Infections
Theresa Coyner
Katrina Nice Masterson
OBJECTIVES
After studying this chapter, the reader will be able to:
Describe the cutaneous presentation of bacterial, viral, and fungal infections.
Discuss factors that may precipitate certain infections.
List appropriate treatment options.
Identify patient education to prevent cutaneous infections and restore skin integrity when infections occur.
KEY POINTS
Infection compromises the barrier function of the skin.
Immunocompromised patients are at higher risk for dissemination of cutaneous infections.
Cutaneous infections can be caused by both extrinsic and intrinsic factors.
Appropriate treatment of cutaneous infections depends upon accurate recognition and diagnosis.
OVERVIEW
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.
BACTERIAL INFECTIONS
I. IMPETIGO
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.) |
PATIENT EDUCATIONBullous Impetigo
Infected children should be isolated briefly until treatment is under way.
Impetigo can spread via fingers, towels, and clothing.
Sodium hypochlorite (bleach) baths may be helpful.
¼ to ½ cup of household bleach added to tub of water.
Soak for 5 to 15 minutes at a frequency of two times weekly.
Mupirocin nasal ointment applied to the nares bid × 5 days to reduce colonization.
Poststreptococcal glomerulonephritis can develop 1 to 3 weeks following impetigo.
Incidence ranges from 2% to 5% of individuals with impetigo.
Children and at-risk adults for development of hematuria and edema should be monitored.
BOX 11-1. Taking the History in the Patient with Cutaneous Infection
In addition to a routine history and physical examination, the following issues must be explored:
Time of onset of lesions (exacerbations, remission, and recurrences)
Site of onset (pattern of spread or dissemination is important to making correct diagnosis)
Change (evolution) in lesions (lesions seen on exam may not be the primary lesion)
Cutaneous symptoms (burning, pruritus, or other discomfort)
Precipitating factors
Previous treatment (self-treatment may alter presentation)
Occupation/hobbies: important to rule out exposure to specific infections
Family history or close contact exposure to similar symptoms or lesions
II. CELLULITIS (FIGURE 11-4)
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.
PATIENT EDUCATIONCellulitis
Burow solution, comprised of an aqueous solution of aluminum acetate (available over the counter), compresses may help alleviate discomfort.
Leg elevation may hasten recovery.
Open wounds should be cleansed with a normal saline irrigation using a 30-gauge syringe attached to an 18-gauge angiocatheter.
III. FURUNCLE/CARBUNCLE (FIGURE 11-5)
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
PATIENT EDUCATIONFuruncle/Carbuncle
Patients should avoid constrictive clothing.
Antibacterial soaps in patients with hyperhidrosis may be considered.
Bleach baths may help to prevent recurrence.
IV. ERYTHRASMA
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
PATIENT EDUCATIONErythrasma
Erythrasma can be a chronic intermittent condition.
Weight loss is recommended for obese patients.
Cotton underwear is recommended, especially boxer shorts for men if erythrasma occurs in the groin area.
Daily washing includes antibacterial soap, pat dry, and use of a handheld hair dryer on cool setting to dry intertriginous areas thoroughly.
V. PITTED KERATOLYSIS (FIGURE 11-6)
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
PATIENT EDUCATIONPitted Keratolysis
Feet should be kept dry and clean by washing at least daily with antibacterial soap and drying thoroughly.
Cotton socks should be worn or socks specifically designed to wick moisture away from the skin; change socks daily or more frequently.
Shoes should be allowed to dry thoroughly prior to the next wear.
VI. FOLLICULITIS (FIGURE 11-7)
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 | ||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
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4. Diagnostic tests
a. Gram stain
b. Culture
c. Histologic analysis
E. Treatment (Table 11-1)
PATIENT EDUCATIONFolliculitis
Occlusive topical steroids should not be used when folliculitis is present.
Constrictive clothing is to be avoided.
Use of a chemical depilatory may be considered.
All shaving techniques must be done with care; an electric razor should be used if possible. Avoid twin, triple, and quadruple blades as these pull and cut the hair below the skin surface. Wet the area to be shaved with warm water and lather with a thick shaving gel. Shave with the grain of the hair. Replace shaving blades frequently as they dull quickly.
Cool compresses may be applied after shaving.
Glycolic acid lotion may be used to reduce hyperkeratosis (elevated bumps).
VII. INFECTIONS WITH POTENTIAL LIFE-THREATENING COMPLICATIONS
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
PATIENT EDUCATIONMeningococcemia
Triage nurses should have high degree of suspicion for patient calls with symptoms of rash, fever, headache, and stiff neck. Urgent visit or refer to emergency department.
Vaccine is available protecting against serotypes A, C, Y, and W-135.
Household members, day caregivers, and close personal contacts should be treated prophylactically with rifampin.
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.
PATIENT EDUCATIONStaphylococcal Scalded Skin Syndrome
Signs of dehydration must be assessed.
All medical and skin care needs individual recommendations.
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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