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Enterococcus faecalis aggravates pyelonephritis caused by Pseudomonas aeruginosa in experimental ascending mixed
N Tsuchimori1, R Hayashi, A Shino
1Pharmaceutical Research Laboratories III, Takeda Chemical Industries, Ltd., Osaka, Japan.
Abstract:
Mixed urinary tract infection was caused by simultaneous inoculation of 10(4) CFU each of Enterococcus faecalis TN2005 and Pseudomonas aeruginosa P9 into the bladders of CBA/J mice. Both organisms proliferated in the kidneys, and viable cell counts of E. faecalis TN2005 reached a peak level of 4.1 x 10(5) CFU per pair of kidneys within the first 24 h, while P. aeruginosa P9 counts increased more slowly. The number of P. aeruginosa P9 cells peaked at 8.3 x 10(6) CFU per pair of kidneys 5 days after infection. Five days after mixed infection, infiltration of neutrophils into the renal pelvis and renal medulla was observed. Immunohistochemical staining revealed the presence of E. faecalis antigen in the renal medulla. P. aeruginosa antigen was detected mainly in the renal pelvis 5 days after infection and in the renal medulla as well as the renal pelvis 14 days after infection. Mixed infection induced pyelonephritis within 5 days after mixed infection, while it was not observed until 14 days after infection with P. aeruginosa P9 alone. P. aeruginosa P9 inoculated together with E. faecalis TN2005 was more resistant to eradication from the kidneys by beta-lactam antibiotics than P. aeruginosa P9 inoculated alone. These results suggest that E. faecalis TN2005 invades the renal medulla first in mixed urinary tract infection and induces histological changes which lead to aggravation of the pyelonephritis caused by P. aeruginosa P9.
Insights
Enterococcus faecalis invades the renal medulla first during mixed urinary tract infections, worsening pyelonephritis caused by Pseudomonas aeruginosa. This co-infection also increases bacterial resistance to antibiotics.
Area of Science:
- Microbiology
- Immunology
- Urology
Background:
- Urinary tract infections (UTIs) are common, often involving multiple bacterial species.
- Understanding polymicrobial UTIs is crucial for effective treatment strategies.
Purpose of the Study:
- To investigate the pathogenic mechanisms of a mixed urinary tract infection (UTI) caused by Enterococcus faecalis and Pseudomonas aeruginosa in a mouse model.
- To determine the role of E. faecalis in the progression of pyelonephritis induced by P. aeruginosa.
Main Methods:
- Simultaneous inoculation of CBA/J mice bladders with E. faecalis TN2005 and P. aeruginosa P9.
- Monitoring bacterial proliferation in kidneys via colony-forming unit (CFU) counts.
- Histopathological examination and immunohistochemical staining for bacterial antigens.
- Assessing antibiotic resistance of P. aeruginosa in the presence of E. faecalis.
Main Results:
- Both E. faecalis and P. aeruginosa proliferated in the kidneys, with E. faecalis counts peaking early and P. aeruginosa counts increasing more slowly.
- Mixed infection led to neutrophil infiltration and pyelonephritis development within 5 days, significantly faster than P. aeruginosa monoinfection.
- E. faecalis antigen was found in the renal medulla, while P. aeruginosa antigen was detected in the renal pelvis and medulla.
- P. aeruginosa in the mixed infection showed increased resistance to beta-lactam antibiotics compared to monoinfection.
Conclusions:
- E. faecalis initiates infection in the renal medulla, contributing to the severity of pyelonephritis caused by P. aeruginosa.
- Mixed UTIs exhibit distinct pathogenic dynamics and altered antibiotic susceptibility compared to single-organism infections.