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In recent years, the number of spinal internal fixation operations has increased significantly, correlating with an elevated risk of postoperative surgical site infection and a rising incidence rate. While the conventional treatment approach involves surgical debridement combined with antibiotic administration, there is a notable gap in reported strategies for Burkholderia cepacia infection and patients exhibiting multidrug resistance.
Surgical site infection occurred in a patient following internal fixation surgery for thoracic vertebral fractures. Despite the application of systemic antibiotics and regular dressing changes, no improvement was observed. Bacterial culture and drug sensitivity experiments revealed a multidrug-resistant Burkholderia cepacia infection. Two comprehensive debridement procedures were performed along with continuous post-operative irrigation combined with antibiotic administration; however, no significant improvement was observed. The patient\'s infection was significantly controlled following treatment with vancomycin loaded bone cement.
Following spinal internal fixation surgery, the management of a B. cepacian infection with multidrug resistance presented a significant challenge, despite the application of debridement procedures and systemic antibiotics. In this case, after 20 days of treatment with vancomycin-loaded bone cement, the patient\'s C-reactive protein level decreased to 54 mg/L, was normalized by February, and normal levels were maintained in the surgical area 1 month and 6 months after bone cement removal.
The use of vancomycin-loaded bone cement proves effective in treating postoperative B. cepacian infection in a multidrug-resistant case following spinal internal fixation surgery.

The Burkholderia cepacia complex (BCC) is a group of opportunistic pathogens, including Burkholderia cepacia, Burkholderia multivorans, Burkholderia vietnamiensis and Burkholderia ambifaria, which can cause severe respiratory tract infections and lead to high mortality rates among humans. The early diagnosis and effective treatment of BCC infection are therefore crucial. In this study, a novel and rapid recombinase-aided amplification (RAA) assay targeting the 16S rRNA gene was developed for BCC detection. The protocol for this RAA assay could be completed in 10 min at 39°C, with a sensitivity of 10 copies per reaction and no cross-reactivity with other pathogens. To characterize the effectiveness of the RAA assay, we further collected 269 clinical samples from patients with bacterial pneumonia. The sensitivity and specificity of the RAA assay were 100% and 98.5%, respectively. Seven BCC-infected patients were detected using the RAA assay, and three BCC strains were isolated from the 269 clinical samples. Our data showed that the prevalence of BCC infection was 2.60%, which is higher than the 1.40% reported in previous studies, suggesting that high sensitivity is vital to BCC detection. We also screened a patient with B. vietnamiensis infection using the RAA assay in clinic, allowing for appropriate treatment to be initiated rapidly. Together, these data indicate that the RAA assay targeting the 16S rRNA gene can be applied for the early and rapid detection of BCC pathogens in patients with an uncharacterized infection who are immunocompromised or have underlying diseases, thereby providing guidance for effective treatment.

This report describes an outbreak of 71 patients developed B. cepacia urinary tract infection (UTI) by contaminated single-use anesthetic gel.
Epidemiological investigation of patients with B. cepacia-positive urine or blood samples between March 19, 2018 and Novemeber 15, 2018 was conducted to identify the source of infection. Microbiological samples from hospital surfaces, endoscopes, disposable items, and the hands of staff were tested for B. cepacia contamination. Pulsed-field gel electrophoresis (PFGE) was used to compare homology in B. cepacia isolates.
During the outbreak, nosocomial B. cepacia UTI was confirmed in 71 patients. Epidemiological investigation showed that 66 patients underwent invasive urological diagnosis and treatment, while the remaining five patients underwent bedside indwelling catheterization, with all patients exposed to single-use anesthetic gel. All batches of anesthetic gel were recalled and the outbreak abated. Overall, 155 samples were collected from environmental surfaces and disposable items, and B. cepacia contamination was confirmed in samples from one used cystoscope and three anesthetic gels from the same batch. PFGE showed homology between 17 out of 20 B. cepacia isolates from patients and three isolates from the contaminated anesthetic gel. All patients achieved cure.
Contaminated single-use anesthetic gel was confirmed as the source of the B. cepacia outbreak, with infection occurring during invasive urological diagnostic and treatments. Thus, investigations of nosocomial outbreaks of B. cepacia infection should consider contamination of diagnostic and treatment items used in infected patients.

Burkholderia cepacia predominantly causes opportunistic infections in hospitalized and immunocompromised patients such as patients with cystic fibrosis, cancer, or human immunodeficiency virus (HIV). Nonetheless, Burkholderia cepacia is infrequently reported to cause infection in hematopoietic stem cell transplantation (HSCT) recipients. Herein, we report a rare case of suppurative parotitis in a 31-year-old patient with T-cell lymphoblastic lymphoma (T-LBL) who underwent auto-HSCT. The secretion from the Stensen duct was collected, and Burkholderia cepacia was detected using the VITEK-2 identification system. Additionally, sensitive antibiotic therapy against this bacterium was also effective. This is the first case of parotitis triggered by Burkholderia cepacia after auto-HSCT, and it is also the first reported domestic case. This case emphasizes the importance of considering bacterial infections in general and Burkholderia cepacia specifically in HSCT patients with post-transplant parotitis.

Contamination of drugs used in minimally invasive treatment may to lead to infection outbreaks and catastrophic public health events that require prompt detection and control. Our aim was to investigate the outbreak of Burkholderia cepacia infection and its source in a tertiary care, general hospital in Beijing, China.
We investigated the outbreak of B cepacia infection from January 2017 to March 2018. The investigation included a detailed review of all cases, and field investigations. Environmental and product cultures were performed at the microbiology laboratory in the hospital. Isolates were evaluated for molecular relatedness using pulsed-field gel electrophoresis performed in an independent laboratory.
In total, 9 patients were infected from November 2017 to March 2018, and all patients had undergone the following surgeries: transurethral resection of the prostate (n = 4), perineal prostate biopsy (n = 2), transurethral resection of bladder tumors (n = 2), and ureteroscopy (n = 1). B cepacia was isolated from the urine of 9 patients, blood of 2 patients, grilles used for puncturing, and 2 samples in 1 batch of analgesic gels. Pulsed-field gel electrophoresis confirmed that the isolates from the patients and gels were homologous.
Our investigation revealed that the outbreak of B cepacia infection was caused by drug contamination.

Quorum sensing (QS) signals are widely used by bacterial pathogens to control biological functions and virulence in response to changes in cell population densities. Burkholderia cenocepacia employs a molecular mechanism in which the cis-2-dodecenoic acid (named Burkholderia diffusible signal factor [BDSF]) QS system regulates N-acyl homoserine lactone (AHL) signal production and virulence by modulating intracellular levels of cyclic diguanosine monophosphate (c-di-GMP). Thus, inhibition of BDSF signaling may offer a non-antibiotic-based therapeutic strategy against BDSF-regulated bacterial infections. In this study, we report the synthesis of small-molecule mimics of the BDSF signal and evaluate their ability to inhibit BDSF QS signaling in B. cenocepacia A novel structural analogue of BDSF, 14-Me-C16:Δ2 (cis-14-methylpentadec-2-enoic acid), was observed to inhibit BDSF production and impair BDSF-regulated phenotypes in B. cenocepacia, including motility, biofilm formation, and virulence, while it did not inhibit the growth rate of this pathogen. 14-Me-C16:Δ2 also reduced AHL signal production. Genetic and biochemical analyses showed that 14-Me-C16:Δ2 inhibited the production of the BDSF and AHL signals by decreasing the expression of their synthase-encoding genes. Notably, 14-Me-C16:Δ2 attenuated BDSF-regulated phenotypes in various Burkholderia species. These findings suggest that 14-Me-C16:Δ2 could potentially be developed as a new therapeutic agent against pathogenic Burkholderia species by interfering with their QS signaling.IMPORTANCE Burkholderia cenocepacia is an important opportunistic pathogen which can cause life-threatening infections in susceptible individuals, particularly in cystic fibrosis and immunocompromised patients. It usually employs two types of quorum sensing (QS) systems, including the cis-2-dodecenoic acid (BDSF) system and N-acyl homoserine lactone (AHL) system, to regulate virulence. In this study, we have designed and identified an unsaturated fatty acid compound (cis-14-methylpentadec-2-enoic acid [14-Me-C16:Δ2]) that is capable of interfering with B. cenocepacia QS signaling and virulence. We demonstrate that 14-Me-C16:Δ2 reduced BDSF and AHL signal production in B. cenocepacia It also impaired QS-regulated phenotypes in various Burkholderia species. These results suggest that 14-Me-C16:Δ2 could interfere with QS signaling in many Burkholderia species and might be developed as a new antibacterial agent.

Since Burkholderia thailandensis is included in the reference spectra of the VITEK MS libraries rather than Burkholderia pseudomallei, B. pseudomallei cannot be correctly identified in the current version of VITEK MS. This study was undertaken to evaluate the utility of matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS) with the VITEK MS plus system in the detection of B. pseudomallei and B. thailandensis isolates. For each species, we increased the reference spectra, and then, a SuperSpectrum was created based on the selection of 39 specific masses. In a second step, we validated the SuperSpectra with 106 isolates identified by 16S rRNA gene sequencing. The results showed that there was 100% agreement between the validation strains analyzed by MALDI-TOF MS and those evaluated using 16S rRNA gene sequencing analysis methods. Therefore, MALDI-TOF MS is a promising, rapid, and economical method to monitor the outbreaks and spread of B. pseudomallei and B. thailandensis isolates.

Immune recognition of pathogen-associated molecular patterns (PAMPs) by pattern recognition receptors often activates proinflammatory NF-κB signalling1. Recent studies indicate that the bacterial metabolite D-glycero-β-D-manno-heptose 1,7-bisphosphate (HBP) can activate NF-κB signalling in host cytosol2-4, but it is unclear whether HBP is a genuine PAMP and the cognate pattern recognition receptor has not been identified. Here we combined a transposon screen in Yersinia pseudotuberculosis with biochemical analyses and identified ADP-β-D-manno-heptose (ADP-Hep), which mediates type III secretion system-dependent NF-κB activation and cytokine expression. ADP-Hep, but not other heptose metabolites, could enter host cytosol to activate NF-κB. A CRISPR-Cas9 screen showed that activation of NF-κB by ADP-Hep involves an ALPK1 (alpha-kinase 1)-TIFA (TRAF-interacting protein with forkhead-associated domain) axis. ADP-Hep directly binds the N-terminal domain of ALPK1, stimulating its kinase domain to phosphorylate and activate TIFA. The crystal structure of the N-terminal domain of ALPK1 and ADP-Hep in complex revealed the atomic mechanism of this ligand-receptor recognition process. HBP was transformed by host adenylyltransferases into ADP-heptose 7-P, which could activate ALPK1 to a lesser extent than ADP-Hep. ADP-Hep (but not HBP) alone or during bacterial infection induced Alpk1-dependent inflammation in mice. Our findings identify ALPK1 and ADP-Hep as a pattern recognition receptor and an effective immunomodulator, respectively.

OBJECTIVE: To investigate the distribution characteristics and clinical features of Burkholderia cepacia infection in children.
METHODS: A retrospective analysis was performed for the clinical data of 16 children with Burkholderia cepacia infection who were hospitalized between June 2012 and September 2017.
RESULTS: All 16 children with Burkholderia cepacia infection were sporadic cases. A total of 16 strains of Burkholderia cepacia were isolated, among which 8 were detected by sputum culture, 5 were detected by blood culture, 2 were detected by tracheal intubation tip culture, and 1 was detected by lung biopsy culture. Of the 16 children, there were 11 boys and 5 girls, with an age of 5 days to 6 years, and the children aged <1 year accounted for 69%. As for department distribution, 10 children were in the PICU/NICU and 6 were in the general wards. As for clinical manifestations, one child had disseminated intravascular coagulation, and the other 15 children had pulmonary infection, among who 11 had severe pneumonia (8 of them underwent mechanical ventilation during treatment). As for underlying diseases, 2 had severe congenital heart disease, 4 had primary immunodeficiency, 3 were highly suspected of immunodeficiency or inherited metabolic diseases, 1 had tracheal stenosis, 1 had Kawasaki disease, 1 was a preterm infant with bronchopulmonary dysplasia, 1 had severe cleft lip and palate, and 3 had no definite underlying diseases. Of all the children, 7 also had infections with adenovirus and Mycoplasma. The average length of hospital stay was 20.3 days for all children, and 12 were improved and 4 died after treatment. All 16 strains of Burkholderia cepacia had a drug resistance rate of 100% to amikacin and gentamicin and ≥80% to ampicillin/sulbactam and ticarcillin/clavulanic acid, as well as the lowest drug resistance rate to levofloxacin.
CONCLUSIONS: Burkholderia cepacia is an opportunistic pathogen often found in immunocompromised children and can produce drug resistance. The presence or absence of underlying diseases should be considered during anti-infective therapy. The children with Burkholderia cepacia infection often have a poor prognosis, and an understanding of the disease spectrum of Burkholderia cepacia infection helps with clinical diagnosis and treatment.