Theresa Coyner

Katrina Nice Masterson


Infections in the skin may range from superficial to deep and may be caused by bacteria, fungi, or viruses. These infections may occur in otherwise healthy individuals.



A. Definition: a common, contagious, superficial skin infection caused by streptococci, staphylococci, or both

1. Bullous impetigo (Figure 11-1)

a. Etiology

(1) Caused by group II Staphylococcus aureus.

(2) Usually not secondarily contaminated by streptococci.

(3) Colonization of the respiratory tract precedes colonization of the skin by days.

b. Pathophysiology

(1) Begins as small vesicles.

(2) Evolves into sharply demarcated bullae without erythematous halo, which eventually rupture.

(3) Nikolsky sign not present.

(4) Shallow erosions result within 1 to 2 days.

(5) Typically occurs on the face in infants and children but may infect any surface and any age group.

(6) Heals with hyperpigmentation with darkskinned individuals.

(7) Characteristic honey-colored crust.

2. Nonbullous impetigo (Figure 11-2)

a. Etiology

(1) Caused by beta-hemolytic streptococci.

(2) Begins with exposure to Streptococcus, which enters the skin via areas of minor trauma.

(3) Often becomes secondarily contaminated with staphylococcus.

b. Pathophysiology

(1) Begins as a small vesicle or pustule.

(2) After rupture, a moist, erythematous base is exposed.

(3) Characteristic honey-colored crust.

(4) Satellite lesions may appear beyond the periphery.

(5) Generally heals without scarring.

3. Ecthyma (Figure 11-3)

a. Etiology

(1) Caused by Streptococcus pyogenes and rapidly contaminated with staphylococcus.

(2) Considered an ulcerated form of nonbullous impetigo.

b. Pathophysiology

(1) Begins like nonbullous impetigo but extends into the dermis.

(2) Shallow ulcer is formed. Generally, 1 to 10 lesions will be present.

(3) Lesion crusts over with a purulent, necrotic base.

(4) Most common on lower extremities in children, elderly, and patients with lymphedema.

B. Assessment

1. History (Box 11-1)

2. Current health status

3. Physical examination

a. Clinical presentation

b. Evidence of trauma (bites, abrasions, lacerations)

c. Gram stain

d. Culture for causative organism(s)

FIGURE 11-1. Bullous impetigo. (Courtesy of Charles E. Lewis, MD.)

C. Treatment

1. Topical

a. Mupirocin: apply to lesions tid for 7 to 10 days.

b. Retapamulin: apply to lesions bid for 5 days.

2. Oral antibiotics for widespread infections

a. Erythromycin 30 to 50 mg/kg/d every 6 to 8 hours

b. Cephalexin 25 to 50 mg/kg/d every 6 to 8 hours

c. Amoxicillin/clavulanate 25 to 45 mg/kg/d every 12 hours

3. Treatment of lesions

a. Wash with antibacterial soap.

b. Keep crusts moistened so they can gently be debrided by washing.

FIGURE 11-2. Nonbullous impetigo. (Courtesy of Charles E. Lewis, MD.)

FIGURE 11-3. Ecthyma. (Courtesy of John K. Randall, MD.)


A. Definition: a diffuse, acute bacterial infection of the skin and subcutaneous tissue

B. Etiology

1. Group A beta-hemolytic streptococci (erysipelas) or staphylococci most common cause.

2. Non-group A streptococcus, Haemophilus influenzae type B, Pseudomonas aeruginosa, and Campylobacter fetus may be the etiology in patients with underlying abnormalities of lymphatics or venous drainage.

C. Pathophysiology

1. Most commonly seen in lower extremities.

2. Infection spreads locally secondary to the release of enzymes.

3. Erythema and edema are present.

4. Skin will be hot and tender to the touch.

5. Lymphangitic streaks may develop specifically in erysipelas.

6. Typically occurs near surgical wounds and cutaneous ulcers or may occur in normal skin. It may occur anywhere in immunocompromised patients.

D. Assessment

1. History (Box 11-1).

2. Evaluate patient’s overall health status.

3. Physical examination.

a. Pain

b. Erythema

c. Increased warmth to palpation

d. Edema

e. Fever

f. Assess for preexisting lesion

g. Lymphadenopathy

FIGURE 11-4. Cellulitis. (From Elder, D. E., et al. (2012). Atlas and synopsis of lever’s histopathology of the skin. Philadelphia, PA: Wolters Kluwer.)

4. Diagnostic tests.

a. CBC with differential

(1) Mild leukocytosis with increase in neutrophils

(2) Mildly elevated sedimentation rate

b. Bacterial culture

E. Treatment

1. Staphylococcal or streptococcal organisms.

a. Dicloxacillin 500 to 1,000 mg every 6 hours

b. Cephalexin 500 mg every 8 hours

2. Recurrent disease: prophylactic antibiotics.

3. Surgical debridement may be indicated if pockets of purulent material are present.


A. Definition: Furuncle is a boil. Carbuncle is an aggregation of interconnected furuncles that drain through several openings in the skin.

B. Etiology

1. Staphylococcal infection

2. May be secondary to ingrown hair or obstruction of sebaceous gland

C. Pathophysiology

1. Abscess of the skin and subcutaneous tissue

2. Central necrosis and suppuration seen

3. Secondary factors that may induce infection

a. Scratching

b. Friction

c. Infestation

FIGURE 11-5. Furunculosis/furuncle. (Courtesy of John K. Randall, MD.)

d. Pressure from restrictive clothing

e. Chemical irritation

f. Hyperhidrosis

g. Occlusion of the follicle with ointments

4. Lesions

a. Primary lesion: small, painful, indurated nodules.

b. Evolves to elevated, tender lesion with shiny erythema and intense pain.

c. Mature lesion.

(1) Fluctuant with yellow or creamy white discharge

(2) Central necrosis

d. May spontaneously rupture.

e. Single or multiple lesions may be present.

5. Systemic signs

a. Fever

b. Malaise

c. Regional adenopathy

D. Assessment

1. History (Box 11-1)

2. Physical examination

3. Note location: lesions commonly seen on the back of the neck, face, buttocks, thighs, perineum, breasts, or axillae.

4. Evaluate the appearance of the lesion(s).

5. Distinguish between furuncle and ruptured epidermal cyst (cyst will have keratinous material).

6. Evaluate the presence of predisposing conditions.

a. Occlusion, especially in hyperhidrosis

b. Follicular abnormalities

c. Colonized skin in patient with atopic dermatitis and scabies

7. Diagnostic tests

a. Gram stain

b. Bacterial culture

E. Treatment

1. Warm compresses

2. Incision, drainage, and packing to promote continuous drainage

3. Antibiotics appropriate for organism cultured


A. Definition: superficial bacterial infection of skin in intertriginous areas

B. Etiology

1. Corynebacterium minutissimum invades the stratum corneum.

2. Growth favored by warm, moist environment.

C. Pathophysiology

1. Lesions most common in the groin but may be seen in any intertriginous area.

2. Irregular erythematous plaque with well-defined borders.

3. Fine scale may cover the lesion.

4. Older lesions will fade to a brown color.

D. Assessment

1. History (Box 11-1)

2. Clinical examination.

a. Assess for signs of hyperhidrosis.

b. Assess for signs of poor personal hygiene.

3. Assess for risk factors including diabetes mellitus, obesity, and exposure to humid climate conditions.

4. Diagnostic tests.

a. Gram stain

b. Wood’s lamp will fluorescence bright coral red.

E. Treatment

1. 11% to 20% topical application of aluminum chloride

2. 2% clindamycin HCl topical solution

3. 2% erythromycin topical gel or solution


A. Definition: noninflammatory bacterial infection on the soles of the feet and/or palms

B. Etiology

1. Causative agent is either Micrococcus sedentarius or Corynebacterium.

2. Produce proteolytic enzymes that digest the stratum corneum.

C. Pathophysiology

1. Crater-like pits will occur on weight-bearing areas of the feet.

2. Pits are 1 to 7 mm in diameter.

3. Erosions may rarely occur.

4. No erythema will be present.

D. Assessment

1. History (Box 11-1)

2. Clinical examination

a. Assess for the characteristic craters.

b. Assess for the presence of hyperhidrosis and malodor.

FIGURE 11-6. Pitted keratolysis. (From Burkhart, C., Morell, D., Goldsmith, L. A., et al. (2009). VisualDx: Essential pediatric dermatology. Philadelphia, PA: Lippincott Williams & Wilkins.)

3. Diagnostic tests

a. Generally, none are performed as this is a clinical diagnosis.

b. Wood’s lamp will not demonstrate fluorescence.

E. Treatment

1. 10 to 25% aluminum chloride solution applied topically

2. 2% clindamycin HCl topical solution

3. 2% erythromycin topical solution


A. Definition: inflammation of the hair follicle

B. Etiology

1. Causative organisms include staphylococcus, dermatophytes, Klebsiella, Proteus, Enterobacter, and Pseudomonas.

2. Drug-induced folliculitis most commonly occurs with use of corticosteroids.

C. Pathophysiology

1. Organisms gain access to the hair follicle due to chemical irritation, physical injury, or occlusion: specifically with topical steroid.

2. Inflammation may be superficial to deep.

3. Pseudofolliculitis barbae caused by shaving.

a. More common in individuals with tightly curled spiral hair

FIGURE 11-7. Folliculitis. (From Goodheart, H. P. (2003). Goodheart’s photoguide of common skin disorders (2nd ed.). Philadelphia, PA: Lippincott Williams & Wilkins.)

D. Assessment

1. History (Box 11-1).

2. Assess shaving practices.

3. Lesions (Table 11-1).

TABLE 11-1 Folliculitis Types, Clinical Presentation, and Treatment


Clinical Presentation


Dermatophyte folliculitis

Erythematous papules and pustules in the beard area with crusting.

Itraconazole 200 mg bid for 1 wk/mo for 2 mo Terbinafine 250 mg/d for 2-3 wk

Griseofulvin microsized 500-1,000 mg/d for 4-6 wk Griseofulvin ultramicrosized 500-700 mg/d for 4-6 wk

Pityrosporum folliculitis

Follicular-based papules and pustules predominantly on the back, chest, and shoulders. Very pruritic.

Topical antifungals Fluconazole 100-200 mg/d for 3 wk

Itraconazole 200 mg/d for 1-3 wk

Drug-induced folliculitis

Erythematous follicular papules and pustules located on the trunk, shoulders, and upper arms. Acute onset.

Stop the offending medication

Topical benzoyl peroxide or clindamycin

Gram-negative folliculitis

Hot tub folliculitis caused by Pseudomonas aeruginosa. Lesions will be pink to erythematous follicular papules and pustules that will appear edematous.

Ciprofloxacin 500 mg bid for 7 d

Bacterial folliculitis

Perifollicular papules and pustules on an erythematous base.

Treatment should be based upon culture results Topical benzoyl peroxide Topical clindamycin Doxycycline 100 mg daily to bid for 2 wk

4. Diagnostic tests

a. Gram stain

b. Culture

c. Histologic analysis

E. Treatment (Table 11-1)


A. Meningococcemia (Figure 11-8)

1. Definition: gram-negative diplococcus skin infection

2. Etiology

a. Causative organism is Neisseria meningitides.

b. Transmitted by respiratory secretions.

c. Present in 10% to 20% of population.

3. Pathophysiology

a. Colonization occurs in nasopharyngeal area.

b. Systemic invasion causes bacteremia.

FIGURE 11-8. Meningococcemia. (Courtesy of John K. Randall, MD.)

c. Organism invades endothelial cells of small vessels and releases endotoxin.

d. Cytokines are released causing hypotension, decreased cardiac output, and increased endothelial permeability.

e. Thirteen strains of N. meningitides and serotypes A, B, C, Y, and W-135 can cause meningococcemia.

f. Predominantly affects young adults and children.

4. Assessment

a. History (Box 11-1).

b. Assess for sudden onset of fever, headache, nausea, vomiting, and stiff neck.

c. Lesion assessment.

(1) Rash occurs in 70% of cases.

(2) Range from pink macules, erythematous papules, to purpuric lesions.

(3) Petechiae and ecchymosis may occur.

(4) Purpuric lesions will have central gunmetal gray discoloration.

d. Diagnostic tests

(1) Blood culture

(2) CSF culture

(3) Gram stain

(4) Histologic analysis: leukocytoclastic vasculitis and thrombi

5. Treatment

a. High-dose penicillin, chloramphenicol for penicillin allergic patients, or third-generation cephalosporin

B. Staphylococcal Scalded Skin Syndrome (SSSS) (Figure 11-9)

1. Definition: staphylococcal epidermolytic toxic syndrome also known as Ritter disease

2. Etiology

a. Epidermolytic toxin acts as a toxin and elicits an antibody reaction.

b. Antibody is present in 75% of people over age 10.

c. Affects young children, immunosuppressed individuals, and patients with chronic renal failure.

3. Pathophysiology

a. Begins with a staphylococcal infection of the conjunctivae, throat, nares, or umbilicus.

b. Toxin is filtered through glomeruli.

FIGURE 11-9. Staphylococcal scalded skin syndrome (SSSS). (From Burkhart, C., Morell, D., Goldsmith, L. A., et al. (2009). VisualDx: Essential pediatric dermatology. Philadelphia, PA: Lippincott Williams & Wilkins.)

c. Individuals with poor renal clearance or low glomeruli filtration rate may develop the toxin systemically.

d. Toxin acts in the epidermis affecting cell-to-cell adhesion.

4. Assessment

a. History (Box 11-1)

b. Lesions

(1) Initially tender, erythematous skin with sandpaper-like appearance.

(2) Skin wrinkles and bullae occur, followed by peeling layers of the skin.

(3) Nikolsky sign will be present.

(4) Yellow crusting will occur followed by skin drying and cracking.

(5) Skin re-epithelializes in 7 to 10 days.

c. Diagnostic tests

(1) Culture of the conjunctivae, nose, throat, and bullae. Often negative in children.

(2) Histologic analysis: dermal-epidermal separation.

5. Treatment.

a. Hospitalization and IV therapy may be needed.

b. Nafcillin 100 to 200 mg/kg/d IV.

c. Less severe cases managed at home with oral antibiotics: dicloxacillin 25 mg/kg/d or cephalosporin for 1 week.

C. Necrotizing Fasciitis (Figure 11-10)

1. Definition: soft tissue infection causing local tissue necrosis and life-threatening sepsis

FIGURE 11-10. Necrotizing fasciitis, postoperative. (Courtesy of John K. Randall, MD.)

2. Etiology

a. Type 1: polymicrobial infection including aerobic and anaerobic organisms

b. Type 2: Streptococcus pyogenes or staphylococcus

c. Vibrio vulnificus and Aeromonas hydrophila, both waterborne organisms, may rarely cause the condition.

3. Pathophysiology

a. Initially appears as a cellulitis.

b. Substances produced by the organism resist phagocytosis.

c. Pyogenic exostosis induces cytokines that mediate fever, shock, and tissue injury.

d. More common in elderly or individuals with chronic conditions. May occur in healthy individuals.

e. Extremities are most likely involved.

4. Assessment

a. History (Box 11-1).

b. Assess for the presence of chronic conditions, specifically diabetes, arterial disease, alcohol abuse, and malnutrition.

c. Assess vital signs: fever often absent initially, and tachycardia will be present.

d. Skin changes.

(1) Initially tender, erythematous, and swollen.

(2) Rapidly progresses from reddish purple appearing to gray-blue in poorly defined patches.

(3) Violaceous bullae may develop.

(4) Thin, malodorous fluid results from necrosis of fascia and fat.

(5) Subcutaneous tissue will feel hard and wooden.

e. Critical diagnostic signs.

(1) Severe pain out of proportion to the initial clinical signs

(2) Vital sign abnormalities

(3) Presence of hemorrhagic bullae indicating occlusion of deep vessels in the fascia

f. Diagnostic studies

(1) Coagulopathy, increased WBC with leukocytosis, and elevated creatinine kinase.

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Mar 9, 2021 | Posted by in NURSING | Comments Off on Infections
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