Skin is the first immune defense mechanism and functions as a barrier against microorganisms. Infections are a significant problem once open wounds compromise this barrier. According to the US National Burn Repository, the four leading causes of burn morbidity are pneumonia, cellulitis, urinary tract infections, and burn wound infections. Infections are a primary factor contributing to mortality, accounting for 51% of deaths in burn patients, as discussed in both Chapters 24 and 26 , on multisystem organ failure and critical care, respectively.

A cutaneous burn is initially sterile as commensal skin flora are killed with the skin in the thermal event. Unfortunately, the burn wound provides optimal bacterial growth conditions due to a reduced blood supply and a nutrient-rich environment, leading to rapid wound colonization.

Interestingly, in a recent porcine study of standard burn wounds, there was no difference in bacterial counts between wounds treated with negative-pressure wound therapy, silver sulfadiazine, or normal saline. These data further demonstrate the need for early wound excision and coverage.

The 2007 American Burn Association (ABA) Consensus Conference defined wound colonization as follows: (1) low concentrations of bacteria on the wound surface, (2) absence of invasive infection, and (3) less than 10 ⁵ organisms per gram of tissue. In a superficial burn, skin flora can survive in hair follicles and sebaceous glands in the same manner as keratinocytes to repopulate a physiologic microbiome. However, burns are customarily colonized by pathogens from the environment, the patient’s gut, or the nasooropharyngeal tract. Ladhani et al. have demonstrated poor specificity for identification of sepsis and septic shock in burn patients. They conclude the best approach is prevention (including wound care, early excision and grafting, antibiotic stewardship, nutrition) and a multidisciplinary support. Meze-Escobar demonstrated that the sepsis definitions in the Third International Consensus Definitions for Sepsis and Septic Shock have better sensitivity and specificity than the 2007 ABA consensus definitions. Ultimately, widely accepted definitions of burn wound infection and sepsis remain elusive, and further work is need to standardize research treatment and discussions. Indeed, Lee et al. found in a systemic review of definitions of burn wound infection 32 different definitions in 29 reviews, making data comparison impossible. This lack of effective definitions and diagnostic criteria to differentiate anticipated systemic inflammatory responses and sepsis continues to beset the field.

A race thus exists between the patient and the pathogen to dominate the wound surface. In the log phase growth, bacteria double two to three times per hour; consequently, a single bacterium can become 10 million in 1 day, far faster than any human cell can multiply. Therefore colonization can quickly become an infection capable of converting partial-thickness into full-thickness burns by causing vessel thrombosis and necrosis in viable tissues in the wound penumbra. Gram-positive bacteria tend to colonize an affected area first, with subsequent colonization by gram-negative bacteria. Delayed treatment risks colonization by extended-spectrum pathogens, bloodstream invasion, and the development of sepsis, all of which increase the likelihood of death.

The model of burn care advocated throughout this text is to rig the race for wound dominance in favor of the patient. Early wound excision eliminates the devitalized tissue that is the main reservoir for pathogen nourishment and habitat. Prompt autografting reestablishes skin barrier function and denies pathogens access to the host. Topical antimicrobials suppress bacterial growth and colony counts while allowing host fibroblasts and keratinocytes to proliferate and cover the wound. Assiduous washing technique allows 2-log reduction in colony counts, breaks down and removes biofilms, and purges the devitalized tissue that pathogens thrive upon. Systemic antimicrobials kill and suppress the invading pathogens accessing perfused areas of tissue. Quantitative wound culturing (QWC) enables effective diagnosis and directed application of the most efficacious antimicrobial with the lowest toxicity. Coordinated critical care, therapy, and nutrition ensure that the wounds have a sufficient supply of nutrients and immune cell–laden blood to clear pathogens, expand skin grafts, and reepithelialize wounds.

Prevention is the optimal way to minimize infection. Pathogens can be carried into or transmitted around the unit by staff, by visitors, or on equipment. Patients should have single rooms separated from other rooms by a door. Positive pressure in the rooms further aids in minimizing bacterial contamination. Patient rooms should undergo a daily cleaning in addition to deep cleaning upon patient discharge. This terminal cleaning should include washing the walls and ceiling and should be done 72 hours prior to admitting another patient to avoid the transfer of more virulent strains. Another important prevention measure is the use of contact precautions with all patients, including gowns and gloves. These items should be donned before entering and doffed prior to exiting the room, regardless of the bacteriologic status of the particular patient. Routine hand hygiene before and after patient interaction is also mandatory to prevent infection. Dressing materials, supplies, devices, and equipment must not be shared between patients. Bathing, showering, tubbing, mobile diagnostic equipment, and operating facilities should be decontaminated between each patient use. Furthermore, fomites, such as ties, rings, watches, and cell phones, should be prohibited because these are possible pathogen vectors. ^, Water and air filters ought to screen particles down to 0.2 and 0.3 μm, respectively, be changed monthly, and be cultured routinely as part of infection control monitoring. By maintaining these strict measures, transmission of infectious organisms between patients can be limited.

Diagnosis of burn infection in burn wounds can be complicated. The typical cytokine and immune cascades that create the typical presentations of infection known to all doctors are often initiated in the burn patient via the elaboration of damage- and pathogen-associated molecular patterns from burn wounds. This complicates diagnoses of infection and sepsis in the burn patient where clinical signs, such as elevated temperature or tachycardia, are normal components of burn pathophysiology (see Chapter 18 for more on hypermetabolism).

Early diagnosis of bloodstream infection in burn patients has been an issue of continuing research. Sadeq et al. performed a retrospective review of 100 pediatric burns over 20% total body surface area (TBSA) comparing events with positive blood cultures to negative cultures. They found a predictive value of bloodstream infection with spikes in heart rate and temperature in the preceding 24 hours with a sensitivity of only 57% and specificity of 44%. They also found that a combination of scored criteria can increase to 93% sensitivity and 81% specificity. In using such criteria, antibiotic stewardship may be improved, though it is as yet unclear if there would be an improvement in clinical outcomes.

Wound culturing remains a critical tool to guide the treatment of burn wounds and to determine what bacteria are colonizing therein. In patients with major burns, the wound usually becomes colonized 5 to 7 days postinjury. Because most initial infections in burn patients derive from endogenous bacteria flora, it is good clinical practice to perform initial wound cultures upon patient admission. This screening should include swabs of both sides of the groin and axilla as well as of the nose and throat. In addition, at each burn excision and whenever suspicion of invasive infection warrants, quantitative tissue cultures may be helpful.

Wound appearance and odor changes can help to diagnose wound colonization vs. wound infection ( Fig. 10.1 ). Kwei et al. described three main methods that exist for culturing a wound: qualitative (presence or absence of growth), semiquantitative (grading of the bacterial presence as scanty, few, moderate, or numerous), and quantitative (an absolute quantity is determined). ^, Swabs are useful but limited because they cannot distinguish between infection and colonization and are only accurate for the region sampled. These problems are mitigated by performing multiple tissue biopsies, which can reveal significant quantitative differences in different areas. Although quantitative cultures are more expensive, bacterial counts have been shown to correlate with histologic evidence of wound infection in approximately 80% of cases after biopsies are taken or after sterilization of the surface with antimicrobials. ^, Histologic examinations can be used to confirm invasive bacterial infection when counts exceed 10 organisms per gram of tissue. If histologic evidence of invasion is present, systemic antibiotics should be administered and the wound excised. ^{, ,}

Burn wound colonization. Flame burn to the left medial knee depicted postburn day 7. The eschar has degraded but is still present; however, the surrounding tissue is not cellulitic.

Studies by Robson and Krizek demonstrated that if burn wound colony counts from biopsies or after cleaning of the surface of the wound are greater than 10 ⁵ /g tissue, the graft survival rate is only 19%, whereas colony counts of less than 10 ⁵ /g tissue are associated with a 94% chance of graft survival. Sensitivities to available antibiotics, both systemic and topical, should instruct therapy. In the setting of resistant organisms, antibiotic synergy testing is advised. Thus the ultimate diagnosis of burn wound infection and the guidance of antimicrobials are directed by culture data.

In practice, the utility of quantitative culturing is limited by the time required for culture growth itself. Williams et al. demonstrated that improved outcomes for septic pediatric burn patients were best obtained by prompt antimicrobial drug administration and source control (as well as early recognition and resuscitation). In clinical practice, the operating surgeon must decide on wound viability and colonization based on experience and clinical judgment because it is impractical to delay source control for confirmatory data. As such, a practical approach is to excisionally treat burn wounds, as described in Chapter 10, while using semiquantitative cultures and patient response to guide postoperative antibiotic management.

Physical examination of the patient also provides valuable insight into the infectious nature of the burn wound. Burn wound erythema is a physiologic phenomenon produced sterilely by the liberation of inflammatory mediators from tissues surrounding the burn area and must not be confused with cellulitis. Normally, this erythema presents within 2 to 3 days of the burn injury and resolves by 1 week postburn ( Fig. 10.2 ). The best differential diagnosis comes from clinical palpation: erythema lacks significant induration or tenderness compared to an infectious process such as cellulitis.

Burn wound erythema. A hot oil scald burn on the lateral thigh is depicted with (A) surrounding erythema noted on postburn day 2. (B) Resolution of redness and healing on postburn day 12.

Cellulitis is a noninvasive infection of the tissues surrounding the burn wound. Cellulitis can be caused by a variety of pathogens. This infection is characterized by edema, hyperesthesia, erythema, induration, and tenderness detectable upon examination ( Fig. 10.3 ). The color of the wound contour and the odor from the wound may also raise suspicion of cellulitis. Furthermore, it can have a lymphangitic component. Particular attention should be given to patients who are elderly or diabetic because of the ease and speed with which infections progress in these populations. Cellulitic burn wounds benefit from systemic antimicrobials to cover likely causative agents in addition to standard burn treatments, such as topical antimicrobials or surgical excision and grafting. Progression of cellulitis despite antibiotics must always trigger suspicions of resistant organisms, such as methicillin-resistant Staphylococcus aureus (MRSA), and these organisms should be covered empirically.

Burn wound cellulitis. Cultures demonstrated Staphylococcus aureus . Clinical findings include increased pain, local inflammatory signs, and fever. Treatment includes systemic and topical antibiotics, excision, and autografting.

Graft ghosting (impetigo) is a wound infection that can cause late graft loss ( Fig. 10.4 ). This phenomenon can occur after spontaneous closure of a partial-thickness wound, following loss of previously adherent graft sites, and in skin donor sites. Characterized by multiple small abscesses, graft ghosting can lead to the complete destruction of the healed wound. The culprit typically responsible for this condition is S. aureus , particularly MRSA. The diagnosis is essentially clinical and can be confirmed by culturing. Treatment requires regular dressing changes, debridement of abscesses, local disinfection, and application of topical antimicrobials, such as mupirocin.

Burn wound impetigo. Right hand in a 13-year-old boy with 85% total body surface area burn, third degree to the hands shown (A) 4 months postburn at hospital discharge. (B) Three weeks later, the patient presented with reopening of the previously taken skin grafts to the hand and clinical impetigo. Cultures were positive for methicillin-resistant Staphylococcus aureus , and the patient was treated with vancomycin, mupirocin, and tub therapy.

Toxic shock syndrome (TSS) is a complication of severe soft tissue infection (SSTI), which occurs predominately in small burns. This syndrome results from colonization with TSS toxin-1–producing S. aureus . This disease is primarily seen in young children with burns covering less than 10% of the TBSA and that would otherwise be expected to heal without problems. The incidence is approximately 2.6% with a mean age of 2 years. TSS is clinically characterized by a prodromal period lasting 1 to 2 days with pyrexia, diarrhea, vomiting, and malaise. Although a rash is often present, at this stage the burn appears clean ( Fig. 10.5 ). Shock subsequently develops in untreated cases, but determining the cause of shock to be TSS can be complicated in this early phase of the patient’s presentation when a litany of potential and more common etiologies of shock exists. Once shock has developed, mortality can be as high as 50%. Awareness and aggressive action are the principal safeguards against the development and progression of TSS. A possible diagnosis of TSS should be considered in small burns when the patient is unexpectedly in shock. Because MRSA has emerged as the most commonly identified cause of SSTI, initiation of empiric anti-MRSA antimicrobials is warranted in all cases of suspected TSS. ^,

Toxic shock syndrome (TSS) rash. Cutaneous rash commonly seen in patients with TSS. This rash does not universally appear in cases of TSS. Patients with small burns developing shock should be evaluated and treated for TSS with excision, grafting, and vancomycin. (A) A 13-year-old girl presenting TSS rash following a 10% total body surface area burn. (B) The typical macular erythroderma lesions. (C) A hematoxylin and eosin (H&E) 4× magnification micrograph of a TSS rash lesion showing an epidermal blister. (D) Further H&E 40× magnification micrograph with low inflammation.

(From Omar P. Sangüeza, MD; Professor and Director of Dermatopathology, Wake Forest University School of Medicine, North Carolina.)

Invasive wound infections manifest clinically with wound color changes, exudate, and odor. Within a short time, partial-thickness burns progress to full-thickness necrosis and begin expanding into unburned tissues. The 2007 ABA Consensus Conference defined invasive infections as follows: “the presence of pathogens in a burn wound at concentrations sufficient in conjunction with depth, surface area involved, and age of patient, to cause suppurative separation of eschar or graft loss, invasion of adjacent unburned tissue or cause the systemic response of sepsis syndrome.” Goal-standard diagnosis is made with histologic examination; however, clinical exam and quantitative cultures usually suffice ( Fig. 10.6 ). It should be noted that sepsis does not always develop during invasive infections ( Fig. 10.7 ). Treatment must be immediate and include aggressive surgical intervention augmented by the administration of systemic and topical antimicrobials. If no culture results are initially available, then a broad-spectrum empirical therapy against fungi and drug-resistant gram-positive and-negative organisms should be initiated until culture data become available. As discussed earlier, these definitions have been demonstrated to be somewhat inadequate in multiple series, but a standard replacement has not yet gained broad acceptance. Surgical extirpation must be aggressive and encompass excision of all necrotic and infected tissue, including fascia and muscle when warranted. Definitive wound coverage is not always indicated in this extirpative operation as dressing changes and hydrotherapy may be needed to further decrease heavy bacterial loads. In cases where tissue has already been excised or there is a life-threatening infection, limb amputation may be indicated. Topical antimicrobials and assiduous washing technique are indicated after extirpation to suppress microbial growth; however, the optimal methodology is to prevent infection, with swift action being taken should an infection arise.

Gram-negative bacilli invading deep viable tissue. Histopathologic confirmation is the gold standard test to diagnose burn wound infection by bacteria in viable tissue. Shown is a typical hematoxylin and eosin–stained section at 1000× magnification.

Invasive burn wound infection. This patient has 75% total body surface area full-thickness burns with wound sepsis due to Enterococcus faecalis and Enterobacter cloacae . Prompt excision, homografting, hemodynamic support, and systemic antibiotics controlled the infection. This patient was subsequently autografted and survived.

Sepsis and septic shock are complicated diagnoses in burn patients because large burns create a systemic inflammatory response syndrome (SIRS) and hypermetabolism of their own (see Chapter 7 on the etiology of shock). This hypermetabolism is a natural part of the body’s compensatory mechanism to burn injury and can last for up to 1 year following the insult, making it difficult to fit shock in burn patients into the definitions of sepsis and septic shock established by the Society of Critical Care Medicine. Patients with high concentrations of bacteria in the burn wounds in conjunction with delayed admission to a burn center or delayed removal of burned tissues are at the greatest risk of developing sepsis. Rapid and complete closure of deep burns is the best defense against this condition. An additional factor influencing the development of sepsis and increasing mortality during hospitalization in patients with equal burn sizes is decreased lean body mass. The identification of parameters associated with sepsis in burn patients is extremely important and ongoing. The 2007 ABA Consensus Conference provided criteria ( Box 10.1 ). These criteria are useful markers and indicators for sepsis but are by no means gospel. A skilled physician must take these factors into account along with changes in the patient’s clinical condition over time to make a presumptive diagnosis of sepsis. Aggressive treatment should be initiated and deescalated based on definitive diagnosis and patient response.

There are no objective laboratory tests to differentiate between inflammatory versus septic shock. To this day, white blood cell count is the most commonly monitored value to provide this insight, though it has low sensitivity and specificity. Procalcitonin (PCT) and C-reactive protein (CRP) are increasingly accepted markers in clinical use as predictors of sepsis in postoperative burn patients. Hassan performed a systematic review of 15 manuscripts finding that both CRP and PCT increase then gradually decrease after burn injury. In the setting of burn wound infection, both continue to rise, and PCT was found to be more reliable than CRP. In another study, it was demonstrated that CRP to albumin ratio at admission was an independent risk factor for sepsis and prognosis in severe burns. Recent multiomic analysis by Huang et al. evaluating genomic, proteomic, and transcriptomic responses in 60 severe burn patients has identified seven novel biomarkers as early warning signs in severe burn–associated sepsis. The protein S100A8 has both warning and therapeutic effects. Further studies continue to develop biomarkers and objective diagnostic panels, but there remains no accepted standard.

Treatment of burn wound infections is multimodal. Surgical debridement and assiduous washing technique decrease the bacterial and nutritive burden. Aggressive grafting denies the pathogens wound surface area to colonize and infect. Topical antimicrobial compounds reduce pathogen burden in the wound and periwound areas while allowing skin grafts to proliferate and cover the wound. Systemic antimicrobials are administered to treat invasive pathogens and prevent or reduce the systemic spread of infection.

S. aureus, gram-positive cocci in clusters, remains the chief cause of burn wound infection and is a well-documented opportunistic pathogen in humans. ^, Colonization with these bacteria in an uninjured individual is usually asymptomatic, but they are a source of opportunistic infection that can lead to severe illness and death, especially in burn patients. Staphylococcus produces virulence factors, such as proteinases, coagulases, and hyaluronidases, that enable it to invade local tissues and disseminate hematogenously, causing generalized systemic infection and sepsis. The most common infections of Staphylococcus spp. are septicemia, cellulitis, impetigo, scalded skin syndrome, and postoperative wound infections. However, puerperal sepsis, pneumonia, osteomyelitis, endocarditis, and burn wound infection are the gravest. Exotoxins, which are produced by pathogenic strains of staphylococci, include a pyrogenic toxin, a dermonecrotizing toxin, and leukocidin. In addition to the exotoxin TSST-1, these organisms can produce enterotoxins A, B, and C, risk factors for TSS in susceptible patients. Staphylococcus spp. generally produce penicillinases that make natural penicillins ineffective and thus require treatment with penicillinase-resistant penicillins, such as oxacillin. MRSA is now the predominant isolate, with rates of infection greater than 50% in burn units. ^, Empiric coverage should be vancomycin for IV therapy or Bactrim and rifampin orally, as detailed earlier, based on the local antibiogram and patient cultures.

Streptococci were once the leading cause of burn wound infection but are now less prevalent. Arranged in chains, these gram-positive cocci are particularly virulent when infecting a burn wound and quantitatively do not require less than 10 ⁵ colony-forming units (CFU)/g of tissue to prevent wound closure. A mere few β-hemolytic streptococci can cause wound infection, failure of a primary closure, and loss of a skin graft. The major infecting species are Streptococcus pyogenes (also referred to as group A streptococci and the most problematic) and S. agalactiae (group B streptococci). Natural penicillins, such as penicillin G and penicillin V, and first-generation cephalosporins are bactericidal to these species. While resistance to these penicillins or cephalosporins has not yet emerged, culture and antibiotic sensitivity data should be followed.

Enterococci are important inciters of gram-positive burn wound infection. Encouragingly, a recent review comparing sepsis mortality between consecutive decades (1989–1999 and 1999–2009) found a steep decline in the rate of infection with enterococci (25%–2%), perhaps stemming from the more liberal use of vancomycin in recent years. However, with the increasing prevalence of VRE, mortality rates from VRE are now greater than those of MRSA (58% and 33%, respectively). While most Enterococcus spp. respond to vancomycin, VRE is treated with linezolid, a combination of ampicillin and aminoglycosides, or quinupristin/dalfopristin (Synercid). Deescalation is advised as soon as indicated by culture data.

Pseudomonas is not just the most ubiquitous gram-negative burn wound pathogen, but also the most likely to be responsible for sepsis leading to burn-related death. ^, Both local environments and gastrointestinal tracts (via translocation of endogenous gastrointestinal flora) are believed to be the primary sources of this bacterium. This species has a predilection for moist environments, and human burn wound exudates have been shown to stimulate the expression of virulence factors of P. aeruginosa , the pathogen chiefly responsible for nosocomial respiratory tract infections. Additionally, it breeds invasive and troublesome wound infections in burn patients. A superficial wound infection caused by P. aeruginosa typically will have a yellow-green color and noxious fruity smell. This may become an invasive infection, ecthyma gangrenosum, causing purplish-blue, punched-out lesions in the skin; if local thrombosis of vessels is present, then the wound requires immediate treatment to remove newly necrotic tissues ( Fig. 10.8 ). Empiric treatment for P. aeruginosa infection has evolved from aminoglycosides to antipseudomonal β-lactams, such as piperacillin/tazobactam, cefepime, and carbapenems. The increasing prevalence of MDRO P. aeruginosa requires the expanding use of antibiotics based on culture data, employment of fifth-generation cephalosporins, use of synergistic antibiotic coverage, and use of colistimethate (see Systemic Antimicrobials in Burn Patients, earlier). This rapidly evolving and virulent pathogen is best eradicated by rapidly closing wounds to deny the bacterium access to any susceptible wound surface.

Ecthyma gangrenosa. A tissue-invasive burn wound infection here seen in a 7-year-old girl transferred to our hospital after a 6-week treatment at another hospital. (A) Note the extensive greenish and slime-coated wound consistent with an invasive wound infection. The patient died subsequently from an overwhelming hematogenously spread pneumonia. (B) The vessel wall at 40× magnification micrograph shows a clear bacterial infiltration. (C) A typical purplish ecthyma gangrenosa lesion in a 35-year-old man.

(C, From Omar P. Sangüeza, MD; Professor and Director of Dermatopathology, Wake Forest University School of Medicine, North Carolina.)

Acinetobacter spp. are gram-negative rods used commercially to convert wine to vinegar and are native flora of the respiratory tract, skin, gastrointestinal tract, and genitourinary tract. This organism may lead to numerous opportunistic infections, including pneumonia and infections of the surgical site and urinary tract. Second only to P. aeruginosa in prevalence, this pathogen has an enhanced capacity for transfer between patients due to its ability to survive in both dry and wet conditions and equally on animate and inanimate objects, whether metal or plastic, making nosocomial transmission a major concern. ^, Acinetobacter spp. have been isolated from diverse clinical sources, including the upper and lower respiratory tracts, the urinary tract, and surgical and burn wounds, as well as in bacteremias secondary to IV catheterization. An agent of low virulence, it has a predilection for infecting patients with dysfunctional host defense mechanisms. Although traditionally susceptible to ceftazidime and ciprofloxacin, Acinetobacter has developed resistance to such an extent that only carbapenems (e.g., imipenem and meropenem) can now be relied on to treat these infections. In cases of MDRO Acinetobacter , colistin has become the rescue treatment, as with Pseudomonas infections. ^,

Stenotrophomonas maltophilia (also known as P. maltophilia or Xanthomonas maltophilia ) is an aerobic gram-negative bacillus responsible for nosocomial infections in immunocompromised patients. Increasingly reported in burn patients, this pathogen causes life-threatening infections that are very difficult to clear due to the particularly obturant biofilm Stenotrophomonas produces. Additionally, S. maltophilia is inherently resistant to a variety of antimicrobial agents, such as aminoglycosides, β-lactam agents, and carbapenems. The most common types of infections caused by S. maltophilia are wound and bacteremia; pneumonia and generalized infections associated with this pathogen are less common. ^, Infections are sensitive to trimethoprim-sulfamethoxazole alone or used with levofloxacin, and sensitivities should be monitored. Aggressive surgical excision and assiduous washing technique with soap and water are vital to combat the resultant biofilm.

Enterobacteriaceae, such as E. coli , Klebsiella spp., Enterobacter spp., Serratia marcescens , and Proteus spp., are often revealed as the cause of burn wound infections and other nosocomial infections in burn patients. Although these pathogens have greater sensitivity to antibiotics than other gram-negative bacteria, emerging resistance patterns to carbapenems and fourth-generation cephalosporins led to a larger array of MDRO and PDRO. Carbapenem-resistant Enterobacteriaceae are increasing in incidence and in many cases require treatment with colistin.

Anaerobic bacteria, such as Bacteroides spp. and Fusobacterium spp., are rarely a cause of invasive burn infection. These bacteria are normal flora from the oropharyngeal cavity to the gastrointestinal tracts. Anaerobic flora are responsible for 2% to 5% of surgical wound infections in the oropharyngeal area ^, and 10% to 15% of wound infections in the gastrointestinal and urogenital tracts. In burn patients, anaerobic infections are usually associated with avascular myonecrosis secondary to electrical injuries, frostbite, or cutaneous flame burns with concomitant crush-type injuries. With the advent of early excision and grafting, the incidence of anaerobic infections in thermal injury has been reduced significantly. If anaerobic infection is suspected, it is vital that collected specimens be placed in appropriate transport tubes void of oxygen. In these cases, broad-spectrum antibiotics covering anaerobes should be given until sensitivities are available to ensure the administration of the appropriate drug. ^,

Fungal wound infection and colonization have become increasingly prevalent following the introduction of topical antibacterials and liberal use of broad-spectrum antibiotics. This has resulted in a surge in invasive fungal infection linked to higher death rates, regardless of the extent of the burn, coincident inhalation injury, or patient age. In a recent review of 15 burn units, fungi were isolated at least once from 6.3% (435/6918) of patients, with positive cultures being most commonly obtained from the wound itself followed by (in order of decreasing frequency) respiratory, urine, and blood specimens. Yeasts are identified primarily on the basis of specific biochemical tests, but both macroscopic and microscopic morphologies are also used to make final identification ( Fig. 10.9 ). Mold identification is based on growth rate, colony structure, microscopic appearance, dimorphism at different incubation temperatures, and inhibition of growth by cycloheximide, as well as various biochemical tests ( Fig. 10.10 ).

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