Author
Lars Grimm, MD, MHS
House Staff
Department of Internal Medicine
Duke University Medical Center
Durham, North Carolina
Disclosure: Lars Grimm, MD, MHS, has disclosed no relevant financial relationships.
Editor
Michael Stuart Bronze, MD
Professor, Stewart G. Wolf Chair in Internal Medicine
Department of Medicine
University of Oklahoma Health Science Center
Oklahoma City, Oklahoma
Disclosure: Michael Stuart Bronze, MD, has disclosed no relevant financial relationships.
Skin rashes caused by bacterial, viral, or fungal etiologies are very common presenting complaints to primary care clinics, emergency departments, and dermatologists. Although many presenting symptoms overlap, discrete identifiable factors for each disease can help aid in diagnosis and treatment. The image shown is from an individual with tinea capitis, caused by an infection with the fungus Microsporum canis.
Herpes zoster, or shingles, is a dermal and neurologic disorder caused by reactivation of the varicella-zoster virus (VZV). VZV is morphologically and antigenically identical to the virus causing varicella, or chickenpox. Individuals with no prior exposure develop varicella, whereas those with circulating antibodies develop zoster. Zoster probably results from a failure of the immune system to contain latent VZV replication. Although radiation, trauma, medications, stress, or other infections have been proposed as triggers, no specific etiology has been clearly established. Zoster typically manifests with a prodrome of pain or anesthesia along a dermatomal distribution. Erythema, regional lymphadenopathy, and grouped herpetiform vesicles (shown) then develop. The cutaneous findings are typically unilateral and do not cross the midline. Image courtesy of the US Centers for Disease Control and Prevention.
Vesicles are initially clear (shown), but then may become cloudy, rupture, crust, and involute. Residual cosmetic defects are uncommon unless significant excoriation or secondary infection occurs. Unfortunately, for some individuals the pain does not resolve and may persist for years, a condition referred to as postherpetic neuralgia. No treatment is required in most individuals, but antiviral agents (eg, acyclovir) given early in the disease course shorten the recovery period and reduce the chance of postherpetic neuralgia. Postherpetic neuralgia treatment is challenging, and many different treatment options are available: gabapentin; topical capsaicin; tricyclic antidepressants; and anesthetic or corticosteroid injections. A vaccine is available and is recommended for all individuals over the age of 60 years by the US Centers for Disease Control and Prevention.
Chickenpox is an infectious vesicular rash caused by primary infection from the double-stranded DNA VZV. Ninety percent of cases occur in children younger than 10 years. Chickenpox is highly contagious and acquired via inhalation of airborne respiratory droplets or direct vesicle contact. The virus first infects the conjunctiva or mucosa of the upper respiratory tract. Proliferation in regional lymph nodes occurs 2-4 days after inoculation with viremia developing on days 4-6. A second round of viral replication develops 14-16 days post infection in the liver and spleen causing a secondary viremia. This viremia invades the capillary endothelial cells and epidermis, producing inter- and intracellular edema, resulting in vesicle formation. The clear vesicles are surrounded by an erythematous halo with subsequent central umbilication and crusting (shown). Patients may report a mild prodrome and then intense pruritus with vesicle formation. On exam, vesicles in all stages of development are typically present. Treatment is for symptomatic relief with topical antipruritic creams or oral antihistamines. Acyclovir is not often prescribed for children. The disease typically resolves spontaneously, but adults may have significant morbidity and are often given antiviral medications.
Herpes simplex viruses (HSVs) are DNA viruses that cause acute skin infections that present as grouped vesicles on an erythematous base. Infection occurs from transmission of body fluids onto a mucous membrane or open skin from an actively shedding individual to a susceptible person. HSV invades and replicates in the neurons and epidermal and dermal cells. Latency is established when virions migrate to a dorsal root ganglion. Recurrent outbreaks occur at or near the same location from viral replication in the sensory ganglia as a result of stress, trauma, immunosuppression, hormonal fluctuations, extremes in temperature, or ultraviolet light. HSV-1 reactivates predominantly in the trigeminal ganglia, called herpes labialis (shown), whereas HSV-2 reactivates in the lumbosacral ganglia, called herpes genitalis. Patients typically report painful ulcerating lesions. Most infections are self-limited but antiviral therapy, such as acyclovir, will shorten the course of symptoms and may help to prevent dissemination and transmission.
Molluscum contagiosum is a cutaneous infection caused by a large DNA poxvirus. Transmission occurs via direct skin contact or by sharing towels, sports equipment, or benches. Most patients are asymptomatic, but others report pruritus, tenderness, and pain. The lesions appear as firm, smooth, umbilicated papules typically 2-6 mm in diameter either clustered or widely distributed (shown). Lesions can be variable in color ranging from flesh, white, translucent, or yellow; range in number from 1 to several hundred; and may persist for several years. Diagnosis is typically made on clinical grounds. Although typically self-limited, therapy may be appropriate for lesions that do not resolve after several months to prevent autoinoculation. Treatment options are not approved by the US Food and Drug Administration (FDA), including topical applications (eg, cantharidin, tretinoin cream), systemic agents (eg, griseofulvin, cimetidine, methisazone), and photodynamic therapy. The overall prognosis is typically excellent.
Hand-foot-and-mouth disease is a viral illness with oral and distal extremity lesions. It is most commonly caused by a coxsackievirus infection. Infections are highly contagious, leading to epidemics from direct contact with nasal and oral secretions or fecal material. Incubation typically averages 3-6 days. Following implantation, regional spread to lymph nodes occurs within 24 hours, and then viremia rapidly ensues. Typically by day 7, neutralizing antibody levels have sufficiently increased and the virus is eliminated. Patients may report a viral prodrome, but the lesions themselves are typically asymptomatic. Children typically have a more severe course and may develop high fevers. The oral lesions are usually 2-3 mm vesicles on an erythematous base. The cutaneous lesions on the hands, feet, and buttocks are 2-mm to 10-mm erythematous macules on which a central, gray, oval vesicle develops. Lesions are typically elliptical with the long axis parallel to skin lines (shown). Care is supportive with antipyretics and anesthetics for symptomatic relief on a case-by-case basis.
Erythema infectiosum, or fifth disease, is a common childhood exanthem caused by human parvovirus B19. Transmission is via aerosolized respiratory droplets with an incubation period of 4-14 days. The illness has 3 distinct phases with a very mild prodrome. In the first phase, which lasts for 2-4 days, bright red erythema develops over the cheeks in a classic slapped-cheek appearance, with sparing of the nasal, periorbital, and perioral regions (shown). In the second phase, which lasts for 1-4 days, an erythematous macular-to-morbilliform eruption occurs predominantly on the extensor surfaces of the extremities. In the final stage, which lasts for several days to weeks, the eruption fades leaving behind a reticulated, lacy pattern. The disease is typically self-limited and resolves without complications or sequelae in children, whereas adults may suffer significant morbidity. Some patients may develop arthralgias or pruritus that can be treated with oral analgesics, antihistamines, or topical antipruritic lotions on a case-by-case basis.
Pityriasis rosea is a benign papulosquamous disease. The exact etiologic organism is not known, but immunologic data suggest a viral etiology. Like many viral exanthems, the incidence increases in the fall and spring. The disease usually begins with a solitary, salmon-colored macule (2-10 cm in diameter) -- termed a herald patch -- that enlarges over several days to become a patch with fine scales and a well-demarcated border. Over the next several weeks, a generalized xanthem develops with bilateral, symmetric macules (0.5-1.5 cm in diameter), oriented along cleavage lines. This usually lasts for 6 weeks. Patients typically only report mild-to-moderate pruritus. Treatment is largely symptomatic for relief of pruritus with topical steroids, oral antihistamines, oatmeal baths, and topical menthol-phenol lotions. Oral steroids are not recommended. Rashes usually resolve within 12 weeks. Image courtesy of Wikimedia Commons.
Tinea is a superficial dermatophyte infection characterized by inflammatory or noninflammatory lesions on the glabrous skin. Classification is based on the region of infection: pedis for feet; corporis for body; capitis for head; and cruris for groin. It may be caused by 1 of 3 dermatophytes: Trichophyton (most common); Microsporum; and Epidermophyton. The dermatophytes preferentially inhabit warm, moist environments. The infections are generally limited to the epidermis and expand in a centrifugal pattern. Transmission is via direct skin-to-skin contact. Patients may be asymptomatic or complain of a pruritic or burning sensation. The lesion appears as an erythematous, scaly plaque that may enlarge rapidly (shown). Scales, crust, papules, vesicles, or bullae may develop along the advancing border. Diagnosis may be made with a KOH preparation from a skin scraping. Topical therapy with either an azole or allylamine is typically sufficient, but systemic therapy with an azole, griseofulvin, or terbinafine may be required for individuals with extensive skin infection, immunosuppression, resistance to topical therapies, or for tinea capitis.
Intertrigo is an inflammatory condition of skin folds, most commonly from candidal infection. Heat, moisture, maceration, friction, or lack of air circulation all provide ideal conditions for infection. It is most common in people with diabetes or who are obese. Intertrigo is typically chronic in nature, with patients reporting itching, burning, and stinging of infected areas. Erythema, weeping, maceration, crusting, fissuring, pustules, and vesicles may all be present depending on the duration of inflammation. Treatment focuses on correcting the causative factors that place patients at risk, including the use of air conditioners, absorbent powders, and moisture-wicking undergarments. Topical steroids and antimycotic agents may be used for severe infections.
Cellulitis is a nonnecrotizing infection of the dermis and hypodermis. The most common organisms involved are Streptococcus pyogenes and Staphylococcus aureus. Small breaks in the skin allow for organisms to gain entrance to the dermis and multiply. In rare cases, hematogenous or metastatic seeding may occur. Patients typically report fevers, chills, pain, swelling, tenderness, erythema, and warmth. The borders of cellulitis are not elevated or sharply demarcated. Lymphangitis or regional lymphadenopathy may develop. Mild cases may be treated in an outpatient setting with oral antibiotics, with activity against staphylococci and streptococci (eg, dicloxacillin, cephalexin, clindamycin, amoxicillin/clavulanate). Intravenous antibiotics are reserved for patients who are severely ill, with facial cellulitis, who are refractory to oral therapy, or who are immunosupressed. There is a growing presence of community-acquired methicillin-resistant S aureus (MRSA), requiring treatment with more potent antibiotics.
Impetigo is a gram-positive bacterial infection of the superficial layers of the epidermis. The most common organisms identified are S aureus and group A beta-hemolytic streptococci. Infection typically occurs via skin breakage from excoriation or other skin diseases. Patients are either colonized in the anterior nares, or organisms pass from one individual to another through direct hand contact. Impetigo may be bullous or nonbullous. Nonbullous impetigo is the more common variety, characterized first by a red macule or papule (2-5 mm in size) that turns into a fragile vesicle that ruptures to become a honey-yellow crusted papule or plaque. In bullous impetigo, bacterial exotoxins cause a loss of cell adhesion in the superficial dermis. An initial vesicle develops into a superficial flaccid bullae (1 cm in size) with minimal surrounding erythema that eventually ruptures, leaving behind a crusty scale (shown). Lesions are usually asymptomatic with occasional pain or pruritus. Treatment is typically with topical antibiotics, such as mupirocin. Oral antibiotics, usually cephalosporins, penicillins, or beta-lactam/beta-lactamase inhibitors, are reserved for more extensive disease. Without treatment, lesions may spread via autoinoculation. Image courtesy of Wikimedia Commons.
Erysipelas is a superficial bacterial skin infection that extends into the cutaneous lymphatics. The most common bacteria responsible are streptococci. Infection occurs via inoculation into an area of local skin trauma. The infection rapidly invades and spreads through the lymphatic vessels, often producing skin streaking and regional lymphadenopathy and tenderness. Erysipelas begins as a small erythematous patch that progresses to a fiery-red, indurated, tense, and shiny plaque (shown). The margins are typically sharply demarcated. In severe infections, vesicles, bullae, petechiae, and frank necrosis may be found. Treatment for 10-20 days is recommended with penicillin, a first-generation cephalosporin, or macrolide in penicillin-allergic patients. Elevation and rest of the affected area may help reduce swelling, and saline wet dressing should be applied to ulcerated and necrotic lesions.
Folliculitis is inflammation within the wall and ostia of a hair follicle creating a pustule. Many different causes have been identified, including infection, trauma, perspiration, and occlusion. The most common infectious organism is S aureus. However, gram-negative organisms are found in patients on chronic antibiotic therapy, and Pseudomonas may be found in patients using hot tubs or wet suits. Acne represents a noninfectious form of folliculitis caused by follicular obstruction from abnormal keratinization. In superficial folliculitis, multiple small papules and pustules on an erythematous base pierced by a central hair are found (shown). Deep folliculitis may present with erythematous, fluctuant nodules. Patients typically report mild pruritus or discomfort. Folliculitis is usually self-limited and does not require treatment, but the use of antibacterial soaps is recommended for recurrent folliculitis. For patients with deep lesions or suspected infectious etiology, empirical treatment with oral or topical antibiotics may be appropriate, such as dicloxacillin, a cephalosporin, or mupirocin.
Author
Lars Grimm, MD, MHS
House Staff
Department of Internal Medicine
Duke University Medical Center
Durham, North Carolina
Disclosure: Lars Grimm, MD, MHS, has disclosed no relevant financial relationships.
Editor
Michael Stuart Bronze, MD
Professor, Stewart G. Wolf Chair in Internal Medicine
Department of Medicine
University of Oklahoma Health Science Center
Oklahoma City, Oklahoma
Disclosure: Michael Stuart Bronze, MD, has disclosed no relevant financial relationships.
