Urinary tract infection (UTI) is the most common and life-threatening bacterial infection among neonates. This study aimed to determine the prevalence, aetiology, and susceptible antimicrobial agents among neonates with UTI.
This was a cross-sectional analytical hospital-based study that included 152 neonates with clinical sepsis who were admitted at Dodoma regional referral hospital from January to June 2020. Bacterial growth of 1 × 103 colony forming units/mL of a single uropathogen was used to define the presence of UTI. Statistical analysis was performed using SPSS version 23.0 and multivariate analysis was used to determine the predicting factors of UTI. P <0.05 was regarded statistically significant.
The prevalence of UTI was 18.4% (28/152). Klebsiella pneumoniae 64.3% (18/28) and Enterobacter spp. 35.7% (10/28) were the bacterial agents isolated. The bacterial isolates were 90%, and 60% sensitive to ciprofloxacin and amikacin, respectively. Low Apgar score (AOR = 12.76, 95% CI = 4.17–39.06, p<0.001), prolonged labour (AOR = 5.36, 95% CI = 1.28–22.52, p = 0.022), positive urine nitrite test (AOR = 26.67, 95% CI = 7.75–91.70, p<0.001), and positive leucocyte esterase test (AOR = 6.64, 95% CI = 1.47–29.97, p = 0.014) were potential predictors of UTI.
The prevalence of UTI confirmed by urine culture among neonates that were included in the present study indicates that this problem is common in the population where the study was conducted. Klebsiella pneumoniae and Enterobacter spp. were the uropathogens which were isolated. Ciprofloxacin, nitrofurantoin, and amikacin were sensitive to the isolated uropathogens.
AbstractCarbapenem-resistant Klebsiella pneumoniae (CRKP) has emerged as a severe global health challenge. We isolate and characterize two previously unidentified lytic phages, P24 and P39, with large burst sizes active against ST11 KL64, a major CRKP lineage. P24 and P39 represent species of the genera Przondovirus (Studiervirinae subfamily) and Webervirus (Drexlerviridae family), respectively. P24 and P39 together restrain CRKP growth to nearly 8 h. Phage-resistant mutants exhibit reduced capsule production and decreased virulence. Modifications in mshA and wcaJ encoding capsule polysaccharide synthesis mediate P24 resistance whilst mutations in epsJ encoding exopolysaccharide synthesis cause P39 resistance. We test P24 alone and together with P39 for decolonizing CRKP using mouse intestinal colonization models. Bacterial load shed decrease significantly in mice treated with P24 and P39. In conclusion, we report the characterization of two previously unidentified lytic phages against CRKP, revealing phage resistance mechanisms and demonstrating the potential of lytic phages for intestinal decolonization.
is a leading cause of healthcare-associated infections, including pneumonia, urinary tract infections, and sepsis. Treatment of
infections is becoming increasingly challenging due to high levels of antibiotic resistance and the rising prevalence of carbapenem-resistant, extended-spectrum β-lactamases producing strains.
As an important member of the
is poorly studied as an emerging human pathogen. We, for the first time, report a unique
isolated from a pediatric patient in China.