• LecturehallDermatology Part I
  • Lecture Transcript
  • TAPE STARTS – [00:00]

    Jaffe Leland: Dermatology is the component of all podiatric physician's practice and this lecture will review some of the major and most common podiatric dermatological conditions that present to our offices on a regular basis. The learning objectives for this lecture will include a review of common fungal and viral skin infections that will present to a podiatric physician's office. Also, we will review inflammatory skin dermatoses including the different types of dermatitis or eczema. And we will begin by reviewing fungal and viral infections of the lower extremity. When we begin discussing fungal organisms of the skin, we must first begin by defining some terminology. Dermatophytosis or dermatophytes are discussing or describing fungal organisms that involve the keratin or the stratum corneum, which is the top layer of our epidermis. These types of fungal organisms are able to infect nonviable keratin but have a limited capacity to invade deeper into our body and cause systemic infections. Per definition, epidermomycosis involves a skin infection, trichomycosis involves hair and hair follicle infection and onychomycosis involves infections of the nail plate involved by fungal organisms. Again on this slide, we are going to review some common terminology that helps us to accurately diagnose these fungal infections involving the skin. Tinea capitis, capitis meaning head or scalp; tinea cruris, which would be the groin or jock itch infection; tinea pedis involving the foot. Anything proximal to the full digit would use the terminology tinea corporis, meaning fungal infection of the body; tinea barbae along the beard and tinea unguium involving the nails. The commonality between all of these types of infections is that they are involved with the same fungal organisms, which are the dermatophytes.


    The dermatophyte organisms synthetize and release an enzyme called keratanase, which enzymatically break down the keratin in the skin allowing these fungal organisms to invade and cause an infection within the skin. There are some predisposing host factors that might make someone more inclined or more predetermined to get a fungal infection. Certainly, genetics can play a role in this infectious process. Also atopy, which is defining a lower threshold for pruritus. Patients that are repeatedly treated with topical or systemic steroids can lower their body's threshold to rid their bodies of these dermatophyte organisms. Ichthyosis, which describes dry scaling, xerotic skin and patients that have collagen vascular disorders also might have a lower threshold to fighting off these organisms and are more susceptible to a dermatophyte infection. Also, some local factors can predispose a patient to developing a dermatophyte fungal infection including but not limited to sweating, which is why often we see this infection involving the feet where there are many eccrine sweat glands and we also tend to accumulate moisture on the foot. Occlusive footwear, occupational exposure, so patients that have repeated exposure to a moisture or moist wound environment and also who live or work in high humidity environment. Diagnostically evaluating for a dermatophyte type skin infection typically begins with a potassium hydroxide type preparation and staining. What this test is doing actually is using potassium hydroxide to dissolve the keratin and other components of the skin and leaving the fungal elements behind, in which we should see fungal hyphae present under the microscope examination. Please keep in mind, however, that this will not identify the species of the fungus present. It will merely demonstrate the morphology of the fungus organism as to whether there is a dermatophyte and also we can often identify a candida type infection with the potassium hydroxide study as well.


    Clinical evaluation for patient suspected of having a fungal infection can also involve the use of a Wood's light examination, which is a specific wavelength of light that will allow certain types of organisms, some fungal, some bacteria to fluoresce certain colors. For example, tinea capitis involving a microsporum infection will fluoresce a greenish light. Erythrasma, which often presents as an inter-digital maceration type infection caused by corynebacterium minutissimum, which a gram-positive organism will fluoresce a coral red. Tinea versicolor, which is actually a yeast that is often a normal skin flora that can over colonize and cause an infection on the skin will fluoresce a yellowish gold color, and finally, a pseudomonas infection, which is a gram-negative rod can fluoresce a greenish color utilizing a Wood's light examination. When we discuss the causative agents of dermatophyte infections, we often discuss trichophyton rubrum, which is the most common cause of fungal infections of our skin. Trichophyton rubrum is often the etiology for patients with chronic moccasin distribution tinea pedis as well as distal subungual or lateral subungual onychomycosis. Trichophyton mentagrophytes is another type of dermatophyte, often presents more as an acute vesicular or acute macerated type tinea pedis infection. Trichophyton tonsurans, which is less commonly seen as well as epidermophyton floccosum is also other types of dermatophytes that may present in these infections involving the lower extremity. When we discuss the different types of tinea pedis, we will first start by discussing moccasin or chronic tinea pedis often involving the plantar aspect of the right and/or left foot. This type of infection often involves central clearing with peripheral scaling and erythema present, which is where there is an advancing edge of the infection. Again, as stated on the previous slide, this type of infection is often caused by trichophyton rubrum, which is a less aggressive type of organism as compared to some of the other dermatophytes.


    And one of the things to be mindful of with type of infection is that it may present as an asymptomatic infection or it could be quite pruritic. The presentation can be different based on each individual patient. The next type of tinea pedis that can be seen clinically is a vesicular type of tinea pedis. Often more aggressive infection again caused by T. mentagrophytes. Patients with this type of infection might have more inflammation, vesicular formations sometimes along the medial longitudinal arch as seen in the picture to the right on the screen. This can be intensely pruritic and quite uncomfortable for patients. Continuing with our discussion of types and distributions of tinea pedis infections, we come to the interdigital tinea pedis. This is a very common skin manifestation seen by the podiatric physician. The interdigital infection can involve any interspace but most commonly is seen in the fourth interdigital space of the right or left foot. This type of presentation can both be a clear dry scaling presentation interdigitally but also can present a macerated fissuring type fashion as seen on the picture on the right hand side of the screen. Patients also have concomitant hyperhidrosis and some significant pruritus clinically with this type of skin infection. One thing to be mindful of though, however, is that the interdigital tinea pedis infection can masquerade as a bacterial infection as discussed on the previous slide as we discussed erythrasma. There also can be other secondary bacterial infection that can present once there is an erosion of skin present. Please keep in mind that the infecting organisms that involve the skin both on the plantar and dorsal aspect of the foot as well as the interspaces are often the same organism that involves the nail unit itself and the nail plate is often a reservoir for fungal infections.


    So it's critically important to treat both infections when dealing with this type of skin infection. One of the less commonly known and less commonly presenting types of dermatophyte infection is an infection called Majocchi's granuloma, which is a dermatophyte infection, however, it's a dermatophyte infection that involves the dermis with a subcutaneous tissue. As we stated previously, dermatophyte infections typically only involve the stratum corneum, which is the top layer of the epidermal skin. This type of dermatophyte infection can invade into the deeper layers of the skin and into the subcutaneous tissue often through a hair follicle. The offending organism with this type of infection also is T. rubrum as discussed earlier and the causative factor here is often trauma to the skin such as shaving the legs or occlusion of the hair follicle. When trying to diagnose this particular condition, it's often important to do a deeper tissue culture as the K-weight staining of superficial stratum corneum or keratin will often not yield any of the T. rubrum organisms as stated previously that they are located deeper into the dermis and subcutaneous tissue layers. The chart pictured on this slide outlines the common topical agents utilized to treat the dermatophyte and candida type infections. The top section of this chart outlines the imidazole, which are fungus static agents, often effective against candida and dermatophyte type organisms. The middle section of this chart outlines the allylamines and benzomines which are fungicidal agents, typically, a better choice for dermatophytes and not as indicated for candidal infections. The bottom part of this slide outlines the polyenes, which are fungus static organisms, Nystatin being the agent from this section, which is a better choice for candida infections with less of an indication to treat dermatophyte skin infections. Transitioning from the skin to the nail unit, we first begin by outlining some common terminology. Onychomycosis, onycho meaning nail, mycosis meaning fungus describes any fungal infection of the toenail.


    When we use the terminology tinea unguium, we are being more specific describing tinea being a dermatophyte infection and unguium being the nail. And candida onychia is describing a yeast or candida infection involving the nail unit, often more aggressive and associated with a paronychia, commonly seen in immune-compromised patients. Onychomycosis can present in multiple different clinical patterns. The most common is the distal subungual onychomycosis or distal lateral subungual onychomycosis. With this type of infection, the fungal organism is invading the nail from the distal aspect of the nail or from the lateral or medial nail folds. Proximal subungual onychomycosis less often seen is an involvement of a fungal infection breaking through the eponychium and involving the proximal aspect of the nail. This is often more seen in patients that have an immuno-compromised status such as HIV AIDS. Superficial wide onychomycosis is another common pattern seen as a superficial white plaque on top of the nail plate and again candida onychomycosis can be another pattern seen clinically usually more inflammatory and associated commonly with a paronychia type infection. A very common pattern of onychomycosis is distal subungual or distal lateral subungual onychomycosis. This infection begins with a break in the hyponychium or in the medial and lateral nail fold in which the offending organism gets underneath the nail plate and involves the nail bed. It can involve the entire nail unit nail plate as it ascends proximally. As seen on this slide, the most common organism is the Trichophyton rubrum dermatophyte organism and this is the clinical picture, 90% of the cases of onychomycosis. As seen pictured on the right, we can see the left hallux toenail with a thickening with onycholysis, which means separation of the nail from the underlying nail bed, hyperkeratosis noted distally as well as yellowish and brown discoloration with nail debris.


    This type of nail infection is almost always involved with a concomitant tinea pedis infection. So this should be evaluated for when patients do have an onychomycosis type infection. The next classical pattern of onychomycosis is superficial wide onychomycosis. This type of infection is often caused by Trichophyton mentagrophytes and as seen here this involves only about 10% of the cases of onychomycosis seen clinically. The difference between superficial wide onychomycosis and distal subungual is that this particular infection involves a direct occultation or invasion of the nail plate by T-mentagrophytes. It looks like a wide chalky plaque substance on top of the nail plate clinically. The final pattern of onychomycosis is proximal subungual onychomycosis. This is an infection where the fungus invades by a break in eponychium proximally. This infection is often caused by T. rubrum and should increase the clinician suspicion for an underlying immuno-compromised status specifically HIV. Clinically, the patient will have leukonychia or white nail that extends distally from underneath the eponychium or the proximal aspect of the nail plate. The next component of this lecture, we will discuss viral skin infections. We will begin our discussion of viral skin infections by reviewing the human papilloma virus, one of the most common viral skin infections in humans. There are many different strains of the HPV infection, some of which cause the very common verucca planus or verucca vulgaris, others which have oncogenic potential and others, which can cause condyloma acuminatum, which is the HPV genital wart type infection.


    The human papilloma virus can invade the basal keratinocytes in the epidermis causing hyperplasia of the epithelium. This can be seen in the clinical picture on the right hand side of the screen where there is a hyperplasia papillomatous type lesion with capillary infiltrate noted within the central aspect of the lesion. These can be solitary lesions or can coalesce to form a larger mosaic type lesion. These types of viral skin infection can be transmitted from skin-to-skin contact. They can survive on inanimate objects and can be transmitted to the patient through a break in the stratum corneum. Also of note, immune-compromised patients do have a lower threshold to fighting off these types of viral infections and are more prone to these types of HPV skin infections. Verruca vulgaris is responsible for about 70% of the cutaneous warts seen in our clinical practice and this is caused by HPV type 1 and type 2 among others but HPV type 1 and type 2 are the most common. The demographic most commonly involved with these types of skin infection is school-aged children from 5 to 20 years of age. These types of skin infections can resolve within one year; however, they are often quite uncomfortable for the patient and could be unsightly and there is concern of spreading either within a family or within friends. The most common location of the verruca vulgaris infection is hands and feet, fingers and palms, toes and soles. So this type of infection can involve both the upper and lower extremity. The common clinical presentation of verruca vulgaris involves a papillomatous lesion that is often hyperkeratotic in appearance. On the plantar aspect or on the palmar surface of the hand, there is often an interruption of skin lines, which is diagnostic for these viral skin infections.


    Also, we will see a capillary infiltrate at the base of the lesion, which represents thrombosed capillary loops, again another diagnostic sign. These types of lesions may koebnerize, which means they can spread to other parts of the body with trauma. Verruca plantaris is a common type of viral skin infection seen on the plantar aspect of the foot, most commonly caused by HPV type 1. These are painful lesions to our patients and often can be confused with a plantar hyperkeratotic lesion. Some of the defining features that indicate a viral wart infection as opposed to a hyperkeratotic lesion is that a wart often will have that brown or dark red capillary infiltrate. Normally, the plantar skin lines are interrupted or disrupted within the lesion itself. Also, there is more pain with side-to-side compression of a viral infection as compared to hyperkeratotic lesion. The clinician should also be mindful as to the weightbearing pressure point areas on the plantar aspect of the foot that might be more prone to developing a hyperkeratotic lesion as opposed to a viral infection. As stated earlier, some strains of HPV do have oncogenic potential, specifically, HPV type 16, which is the most common variant that can lead to cervical cancer. This strain also has the ability to cause squamous cell carcinoma whether it's an in situ or invasive type strain. Therefore, it's important for the clinician when removing skin suspected of being a viral skin infection, that skin should be sent for histopathological evaluation to confirm the presence of a benign lesion versus a carcinoma type lesion. The next type of viral skin infection, I will discuss, is hand, foot and mouth disease. Hand, foot and mouth disease is caused by an enterovirus specifically Coxsackie A16 virus.


    This is a systemic infection usually infecting patients less than 10 years of age. It is a highly contagious infection that presents with ulcerative oral lesions and a vesicular infection involving the distal extremities and plantar aspect of the feet. Often, there is only very mild constitutional symptoms and this is a self-limiting disease usually only lasting about one week in duration. The next viral skin infection will be presented to the use of a case study. In this case, a 7-year-old female was seen in clinic for evaluation of multiple bumps on the side of right and left thigh as well as on the posterior aspect of the right and left popliteal fossa. There was positive pruritus with no systemic signs or symptoms, no pertinent medical history and the patient appears well-nourished and healthy. And if you look at the clinical appearance picture on the right side of this slide, we can see multiple papules with central umbilication within these lesions. This case presentation was describing a 7-year-old patient that was diagnosed to have molluscum contagiosum. Molluscum contagiosum is a self-limited epidermal viral infection. The classic appearance of this type of viral skin infection is a papule with central umbilication. The most common demographics affiliated with this condition is young children as well as sexually active adults as well as people with an immuno-compromised status including HIV and AIDS. This is a highly contagious skin infection transmitted by skin-to-skin contact and involving the lower extremities, it's commonly seen on the right and left thigh as well as posterior aspect of the knee because that's where their skin tends to rub against one another. In HIV infected individuals, we often see more widespread involvement, face involvement, and these lesions often do not spontaneously regress as compared to skin lesions and people with an immunocompetent immune status.


    Molluscum contagiosum is a type of double-stranded poxvirus, again an epidermal viral skin infection with a classic clinical appearance of a papule with central umbilication common on the head and neck as well as on the lower extremity. In most patients, again with an immunocompetent immune status, there should be a spontaneous resolution of this condition; however, it may take up to two years in duration. If treatment is necessary, first line of therapy may include liquid nitrogen therapy, topical salicylic acid treatments as well as topical cantharidin. Let's now transition from the infectious fungal and viral skin infections to some of the common inflammatory dermatosis seen by the foot and ankle physician. The first type of inflammatory skin condition that will be discussed in this lecture is dermatitis or eczema. Please understand that these two terms can be used interchangeably. This is a list of different types of dermatitis that may present to the clinician's office. A number of different types of dermatitis belong to a grouping called spongiotic dermatitis. This includes nummular, dyshidrotic, allergic, contact, auto-sensitization as well as atopic dermatitis. Spongiosis is a terminology meaning intercellular edema within the epidermis as seen on histopathological evaluation of a tissue specimen. The first type of dermatitis that will be reviewed in this lecture is atopic dermatitis. Atopic dermatitis is often seen in infancy as well as young childhood. In this clinical presentation, the patient has a lower cutaneous threshold to pruritus and clinically we see an itch scratch cycle where the patient constantly is rubbing and scratching, which leads to lichenification, which leads to skin breakdown, which leads to further scratching and itching. This is typically a clinical diagnosis. If a lab evaluation is performed, we will typically see eosinophilia with elevated serum IgE levels.


    Patients with atopic dermatitis often present with the classic atopic triad, which includes asthma, allergic rhinitis or Hay fever and the skin condition of atopic dermatitis. When reviewing the epidemiology of atopic dermatitis, it is important to understand that the onset of this condition is usually present by the first year of life. In fact, in about 60% of patients this is true. As patients become older, the prevalence of the onset of this condition decreases and there is a rare development of atopic dermatitis in adults. When reviewing the exacerbating factors, we will first begin by discussing the alteration of the skin microbiome. An asterisk is placed by this line because this discussion is beyond the scope of this lecture; however, it's important to understand that there is emerging evidence and research that suggest that a dysregulation of the normal skin flora as well as normal healthy bacteria that live in our GI system can predispose the patient and make them more susceptible to developing autoimmune conditions such as atopic dermatitis. Other exacerbating factors could include allergens, foods that can elicit an allergic response, dehydration of the skin, which may occur with frequent bathing of these children, superficial skin infections like staph and strep or impetigo, clothing that may elicit an immune response, a patient with emotional stress as well as there are seasonal conditions that can cause flares in the winter where the skin does dehydrate and dry. As introduced on the previous slide, the pathogenesis of atopic dermatitis is a complex one involving multiple factors including a skin barrier breakdown, which can include either a skin infection or dehydration of the skin caused by frequent bathing. There is a genetic predisposition to the development of this autoimmune condition.


    Other environmental and immunological factors also may play a role. Also as introduced in the previous slide and ulceration on the skin microbiome where the normal skin flora may predispose the patient to dysregulation of the immune system, which may cause the onset of this autoimmune condition. Atopic dermatitis is a type 1 IgE mediated hypersensitivity reaction involving the activation of mast cell and basophils releasing vasoactive substances on the skin surface causing this eczematous reaction. As atopic dermatitis progresses and becomes more chronic in nature, the patient will often develop lichenification of the skin, which is a thickening of the skin with exaggerated skin lines. This is caused by a repetitive rubbing and scratching causing a hypertrophy of the skin surface. Often this will develop in patients greater than 20 years of age and females have a higher prevalence than males to develop this chronic condition. The next type of dermatitis that will be reviewed is contact dermatitis and this can be broken down into irritant contact as well as allergic contact dermatitis. Irritant contact dermatitis is caused by chemical irritant causing direct damage to the skin. This is a non-immunologic skin reaction with no sensitization phase. Single exposure to the chemical irritant will cause a skin reaction and often the skin reaction is confined to the area of exposure with sharp well-demarcated borders. On a contrary, allergic contact dermatitis is caused by exposure to an allergen. This is a type 4 delayed hypersensitivity reaction. Often the first exposure to the allergen causes minimal to no skin reaction; however, the skin reaction can spread beyond the original site of contact in direct contrary to the irritant contact dermatitis. This is a clinical photograph of a patient with a full thickness ulceration at the lateral aspect of the right foot.


    This patient was treated with wound VAC therapy with the wound VAC bridged to the proximal calf. Underneath the bridging foam, adhesive was placed on the skin and you can see that this patient did develop a contact dermatitis in the direct distribution where the adhesive was placed on the patient's skin. Prior to this treatment, the patient was unaware that they did have an allergy to adhesives. The classic type of allergic contact dermatitis is poison IV or rust dermatitis, which is a delayed type for hypersensitivity reaction. With this type of dermatitis, an antigen is exposed to the Langerhans cells, which are located in the epidermal layer of the skin. The antigen is then carried to the lymph nodes presented to helper T cells and then T cells proliferate. At this point, the patient is then sensitized and second exposure to this allergen will create a skin reaction. The skin reaction often develops within 12 to 24 hours and may persist for up to three to four weeks' duration. The next type of dermatitis that will be reviewed is seborrheic dermatitis, which otherwise may be known as cradle cap in the infant population or pityriasis sicca in patients of an older demographic. This skin condition is characterized by erythema and scaling in areas of the body where sebaceous glands are most active including the face, scalp, presternal area or other body folds. The next type of dermatitis that will be reviewed is dyshidrotic eczema, also might be known as pompholyx. This is a vesicular type of hand and/or foot dermatitis often associated with intense pruritus. This is characterized by deep-seated pruritic tapioca-like vesicles that might present on the medial and lateral aspect of the digit as well as thenar eminence of the hand that's spontaneously developed. The name dyshidrotic is a misnomer as sweating does not play a role in the pathogenesis of this condition.


    This condition might be seen with pruritic tapioca-like vesicles and later on in the progression of this condition, the patient may develop fissures, erosions as well as lichenification of the skin. There are multiple different clinical presentations of dyshidrotic eczema. In the acute stage, the patient often presents with deep-seated tapioca-like vesicles that arise spontaneously and rapidly on the medial or lateral aspect of the fingers and toes. As the vesicle is resolved and ruptured and leaves the patient with hyperkeratosis present, and finally, if it does progress to the chronic stage, which is uncommon, the patient will be left with hyperkeratosis with lichenification of the skin. Moving along the next type of spongiotic dermatitis is nummular eczema. Nummular eczema also may be known as discoid eczema and presents as a chronic pruritic inflammatory dermatitis. Clinically is seen as coin-shaped plaques with small papules or vesicles on erythematous base. The distribution can present either on the lower legs, especially in older males during the winter months. It also may present on the fingers or toes in adolescence or younger demographic of patients. This is a classic presentation of nummular eczema with a circular coin-shaped plaque on the medial aspect of the patient's left calf with papules present within the central aspect of the lesion. Moving along, we will discuss the Id reaction or the auto-sensitization dermatitis, which is a type of spongiotic dermatitis. The auto-sensitization reaction is defined as a pruritic papulovesicular dermatitis. This condition develops due to a primary skin condition or skin lesion that may be of infectious or inflammatory etiology. The pathogenesis of this condition involves inflammatory cytokines spreading from the original skin lesion through the lymphatics to a distant site casing a skin reaction.


    This skin reaction often will persist until the primary skin lesion is effectively treated. Again, understand that this may be due to a primary infectious condition such as acute tinea or inflammatory condition such as a primary dermatitis reaction. In summary, this review dermatology lecture initially began with a discussion of fungal and viral type skin infections and this was followed by discussion of the different types of dermatitis or eczema. When considering treatment and diagnostics for dermatitis and eczema, a punch biopsy is often the biopsy of choice if we are trying to differentiate this inflammatory skin condition as compared to some of the other inflammatory skin condition such as psoriasis, lichen planus or inflammatory conditions like tinea pedis. Once an appropriate diagnosis has been made, then the clinician can then initiate appropriate treatment for their patients. Thank you for your time and interest in this lecture and if you have any questions, I can be reached via email at leland.jaffe@rosalindandfranklin.edu. Thank you once again.

    TAPE ENDS - [31:12]