Investigations of patients with suspected Mycoplasma pneumoniae infection have been undertaken in England since the early 1970s. M. pneumoniae is a respiratory pathogen that is a common cause of pneumonia and may cause serious sequelae such as encephalitis and has been documented in children with persistent cough. The pathogen is found in all age groups, with higher prevalence in children aged 5-14 years. In England, recurrent epidemic periods have occurred at ~4-yearly intervals. In addition, low-level sporadic infection occurs with seasonal peaks from December to February. Voluntarily reports from regional laboratories and hospitals in England from 1975 to 2015 were collated by Public Health England for epidemiological analysis. Further data pertaining cases of note and specimens submitted to Public Health England from 2005 to 2015 for confirmation, molecular typing is included.

/pdf/mycoplasma-pneumoniae-epidemiology-in-england-and-wales-a-4h4db5bd32.pdf

Mycoplasma pneumoniae epidemiology in England and Wales: a national perspective

Repurposing of the gold drug auranofin and a review of its derivatives as antibacterial therapeutics.

Within-host resistance evolution of a fatal ST11 hypervirulent carbapenem-resistant Klebsiella pneumoniae.

Antimicrobials used to treat burn wound infections have become multidrug-resistant, thus delaying wound healing. When combined with silver nanoparticles, antibiotics create a multifaceted antibacterial mechanism of action to which bacteria are incapable of developing resistance. Similarly, the amniotic membrane has been found to lower the bacterial number. The purpose of the current study was to observe the antibacterial activity of combined topical colistin with silver nanoparticles and decellularized human amniotic membrane as a dressing in burn wounds infected with bacteria with the goal of promoting faster healing. Bacteria commonly isolated from burn wounds and the most sensitive topical antibiotic were identified. Colistin, silver nanoparticles and combined colistin with silver nanoparticles were impregnated into decellularized human amniotic membranes. These wound dressings were evaluated in third-degree multidrug-resistant bacterial infected thermal burns induced in rats. Out of a total of 708 pus samples from burn wounds, Pseudomonas aeruginosa was the most prevalent pathogen 308 (43.5%), followed by Klebsiella pneumoniae 300 (42.4%). Topical colistin was 100% sensitive for both bacteria. Overall, maximum wound contraction (p < 0.05), and increased collagen deposition (+++) with no isolation of bacteria from wound swabs were noted on day 21 for the combined colistin with silver nanoparticle-loaded human amniotic membrane dressing group. Our study concluded that the increased antimicrobial activity of the novel combination of colistin and silver nanoparticle-loaded decellularized human amniotic membrane manifested its potential as an effective burn wound dressing. 

/pdf/synergistic-efficacy-of-colistin-and-silver-nanoparticles-12txquyu.pdf

Synergistic efficacy of colistin and silver nanoparticles impregnated human amniotic membrane in a burn wound infected rat model

Molecular mechanisms and clinical implications of the gold drug auranofin

We describe in vivo evolution of carbapenem and ceftazidime-avibactam resistance by analyzing four longitudinal Klebsiella pneumoniae clinical isolates from a patient with pneumonia following antimicrobial treatment. The patient had fever, cough associated with expectoration, and new infiltration was found on the chest CT. Antimicrobial susceptibility was determined, and whole genome sequencing (WGS) was performed to investigate its dynamic change of resistance phenotype. Population analysis profile was performed to investigate the population of Klebsiella pneumoniae. The infection started with a KPC-2-producing K. pneumoniae (ZRKP01, ceftazidime-avibactam-S/carbapenem-R). Then, after ceftazidime-avibactam treatment, the strain switched to D179Y mutant that is KPC-33 (ZRKP02, ceftazidime-avibactam-R/carbapenem-S), which restored carbapenem susceptibility. However, the restored carbapenem susceptibility in vivo was not stable and the subsequent use of imipenem against KPC-33-producing K. pneumoniae infection resulted in a reversion of KPC-2 producers (ZRKP03 and ZRKP04, ceftazidime-avibactam-S/carbapenem-R). Genetic analysis demonstrated that all four K. pneumoniae isolates belonged to sequence type 11and had identical capsular polysaccharide (KL47), identical porin genes, and same plasmid replicon types. Phylogenetic analysis indicated that four K. pneumoniae isolates showed a high degree of relatedness. Single nucleotide polymorphisms analysis indicated that the number of mutations observed in the KPC-33 isolate was more than in the wild-type KPC-2 isolates and the four KPC-Kp isolates evolved from a longitudinal evolution of K. pneumoniae harboring bla KPC-2 gene. This is the first report to observe the in vivo evolution of wild-type KPC-2 to KPC-33 and then the reversion to its original wild-type KPC-2. Through WGS, we demonstrated the role of selective pressure of antibiotic in the mutation and reversion of bla KPC genes, which leading to the dynamic change of KPC enzymes and the dynamic emergence of resistance to ceftazidime-avibactam and carbapenems. Statement: Recently, studies reported the emergence of ceftazidime-avibactam-resistant strains. The KPC mutations mediating ceftazidime-avibactam resistance are generally associated with the restoration of carbapenem susceptibility. However, clinical significance of this observation is unclear. In this manuscript, we demonstrate the role of selective pressure of antibiotic in the mutation and reversion of bla KPC genes, which leading to the dynamic change of KPC enzymes and the dynamic emergence of resistance to ceftazidime-avibactam and carbapenems. To the best of our knowledge, this is the first report to observe the in vivo evolution of wild-type KPC-2 to KPC-33 and then the reversion to its original wild-type KPC-2. It should be noted that understanding the clinical significance of this observation is of critical importance, and reversion to carbapenem susceptibility would not imply a potential role for carbapenems monotherapy. We hope our study will draw attention to clinicians, so that this agent can be used most effectively for the longest period of time.

/pdf/in-vivo-selection-of-imipenem-resistance-among-ceftazidime-35gnzuq54e.pdf

In vivo Selection of Imipenem Resistance Among Ceftazidime-Avibactam-Resistant, Imipenem-Susceptible Klebsiella pneumoniae Isolate With KPC-33 Carbapenemase.

T the editor: A 31-year-old previous healthy male patient was admitted to the hospital with fever (Tmax 41°C) and nonproductive cough for seven days and dyspnea for three days. On day 4 after disease onset, his chest X-ray showed right upper lung small opacity and left lung large opacity (Figure 1A). The patient has been administrated levofloxacin for two days before he came into our hospital. Upon physical examination, blood pressure was 76/45 mmHg, pulse rate was 110/minute, respiratory rate was 35 breaths/min and temperature was 39.0°C. Chest examination showed bilateral fine moist rales and sporadic dry rales. Lab results showed that white blood cell (WBC) count was 8.86×10 with 82.7% neutrophils, platelet count 127×10/mm and hemoglobin 133 g/dl. Blood chemistry including liver profile, kidney profile, and coagulation studies were within normal limits. The chest X-ray showed progressive infiltration with left lung extensive consolidation (Figure 1B). Artery blood gas on non-rebreath oxygen face mask with 10 L/min oxygen flow rate showed PH 7.457, PaO2 77.8 mmHg, PaCO2 29.7 mmHg, and HCO3 –21.2 mmol/L. Infection work-ups were initiated thoroughly and finally sputum PCR for Mycoplasma pneumoniae (M. pneumoniae) was strong positive and serum IgM antibody for M. pneumoniae was also positive. Upon coming into our hospital, only moxifloxacin (0.4 g once daily intravenously) and oxygen therapy were administrated. Three days later on day 10 after onset, patient symptoms were significantly improved. However, at night on day 10, the patient presented passing dark urine and jaundice next early morning. Lab analysis showed WBC count was 28.87×10 with 67% neutrophils, platelet count 127×10/mm and hemoglobin 82 g/dl, high LDH level (1388 U/L) and hyperbilirubinemia (TBIL 73.9 μmol/L, IBIL 47.40 μmol/L, and DBIL 26.50 μmol/L). The blood smear showed red cell agglutination (Figure 1C). So hemolytic anemia was concerned and was treated by intravenous methylprednisolone (80 mg, Q12h) and immunoglobulin (35 g/d). Unfortunately, the hemoglobin quickly dropped to 3.2 g/dl in the following 36 hours and IBIL elevated to 9.56 μmol/L even received 240 mg methylprednisolone. A Coombs test was positive only for complement. The patient was transferred into ICU for plasmapheresis. After three-time plasmapheresis and steroids decrement to 40 mg/d, the patient’s hemoglobin did not drop again and gradually went up to 4.3 g/L and bilirubin came down to normal level and went back general ward. He was discharged with hemoglobin 8.2 g/dl on day 23. Before he was discharged, a cold agglutinin test was found to be positive with antibody titre 1: 512. The patient was followed on day 30 after onset. He recovered very well and hemoglobin reached 12.3 g/dl. Lung field was also clear (Figure 1D).

A case of lethal hemolytic anemia associated with severe pneumonia caused by Mycoplasma pneumoniae.

Colistin-resistant (Col-R) bacteria are steadily increasing, and are extremely difficult to treat. New drugs or therapies are urgently needed to treat infections caused by these pathogens. Combination therapy with colistin and other old drugs, is an important way to restore the activity of colistin. This study aimed to investigate the activity of colistin in combination with the anti-rheumatic drug auranofin against Col-R Gram-negative bacteria. The results of checkerboard analysis demonstrated that auranofin synergized with colistin against Col-R Gram-negative bacteria. Time-kill assays showed significant synergistic antimicrobial activity of colistin combined with auranofin. Electron microscopy revealed that the combination resulted in more cellular structural alterations compared to each drug alone. Auranofin enhanced the therapeutic effectiveness of colistin in mouse peritoneal infection models. These results suggested that the combination of colistin and auranofin might be a potential alternative for the treatment of Col-R Gram-negative bacterial infections.

/pdf/synergistic-activity-of-colistin-combined-with-auranofin-56jiwei4hr.pdf

Synergistic Activity of Colistin Combined With Auranofin Against Colistin-Resistant Gram-Negative Bacteria

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In vivo Selection of Imipenem Resistance Among Ceftazidime-Avibactam-Resistant, Imipenem-Susceptible Klebsiella pneumoniae Isolate With KPC-33 Carbapenemase.

A case of lethal hemolytic anemia associated with severe pneumonia caused by Mycoplasma pneumoniae.

Synergistic Activity of Colistin Combined With Auranofin Against Colistin-Resistant Gram-Negative Bacteria