Chapter 11 Cellulitis and Diabetic Foot Infections
Risk Factor | Potential Infectious Organism | Treatment |
---|---|---|
Cat bite | Pasteurella multocida | Amoxicillin-clavulanate, ampicillin-sulbactam, cefoxitin |
P. multocida is resistant to dicloxacillin and nafcillin | ||
Dog bite | P. multocida, Capnocytophaga canimorsus, Staphylococcus intermedius | Amoxicillin-clavulanate, ampicillin-sulbactam, cefoxitin |
P. multocida is resistant to dicloxacillin and nafcillin | ||
Human bite | Eikenella corrodens, Fusobacterium, Porphyromonas, Prevotella, S. pyogenes | Amoxicillin- clavulanate, ampicillin-sulbactam, cefoxitin |
Hot tub exposure | Pseudomonas aeruginosa | Aminoglycosides, third-generation cephalosporins, ticarcillin, mezlocillin, piperacillin, fluoroquinolones (in adults) |
Diabetes mellitus or peripheral vascular disease | Group B streptococci | Penicillin or erythromycin |
Periorbital cellulitis in children | Haemophilus influenzae | Third-generation cephalosporin |
Saphenous venectomy site | Groups C and G streptococci | Penicillin or erythromycin |
Fresh water laceration | Aeromonas hydrophilia | Trimethoprim- sulfamethoxazole, fluoroquinolones, aminoglycosides, chloramphenicol, third-generation cephalosporins; resistant to ampicillin |
Sea water exposure, raw oysters, and cirrhosis | Vibrio vulnificus | Tetracyclines |
Stasis dermatitis or lymphedema | Groups A, C, G streptococci | Penicillin or erythromycin |
Cat scratch, or bacillary angiomatosis in an HIV patient | Bartonella henselae, B. quintana | Erythromycin |
Fish mongering, bone rendering | Erysipelothrix rhusiopathiae | Erythromycin, clindamycin, tetracycline, cephalosporins; resistant to sulfonamides, chloramphenicol |
Fish tank exposure | Mycobacterium marinum | Rifampin and ethambutol |
Contact with others with soft tissue infections | Methicillin-resistant S. aureus | Vancomycin |
Compromised host with ecthyma gangrenosum | P. aeruginosa | Aminoglycosides, third-generation cephalosporins, ticarcillin, mezlocillin, piperacillin, fluoroquinolones (in adults) |
Stevens DL. Cellulitis, pyoderma, abscesses and other skin and subcutaneous infections. In: Cohen J, Powderly WG, Berkley SF, et al. Infectious Diseases, 2nd ed. Philadelphia: Mosby; 2004. p. 133.
Definition and Epidemiology
Cellulitis is a skin and subcutaneous tissue infection that can affect any part of the body. Cellulitis is most commonly caused by Staphylococcus aureus and Streptococcus pyogenes. However, other infectious agents may predominate in different clinical situations (Table 11-1). Although cellulitis is quite common, accurate incidence information is not available. Some estimates suggest that cellulitis accounts for approximately 2% of outpatient office visits, or up to 158 visits per 10,000 person-years.
Pathogenesis
Risk Factors for Cellulitis
General
Risk factors for cellulitis include obesity, vascular or lymphatic compromise (e.g., venous insufficiency, saphenous venectomy, or lymph node dissection after surgery for breast cancer), lower extremity edema, diabetes mellitus, and skin trauma (e.g., pressure ulcers, trauma or tinea pedis).
Patients without vascular or immune defects will likely be infected by S. aureus or group A streptococci. Pseudomonas, enterococci, or other bacteria may cause cellulitis in patients with an immune or vascular defect, or loss of significant skin integrity (e.g., burns).
Breast Cancer
Women who have undergone surgery for breast cancer with axillary lymph node dissection are at risk for recurrent cellulitis in the ipsilateral breast and upper extremity. Disruption of normal lymphatic drainage is thought to play a role in pathogenesis.
Pathogenesis of Cellulitis
Bacteria penetrate the cutaneous barrier through breaks in the skin or via hair follicles. Microbial cell wall components (e.g., endotoxins, peptidoglycans) stimulate production of chemotactic factors, which attract neutrophils to the region. Continued production of pro-inflammatory cytokines causes fever and local changes of erythema, edema, warmth, and pain.
Patients with decreased tissue perfusion as a result of vascular disease (e.g., atherosclerosis, diabetes) may have an increased susceptibility to cellulitis and are predisposed to deeper soft tissue infections.
Risk Factors for Diabetic Foot Infections
Diabetic foot infections occur as a result of multiple risk factors that result in an initial break in the protective skin barrier and an increased susceptibility to infection:
Pathogenesis and Microbiology of Diabetic Foot Infections
The initial break in overlying skin is usually caused by trauma or pressure ulceration. The area becomes colonized with bacteria, and becomes infected over a period of hours to days.
Clinical Features and Diagnosis
Cellulitis
History
Patients may or may not report a history of trauma to the region. Exposure history may provide clues to specific infections, as detailed in Table 11-1. Risk factors such as a history of tinea pedis, diabetes mellitus, surgery for breast cancer with lymph node dissection, saphenous venectomy, or peripheral vascular disease should be determined.
Patients in close contact with other persons who have soft-tissue infections may be at higher risk for methicillin-resistant S. aureus (MRSA) infections.