Chapter 12: Bacterial Infections

Most common bacterial skin infections are caused by coagulase-positive Staphylococcus aureus or group A beta-hemolytic streptococci. Before the widespread availability of antibiotics, many common skin infections resulted in serious illness and even death. In the 1950s following the widespread use of antibiotics, most staphylococcal and streptococcal skin infections responded well to the use of the penicillins. However, scattered cases of methicillin-resistant Staphylococcus aureus (MRSA) were already being reported by the early 1960s. From late 1960s to the mid-1990s, MRSA infections became a major problem especially in large urban hospitals. In the past decade, hospital-acquired MRSA infections began to decrease as hospitals instituted more aggressive infection control measures, but during that same time community-acquired MRSA infections increased.

Syphilis has been called "the great masquerader" and "the great imitator" based on the many varied presentations of the cutaneous and other organ system findings. Patients with secondary syphilis usually present with rashes that mimic common papulosquamous skin diseases, but can present with skin findings that mimic almost any cutaneous disorder.

Introduction

Impetigo is a common, highly contagious, superficial skin infection that presents with either a bullous or nonbullous appearance. Nonbullous impetigo accounts for the majority of cases. It occurs in children of all ages, as well as adults, whereas the bullous form is most common in newborns. Impetigo is limited to the epidermis.

Pathophysiology

Coagulase-positive Staphylococcus aureus is the most common cause of bullous and nonbullous impetigo. Group A beta-hemolytic streptococci including the nephritogenic strains may also cause impetigo.^1,2

Nonbullous impetigo represents a host response to the infection, whereas staphylococcal toxin causes bullous impetigo and no host response is required to manifest clinical disease.³

Clinical Presentation

History and Physical Examination

• Nonbullous impetigo begins as a single lesion typically manifesting as a red macule or papule that quickly becomes a vesicle. The vesicle ruptures, forming an erosion and the contents dry to form the characteristic honey-colored crust commonly seen with impetigo (Figure 12-1). Nonbullous impetigo usually occurs on the face or extremities. Impetigo may occur concomitantly with herpes simplex and atopic dermatitis.

• Bullous impetigo begins as a superficial vesicle that rapidly progresses to a flaccid bulla, with sharp margins and no surrounding erythema. When the bulla ruptures, a moist yellow crust forms. Impetigo is often spread to surrounding areas by autoinoculation. Bullous impetigo usually arises on grossly normal skin and favors moist intertriginous areas, such as the diaper area, axillae, and neck folds.

• Ecthyma is an uncommon variant of impetigo that initially presents as a typical impetigo infection that spreads into the dermis. It usually presents on the lower legs with thick crusts overlying superficial ulcers. It is more common in young children, immunosuppressed patients, and in patients with poor hygiene.

Laboratory Findings

Bacterial cultures from the infected areas are usually positive for S. aureus or streptococci.

Diagnosis

The key diagnostic clinical features of impetigo are honey-colored crusts or bullae.

Differential Diagnosis

• ✓ Herpes simplex: Presents with grouped vesicles on the lips, perioral, and genital region.

• ✓ Atopic dermatitis: Presents with pruritic, scaly, or crusted papules and plaques in patients with a history of atopy.

• ✓ Varicella (chicken pox): Presents with fever and widespread vesicles with surrounding erythema.

• ✓ Other: Perioral dermatitis, insect bites, tinea infections, abrasions, lacerations, thermal burns, erythema multiforme, dermatitis herpetiformis, burns, bullous fixed drug eruptions, staphylococcal scalded skin syndrome, bullous tinea pedis, and bullous insect bites. In adults, bullous pemphigoid and pemphigus are in the differential.

Management

The superficial crusts should be removed with gentle cleansing with an antibacterial soap. Wet dressings could also be applied to remove thicker crusts (Table 6-5). Localized impetigo can be treated with topical medications including:

• Bacitracin ointment 3 times a day for 3 to 5 days.

• Mupirocin (Bactroban) ointment 3 times a day for 3 to 5 days.

• Retapamulin (Altabax) ointment twice a day for 5 days.

Severe or more widespread impetigo may require oral antibiotics, such as first-generation cephalosporins, dicloxacillin, amoxicillin/clavunate, or azithromycin.^1,3 Impetigo usually responds well to treatment, but may be recurrent.

Indications for Consultation

Severe or persistent disease that does not respond to therapy.

Patient Information

PubMed Health: www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001863/

Introduction

A boil (furuncle) is a deep-seated inflammatory nodule that develops around a hair follicle, often from a preceding more superficial folliculitis. A carbuncle is two or more confluent boils.

Pathophysiology

Coagulase-positive Staphylococcus aureus (SA) is the most common cause of boils and carbuncles. The organism may be methicillin sensitive (MSSA) or methicillin resistant (MRSA).

MRSA infections may be acquired in health care facilities such as hospitals and nursing homes or now more commonly in the community. In one study of 12 United States' emergency departments, MRSA infections were responsible for 38% to 84% of purulent skin and soft tissue infections.⁴

Clinical Presentation

History

Patients usually give a history of a rapidly enlarging tender "pimple" or boil. The patient may give a history of risk factors such as crowded living conditions, infected family members, diabetes, obesity, atopic dermatitis, or inherited or acquired immune deficiency.

Physical Examination

A boil starts as a hard, tender, red, follicular centric nodule. The nodule enlarges and becomes painful and fluctuant after several days (Figure 12-2). Rupture may occur, with extrusion of pus.

Laboratory Findings

Cultures from pus within the lesion or from drainage are usually positive for MSSA or MRSA.

Diagnosis

The key diagnostic clinical feature of a boil is a tender, fluctuant cyst or nodule.

Differential Diagnosis

• ✓ Ruptured epidermal inclusion cyst: This may very closely resemble a staphylococcal boil, but when lanced, the cyst contains thick white keratinous material.

• ✓ Acne cyst: This may also closely resemble a staphylococcal boil, but other signs of acne such as comedones should be present.

• ✓ Hidradenitis suppurativa: Presents with cysts limited to intertriginous areas of the body.

• ✓ Other: Deep fungal infections, dental abscess, kerion.

Management

The primary and most important management of boils and carbuncles is simple incision with a number 11 scalpel blade and drainage with evacuation of the pus, probing the cavity to break up loculations. Bacterial cultures may also be performed if a MRSA infection is suspected. The wound can be packed with iodoform gauze to encourage further drainage. The surgical site should be covered with a dry dressing.

Patients with central facial disease, multiple lesions, immunosuppression, lesions greater than 5 cm, or with surrounding cellulitis or fever may require systemic antibiotics. Patients who are very young or very old may also require systemic antibiotics. Recommended oral antibiotics for MSSA infections include dicloxacillin, cephalexin, clindamycin, doxycycline, minocycline, and trimethoprim sulfamethoxazole.⁵ Medications recommended for MRSA include clindamycin, doxycycline, minocycline, and trimethoprim sulfamethoxazole.⁵

In addition, carriers of MSSA and MRSA should be treated with intranasal mupirocin (Bactroban) ointment twice a day for 5 days and 4% chlorhexidine (Hibiclens) wash daily.

Indications for Consultation

Severe or persistent or recurrent disease that does not respond to therapy.

Patient Information

• Centers of Disease Control and Prevention: www.cdc.gov/mrsa/

• MedlinePlus/carbuncles: www.nlm.nih.gov/medlineplus/ency/article/000825.htm

• MedlinePlus/boils: www.nlm.nih.gov/medlineplus/ency/article/001474.htm

Introduction

Cellulitis is an acute infection of the dermis and subcutaneous tissue. It is a common cause of inpatient hospital admissions, accounting for 10% of infectious disease-related US hospitalizations from 1998 to 2006.⁶

Pathophysiology

Most cases of cellulitis are caused by S. aureus and group A Streptococcus.⁷ However, in certain situations other organisms may be involved, such as gram-negative organisms in cellulitis originating from a toe web fissure or Hemophilus influenza in young infants.

Risk factors for cellulitis include skin trauma or an underlying lesion such as a leg ulcer or fissured toe webs that can serve as a portal of entry for pathogenic bacteria. Other risk factors include chronic venous or arterial insufficiency, edema, surgery, intravenous drug use, body piercing, human and animal bites, diabetes, hepatic cirrhosis, immunosuppression, and neutropenia.^6,8

Clinical Presentation

History

Cellulitis typically presents with rubor (erythema), dolor (pain), calor (warmth), and tumor (edema).

Physical Examination

Cellulitis typically begins with the acute onset of localized erythema and tenderness. The borders may be ill-defined and surface crusts may develop (Figure 12-3). Other symptoms include fever, malaise, and chills. Less common findings include ascending lymphangitis and regional lymphadenopathy. Cellulitis usually presents in a unilateral distribution. Some other clinical presentations of less common types of cellulitis are listed in Table 12-1.

Laboratory Findings

The diagnosis of cellulitis is generally made in the clinical setting. If indicated, cultures from exudate or blistered areas can be done with a culturette swab or cultures can be obtained by aspirating the affected skin. A skin punch biopsy of affected skin may also be cultured. However, these techniques often do not isolate the pathogenic organism.⁹ If cultures are positive, they usually show gram-positive microorganisms, primarily Staphylococcus aureus, group A or group B streptococci, Streptococcus viridans, Streptococcus pneumoniae, Enterococcus faecalis, and, less commonly, gram-negative organisms such as Hemophilus influenzae and Pseudomonas aeruginosa.^8,9

Diagnosis

The key diagnostic clinical feature of cellulitis is a painful, warm, red, edematous plaque.

Differential Diagnosis

• ✓ Acute allergic contact dermatitis: Usually presents with pruritic, but not painful red plaques, with more than one area involved.

• ✓ Stasis dermatitis: Presents with bilateral chronic dermatitis on the lower legs, with red/brown pigment.

• ✓ Thrombophlebitis/deep vein thrombosis (DVT): Presents with calf pain, erythema, usually no fever or chills, abnormal ultrasound of the leg veins.

• ✓ Other: Insect bite, erythema migrans, erythema nodosum, Sweet's syndrome, panniculitis, eosinophilic cellulitis, fixed drug eruption, lipodermatosclerosis, and polyarteritis nodosum.

Management

Treatment for the most common forms of cellulitis that is likely caused by methicillin-sensitive Staphylococcus aureus includes empiric treatment with a penicillinase-resistant penicillin, first-generation cephalosporin, amoxicillin-clavulanate, a macrolide, or a fluoroquinolone antibiotic.^8,9 Treatment for MRSA and other organisms and other forms of cellulitis are summarized in references 8 and 9.

Localized disease can be treated in the outpatient setting, whereas extensive disease requires intravenous administration in an inpatient setting. Ancillary measures include elevation and immobilization of the involved limb to reduce swelling. One should also identify and treat the underlying portal of entry of the cellulitis (eg, tinea pedis, leg ulcer). Imaging studies may be needed, if crepitant or necrotic cellulitis is suspected.

Indications for Consultation

Severe or persistent disease that does not respond to treatment. Patients with high fevers, crepitant, or necrotic cellulitis should be hospitalized.

Patient Information

PubMed Health: www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001858/

Introduction

Syphilis is a sexually transmitted disease with worldwide distribution. Incidence dropped dramatically after introduction of penicillin as a treatment, but the CDC has reported resurgence in recent years, mostly in black and hispanic populations and in men who have sex with men.¹⁰ The skin eruption may manifest various morphologies, often mimicking other skin conditions, such as pityriasis rosea, psoriasis, lichen planus, exanthems, etc., giving cutaneous secondary syphilis the name "the great masquerader."

Pathophysiology

Syphilis is caused by Treponema pallidum, a spirochetal bacterium. Approximately one-third of persons who come in contact with a lesion become infected. After inoculation through skin or mucous membranes, the bacterium spreads throughout the body via the lymphatic system and blood.

Clinical Presentation

History and Physical Examination

Syphilis progresses through active and latent stages and in some cases progresses to a tertiary stage.

• Primary stage: At the site of entry, 10 to 90 days (average 3 weeks) after infection, a dusky red macule appears and evolves into a papule. Surface necrosis occurs with progression to a nontender, indurated, firm ulcer (chancre), with a raised border (Figure 12-5). Prominent regional lymphadenopathy may be present. The ulcer spontaneously heals in 2 to 10 weeks.

• Secondary stage and latent stages: Systemic symptoms such as fever, malaise, sore throat, generalized lymphadenopathy, myalgia, and headache develop 4 to 10 weeks after onset of infection. Within a few days, a pink, violaceous or red-brown macular, papular or more typically a papulosquamous eruption appears on the face, trunk (Figure 12-6), and extremities; often including the palms and soles (Figure 12-7). The eruption may become follicular, pustular, annular, nodular, or plaque-like and may be pruritic. A patchy, "moth-eaten" and/or diffuse alopecia may develop. Superficial erosions (mucous patches) are seen in the mouth, throat, and genitalia. Wart-like moist papules (condylomata lata) may appear in the anogenital area. Without treatment, the symptoms and eruptions clear within 3 to 12 weeks, but may relapse at a later time. Most relapses occur within 1 year (early latent stage). After 1 year (late latent stage), relapse is unlikely.

• Tertiary syphilis: Only a small percentage of patients with syphilis go on to develop tertiary syphilis that primarily affects the central nervous system and the cardiovascular system.

Laboratory Findings

Nontreponemal blood tests, such as the rapid plasma regain (RPR) or venereal disease research laboratory test (VDRL), are useful for screening, but may be negative in early primary syphilis, or show false-positive results. Biologic false-positive results can occur, usually with a low titer (<1:8). Positive reactions need to be confirmed with a Treponemal pallidum particle agglutination assay (TPPA) for IgM and IgG antibodies to T. pallidum proteins.¹¹

The spirochete can be detected by dark-field microscopic examination of serous material obtained from a chancre. A skin biopsy of primary or secondary lesions may detect T. pallidum, using special stains.

Diagnosis of Primary Syphilis

The diagnostic feature is a painless indurated ulcer on the genitals.

Differential Diagnosis of Primary Syphilis

• ✓ Chancroid: Presents with very painful ulcers or erosions that are not indurated.

• ✓ Herpes simplex: Presents with grouped vesicles or erosions. Cultures and Tzanck smear are diagnostic.

• ✓ Other: Lymphogranuloma venereum, trauma, fixed drug eruption, and ulcerated genital carcinoma.

Diagnosis of Secondary Syphilis

The diagnostic features are pink to rust colored macules and/or papules on the trunk, palms, and soles.

Differential Diagnosis of Secondary Syphilis

• ✓ Pityriasis rosea: Presents with oval, scaly papules, or plaques with a collarette scale located on the trunk in a parallel sloping arrangement similar to evergreen branches. A larger herald lesion is usually present and palms and soles are not involved.

• ✓ Guttate psoriasis: Presents with pink papules or plaques with subtle to silvery scale, primarily on the trunk. Palms and soles are usually not involved with this form of psoriasis.

• ✓ Other: Tinea corporis, tinea versicolor, lichen planus, pityriasis lichenoides, drug eruptions, primary HIV infection, erythema multiforme, viral exanthems, nummular dermatitis, folliculitis, and alopecia areata. Mucous membrane lesions may mimic lichen planus, aphthae, hand-foot-mouth disease, herpangina, and angular cheilitis.

Management

A single intramuscular dose of Benzathine penicillin G 2.4 million units is recommended for primary, secondary, and early latent syphilis. See CDC publication for treatment of penicillin allergic individuals or for special cases.¹¹ Follow-up laboratory testing is recommended at 3 and 6 months after treatment, then every 6 months for 2 years. Patients with syphilis often have other sexually transmitted diseases and should be evaluated and treated for these diseases and counseled on safe sex practices. Cases of syphilis should be reported to the local health department for follow up and identification of sexual contacts.

Indications for Consultation

Significant doubt about the diagnosis, immunosuppressed patient, or patient with advanced disease.

Patient Information

Centers for Disease Control and Prevention: www.cdc.gov/std/syphilis/default.htm