Infections characterized by a minimal or moderate immunologic response

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Human papillomaviruses (HPVs) are double-stranded DNA viruses that infect basal epithelial cells. HPVs can be divided into at least 65 genotypes.

Table 1 Skin disorders and their causative organisms

Disorder

Infectina oraanism

Skin infections characterized by a mild or minimal immunologic response

Verruca vulgaris Molluscum contagiosum Erythrasma Tinea versicolor Cryptococcosis Cysticercosis (viable larvae) Follicle mites

Human papillomavirus Molluscum contagiosum poxvirus Corynebacterium minutissimum Malassezia furfur Cryptococcus neoformans Cysticercus cellulosae (larval stage of Taenia solium) Demodex folliculorum

Skin infections characterized by a polymorphonuclear inflammatory response

Impetigo Group A streptococci, and others

Bullous impetigo Staphylococcus aureus

Ecthyma Streptococcus spp., Pseudomonas spp. and others Erysipelas Streptococcus spp.

Cellulitis Many bacterial species (e.g.

Staphyloccus spp., Streptococcus spp., Clostridium spp., Vibrio spp., Aeromonas spp., etc.)

Folliculitis (including Staphylococcus aureus and furuncles and others, including Pseudomonas carbuncles) aeruginosa

Candidiasis Various Candida spp.

Skin infections characterized by an eosinophil IgE-mediated immunologic response

Scabies Sarcoptes scabiei

Onchocerciasis Onchocerca volvulus

Cutaneous larva migrans Various nonhuman hookworm species (e.g. Ancylostoma braziliense, A. caninum) Cercarial dermatitis Nonhuman schistosomal (e.g.

avian) cercariae

Skin infections characterized by the presence of a monocyte/macrophage immunologic response

Diffuse histiocytic Lepromatous leprosy Mycobacterium leprae Diffuse cutaneous Leishmania spp leishmaniasis Granulomatous Tuberculoid leprosy M. leprae Cutaneous tuberculosis M. tuberculosis Leishmania recidivans Leishmania spp. (usually L. tropica)

Tertiary syphilis Treponema pallidum

(gumma)

Dermatomycoses due Various fungal spp. (e.g. to primary invasive Blastomyces dermatitidis, systemic fungi Histoplasma capsulatum,

Sporothrix schenckii)

A nongenital HPV lesion of the skin is usually caused uy HPV-l, 2, 3 or 4. In its most common manifestation, HPV infection of the skin presents as verruca vulgaris, the common wart. The immunologic response to HPV infection is poorly understood. A cellular response is undoubtedly important in preventing or limiting infection since individuals deficient in cell-mediated immunity are not only predisposed to HPV infection and dissemination, but also HPV infections in such individuals are often refractory to treatment. Additionally, patients with epidermodysplasia verruciformis, who are congeni-tally susceptible to disseminated HPV infection of the skin, appear to have a specific defect in cell-mediated immunity. Although affected individuals are not predisposed to infectious processes in general, T cell and natural killer cell responses directed against HPV-encoded antigens have been shown to be defective in vitro in such patients. The successful use of the cellular immunity-boosting glycoprotein interferon a in the treatment of HPV-infected individuals also suggests the importance of cell-mediated immunity in controlling HPV infections of the skin.

Even in normal individuals, verruca vulgaris induces minimal inflammatory changes and can persist for months or years. Histopathologic examination of involved skin can disclose an acanthoid dermis with papillomatosis, hyperkeratosis and parakeratosis. Despite the fact that viral HPV DNA and antigens are easily detected in many epithelial cells, a host immune inflammatory response is usually minimal (a mild mononuclear infiltrate may be present) or absent.

Tinea versicolor is another dermatological infection that elicits only minimal apparent immunologic change. The scaly hypo- or hyperpigmented macules of tinea versicolor are caused by the dimorphic, lipophilic fungus Malassezia furfur (formerly designated Pityrosporum orbiculare). Since the organism is part of the normal skin flora, it is unclear what allows the fungus to cause clinical disease. Defects or alterations in cellular immunity probably play a central role. Histopathological examination of involved skin demonstrates proliferating M. furfur organisms in stratum corneum with only minimal, if any, immunological infiltrate.

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