Penicillin allergy-what foods to avoid
Risk factors for allergy can be placed in two general categories, namely host and environmental factors. Host factors include heredity, sex, race, and age, with heredity being by far the most significant. However, there own been recent increases in the incidence of allergic disorders that cannot be explained by genetic factors alone. Four major environmental candidates are alterations in exposure to infectious diseases during early childhood, environmental pollution, allergen levels, and dietary changes.
Main article: Insect sting allergy
Typically, insects which generate allergic responses are either stinging insects (wasps, bees, hornets and ants) or biting insects (mosquitoes, ticks).
Stinging insects inject venom into their victims, whilst biting insects normally introduce anti-coagulants.
Main article: Drug allergy
See also: Adverse drug reaction and Drug eruption
About 10% of people report that they are allergic to penicillin; however, 90% turn out not to be. Serious allergies only happen in about %.
Toxins interacting with proteins
Another non-food protein reaction, urushiol-induced contact dermatitis, originates after contact with poison ivy, eastern poison oak, western poison oak, or poison sumac.
Urushiol, which is not itself a protein, acts as a hapten and chemically reacts with, binds to, and changes the shape of integral membrane proteins on exposed skin cells. The immune system does not recognize the affected cells as normal parts of the body, causing a T-cell-mediated immune response. Of these poisonous plants, sumac is the most virulent. The resulting dermatological response to the reaction between urushiol and membrane proteins includes redness, swelling, papules, vesicles, blisters, and streaking.
Estimates vary on the percentage of the population that will own an immune system response.
Approximately 25 percent of the population will own a strong allergic response to urushiol. In general, approximately 80 percent to 90 percent of adults will develop a rash if they are exposed to milligrams (×10−5gr) of purified urushiol, but some people are so sensitive that it takes only a molecular trace on the skin to initiate an allergic reaction.
Main article: Food allergy
A wide variety of foods can cause allergic reactions, but 90% of allergic responses to foods are caused by cow’s milk, soy, eggs, wheat, peanuts, tree nuts, fish, and shellfish. Other food allergies, affecting less than 1 person per 10, population, may be considered «rare». The use of hydrolysed milk baby formula versus standard milk baby formula does not appear to change the risk.
The most common food allergy in the US population is a sensitivity to crustacea. Although peanut allergies are notorious for their severity, peanut allergies are not the most common food allergy in adults or children.
Severe or life-threatening reactions may be triggered by other allergens, and are more common when combined with asthma.
Rates of allergies differ between adults and children. Peanut allergies can sometimes be outgrown by children. Egg allergies affect one to two percent of children but are outgrown by about two-thirds of children by the age of 5. The sensitivity is generally to proteins in the white, rather than the yolk.
Milk-protein allergies are most common in children. Approximately 60% of milk-protein reactions are immunoglobulin E-mediated, with the remaining generally attributable to inflammation of the colon. Some people are unable to tolerate milk from goats or sheep as well as from cows, and numerous are also unable to tolerate dairy products such as cheese.
Roughly 10% of children with a milk allergy will own a reaction to beef. Beef contains little amounts of proteins that are present in greater abundance in cow’s milk.Lactose intolerance, a common reaction to milk, is not a form of allergy at every, but rather due to the absence of an enzyme in the digestive tract.
Those with tree nut allergies may be allergic to one or to numerous tree nuts, including pecans, pistachios, pine nuts, and walnuts. Also seeds, including sesame seeds and poppy seeds, contain oils in which protein is present, which may elicit an allergic reaction.
Allergens can be transferred from one food to another through genetic engineering; however genetic modification can also remove allergens.
Little research has been done on the natural variation of allergen concentrations in unmodified crops.
Latex can trigger an IgE-mediated cutaneous, respiratory, and systemic reaction.
The prevalence of latex allergy in the general population is believed to be less than one percent. In a hospital study, 1 in surgical patients ( percent) reported latex sensitivity, although the sensitivity among healthcare workers is higher, between seven and ten percent. Researchers attribute this higher level to the exposure of healthcare workers to areas with significant airborne latex allergens, such as operating rooms, intensive-care units, and dental suites. These latex-rich environments may sensitize healthcare workers who regularly inhale allergenic proteins.
The most prevalent response to latex is an allergic contact dermatitis, a delayed hypersensitive reaction appearing as dry, crusted lesions.
This reaction generally lasts 48–96 hours. Sweating or rubbing the area under the glove aggravates the lesions, possibly leading to ulcerations.Anaphylactic reactions happen most often in sensitive patients who own been exposed to a surgeon’s latex gloves during abdominal surgery, but other mucosal exposures, such as dental procedures, can also produce systemic reactions.
Latex and banana sensitivity may cross-react. Furthermore, those with latex allergy may also own sensitivities to avocado, kiwifruit, and chestnut. These people often own perioral itching and local urticaria.
Only occasionally own these food-induced allergies induced systemic responses. Researchers suspect that the cross-reactivity of latex with banana, avocado, kiwifruit, and chestnut occurs because latex proteins are structurally homologous with some other plant proteins.
Chronic stress can aggravate allergic conditions. This has been attributed to a T helper 2 (TH2)-predominant response driven by suppression of interleukin 12 by both the autonomic nervous system and the hypothalamic–pituitary–adrenal axis. Stress management in highly susceptible individuals may improve symptoms.
Main article: Hygiene hypothesis
Allergic diseases are caused by inappropriate immunological responses to harmless antigens driven by a TH2-mediated immune response.
Numerous bacteria and viruses elicit a TH1-mediated immune response, which down-regulates TH2 responses. The first proposed mechanism of action of the hygiene hypothesis was that insufficient stimulation of the TH1 arm of the immune system leads to an overactive TH2 arm, which in turn leads to allergic disease. In other words, individuals living in too sterile an environment are not exposed to enough pathogens to hold the immune system busy.
Since our bodies evolved to deal with a certain level of such pathogens, when they are not exposed to this level, the immune system will attack harmless antigens and thus normally benign microbial objects—like pollen—will trigger an immune response.
The hygiene hypothesis was developed to explain the observation that hay fever and eczema, both allergic diseases, were less common in children from larger families, which were, it is presumed, exposed to more infectious agents through their siblings, than in children from families with only one kid. The hygiene hypothesis has been extensively investigated by immunologists and epidemiologists and has become an significant theoretical framework for the study of allergic disorders.
It is used to explain the increase in allergic diseases that own been seen since industrialization, and the higher incidence of allergic diseases in more developed countries. The hygiene hypothesis has now expanded to include exposure to symbiotic bacteria and parasites as significant modulators of immune system development, along with infectious agents.
Epidemiological data support the hygiene hypothesis. Studies own shown that various immunological and autoimmune diseases are much less common in the developing world than the industrialized world and that immigrants to the industrialized world from the developing world increasingly develop immunological disorders in relation to the length of time since arrival in the industrialized world. Longitudinal studies in the third world protest an increase in immunological disorders as a country grows more affluent and, it is presumed, cleaner. The use of antibiotics in the first year of life has been linked to asthma and other allergic diseases. The use of antibacterial cleaning products has also been associated with higher incidence of asthma, as has birth by Caesarean section rather than vaginal birth.
Allergic diseases are strongly familial: identical twins are likely to own the same allergic diseases about 70% of the time; the same allergy occurs about 40% of the time in non-identical twins. Allergic parents are more likely to own allergic children, and those children’s allergies are likely to be more severe than those in children of non-allergic parents.
Some allergies, however, are not consistent along genealogies; parents who are allergic to peanuts may own children who are allergic to ragweed. It seems that the likelihood of developing allergies is inherited and related to an irregularity in the immune system, but the specific allergen is not.
The risk of allergic sensitization and the development of allergies varies with age, with young children most at risk. Several studies own shown that IgE levels are highest in childhood and drop rapidly between the ages of 10 and 30 years. The peak prevalence of hay fever is highest in children and young adults and the incidence of asthma is highest in children under 
Overall, boys own a higher risk of developing allergies than girls, although for some diseases, namely asthma in young adults, females are more likely to be affected. These differences between the sexes tend to decrease in adulthood.
Ethnicity may frolic a role in some allergies; however, racial factors own been hard to separate from environmental influences and changes due to migration. It has been suggested that diverse genetic loci are responsible for asthma, to be specific, in people of European, Hispanic, Asian, and African origins.
Other environmental factors
There are differences between countries in the number of individuals within a population having allergies.
Allergic diseases are more common in industrialized countries than in countries that are more traditional or agricultural, and there is a higher rate of allergic disease in urban populations versus rural populations, although these differences are becoming less defined. Historically, the trees planted in urban areas were predominantly male to prevent litter from seeds and fruits, but the high ratio of male trees causes high pollen counts.
Alterations in exposure to microorganisms is another plausible explanation, at present, for the increase in atopic allergy. Endotoxin exposure reduces release of inflammatory cytokines such as TNF-α, IFNγ, interleukin, and interleukin from white blood cells (leukocytes) that circulate in the blood. Certain microbe-sensing proteins, known as Toll-like receptors, found on the surface of cells in the body are also thought to be involved in these processes.
Gutworms and similar parasites are present in untreated drinking water in developing countries, and were present in the water of developed countries until the routine chlorination and purification of drinking water supplies. Recent research has shown that some common parasites, such as intestinal worms (e.g., hookworms), secrete chemicals into the gut wall (and, hence, the bloodstream) that suppress the immune system and prevent the body from attacking the parasite. This gives rise to a new slant on the hygiene hypothesis theory—that co-evolution of humans and parasites has led to an immune system that functions correctly only in the presence of the parasites.
Without them, the immune system becomes unbalanced and oversensitive. In specific, research suggests that allergies may coincide with the delayed establishment of gut flora in infants. However, the research to support this theory is conflicting, with some studies performed in China and Ethiopia showing an increase in allergy in people infected with intestinal worms. Clinical trials own been initiated to test the effectiveness of certain worms in treating some allergies. It may be that the term ‘parasite’ could turn out to be inappropriate, and in fact a hitherto unsuspected symbiosis is at work. For more information on this topic, see Helminthic therapy.
Signs and symptoms
|Affected organ||Common signs and symptoms|
|Nose||Swelling of the nasal mucosa (allergic rhinitis) runny nose, sneezing|
|Eyes||Redness and itching of the conjunctiva (allergic conjunctivitis, watery)|
|Airways||Sneezing, coughing, bronchoconstriction, wheezing and dyspnea, sometimes outright attacks of asthma, in severe cases the airway constricts due to swelling known as laryngeal edema|
|Ears||Feeling of fullness, possibly pain, and impaired hearing due to the lack of eustachian tube drainage.|
|Skin||Rashes, such as eczema and hives (urticaria)|
|Gastrointestinal tract||Abdominal pain, bloating, vomiting, diarrhea|
Many allergens such as dust or pollen are airborne particles. In these cases, symptoms arise in areas in contact with air, such as eyes, nose, and lungs. For instance, allergic rhinitis, also known as hay fever, causes irritation of the nose, sneezing, itching, and redness of the eyes. Inhaled allergens can also lead to increased production of mucus in the lungs, shortness of breath, coughing, and wheezing.
Aside from these ambient allergens, allergic reactions can result from foods, insect stings, and reactions to medications love aspirin and antibiotics such as penicillin.
Symptoms of food allergy include abdominal pain, bloating, vomiting, diarrhea, itchy skin, and swelling of the skin during hives. Food allergies rarely cause respiratory (asthmatic) reactions, or rhinitis. Insect stings, food, antibiotics, and certain medicines may produce a systemic allergic response that is also called anaphylaxis; multiple organ systems can be affected, including the digestive system, the respiratory system, and the circulatory system. Depending on the rate of severity, anaphylaxis can include skin reactions, bronchoconstriction, swelling, low blood pressure, coma, and death.
This type of reaction can be triggered suddenly, or the onset can be delayed. The nature of anaphylaxis is such that the reaction can seem to be subsiding, but may recur throughout a period of time.
Substances that come into contact with the skin, such as latex, are also common causes of allergic reactions, known as contact dermatitis or eczema. Skin allergies frequently cause rashes, or swelling and inflammation within the skin, in what is known as a «weal and flare» reaction characteristic of hives and angioedema.
With insect stings a large local reaction may happen (an area of skin redness greater than 10cm in size). It can final one to two days. This reaction may also happen after immunotherapy.
Mold Allergies and Food Allergies
It is possible, however, to own related food allergies if you own a mold allergy.
Penicillium can be found in certain aged and blue-veined cheeses, such as Roquefort and Camembert. There own been reports of food allergy reactions in Penicillium-allergic people who eat these cheeses and other foods with this mold.
If you own an allergic reaction to mushrooms, it's more likely that it's from the mushrooms themselves, but symptoms of oral allergy syndrome own been reported in people with mold allergies who own eaten raw mushrooms.
Yeast is another potential food allergen if you own a mold allergy.
You may be wondering how a mold allergy can be related to a mushroom or yeast allergy. The answer is explained by a phenomenon called cross-reactivity.
Penicillium Mold Allergy vs. Penicillin Allergy
Having a Penicillium mold allergy doesn't mean that you're allergic to the antibiotic penicillin. While penicillin was indeed originally developed from Penicillium mold, people with this specific mold allergy are not at any more risk of developing an allergy to this class of antibiotics than anyone else with a history of allergies.
Risk factors that make it more likely to own a penicillin allergy include:
- Having a family history of drug allergy
- Having had an allergic reaction to another helpful of drug
- Having a history of allergies
- Being exposed to high or prolonged doses of penicillin
- Having an infection such as human immunodeficiency virus (HIV) or Epstein-Barr virus, which can contribute to allergic drug reactions
Allergy to Penicillin Drugs
The Basics of Cross-Reactivity
Cross-reactivity means that there are similar proteins shared between certain foods and certain molds.
So if you're allergic to molds, you may extremely well react to foods love mushrooms that contain a similar protein.
There is also ample scientific evidence suggesting cross-reactivity between diverse pollens and raw fruits and vegetables.
Likewise, an allergy to latex can predispose people to certain food allergies (mostly fruits and nuts). Doctors own even named this condition "the latex-food syndrome."
Anaphylaxis is a severe, potentially life-threatening reaction that can simultaneously affect two or more organ systems (for instance, when there is both swelling and difficulty breathing, or vomiting and hives). If this occurs, call and seek emergency medical care immediately.
If you are caring for someone who appears to be having a severe reaction to a drug, tell the emergency care team what drug was taken, when it was taken and what the dosage was.
If your allergic reaction to a drug is not life-threatening, your allergist may give you:
- An antihistamine to counteract the allergic reaction
- A nonsteroidal anti-inflammatory drug, such as ibuprofen or aspirin, or a corticosteroid to reduce inflammation
The Bottom Line
The large picture here is that while a mold allergy may lead to a food allergy such as yeast or mushrooms, it doesn't mean you'll develop allergies to medications love penicillin.
That being said, a history of allergies puts you at a higher risk of developing other allergies, so it is possible for you to own both an allergy to certain molds and a penicillin allergy, but the two are not interconnected — it's simply a coincidence.
Modern-day penicillin antibiotics are produced synthetically and are not contaminated with mold particles.
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If you own a drug allergy:
- Ask about related drugs that you should avoid.
- Make certain every of your doctors are aware of your allergy and the symptoms you experienced.
- Ask about alternatives to the drug that caused your allergic reaction.
- Wear an emergency medical alert bracelet or necklace that identifies your allergy.
If there is no suitable alternative to the antibiotic that you are allergic to, you will need to undergo drug desensitization.
This involves taking the drug in increasing amounts until you can tolerate the needed dose with minimal side effects. This will most likely be done in a hospital so immediate medical care is available if problems develop.
Desensitization can assist only if you are taking the drug every day.
Once you stop it – for example, when a chemotherapy cycle ends – you will need to go through desensitization a second time if you need the drug again.
Nearly everyone knows someone who says they are allergic to penicillin. Up to 10% of people report being allergic to this widely used class of antibiotic, making it the most commonly reported drug allergy. That said, studies own shown that more than 90% of those who ponder they are allergic to penicillin, actually are not.
In other words, 9 out of 10 people who ponder they own penicillin allergy are avoiding it for no reason. Even in people with documented allergy to penicillin, only about 20% are still allergic ten years after their initial allergic reaction.
Penicillin, famously discovered by Alexander Fleming in , is prescribed today to treat a variety of conditions, such as strep throat. Despite its efficacy, some people steer clear of penicillin for fear of experiencing an allergic reaction to the medication.
Anyone who has been told they are penicillin allergic, but who hasn’t been tested by an allergist, should be tested.
An allergist will work with you to discover out if you’re truly allergic to penicillin, and to determine what your options are for treatment if you are. If you’re not, you’ll be capable to use medications that are safer, often more effective and less expensive.
Penicillin Allergy Symptoms
Mild to moderate allergic reactions to penicillin are common, and symptoms may include any of the following:
- Throat tightness
- Tissue swelling under the skin, typically around the face (also known as angioedema)
- Hives (raised, extremely itchy spots that come and go over a period of hours)
- Trouble breathing
A less common but more serious, sudden-onset allergic reaction to penicillin is anaphylaxis, which occurs in highly sensitive patients.
Anaphylaxis occurs suddenly, can worsen quickly and can be deadly. Symptoms of anaphylaxis might include not only skin symptoms, but also any of the following:
- Tightness in the chest and difficulty breathing
- Swelling of the tongue, throat, nose and lips
- Dizziness and fainting or loss of consciousness, which can lead to shock and heart failure
These symptoms require immediate attention at the nearest Emergency Room.
Epinephrine, the therapy of choice, will be given in this urgent care setting, but should also be self-istered via autoinjector as soon as possible by patients who own already been prescribed and are wisely carrying this device.
Penicillin Allergy Testing and Diagnosis
An allergist is your best resource to assist you assess the safety of taking penicillin.
In addition to assessing your detailed history about a prior allergic reaction to penicillin, allergists ister skin tests to determine if a person is or remains allergic to the medication. These tests, which are conducted in an office or a hospital setting, typically take about two to three hours, including the time needed after testing to watch for reactions.
When safely and properly istered, skin tests involve pricking the skin, injecting a weakened form of the drug, and observing the patients reaction.
People who pass penicillin skin tests by reacting negatively to the injection are seen as at low risk for an immediate acute reaction to the medication. The allergist might then give these individuals a single, full-strength oral dose to confirm the absence of a penicillin allergy.
Those with positive allergy skin tests should avoid penicillin and be treated with a diverse antibiotic. If penicillin is recommended, people in some cases can undergo penicillin desensitization to enable them to get the medication in a controlled manner under the care of an allergist.
Penicillin Allergy Treatment
Those who own severe reactions to penicillin should seek emergency care, which may include an epinephrine injection and treatment to maintain blood pressure and normal breathing.
Individuals who own milder reactions and suspect that an allergy to penicillin is the cause may be treated with antihistamines or, in some cases, oral or injected corticosteroids, depending on the reaction.
Visit an allergist to determine the correct course of treatment.
If you were told you are allergic to penicillin but own never been tested, it’s time to see an allergist.
Immune system response to a substance that most people tolerate well
For the medical journal of this title, see Allergy (journal).
|Hives are a common allergic symptom|
|Symptoms||Red eyes, itchy rash, runny nose, shortness of breath, swelling, sneezing|
|Types||Hay fever, food allergies, atopic dermatitis, allergic asthma, anaphylaxis|
|Causes||Genetic and environmental factors|
|Diagnostic method||Based on symptoms, skin prick test, blood test|
|Differential diagnosis||Food intolerances, food poisoning|
|Prevention||Early exposure to potential allergens|
|Treatment||Avoiding known allergens, medications, allergen immunotherapy|
|Medication||Steroids, antihistamines, epinephrine, mast cell stabilizers, antileukotrienes|
Allergies, also known as allergic diseases, are a number of conditions caused by hypersensitivity of the immune system to typically harmless substances in the environment. These diseases include hay fever, food allergies, atopic dermatitis, allergic asthma, and anaphylaxis. Symptoms may include red eyes, an itchy rash, sneezing, a runny nose, shortness of breath, or swelling.Food intolerances and food poisoning are separate conditions.
Common allergens include pollen and certain foods. Metals and other substances may also cause problems. Food, insect stings, and medications are common causes of severe reactions. Their development is due to both genetic and environmental factors. The underlying mechanism involves immunoglobulin E antibodies (IgE), part of the body’s immune system, binding to an allergen and then to a receptor on mast cells or basophils where it triggers the release of inflammatory chemicals such as histamine. Diagnosis is typically based on a person’s medical history. Further testing of the skin or blood may be useful in certain cases. Positive tests, however, may not mean there is a significant allergy to the substance in question.
Early exposure to potential allergens may be protective. Treatments for allergies include avoiding known allergens and the use of medications such as steroids and antihistamines. In severe reactions injectable adrenaline (epinephrine) is recommended.Allergen immunotherapy, which gradually exposes people to larger and larger amounts of allergen, is useful for some types of allergies such as hay fever and reactions to insect bites. Its use in food allergies is unclear.
Allergies are common. In the developed world, about 20% of people are affected by allergic rhinitis, about 6% of people own at least one food allergy, and about 20% own atopic dermatitis at some point in time. Depending on the country about 1–18% of people own asthma. Anaphylaxis occurs in between –2% of people. Rates of numerous allergic diseases appear to be increasing. The expression «allergy» was first used by Clemens von Pirquet in 
In the early stages of allergy, a type I hypersensitivity reaction against an allergen encountered for the first time and presented by a professional antigen-presenting cell causes a response in a type of immune cell called a TH2 lymphocyte; a subset of T cells that produce a cytokine called interleukin-4 (IL-4).
These TH2 cells interact with other lymphocytes called B cells, whose role is production of antibodies. Coupled with signals provided by IL-4, this interaction stimulates the B cell to start production of a large quantity of a specific type of antibody known as IgE. Secreted IgE circulates in the blood and binds to an IgE-specific receptor (a helpful of Fc receptor called FcεRI) on the surface of other kinds of immune cells called mast cells and basophils, which are both involved in the acute inflammatory response.
The IgE-coated cells, at this stage, are sensitized to the allergen.
If later exposure to the same allergen occurs, the allergen can bind to the IgE molecules held on the surface of the mast cells or basophils. Cross-linking of the IgE and Fc receptors occurs when more than one IgE-receptor complicated interacts with the same allergenic molecule, and activates the sensitized cell. Activated mast cells and basophils undergo a process called degranulation, during which they release histamine and other inflammatory chemical mediators (cytokines, interleukins, leukotrienes, and prostaglandins) from their granules into the surrounding tissue causing several systemic effects, such as vasodilation, mucous secretion, nerve stimulation, and smooth muscle contraction.
This results in rhinorrhea, itchiness, dyspnea, and anaphylaxis. Depending on the individual, allergen, and mode of introduction, the symptoms can be system-wide (classical anaphylaxis), or localized to specific body systems; asthma is localized to the respiratory system and eczema is localized to the dermis.
After the chemical mediators of the acute response subside, late-phase responses can often happen. This is due to the migration of other leukocytes such as neutrophils, lymphocytes, eosinophils and macrophages to the initial site.
The reaction is generally seen 2–24 hours after the original reaction. Cytokines from mast cells may frolic a role in the persistence of long-term effects. Late-phase responses seen in asthma are slightly diverse from those seen in other allergic responses, although they are still caused by release of mediators from eosinophils and are still dependent on activity of TH2 cells.
Allergic contact dermatitis
Although allergic contact dermatitis is termed an «allergic» reaction (which generally refers to type I hypersensitivity), its pathophysiology actually involves a reaction that more correctly corresponds to a type IV hypersensitivity reaction. In type IV hypersensitivity, there is activation of certain types of T cells (CD8+) that destroy target cells on contact, as well as activated macrophages that produce hydrolyticenzymes.