The preparation of food in restaurant kitchens carries a high risk of occupational dermatoses. Analysis of 33 cases revealed four different etiological types. Simple irritant dermatitis was rare (2 cases), plain contact dermatitis was more common (6 cases). Fifteen patients had relevant patch tests and scratch tests; ten had positive scratch tests only to explain the cause of their dermatitis. The last type was termed protein contact dermatitis. The major type IV allergens incriminated were metals, onion and garlic. The major proteinaceous allergens indicated by history and test results were fish and shell-fish. Open patch tests with the incriminated foods may cause erythema or oedema on normal skin after 20 minutes. Previously eczematous, now normal looking, skin often responds with a crop of dyshidrotic vesicles preceded by erythema and itching 30 minutes after the application of an open test. Examination for specific IgE is not always positive in such cases. Inhalant allergy was rare. The results indicate that food handlers are sensitized by the protein they touch, and then react to later contact with the proteins. Protein contact dermatitis is similarly common among veterinary surgeons, while the importance in other occupational groups remains to be studied.

Occupational protein contact dermatitis in food handlers.

The last decade has witnessed remarkable advances in the therapy for cutaneous fungal diseases. These will have a major impact on the choice of antifungal therapy. To understand these advances traditional therapies for fungal diseases, the polyenes, griseofulvin, older topical agents and the older azoles, will be reviewed first. Part II will focus on recent advances.

https://www.jaad.org/article/S0190-9622(08)81495-8/pdf

Antifungal agents: An overview. Part II

Atopic dermatitis is a disease of fascination and frustration to medical practitioners and researchers. This very common disorder is confusing from several standpoints. The confusion begins with nomenclature; in discussions with American nondermatologic physicians, we might hear atopic dermatitis referred to as "eczema," allergic dermatitis, allergic eczema, or even neurodermatitis. Many Europeans continue to use the term prurigo Besnier. Diagnostic features of atopic dermatitis are another source of confusion. The skin lesions a pediatrician sees on a child's skin may be vastly different from the lesions the general practitioner sees on that same individual 15 years later. There may be no single distinguishing characteristic; diagnosis may depend on a combination of morphologic, distributional, and historical features. Histological findings provide very little aid in diagnosis, though a recent preliminary report by Mihm et al 1 raises the hope that new histologic techniques may reveal distinct histopathologic features in atopic dermatitis. With

Newer concepts of atopic dermatitis.

Tissue sections from involved and uninvolved skin of nine patients with atopic dermatitis (AD) were investigated by light microscopy, electron microscopy, and an immunoperoxidase method using monoclonal antibodies to cell-surface antigens. Acute lesions were characterized by spongiotic epidermis, with increased numbers of infiltrating mononuclear cells consisting predominantly of lymphocytes. Perivascular dermal infiltrates consisted of lymphocytes and a few monocytes-macrophages. Capillary endothelial cells were not enlarged. In chronic lesions the epidermis was hyperplastic, with virtually no cellular infiltrate. The perivascular dermal infiltrates consisted primarily of monocytes-macrophages intermixed with lymphocytes. Capillary lumens were narrowed by enlarged endothelial cells. The majority of the infiltrating lymphocytes in all skin biopsy specimens from AD patients were stained with anti-T3, anti-Leu-1, anti-T4, and anti-Leu-3 antibodies, suggesting that most of the infiltrating lymphocytes were T cells possessing the helper/inducer phenotype. In contrast, a smaller number of infiltrating cells reacted with anti-T8 or anti-Leu-2 antibodies, which define the suppressor/cytotoxic T cell population. Langerhans cells, as defined by reactivity with anti-T6 monoclonal antibody, were increased in the diseased skin of AD patients. The presence of increased numbers of Langerhans cells and T cells of the helper/inducer phenotype may reflect increased antigen processing in the diseased skin of patients. In addition, the smaller number of T8+ cells infiltrating into the skin suggests that the depression of circulating T8+ cells observed in the majority of patients with AD is not due to the selective migration of these T8+ cells into the skin.

Characterization of the mononuclear cell infiltrate in atopic dermatitis using monoclonal antibodies

1 History and Nomenclature.- 1.1 History.- 1.2 Nomenclature.- References.- 2 Clinical Aspects.- 2.1 Prevalence.- 2.1.1 Worldwide Distribution.- 2.1.2 Sex Incidence.- 2.2 Course.- 2.2.1 Onset, Phases, and Morphological Characteristics.- 2.2.2 Infantile Phase.- 2.2.3 Childhood Phase.- 2.2.4 Adolescent/Young Adult Phase.- 2.2.5 Onset at Elder Age.- 2.3 Prognosis.- 2.3.1 Phases and Prognostic Problems.- 2.3.2 Cases Healed After the Infantile Phase.- 2.3.3 Clearing of the Disease.- 2.4 Basic Clinical Features.- 2.4.1 Primary Trait.- 2.4.2 Prurigo.- 2.4.3 Lichenification.- 2.4.4 Eczematous Lesions.- 2.4.5 Correlation Between Itch and Major Features.- 2.5 Morphology and Distribution.- 2.5.1 Sites of Predilection.- 2.5.2 Head and Face.- 2.5.3 Body.- 2.5.4 Hands.- 2.5.5 Feet.- 2.6 Other Essential Features.- 2.6.1 Dry Skin.- 2.6.2 Photosensitivity.- 2.7 Special Clinical Types.- 2.7.1 Follicular Type.- 2.7.2 Inhalative (Hand) Eczema.- 2.8 Correlations Between Distribution and Pathomechanism.- 2.9 Complications Caused by Living Agents.- 2.9.1 Staphylococcal Infections.- 2.9.2 Viral Infections.- 2.9.3 Dermatophytosis and Candida.- 2.9.4 Scabies and House Dust Mite.- 2.9.5 Pityrosporon Orbiculare.- 2.10 Complication of the Malfunctioning Immunomechanisms.- 2.10.1 Atopic Erythroderma.- 2.10.2 Some Types of Cutaneous Lymphoma.- 2.10.3 Alopecia Areata and Vitiligo.- 2.11 Other Complications.- 2.11.1 Atopic Cataract.- 2.12 Associated Conditions Proven Correlations.- 2.12.1 Atopic Correlations.- 2.12.2 Bronchial Asthma.- 2.12.3 Atopic Rhinoconjunctivitis.- 2.12.4 Oral Symptoms.- 2.12.5 Gastrointestinal Symptoms.- 2.13 Xerosis-Ichthyosis Group.- 2.14 Probable Correlations.- 2.14.1 Drug Reactions of the Immediate Type.- 2.14.2 Systemic Diseases (Related to Impaired Cell-Mediated Immunity).- 2.14.3 Certain Types of Urticaria.- 2.15 Possible Correlations.- 2.15.1 Some Genetic Disorders with Eczematous Lesions.- 2.15.2 Adult Celiac Disease/Dermatitis Herpetiformis.- 2.15.3 Other Conditions.- 2.16 Coexistence of AD with Common Skin Diseases.- References.- 3 Itch.- 3.1 Short Survey.- 3.1.1 Itch and Pain.- 3.1.2 Mediator of Itch.- 3.1.3 Nonchemical Stimuli.- 3.1.4 Itch and Late Cutaneous Reactions.- 3.2 Role of Itch in AD.- 3.2.1 Itch as the Essential Symptom of AD.- References.- 4 Histopathological and Laboratory Findings.- 4.1 Histopathological Findings.- 4.2 Laboratory Findings.- References.- 5 Pathomechanism: Genetic and Immunological Factors.- 5.1 Genetic Factors.- 5.1.1 Mode of Inheritance.- 5.1.2 Transmission of IgE and Other Features.- 5.1.3 Practical Consequences for the Clinician.- 5.2 Atopic Allergens.- 5.2.1 General Remarks.- 5.2.2 Skin Testing.- 5.2.3 Inhalants: Pollen.- 5.2.4 Inhalants: Animal Hair.- 5.2.5 Inhalants: Human Dandruff.- 5.2.6 Inhalants: House Dust and House Dust Mites.- 5.2.7 Inhalants: Molds.- 5.2.8 Other Inhalants.- 5.2.9 Inhalants Eliciting Contact Reaction.- 5.3 Foods.- 5.3.1 General Remarks.- 5.3.2 Food Reactivity.- 5.3.3 Frequent Food Allergens.- 5.3.4 Skin Reactivity.- 5.3.5 Challenge Tests.- 5.3.6 Late and Non-IgE-Mediated Food Reactions.- 5.3.7 Concluding Remarks.- 5.4 Other Allergens from Living Agents.- 5.4.1 Staphylococci and Other Bacteria.- 5.4.2 Dermatophytes and Candida.- 5.4.3 Scabies Mite, Insects, and Helminths.- 5.5 The Atopic Antibody.- 5.5.1 General Remarks.- 5.5.2 IgE in AD.- 5.5.3 RAST.- 5.5.4 Non-IgE Antibodies.- 5.5.5 Evaluation of Immediate Type Skin Reactions.- 5.6 Contact Reactivity.- 5.6.1 Allergic Contact Dermatitis.- 5.6.2 Irritative Contact Dermatitis.- 5.7 Delayed (Tuberculin-Type) Reactivity.- 5.7.1 In Vivo Reactivity.- 5.7.2 In Vitro Reactivity.- 5.7.3 Leukocytes and Monocytes.- 5.7.4 Antigen-Presenting Cells.- 5.7.5 Skin Infiltrate.- 5.7.6 Anti-Infectious Resistance.- 5.7.7 Cell-Mediated Immunity in Respiratory Atopies.- 5.8 Other Reaction Types.- 5.9 Concluding Remarks.- References.- 6 Pathomechanism: Cells and Mediators.- 6.1 Mast Cells and Histamine.- 6.1.1 Mast Cells.- 6.1.2 Histamine.- 6.1.3 Histamine Inhibition.- 6.2 Eosinophils and Their Products.- 6.3 Cyclic Nucleotides.- 6.3.1 Introduction.- 6.3.2 Conditions in Atopy/AD.- 6.3.3 Concluding Remarks.- 6.4 Eicosanoids.- 6.4.1 Prostaglandins.- 6.5 Complement.- 6.6 Other Mediators.- 6.6.1 Acetylcholine.- 6.6.2 Kinins.- 6.6.3 Miscellaneous.- References.- 7 Pathomechanism: The Altered Skin.- 7.1 Itch.- 7.2 Alteration of Skin Structure and Some Consequences.- 7.2.1 Epidermodermal Changes.- 7.3 Water Exchange.- 7.3.1 Sweat Secretion.- 7.3.2 Transepidermal Water Loss.- 7.3.3 Sebum Excretion.- 7.3.4 Skin Dryness.- 7.4 Paradoxical Vascular Responses.- 7.4.1 White Dermographism.- 7.4.2 Nicotinate Reactions.- 7.4.3 Delayed Blanch and Comments.- 7.4.4 Further Vascular Changes.- 7.5 Other Alterations.- 7.5.1 Pilomotor Reaction.- 7.5.2 Endocrine Alterations.- 7.6 Concluding Remarks.- References.- 8 Pathomechanism: Attempt at Synthesis.- 8.1 Animal Models.- 8.2 Attempt at Synthesis.- References.- 9 Factors Influencing the Course of AD.- 9.1 Seasonal Dependence.- 9.2 Climatic Factors.- 9.3 Some Environmental Factors.- 9.4 Socioeconomic Environment.- 9.5 Occupation.- 9.6 Psychological Factors.- 9.7 Other Factors.- 9.7.1 Military Service and Sports.- 9.7.2 Hormonal Influences.- 9.7.3 Infections.- 9.7.4 Problems with Schooling in Young AD Patients.- References.- 10 Diagnosis and Grading (Severity).- 10.1 Diagnostic Criteria.- 10.2 Differential Diagnosis.- 10.3 Grading (Severity).- References.- 11 Prophylaxis.- 11.1 Food Avoidance.- 11.1.1 Sensitization in Utero.- 11.1.2 Breast Feeding.- 11.1.3 Avoidance Diets.- 11.2 Inhalant Allergens.- 11.3 Occupational Prophylaxis.- 11.4 Other Measures.- References.- 12 Management of AD.- 12.1 Specific and Immunological Therapy.- 12.2 General Measures.- 12.2.1 Climatotherapy.- 12.2.2 Hospitalization.- 12.3 Systemic Therapy.- 12.3.1 Antipruritics.- 12.3.2 Anti-Inflammatory Agents.- 12.3.3 Light Therapy.- 12.3.4 Chromones.- 12.3.5 Essential Fatty Acids.- 12.3.6 Anti-Infectious Agents.- 12.4 Topical Therapy.- 12.4.1 Antipruritics and Tars.- 12.4.2 Topical Corticosteroids.- 12.4.3 Treatment of Acute Eczematous Reaction.- 12.4.4 Measures Against Dryness.- 12.4.5 Antibacterial and Antimycotic Agents.- 12.4.6 Special Points for Infantile Eczema.- 12.4.7 Newer Topical Therapy.- 12.5 Concluding Remarks.- References.

Essential Aspects of Atopic Dermatitis

Summary.— Tests of immune function over a 12-month period in a young woman and a young man with life-long atopic dermatitis showed depressed cell-mediated immunity (CMI) (delayed-type skin test unresponsiveness, inability to be sensitized to DNCB, diminished responsiveness of cultured lymphocytes to phytohaemagglutinin, enlarged subcutaneous lymph nodes without any cell-mediated immunopathology, but with the structure of a node involved in humoral antibody production). Direct immunofluorescence localized IgE in the germinal centres of these subcutaneous lymph nodes. No anti-immunoglobulin or anti-C3 complement fluorescent conjugates were localized in their involved or uninvolved skin. Cells corresponding to small-and medium-sized lymphocytes in concentrated peripheral leucocyte smears stained with FITC antiserum to human IgE. The woman's lymphocyte transformation suppression improved during a remission and relapsed during an exacerbation of the dermatitis.

Suppressed cell-mediated immunity in two adults with atopic dermatitis.

SUMMARY

Patients with Trichophyton mentagrophytes and T. rubrum infections were compared in terms of cutaneous responses and in vitro lymphocyte reactivity to trichophytin and other antigens. Twelve out of fourteen T. mentagrophytes patients exhibited delayed cutaneous hypersensitivity to trichophytin. Most T. rubrum patients (thirty-seven out of forty-nine) lacked delayed reactions to trichophytin specifically, but these patients frequently manifested immediate weal reactions to this antigen. Positive lymphocyte responses correlated with the presence of delayed but not immediate cutaneous reactions. Serum from chronic T. rubrum patients failed to inhibit lymphocyte responses. Possible mechanisms for selective anergy in chronic T. rubrum patients are discussed.

Immunological reactivity in dermatophytosis

HEREDITARY disorders of amiiao-acid metabolism, central nervous system function and development, skeletal growth, ectodermal differentiation and chromosomal abnormalities are associated with abnormal hair development. In this paper we will consider tbose genetic disorders which involve hair in relation to the essential biochemical, anatomical, physiological and genetic factors producing the hair's defect. We will also emphasize the usefulness of hair aa a genetic marker. Various pelages, the rates of bair growth, structure of tbe hair shaft and hair follicle, and tbe regional variations of hair growth and structure are of primary importance when one evaluates hair in genetic disorders. Tbe abnormalities of bair should be divided into those that involve its texture, its density and its colour. Abnormalities which exclusively involve hair colour are purposely omitted from tbis paper because an entirely different genetic system regulates melanin synthesis; and we will not address ourselves to this. The regulation of the human hair cycle is one of the most mysterious biological events. Hair follicles develop in the 2nd-5th month of intra-uterine life (Pinkus, 1958). Thia first pelage (all Ianugo) is shed iu 7tb-8tb foetal month. After birth no new hair foUicles are formed unless as a response to severe trauma (Rook, 1060). The scalp hair grows for 1000 days (anagen), and will then rest for 100 days (telogen). However, the cycle can vary from 120 days to 7 years (Goodwin, 1059). There are 80-90 hairs in anagen to every 10-20 hairs in telogen. In man, this time of resting and growing differs from follicle to follicle; each is autonomous. In contrast tlie growth is synchronous in sheep, all follicles resting at one time; in rats and mice there is a wave of telogen whicb spreads from the ventral to the dorsal and then from anterior to posterior. At a certain time in life haii's change character (Duggins and Trotter, 1051; Wynlioop, 1029; Pecoraro et al., 1064). Some ofthe fine, short, wavy, lightly-pigmented hairs (vellus) of childhood become the long, dark, thick hairs (terminal hairs) of the body and face of the adult. Some become intermediate, neither vellus nor terminal. These changes are produced by numerous factors. For example, Garn (1951) has even proposed a classification of hair baaed on the effect of steroid hormones (Table I). hi general, the diameter, the rates of hair growtii, and hair pigmentation increases with age. There are regional exceptions (Danfort-b, 1025), most notable of whicb is man's scalp. Little tias been written ofthe hair root itself, yet it is here that abnormalities in hair synthesis are first reflected. The ratio of anagen to telogen hairs ia a simple matter to determine (Rook, 1065). Anagen bair has a well developed internal and

Human hair: a genetic marker.

On page 145 of this issue there is an article associating the diseases psoriasis vulgaris and pustular psoriasis with antigens of the major human histocompatibility system, HL-A. The premise for investigating the frequency of the antigens of the HL-A system was originally based on solid evidence from studies in mice showing that the susceptibility to certain oncogenic viruses is partly controlled by the major histocompatibility system (H-2) of that species (Lilly, 1973). Since there is considerable similarity between the H-2 system of mice and the HL-A system of man, it was quite natural to expect that some HL-A antigens would occur with increased or decreased frequencies in various diseases. Furthermore, there is historical precedent for such expectations. In 1945, the distinguished British geneticist, E.B. Ford, suggested studying blood-group frequencies in himian diseases because the genetic theory of natural selection assumes that no genes are likely to have only neutral effects (Fisher, 1930). Ford's prediction was proved correct by the discovery of a higher frequency of blood group O in patients with duodenal ulcer and of blood group A in patients with gastric carcinoma (Aird, Bentall & Frazer Roberts, 1953; Aird, et al., 1954). The HL-A system (major human histocompatibility system) consists of a large number of known and a still totally unlmown number of closely linked loci on chromosome number 6 (Lamm et al., 1974). These gene loci pass on information through RNA to the cell's surface membrane as gene products. Such gene products are most likely proteins and are easily detected as antigens on peripheral blood ljnnphocytes by means of humoral antibodies that have arisen during previous immunizations by blood transfusions and pregnancies. These antigens (gene products) are inherited as stable codominant characters controlled by two series of allelic genes on chromosome number 6. One series is called LA (or First) and the other FOUR (or Second). These names have been acquired for historical reasons not pertinent to this discussion. Since the surface antigens (gene products) are inherited as stable co-dominant characters, and since they are controlled by allelic genes within each of the two series, LA and FOUR, each individual can have only two antigens from each series. However, as there are at least fourteen different LA and twenty diflFerent FOUR antigens in the population they can be combined in many thousands of ways. The individual HL-A antigens have frequencies in the populations varying from about 50% to less than 1%. Table i lists the HL-A antigens (also called HL-A determinants) with the per cent and gene frequencies of the two series, LA and FOUR. In addition to the numbered HIL-A antigens (eg. HL-Ai, HL-A5) there are some numbers prefixed by the letter W (eg. W19, W5). These are current designations given by the WHO Nomenclature Committee to identify these HL-A antigens at the present time. For even more recently discovered antigens local designations are used (e.g. MK and TY). Also, it should be recalled that gene loci on chromosomes are paired, one on each of the homologous chromosomes opposite each other. The genetic HL-A information carried by one chromosome is called a haplotype and comprises one LA and one FOUR gene. One of the two haplotypes is handed on from each parent to the child usually in an unaltered form (Fig. i). These haplotype frequencies can be determined. As one might expect, cross-overs from within one haplotype to another may occur and the frequency with which this happens is reported as the recombination frequency. For clinical studies, the HL-A typing which is performed on freshly drawn blood uses most but rarely all of the HL-A antigens presently identified. In the study reported, all individuals were investigated for the LA series antigens HL-Ai, 2, 3, 9, 10, 11, W28, and W19, and for the FOUR

Walter C. Lobitz

Papers

Suppressed cell-mediated immunity in two adults with atopic dermatitis.

Immunological reactivity in dermatophytosis

Human hair: a genetic marker.

HL-A histocompatibility antigens and skin diseases.