# Lecture 9: Skin Infections ## Unit 2.10: Musculoskeletal System/Dermatology --- ## Learning Objectives By the end of this lecture, students will be able to: 1. Describe the clinical features and treatment of bacterial skin infections 2. Explain the diagnosis and management of viral skin infections 3. Describe superficial and deep fungal skin infections 4. Explain parasitic skin infestations 5. Describe the approach to necrotizing soft tissue infections 6. Explain special considerations in immunocompromised patients --- ## Lecture Outline ### I. Bacterial Skin Infections - Superficial Impetigo is the most common superficial bacterial skin infection, caused primarily by Staphylococcus aureus (the most common pathogen) and less frequently by Group A streptococcus, and it predominantly affects children with a predilection for the face and extremities. Two clinically distinct forms are recognized: non-bullous (crusted) impetigo is the more common variant, presenting with the characteristic honey-colored crusts on an erythematous base that result from drying of serous exudate, and this form may be caused by either S. aureus or Group A streptococcus. Bullous impetigo is caused exclusively by S. aureus strains that produce exfoliative toxins (epidermolytic toxins A and B) that cleave desmoglein 1 in the superficial epidermis, producing flaccid bullae that rupture easily and leave shallow erosions with a collarette of scale. Treatment of limited impetigo consists of topical mupirocin applied three times daily for five to seven days, while more extensive disease or lesions in multiple anatomic locations warrants oral antibiotics with activity against S. aureus and streptococci. Ecthyma represents a deeper extension of impetigo through the epidermis into the superficial dermis, producing ulcerative lesions with a more indolent course. Group A streptococcus is the primary pathogen, though S. aureus may be involved as a co-pathogen. The characteristic lesion is a punched-out ulcer with an adherent crust or eschar that, when removed, reveals a shallow ulcer with raised, violaceous borders. Ecthyma occurs most commonly on the lower extremities and is associated with poor hygiene, neglected wounds, and conditions that compromise the skin barrier. Unlike impetigo, which heals without scarring, ecthyma extends into the dermis and heals with scar formation, making prompt treatment with oral antibiotics important to minimize tissue destruction. Folliculitis is a common infection of hair follicles that presents as small pustules centered on follicular openings, each surrounded by a rim of erythema. Staphylococcus aureus is the most common causative organism in typical folliculitis, though Pseudomonas aeruginosa causes a distinctive form known as hot tub folliculitis that occurs 24 to 48 hours after exposure to inadequately chlorinated hot tubs, whirlpools, or swimming pools. The pustules of folliculitis are typically superficial, involving only the infundibulum of the follicle, and are distributed in areas of friction, occlusion, or shaving. Treatment of limited folliculitis consists of topical antibiotics such as mupirocin or clindamycin, while extensive involvement may require oral antibiotics, and Pseudomonas folliculitis is generally self-limited, resolving spontaneously within 7 to 10 days. Furuncles and carbuncles represent deeper infections of hair follicles that extend into the surrounding dermis and subcutaneous tissue. A furuncle, commonly known as a boil, is a deep follicular abscess that presents as a painful, erythematous, fluctuant nodule with a central pustule that eventually points and drains spontaneously or requires incision and drainage. A carbuncle is a larger, deeper infection consisting of multiple interconnected furuncles that drain through multiple sinus tracts, often associated with systemic symptoms including fever and malaise. Staphylococcus aureus is the causative organism in virtually all cases, with community-acquired methicillin-resistant S. aureus (CA-MRSA) being increasingly prevalent in furuncles and carbuncles. Treatment centers on incision and drainage, which is the most important therapeutic intervention, with oral antibiotics added when there are systemic symptoms, surrounding cellulitis, or involvement of high-risk anatomic sites. Panel A: Impetigo showing non-bullous type with characteristic honey-colored crusts on erythematous base and bullous type with flaccid fluid-filled bullae from staphylococcal exfoliative toxin. Panel B: Folliculitis with pustules centered on hair follicles, showing superficial involvement and typical distribution on trunk and extremities. Panel C: Furuncle (boil) as deep follicular abscess with surrounding erythema and induration, showing progression to central pustule and drainage. Panel D: Carbuncle demonstrating multiple interconnected furuncles with multiple drainage points, deeper tissue involvement, and surrounding cellulitis. --- ### II. Bacterial Skin Infections - Deep Cellulitis is an acute infection of the dermis and subcutaneous tissue that presents with the cardinal signs of inflammation and represents one of the most common reasons for dermatologic-related hospital admissions. The most common causative organisms are beta-hemolytic streptococci, particularly Group A streptococcus (GAS), and Staphylococcus aureus, with the relative contribution of each pathogen varying by clinical presentation. The hallmark clinical features include diffuse erythema, warmth, swelling, and tenderness over the affected area, with borders that are characteristically poorly demarcated and blend gradually into uninvolved skin. Systemic signs may include fever, chills, malaise, and lymphangitis manifesting as erythematous streaking along lymphatic channels proximal to the infection site. Treatment consists of oral antibiotics for mild-to-moderate cases and intravenous antibiotics for severe infections, patients with systemic toxicity, or those who fail outpatient therapy. Erysipelas is a distinct form of superficial cellulitis involving the upper dermis and superficial lymphatic vessels that is almost always caused by Group A streptococcus. The clinical presentation is distinctive, featuring a bright red, raised, indurated plaque with sharply demarcated borders that distinguish it from the poorly defined margins of deeper cellulitis. The advancing border is often palpably elevated, and the surface may show a peau d'orange texture due to lymphatic involvement and dermal edema. Erysipelas has a predilection for the face and lower extremities and is associated with portal-of-entry lesions such as tinea pedis, venous stasis ulcers, and surgical wounds. Treatment with penicillin or a first-generation cephalosporin targeting streptococcal organisms is typically effective, with the approach similar to that used for cellulitis. Community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) has emerged as a major cause of purulent skin and soft tissue infections over the past two decades. CA-MRSA characteristically produces abscesses rather than cellulitis, and patients frequently present with a history of a "spider bite" that actually represents a staphylococcal abscess. Risk factors for CA-MRSA include participation in contact sports, incarceration, men who have sex with men (MSM), military personnel, and close contacts of known MRSA carriers. Treatment of CA-MRSA abscesses requires incision and drainage as the primary intervention, with antibiotics such as trimethoprim-sulfamethoxazole (TMP-SMX) or doxycycline added for surrounding cellulitis or systemic symptoms. For patients with recurrent MRSA infections, decolonization protocols using intranasal mupirocin and chlorhexidine body washes may be beneficial. Antibiotic selection for skin and soft tissue infections should be guided by the clinical presentation, specifically whether the infection is purulent (suggesting staphylococcal etiology) or non-purulent (suggesting streptococcal etiology). Non-purulent cellulitis without abscess formation is most commonly caused by streptococci and is appropriately treated with cephalexin or penicillin, which provide reliable streptococcal coverage. Purulent infections and abscesses suggest MRSA involvement and should be treated with TMP-SMX or doxycycline in addition to incision and drainage to provide MRSA coverage. Severe infections presenting with systemic toxicity, rapid progression, or failure of outpatient therapy warrant hospitalization and intravenous antibiotics such as vancomycin combined with piperacillin-tazobactam for broad coverage. Facial cellulitis deserves special consideration and often warrants hospitalization due to the risk of cavernous sinus thrombosis, orbital complications, and the cosmetic importance of the area. Panel A: Cellulitis showing poorly demarcated erythema, warmth, and swelling extending through dermis and subcutaneous tissue with associated lymphangitis streaking. Panel B: Erysipelas demonstrating sharply demarcated, raised, bright red plaque with peau d'orange texture due to superficial lymphatic involvement and typical facial or leg location. Panel C: Cross-sectional comparison showing cellulitis extending deeper into subcutaneous fat versus erysipelas confined to upper dermis and superficial lymphatics. Panel D: Treatment algorithm distinguishing non-purulent cellulitis (streptococcal coverage with cephalexin) from purulent infections/abscesses (MRSA coverage with TMP-SMX or doxycycline plus drainage). --- ### III. Necrotizing Soft Tissue Infections Necrotizing soft tissue infections (NSTIs) represent rapidly progressive, life-threatening infections that cause destruction of skin, subcutaneous tissue, fascia, and potentially muscle, with mortality rates of 20-40% even with optimal management. The two main types are necrotizing fasciitis, in which destruction spreads rapidly along fascial planes, and gas gangrene (clostridial myonecrosis), in which clostridia produce toxins causing massive muscle necrosis. NSTIs are classified microbiologically as Type I (polymicrobial, involving a mixture of aerobic and anaerobic organisms including streptococci, staphylococci, gram-negative rods, and anaerobes) or Type II (monomicrobial, most commonly caused by Group A streptococcus, which may also produce streptococcal toxic shock syndrome). Necrotizing soft tissue infections constitute a surgical emergency in which the critical intervention is operative debridement rather than antibiotic therapy alone. The clinical features of NSTIs evolve rapidly over hours and must be recognized emergently to prevent fatal outcomes. Pain out of proportion to the physical examination findings is the most important early clinical clue, as the infection spreads along the deep fascia before producing visible skin changes, creating a disconnect between the patient's severe pain and relatively unremarkable surface appearance. Skin changes evolve in a characteristic progression from initial erythema through dusky, violaceous discoloration with hemorrhagic bullae to frank black necrosis and eschar formation, reflecting progressive thrombosis of perforating vessels. Crepitus, palpable as a crackling sensation in the tissues, indicates gas production by anaerobic organisms and is highly suggestive of NSTI when present, though its absence does not exclude the diagnosis. Systemic toxicity develops rapidly with fever, tachycardia, hypotension, and altered mental status reflecting the massive inflammatory response and sepsis that accompany these infections. Risk factors for NSTIs include both patient-related and local factors that impair host defenses and create portals of entry for infection. Patient factors include diabetes mellitus, immunocompromise from any cause, obesity, chronic liver disease, and peripheral vascular disease, all of which impair the immune response and tissue perfusion. Local factors include trauma, recent surgery, injection drug use, and minor skin breaks that provide portals of entry for organisms into the deep soft tissues. An important clinical consideration specific to Type II (GAS) necrotizing fasciitis is that NSAIDs may mask early symptoms by suppressing pain and fever, and this type can occur in previously healthy patients without traditional risk factors, making a high index of suspicion essential. Management of NSTIs requires a coordinated, multidisciplinary approach emphasizing rapid resuscitation, broad-spectrum antibiotics, and urgent surgical debridement. Hemodynamic resuscitation with aggressive intravenous fluids and vasopressors is initiated immediately, as septic shock is common at presentation. Broad-spectrum empiric antibiotics should be started immediately and typically consist of vancomycin (for MRSA coverage) plus piperacillin-tazobactam (for broad gram-negative and anaerobic coverage) plus clindamycin, the latter added specifically for its ability to inhibit toxin production by Group A streptococcus and clostridia. Urgent surgical debridement is the most critical intervention and must not be delayed for imaging studies; surgery should be performed as soon as possible with aggressive resection of all necrotic tissue back to viable, bleeding margins, with repeat debridements at 24-48 hour intervals as needed. CT imaging may demonstrate fascial thickening, enhancement, gas tracking along fascial planes, and fluid collections, but should not delay surgical intervention when clinical suspicion is high. Intravenous immunoglobulin (IVIG) should be considered for cases associated with streptococcal toxic shock syndrome, where it may neutralize circulating superantigens. Panel A: Clinical progression of necrotizing fasciitis from initial erythema and pain out of proportion to exam, through dusky discoloration with bullae, to frank necrosis with black eschar. Panel B: CT imaging findings showing fascial thickening with enhancement, gas tracking along fascial planes, and fluid collections indicating need for surgical exploration. Panel C: Surgical debridement demonstrating necrotic fascia, dishwater-gray purulent material, and extent of tissue involvement requiring aggressive resection to viable bleeding margins. Panel D: Management algorithm emphasizing rapid resuscitation, broad-spectrum antibiotics (vancomycin plus piperacillin-tazobactam plus clindamycin), and emergent surgical debridement as the critical intervention. --- ### IV. Viral Skin Infections - Herpes Viruses Herpes simplex virus (HSV) infections are among the most common viral skin infections, with HSV-1 typically causing oral herpes (herpes labialis) and HSV-2 typically causing genital herpes, though either serotype can infect either site. Primary HSV infection is generally more severe than recurrent episodes, presenting with more numerous lesions, more prominent systemic symptoms including fever and malaise, and a longer duration of viral shedding and clinical illness. Recurrent infections are less severe and are often preceded by a prodrome of tingling, burning, or itching at the site of the impending eruption, reflecting viral reactivation from the sensory ganglion where latency is established. The characteristic lesion of HSV infection is a cluster of grouped vesicles on an erythematous base that evolve through stages of vesiculation, ulceration, crusting, and healing over approximately 7 to 10 days. Treatment with acyclovir or valacyclovir is effective for both primary and recurrent infections, with chronic suppressive therapy recommended for patients with frequent recurrences. Herpes zoster (shingles) results from reactivation of varicella-zoster virus (VZV) latent in the dorsal root ganglia following primary varicella infection and produces a characteristically dermatomal eruption. The distribution is strictly unilateral and confined to one or occasionally two adjacent dermatomes, a pattern that is virtually pathognomonic for this diagnosis. A prodrome of pain, burning, or paresthesias in the affected dermatome typically precedes the rash by 1 to 5 days and may be mistaken for cardiac, pulmonary, or abdominal disease depending on the involved dermatome. The eruption consists of grouped vesicles on an erythematous base that evolve over several days, with new lesions continuing to appear for up to one week. Complications include postherpetic neuralgia (PHN), which is chronic neuropathic pain persisting beyond 90 days after rash onset and is the most common complication; dissemination in immunocompromised patients; and ocular involvement (herpes zoster ophthalmicus) when the ophthalmic division of the trigeminal nerve is affected. Antiviral therapy with acyclovir, valacyclovir, or famciclovir should be initiated within 72 hours of rash onset to reduce the duration of illness and the risk of postherpetic neuralgia, and pain management may require multimodal analgesia. Varicella (chickenpox) is the primary infection caused by VZV and presents with a distinctive exanthem characterized by vesicles described as having a "dewdrop on a rose petal" appearance. The rash has a centripetal distribution, meaning that lesion density is greatest on the trunk and proximal extremities with relative sparing of distal sites, and a hallmark feature is the presence of lesions in different stages of evolution (macules, papules, vesicles, and crusts) simultaneously. Complications include secondary bacterial skin infection (the most common complication), varicella pneumonia (more common in adults and immunocompromised patients), and encephalitis. Prevention through vaccination with the live attenuated varicella vaccine has dramatically reduced the incidence of primary varicella and its complications. Other herpesviruses produce a variety of mucocutaneous manifestations with clinical significance. Epstein-Barr virus (EBV) causes infectious mononucleosis, and patients who receive ampicillin or amoxicillin during active mononucleosis develop a characteristic widespread maculopapular rash that is not a true drug allergy but rather reflects an interaction between the virus and the antibiotic. Cytomegalovirus (CMV) produces cutaneous manifestations primarily in immunocompromised patients, including oral and perianal ulcers that may be difficult to distinguish from HSV without biopsy and immunohistochemistry. Human herpesvirus 6 (HHV-6) causes roseola infantum (exanthem subitum), a common childhood illness characterized by several days of high fever followed by the appearance of a diffuse maculopapular rash coinciding with defervescence. Human herpesvirus 8 (HHV-8) is the causative agent of Kaposi sarcoma, a vascular neoplasm most commonly seen in HIV/AIDS patients presenting as violaceous plaques and nodules. Panel A: Herpes simplex showing grouped vesicles on an erythematous base at the vermilion border (cold sore) and genital presentation with painful erosions and ulcerations. Panel B: Herpes zoster with dermatomal distribution of vesicles on erythematous base, showing unilateral involvement respecting midline and typical thoracic dermatome pattern. Panel C: Varicella (chickenpox) demonstrating "dewdrop on rose petal" vesicles, centripetal distribution with higher density on trunk, and lesions in different stages of evolution. Panel D: Tzanck smear preparation showing multinucleated giant cells indicative of herpesvirus infection used for rapid bedside diagnosis. --- ### V. Viral Skin Infections - Other Human papillomavirus (HPV) causes a spectrum of warty lesions whose clinical appearance and significance depend on the viral type and anatomic site of infection. Common warts (verruca vulgaris) are the most prevalent manifestation, presenting as rough, hyperkeratotic, dome-shaped papules most commonly on the hands and fingers, caused primarily by HPV types 2 and 4. Plantar warts occur on the soles of the feet where the body's weight drives them endophytically, producing painful lesions with characteristic thrombosed capillaries (black dots) visible on the surface. Flat warts (verruca plana) present as smooth, flat-topped, flesh-colored to slightly brown papules typically on the face and arms of children, caused by HPV types 3 and 10. Genital warts (condylomata acuminata) are soft, cauliflower-like growths on the anogenital skin caused primarily by HPV types 6 and 11, while high-risk types 16 and 18 are associated with cervical, anal, and oropharyngeal carcinoma. Treatment options include cryotherapy with liquid nitrogen, topical salicylic acid, and topical imiquimod, which stimulates the local immune response against the virus. Molluscum contagiosum is caused by a poxvirus and produces distinctive skin lesions that are among the most recognizable in dermatology. The characteristic lesion is an umbilicated, dome-shaped, pearly papule with a central dell or dimple that contains a cheesy core of molluscum bodies (Henderson-Paterson bodies). The infection occurs in two main demographic groups: children, in whom it typically presents as scattered papules on the trunk and extremities spread by direct contact and fomites, and sexually active adults, in whom genital molluscum represents a sexually transmitted infection. The clinical course is self-limited in immunocompetent individuals, though resolution may take months to years, and treatment options include observation, curettage, and cryotherapy depending on patient preference and the number and location of lesions. Hand-foot-and-mouth disease is a common childhood viral illness caused by Coxsackievirus A16 and enterovirus 71, characterized by a distinctive pattern of oral and cutaneous lesions. The oral component presents as painful ulcers on the palate, tongue, and buccal mucosa that may interfere with feeding in young children. The cutaneous component consists of oval vesicles with a surrounding rim of erythema distributed on the palms, soles, and often the buttocks. The disease is highly contagious, spread through fecal-oral and respiratory routes, and the clinical course is self-limited with resolution typically occurring within 7 to 10 days. Treatment is supportive, focusing on pain management and maintenance of hydration. The classic childhood viral exanthems each produce characteristic cutaneous findings that enable clinical diagnosis. Measles (rubeola), caused by morbillivirus, produces a maculopapular rash that begins on the face and spreads cephalocaudally, preceded by the pathognomonic Koplik spots (blue-white papules on the buccal mucosa opposite the molars). Rubella (German measles) produces a finer maculopapular rash with characteristic postauricular and suboccipital lymphadenopathy. Erythema infectiosum (fifth disease), caused by parvovirus B19, is distinguished by the "slapped cheek" appearance with bright erythema of both cheeks sparing the nose and perioral area, followed by a lacy, reticular rash on the trunk and extremities. Roseola infantum (sixth disease), caused by HHV-6, presents with several days of high fever followed by the appearance of a diffuse maculopapular rash coinciding with defervescence, a temporal pattern that is diagnostically distinctive. Panel A: HPV warts showing verruca vulgaris (rough, hyperkeratotic papule on hand), plantar wart (endophytic with thrombosed capillaries), and condyloma acuminata (genital, cauliflower-like). Panel B: Molluscum contagiosum with characteristic umbilicated, dome-shaped, pearly papules showing central dell and typical grouped distribution. Panel C: Hand-foot-mouth disease showing oral ulcerations on palate and tongue, oval vesicles on palms and soles with surrounding erythema, and buttock involvement. Panel D: Viral exanthems comparing measles (morbilliform rash with Koplik spots), erythema infectiosum (slapped cheek appearance), and roseola (fever followed by rash on defervescence). --- ### VI. Fungal Skin Infections - Superficial Dermatophyte infections, collectively termed tinea, are superficial fungal infections caused by three genera of keratinophilic fungi (Trichophyton, Microsporum, and Epidermophyton) that invade the stratum corneum, hair, and nails. These infections are named according to the anatomic site of involvement: tinea capitis affects the scalp, tinea corporis the body, tinea cruris the groin (commonly known as jock itch), tinea pedis the feet (athlete's foot), tinea unguium the nails (onychomycosis), and tinea manuum the hands. The clinical presentation varies by site but shares the common feature of a superficial infection confined to keratinized tissue, reflecting the dermatophytes' inability to invade living tissue or survive at core body temperature. The clinical features of dermatophyte infections are distinctive at each anatomic location. Tinea corporis classically presents as an annular plaque with a raised, erythematous, scaling border and central clearing, producing the characteristic "ringworm" appearance despite having no helminthic etiology. Tinea capitis presents as areas of scaling and hair loss on the scalp, and may produce a kerion, which is a severely inflammatory, boggy, pustular mass that represents a vigorous host immune response to the fungal infection. Tinea pedis is the most common dermatophyte infection in adults and presents in several patterns including interdigital maceration between the toes and a chronic, diffuse, hyperkeratotic "moccasin" distribution involving the soles and lateral feet. Onychomycosis (tinea unguium) produces thickened, discolored (yellow-white), and crumbly nails, typically beginning at the distal or lateral nail edge and progressing proximally over months to years. Diagnosis of dermatophyte infections relies on clinical recognition supplemented by several confirmatory laboratory methods. Potassium hydroxide (KOH) preparation is the most practical bedside test, in which skin scrapings from the active, scaling border of the lesion are treated with KOH to dissolve keratinocytes, revealing the branching, septate hyphae crossing cell borders that are characteristic of dermatophyte infection. Fungal culture on dermatophyte test medium or Sabouraud agar provides definitive identification of the species but requires 2 to 4 weeks for growth. Wood lamp examination using ultraviolet light causes certain Microsporum species to fluoresce a bright green-yellow color, though it is not useful for Trichophyton infections, which are the most common dermatophytes. Dermoscopy of tinea capitis may reveal comma hairs (short, broken hairs with a curved shape) that are characteristic of dermatophyte infection of the hair shaft. Treatment of dermatophyte infections depends on the site and extent of involvement. Tinea corporis, tinea cruris, and tinea pedis affecting limited areas respond well to topical antifungal agents including terbinafine cream and azole antifungals (clotrimazole, miconazole, ketoconazole), applied twice daily for 2 to 4 weeks. Tinea capitis requires oral antifungal therapy because topical agents cannot penetrate the hair follicle to reach the site of infection, with griseofulvin or terbinafine being the standard oral agents. Onychomycosis requires prolonged oral antifungal therapy with terbinafine (typically 6 weeks for fingernails and 12 weeks for toenails) or itraconazole, as the avascular nail plate prevents adequate penetration of topical medications. Extensive or recalcitrant dermatophyte infections at any site may also require oral therapy. Panel A: Tinea corporis showing annular plaque with raised, scaly, advancing border and central clearing giving the classic ringworm appearance. Panel B: KOH preparation microscopy demonstrating septate, branching hyphae crossing cell borders, confirming dermatophyte infection. Panel C: Tinea unguium (onychomycosis) with distal subungual involvement showing yellow discoloration, onycholysis, subungual debris, and nail plate thickening. Panel D: Tinea variants by location including tinea capitis (scalp with alopecia and scale), tinea pedis (interdigital maceration and moccasin pattern), and tinea cruris (groin sparing scrotum). --- ### VII. Fungal Skin Infections - Yeast Candidiasis is caused by Candida species, most commonly Candida albicans, and produces a spectrum of mucocutaneous infections whose presentation depends on the site of involvement and the host's immune status. Oral candidiasis (thrush) presents as white, curd-like plaques on an erythematous base that can be scraped off with a tongue blade, leaving a raw, erythematous surface, and is seen in immunocompromised patients, those receiving inhaled corticosteroids, and neonates whose immune systems are immature. Cutaneous candidiasis occurs in intertriginous areas (intertrigo) where moisture, warmth, and skin-on-skin friction create a favorable environment for yeast proliferation, producing beefy red erythema with maceration and the characteristic satellite pustules or papules beyond the advancing border that are virtually pathognomonic. Candidal diaper dermatitis is distinguished from irritant diaper rash by the presence of satellite pustules extending beyond the main area of erythema. Vulvovaginitis caused by Candida presents with thick, white, cottage cheese-like vaginal discharge accompanied by intense pruritus and vulvar erythema. Candidal paronychia is an infection of the nail fold producing erythema, swelling, and tenderness, typically seen in patients whose hands are chronically exposed to moisture. Treatment of candidiasis varies by site and severity. Oral candidiasis is treated with nystatin suspension used as a swish-and-swallow preparation for mild cases, while fluconazole is preferred for moderate-to-severe disease or in immunocompromised patients. Cutaneous candidiasis responds to topical antifungal agents including azoles (clotrimazole, miconazole, ketoconazole) and nystatin cream, with attention to keeping the affected area dry and reducing moisture through absorbent powders. Extensive or recalcitrant cutaneous candidiasis, as well as esophageal or disseminated disease, requires systemic treatment with oral fluconazole. Pityriasis versicolor (formerly tinea versicolor) is a common superficial fungal infection caused by Malassezia species, lipophilic yeasts that are part of the normal skin flora but can proliferate and cause clinical disease under favorable conditions. The characteristic presentation consists of hypo- or hyperpigmented macules and patches with a fine, powdery scale, distributed predominantly on the trunk, shoulders, and upper arms. The pigmentary alteration results from Malassezia's production of azelaic acid, which inhibits melanocyte tyrosinase, producing hypopigmented lesions that become more apparent after sun exposure when surrounding skin tans but the affected areas do not. KOH preparation demonstrates the characteristic "spaghetti and meatballs" appearance of short, stubby hyphae intermixed with round yeast forms that is diagnostic. Treatment options include topical azole antifungals, selenium sulfide shampoo applied as a body wash, and oral fluconazole for extensive or recalcitrant cases, though patients should be counseled that pigmentary changes may persist for weeks to months after successful eradication of the organism. Piedra is a rare fungal infection of the hair shaft caused by specific organisms depending on the geographic and clinical type. Black piedra, caused by Piedraia hortae, affects the scalp hair in tropical regions and produces dark, firmly adherent nodules along the hair shaft. White piedra, caused by Trichosporon species, affects the beard, groin, and axillary hair and produces softer, white-to-tan nodules that are more loosely attached to the hair shaft. Both conditions are treated by shaving the affected hair and applying topical antifungal agents. Panel A: Oral candidiasis (thrush) showing white, curd-like plaques on erythematous base that can be scraped off, involving tongue and buccal mucosa. Panel B: Candidal intertrigo in intertriginous areas (axillae, groin, inframammary) with beefy red erythema, maceration, and characteristic satellite pustules at periphery. Panel C: Pityriasis (tinea) versicolor showing hypo- and hyperpigmented macules with fine scale on trunk and shoulders, more apparent after sun exposure. Panel D: KOH preparation of pityriasis versicolor demonstrating "spaghetti and meatballs" appearance with short hyphae and round yeast forms of Malassezia. --- ### VIII. Parasitic Infestations Scabies is an intensely pruritic skin infestation caused by the mite Sarcoptes scabiei var. hominis, transmitted through prolonged close personal contact and affecting all socioeconomic groups worldwide. The cardinal symptom is intense pruritus that is characteristically worse at night, when the warmth of bedding increases mite activity and the absence of daytime distractions amplifies the perception of itch. The pathognomonic lesion is the burrow, a short (2-10 mm), thin, wavy, grayish-white line that represents the tunnel excavated by the female mite as she lays eggs within the stratum corneum, most commonly found in the finger web spaces and wrists. The characteristic distribution includes the finger webs, wrists, axillae, periumbilical area, waistband, and genitals, with the head and neck typically spared in adults but potentially involved in infants. Norwegian (crusted) scabies is a severe variant occurring in immunocompromised patients, the elderly, and those with neurologic conditions that impair the itch response, characterized by thick, hyperkeratotic plaques harboring thousands to millions of mites and making this form extraordinarily contagious compared to typical scabies with its low mite burden of 10-15 organisms. Treatment of scabies must address the patient, close contacts, and the environment simultaneously to prevent reinfection. Permethrin 5% cream is the first-line treatment, applied from the neck down to all skin surfaces including under fingernails and in skin folds, left on for 8 to 14 hours before washing off, and repeated in one week to kill newly hatched mites from surviving eggs. Oral ivermectin is an effective alternative that offers the convenience of a single oral dose (repeated in one to two weeks), is the treatment of choice for crusted scabies where the thick scale prevents adequate penetration of topical therapy, and may be preferred for institutional outbreaks. All household members and close contacts should be treated simultaneously regardless of whether they have symptoms, as the incubation period for primary scabies is 4 to 6 weeks during which transmission can occur. Bed linens and clothing worn in the preceding three days should be washed in hot water and dried on high heat. Importantly, the pruritus of scabies may persist for two to four weeks after successful treatment due to the ongoing immune response to dead mites and fecal material, and this should not be mistaken for treatment failure. Pediculosis (lice infestations) is caused by three species of obligate human ectoparasites that affect different body regions. Head lice (Pediculus humanus capitis) infest the scalp hair, predominantly in school-aged children, and are treated with topical permethrin, oral ivermectin, or dimethicone-based products, with manual nit removal complementing chemical treatment. Body lice (Pediculus humanus corporis) are unique in that they live in the seams of clothing rather than on the body, laying eggs in fabric and moving to the skin only to feed, and treatment therefore centers on hygiene measures and washing clothes in hot water rather than topical pediculicides. Pubic lice (Phthirus pubis, commonly known as crabs) infest the coarse hair of the genital region and are transmitted through sexual contact, treated with topical permethrin, and sexual partners must be simultaneously treated to prevent reinfection. Cutaneous larva migrans is a parasitic skin condition caused by the percutaneous penetration of animal hookworm larvae, most commonly Ancylostoma braziliense from dogs and cats. Infection occurs through direct skin contact with contaminated soil or sand, typically when walking barefoot on beaches in tropical and subtropical regions. The characteristic presentation is a serpiginous (snake-like), erythematous, intensely pruritic track that advances 1 to 2 centimeters daily as the larva migrates through the superficial layers of the skin, unable to penetrate into the deeper tissues of the non-definitive human host. Treatment is highly effective with oral ivermectin as a single dose or albendazole for 3 days, and the infection is self-limited even without treatment as the larvae eventually die without completing their life cycle. Panel A: Scabies showing linear burrows in finger web spaces, excoriated papules from intense pruritus, and distribution on wrists, axillae, and genitals. Panel B: Microscopic view of Sarcoptes scabiei mite from skin scraping, and Norwegian (crusted) scabies with hyperkeratotic plaques in immunocompromised patient. Panel C: Pediculosis with head louse attached to hair shaft, nits (eggs) cemented to hair, and pubic louse (crab) with characteristic morphology. Panel D: Cutaneous larva migrans showing serpiginous, erythematous, pruritic track from migrating hookworm larva, advancing 1-2 cm daily, typically on foot after beach exposure. --- ### IX. Skin Infections in Immunocompromised Immunocompromised patients face a dramatically expanded spectrum of potential skin pathogens and present with more severe, atypical, and treatment-resistant infections that challenge even experienced clinicians. Bacterial infections in immunocompromised hosts include typical organisms such as S. aureus and Pseudomonas aeruginosa that may cause more extensive or invasive disease, as well as opportunistic organisms that rarely cause skin infections in immunocompetent individuals. Viral infections, particularly with herpesviruses, may present with severe, prolonged, or disseminated disease, with HSV producing large, chronic ulcers and VZV potentially disseminating across multiple dermatomes or becoming viscerally involved. Fungal infections extend beyond the superficial dermatophytes and yeasts to include invasive molds such as Aspergillus and Mucor that can cause rapidly progressive, life-threatening infections. Atypical organisms including non-tuberculous mycobacteria, Nocardia, and other environmental organisms that rarely infect immunocompetent hosts must be considered in the differential diagnosis. Several specific infections in immunocompromised patients warrant particular attention due to their clinical significance and distinctive presentations. Ecthyma gangrenosum is a characteristic skin manifestation of Pseudomonas sepsis, typically occurring in neutropenic patients, presenting as hemorrhagic bullae that rapidly progress to necrotic ulcers with black eschar and surrounding erythema, reflecting vascular invasion by the organism. Disseminated zoster occurs when VZV reactivation spreads beyond the initial dermatome to involve multiple dermatomes or the entire skin surface, with risk of visceral involvement including pneumonitis, hepatitis, and encephalitis. Invasive aspergillosis may produce black necrotic skin lesions (eschars) reflecting angioinvasion, often in association with underlying pulmonary aspergillosis in neutropenic patients. Mucormycosis (zygomycosis) is a rapidly progressive infection caused by Mucor and Rhizopus species that classically presents as rhino-orbital-cerebral disease in diabetic patients with ketoacidosis or neutropenic patients, producing black necrotic tissue on the nasal mucosa or palate with rapid extension into the orbit and brain. Kaposi sarcoma is a vascular neoplasm caused by HHV-8 that is strongly associated with HIV/AIDS and represents one of the AIDS-defining illnesses. The characteristic lesions are violaceous (purple) plaques and nodules that can occur anywhere on the skin, with a predilection for the lower extremities, face, and oral mucosa. The lesions are typically non-tender and non-pruritic, and may be solitary or widespread depending on the degree of immunosuppression. Treatment of HIV-associated Kaposi sarcoma begins with initiation or optimization of antiretroviral therapy (ART), which often produces significant regression of lesions through immune reconstitution, with chemotherapy reserved for extensive or viscerally involved disease. The evaluation of skin infections in immunocompromised patients requires a systematic approach that differs from the approach used in immunocompetent hosts. The differential diagnosis must be broadened to consider unusual organisms that would not typically be considered in immunocompetent patients, including opportunistic fungi, atypical mycobacteria, and parasites. Skin biopsy is critically important and should be performed early in the evaluation, with tissue sent for both culture (bacterial, fungal, mycobacterial) and histopathologic examination to maximize diagnostic yield. Imaging studies should be obtained to assess for deep tissue involvement and systemic dissemination of infection. Early empiric therapy should be initiated while awaiting diagnostic results, given the potential for rapid progression of infections in the setting of impaired immunity. Panel A: Ecthyma gangrenosum showing hemorrhagic bullae progressing to necrotic ulcer with black eschar and surrounding erythema, characteristic of Pseudomonas sepsis in neutropenic patients. Panel B: Kaposi sarcoma with violaceous plaques and nodules on skin, associated with HHV-8 in HIV/AIDS patients, showing typical distribution on lower extremities and face. Panel C: Mucormycosis showing rhino-orbital-cerebral presentation with black eschar on nasal mucosa or palate, periorbital swelling, and rapid progression in diabetic or neutropenic patients. Panel D: Approach to skin infections in immunocompromised patients emphasizing broad differential, early biopsy for culture and histopathology, and aggressive empiric therapy while awaiting diagnosis. --- ### X. Approach to Skin Infections A systematic history is essential for narrowing the differential diagnosis and guiding the evaluation of skin infections. The onset and progression of the infection provide critical information about whether the process is acute or chronic, with acute bacterial infections typically evolving over hours to days and fungal infections developing over weeks to months. Exposure history should explore recent travel to endemic regions, contact with animals, exposure to known infected individuals, and occupational or recreational activities that may predispose to specific infections. The patient's immune status must be assessed, including diabetes mellitus, HIV infection, medications causing immunosuppression (corticosteroids, chemotherapy, biologic agents), and other conditions that alter host defenses. A history of prior episodes may reveal a recurrence pattern that suggests specific organisms (recurrent HSV) or underlying host factors (recurrent staphylococcal abscesses suggesting MRSA carriage). Physical examination of skin infections should systematically characterize the morphology, distribution, and associated findings to guide the differential diagnosis. The primary lesion morphology provides the most important diagnostic clue, distinguishing between vesicular eruptions (suggesting viral etiology), pustular eruptions (bacterial or fungal), and nodular or plaque-like lesions (deep infections or atypical organisms). The distribution pattern may be localized (suggesting a point source such as a wound infection or local inoculation), widespread (suggesting hematogenous dissemination or a diffuse process), or follow a specific pattern such as dermatomal (herpes zoster) or intertriginous (candidiasis). Associated findings including regional lymphadenopathy, fever, and other systemic signs suggest deeper or more extensive infection requiring aggressive evaluation and treatment. Signs of deep tissue involvement such as disproportionate pain, crepitus, and systemic toxicity should raise immediate concern for necrotizing soft tissue infection requiring emergent surgical evaluation. Diagnostic testing should be directed by the clinical presentation and the organisms most likely to be responsible. Gram stain and culture of wound fluid or aspirate remain the cornerstone of bacterial infection diagnosis, providing both immediate Gram stain information to guide empiric therapy and definitive culture results for antibiotic optimization. KOH preparation of skin scrapings is the primary diagnostic test for dermatophyte infections, demonstrating the characteristic branching, septate hyphae. The Tzanck smear is a rapid bedside test for herpesvirus infections in which cells scraped from the base of a vesicle are stained and examined for multinucleated giant cells, providing immediate results though it cannot distinguish between HSV and VZV. Skin scraping with mineral oil preparation is used to identify scabies mites, eggs, and fecal pellets (scybala). Skin biopsy is indicated for deep infections, immunocompromised patients, and cases where the diagnosis remains uncertain despite initial testing, with tissue sent for both culture and histopathologic examination. Treatment of skin infections should be guided by several fundamental principles. Appropriate antimicrobial coverage should be selected based on the most likely causative organism, guided by the clinical presentation, Gram stain results, and knowledge of local resistance patterns. Source control through incision and drainage of abscesses and debridement of necrotic tissue is essential and often more important than antibiotic selection, as antibiotics cannot penetrate undrained collections or devascularized tissue. The duration of treatment should be appropriate to the specific infection, with premature discontinuation risking relapse and unnecessarily prolonged courses contributing to antimicrobial resistance and adverse effects. Follow-up should be arranged to ensure resolution of infection, particularly for deep or severe infections where clinical deterioration may indicate treatment failure, abscess formation, or an alternative diagnosis requiring reassessment. Panel A: Diagnostic algorithm beginning with history (onset, exposures, immune status) and physical examination (morphology, distribution, systemic signs) to narrow differential diagnosis. Panel B: Bacterial infection diagnostics showing Gram stain and culture technique, wound swab versus tissue culture, and blood cultures for systemic involvement. Panel C: Fungal and parasitic diagnostics including KOH preparation technique, fungal culture on dermatophyte test medium, and skin scraping for scabies mite identification. Panel D: Viral diagnostics showing Tzanck smear preparation for herpesviruses, viral culture indications, and PCR testing for definitive identification when needed. --- ## Summary - Impetigo: superficial; honey-colored crusts; S. aureus, GAS - Cellulitis: deep dermis/subcutaneous; poorly demarcated erythema - NSTI: pain out of proportion, rapid progression; surgical emergency - HSV: grouped vesicles on erythematous base; acyclovir treatment - Herpes zoster: dermatomal; antivirals within 72 hours - Dermatophytes: KOH shows hyphae; topical for limited, oral for scalp/nails - Candidiasis: satellite lesions; intertriginous areas - Scabies: intense pruritus, burrows; permethrin or ivermectin - Immunocompromised: broader differential; biopsy important - NSTI red flags: pain disproportionate to exam, rapid spread, systemic toxicity --- ## Key Terms | Term | Definition | |------|------------| | Impetigo | Superficial bacterial skin infection with crusts | | Cellulitis | Infection of dermis and subcutaneous tissue | | Erysipelas | Superficial cellulitis with sharply demarcated borders | | Necrotizing fasciitis | Rapidly progressive deep soft tissue infection | | Dermatophyte | Fungus causing tinea infections | | KOH preparation | Microscopic exam for fungal elements | | Scabies | Sarcoptes scabiei mite infestation | | Burrow | Linear track from scabies mite | --- *This content is subject to the [MIT License](https://opensource.org/licenses/MIT). © 2024–2026 Hibbert School of Medicine.*