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Tinea pedis with bacterial infection,ear nose & throat associates 2014,ringing ears 3 days rhye - Downloads 2016

Author: admin | 15.05.2014 | Category: Tinnitus Causes And Treatments

This is tinea pedis, a presentation known as "moccasin" tinea because it encases the foot like a moccasin slipper. Because foot eczema and psoriasis can resemble moccasin tinea, the diagnosis should always be confirmed by scraping the affected skin for microscopy using potassium hydroxide and fungal culture.
This dermatology case history quiz was also published by ADIS International in in July 2001. AbstractTinea pedis is a chronic fungal infection of the feet, very often observed in patients who are immuno-suppressed or have diabetes mellitus. IntroductionDermatophytic infection of the skin can manifest in different anatomical regions of the body and have been accordingly named. PathogensThree species of fungi, Trichophyton rubrum, Trichophyton mentagrophytes, and Epidermophyton floccosum are together responsible for the vast majority of cases of tinea pedis throughout the world. Clinical syndromesDepending on the pathogen and anatomical distribution, tinea pedis may present in a given patient as one of several syndromes.
Interdigital tinea pedis is the most common form and usually manifests in the interspace of the fourth and fifth digits and may spread to the underside of the toes (Figure 1) [4, 8]. In some cases as described recently, tinea pedis may mimic bacterial cellulitis due to the inflammatory component [11].
The moccasin type is a more severe, prolonged form of tinea pedis that covers the bottom and lateral aspects of the foot. Over the past decade, many fungi that were once thought not to infect humans have suddenly emerged as human pathogens. Cellulitis is a bacterial infection of the subcutaneous layers of the skin, which usually stems from a skin lesion or wound. Semel and Goldin describe 24 episodes of lower extremity cellulitis in 22 patients, 20 of which had tinea pedis [12]. Saphenous venectomy has also been associated with increased incidence of cellulitis and tinea pedis infection may be a complicating factor [16, 17].
Tinea unguium is a fungal infection, usually with a dermatophyte, on the matrix, plate, or nail bed commonly associated with tinea pedis. Dermatophytid, also referred to as the "ID" reaction, is an immunological reaction secondary to tinea pedis along with other tinea infections. Molecular immunopathogenesisThe relationship between fungal dermatitis and atopic disease is interesting.
TreatmentTinea Pedis usually responds to topical antifungal agents such as ketoconazole, terbinafine, econazole, or cicloprox creams. Non-pharmacological treatment focuses on educating patients about the predisposing factors, and the chronic nature of disease. Data has shown that topical antifungal treatment fails to cure about one-third of patients with tinea pedis [38]. Systemic treatment may be required for patients who have failed with topical antifungal therapy. Griseofulvin concentrates in the stratum corneum of the skin and causes mitotic arrest during microtubule spindle formation in actively growing fungi [41].
AcknowledgmentsThis report was supported by NIH grants AI-43310 and HL-63070, and the Department of Internal Medicine at East Tennessee State University.
Moccasin tinea may be resistant to topical antifungal agents, but these should be recommended initially for a period of several weeks. Thus, tinea capitis affects the scalp, tinea barbae- the face, tinea unguum- the nails, tinea manuum- the hands, and tinea cruris- the groin area.
Of these keratinophilic organisms, Trichophyton rubrum is the most common pathogen associated with chronic tinea pedis, while other fungal pathogens have also been associated with the disorder and are listed in Table 1. Typically, three variants are seen and include the interdigital (Figure 1), moccasin (Figures 2A and 2B), and vesicobullous forms (Figure 3) of the disease. Moccasin type tinea pedis is a more prolonged form of tinea infection that surrounds the sole and lateral aspects of the foot in a slipper or moccasin distribution. This type of tinea pedis usually causes pustules or vesicles on the instep and plantar surfaces of the feet. Patients often complain of itching and burning sensations on the feet accompanied by malodor.
Its appearance is that of a slipper or moccasin covering the foot, hence the name (Figures 2A and 2B). A number of host factors have contributed to the growing incidence of these fungi in tinea pedis infections (Table 2). Common predisposing factors for cellulitis include trauma, ulceration, venous and lymphatic insufficiency, and peripheral vascular disease.
Of the 20 patients with athlete's foot, all had gram-positive bacteria isolated from their ipsilateral interdigital web space, and 85% (17 of the 20 cases) of these had ?-hemolytic streptococci present. Gram-positive bacteria usually dominate the interdigital spaces of the feet and upon infection with dermatophytes, bactericidal products similar to penicillin may inhibit their growth.
It most often causes vesicular or pustular eruptions near the site of infection or on the palms and fingers of the hands [14].
Ward and coworkers described "Trichophyton asthma" in 12 adult patients with chronic rhinitis and asthma who also demonstrated immediate hypersensitivity to Trichophyton spp [20].
In one study, peripheral blood mononuclear cells from some patients with atopic dermatitis released interleukin-5 (IL-5) in response to stimulation by fungal antigens [34]. 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. However, complete identification of the causative fungi should be established to confirm diagnosis and ensure proper treatment. In the case of interdigital infection, antifungal powder preparations may be more effective. 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.
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].
These drugs act by destroying the fungal cell wall at a much earlier stage in its development than the azoles. Classifying the type and causative organism of tinea pedis is important for proper treatment of the patient.
As moccasin tinea is relatively asymptomatic, patients frequently present when a dermatophyte infection develops at another body site such as toenails or the groin.
Most cases will require oral treatment, either terbinafine 250 mg daily or oral itraconazole 200mg twice daily for 7 to 30 days. Tinea pedis, also known as athlete's foot, is a chronic fungal infection of the feet and is the focus of this review.
The factors affecting the transmission of these dermatophytic pathogens are dependent on the source of infection, which is usually either human (anthropophilic), animal (zoophilic) or soil (geophilic).The most common anthropophilic dermatophyte infection seen is T. Some patients may present with recurrent cellulitis and aggressive attempts have to be made to identify the presence of tinea pedis as therapy for this condition can alleviate recurrences of cellulitis.
As summarized by Semel and Golden, tinea pedis was discovered in 20 of 24 episodes (84%) of cellulitis studied [12]. This type comprises pustules or vesicles on the instep and adjacent plantar surfaces of the feet and is less common (Figure 3) [8].
Due to an increase in immune deficiency diseases (AIDS) and increased numbers of patients receiving chemotherapy, steroids, organ transplants, and parenteral nutrition, the incidence of tinea pedis has increased [6].


Tinea pedis infections, most often interdigital type, may be complicated by cellulitis and has been discussed in the article earlier.
This may result in a predominant growth of gram-negative bacteria like pseudomonas, proteus, and klebsiella, leading to gram-negative cellulitis [18]. 10 out of the 12 patients also demonstrated positive immediate broncho-constrictive reactions to extracts of T.
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. Topical treatment may need to be continued for at least 4 weeks and recurrences are common. So it must be emphasized that the patient should continue topical treatment at least one week after symptoms have resolved.
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 easiest way to test for fungal presence is by microscopy of a KOH preparation, but complete identification of the organism requires culturing. In other patients, tinea pedis may complicate allergy and asthma and may contribute to refractory atopic disease.
Tinea pedis is estimated to be the second most common skin disease in the United States, behind acne [1], and up to 15% of the population may manifest the disease [2, 3].
Common bacterial coinfection in descending order of frequency in their study included beta hemolytic streptococci (85%), Staphylococcus aureus (45%) and enterobacteriaceae (35%). The overall health of the patient is another important risk factor in developing tinea pedis. Wet, occlusive conditions developing in the infected interspaces lead to maceration and fissuring of the skin.
No ?-hemolytic streptococci were isolated from control patients without tinea pedis or cellulitis. A thorough examination of the patient's feet and inter-digital spaces will often reveal evidence of recent or active tinea pedis. In such situations, demonstration of fungal elements may become difficult as excessive gram-negative bacterial presence may inhibit fungal growth and make it harder to detect fungal hyphae on KOH preparations. Kanda and colleagues also demonstrated expression of the Th2 cytokine IL-4 from peripheral blood mononuclear cells in response to stimulation by Trichophyton rubrum [35].
IgE in the presence of antigen can cross-link mast cells leading to further cytokine, chemokine and mediator production. Scrapings from the outer edge of a tinea lesion should be taken with a sterile scalpel, placed on a slide and KOH applied. Ketoconazole treatment is indicated when griseofulvin therapy has failed or when the patient cannot tolerate it. Tinea pedis infection can contribute not only to fungal dermatitis but also to flares of eczema and asthma. Tinea pedis presents as pruritic, erythematous, inflamed regions on the feet that may be located on the sole (vesicular type) or lateral aspects (moccasin type) of the foot and sometimes between the toes (interdigital type). These authors suggested that cultures of interdigital areas for fungal pathogens combined with antistreptolysin-O titers (ASO titers) may provide more useful information in patients with recurrent cellulitis than other routine studies [12]. The skin of the inflamed area in this type of infection is often scaly and hyperkeratotic with erythema around the soles and sides of the foot [4, 8]. Fluid filled vesicles are usually clear but pus usually indicates secondary bacterial infection, most often with Staphylococcus aureus or group A Streptococcus.
Patients who are obese, elderly, or have systemic problems (diabetes mellitus) are at increased risk [6]. This weakens the natural barrier of the skin and may serve as an entry point for several kinds of pathogenic bacteria. They conclude, but do not prove, that athlete's foot may be a common entry point for bacteria that cause cellulitis. Antifungal agents released from the gram-negative bacteria may also contribute to decreased presence of fungus.
Onychomycosis accounts for about one third of fungal skin infections but only about half of onychomycosis infections are caused by a dermatophyte [19]. These patients had eosinophilia and chronic rhinosinusitis in addition to features compatible with "intrinsic or late onset asthma". 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-13) in peripheral blood mononuclear cells [36].
The other cytokine, IL-5, enhances eosinophil production from the bone marrow, eosinophil activation, survival, recruitment and degranulation.
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].
KOH dissolves the epithelial cells seen in the background and leaves the fungus to be viewed by microscopy.
Treatment options and dosing are explained in greater detail below and are reviewed in Table 3. Many studies have compared the efficacy and rate of relapse upon applying different topical antifungal agents.
Blood counts, platelet count, and liver enzymes should be repeated every 4–6 weeks with this therapy.
From a molecular standpoint, superficial fungal infections may induce a type2 T helper cell response (Th2) that can aggravate atopy. Three main genera of fungi may cause tinea pedis, Trichophyton, Epidermophyton, and Microsporum. A similar syndrome of recurrent cellulitis with tinea pedis in patients who have undergone saphenous vein grafting for coronary artery disease has been described almost two decades ago [13]. Other local factors that may contribute infection are trauma, excessive moisture, occlusive clothing, and frequent usage of public showers and pools. ?-hemolytic streptococci (group A, B C, F, and G), Staphylcoccus aureus, Streptococcus pneumoniae, and gram negative bacilli have all been associated with cellulitis, with ?-hemolytic streptococci being the most prevalent [16]. Evaluation for and treatment of any underlying disorders that led to a predisposition to tinea pedis (such as diabetes mellitus, obesity, hygiene) will also be necessary.
Hence, cultures of skin scraping may demonstrate gram-negative bacteria but no fungal pathogens. The possible interactions of dermatophytes with T-cells and triggering of atopic disease is shown in Figure 4. These processes can result in expression of atopic disease, from rhinitis and asthma to atopic dermatitis. Malassezia furfur and Corynebacterium minutissimum both fluoresce under ultraviolet light while other common dermatophytes do not.
Oral treatment with griseofulvin, itraconazole, fluconazole, and terbinafine may all be effective for this disease.
Aggressive treatment of tinea pedis can be associated with improvements in atopic dermatitis, asthma and cellulitis in affected individuals. Th2 cytokines may induce eosinophil recruitment and immunoglobulin E (IgE) class switching by B cells, thereby leading to exacerbation of atopic conditions. Other, nondermatophtye, fungi like Malassezia furfur, corynebacterium minutissimum, and Candida species may also cause tinea pedis but fall outside the scope of this review [4, 5].
The spread of infections with this pathogen have been attributed to large population movements during World War II.


Besides tinea pedis, other interdigital inflammatory conditions need to be included in the differential diagnosis and include erythrasma, impetigo, pitted keratolysis, Candida intertrigo, and Pseudomonus aeruginosa interdigital infection [14]. Aggressive treatment of the underlying fungal as well as the gram-negative bacterial infection can, however, lead to amelioration of cellulitis in these patients. Drug resistance, adverse effects of medications and drug interactions are all major hurdles to successful completion of therapy. Absorption is improved by food, so food intake should be encouraged with the ketoconazole treatment. Three groups of fungal pathogens, referred to as dermatophytes, have been shown to cause tinea pedis: Trychophyton sp, Epidermophyton sp, and Microsporum sp. Outbreaks of infection of glabrous skin have been associated with contact with infected, desquamated skin scales.
Dermatophytosis complex, as it is called, may have fissuring of the interspace along with hyperkeratosis, leukokeratosis, or erosions [9].
These can often be differentiated by clinical features, gram stains, and cultures of aspirated material.
Subungual onychomycosis coexisting with moccasin type dermatophytosis is most often caused by T.
Bullous impetigo, allergic contact dermatitis, dyshidrotic eczema, and bullous disease all need to be considered in the differential diagnosis [14].
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. An evaluation for etiologies for immunosupression such as new onset diabetes or malignancy may be indicated in selected patients. Due to its structural difference, itraconazole has greater efficacy and less toxicity as compared with other azoles. The disease manifests as a pruritic, erythematous, scaly eruption on the foot and depending on its location, three variants have been described: interdigital type, moccasin type, and vesiculobullous type.
Wet conditions along with fungal invasion increases the incidence of bacterial infection in these patients by breaching cutaneous integrity.
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. Possible drug-drug interactions are listed in Table 4, adapted from "Oral antifungal drug interactions" by Katz and Gupta [37]. Another randomized, double-blind parallel group study compared efficacy and tolerability of topical terbinafine 1% cream, twice a day for one week, with clotrimazole 1% cream, twice a day for 3 weeks, and showed that terbinafine achieves a cure rate more rapidly than clotrimazole and in a shorter amount of time [3]. Tinea pedis may be associated with recurrent cellulitis, as the fungal pathogens provide a portal for bacterial invasion of subcutaneous tissues. It may complicate the management of the atopic patient and fungal pathogens themselves may aggravate asthma or atopic dermatitis. IgE in the presence of antigen can cross-link mast cells leading to further cytokine, chemokine, and mediator production. 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.
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. In some cases of refractory asthma, treatment of the associated tinea pedis infection may induce remission in airway disease. Occasionally, a patient may be referred for evaluation of recurrent cellulitis resulting from a tinea pedis infection rather than from immune deficiency. The first is typically white and fluffy in appearance with several aerial hyphae and is called the "downy form". The other cytokine, IL-5, enhances eosinophil production from the bone marrow, eosinophil activation, survival, recruitment, and degranulation. One to two drops of 10% KOH solution is dropped onto the slide and heated gently to dissolve skin cells while keeping the fungal hyphae intact (Figure 5). With long-term use of topical glucocorticosteroids atrophy and steroid-induced rosacea and striae may occur.
Fluconazole has more potency, less toxicity, and wider spectrum of action than earlier azoles.
These investigators suggested that patients with intrinsic asthma needed to be tested for sensitivity to Trichophyton spp. These combination agents are relatively contraindicated in children under12 years of age [1].
An evaluation for underlying immuno-suppression or diabetes may be indicated in patients with refractory disease. This review will discuss the clinical features of tinea pedis infection, the pathogens incriminated, and the current treatment options for patients with this disease.
Other investigators have also discussed a possible relationship between dermatophytic infections and asthma [22, 23]. Fluconazole and itroconazole should not be given together with terfenadine, astemizole, and cisapride in view of the risk of cardiac arrhythmia. The allergic disease improved rapidly when the patients were treated with terbinafine and relapsed rapidly after this therapy was discontinued.
Klein and coworkers described a patient with atopic dermatitis and concurrent tinea pedis and onychomycosis [24]. Conidia are asexual spores that form at the tip of conidiophores; in the same species, these are either large (macroconidia) or small (microconidia).
As reviewed by Leyden, mocassin-type tinea pedis occurs more often in patients with an atopic background [25]. Byrld and coworkers found an association between tinea pedis and risk for vesicular eruption on the hands of patients [26]. Both have a downy or granular appearance and are sometimes indistinguishable under the microscope. The use of systemic antifungal therapies and ketoconazole shampoos led to improvement in 5 patients with atopic dermatitis complicated by dermatophytosis [27].
The role of Mallasezia (pityrosporium species) in atopic eczema has been extensively reviewed by several investigators [28–31]. Ward and coworkers demonstrated that treatment of 11 patients with late onset asthma complicated by dermatophytosis with fluconazole led to improved lung function and symptoms, and decreased steroid usage [32]. Microsporum canis, however, is probably the most prevalent of the zoophilic dermatophytes.Trichophyton tonsurans is another anthropophilic fungus that causes tinea pedis. Mandez and colleagues also reported on one patient with urticaria complicating dermatophytosis [33]. Cultures of this fungus have short, septate hyphae with several microconidia that vary from tear drop to club shape. Many chlamydoconidia, asexual conidia produced from the hyphae, may be seen but macroconidia are usually rare. No microconidia are observed in this species, but chlamydoconidia can sometimes be seen in older colonies [7].Microsporum canis is a zoophilic fungus contracted from dogs that is a rarer cause of tinea pedis infections [6].
Their hyphae are septate, their microconidia are club shaped, they have many macroconidia, and their cell wall is usually thick [7].



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