Skin Disorders

(A from Lookingbill D, Marks J: Principles of Dermatology, 3rd ed. Philadelphia, WB Saunders, 2000, p 68, Fig. 6-1A; B and G from Savin JA, Hunter JAA, Hepburn NC: Diagnosis in Color: Skin Signs in Clinical Medicine. London, Mosby-Wolfe, 1997, pp 79 and 6, Figs. 2-47 and 1-10, respectively; C from Centers for Disease Control and Prevention Web site—Public Health Image Library. Image #4500. Available at http://phil.cdc.gov/phil/details.asp; D from Zitelli B: Atlas of Pediatric Physical Diagnosis, 3rd ed. St. Louis, Mosby, 1997; E from Eisen D, Lynch DP: The Mouth: Diagnosis and Treatment. St. Louis, Mosby, 1998; F courtesy of Dr. Michael Sherlock; H from Paller AS, Mancinin AJ [eds]: Hurwitz Clinical Pediatric Dermatology, 3rd ed. Philadelphia, Elsevier, 2006, p 434; I courtesy of The Honickman Collection of Medical Images in memory of Elaine Garfinkel and The Jefferson Clinical Images Collection [through the generosity of JMB, AKR, LKB and DA]; J from Forbes C, Jackson W: Color Atlas and Text of Clinical Medicine, 2nd ed. St. Louis, Mosby, 2003, p 29, Fig. 1-85.)

Molluscum contagiosum: poxvirus; umbilicated lesions with viral particles

• Depression contains viral particles called molluscum bodies.

3. Transmission

a. Can be sexually transmitted in adults (common in AIDS)

Molluscum contagiosum: common in AIDS

b. Self-inoculation by scratching the infective viral particles out of the crater

4. Treatment

a. Spontaneous remission occurs in 6 to 9 months if immunocompetent.

• Cell-mediated immunity

b. Cryotherapy

C. Rubeola (measles)

Rubeola: regular measles

1. RNA paramyxovirus

2. Vaccination has reduced the incidence of rubeola.

3. Prodrome

Prodrome 3 Cs: cough, coryza, conjunctivitis

• Fever, cough, coryza (runny nose), conjunctivitis

4. Koplik spots develop on the buccal mucosa.

• Koplik spots are white spots overlying an erythematous base (Fig. 24-1C).

Rubeola: rash after Koplik spots disappear

5. Maculopapular rash develops after Koplik spots disappear (Fig. 24-1D).

a. Cytotoxic T cell damage of endothelial cells containing the virus

b. Typically begins on the head and then to the trunk and extremities

c. Tends to become confluent on face and trunk but discrete on extremities

6. Complications

Rubeola: giant cell pneumonia; acute appendicitis (children); otitis media

a. Giant cell pneumonia

• Warthin-Finkeldey multinucleated giant cells

b. Acute appendicitis in children

c. Otitis media

d. Encephalitis

• Before immunization, encephalitis was a common cause of death in measles.

e. Not teratogenic

7. Prevented through vaccinations

D. Rubella (German measles)

1. RNA togavirus

• Produces “3-day measles”

2. Vaccination has reduced the incidence of rubella.

3. Forchheimer’s spots (see Fig. 21-1E)

a. Dusky red spots that develop on posterior soft/hard palate

b. Develop at beginning of the rash

Rubella: maculopapular rash with discrete lesion; not confluent; fades in 3 days

4. Maculopapular rash lasts 3 days (see Fig. 21-1F).

a. Pinkish, red maculopapular eruption

b. Begins first at hairline and rapidly spreads cephalocaudally

c. Unlike rubeola, the macules and papules are discrete and do not become confluent.

d. Fades in 3 days

5. Painful postauricular lymphadenopathy (characteristic)

Rubella: painful postauricular lymphadenopathy

6. Polyarthritis is common in adults.

7. Infection during first trimester may produce congenital anomalies (refer to Chapter 5).

8. Prevent through vaccination

Rubella: teratogenic

E. Erythema infectiosum (fifth disease)

1. Caused by parvovirus B19 (DNA virus)

2. Most often occurs in school age children

• Often occurs in epidemics

3. Confluent net-like erythema type of rash

a. Begins on the cheeks (“slapped face” appearance; Fig. 24-1G)

Erythema infectiosum: parvovirus; slapped face appearance

b. Extends to the trunk and proximal extremities

4. Polyarthritis is common in adults.

Polyarthritis in adults: rubella and parvovirus

Other disorders caused by parvovirus B19 include pure red blood cell aplasia and aplastic anemia in chronic hemolytic diseases (e.g., hereditary spherocytosis) and chronic arthritis. Pregnant mothers exposed to a child with the infection may abort the fetus.

F. Roseola infantum

1. Caused by human herpesvirus 6 (DNA virus)

Roseola: HHV-6; most common viral exanthem children < 2 years old

2. Most common viral exanthem in children < 2 years old

3. Erythematous macules develop on soft palate 48 hours before rash.

4. Maculopapular rash occurs abruptly after 3 to 7 days of high fever (Fig. 24-1H).

Roseola: common cause of febrile convulsions

5. High fever may precipitate a febrile convulsion.

G. Disorders caused by varicella-zoster virus

1. DNA herpesvirus

• Remains latent in cranial and thoracic sensory ganglia

2. Varicella (chickenpox)

a. Predominantly a childhood disease

Varicella: predominantly a childhood disease

(1) Approximately 90% of cases occur in those <10 years of age.

(2) Peaks in spring months

b. Incubation 2 to 3 weeks

c. Patient is infectious 1 week before the rash appears.

• Infectious an additional 4 to 5 days until vesicles become crusted

Infectious: week before rash; week after rash until vesicles become crusted

d. Pruritic rash progresses from macules, to vesicles, to pustules (Fig. 24-1I).

(1) All stages of development are simultaneously present.

(2) Lesions are most prominent on the trunk.

(a) Also involves extremities (including palms and soles), mucous membranes in mouth, conjunctiva

(b) Vesicles are often umbilicated (depressed center) and hemorrhagic.

Varicella: macules, vesicles, pustules

e. Positive Tzanck test similar to herpes simplex virus (refer to Chapter 21)

f. Complications

(1) Association with Reye syndrome

(2) Pneumonia, self-limited cerebellitis

Complications: children—Reye syndrome, cerebellitis; adult—pneumonia, encephalitis, hepatitis

(3) In adults—hepatitis, pneumonia, encephalitis

• Treated with acyclovir

g. Treatment

(1) Prevention with immunization

(2) Antihistamine; oatmeal bath; calamine lotion

3. Herpes zoster (shingles)

a. Occurs in ∼︀10% to 20% of people in their lifetime.

b. Incidence increases with age.

Herpes zoster: incidence increases with age; cancer; immunocompromised state

c. Incidence increased in patients with cancer and AIDS

d. Prodrome of radicular pain and itching before rash occurs

e. Eruption characterized by groups of vesicles on an erythematous base

Herpes zoster: painful vesicles/pustules follow sensory dermatomes

(1) Rash follows sensory dermatomes in the distribution of cranial nerves or spinal nerves (Fig. 24-1J).

(2) Like varicella, pustules form that rupture, causing crusting and weeping.

f. Treatment

(1) Prevention with previous immunization for varicella

(2) Prevention with zoster vaccine

• Greater than 50% reduction in infection

(3) Analgesics commensurate with amount of pain

(4) Immunocompromised patients are often treated with acyclovir, valacyclovir, or famiciclovir.

• Best started before the rash has erupted

III. Selected Bacterial Disorders

A. Staphylococcus aureus skin infections

1. Gram-positive coccus (Fig. 24-2A)

24-2: Bacterial infections. A, Gram stain of Staphylococcus aureus. Note the gram-positive cocci, some of which are forming clusters. B, Impetigo of the face showing “honey-colored” crusts overlying an erythematous base. C, Gram stain of Streptococcus pyogenes. Note the gram-positive cocci in chains. D, Tuberculoid leprosy. Note the hypopigmented macule, an early finding in tuberculoid leprosy. E, Lepromatous leprosy. Note the nodular lesions on the face giving the patient a leonine facies. F, Acne vulgaris. Note the severe facial acne with inflamed papules and cystic lesions.

(A from McPherson R, Pincus M: Henry’s Clinical Diagnosis and Management by Laboratory Methods, 21st ed. Philadelphia, WB Saunders, 2007, p 1018, Fig. 56-2; B from Lookingbill D, Marks J: Principles of Dermatology, 3rd ed. Philadelphia, WB Saunders, 2000, pp 217 and 213, Figs. 13-9 and 13-4A, respectively; C from Murray PR, Shea YR: Medical Microbiology, 2nd ed. St. Louis, Mosby, 2002, p 238, Fig. 23-1; D from Cohen J: Infectious Disease, 2nd ed. St. Louis, Mosby, 2003; E and F from Savin JA, Hunter JAA, Hepburn NC: Diagnosis in Color: Skin Signs in Clinical Medicine. London, Mosby-Wolfe, 1997, pp 23 and 135, Figs. 1-48 and 5-20, respectively.)

S. aureus: gram-positive coccus in clumps

2. Toxic shock syndrome

a. Production of toxic shock syndrome toxin (TSST)

TSST: produces desquamating sunburn-like rash

• Superantigen that stimulates release of cytokines

b. Usually occurs in tampon-using menstruating women

c. Clinical findings

(1) Fever, hypotension

(2) Desquamating, sunburn-like rash

3. Other infections

a. Skin abscess (see Fig. 2-6)

• Treatment: trimethoprim-sulfamethoxazole (TMP-SMX; community acquired)

b. Hidradenitis suppurativa

(1) Chronic condition characterized by:

(a) Swollen, painful, inflamed apocrine glands usually in the axillae and groin

(b) Infection can also involve adjacent subcutaneous tissue and fascia.

(2) Must aspirate and culture pus

(3) Difficult to treat; may require surgery

S. aureus infections: abscess, postsurgical wound infection; hidradenitis; impetigo

c. Postsurgical wound infection (most common pathogen)

(1) If not septic, treat with TMP-SMX double strength.

(2) If septic, treat with IV vancomycin.

d. Impetigo

(1) Most often caused by Staphylococcus aureus

• Streptococcus pyogenes second most common cause

(2) Rash usually begins on the face (Fig. 24-2B).

• Vesicles and pustules rupture to form honey-colored, crusted lesions.

(3) Bullae commonly occur.

(4) Treatment

• Mupirocin ointment + dicloxacillin (or oxacillin, amoxicillin-clavulanate, azithromycin)

B. Streptococcus pyogenes skin infections

1. Gram-positive coccus (Fig. 24-2C)

S. pyogenes: gram-positive coccus in chains

2. Scarlet fever

a. Particular strains of S. pyogenes produce an erythrogenic toxin.

b. Patients are febrile and have a sore throat due to streptococcal pharyngitis.

c. An erythematous rash develops that involves the skin and tongue.

Scarlet fever: erythrogenic toxin; erythematous sandpapery rash that desquamates

(1) It initially occurs on the face and neck before spreading to other parts of the body.

(2) It spares the mouth producing conspicuous circumoral pallor.

(3) It has a sandpapery feeling.

(4) The tongue is covered by a white exudate studded with prominent red papillae.

(5) The rash begins to fade after 6 days and desquamation (peeling) begins, which may last up to 10 days.

(6) The white exudate on the tongue disappears; tongue is beefy red, hence the term “strawberry tongue.”

Scarlet fever: ↑ risk poststreptococcal glomerulonephritis, rheumatic fever

d. Increased risk for developing poststreptococcal glomerulonephritis (refer to Chapter 19) and rheumatic fever (refer to Chapter 10)

e. Treatment is penicillin V.

3. Erysipelas

a. Type of cellulitis

(1) Border is raised and surface appears like an orange peel (see Fig. 2-1).

(2) Skin surface is hot and bright red (rubor of acute inflammation).

Erysipelas: cellulitis with raised borders

b. Commonly occurs on the face and lower extremities

c. Patient feels ill and is febrile.

d. Treatment is IV penicillin G if on extremities; vancomycin if on the face

C. Leprosy

1. Caused by Mycobacterium leprae

• Grows in footpads of mice and armadillos; cannot be cultured

2. Tuberculoid type

a. Granulomas present

Tuberculoid: granuloma; intact cellular immunity; + lepromin skin test

• Very few acid-fast bacteria are present in the granulomas.

b. Positive lepromin skin test

• Indicates intact cellular immunity

c. Localized skin lesions with nerve involvement

(1) Autoamputation of digits

Tuberculoid: digital autoamputation; hypopigmented skin

(2) Anesthetic macules with hypopigmentation (Fig. 24-2D)

d. Treatment

• Dapsone + rifampin

3. Lepromatous type

a. Absence of granulomas

Lepromatous: organisms present; impaired cellular immunity; − lepromin skin test

(1) Numerous bacteria are present in foamy macrophages.

(2) Macrophages are located under a subepidermal zone free of organisms.

• Called the Grenz zone

b. Negative lepromin skin test

• Indicates a lack of cellular immunity

Lepromatous: leonine facies

c. Nodular lesions produce the classic leonine facies (Fig. 24-2E).

d. Treatment

• Dapsone + rifampin + clofazimine

D. Acne vulgaris

1. Chronic inflammation of the pilosebaceous unit

Acne vulgaris: chronic inflammation of pilosebaceous unit

2. Most common disease seen by dermatologists

3. Begins at an early age (9–11 years old)

4. Increases in severity in teenage years

5. Clinical lesions

• Inflammatory papules, pustules, nodules, cysts

6. Noninflamed comedones

a. Plugging of the outlet of a hair follicle by keratin debris

Comedones: open (“blackhead”), closed (“whitehead”)

b. Open comedone is called a “blackhead.”

c. Closed comedone is called a “whitehead.”

7. Inflammatory type

a. Abnormal keratinization of the follicular epithelium

Acne vulgaris: androgen receptors located on sebaceous glands

b. Increased sebum production (androgen-dependent)

c. Bacterial lipase (Propionibacterium acnes) produces irritating fatty acids.

• Produces the inflammatory reaction (Fig. 24-2F)

Acne vulgaris: Propionibacterium acnes produces lipase

8. Treatment

a. Topical agents—e.g., topical retinoid + benzoyl peroxide

b. Systemic antibiotics—e.g., tetracycline (first choice); erythromycin

c. Systemic retinoids—isotretinoin (decreases follicular keratinization, sebum production, bacterial count)

d. Hormonal therapy—oral contraceptives (women; reduce free testosterone levels); antiandrogens (spironolactone)

IV. Selected Fungal Disorders

A. Superficial mycoses (dermatophytoses)

1. Fungi confined to the stratum corneum or its adnexal structures

Superficial dermatophytes: live in stratum corneum

a. Incidence increases in warm, humid climates.

b. Most infections present with a scaling rash.

c. Tinea actually means “worm” in Latin, but is applied to describe superficial fungal infections.

(1) Tinea is followed by a word that qualifies its location (e.g., capitis, pedis, corporis)

(2) Most common infections in decreasing order—tinea pedis (foot), tinea unguim (nail), tinea versicolor (describes color variation rather than location), tinea cruris (groin)

Wood’s lamp and potassium hydroxide (KOH)–treated skin scrapings from lesions are commonly used for diagnosis of the dermatophytoses. Wood’s lamp (ultraviolet A light) detects fluorescent metabolites produced by organisms (e.g., fungi, some bacteria). KOH preparations identify yeasts and hyphae in the stratum corneum or hair shafts (Fig. 24-3A).

24-3: A, Potassium hydroxide (KOH) preparation of skin scrapings showing hyphae and yeasts. B, Tinea capitis due to Trichophyton tonsurans. Note the area of alopecia (hair loss) with black dots representing broken off hairs and scaling of the skin. C, Tinea corporis showing annular lesions with erythematous margins and clear centers. D, Tinea cruris. Note the scaly, erythematous rash in the groin. E, Tinea versicolor showing skin with pink-tan patches (hyperpigmentation) intermixed with normal skin. The hyperpigmented lesions should be scraped for a KOH preparation. F, Malassezia furfur. Note the classic spaghetti (hyphae) and meatball (yeasts) morphologic appearance. G, Seborrheic dermatitis. Note the erythematous, greasy scaling rash in the nasolabial fold. It is caused by M. furfur. H, Lymphocutaneous sporotrichosis showing a linear array of suppurating subcutaneous nodules.

(A and B from Goldstein BG: Practical Dermatology, 2nd ed. St. Louis, Mosby, 1997, pp 24, 97, Fig. 3-2 and Fig. 10-1, respectively; C from Forbes C, Jackson W: Color Atlas and Text of Clinical Medicine, 2nd ed. St. Louis, Mosby, 2003, p 97, Fig. 2-57; D and G from Savin JA, Hunter JAA, Hepburn NC: Diagnosis in Color: Skin Signs in Clinical Medicine. London, Mosby-Wolfe, 1997, pp 123 and 9, Figs. 4.78 and 1.17, respectively; E from Lookingbill D, Marks J: Principles of Dermatology, 3rd ed. Philadelphia, WB Saunders, 2000, p 227, Fig. 14-2; F from Midgley G, Clayton Y, Hay RJ: Diagnosis in Color: Medical Mycology. London, Mosby-Wolfe, 1997, p 73, Fig. 93; H from Murray PR, Shea YR: Medical Microbiology, 2nd ed. St. Louis, Mosby, 2002, p 163, Fig. 43-14.)

Wood’s lamp: detects fluorescent fungal metabolites

2. Tinea capitis

a. Superficial fungal infection of scalp

b. Pathogens