Emergence of K1 ST23 and K2 ST65 hypervirulent klebsiella pneumoniae as true pathogens with specific virulence genes in cryptogenic pyogenic liver abscesses Shiraz Iran.

Hypervirulent Klebsiella pneumoniae (hvKp) pathotype is emerging worldwide in pyogenic liver abscesses (PLAs). However, the role of virulence factors in pathogenicity remains unclear. On the other hand, the epidemiology of PLAs in Iran is unknown. From July 2020 to April 2022, bacterial species were isolated and identified from the drainage samples of 54 patients with PLAs. K. pneumoniae as the most common pathogen of pyogenic liver abscesses was identified in 20 (37%) of the 54 patients. We analyzed the clinical and microbiological characteristics of K. pneumoniae-related pyogenic liver abscesses. Antibiotic susceptibility testes and string test were performed. 16S rRNA, antibiotic resistance, and virulence genes were determined by polymerase chain reaction amplification. Clonal relatedness of isolates was identified by multilocus sequence typing. Virulence levels were assessed in the Galleria mellonella larval infection model. Four hvKp isolates (K1/K2) were found to be responsible for cryptogenic PLAs, and 16 classical K. pneumoniae isolates (non-K1/K2) were associated with non-cryptogenic PLAs. Three capsular serotype K1 strains belonged to sequence type 23 (ST23) and one K2 strain to ST65. Meanwhile, the non-K1/K2 strains belonged to other STs. ST231 was the most common strain among the classical K. pneumoniae strains. Compared with the non-K1/K2 strains, capsular serotypes K1/K2 strains were less resistant to antibiotics, had positive string test results, and had more virulence genes. In Galleria mellonella, a concentration of 106 colony-forming units of the K1 hvKp strain resulted in 100% death at 24 hours, confirming the higher virulence of the hvKp strain compared with cKp. K. pneumoniae isolates represented that the acquisition of any plasmid or chromosomal virulence genes contributes to pathogenicity and high prevalence in PLAs. Meanwhile, hvKp isolates with a specific genetic background were detected in cryptogenic PLAs.

Relationships among serum receptor of nuclear factor-kappaB ligand, osteoprotegerin, high-sensitivity C-reactive protein, and bone mineral density in postmenopausal women: osteoimmunity versus osteoinflammatory.

OBJECTIVE: The aim of this study was to investigate the correlations among circulating osteoprotegerin (OPG), the receptor activator of nuclear factor-kappaB ligand (RANKL), high-sensitivity C-reactive protein (hsCRP), and bone mineral density (BMD) in healthy postmenopausal women. METHODS: In a population-based study, highly specific enzyme-linked immunosorbent assay methods were used to evaluate the sera of 382 healthy Iranian postmenopausal women (mean age +/- SD, 58.7 +/- 7.5 y) for RANKL, OPG, hsCRP, degradation products of C-terminal telopeptides of type I collagen, and osteocalcin. BMD was determined for the lumbar spine (L2-L4) and the proximal femur using dual-energy x-ray absorptiometry. RESULTS: Circulating levels of OPG (r = 0.30, P < 0.001) and the RANKL/OPG ratio (r = -0.17, P < 0.001) were significantly associated with age. The geometric mean of hsCRP was 1.89 mg/L (SE, 1.05) in the population studied. There was a significant correlation between log(hsCRP) levels and body mass index (BMI; r = 0.36, P < 0.001). Multivariate linear analyses revealed that age (beta = -0.295, P < 0.001), BMI (beta = 0.464, P < 0.001), RANKL (beta = -0.105, P = 0.014), and OPG (beta = 0.098, P = 0.029) were the independent determinants for lumbar BMD (R(2) = 0.35). Age (beta = -0.250, P < 0.001), BMI (beta = 0.486, P < 0.001), and RANKL (beta = -0.110, P = 0.009) were independently correlated with femoral neck BMD (R(2) = 0.36). Age- and BMI-adjusted analysis by quartiles of log-transformed hsCRP did not reveal an association with BMD, serum levels of biochemical markers of bone turnover, RANKL, or OPG. CONCLUSIONS: The circulating levels of the RANKL/OPG osteoimmunity system have an association with BMD, but subclinical systemic inflammation may not be involved in bone mass in healthy postmenopausal women.