Dermatophytes grow extensions that infect the top layer of the skin. The base layer of the skin makes more skin cells than normal and the cells are moved to the surface which causes the skin to become scaly and thicken.
A dermatophyte attacks the skin. A dermatophyte develops colonies on the skin of the foot. Johansson and coworkers showed that a positive response to patch testing with Malassezia furfur in atopic dermatitis patients correlated with a Th2 cytokine response IL-4, IL-5, and IL in peripheral blood mononuclear cells [ 36 ]. The possible interactions of dermatophytes with T-cells and triggering of atopic disease is shown in Figure 4.
The first two cytokines can lead to two pivotal effects: synthesis of IgE by B cells and endothelial activation leading to eosinophil recruitment by a vascular cell adhesion molecule VCAM -very late activating antigen 4 VLA-4 adhesion molecule pathway. Both IgE and eosinophils play a prominent role in atopic disease. IgE in the presence of antigen can cross-link mast cells leading to further cytokine, chemokine, and mediator production.
The other cytokine, IL-5, enhances eosinophil production from the bone marrow, eosinophil activation, survival, recruitment, and degranulation. These processes can result in expression of atopic disease, from rhinitis and asthma to atopic dermatitis.
The first 2 cytokines can lead to two pivotal effects: Synthesis of IgE by B cells and endothelial activation leading to eosinophil recruitment by a vascular cell adhesion molecule VCAM -very late activating antigen 4 VLA-4 adhesion molecule pathway. IgE in the presence of antigen can cross-link mast cells leading to further cytokine, chemokine and mediator production.
The other cytokine, IL-5, enhances eosinophil production from the bone marrow, eosinophil activation, survival, recruitment and degranulation. Tinea pedis infections are typically easy to distinguish and diagnose. However, complete identification of the causative fungi should be established to confirm diagnosis and ensure proper treatment. Diagnosis of tinea pedis is based on history and clinical appearance of the feet in addition to direct microscopy of a potassium hydroxide KOH preparation.
Cultures or histological examinations are rarely required. A Wood's lamp is not usually helpful in diagnosing tinea pedis but can be used to rule out other diagnoses like infection with Malassezia furfur [ 1 ] or erythrasma [ 14 ]. Malassezia furfur and Corynebacterium minutissimum both fluoresce under ultraviolet light while other common dermatophytes do not. KOH preparations are simple, inexpensive, efficient, and widely used.
The KOH preparation also has an excellent positive predictive value. Occasionally, false negative results may be obtained, especially if treatment has already begun. To prepare a KOH slide of the suspected fungi, the procedure has to be followed carefully. First of all, skin cells from the periphery of the affected area are scrapped off onto a glass microscope slide with a sterile scalpel blade.
Slide preparations should then be examined under low or medium power of a microscope. If a vesicle is being examined, it may be unroofed so the inside material may be examined. KOH preparation of fungal hyphae. This slide shows the branched hyphae of T. Scrapings from the outer edge of a tinea lesion should be taken with a sterile scalpel, placed on a slide and KOH applied.
KOH dissolves the epithelial cells seen in the background and leaves the fungus to be viewed by microscopy. Tinea Pedis usually responds to topical antifungal agents such as ketoconazole, terbinafine, econazole, or cicloprox creams. In the case of interdigital infection, antifungal powder preparations may be more effective. Topical treatment may need to be continued for at least 4 weeks and recurrences are common.
For refractory or resilient disease, oral antifungals may be required. Treatment options and dosing are explained in greater detail below and are reviewed in Table 3. Oral treatment with griseofulvin, itraconazole, fluconazole, and terbinafine may all be effective for this disease. Drug resistance, adverse effects of medications and drug interactions are all major hurdles to successful completion of therapy. An evaluation for etiologies for immunosupression such as new onset diabetes or malignancy may be indicated in selected patients.
Possible drug-drug interactions are listed in Table 4 , adapted from "Oral antifungal drug interactions" by Katz and Gupta [ 37 ]. Non-pharmacological treatment focuses on educating patients about the predisposing factors, and the chronic nature of disease. Also, measures that are aimed at eliminating the moisture that provides the environment for infection and its recurrence should be discussed fully with the patients. Instructions about wearing open-toed shoes and avoiding skin maceration are essential.
Data has shown that topical antifungal treatment fails to cure about one-third of patients with tinea pedis [ 38 ]. However, most of the relapses were due to poor compliance. So it must be emphasized that the patient should continue topical treatment at least one week after symptoms have resolved.
The application area should include normal skin about 2 cm beyond the affected area. Many studies have compared the efficacy and rate of relapse upon applying different topical antifungal agents. A comparison study by Suschka et al. Topical corticosteroids combined with topical antifungal agents for example, in the form of clotrimazole-betamethasone provide rapid symptomatic relief in addition to eradication of the causative organism. With long-term use of topical glucocorticosteroids atrophy and steroid-induced rosacea and striae may occur.
These combination agents are relatively contraindicated in children under12 years of age [ 1 ]. Systemic treatment may be required for patients who have failed with topical antifungal therapy. It can also be used as a first line therapy in patients with severe disease like hyperkeratotic lesions or in patients who are immunosuppressed [ 40 ]. A list of common oral therapies and their dosages are listed in Table 3. Griseofulvin concentrates in the stratum corneum of the skin and causes mitotic arrest during microtubule spindle formation in actively growing fungi [ 41 ].
Cure is difficult to achieve and the recurrence rate is high. Blood counts and serum chemistry including renal and hepatic function should be checked regularly throughout treatment, as Griseofulvin may have toxic effects on the liver. The azoles, as a group, include ketoconazole, itraconazole, and fluconazole. Doses, indications for usage, and adverse effects are all readily available in textbooks. Ketoconazole treatment is indicated when griseofulvin therapy has failed or when the patient cannot tolerate it.
Blood counts and serum chemistry should be monitored more frequently during this therapy. Dosage adjustment may not be necessary in patients with renal failure. Absorption is improved by food, so food intake should be encouraged with the ketoconazole treatment. Due to its structural difference, itraconazole has greater efficacy and less toxicity as compared with other azoles. Also its absorption is enhanced by coadministration with food.
No dose adjustment is needed in renal failure. Fluconazole has more potency, less toxicity, and wider spectrum of action than earlier azoles. Fluconazole and itroconazole should not be given together with terfenadine, astemizole, and cisapride in view of the risk of cardiac arrhythmia. Another group of drugs classified as allylamines include terbinafine as a member. These drugs act by destroying the fungal cell wall at a much earlier stage in its development than the azoles.
Terbinafine may be the most effective treatment for tinea pedis. However, as a cost-effective option it is not the first line of therapy. Blood counts, platelet count, and liver enzymes should be repeated every 4—6 weeks with this therapy. Allylamines must be stopped if liver enzyme measurement exceeds twice the normal level. Tinea pedis is a common dermatophyte infection of the feet. Classifying the type and causative organism of tinea pedis is important for proper treatment of the patient.
The easiest way to test for fungal presence is by microscopy of a KOH preparation, but complete identification of the organism requires culturing. Tinea pedis infection can contribute not only to fungal dermatitis but also to flares of eczema and asthma. Tinea pedis may lead to severe bacterial cellulitis. Aggressive treatment of tinea pedis can be associated with improvements in atopic dermatitis, asthma and cellulitis in affected individuals. Weinstein A, Berman B: Topical treatment of common superficial tinea infections.
Am Fam Physician. PubMed Google Scholar. Cochrane Database Syst Rev. Google Scholar. The nail becomes thick, opaque, whitish, and crumbly. There may be pain and inflammation in the skin under the nail. Untreated toenail infections may eventually lead to more pain and problems wearing shoes, or even walking.
Secondary bacterial infection: If this develops the foot may become painful, hot, and swollen. Infected lymph system: The infection can sometimes spread to the lymph system. Lymphangitis is an infection of the lymph vessels, and lymphadenitis is an infection of the lymph nodes. Cellulitis: This is a bacterial infection deep in the skin. Skin, fat, and soft tissue may be affected. Untreated cellulitis can lead to serious complications, such as septicemia blood poisoning or bone infection.
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It's easy! Click here to learn about editing. Editor-In-Chief: C. Michael Gibson, M. Young, Inc. Tinea pedis became more popular in the US and United Kingdom because of the popularisation of occlusive footwear and the habit of wearing socks which retained moisture around the feet. Prior to this, tinea affecting the feet was very rare. Tinea pedis interestingly affected members of the British Army who bathed more often and maintained general personal hygiene.
The number of people infected only increased during WW2, with it being rampant among the troops stationed in the tropics.
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