T he thin-layer rapid use epicutaneous (T.R.U.E) Test of 23 common allergens is a valuable, first-line screening tool used by many dermatologists. Although the test focuses on common allergens, frequent questions have arisen from colleagues and patients as to where a specific allergen is derived or what products patients should avoid. With this in mind, this column was developed to provide educational information about the T.R.U.E. Test allergens. A rich, interesting history accompanies each of the 23 allergens, and understanding these historic perspectives can help to better educate patients. Each column will also highlight appropriate products that patients should avoid when they are allergic to a specific allergen. Contact Dermatides Allergic Contact dermatitis [ACD] is an important disease with high impact both in terms of patient morbidity and economics. ACD represents a T-helper cell Type 1 [Th1] dependent delayed-type (Type IV) hypersensitivity reaction. The instigating exogenous antigens are primarily small lipophilic chemicals (haptens) with a molecular weight less than 500 Da.1 On direct antigen exposure to the skin or mucosa, an immunologic cascade is initiated which includes cytokines, i.e. interleukin 2 [IL-2] and interferon gamma [IFN-g], T cells and Langerhan cells. This complex interaction leads to the clinical picture of ACD. The contact dermatides include allergic contact dermatitis, irritant contact dermatitis and contact urticaria. Irritant contact dermatitis, the most common form, accounts for approximately 80% of environmental-occupational based dermatoses. Contact urticaria (wheal and flare reaction) represents an IgE and mast cell-mediated immediate-type hypersensitivity reaction that can lead to anaphylaxis. The foremost example of this would be latex hypersensitivity. While this is beyond the scope of this section, we acknowledge this form of hypersensitivity due to the severity of the potential reactions and direct the reader to key sources.2,3 The primary focus of this section is to highlight the educational and pathophysiological component of allergic contact dermatitis. Clinical Illustration An atopic patient was referred to the University of Miami Allergic Contact Dermatitis Clinic by family medicine for comprehensive patch testing. The patient suffered from sustained hand and foot dermatitis for the better part of the last 8 years. He notably applied corticosteroids to his entire hands and feet, in addition to regular application of neomycin to the fissures. Neomycin: A Historical Perspective Since ancient times, preparations derived from living matter have been applied to wounds to destroy infection. Beginning around 1550 B.C. the Egyptians used a mixture of lard, honey, and lint as a wound ointment. Euro-peans began producing essential oils, which were known to have anti-bacterial activity, in the twelfth century.4 Despite this long history of caring for wound infections, the idea that a microorganism was capable of destroying another microbiotic species was not established until the latter half of the nineteenth century. It was then that Louis Pasteur’s observation of the antagonistic effect of saprophytic (soil) bacteria on the growth of anthrax bacteria spurred the notion that this interaction might be put to therapeutic use. In 1928, Sir Alexander Fleming, a Scottish biologist, observed that the common mold Penicillium notatum could destroy staphylococcus bacteria in culture5 and, in 1939, penicillin was finally isolated. In that same year the American microbiologist René Dubos found that the saprophyte Bacillus brevis was capable of decomposing the capsule of the pneumococcus bacterium, without which this pathogen loses its infectivity.5 The race was on to discover antibiotics, especially one with gram-negative class bioactivity. In 1944, two American microbiologists saw this dream to fruition; Selman Waksman and Albert Schatz isolated streptomycin from the actinomycete (a bacteria-like organism found in the soil) Streptomyces griseus.3 Streptomycin, the first antibiotic in its class, revolutionized the treatment of tuberculosis and other previously untreatable bacterial infections. Waksman proceeded to discover a new member of the aminoglycoside-streptomycin class of antibiotics, neomycin, in 1949, from the actinomycete Streptomyces fradiae.6 Neomycin had better bioactivity than its predecessor against gram-negative bacilli; however, the use was limited by its renal toxicity. Additionally, neomycin was not well absorbed from the gastrointestinal tract, limiting its bioavailability and indicating its utility as a topical preparation for skin and mucous membrane infections, wounds and burns. Commercial production of neomycin began in 1952.7 To this day, the aminoglycosides are the most commonly used antibiotics worldwide, due to their high efficacy and low cost. Neomycin is active against gram-negative organisms, including Escherichia coli, Proteus sp., Klebsiella sp., and Enterobacter sp.8 Aminoglycosides are irreversible inhibitors of protein synthesis. After passive diffusion via porin channels across the outer membrane of bacteria, these drugs are actively transported across the cell membrane into the cytoplasm, where they bind to specific 30S-subunit ribosomal proteins.8 This inhibits protein synthesis and is lethal for the bacterial cell. Aside from neomycin-containing creams and eye drops (see Table 1),9 other sources of exposure include dental root canal work, pet food, veterinary products, and rarely deodorants, soaps and cosmetics. Checking product labels for ingredients is imperative. Treatment of neomycin allergy requires removal and avoidance of the causative agent. Importantly, allergy to neomycin may cause cross-sensitivity to other related antibiotics, such as gentamicin, kanamycin, paromomycin, and streptomycin, and products containing any of these substances should be avoided as well. Unlike the relatives of the aminoglycoside family, which cross-react, Bacitracin, in a different antibiotic class, is a common co-sensitizer as they are often used together in products such as Neosporin and triple antibiotic creams. Testing for Neomycin Sensitivity Allergen patch testing for neomycin can be accomplished with the T.R.U.E. test [site #3]. The patient had unwittingly continued to use his allergen, neomycin, on his open-hand fissures. Once the patient was educated about his allergy and given alternative therapeutic options (See Table 2), his dermatitis cleared. Allergen identification and patient education are of the utmost importance because the mainstay of treatment for allergic contact dermatitis is avoidance. Patch testing support and patient education materials are available through the American Contact Dermatitis Society (ACDS) through the newly developed Contact Allergen Replacement Database (C.A.R.D.).
Focus on T.R.U.E. Test Allergen #3: Neomycin
T he thin-layer rapid use epicutaneous (T.R.U.E) Test of 23 common allergens is a valuable, first-line screening tool used by many dermatologists. Although the test focuses on common allergens, frequent questions have arisen from colleagues and patients as to where a specific allergen is derived or what products patients should avoid. With this in mind, this column was developed to provide educational information about the T.R.U.E. Test allergens. A rich, interesting history accompanies each of the 23 allergens, and understanding these historic perspectives can help to better educate patients. Each column will also highlight appropriate products that patients should avoid when they are allergic to a specific allergen. Contact Dermatides Allergic Contact dermatitis [ACD] is an important disease with high impact both in terms of patient morbidity and economics. ACD represents a T-helper cell Type 1 [Th1] dependent delayed-type (Type IV) hypersensitivity reaction. The instigating exogenous antigens are primarily small lipophilic chemicals (haptens) with a molecular weight less than 500 Da.1 On direct antigen exposure to the skin or mucosa, an immunologic cascade is initiated which includes cytokines, i.e. interleukin 2 [IL-2] and interferon gamma [IFN-g], T cells and Langerhan cells. This complex interaction leads to the clinical picture of ACD. The contact dermatides include allergic contact dermatitis, irritant contact dermatitis and contact urticaria. Irritant contact dermatitis, the most common form, accounts for approximately 80% of environmental-occupational based dermatoses. Contact urticaria (wheal and flare reaction) represents an IgE and mast cell-mediated immediate-type hypersensitivity reaction that can lead to anaphylaxis. The foremost example of this would be latex hypersensitivity. While this is beyond the scope of this section, we acknowledge this form of hypersensitivity due to the severity of the potential reactions and direct the reader to key sources.2,3 The primary focus of this section is to highlight the educational and pathophysiological component of allergic contact dermatitis. Clinical Illustration An atopic patient was referred to the University of Miami Allergic Contact Dermatitis Clinic by family medicine for comprehensive patch testing. The patient suffered from sustained hand and foot dermatitis for the better part of the last 8 years. He notably applied corticosteroids to his entire hands and feet, in addition to regular application of neomycin to the fissures. Neomycin: A Historical Perspective Since ancient times, preparations derived from living matter have been applied to wounds to destroy infection. Beginning around 1550 B.C. the Egyptians used a mixture of lard, honey, and lint as a wound ointment. Euro-peans began producing essential oils, which were known to have anti-bacterial activity, in the twelfth century.4 Despite this long history of caring for wound infections, the idea that a microorganism was capable of destroying another microbiotic species was not established until the latter half of the nineteenth century. It was then that Louis Pasteur’s observation of the antagonistic effect of saprophytic (soil) bacteria on the growth of anthrax bacteria spurred the notion that this interaction might be put to therapeutic use. In 1928, Sir Alexander Fleming, a Scottish biologist, observed that the common mold Penicillium notatum could destroy staphylococcus bacteria in culture5 and, in 1939, penicillin was finally isolated. In that same year the American microbiologist René Dubos found that the saprophyte Bacillus brevis was capable of decomposing the capsule of the pneumococcus bacterium, without which this pathogen loses its infectivity.5 The race was on to discover antibiotics, especially one with gram-negative class bioactivity. In 1944, two American microbiologists saw this dream to fruition; Selman Waksman and Albert Schatz isolated streptomycin from the actinomycete (a bacteria-like organism found in the soil) Streptomyces griseus.3 Streptomycin, the first antibiotic in its class, revolutionized the treatment of tuberculosis and other previously untreatable bacterial infections. Waksman proceeded to discover a new member of the aminoglycoside-streptomycin class of antibiotics, neomycin, in 1949, from the actinomycete Streptomyces fradiae.6 Neomycin had better bioactivity than its predecessor against gram-negative bacilli; however, the use was limited by its renal toxicity. Additionally, neomycin was not well absorbed from the gastrointestinal tract, limiting its bioavailability and indicating its utility as a topical preparation for skin and mucous membrane infections, wounds and burns. Commercial production of neomycin began in 1952.7 To this day, the aminoglycosides are the most commonly used antibiotics worldwide, due to their high efficacy and low cost. Neomycin is active against gram-negative organisms, including Escherichia coli, Proteus sp., Klebsiella sp., and Enterobacter sp.8 Aminoglycosides are irreversible inhibitors of protein synthesis. After passive diffusion via porin channels across the outer membrane of bacteria, these drugs are actively transported across the cell membrane into the cytoplasm, where they bind to specific 30S-subunit ribosomal proteins.8 This inhibits protein synthesis and is lethal for the bacterial cell. Aside from neomycin-containing creams and eye drops (see Table 1),9 other sources of exposure include dental root canal work, pet food, veterinary products, and rarely deodorants, soaps and cosmetics. Checking product labels for ingredients is imperative. Treatment of neomycin allergy requires removal and avoidance of the causative agent. Importantly, allergy to neomycin may cause cross-sensitivity to other related antibiotics, such as gentamicin, kanamycin, paromomycin, and streptomycin, and products containing any of these substances should be avoided as well. Unlike the relatives of the aminoglycoside family, which cross-react, Bacitracin, in a different antibiotic class, is a common co-sensitizer as they are often used together in products such as Neosporin and triple antibiotic creams. Testing for Neomycin Sensitivity Allergen patch testing for neomycin can be accomplished with the T.R.U.E. test [site #3]. The patient had unwittingly continued to use his allergen, neomycin, on his open-hand fissures. Once the patient was educated about his allergy and given alternative therapeutic options (See Table 2), his dermatitis cleared. Allergen identification and patient education are of the utmost importance because the mainstay of treatment for allergic contact dermatitis is avoidance. Patch testing support and patient education materials are available through the American Contact Dermatitis Society (ACDS) through the newly developed Contact Allergen Replacement Database (C.A.R.D.).
T he thin-layer rapid use epicutaneous (T.R.U.E) Test of 23 common allergens is a valuable, first-line screening tool used by many dermatologists. Although the test focuses on common allergens, frequent questions have arisen from colleagues and patients as to where a specific allergen is derived or what products patients should avoid. With this in mind, this column was developed to provide educational information about the T.R.U.E. Test allergens. A rich, interesting history accompanies each of the 23 allergens, and understanding these historic perspectives can help to better educate patients. Each column will also highlight appropriate products that patients should avoid when they are allergic to a specific allergen. Contact Dermatides Allergic Contact dermatitis [ACD] is an important disease with high impact both in terms of patient morbidity and economics. ACD represents a T-helper cell Type 1 [Th1] dependent delayed-type (Type IV) hypersensitivity reaction. The instigating exogenous antigens are primarily small lipophilic chemicals (haptens) with a molecular weight less than 500 Da.1 On direct antigen exposure to the skin or mucosa, an immunologic cascade is initiated which includes cytokines, i.e. interleukin 2 [IL-2] and interferon gamma [IFN-g], T cells and Langerhan cells. This complex interaction leads to the clinical picture of ACD. The contact dermatides include allergic contact dermatitis, irritant contact dermatitis and contact urticaria. Irritant contact dermatitis, the most common form, accounts for approximately 80% of environmental-occupational based dermatoses. Contact urticaria (wheal and flare reaction) represents an IgE and mast cell-mediated immediate-type hypersensitivity reaction that can lead to anaphylaxis. The foremost example of this would be latex hypersensitivity. While this is beyond the scope of this section, we acknowledge this form of hypersensitivity due to the severity of the potential reactions and direct the reader to key sources.2,3 The primary focus of this section is to highlight the educational and pathophysiological component of allergic contact dermatitis. Clinical Illustration An atopic patient was referred to the University of Miami Allergic Contact Dermatitis Clinic by family medicine for comprehensive patch testing. The patient suffered from sustained hand and foot dermatitis for the better part of the last 8 years. He notably applied corticosteroids to his entire hands and feet, in addition to regular application of neomycin to the fissures. Neomycin: A Historical Perspective Since ancient times, preparations derived from living matter have been applied to wounds to destroy infection. Beginning around 1550 B.C. the Egyptians used a mixture of lard, honey, and lint as a wound ointment. Euro-peans began producing essential oils, which were known to have anti-bacterial activity, in the twelfth century.4 Despite this long history of caring for wound infections, the idea that a microorganism was capable of destroying another microbiotic species was not established until the latter half of the nineteenth century. It was then that Louis Pasteur’s observation of the antagonistic effect of saprophytic (soil) bacteria on the growth of anthrax bacteria spurred the notion that this interaction might be put to therapeutic use. In 1928, Sir Alexander Fleming, a Scottish biologist, observed that the common mold Penicillium notatum could destroy staphylococcus bacteria in culture5 and, in 1939, penicillin was finally isolated. In that same year the American microbiologist René Dubos found that the saprophyte Bacillus brevis was capable of decomposing the capsule of the pneumococcus bacterium, without which this pathogen loses its infectivity.5 The race was on to discover antibiotics, especially one with gram-negative class bioactivity. In 1944, two American microbiologists saw this dream to fruition; Selman Waksman and Albert Schatz isolated streptomycin from the actinomycete (a bacteria-like organism found in the soil) Streptomyces griseus.3 Streptomycin, the first antibiotic in its class, revolutionized the treatment of tuberculosis and other previously untreatable bacterial infections. Waksman proceeded to discover a new member of the aminoglycoside-streptomycin class of antibiotics, neomycin, in 1949, from the actinomycete Streptomyces fradiae.6 Neomycin had better bioactivity than its predecessor against gram-negative bacilli; however, the use was limited by its renal toxicity. Additionally, neomycin was not well absorbed from the gastrointestinal tract, limiting its bioavailability and indicating its utility as a topical preparation for skin and mucous membrane infections, wounds and burns. Commercial production of neomycin began in 1952.7 To this day, the aminoglycosides are the most commonly used antibiotics worldwide, due to their high efficacy and low cost. Neomycin is active against gram-negative organisms, including Escherichia coli, Proteus sp., Klebsiella sp., and Enterobacter sp.8 Aminoglycosides are irreversible inhibitors of protein synthesis. After passive diffusion via porin channels across the outer membrane of bacteria, these drugs are actively transported across the cell membrane into the cytoplasm, where they bind to specific 30S-subunit ribosomal proteins.8 This inhibits protein synthesis and is lethal for the bacterial cell. Aside from neomycin-containing creams and eye drops (see Table 1),9 other sources of exposure include dental root canal work, pet food, veterinary products, and rarely deodorants, soaps and cosmetics. Checking product labels for ingredients is imperative. Treatment of neomycin allergy requires removal and avoidance of the causative agent. Importantly, allergy to neomycin may cause cross-sensitivity to other related antibiotics, such as gentamicin, kanamycin, paromomycin, and streptomycin, and products containing any of these substances should be avoided as well. Unlike the relatives of the aminoglycoside family, which cross-react, Bacitracin, in a different antibiotic class, is a common co-sensitizer as they are often used together in products such as Neosporin and triple antibiotic creams. Testing for Neomycin Sensitivity Allergen patch testing for neomycin can be accomplished with the T.R.U.E. test [site #3]. The patient had unwittingly continued to use his allergen, neomycin, on his open-hand fissures. Once the patient was educated about his allergy and given alternative therapeutic options (See Table 2), his dermatitis cleared. Allergen identification and patient education are of the utmost importance because the mainstay of treatment for allergic contact dermatitis is avoidance. Patch testing support and patient education materials are available through the American Contact Dermatitis Society (ACDS) through the newly developed Contact Allergen Replacement Database (C.A.R.D.).
