Chapter 27 Bacterial infections
3. Is Staphylococcus aureus the only bacterium that causes impetigo?
Older textbooks state that the most common cause of impetigo (impetigo contagiosum) is group A β-hemolytic Streptococcus. In recent years, most infections in the United States have been due to S. aureus, but the prevalence varies geographically. Although impetigo may be due to either organism, in many cases, both can be cultured. In these cases, it is thought that the streptococci are the primary infection and the staphylococci are secondary invaders after the infection has damaged the skin.
4. What does staphylococcal impetigo look like?
Early lesions of staphylococcal impetigo appear as thin, flaccid blisters that may demonstrate cloudy contents or layering of pus (Fig. 27-1). The base of the blister may demonstrate variable erythema. Histologically, the blisters are very superficial; the split occurs beneath the stratum corneum. For this reason, the blisters quickly collapse and may demonstrate a shiny lacquered appearance. Older lesions demonstrate a yellowish crust.
5. Why is staphylococcal impetigo frequently bullous?
Bullous impetigo is caused by staphylococci that produce toxins (exfoliative toxins A and B) capable of causing the split in the epidermis by targeting the epidermal adhesion molecule, desmoglein 1 (Dsg-1). Group II staphylococci are most commonly implicated.
6. How is bullous impetigo diagnosed?
The clinical appearance is usually suggestive but not diagnostic, and other superficial blistering or pustular disorders need to be considered, such as pemphigus, some bullous drug eruptions, and subcorneal pustular dermatosis. A Gram stain of the blister contents should demonstrate abundant Gram-positive cocci, but the definitive test is a culture that not only establishes the cause but also provides sensitivities to different antibiotics. The diagnosis can also be established by doing a biopsy, which demonstrates a subcorneal blister with neutrophils and cocci in the blister cavity.
7. How is bullous impetigo treated?
Oral dicloxacillin or cephalexin is the antibiotic of choice for severe infections. Oral erythromycin is frequently used in penicillin-allergic patients, although up to 20% or more of all staphylococci are resistant. Topical mupirocin is also effective and can be used if the patient cannot take oral antibiotics or if the infection is localized to a small area.
9. How do furuncles present?
Furuncles may be solitary or multiple and present as painful, erythematous, deep-seated follicular abscesses (Fig. 27-2). Patients may demonstrate mild constitutional symptoms in severe cases, or lesions may progress into carbuncles or staphylococcal cellulitis.
10. What is the best way to treat furuncles?
Nonsuppurative solitary lesions are best treated with local heat until they become fluctuant. Fluctuant furuncles should be opened and drained. Smaller lesions may be punctured with a no. 11 blade and the contents drained, while large abscesses may require a larger incision, drainage, and a wick. Patients with many lesions, evidence of surrounding cellulitis or with systemic symptoms should be considered for oral antibiotics.
As always, the diagnosis should be confirmed with a culture and antibiotic sensitivities performed at the initial visit, since not all follicular-based abscesses are due to staphylococci. The initial antibiotic choice before the culture and antibiogram results is usually oral dicloxacillin, oral cephalexin, or oral amoxicillin/clavulanate. Oral erythromycin, azithromycin, or clarithromycin can be used if the patient is allergic to penicillin. However, if MRSA infection is clinically suspected then the initial antibiotic choice is different (see question 16).
11. Why do some patients develop recurrent staphylococcal impetigo or recurrent furunculosis?
Recurrent infections occur when Staphylococcus aureus establishes itself as a part of the resident microbial flora. This occurs in up to 20% of individuals. The most common sites of carriage are the anterior nasal vestibule, axilla, groin, and feet. Patients who have virulent strains are prone to the development of recurrent impetigo or furunculosis, depending on the strain. A variety of host factors, such as abnormal neutrophil chemotaxis (e.g., hypergammaglobulinemia IgE syndrome), deficient intracellular killing (e.g., chronic granulomatous disease), and immunodeficiency states (e.g., AIDS), are important in a minority of patients. Diabetes mellitus is listed in many references as being associated with recurrent furunculosis, but this is controversial.
El-Gilany AH, Fathy H: Risk factors of recurrrent furunculosis, Dermatol Online J 15:16, 2009.
12. How is staphylococcal carriage eliminated?
Standard treatment regimens, such as oral dicloxacillin, oral cephalexin, oral erythromycin, or even intravenous vancomycin, eliminate active infection but not staphylococcal carriage. The most commonly used regimen to eliminate staphylococcal carriage is rifampin in combination with dicloxacillin. Less common regimens utilize oral clindamycin, topical mupirocin ointment, or replacement of the microflora with a less pathogenic strain of S. aureus (strain 502A). The success of these regimens varies from 50% to 70%; however, recolonization is common.
13. What is staphylococcal scalded-skin syndrome?
Staphylococcal scalded-skin syndrome typically occurs in neonates, infants, or immunocompromised adults. Like bullous impetigo, it is due to group II staphylococci that produce an exfoliatoxin; however, it differs in that the infection occurs at a distant site, such as a conjunctivitis or abscess. In neonates and infants, the kidneys are not able to excrete the exfoliatoxin adequately. The high level of exfoliatoxin produces diffuse, tender erythema associated with fever that rapidly progress to flaccid bullae; the bullae wrinkle and exfoliate, leaving an oozing erythematous base (Fig. 27-3). Mortality in neonates is usually not due to the infection but is secondary to impaired temperature regulation or fluid balance.
14. Describe the presentation of toxic shock syndrome.
Toxic shock syndrome is an acute febrile illness due to Staphylococcus aureus strains that produce pyrogenic exotoxins. These toxin-producing strains have been isolated classically from superabsorbent tampons in menstruating women but are also found in abscesses, wound infections, or the vaginas of nonmenstruating women.
15. Why is S. aureus frequently found in secondary infections of dermatitis and wounds?
S. aureus has receptors that allow it to bind to fibrin that is found in abundance on wound surfaces and in dermatitic skin.
17. What is the difference between HA-MRSA and CA-MRSA?
In the past, most cases of MRSA were hospital acquired but, in recent years, a distinct subtype of MRSA has emerged in the community setting. The two MRSA types are known as hospital acquired and community acquired (HA and CA-MRSA). HA-MRSA tends to cause invasive and disseminated infections in hospitalized patients, hemodialysis patients, long-term care facility patients, and patients with implanted medical devices. These strains tend to exhibit resistance to a greater number of antibiotic classes than CA-MRSA. CA-MRSA causes the same spectrum of skin infections as methicillin-sensitive (MSSA) S. aureus, most commonly furuncules, boils, and abscesses; however, severe, invasive infections with CA-MRSA have been reported. Additionally, CA-MRSA tends to display a narrower spectrum of antibiotic resistance than HA-MRSA. Trimethoprim-sulfamethoxazole, tetracycline, and clindamycin are antibiotics that will often cover CA-MRSA, although inducible clindamycin resistance is fairly common in CA-MRSA isolates. Therapy is dependent on the severity of infection and the strain susceptibility, with empiric antibiotic coverage determined by prevalence of CA-MRSA in a given community. More serious and hospital-acquired cases are usually treated with vancomycin or linezolid.
19. How does streptococcal impetigo present?
Streptococcal impetigo presents as superficial, stuck-on, honey-colored crusts overlying an erosion (Fig. 27-4). The most common location is the face, but any area may be involved. In contrast to staphylococcal impetigo, blisters are absent.
20. What is ecthyma?
Ecthyma is a severe form of streptococcal impetigo in which there is a thick crust overlying a punched-out ulceration of the epidermis (Fig. 27-5). Typically, it is surrounded by a zone of erythema. In contrast to streptococcal impetigo, which is usually found on the face and does not produce scarring, ecthyma is more commonly located on lower extremities and may heal with scarring.
21. What is blistering distal dactylitis?
Blistering distal dactylitis is an uncommon infection typically caused by Streptococcus pyogenes but occasionally caused by Staphylococcus aureus. It typically presents in young children as one or more tender superficial bullae on an erythematous base on the volar fat pad of a finger (Fig. 27-6). In rare instances, toes may be affected.
22. What is erysipelas?
Erysipelas, or St. Anthony’s fire, is a form of cellulitis usually caused by β-hemolytic streptococci, rarely by Staphylococcus aureus. Patients often have a prodrome of malaise, fever, and headache. Typically, erysipelas presents on the face as an erythematous indurated plaque with a sharply demarcated border and a “cliff-drop” edge (Fig. 27-7). In severe cases, the epidermis may become bullous, pustular, or necrotic. Untreated erysipelas can be fatal due to vascular thrombosis, bacteremia, or toxin release. Streptococcal cellulitis is a more generic term that includes erysipelas but also cellulitis that lacks the characteristic cliff-drop border. Known commonly as “blood poisoning,” it is most often found on extremities and is associated with lymphangitis (Fig. 27-8).
24. How is erysipelas treated?
Mild or early cases may be treated with an oral penicillin or oral erythromycin. Oral dicloxacillin is the best choice because it provides better antistaphylococcal coverage for the rare case of staphylococcal erysipelas. Severe cases or cases with central facial involvement should be hospitalized and treated with intravenous antibiotics, such as vancomycin. Erysipelas usually improves within 48 hours after institution of antibiotic therapy.
Figure 27-6. Blistering distal dactylitis demonstrating a characteristic tender superficial blister on the volar fat pad.
25. Describe the cutaneous manifestations of Lyme disease.
Lyme disease is a multisystem disease caused by Borrelia burgdorferi that is transmitted to humans by ticks of the genus Ixodes. One to 30 days after the tick bite, patients present with variable constitutional symptoms, including fever, malaise, headache, and arthralgias. Approximately three fourths of patients develop erythema chronicum migrans that begins as an erythematous papule at the bite site and progresses to an annular erythema that may reach 20 cm or more in size (Fig. 27-9).
26. A patient living in an endemic area for Lyme disease reports a history of a tick bite. Should that patient receive antibiotic prophylaxis?
The question of whether or not patients with tick bites in endemic areas should receive antibiotic prophylaxis is controversial. Randomized controlled trials only support the use of a 200 mg oral dose of doxycycline in a child >8 years of age when all of the following criteria are met: 1) The attached tick can be identified as a nymphal or adult form of Ixodes scapularis that has been attached for >36 hours, estimated by exposure or degree of tick engorgement; 2) prophylaxis can be started within 72 hours of when tick was removed; 3) ecologic information shows that local prevalence of infection of ticks with Borellia burgdorferi is greater than 20%; and 4) doxycycline is not contraindicated.
Wormser GP, Dattwyler RJ, Shapiro ED, et al: The clinical assessment, treatment, and prevention of Lyme disease, human granulocytic anaplasmosis, and babesiosis: clinical practice guidelines by the Infectious Diseases Society of America, Clin Infect Dis 43:1089–1134, 2006.
27. What types of skin infections does Pseudomonas aeruginosa produce?
28. How does ecthyma gangrenosum differ from ecthyma?
• Ecthyma is caused by β-hemolytic streptococci, while ecthyma gangrenosum is most commonly caused by P. aeruginosa.
29. Where do you usually acquire Pseudomonas folliculitis?
In your hot tub. Pseudomonas folliculitis is typically associated with hot tub use (hot tub folliculitis). Less commonly, it is associated with whirlpools or swimming pools. It is usually associated with P. aeruginosa serotype O:11, although other serotypes have also been reported. Pseudomonas folliculitis has also been reported as a complication of depilatories used for the removal of leg hair.
30. How does Pseudomonas folliculitis present?
Clinically, it occurs 1 to 3 days after exposure, presenting as a diffuse truncal eruption (Fig. 27-11). The primary lesion is a follicular-based erythematous papule that frequently demonstrates a follicular pustule. Less commonly, patients may also demonstrate mastitis, abscesses, lymphangitis, and fever. Another variation is those patients that present with painful indurated lesions of the feet and/or hand that may become pustular (“Pseudomonas hot hand-foot syndrome”). The disease is usually self-limited, although rare patients may continue to develop recurrent folliculitis or abscesses for up to 2 months.
31. What is the best treatment for Pseudomonas folliculitis?
Most cases are self-limited and do not require treatment. Severe or recurrent cases can be treated with oral ciprofloxacin. Ultimately, the best treatment is prevention of infection. The most effective measures are frequent drainage of the hot tub or whirlpool to remove the buildup of desquamated skin cells that serve as the prime source of nutrients. Adequate chlorination and bromination are also necessary.
33. What causes tularemia? Where did the name tularemia come from?
Tularemia is caused by Francisella (formerly Pasteurella) tularensis, a Gram-negative coccobacillus. The infection is acquired through handling of infected animals (squirrels and rabbits), tick bites, and deerfly bites. Tularemia gets its name from Tulare County in California, the site where researchers isolated the organism from ground squirrels in 1911. The term was first used by Dr. Francis, who was subsequently honored by having the genus named after him.
34. Describe the skin lesions of tularemia.
Tularemia has six presentations: ulceroglandular, glandular, oculoglandular, oropharyngeal, typhoidal, and pneumonic forms. The ulceroglandular form is the most common presentation and the one that typically demonstrates skin lesions. The primary skin lesion begins as a small papule at the inoculation site that rapidly necroses. The papule may be surrounded by an area of cellulitis and is characteristically associated with painful regional lymphadenopathy (Fig. 27-12). Systemic symptoms include fever, chills, headache, and malaise.
36. What is trichomycosis axillaris?
Trichomycosis axillaris is a superficial infection of the hair shaft that most commonly affects the axillary hair and, less commonly, the pubic hair. It is most commonly produced by Corynebacterium tenuis although other Corynebacterium species are also frequently implicated. It is an asymptomatic infection characterized by tan or, less commonly, yellow, red, or black concretions of tightly packed bacteria that grow on and within the hair (Fig. 27-13). Treatment options include cutting the affected hair, topical aluminum chloride, topical erythromycin, or topical clindamycin.
