Pseudomonas aeruginosa is the most common pathogen of burn wound infection. It can encode a variety of virulence factors and is highly pathogenic, which can lead to poor prognosis and high mortality. In order to research a new method to combat Pseudomonas aeruginosa infection, researchers have observed a wide range of interactions between the bacteriophages and the host. Bacteriophages influence and even dominate the structure, movement, and metabolism of host bacteria through a variety of mechanisms, catalyze the evolution of the host, and are also an important factor in host environmental adaptability and pathogenicity. In this paper, the interaction between Pseudomonas aeruginosa bacteriophages and the host is reviewed from the single cell level and the population level. Understanding these interactions could provide new idea for the treatment of Pseudomonas aeruginosa clinical infections, provides a basis for future development of antimicrobial agents and guides the treatment of burn infections.
Bacteriophages ; Burns/therapy* ; Humans ; Pseudomonas Infections/microbiology* ; Pseudomonas Phages ; Pseudomonas aeruginosa ; Virulence Factors

Objective: To investigate the application and clinical efficacy of ultrasound debridement method in residual burn wounds. Methods: A retrospective cohort study was conducted. From August 2017 to August 2021, 64 patients with residual burn wounds who met the inclusion criteria were admitted to the 980^th Hospital of the Joint Logistic Support Force of PLA. According to the debridement method adopted for the residual wounds, the patients were divided into ultrasound debridement group (34 cases, 22 males and 12 females, aged (31±13) years) and traditional debridement group (30 cases, 19 males and 11 females, aged (32±13) years). After the corresponding debridement, the wounds of patients in the two groups were selected for stamp skin grafting or large skin grafting according to the wound site and skin donor status. For unhealed wounds after stage Ⅰ surgery, secondary debridement and skin grafting were be performed, with the wound debridement methods in the 2 groups being the same as those of stage Ⅰ, respectively. On postoperative day 3, drug-sensitive test was used to detect the bacteria in the wound and the positive rate of bacteria was calculate. On postoperative day 7, the survival rate of skin slices in wound and the incidence of subcutaneous hematoma were calculated. At discharge, wound healing time and debridement times of patients were counted, and the secondary debridement rate was calculated. Data were statistically analyzed with independent sample t test or chi-square test. Results: On postoperative day 3, the wounds in ultrasound debridement group were infected with Staphylococcus aureus in 2 cases and Pseudomonas aeruginosa in 2 cases, and the wounds in traditional debridement group were infected with Staphylococcus aureus in 5 cases, Pseudomonas aeruginosa in 3 cases, Acinetobacter baumannii in 1 cases, Klebsiella pneumoniae in 1 cases, and Enterobacter cloacae in 1 cases. The positive rate of bacteria of wound in ultrasound debridement group was significantly lower than that in traditional debridement group (χ²=5.51, P<0.05). On postoperative day 7, the survival rate of skin grafts in ultrasound debridement group was (92±5) %, which was significantly higher than (84±10) % in traditional debridement group (χ²=6.78, P<0.01); the incidence of subcutaneous hematoma in ultrasound debridement group was 17.6% (6/34), which was significantly lower than 40.0%( 12/30) in traditional debridement group, χ²=3.94, P<0.05. At discharge, the wound healing time in ultrasound debridement group was (11.0±2.0) d, which was significantly shorter than (13.0±3.1) d in traditional debridement group (t=3.81, P<0.01); the secondary debridement rate of wounds in ultrasound debridement group was 2.9% (1/34), which was significantly lower than 20.0% (6/30) in traditional debridement group (χ²=4.76, P<0.05). Conclusions: Ultrasound debridement method can significantly reduce the bacterial load of residual burn wounds, reduce postoperative hematoma formation, and promote the survival of skin grafts to shorten the course of disease of patients.
Male ; Female ; Humans ; Debridement/methods* ; Retrospective Studies ; Treatment Outcome ; Bacteria ; Burns/microbiology* ; Hematoma

The incidence and mortality of infective endocarditis (IE) in patients with severe burn remain high, which are attributed to invasive procedures, bacteremia, and wound infection after burns. Clinical clues for IE in burns are usually masked by burn-related manifestations, so the diagnosis of IE may be delayed or missed. For burned patients with persistent bacteremia of unknown source, especially Staphylococcus aureus-induced bacteremia, the diagnosis of IE should be considered according to the Duke criteria, and early echocardiography performance is particularly important. Antibiotic therapy is the mainstay initial management, and early surgical intervention is strongly recommended once IE is clearly diagnosed in patients with burns. In order to lower the incidence and mortality of IE in burns, it is very important to take prophylactic procedures along with the whole course of burn management.
Bacteremia ; epidemiology ; Burn Units ; Burns ; complications ; mortality ; surgery ; Endocarditis, Bacterial ; complications ; diagnosis ; microbiology ; mortality ; Humans ; Incidence ; Severity of Illness Index ; Staphylococcal Infections ; complications ; diagnosis ; Staphylococcus aureus ; isolation & purification ; Surgery, Plastic ; Wound Infection ; etiology ; mortality

Wound sepsis is one of the main causes of death in patients with severe burn and trauma. The high incidence of burn wound sepsis in children is attributed to their imperfect immune system function, poor resistance against infection, and the weakened skin barrier function after burn. The key to reduce the mortality of pediatric patients with burn wound sepsis is to enhance the understanding of its etiology, epidemiology, pathogenesis, and diagnostic criteria, in order to improve its early diagnosis and treatment.
Burns ; complications ; prevention & control ; therapy ; Child ; Humans ; Sepsis ; diagnosis ; etiology ; mortality ; therapy ; Skin ; microbiology ; pathology ; Survival Rate ; Wound Infection ; mortality ; prevention & control ; therapy

OBJECTIVETo study the drug resistance of Acinetobacter baumannii (AB) producing VIM-2-type metallo-β-lactamase (MBL) isolated from burn patients of our ward against carbapenem antibiotics and its homology.

METHODSA total of 400 strains of AB (identified) were isolated from sputum, urine, blood, pus, and wound drainage. of burn patients hospitalized in our ward from September 2011 to March 2014. Drug resistance of the 400 strains of AB to 15 antibiotics, including compound sulfamothoxazole, aztreonam, etc. , was tested using the automatic microorganism identifying and drug sensitivity analyzer. Among the carbapenems-resistant AB isolates, modified Hodge test was applied to screen carbapenemase-producing strains. The carbapenemase genes of the carbapenemase-producing strains, and the mobile genetic elements class I-integron (Intl1) gene and conserved sequence (CS) of carbapenemase-producing strains carrying blaVIM-2 gene were determined with PCR and DNA sequencing. For carbapenemase-producing strains carrying blaVIM-2 gene, synergism test with imipenem-ethylene diamine tetraacetic acid (EDTA) and enhancement test with imipenem-EDTA and ceftazidime-EDTA were used to verify the MBL-producing status. Drug resistance of the VIM-2-type MBL-producing AB strains was analyzed. For VIM-2-type MBL-producing AB strains, plasmid conjugation experiment was used to explore the transfer of plasmid; outer membrane protein (OMP) CarO gene was detected by PCR. For VIM-2-type MBL-producing AB strains carrying CarO gene, the protein content of CarO was analyzed with sodium dodecyl sulfate polyacrylamide gel electro- phoresis. The repetitive consensus sequence of Enterobacteriaceae genome PCR (ERIC-PCR) was carried out for gene typing of VIM-2-type MBL-producing AB strains to analyze their homology.

RESULTS(1) The resistant rates of the 400 strains of AB against levofloxacin and compound sulfamethoxazole were low. A total of 381 carbapenems-resistant AB strains were screened, including 240 carbepenemase-producing strains. (2) Out of the 240 carbepenemase-producing strains, 18 strains were found to harbor the blaVIM-2 gene, accounting for 7.5%; 133 strains carried the blaTEM-1 gene, accounting for 55.42%; 195 strains carried the blaOXA23 gene, accounting for 81.25%; 188 strains carried the bla(armA) gene, accounting for 78.33%. (3) Eighteen carbepenemase-producing strains which carried the bla(VIM-2) gene were found to carry the Intl1 gene, showing the Intl1-VIM linkage. Simultaneously, Intl1 variable area CS showed diversity. (4) Eighteen carbepenemase-producing strains which carried the blaVIM-2 gene were verified to produce MBL. The resistant rates of the 18 strains of AB against compound sulfamethoxazole were the lowest, followed by levofloxacin and cefoperazone/sulbactam, and those against the other antibiotics were above 60.00%. (5) Through multiple joint tests, plasmid conjugation experiment positive transfer strain was not found in 18 VIM-2-type MBL-producing AB strains. (6) Nine out of the 18 VIM-2-type MBL-producing AB strains were found to carry CarO gene. The OMP CarO of VIM-2-type MBL-producing AB strains carrying CarO gene was lost or lowered in the protein content. (7) The 18 VIM-2-type MBL-producing AB strains were classified into 6 genotypes by the ERIC-PCR. There were respectively 6, 4, 3, and 1 stain (s) in genotypes A, B, C, and F, and there were 2 strains in genotypes D and E respectively.

CONCLUSIONSThe resistance mechanism of AB against carbapenems is mainly mediated by blaTEM-1, blaOXA-23, and bla(arma); meanwhile, VIM-2-type MBL-producing and lack or change in OMP CarO are attributable to carbapenems resistance of clinically isolated AB from burn wards, and the Intl1 gene may take a part in blaVIM-2 gene transmission.

Acinetobacter baumannii ; drug effects ; enzymology ; genetics ; isolation & purification ; Anti-Bacterial Agents ; pharmacology ; therapeutic use ; Bacterial Proteins ; Burns ; drug therapy ; microbiology ; Carbapenems ; pharmacology ; Drug Resistance, Bacterial ; Genes, Bacterial ; Humans ; Imipenem ; pharmacology ; Microbial Sensitivity Tests ; Sulbactam ; pharmacology ; beta-Lactamases ; genetics

OBJECTIVETo analyze the detection, drug resistance, and status of infection of Acinetobacter baumannii (AB) in burn ICU during 3 years.

METHODSA total of 2 010 specimens of wound secretion, blood, venous catheter attachment, sputum, stool and urine were collected from 505 burn patients hospitalized in our burn ICU from January 2011 to December 2013, and bacterial culture was performed. Pathogens were identified by automatic microorganism identifying and drug sensitivity analyzer. Drug resistance of all the obtained AB to 16 antibiotics commonly used in clinic, including cefoperazone/sulbactam, polymyxin, etc., was tested with K-B paper disk diffusion method. Patients with AB infection were ascertained. The WHONET 5.6 software was used to analyze the distribution of pathogens during 3 years, the isolation of AB with different sources and the status of drug resistance of AB to 16 antibiotics each year, and the status of patients with AB infection, and their outcome.

RESULTSA total of 961 strains of pathogens were isolated, among which 185 (19.25%) strains were Gram positive cocci, 728 (75.75%) strains were Gram negative bacilli, and 48 (4.99%) strains were fungi. A total of 172 strains of AB were isolated, ranking the second place among all the detected pathogens, with 67 (38.95%) strains from wound secretion, 11 (6.40%) strains from blood, 23 (13.37%) strains from venous catheter attachment, and 71 (41.28%) strains from sputum, no AB strain was isolated from feces or urine. The AB strains were found sensitive to polymyxin and with relatively low drug resistance rate to minocycline, while the drug resistance rates were over 80.0% to the other 14 antibiotics commonly used in clinic in 2013. AB culture of wound secretion was positive in 27 patients. Among them, 7 patients suffered from wound infection, and the wound infection was caused by AB in 1 out of the 7 patients. AB culture of blood was positive in 7 patients. Among them, 3 patients suffered from bloodstream infection, and the infection was due to AB invasion in 1 out of the 3 patients. AB culture of venous catheter attachment was positive in 20 patients. Among them, 8 patients suffered from bloodstream infection, and the infection was due to AB invasion in 1 out of the 8 patients. AB culture of sputum was positive in 35 patients. Among them, 13 patients suffered from ventilatory associated pneumonia, and 2 out of the 13 patients were diagnosed as AB infection. A total of 69 patients were AB culture positive, among them 64 patients were cured, 2 patients were transferred to other hospitals, and 3 patients died, with the mortality rate of 4.35%.

CONCLUSIONSAB in our burn ICU has a high detection rate and extensive drug resistance in above-mentioned 3 years. However, AB was mainly colonized in patients with extensive burns with a low mortality rate.

Acinetobacter Infections ; drug therapy ; epidemiology ; microbiology ; Acinetobacter baumannii ; drug effects ; isolation & purification ; Anti-Bacterial Agents ; pharmacology ; Burns ; microbiology ; Cross Infection ; Drug Resistance ; Gram-Negative Bacteria ; isolation & purification ; Humans ; Intensive Care Units ; Microbial Sensitivity Tests

The emergence and spread of carbapenems-resistant Klebsiella pneumoniae (CRKP) in burn ward is an important threat to burn management. CRKP isolates are resistant to almost all available antibiotics and are susceptible only to polymyxins and tigecycline. The mechanism of the drug resistance of CRKP is associated with the plasmid-encoded carbapenemase Klebsiella pneumoniae carbapenemase (KPC), a carbapenem-hydrolyzing β-lactamase. Antibiotics which can currently be used to treat CRKP infection include polymyxins, tigecycline, and some aminoglycosides. The efficacy of using antibiotics in combination is better than that of single-agent therapy for the treatment of CRKP infection in bloodstream. In order to control CRKP infection in burn patients, strategies for preventing CRKP dissemination in burn ward are strongly advocated.
Anti-Bacterial Agents ; therapeutic use ; Bacterial Proteins ; Burns ; drug therapy ; Carbapenems ; pharmacology ; Drug Resistance, Bacterial ; Humans ; Klebsiella Infections ; drug therapy ; microbiology ; prevention & control ; Klebsiella pneumoniae ; drug effects ; Microbial Sensitivity Tests ; Minocycline ; analogs & derivatives ; therapeutic use ; beta-Lactam Resistance ; beta-Lactamases

BACKGROUND: Burn wounds lack normal barriers that protect against pathogenic bacteria, and burn patients are easily colonized and infected by Staphylococcus aureus. Toxic shock syndrome (TSS) is a rare but fatal disease caused by S. aureus. A lack of detectable antibodies to TSS toxin-1 (TSST-1) in serum indicates susceptibility to TSS. METHODS: A total of 207 patients (169 men and 38 women; median age, 42.5 yr) admitted to a burn center in Korea were enrolled in this study. The serum antibody titer to TSST-1 was measured by sandwich ELISA. S. aureus isolates from the patients' nasal swab culture were tested for TSST-1 toxin production by PCR-based detection of the TSST-1 toxin gene. RESULTS: One hundred seventy-four (84.1%) patients showed positive results for antibody against TSST-1. All patients aged > or =61 yr (n=28) and <26 months (n=7) were positive for the anti-TSST-1 antibody. S. aureus was isolated from 70 patients (33.8%), and 58.6% of the isolates were methicillin resistant. Seventeen patients were colonized with TSST-1-producing S. aureus. The antibody positivity in these 17 carriers was 88.2%, and the positivity in the non-carriers was 83.7%. CONCLUSIONS: Most burn patients had antibody to TSST-1, and nasal colonization with TSST-1-producing S. aureus was associated with positive titers of anti-TSST-1 antibody. Additionally, patients with negative titers of anti-TSST-1 antibody might be susceptible to TSS.
Adolescent ; Adult ; Aged ; Aged, 80 and over ; Antibodies, Bacterial/*blood ; Bacterial Toxins/genetics/immunology/*metabolism ; Burns/blood/*immunology/*microbiology/pathology ; Child ; Child, Preschool ; Enterotoxins/genetics/immunology/*metabolism ; Enzyme-Linked Immunosorbent Assay ; Female ; Humans ; Infant ; Male ; Middle Aged ; Nasal Cavity/microbiology ; Polymerase Chain Reaction ; Prevalence ; Staphylococcal Infections/epidemiology ; Staphylococcus aureus/isolation & purification/*metabolism ; Superantigens/genetics/immunology/*metabolism ; Young Adult

OBJECTIVETo investigate the genotype of staphylococcal chromosomal cassette mec (SCCmec) in methicillin-resistant Staphylococcus aureus (MRSA) isolated from burn wards and its current status of drug resistance.

METHODSOne hundred and seventy-nine strains of Staphylococcus aureus were isolated from wound excretion, blood, and sputum samples of patients that were admitted to ICU or public wards of our Department of Burns and Plastic Surgery from September 2012 to September 2013. Among them, 68 strains were from ICU and 111 strains from public wards. The MRSA phenotype of Staphylococcus aureus was detected with cefoxitin K-B disk diffusion method, and the isolation rates of MRSA in ICU and public wards were compared. Genotyping of SCCmec was performed by PCR in strains of MRSA. In the meantime, the identification result of MRSA by K-B method was verified through detecting methicillin-resistant determinant mecA. The antimicrobial resistance of MRSA and methicillin-sensitive Staphylococcus aureus (MSSA) to 23 kinds of commonly used antibiotics in clinic were detected by K-B disk diffusion method. Except for the antibiotics to which the resistant rates of MRSA were 100.0% or 0, the resistant rates of SCCmecIII MRSA and non-SCCmec III MRSA to the rest of antibiotics were compared. Data were processed with Pearson chi-square test or corrected chi-square test.

RESULTSOne hundred and forty-eight strains out of the 179 Staphylococcus aureus were identified as MRSA (accounting for 82.7%), among which 62 were originated from ICU and 86 from public wards. The rest 31 strains of Staphylococcus aureus were MSSA, accounting for 17.3%. The percentage of MRSA in the isolated Staphylococcus aureus was 91.2% (62/68) in ICU, which was significantly higher than that in the public wards [77.5% (86/111), χ2 = 5.526, P = 0.019]. PCR detection showed that the 148 strains of MRSA harbored the mecA gene, out of which 106 strains were SCCmec III positive, accounting for 71.6%. The percentages of SCCmec III type MRSA in MRSA isolated from ICU and public wards were respectively 72.6% (45/62) and 70.9% (61/86), showing no statistically significant difference (χ2 = 0.048, P = 0.826). The 148 strains of MRSA were 100.0% resistant to a total of 8 kinds of antibiotics including penicillin and cephalosporins, but it was 0 for vancomycin, teicoplanin, linezolid, tigecycline, nitrofurantoin, and quinupristin/dalfopristin. Except for the 6 kinds of antibiotics to which the resistant rates of MRSA and MSSA were 0, resistant rates of MRSA to the remaining 17 kinds of antibiotics were significantly higher than those of MSSA (with χ2 values from 4.091 to 138.546, P < 0.05 or P < 0.01). Resistant rates of the 106 strains of SCCmecIII type MRSA to levofloxacin, ciprofloxacin, rifampicin, tetracycline, erythrocin, lincomycin, gentamicin, clindamycin were respectively 56.6% (60/106), 85.8% (91/106), 89.6% (95/106), 86.8% (92/106), 84.9% (90/106), 78.3% (83/106), 92.5% (98/106), 74.5% (79/106), and they were significantly higher than those of the 42 strains of non-SCCmec III type MRSA [33.3% (14/42), 61.9% (26/42), 71.4% (30/42), 66.7% (28/42), 69.0% (29/42), 57.1% (24/42), 71.4% (30/42), 52.4% (22/42), with χ2 values from 4.801 to 11.377, P < 0.05 or P < 0.01].

CONCLUSIONSIsolation rate of MRSA from burn wards in our hospital is high, and drug resistance status of this strain against antibiotics is very serious. SCCmec III is the major genotype of the isolated MRSA, but no strains resistant to the glycopeptide antibiotics are found.

Anti-Bacterial Agents ; pharmacology ; Burns ; microbiology ; Drug Resistance, Bacterial ; genetics ; Drug Resistance, Multiple ; Genes, Bacterial ; genetics ; Genotype ; Humans ; Methicillin-Resistant Staphylococcus aureus ; drug effects ; genetics ; isolation & purification ; Microbial Sensitivity Tests ; Staphylococcal Infections ; drug therapy ; epidemiology

OBJECTIVETo investigate the effects of recombinant human granulocyte macrophage colony-stimulating factor (rhGM-CSF) on wound healing and microRNA expression in diabetic rats.

METHODSEighteen male SD rats of clean grade were used to reproduce diabetes model. Four weeks later, a total of 64 full-thickness skin wounds were created on the back of 16 rats with established diabetes, with 4 wounds on each rat. Two symmetrical wounds on either side of the spine were created as a pair according to paired design. Then the wounds were divided into groups A and B according to the random number table and blind method (red and blue tags on the rhGM-CSF or the gel vehicle), with 32 wounds in each group. The ointment with red tag was applied on the wounds of group A and the blue one on group B. The application was conducted once a day, with a thickness of 3 mm, up to post injury day (PID) 14. Gross observation of wound healing was conducted on PID 3, 7, 14. The wound healing rate was determined on PID 3 and 7. On PID 3, 7, 14, tissues from 2, 4, and 8 wounds were harvested from each group respectively for the observation of the histopathological changes with HE staining, and also for analyzing the expression of proliferating cell nuclear antigen (PCNA) and CD31 with immunohistochemical staining (denoted as absorbance value). On PID 7, tissues from 6 wounds in each group were harvested for microarray gene chip to screen the differentially expressed microRNAs. Enrichment analysis of Kyoto encyclopedia of genes and genomes (KEGG) signaling pathway on the differentially expressed microRNAs were performed after the microRNA screening results were validated by real-time fluorescent quantitative RT-PCR. Data were processed with paired t test or two-sample t test.

RESULTS(1) On PID 3, the wound area was significantly decreased, and the wound granulation was significantly proliferated in both groups. On PID 7, the wound area was further decreased, and the wound area was almost filled by granulation in both groups; the conditions in group A were better. On PID 14, all the wounds in group A were almost healed, while a small area of raw wound with incrustation still remained in some wounds of group B. On PID 3 and 7, the wound healing rates of group A were (41 ± 5)% and (75 ± 4)%, significantly higher than those of group B [(31 ± 9)% and (71 ± 4)%, with t values respectively 10.13 and 8.06, P values below 0.001]. (2) On PID 3, the epidermal cells, endothelial cells, and Fbs in the wounds of 2 groups were sparse, with heavy infiltration of inflammatory cells. The above condition in the wounds was better in group A than in group B. On PID 7, the epidermal cells, endothelial cells, and Fbs were gradually well arranged in group A; infiltration of inflammatory cells decreased, and the condition was better than that of group B. On PID 14, the wounds of group A were completely covered by epidermis, while infiltration of inflammatory cells still remained in some wounds of group B. (3) On PID 3, 7, 14, the positive expressions of CD31 and PCNA in group A were respectively 0.275 ± 0.018, 0.345 ± 0.034, 0.305 ± 0.023; 0.406 ± 0.063, 0.223 ± 0.011, 0.045 ± 0.022. They were significantly higher than those of group B (0.222 ± 0.020, 0.229 ± 0.018, 0.197 ± 0.015; 0.324 ± 0.039, 0.162 ± 0.012, 0.018 ± 0.020, with t values from 2.281 to 9.652, P < 0.05 or P < 0.01). (4) According to the microRNAs detection and screening, as compared with group B, 18 microRNAs were up-regulated while 13 were down-regulated in the wounds of group A. (5) The results of real-time fluorescent quantitative RT-PCR had good consistency with the results of microRNAs detection. (6) Enrichment analysis of KEGG signaling pathway showed that among the 31 differentially expressed microRNAs, 4 took part in the MAPK signaling pathway, 3 took part in the Wnt signaling pathway, 1 took part in the TGF-β signaling pathway, 3 took part in the epidermal growth factor receptor signaling pathway, 2 took part in the cell cycle pathway, 5 took part in the axon guidance signaling pathway, 6 took part in the focal adhesion pathway, 3 took part in the regulation of actin cytoskeleton pathway, 1 took part in the extracellular cell matrix receptor pathway, 3 took part in the adherens junction pathway, and 1 took part in the cell adhesion molecules pathway. After disclosing the blind, it showed that the ointment with red tag was the rhGM-CSF gel and the blue one was gel vehicle.

CONCLUSIONSThe rhGM-CSF gel can promote wound healing in diabetic rats, producing significant differential microRNA expression in wounds, and they may be the target at gene post-transcriptional level of rhGM-CSF gel in promoting wound healing.

Animals ; Bacteria ; isolation & purification ; Burns ; drug therapy ; microbiology ; pathology ; Diabetes Mellitus, Experimental ; complications ; Granulocyte-Macrophage Colony-Stimulating Factor ; pharmacology ; Humans ; Male ; MicroRNAs ; genetics ; Proliferating Cell Nuclear Antigen ; metabolism ; Rats ; Recombinant Proteins ; Signal Transduction ; Wound Healing ; drug effects