A Mouse Model of Trichophyton Inflammation Based on Trichophytin-induced Contact Hypersensitivity.

The prevalence of Trichophyton-induced superficial skin mycosis is very high among human patients. Dermatophytes generally infect the epidermis, especially the stratum corneum, forming scales, hyperkeratosis, and vesicles. The important roles played by the immune system in Trichophyton infection are detection of fungal invasion and elimination of fungi.These immune mechanisms are presumed to involve not only innate immunity but also acquired immunity. Therefore, there is a substantial need for studies on treatment methods based on new basic knowledge, and the elucidation of immunological mechanisms of Trichophyton-induced inflammatory reactions is especially important.However, since Trichophyton cannot colonize on the mouse skin, we tried to develop a model for Trichophyton inflammation induced by trichophytin extracted from Trichophyton mentagrophytes using a method based on contact hypersensitivity.Trichophytin is a crude extract that mainly contains fungal cell wall constituents including ß-glucan and zymosan. In this model, TLR2, TLR4, and dectin-1 were highly expressed, and production of IL-17A and IL23 was observed. This indicates that we succeeded in inducing fungal-specific inflammation in the mice.In this review, we introduce a mouse Trichophyton inflammation model developed to investigate the immunological mechanisms of Trichophyton-induced inflammatory reactions. In addition, we report results of evaluation of anti-inflammatory and anti-itching effects of anti-fungal agents using the inflammation model.

Itching in a trichophytin contact dermatitis mouse model and the antipruritic effect of antifungal agents.

BACKGROUND: Tinea is an infectious disease by dermatophytes, of which Trichophyton species accounts for the overwhelming majority of case. Tinea often causes itching with inflammation. In terms of pruritus by fungal infection, however, tinea has not been investigated sufficiently to date. AIM: To evaluate itch caused by Trichophyton infection and the effect of antifungal agents on the infection, by measuring scratch behaviour and profiles of inflammatory cytokines and chemokines. METHODS: We used a previously established mouse model of contact hypersensitivity induced by trichophytin, a crude extract from Trichophyton mentagrophytes. Scratching behaviour was recorded using a counting device that measured an electric current induced in a coil by movement of magnets that had been inserted into the hind paws of each animal. We investigated expression of various genes in lesional skin of mice and in normal human epidermal keratinocytes. We also investigated the antipruritic effects of the corticosteroid dexamethasone (DEX) and three antifungal agents: ketoconazole (KCZ), terbinafine (TBF) and liranaftate (LNF). RESULTS: Biphasic peaks of scratching were observed at 1 h and at 6-7 h during an observation period of 14 h after trichophytin induction. For lesional skin, RNA was extracted 24 h after trichophytin challenge, and increased expression was seen in the genes for interleukin (IL)-17A, interferon-γ, tumour necrosis factor (TNF)-α, macrophage inflammatory protein (MIP)-2 and Dectin-1, whereas there was no obvious change in the genes for IL-31 and prostaglandin (PG)E2. Furthermore, KCZ inhibited histidine decarboxylase (HDC) expression in vitro and in vivo, and inhibited scratching in the very early phase. LNF inhibited expression of thymic stromal lymphopoietin (TSLP) and IL-8 in vitro, and TSLP, TNF-α, IL-1α and MIP2 in vivo, and also scratching in the early phase. TBF did not induce any significant alterations in either gene expression or scratching. DEX suppressed expression of all the chemical mediators except HDC in vitro and in vivo, and inhibited scratching. CONCLUSION: Antifungals can inhibit itching induced by fungal infection through different mechanisms.

Glycyrrhetinic acid inhibits contact hypersensitivity induced by trichophytin via dectin-1.

Trichophyton infection is highly prevalent and tends to be recurrent. Therefore, it is important to develop new therapeutic agents. Previously, we established a mouse model of Trichophyton-induced contact hypersensitivity (CHS) and demonstrated that dectin-1 was involved in inflammation induced by trichophytin, the Trichophyton antigen. Here, we used that model to investigate glycyrrhetinic acid (GA) from plants of the genus Glycyrrhiza as a potential anti-inflammatory agent against superficial mycoses. GA suppressed swelling and the expression of inflammatory cytokines, including macrophage inflammatory protein (MIP)-2, interleukin (IL)-6, tumor necrosis factor (TNF)-α and interferon (IFN)-γ mRNA. Anti-MIP-2 antibody suppressed trichophytin-induced inflammation, and antidectin-1 antibody suppressed zymosan-induced MIP-2 production in keratinocyte cells. These results suggest that MIP-2 is produced by dectin-1 activation and is involved in inflammation associated with CHS to trichophytin. GA also suppressed zymosan-induced MIP-2 and interleukin (IL)-8, production in mouse and human macrophages and keratinocytes. Furthermore, GA suppressed the phosphorylation of spleen tyrosine kinase (Syk) and inhibitor of nuclear factor-kappa B (IκBα) and the degradation of IκBα in zymosan-simulated RAW264.7 cells. The results of this study suggest that GA suppresses inflammation induced by trichophytin, partly by the downregulation of Syk phosphorylation.

Possible Role of Trichophytin Antigen in Inducing Impaired Immunological Clearance of Fungus in Onychomycosis.

The immunology of onychomycosis is poorly understood. Th1 and Th17 are the principal effector cells responsible for protective immunity against fungi, while it is assumed that Th2 responses are associated with deleterious effects. The study was conducted to appraise the role of interleukin-6 (IL-6), transforming growth factor ß (TGF-ß) and immunoglobulin E (IgE) in onychomycosis patients and to study skin reactivity to trichophytin antigen in them. Serum samples of 60 cases of chronic onychomycosis and 30 healthy controls were assayed for serum IgE, IL-6 and TGF-ß levels using specific immunoassay kits; 0.01 ml of trichophytin antigen, Candida antigen and phosphate-buffered saline using separate syringes were injected intradermal at three independent sites of the forearm in cases and controls. Serum IL-6 levels were significantly lower in cases as compared to controls, while serum TGF-ß levels in both cases and controls were comparable. Serum IgE levels in cases were significantly higher when compared with controls. Thirty-eight patients showed immediate hypersensitivity response to trichophytin antigen, while none showed delayed hypersensitivity reaction to trichophytin antigen. Constant fungal antigenic stimuli induce a state of anergy as indicated by low serum IL-6 levels and the absence of delayed hypersensitivity reaction to trichophytin antigen in cases, leading to chronicity of infection. High total IgE may indicate a high probability of prior fungal sensitization.

Candidin and trichophytin stimulate the production of Th1 and regulatory cytokines by peripheral blood mononuclear cells: implication for their use as adjuvants in immunotherapy.

AIM: This study's objective was to investigate whether candidin or trichophytin elicit recall immune responses that could potentially inhibit a Th2 response. MATERIALS & METHODS: Peripheral blood mononuclear cells from nine allergic and seven nonallergic individuals were cultivated in vitro in the presence or absence of these fungal extracts. RESULTS: Trichophytin or candidin, or both, stimulated the production of regulatory cytokines (TGF-ß and/or IL-10), accompanied or not by stimulation of production of cytokines associated with the Th1 response (TNF-α, IL-12 and IFN-γ), but without stimulation of Th2 cytokines (IL-5 and IL-13) and IL-17, by peripheral blood mononuclear cells of most allergic and nonallergic individuals. CONCLUSION: These results indicate that these fungal extracts could be used as adjuvants in personalized therapeutic vaccines in a fair proportion of individuals. In addition, they justify the carrying out of investigations aimed at identifying molecules in these extracts that might exclusively induce Treg and/or Th1 immune responses.

Analysis of Trichophyton antigen-induced contact hypersensitivity in mouse.

BACKGROUND: Trichophyton-induced superficial skin mycosis is a common infectious human disease, but the immunological mechanism against Trichophyton infection is unclear with regard to many points. Since Trichophyton cannot colonize mice, guinea pigs were used in previous experiments on Trichophyton infection. However, it is difficult to perform immunological and genetic analyses in guinea pigs. OBJECTIVE: The objective of this study was to establish a mouse Trichophytin-associated inflammation model of superficial skin mycosis in which immunological and genetic analyses can be performed. METHODS: We established a mouse Trichophyton-induced contact hypersensitivity model by applying Trichophytin, the Trichophyton antigen, extracted from Trichophyton mentagrophytes, to mice. Using a Th1-dominant strain, C57BL/6, and a Th2-dominant strain, BALB/c, we investigated the expression of inflammatory cytokines and receptors of the innate immune system for fungi, TLR4, TLR2, and dectin-1, and their influences on responses of the acquired immune system. RESULTS: In C57BL/6 mice, expressions of IFN-γ and IL-17 A in regional lymph nodes and IL-1ß, IFN-γ, IL-6, and IL-23 in the inflammatory auricular skin were enhanced by Trichophytin challenge, suggesting that not only Th1 cells but also Th17 cells were induced. In BALB/c mice, expressions of IL-4 in regional lymph nodes, and TSLP and IL-4 in the auricular skin were enhanced by Trichophytin challenge. Interestingly, dectin-1-neutralizing antibody inhibited the promotion of IFN-γ production in C57BL/6 mice, and dectin-1-expressing immune cells had crucial actions in Trichophyton-induced IFN-γ production. CONCLUSION: These results suggest that inflammatory mediators differently regulate Trichophytin-induced contact hypersensitivity on the basis of the status of host immunity.

[Erythema multiforme secondary to cutaneous Trichophyton mentagrophytes infection]. / Eritema multiforme secundario a infección por Trichophyton mentagrophytes.

Erythema multiforme is an acute self-limited cutaneous syndrome associated in more than 50% of the cases with herpes simplex virus infection; but it can also be a consequence of other infectious agents or drugs. We report on a 24 year-old female patient with erythema multiforme secondary to Trichophyton mentagrophytes var. mentagrophytes cutaneous infection acquired from contact with animals in a research laboratory.

Intradermorreacciones y su aplicación: revisión bibliográfica / Skin and its application: literature review

Las intradermorreacciones consisten en la aplicación intradérmica de una sustancia conocida con la finalidad de evaluar la hipersensibilidad retardada (HSR). Se utilizan con fines diagnósticos y pronósticos en algunas enfermedades. En esta revision se identifican las características relevantes de estas pruebas

[Anti-fungal drug liranaftate suppresses fungal element-promoted production of IL-8 in normal human keratinocytes].

Dermatophytes reside in the stratum corneum of the epidermis, and one scenario in superficial dermatophytosis is that fungi stimulate keratinocytes to secrete chemokines, thereby attracting inflammatory cells. We investigated the effect of the cytokine / chemokine production of keratinocytes solely stimulated by fungal elements. The fungal elements beta-D-glucan and trichophytin from Trichophyton rubrum and Trichophyton mentagrophytes augmented production of IL-8 and IL-1 alpha of cultured normal human epidermal keratinocytes. It was found that keratinocytes can recognize elements of dermatophytes as a pathogen. Next we examined the effect of liranaftate, a representative Japanese thiocarbamate antifungal agent, on the production of IL-8 and IL-1 alpha. Keratinocytes were incubated with this antifungal drug in the presence of beta -glucan or trichophytin. Augmented production of IL-8 was profoundly suppressed by the addition of liranaftate to the culture in a dose-dependent manner. Clinically, liranaftate an antifungal drug with IL-8-decreasing activity may reduce infiltration of neutrophils in the skin and their invasion into the epidermis.

Tiñas multifocales y localizadas en pacientes inmunosuprimidos / Multicentric and localized tineas in immunocompromised patients

Desde el punto de vista dermatológico, las tiñas multifocales o multicentricasson infecciones extensas causadas por dermatofitos que abarcan dos o mássegmentos corporales. En el paciente inmunosuprimido, estas lesiones sonatípicas y los factores de riesgo asociados no han sido bien determinados.Los objetivos del presente estudio fueron determinar los factores de riesgoasociados a las tiñas multicentricas en pacientes inmunosuprimidos,determinar su etiología y evaluar la respuesta inmune a través de laintradermorreacción y la cuantificación de algunas interleucinas séricas.Treinta y seis pacientes con tiñas multifocales y 37 con tiñas localizadas,ambos grupos de pacientes inmunosuprimidos, fueron estudiados. Por mediode un cuestionario se identificaron los factores de riesgo; se aplicó tricofitina ycandidina por vía intradérmica. Se realizó examen directo y cultivo micológico.Se cuantificaron las interleucinas séricas IL-2, IL-4, IL-10 e interferón gammapor ELISA. Para el análisis estadístico se emplearon las pruebas de X2, U deMann Whitney y análisis de regresión logística.En los pacientes con tiña multicentricas se observó un predominio de mujeres(69%) respecto a los pacientes con tiña localizada (30%). La prednisona,azatioprina y ciclofosfamida fueron factores asociados a la tiña multicentrica.La tricofitina fue negativa en todos los casos de tiña multifocal y positivasolamente en tres casos de tiña localizada; la candidina fue positiva en seis yocho casos de tiña multicentrica y localizada, respectivamente. Trichopytonrubrum fue el principal agente causal. No se encontraron diferencias en lacuantificación de interleucinas.El género femenino y algunos tratamientos inmunosupresores se asociaronsignificativamente a tiñas multicentricas(AU)

From the dermatological point of view, multifocal or multicentric tineas arewidespread dermatophytic infections affecting two or more anatomical areas.In the immunosuppressed patient, these lesions are frequently atypical and therisk factors are not well established. The aims of this study were: to determinethe risk factors associated to multicentric tinea in immunecompromisedpatients; to evaluate the immune response by trichophytin and candidin skintest, to determine the etiological agent and to quantify some seruminterleukines.Thirty-six multicentric tinea and 37 localized tinea patients, both withimmunocompromised factors, were included. By means of a questionnaireseveral risk factors were identified; the trichophytin and candidin skin test wasevaluated after 48 hours. Mycological direct examination and culture wereperformed. The interleukins IL-2, IL-4, IL-10 and interferon gamma werequantified by ELISA. Statistical analysis was made by X2, U Mann Whitney andlogistic regression. In disseminated tinea patients a predominance of females (69%) versuslocalized tinea patients (30%) was observed. Prednisone, azathioprine andcyclophosphamide treatment was associated to multicentric tinea. Trichophytinwas negative in all disseminated tinea patients and positive in only threelocalized tinea cases, candidin was positive in six and eight cases ofmulticentric and localized tinea respectively. Trichophyton rubrum was themost frequent etiological agent. No differences in interleukin concentrationswere found.Female gender and some immunosuppressor treatments were associated witha high probability to develop multicentric tinea. In this study a defect in thecellular immune response was the possible explanation fo the extensivereactions(AU)

Associacao entre reatividade a tricofitina, dermatofito isolado e grupo sanguineo ABO nas dermatofitoses / Association between reactivity the trichophytin, isolated dermatofito and blood group ABO in dermatofitoses

As dermatofitoses sao infeccoes causadas por fungos que parasitam a queratina da pele, pelos e unhas. A designacao dermatofito compreende tres generos de fungos: Trichophyton, Microsporum e Epidermophyton, com caracteristicas morfologicas, fisiologicas e antigenicas que os relaciona entre si. Os estudos envolvendo a parede celular dos dermatofitos tem demonstrado que os fungos T. mentagrophytes, T. rubrum e E. floccosum possuem glicoproteinas antigenicamente semelhantes ao isoantigeno A dos eritrocitos humanos, o que tornaria esses individuos mais suscetiveis ao desenvolvimento de dermatofitoses generalizadas e resistentes ao tratamento do que aqueles desprovidos desses antigenos. Neste estudo os autores investigaram uma possivel associacao entre dermatofitose, grupo sanguineo ABO e reatividade a tricofitina atraves de identificacao do grupo sanguineo e do subgrupo A1, avaliacao da resposta imune celular especifica e identificacao do dermatofito envolvido. Assim, 39 pacientes caucasoides com dermatofitose diagnosticados atraves de sinais clinicos e laboratoriais foram submetidos a tipagem sanguinea e ao teste da tricofitina. Os resultados obtidos mostraram que o fungo T. rubrum foi isolado de 83% dos pacientes e o teste da tricofitina (reacao de hipersensibilidade tardia - 48 horas) foi positivo em 10%. A presenca de reacao imediata a tricofitina (reacao de hipersensibilidade imediata - 30 minutos) foi verificada em 51% dos pacientes. A distribuicao do grupo sanguineo entre pacientes e o grupo controle foi respectivamente: O=41% x 50%; A= 38,5% x36,0; B= 13,0% x 11,0%; AB= 7,5% x 3,0%; sendo o subgrupo A1: 61,0% x 79,0%. A classificacao da micose em aguda e cronica levando-se em consideracao o tempo em que os pacientes apresentavam as manifestacoes clinicas, revelou que 64% apresentavam lesoes ha pelo menos 1 ano. Desses pacientes, 44% pertenciam ao grupo sanguineo A, sendo 73% do subgrupo A1, e 36% pertenciam ao grupo O. Em conjunto, os resultados obtidos se...

Reactivity to trichophytin antigen in patients with onychomycosis: effect of terbinafine.

BACKGROUND: Many patients with chronic dermatophytosis and onychomycosis have depressed cell-mediated immunity (CMI) to trichophytin. OBJECTIVE: The fungicidal properties of oral terbinafine provide a unique opportunity to explore whether elimination of antigen could restore CMI response in these patients. METHODS: A double-blind, placebo-controlled study evaluated the effect of terbinafine (250 mg/d for 12 weeks) on skin immunoreactivity to intradermal trichophytin antigen (TRIPA), mycologic status of the nail, and nail growth in patients with toenail onychomycosis. RESULTS: Skin reactivity, in an optimized, dose response challenge series to TRIPA was inversely related to disease chronicity. Mycologic/clinical response rates were 72%/84% for terbinafine and 0%/7% for placebo. Terbinafine increased the number of TRIPA reactors 2-fold and the mean TRIPA reaction area 4-fold; responses in placebo-treated patients were relatively unchanged. Of the 7 (of 25) patients receiving terbinafine who still had positive mycology 6 months after treatment, all were anergic to TRIPA at baseline and all but one remained so after treatment. CONCLUSION: Terbinafine treatment enhances and restores CMI to TRIPA in patients with Trichophyton rubrum onychomycosis and may thereby reduce susceptibility to reinfection. Terbinafine reversal of immunologic anergy may be an important model of microbial tolerance in chronic dermatophyte infections.

Interferon-gamma production in peripheral lymphocytes of patients with tinea pedis: comparison of patients with and without tinea unguium.

The precise mechanism of the host defense that protects the nail from dermatophyte invasion is not known. Recent immunological findings in dermatophytosis suggest the hypothesis that the T helper 1 (Th1) response may play a role in protecting the nail from dermatophyte invasion. Our present study focused on interferon-gamma (IFN-gamma) release in patients with tinea pedis with or without tinea unguium, and pathogenesis of tinea unguium is discussed in relation to the association with a possible deficiency of Th1 response in the host defense mechanism. The production of IFN-gamma by peripheral blood mononuclear cells from the patients with tinea unguium in response to stimulation with trichophytin was not impaired in contrast to that from the patients without tinea unguium. Comparable lymphocyte proliferation to trichophytin was observed in both groups. Normal healthy persons with no clinical evidence of tinea could be divided into two groups based on lymphocyte proliferation and IFN-gamma production in response to trichophytin: high responder and low responder, with high responders being correlated with a clinical history of previous tinea pedis. In this study, a lack of a Th1 response to dermatophyte antigen was not shown in patients with tinea unguium by measuring the release of IFN-gamma, which plays a role in the effector phase of the delayed-type hypersensitivity reaction. A deficiency in the Th1 response to dermatophyte antigen, therefore, does not appear to play an important role in the establishment of tinea unguium.

Cutaneous Immune Reactions to Trichophytin in Dermatophytosis / 대한의진균학회지

BACKGROUND: The cell mediate immunity is of importance for the development of host resistance to dermatophytic infection. OBJECTIVE: The aim of this study was to estimate the clinical usefulness of purified trichophytin and to correlate cell mediate immunity to the clinical parameters of dermatophytosis, i. e. duration of infection, localization of infection and the type of dermatophyte involved. METHODS: For evaluation of cell mediate immunity in dermatophytosis, cutaneous immune reaction was measured in 102 patients with dermatophytosis (75 patients with chronic dermatophytosis and 27 patients with non-chronic dermatophytosis) by means of intradermal injection of purified trichophytin extracted from Trichophyton(T.) mentagrophytes. RESULTS: The results are summarized as follows: Patients with chronic dermatophytosis were positive in 10.7% of cases, while 51.9% of the patients with non-chronic dermatophytosis showed positive delayed cutaneous reactions (p<0.05). Of the dermatophytes isolated, 81.4% of the patients were chronically infected by T. rubrum. Delayed cutaneous reactions occured in infections with T. rubrum in only 17.1% of cases, but this difference was not statistically significant (p=0.06). Of the patients with tinea cruris, delayed cutaneous reactions were registered in 50%, but only in 15.1% those with tinea unguium (p<0.05). The significant difference in the rate of positivity in delayed reactions was not shown between the patients group with nail infection (15.1%) and the patients group without nail infection (28.6%). The rate of positivity in immediate and delayed reactions of the patients group in the multiple lesions (50%, 13.2%, respectively) was higher than that of the patients group in the single lesion (46.9%, 26.6%, respectively). CONCLUSION: The present study reinforced the hypothesis that susceptibility to chronic dermatophytosis is related to a lack of cell mediate immunity to the infectious agents and clinically, purified trichophytin is good for the evaluation of host sensitization to dermatophyte antigens as well as cell mediate immunity in dermatophytosis.

Dermatophytosis: association between ABO blood groups and reactivity to the trichophytin.

The authors investigated the relationship between dermatophytosis and ABO blood groups through blood typing, identification of isolated dermatophytes and specific cellular immune response of 40 individuals carriers of this mycosis. They verified that the fungus Trichophyton rubrum, isolated from 54.5% of the patients, was more frequent in individuals belonging to blood group A. The cellular immune response, evaluated through the trichophytin antigen, was positive in 25% of the studied patients; the presence of immediate reactions (30 minutes) was verified in 35%. The blood group distribution among patients with dermatophytosis and control groups was, respectively: 47.5% X 36% in group A, 40% X 50% in group O, 12. 5% X 11% in group B. Even though the authors have found a higher number of patients belonging to blood group A infected by T. rubrum, these results suggest that there is no statistical evidence that these individuals are more susceptible to dermatophytosis.

Dermatophytosis: association between ABO blood groups and reactivity to the trichophytin

The authors investigated the relationship between dermatophytosis and ABO blood groups through blood typing, identification of isolated dermatophytes and specific cellular immune response of 40 individuals carriers of this mycosis. They verified that the fungus Trichophyton rubrum, isolated from 54.5 percent of the patients, was more frequent in individuals belonging to blood group A. The cellular immune response, evaluated through the trichophytin antigen, was positive in 25 percent of the studied patients; the presence of immediate reactions (30 minutes) was verified in 35 percent. The blood group distribution among patients with dermatophytosis and control groups was, respectively: 47.5 percent X 36 percent in group A, 40 percent X 50 percent in group O, 12.5 percent X 11 percent in group B. Even though the authors have found a higher number of patients belonging to blood group A infected by T. rubrum, these results suggest that there is no statistical evidence that these individuals are more susceptible to dermatophytosis

Dermatophytosis: association between ABO blood groups and reactivity to the trichophytin / Dermatofitose: associação entre grupos sanguíneos ABO e reatividade à tricofitina

The authors investigated the relationship between dermatophytosis and ABO blood groups through blood typing, identification of isolated dermatophytes and specific cellular immune response of 40 individuals carriers of this mycosis. They verified that the fungus Trichophyton rubrum, isolated from 54.5 percent of the patients, was more frequent in individuals belonging to blood group A. The cellular immune response, evaluated through the trichophytin antigen, was positive in 25 percent of the studied patients; the presence of immediate reactions (30 minutes) was verified in 35 percent. The blood group distribution among patients with dermatophytosis and control groups was, respectively: 47.5 percent X 36 percent in group A, 40 percent X 50 percent in group O, 12.5 percent X 11 percent in group B. Even though the authors have found a higher number of patients belonging to blood group A infected by T. rubrum, these results suggest that there is no statistical evidence that these individuals are more susceptible to dermatophytosis

Os autores investigaram a relação entre dermatofitose e grupos sanguíneos ABO por meio da tipagem sanguínea, identificação de dermatófitos isolados e resposta imune celular específica de 40 indivíduos portadores dessa micose. Verificaram que o fungo Trichophyton rubrum, isolado de 54,5 por cento dos pacientes, era mais frequente em indivíduos pertencentes ao grupo sanguíneo A. A resposta imune celular, avaliada pelo antígeno tricofitina, foi positiva em 25 por cento dos pacientes estudados; a presença de reações imediatas (30 minutos) foi verificada em 35 por cento. A distribuição do grupo sanguíneo entre os pacientes com dermatofitose e grupos controle foi, respectivamente: 47,5 por cento X 36 por cento no grupo A, 40 por cento X 50 por cento no grupo O, 12,5 por cento X 11 por cento no grupo B. Mesmo que os autores encontraram um maior número de pacientes pertencentes ao grupo sanguíneo A infectado por T. rubrum, estes resultados sugerem que não há evidências estatísticas de que esses indivíduos sejam mais suscetíveis à dermatofitose

Prevalence of undetected tinea capitis in a school survey in Spain.

From October 1994 to November 1995, a prospective study aiming to detect dermatophytes on the scalp was undertaken in 5000 unselected school children aged between 3 and 16 years (mean age 8.34 years, SD +/- 3.83). Thirty-two (0.64%) had dermatophytes in the scalp, 22. (0.44%) had tinea capitis and 10 were asymptomatic scalp carriers. It is important to point out that 33% of the patients with tinea capitis and 60% of the asymptomatic scalp carriers also had ringworm in other body sites. There was a significantly higher proportion of cases of tinea capitis (P < 0.001)(particularly due to Trichophyton tonsurans, P < 0.001) and of cases of asymptomatic scalp carriers (P < 0.05) (particularly due to Trichophyton tonsurans, P < 0.001) in the immigrant population of African origin. In all the child index cases with positive scalp cultures (tinea capitis and carriers), the household members were studied clinically and mycologically. One child had a body ringworm caused by Microsporum canis. Twelve adults had positive cultures with dermatophytosis (one tinea capitis and eleven body ringworm). Three adult patients were also carriers of dermatophytes in other body sites. Our data indicate a change in the causative agents of tinea capitis seen in Madrid over a 12-month period, with cases due to antropophilic species (T. tonsurans, T. soudanense, M. audouinii and T. violaceum) occurring in the immigrant population from Africa; as a consequence, there is an emergence of T. tonsurans in the Spanish population.