do so. Labour itself is very strenuous of course, but problems during the birth are uncommon. If anaphylaxis does occur, the reaction is usually quite mild – nettle rash only – and the baby is delivered alive and well. However, many women find that the attacks of exercise-induced anaphylaxis are more frequent and severe when they start exercising again after the baby is born. It is best to resume exercise very gradually.
Eczema and other skin problems
Atopic eczema may improve during pregnancy, probably because the body produces slightly more of its own natural steroid, hydrocortisone. Contact dermatitis may either improve or flare up.
Stretch marks often itch a great deal, and widespread itchy skin, with or without a rash, is a common problem during pregnancy. These are not usually allergic reactions, and no cause can be identified in most cases. The skin tends to recover a few days after the birth.
If there is itching in the vulva) area, this could be due to a Candida infection (your doctor can prescribe a safe treatment) or it might be just another of those unexplained itches of pregnancy.
Hayfever and other nasal allergies
The natural hormone changes of pregnancy affect the nose, which can become more blocked. If you have allergic rhinitis this will add to your woes. See your doctor and make sure that your drug treatment is adequate (see p. 29). The nose-clearing exercises on pp. 230-31 might also help.
Asthma
Severe asthma can be bad for both the pregnant mother and the unborn child. Uncontrolled asthma increases the risk of the baby being born prematurely – and premature babies are more likely to develop asthma themselves. The death rate for newborn babies is also higher if the mother has poorly controlled asthma.
Treating a severe asthma attack promptly helps to prevent any damage to the baby, so don’t hesitate to call an ambulance –and tell the operator you are pregnant. The ambulance should be carrying oxygen which is particularly important for helping the unborn baby through the attack.
If you have asthma, don’t stop using your drugs or reduce the dose unless advised to do so by a doctor. Because it is so important to keep asthma under control during pregnancy, your doctor may want to add, or increase, preventer drugs such as inhaled corticosteroids or sodium cromoglycate (see p. 148). It
also makes sense to monitor your peak flow twice a day (see p. 97) so that you have advance warning of serious attacks.
Unfortunately, some asthmatics – usually those who have severe asthma to begin with – get much worse during their pregnancy. In such cases, careful monitoring and increased use of preventer medicines are essential. The symptoms usually increase from week 24 to week 36 of the pregnancy. The last four weeks tend to be much better, and things are back to normal by about three months after the birth.
Some women with asthma have fewer symptoms while they are pregnant, and for others their asthma stays about the same.
Asthma can also appear for the first time during pregnancy, and may be quite severe. However, a relatively mild breathlessness can be due simply to the fact that, as the pregnancy advances, the chest cavity, and therefore the lungs, become compressed. This is not necessarily asthma.
This simple physical effect can also add to the difficulties experienced by women who were already asthmatic before they became pregnant.
GER (acid reflux) – see p. 38 – can contribute to asthma during pregnancy, and treating this problem may help.
Asthma attacks during the birth
Severe asthma attacks very rarely occur during labour, but it is still important that all the medical staff in attendance know you have asthma. They should also be told if you have taken steroid tablets during the previous two years. A record of when you took steroids, how long for, and at what dose, will be valuable. You may need a low dose of steroid to get you through the physical stress of labour (see p. 142). Some doctors believe that patients who have been using high-dose inhaled steroids should be treated in the same way.
Smoking
Smoking is a bad idea if you have allergies or any allergic tendency in the family. Smoking is a very bad idea indeed if you are pregnant, or a parent. This is the moment, if ever there was one, to give up.
Enlist your doctor’s help, and ask if counselling, psychotherapy or other forms of support are available. If you have tried all this before, and failed, then talk to your doctor about the possibility of using nicotine patches. Some doctors believe that, for pregnant women who smoke 20 cigarettes or more a day, the advantages of nicotine patches outweigh the risks to the foetus. Nicotine levels in the blood are lower with patches than with heavy smoking, and your baby is not enduring the hundreds of other toxins found in cigarette smoke.

`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 .