eMedicine Specialties > Infectious Diseases > Skin and Soft-Tissue Infections
Burn Wound Infections
Updated: Apr 16, 2008
Introduction
Background
Approximately 500,000 persons seek medical treatment for burns every year in the United States. Of these, approximately 40,000 are hospitalized for burn injuries, including 25,000 admissions to the approximately 125 medical centers that specialize in burn care. Typically, 4,000 people die from fire and burns every year; of these, approximately 3,500 deaths are due to residential fires, and 500 are due to motor vehicle and aircraft accidents, electrical injuries, chemical exposures, or hot-liquid and substance spills. Among fatalities, nearly 75% die at the scene of the incident or during initial transport. Of those who reach medical care, infection is a major cause of morbidity and mortality.
The skin, one of the largest organs in the body, performs numerous vital functions, including fluid homeostasis, thermoregulation, immunologic functions, neurosensory functions, and metabolic functions (eg, vitamin D). The skin also provides primary protection against infection by acting as a physical barrier. When this barrier is damaged, pathogens have a direct route to infiltrate the body, possibly resulting in infection.
In addition to the nature and extent of the thermal injury influencing infections, the type and quantity of microorganisms that colonize the burn wound appear to influence the future risk of invasive wound infection. The pathogens that infect the wound are primarily gram-positive bacteria such as methicillin-resistant Staphylococcus aureus (MRSA) and gram-negative bacteria such as Acinetobacter baumannii-calcoaceticus complex , Pseudomonas aeruginosa, and Klebsiella species. These latter pathogens are notable for their increasing resistance to a broad array of different antimicrobial agents. In addition, burn wounds are commonly infected with fungal pathogens.
Factors that are associated with improved outcome and prevention of infection likely include early burn-eschar excision, topical and prophylactic antibiotics, and aggressive infection-control measures.
Pathophysiology
The burn wound typically has 3 characteristic areas of involvement. The first is the zone of coagulation, which is nearest the heat source and includes dead tissue that forms the burn eschar. The second is the zone of stasis, which is adjacent to the area of necrosis; this area is viable but is at a substantial risk for ongoing necrosis and ischemic damage due to perfusion defects. The third is the zone of hyperemia, which includes relatively healthy skin with increased blood flow and vasodilation in response to the injury; the cellular injury in this area is minimal.
Wounds reflect the mechanism of the burn. In thermal burns, the degree of cellular damage varies based on the duration and temperature of exposure. Increasing temperatures alter molecular confirmation, destroy cell membranes, denature protein, and release oxygen-free radicals, all resulting in cell death and burn eschar. Types of chemical burns differ and include those due to reducing agents (eg, hydrochloric acid), oxidizing agents (eg, sodium hypochlorite), and corrosive agents (eg, phenol); each causes burn injuries with varying modes of action.
Burns alter not only the innate immune character of the skin but also other arms of the immune system. Overall, T-cell activity is reduced through an increase in the number of suppressor cells and a decrease in the number of helper cells. The levels of inflammatory cytokines and complement are also decreased. In addition, burn decrease the chemotaxis and phagocytic and bactericidal activity of neutrophils. One of the primary concerns associated with burn injuries is that the eschar is avascular, preventing immune cells and systemically administered antibiotics from being delivered to the site of infection.
Immediately following a thermal burn, the surface of the burn wound is free of microorganisms. However, deep cutaneous structures that survive the initial burn injury (eg, sweat glands, hair follicles) often contain staphylococci, which colonize the wound surface during the subsequent 48 hours. Over the following 5-7 days, other microbes, including gram-negative and gram-positive bacteria, colonize the wound. These potential pathogens typically come from the patients’ gastrointestinal tract, upper respiratory tract, or the hospital environment, transferring through contact with health care workers.
Fungal infections often develop later, after broad-spectrum antibiotics have been administered or after wound care has been delayed. Infections with anaerobes are rare, except after electrical injuries. Infections with viruses such as herpes simplex virus and varicella-zoster virus rarely complicate burn wounds.
Frequency
United States
According to the National Fire Protection Agency, US fire departments responded to 1.64 million fires during 2006. There were a total of 3,245 civilian fire-related deaths and 16,400 civilian fire-related injuries, resulting in one fire death every 162 minutes and one injury every 32 minutes. The total economic impact was estimated at $11.3 billion.
International
At the beginning of the 21st century, the Centre of Fire Statistics estimated that the average number of fires worldwide was 7-8 million, resulting in 70,000-80,000 fire deaths and 500,000-800,000 fire injuries. In Europe, 2-2.5 million fires were reported, resulting in 20,000-25,000 fire deaths and 250,000-500,000 fire injuries. The World Fire Statistics from the Geneva Association reported that, by country, the highest number of fire deaths in 2004 occurred in the United States (4,250), followed by Japan at 2,050 and the United Kingdom at 530. When adjusted for deaths per 100,000 persons between 2002 and 2004, of the 25 countries that reported data, the highest rate was in Hungary (2.1); Japan reported 1.79, the United States reported 1.39, the United Kingdom reported 0.97, Spain reported 0.61, and Singapore reported 0.08.
Mortality/Morbidity
According to the National Burn Repository’s 10-year rolling data collection from January 1, 1996, through June 30, 2006, the mortality rate associated with burns was 5.3% overall, with older age and higher-percentage total body surface area (TBSA) burned correlating with higher mortality rates.1 The causes of death were reported in 3,463 cases; 27% died of multiple organ failure, 14% died from withheld treatment, 12% died from trauma wounds, 12% died from burn shock, 11% died from pulmonary failure/sepsis, 11% died from cardiovascular failure, 5% died from other causes, and 4% died from sepsis burn wound. Burns covering 1-10% of the TBSA carried the lowest risk of mortality (0.7%), increasing as the percentage of TBSA burned increased. The mortality rate was 78% in patients with 90% of their TBSA burned.
Among the 19,655 reported cases of complications included in the analysis, pulmonary complications including pneumonia (3,361), acute respiratory distress syndrome (885), and respiratory failure (1,944) constituted the greatest percentage of cases (31%). Cellulitis (1,988) and wound infections (1,950) were responsible for 17% of the complications. Septicemia (1,672) and other infections (1,250) were the other categories that included infectious complications (15%).
Race
Among 142,318 patients with burns reported in the National Burn Registry, 58% were white, 17.4% were African American, 12.8% were Hispanic, 2% were Asian, 0.6% were Native American, 1.8% were classified as other, and data were missing for 7.3%.
Sex
Among 142,318 burn patients reported in the National Burn Registry, 69.7% were male and 30.3% were female.
Age
Most burns occur in persons aged 5-30 years, with only 8% occurring in persons older than 70 years. Younger individuals are more likely to have scald burns, while older individuals are more likely to be burned by fire. With the same percentage of TBSA burned, older patients have a higher mortality rate.
Clinical
History
The American Burn Association (ABA) recently published criteria for sepsis and wound infections. Regular monitoring of burn wounds allows for the early recognition of infection. Local signs of burn wound infection include conversion of a partial-thickness injury to full-thickness wound, worsening cellulitis of surrounding normal tissue, eschar separation, and tissue necrosis.
According to the ABA, the various types of burn wound infections include wound colonization, wound infection, invasive infection, cellulitis, and necrotizing infection/fasciitis.
- Wound colonization is characterized by the presence of low concentrations of bacteria on the surface without invasion or systemic signs or symptoms of infection. Tissue biopsies obtained from colonized but not infected skin usually reveal less than 105 bacteria per gram of tissue.
- Wound infection is associated with higher concentration of bacteria (>105 bacteria per gram of tissue) within the wound or wound eschar but not a deeply invasive infection.
- An invasive infection includes concentrations of bacteria (frequently >105 bacteria per gram of tissue) at an appropriate depth of the burn wound to cause suppurative separation of the eschar or graft loss with involvement of unburned tissue or the presence of a systemic response consistent with sepsis.
- Cellulitis manifests as erythema, induration, warmth, and tenderness in the tissue surrounding the burn wound or wound eschar and occasionally the presence of sepsis. Erythema alone may not indicate cellulitis.
- Necrotizing infection/fasciitis involves an aggressive invasive infection with involvement of structures below the skin.
Physical
- Wound infection
- Suppurative separation of the eschar
- Graft loss with involvement of unburned tissue or the presence of a systemic response consistent with sepsis
- Change in wound color (focal areas of red, brown, or black)
- Green discoloration of the subcutaneous fat
- Cellulitis
- Erythema (Erythema alone may not require treatment.)
- Induration
- Warmth
- Tenderness
- Sepsis (occasionally)
- Necrotizing infection/fasciitis - Aggressive invasive infection with involvement of structures below the skin (eg, muscle, bone, organs)
- Signs of sepsis
- Temperature greater than 39o C or less than 36.5o C
- Progressive tachycardia (>110 beats per minute)
- Progressive tachypnea
- More than 25 breaths per minute without assisted ventilation
- Minute ventilation greater than 12 L per minute min if intubated and mechanically ventilated
- Thrombocytopenia (<100,000/μL; does not apply immediately after initial resuscitation)
- Hyperglycemia (in the absence of pre-existing diabetes mellitus)
- Plasma glucose levels greater than 200 mg/dL in the absence of treatment
- Significant resistance to insulin (>25% increase in insulin requirement)2
- Inability to continue enteral feedings for more than 24 hours
- Abdominal distension
- High gastric residuals
- Uncontrollable diarrhea
Causes
- Risk factors for the development of a burn wound infection
- Extremes of age
- Comorbidities such as obesity and diabetes
- Immunosuppression (eg, due to AIDS)
- Invasive devices (eg, catheters)
- Burns involving greater than 30% TBSA
- Full-thickness burns
- Failure to cover burns or failed skin graft resulting in prolonged open burn wounds
- Improper early burn care
- Organisms frequently causing invasive burn wound infection
- Gram-positive bacteria
- S aureus, including MRSA
- Coagulase-negative S taphylococcus species
- Enterococcus species, including vancomycin-resistant species
- Gram-negative bacteria
- P aeruginosa
- Klebsiella species
- Acinetobacter species
- Escherichia coli
- Serratia marcescens
- Enterobacter species
- Proteus species
- Fungi (Burn wounds complicated by fungal infections constitute an independent predictor for mortality in patients with a burned TBSA of 30-60%.3 )
- Candida species
- Aspergillus species
- Fusarium species
- Phaeohyphomycetes(dark molds)
- Zygomycetes (eg, Rhizopus, Mucor, Absidia)
- Viruses (Cutaneous disease typically occurs in healing partial-thickness burns and donor sites.)
- Herpes simplex virus
- Varicella-zoster virus
- Gram-positive bacteria
Differential Diagnoses
Cellulitis
Toxic Epidermal Necrolysis
Workup
Laboratory Studies
Diagnosis of wound infection should focus on a careful physical examination that is performed frequently by personnel trained in the management of burns.
- Laboratory tests or changes in laboratory values such as WBC count, neutrophil percentage, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP) level are of low yield in detecting or predicting burn infections because of the inflammatory response associated with the burn itself.4
- Diagnosis relies on clinical examination as outlined above (see Clinical) and culture data, including the following:
- Quantitative biopsy can be used to confirm infection but is not reliable. This procedure is useful in identifying the infecting pathogen.
- Quantitative swab is of limited value but may aid in identifying the infecting pathogen.5
- Tissue histopathology allows for quantification and evaluation of infection depth and involvement of non-burned skin.
- The use of routine wound cultures as part of surveillance procedures has been proposed to provide early identification of organisms colonizing the wound, to monitor response to therapy, to guide empiric therapy, and to evaluate for nosocomial transmission. However, this has not been shown to improve patient outcomes, and routine application has been brought into question.
Imaging Studies
None imaging studies have been identified as useful for detecting wound infections.
Procedures
- Biopsies
- Multiple samples from several areas of the burn wound should be obtained and sent for histopathology and microbiological workup of the pathogens and their resistance profiles.
- After cleaning the wound with isopropyl alcohol, 2 parallel incisions 1-2 cm in length and 1.5 cm apart with a depth to obtain a portion of the underlying fat are made in the skin. Alternatively, biopsy samples typically weighing 0.02-0.5 g may be obtained with a 3-mm punch-biopsy technique.
- Biopsy is a commonly bypassed procedure because of technical difficulty within the microbiology section working up these types of samples or a lack of local histopathological expertise.
Histologic Findings
- Bacteria are detected using Gram stain.
- Fungus are detected based on standard morphological appearance on various stains (periodic acid-Schiff [PAS] and Gomori methenamine silver [GMS]), but cultures must be obtained to definitively identify the pathogen.
- Aspergillus -like morphology - Presence of parallel-walled, branching, septate hyphae (eg, Aspergillus species, Fusarium species, Phaeohyphomycetes)
- Mucor -like morphology (zygomycosis/mucormycosis) - Presence of wide, ribbonlike, rarely septate hyphae (eg, Rhizopus, Mucor, Rhizomucor, Absidia)
- Yeastlike morphology - Presence of budding yeasts or rounded, yeastlike structures (Many yeasts, including most Candida species also produce hyphae and pseudohyphae in tissue.)
- Virus: Herpes simplex virus can be isolated via identification of inclusions on light or electron microscopy or other viral particles on biopsy specimen or lesion scrapings.
Staging
The various stages used to diagnose burn wound infections are as follows:
- Stage I - Colonization
- Superficial - Microorganisms present only on burn wound surface
- Penetrating - Variable depth of microbial penetration of eschar
- Proliferating - Variable level of microbial proliferation at nonviable–viable tissue interface (subeschar space)
- Stage II - Invasion
- Microinvasion - Microorganisms present in viable tissue immediately subjacent to subeschar space
- Deep invasion - Penetration of microorganisms to variable depth and expanse within viable subcutaneous tissue
- Microvascular involvement - Microorganisms within small blood vessels and lymphatics (thrombosis of vessels is common)
Treatment
Medical Care
The focus of medical care is to prevent infection. Once infection develops, aggressive surgical excision involving wound closure with autograft, allograft, or skin substitutes and antimicrobial therapy are needed.
Although early excision appears to be the primary surgical method for improving infection outcomes, the cumulative data for this are not very strong. However, a recent meta-analysis of all available randomized controlled studies found that early excision reduced mortality rates in all patients with burns who did not have an inhalation injury.6
Wound care should be directed at thoroughly removing devitalized tissue, debris, and previously placed topical antimicrobials. A broad-spectrum surgical antimicrobial topical scrub such as chlorhexidine gluconate should be used along with adequate analgesia and preemptive anxiolytic in order to permit adequate wound care. The most commonly used topical antimicrobials for the prevention and treatment of burn wound infection include mafenide acetate, silver sulfadiazine, silver nitrate solution, and silver-impregnated dressings. These various therapies differ in their ability to penetrate eschars, antimicrobial activities, and adverse-event profiles. However, they may be associated with drug pressure, resulting in infections with resistant bacteria or fungus.
Antibiotic prophylaxis has also been studied in burn surgery at the time of wound manipulation, but few studies have supported this use of systemic antibiotics during acute burn surgery. Antibiotics appear to be of no value in the prophylaxis of wound infections accompanying surgery for small to moderate burns. However, few studies have evaluated surgical prophylaxis in patients with burns over more than 40% TBSA.
When an infection is identified, antimicrobial therapy should be directed at the pathogen recovered on culture. In the setting of invasive infection or evidence of sepsis, empiric therapy is often initiated. A local burn facility's antibiogram must be established to help direct empiric therapy. If fungus is detected on histopathology, culture samples to detect the infecting genus and species are necessary because the growing armamentarium of antifungal agents have varying activity. Amphotericin B was once the agent of choice, but some facilities have seen increased rates of infections with Fusarium species and Aspergillus terreus, which are innately resistant to amphotericin B. In these cases, voriconazole is often used. A new agent, posaconazole, may have broader antifungal activity but is limited as it is available only in an oral formulation.
Patients with burns are also at risk for tetanus. Tetanus vaccination plus antitetanus immunoglobulin should be administered to patients who have no history of vaccination with booster tetanus toxoid vaccination given at 4 weeks and 6 months.
Surgical Care
This is fundamental to the care of the patient. Systemic and local antibiotics have limited effect in improving morbidity and mortality unless they are used in combination with adequate surgical care.
Consultations
Consultation with an infectious disease specialist is suggested if multidrug-resistant bacteria are present.
Diet
The basal metabolic rate increases as the percentage of TBSA burned increases. Early enteral feeds should be started.7
Activity
Patients may be as active as they can tolerate. Aggressive physical and occupational therapy of extremity injuries is necessary to prevent long-term morbidity.
Medication
The goals of antimicrobial therapy are to treat an underlying infection, to reduce morbidity, and to prevent mortality. Topical therapy is often applied to prevent infection and to treat ongoing infections or used as an adjunct to surgical treatment and systemic antibiotics. Systemic antimicrobial agents should be directed at the underlying pathogen recovered from culture or determined empirically from the local burn unit’s antibiogram while culture results are pending.
Antifungal agents may also be used. However, pathogen identification is necessary in order to determine the ideal antifungal agent, as amphotericin B is not active against all fungal infections.
Antibacterial, Topical
Topical therapy is typically applied to prevent infection and to treat infection when adequate surgical management is not possible.
Silver sulfadiazine (Silvadene, SSD, SSD-AF, Thermazene)
Useful in prevention of infections from second- or third-degree burns. Has bactericidal activity against many gram-positive and gram-negative bacteria, including yeast. It has poor eschar penetration.
Dosing
Adult
Apply qd/bid to a thickness of 1/16th; burned area should be covered with medication continuously
Pediatric
Apply as in adults
Interactions
Effect of proteolytic enzymes is reduced when used concomitantly with this product
Contraindications
Documented hypersensitivity; neonates and infants <2 years
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in G-6-PD deficiency and renal insufficiency; a decrease in the neutrophil count has been observed with initiation of therapy (this effect typically resolves even when the agent is continued and rarely necessitates discontinuation of therapy)
Silver nitrate
Coagulates cellular protein and removes granulation tissue. It exhibits activity against gram-positive bacteria, gram-negative bacteria, and Candida species. The major drawbacks are that it has poor penetration of eschar, requires the use of occlusive dressings, and turns black upon contact with tissues.
Dosing
Adult
Apply to affected area or lesion for approximately 5 d
Pediatric
Apply as in adults
Interactions
Decreases effects of sulfacetamide preparations
Contraindications
Documented hypersensitivity; broken skin or cuts
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Not for internal use; depletes cations due to leeching across open wound into hypotonic solution (phenomenon may result in hyponatremia, hypocalcemia, hypokalemia, and hypomagnesemia; close monitoring of electrolytes is necessary)
Mafenide (Sulfamylon)
Topical sulfonamide. Diffuses freely into the eschar and is highly effective against gram-negative organisms, including Pseudomonas species.
Dosing
Adult
Apply cream to open wounds bid/tid
Pediatric
Apply as in adults
Interactions
None reported
Contraindications
Documented hypersensitivity; renal impairment
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Pain or burning may occur upon application; metabolized to a carbonic anhydrase inhibitor (p-carboxybenzene-ulfonamide), which may result in metabolic acidosis
Follow-up
Further Inpatient Care
A primary focus during hospitalization is to prevent nosocomial transmission of multidrug-resistant pathogens, especially in patients with a greater percentage of TBSA burn (approximately 30%) or who are known to be colonized with multidrug-resistant bacteria such as MRSA, vancomycin-resistant Enterococcus species, or gram-negative bacteria known to develop resistance (eg, Pseudomonas, Klebsiella, Acinetobacter species).
Hand hygiene should be aggressively implemented. Standard precautions should be used in the care of all patients with burn injuries. Patients should be managed in single rooms, if possible, with use of contact precautions. Gowns and gloves should be used when contact is expected with infected material or open wounds. Masks and caps should be implemented based on the presence of multidrug-resistant bacteria. The use of individual-patient equipment should be considered.
Further Outpatient Care
Patients will require prolonged occupational and physical therapy support based on the site of burn.
Transfer
Aggressive infection-control procedures should be undertaken when transferring patients between facilities because of the risk of transferring multidrug-resistant bacteria.
Deterrence/Prevention
The prevention of burn wound infection is a team approach that includes the support of surgeons, nurses, infection-control providers, and infectious disease physicians. Emphasis on early wound care, infection-control practices, and long-term rehabilitative care is necessary to improve the morbidity and mortality associated with burns.
Early removal of full-thickness burned tissue, as well as early definitive wound closure and strict enforcement of infection-control procedures, is necessary to mitigate poor outcomes.
Complications
- Burn wound infections are often the source of bacteria responsible for other systemic infections including bloodstream infections and pneumonia. This can lead to multisystem organ failure and death.
- Sepsis can contribute to multisystem organ failure and death.
- Early wound excision is associated with bleeding complications that require transfusions. Given the evidence that increased blood transfusion is associated with higher infection rates in the general trauma population, further data is needed to evaluate the overall utility of early excision especially as the overall data supporting this technique is limited although it is considered standard of care in most burn facilities.
Prognosis
The overall prognosis depends on numerous factors, including the patient’s age, percentage of TBSA burned, comorbidities, initial management strategies, and the support necessary for long-term rehabilitative care.
Patient Education
- For excellent patient education resources, visit eMedicine's Burns Center. Also, see eMedicine's patient education article Thermal (Heat or Fire) Burns.
Miscellaneous
Medicolegal Pitfalls
Burn care involves a multisystem approach, requiring numerous health care providers to be involved in the process. The treatment of such infections is often prolonged and is associated with an increased risk for complications, including iatrogenic episodes. As such, continued diligence is needed.
References
Latenser BA, Miller SF, Bessey PQ, Browning SM, Caruso DM, Gomez M, et al. National Burn Repository 2006: a ten-year review. J Burn Care Res. Sep-Oct 2007;28(5):635-58. [Medline].
Pidcoke HF, Wade CE, Wolf SE. Insulin and the burned patient. Crit Care Med. Sep 2007;35(9 Suppl):S524-30. [Medline].
Horvath EE, Murray CK, Vaughan GM, Chung KK, Hospenthal DR, Wade CE, et al. Fungal wound infection (not colonization) is independently associated with mortality in burn patients. Ann Surg. Jun 2007;245(6):978-85. [Medline].
Murray CK, Hoffmaster RM, Schmit DR, Hospenthal DR, Ward JA, Cancio LC, et al. Evaluation of white blood cell count, neutrophil percentage, and elevated temperature as predictors of bloodstream infection in burn patients. Arch Surg. Jul 2007;142(7):639-42. [Medline].
Uppal SK, Ram S, Kwatra B, Garg S, Gupta R. Comparative evaluation of surface swab and quantitative full thickness wound biopsy culture in burn patients. Burns. Jun 2007;33(4):460-3. [Medline].
Ong YS, Samuel M, Song C. Meta-analysis of early excision of burns. Burns. Mar 2006;32(2):145-50. [Medline].
Wolf SE. Nutrition and metabolism in burns: state of the science, 2007. J Burn Care Res. Jul-Aug 2007;28(4):572-6. [Medline].
Albrecht MC, Griffith ME, Murray CK, Chung KK, Horvath EE, Ward JA, et al. Impact of Acinetobacter infection on the mortality of burn patients. J Am Coll Surg. Oct 2006;203(4):546-50. [Medline].
Church D, Elsayed S, Reid O, Winston B, Lindsay R. Burn wound infections. Clin Microbiol Rev. Apr 2006;19(2):403-34. [Medline].
Esselman PC. Burn rehabilitation: an overview. Arch Phys Med Rehabil. Dec 2007;88(12 Suppl 2):S3-6. [Medline].
Greenhalgh DG, Saffle JR, Holmes JH 4th, Gamelli RL, Palmieri TL, Horton JW, et al. American Burn Association consensus conference to define sepsis and infection in burns. J Burn Care Res. Nov-Dec 2007;28(6):776-90. [Medline].
Mayhall CG. The epidemiology of burn wound infections: then and now. Clin Infect Dis. Aug 15 2003;37(4):543-50. [Medline].
Regules JA, Carlson MD, Wolf SE, Murray CK. Analysis of anaerobic blood cultures in burned patients. Burns. Aug 2007;33(5):561-4. [Medline].
Regules JA, Glasser JS, Wolf SE, Hospenthal DR, Murray CK. Endocarditis in burn patients: Clinical and diagnostic considerations. Burns. Oct 26 2007;[Medline].
Schofield CM, Murray CK, Horvath EE, Cancio LC, Kim SH, Wolf SE, et al. Correlation of culture with histopathology in fungal burn wound colonization and infection. Burns. May 2007;33(3):341-6. [Medline].
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Keywords
burn wound cellulitis, burn wound infection, invasive burn wound infection, burn injury, thermal injury, wound colonization, necrotizing infection/fasciitis, house fire, electrical injury, chemical exposure, burn infection, burn complications
Contributor Information and Disclosures
Author
Clinton Murray, MD, Program Director, Infectious Disease Fellowship, San Antonio Uniformed Services Health Education Consortium
Clinton Murray, MD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Association of Military Surgeons of the US, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.
Coauthor(s)
Duane R Hospenthal, MD, PhD, Chief, Infectious Disease Service, Brooke Army Medical Center and Associate Professor, Department of Medicine, Uniformed Service University of Health Sciences
Duane R Hospenthal, MD, PhD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Association of Military Surgeons of the US, Infectious Diseases Society of America, International Society for Infectious Diseases, International Society of Travel Medicine, Medical Mycology Society of the Americas, and Sigma Xi
Disclosure: Merck Honoraria Speaking and teaching; Pfizer Honoraria Speaking and teaching
Medical Editor
Fred A Lopez, MD, Associate Professor and Vice Chair, Department of Medicine, Assistant Dean for Student Affairs, Louisiana State University School of Medicine
Fred A Lopez, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, Infectious Diseases Society of America, and Louisiana State Medical Society
Disclosure: Nothing to disclose.
Pharmacy Editor
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.
Managing Editor
Charles V Sanders, MD, Edgar Hull Professor and Chairman, Department of Internal Medicine, Professor of Microbiology, Immunology and Parasitology, Louisiana State University School of Medicine at New Orleans; Medical Director, Medicine Hospital Center, Charity Hospital and Medical Center of Louisiana at New Orleans; Consulting Staff, Ochsner Medical Center
Charles V Sanders, MD is a member of the following medical societies: Alliance for the Prudent Use of Antibiotics, Alpha Omega Alpha, American Association for the Advancement of Science, American Association of University Professors, American Clinical and Climatological Association, American College of Physician Executives, American College of Physicians, American Federation for Medical Research, American Foundation for AIDS Research, American Geriatrics Society, American Lung Association, American Medical Association, American Society for Microbiology, American Thoracic Society, American Venereal Disease Association, Association for Professionals in Infection Control and Epidemiology, Association of American Medical Colleges, Association of American Physicians, Association of Professors of Medicine, Infectious Disease Society for Obstetrics and Gynecology, Infectious Diseases Society of America, Louisiana State Medical Society, Orleans Parish Medical Society, Royal Society of Medicine, Sigma Xi, Society of General Internal Medicine, Southeastern Clinical Club, Southern Medical Association, Southern Society for Clinical Investigation, and Southwestern Association of Clinical Microbiology
Disclosure: Nothing to disclose.
CME Editor
Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.
Chief Editor
Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.