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Ecthyma Gangrenosum

Early Ecthyma Gangrenosum

Ecthyma gangrenosum describes a cutaneous infection with Pseudomonas aeruginosa that is manifested by necrotic plaques with an eschar. The infection usually occurs in immunosuppressed patients. Three to six percent of Pseudomonas septicemia is complicated by ecthyma gangrenosum (1). The term ecthyma gangrenosum was given by Hitschmann and Kreibich in 1897 in Germany to describe necrotic cutaneous plaques due to cutaneous involvement in disseminated Pseudomonas infection. However, ecthyma gangrenosum is now known to be a morphologic pattern of cutaneous infection caused by a wide variety of organisms. Ecthyma gangrenosum usually starts as an erythematous macule, which subsequently forms a vesicle. Multiple lesions may occur. Lesions rapidly become indurated and may develop pustules or bullae, which slough and leave an ulcer. An eschar forms, with a rim of erythema (Figure 25.1). The disease has a strong predilection for axillae, inguinal folds, and perineum, so-called apocrine areas....

Impetigo

Bullous Impetigo Eyelid

INTRODUCTION Impetigo represents a superficial invasion of the skin by pathogenic streptococci, staphylococci, or sometimes a mixture of both. Infections tend to occur in areas of previously compromised or diseased skin, such as skin affected by dermatitis, especially eczema, or in a recently lasered resurfaced skin. Owing to the superficial location there is rarely any systemic reaction of consequence. However, in rare instances the bacterial infection may result in the formation of antigen-antibody complexes that can lead to a life-threatening nephritis. CLINICAL PRESENTATION Impetigo can begin in either a bullous or vesicular form, with both types eventuating in pustule formation and then in ulceration. Invasion of the superficial regions of the skin by pathogenic streptococci or staphylococci produces small erythe-matous macules followed by dissolution of the basal epithelial layers and the formation of superficial vesicles or bullae ranging from 2 to 20 mm in diameter and...

Clinical manifestation

Differential diagnosis Bullous pemphigoid linear IgA dermatosis erythema multiforme Stevens-Johnson syndrome epidermolysis bullosa epider-molysis bullosa acquisita dermatitis herpe-tiformis impetigo pemphigus foliaceus pemphigus vulgaris herpes simplex virus infection herpes zoster

Microdistribution None

Scabies must be considered in the differential diagnosis of any generalized pruritic skin disorder especially with a history of nocturnal itching that interrupts sleep. Atopic dermatitis, generalized drug reactions, and widespread impetigo all show common features. A high index of suspicion that leads to a search for primary lesions is important to maintain. Crusted scabies can simulate eczema, psoriasis, or on rare occasions, an ery-throderma.

Conditions That May Simulate Tinea

An active impetigo of the scalp, on rare occasions, can produce enough inflammation to cause hair loss and may simulate a kerion. Hairs can be readily epilated but come out by the root rather than by breakage. Whenever there is a question, hair KOH exam and fungal culture are indicated. Patches of nummular eczema, early lesions of psoriasis, patches of impetigo, pityriasis alba in its early inflammatory phase, and the herald patch of pityriasis rosea can all be confused with TC. When other diagnostic features of these conditions are absent, a simple KOH exam should distinguish them.

Taxonomy and Classification

The genus Parapoxvirus belongs to the subfamily Chordo-poxvirinae of the family Poxviridae. The type species of the genus is Orf virus, and the other species recognized as members are Bovine papular stomatitis virus, Pseudocowpox virus, Squirrel parapoxvirus, and a recently identified member, Parapoxvirus of red deer in New Zealand. Synonyms for the viruses include contagious pustular dermatitis virus and contagious ecthyma virus for ORFV and milker's nodule virus and paravaccinia virus for PCPV. Tentative species of this genus are Auzduk disease virus (camel contagious ecthyma virus), chamois contagious ecthyma virus, and sealpox virus. A virus that infects red squirrels and induces a pustular skin disease was thought to be a PPV, but recent DNA sequence data suggest that this is not the case.

Differential diagnosis

Atopic dermatitis dermatitis herpeti-formis pityriasis lichenoides lichen pla-nus insect bite reaction contact dermatitis psoriasis ecthyma impetigo xerotic eczema transient acantholytic dermatosis linear IgA bullous dermatosis seborrheic dermatitis erythroderma from other causes such as Sezary syndrome and pemphigus foliaceus Langerhans cell histiocy-tosis fiberglass dermatitis dyshidrotic eczema pityriasis rosea animal scabies pediculosis delusions of parasitosis metabolic pruritus

Clinical Application Questions

A 14-year-old girl presents at your afternoon clinic accompanied by her mother for evaluation of oozing blisters on the left upper thigh starting at the level of the gluteal crease. Onset was sudden with rapid progression over 3 days, and the lesions are both tender and pruritic. The mother is concerned about some sort of insect-bite reaction and about the rapid progression of the lesions. You suspect impetigo. 1. With what primary form of impetigo is this clinical course most consistent 3. What are the primary lesions of bullous impetigo 4. What are the secondary lesions of bullous impetigo

Dermatologic Physical Exam

Nonbullous impetigo Thin-walled, small, transient vesicles that rupture easily (see Photo 1) burnished, moist, deep-red macules 0.5 to 1.0 cm that may enlarge as they coalesce (see Photo 2). 2. Bullous impetigo Bullae 1 to 2 cm in size that are clear at first and later become cloudy (see Photos 3,4) scaling and red plaques 1 to 2 cm or more in size that show central resolution (see Photo 5).

Indicated Supporting Diagnostic Data

This simple test is positive in staphylococcal bullous impetigo, and shows clumps of Gram-positive cocci. In nonbullous impetigo, smears can be of value if early vesicles are still present. Chains of Gram-positive cocci may be seen. Figure 1 Macrodistribution of nonbullous impetigo. Figure 1 Macrodistribution of nonbullous impetigo. 2. The impetigo does not respond to antimicrobial treatment, suggesting a resistant organism. 3. Cases of bullous impetigo where therapy will be initiated with erythromycin because of penicillin allergy. If the organism recovered is erythromycin-resistant, then treatment can be promptly corrected. This cost-effective test should be done when streptococcal-type impetigo is diagnosed, and then repeated 2 to 3 weeks post-therapy to screen for any sign of acute glomerulonephritis. This is especially pertinent during epidemics. Figure 2 Macrodistribution of bullous impetigo. Figure 2 Macrodistribution of bullous impetigo. Topical 2 mupirocin ointment applied in...

Appendix A Table of Primary Lesions and Related Disorders

Erysipelas Part III Erythema multiforme Part III Fixed drug eruption Part III Impetigo Part VI Actinic keratosis (erythematous) Part V Atypical nevi Part V Common benign nevi (pigmented) Part V Ephelides Part V Erysipelas (erythematous) Part III Erythema multiforme (erythematous) Part III Erythrasma Part III Fixed drug eruption Part III Halo nevi Part V Impetigo (deep red) Part VI Lentigines Part V Malignant melanoma Part V Nodules Impetigo (red) Part VI Impetigo (small, transient) Part VI

Phylum Firmicutes The low GC Grampositive bacteria

The cells of staphylococci occur in irregular bunches rather than ordered chains. They also produce lactic acid but can additionally carry out aerobic respiration involving cytochromes, and lack the complex nutritional requirements of the lactic acid bacteria. They are resistant to drying and able to tolerate relatively high concentrations of salt. These properties allow Staphylococcus aureus to be a normal inhabitant of the human skin, where it can sometimes give rise to dermatological conditions such as acne, boils and impetigo. It is also found in the respiratory tract of many healthy individuals, to whom it poses no threat, but in people whose immune system has been in some way compromised, it can cause serious respiratory infections. S. aureus can also cause a type of food poisoning and is the causative agent of toxic shock syndrome. Widespread antibiotic use has been largely responsible for the development of resistant forms of S. aureus, which have become ubiquitous inhabitants...

Conditions That May Simulate Herpes Simplex Recidivans

Impetigo (Nonbullous) Both diseases are common in the central facial region, and both begin with small clear vesicles on an inflammatory base. Herpetic lesions tend to remain fixed and discrete, and the vesicles are small, 1 to 2 mm across, tightly grouped, and persist for longer periods. Facial HSV occasionally develops secondary impetigo, causing some diagnostic confusion. A smear with a Gram stain will often show bacteria with cases of impetigo. A Tzanck smear of a blister base will show herpes virus cytopathic effect with herpes labialis. RIF test is also positive with herpes. Bacterial and viral cultures are expensive and are seldom justified.

Fogo selvagem

Impetigo lupus erythematosus pemphigus vulgaris seborrheic dermatitis atopic dermatitis subcorneal pustular dermatosis epidermolysis bullosa glucagonoma syndrome erythema multiforme Other causes of erythroderma drug reaction cutaneous T-cell lymphoma psoriasis pityriasis rubra pilaris contact dermatitis

Anthrax Infection

Anthrax Disease

The differential diagnosis of cutaneous anthrax is considerable, and includes ecthyma, insect or arachnid bite reaction, tularemia, glanders, rickettsialpox, diphtheria, syphilitic chancre, ecthyma gangrenosum, and orf. In endemic or occupational settings, history of contact with animals or animal products is expected in cases of anthrax. Clinical features that may point to anthrax include relative lack of symptoms given impressive clinical findings, and prominent edema. Gram stain and culture of cutaneous vesicles or ulcers will yield the organism in the majority of cases. Skin biopsy specimens of Bacillus anthracis infection have prominent superficial dermal edema with variable epidermal necrosis, and an infiltrate of neutro-phils throughout the dermis, with abscess formation. There is prominent dermal fibrin, with foci of vasculitis. Gram stain reveals gram-positive rods within the dermis (Figure 24.2A, 24.2B, and 24.2C) (14,15). Should there be

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