Analysis of Hospital Acquired Severe Pneumonia with Pseudomonas Aeruginosa Infection

2021 ◽  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Severe Pneumonia ◽  
Pseudomonas Aeruginosa Infection ◽  
Hospital Acquired

scholarly journals Effectiveness of Ciprofloxacin and Levofloxacin in treatment of Pseudomonas Aeruginosa infection

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Imtiaz Ahmad ◽  
Wasil Khan ◽  
Aleem ur Rashid ◽  
Samiullah , ◽  
Abdul Ahad ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Oral Treatment ◽  
Tracheal Aspirate ◽  
Cross Sectional Study ◽  
Cross Sectional ◽  
Hospital Acquired Infections ◽  
Sensitivity Report ◽  
Bronchial Washing ◽  
Pseudomonas Aeruginosa Infection ◽  
Hospital Acquired

Background: Pseudomonas aeruginosa is the most troublesome and feared pathogen in medical field. It is the sixth mostcommon cause of hospital-acquired infections and the cause of ventilator-associated pneumonia. The most common multidrugresistantgram-negative pathogen in Ventilated Assisted Patient. In our study in 100 patients culture and sensitivity report only 46%were sensitive to oral treatment while 54% of the pseudomonas were resistant to ciprofloxacin and 34% sensitive and 66%resistant to levofloxacin.Objective: To find out resistance of pseudomonas to oral medication.Material and Methods: A cross-sectional study, conducted in Saidu Group of Teaching Hospital from January 2018 to July 2019. ).100 patient samples (tracheal aspirate, bronchial washing, sputum, pus, urine and blood) were cultured for pseudomonas and itssensitivity to oral medication ciprofloxacin and levofloxacin was recorded.Results: Sensitivity to 46% were samples was observed to oral treatment while 54% of the pseudomonas were resistant tociprofloxacin and 34% sensitive and 66% resistant to levofloxacin respectively.Conclusion: It was found that 54% pseudomonas were resistant to Ciprofloxacin and 66% resistant to levofloxacin. So we shouldalways consider for combination therapy.

The effect of the antiinflammatory IL-1R antagonist anakinra in mice with CF-like lung disease and Pseudomonas aeruginosa infection

Pneumologie ◽  
2016 ◽  
Vol 70 (07) ◽  
Author(s):  
A Schütte ◽  
Z Zhou-Suckow ◽  
J Schatterny ◽  
S Schmidt ◽  
S Hassel ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Lung Disease ◽  
Pseudomonas Aeruginosa Infection

scholarly journals Epidemiology of first/new Pseudomonas aeruginosa infection in cystic fibrosis patients

2010 ◽  
Vol 9 ◽  
pp. S29 ◽  
Author(s):  
L. Zavataro ◽  
G. Taccetti ◽  
L. Cariani ◽  
N. Ravenni ◽  
G. Braccini ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Pseudomonas Aeruginosa ◽  
Pseudomonas Aeruginosa Infection

scholarly journals Rapid evolution and host immunity drive the rise and fall of carbapenem resistance during an acute Pseudomonas aeruginosa infection

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Rachel Wheatley ◽  
Julio Diaz Caballero ◽  
Natalia Kapel ◽  
Fien H. R. de Winter ◽  
Pramod Jangir ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Efflux Pump ◽  
Rapid Evolution ◽  
Carbapenem Resistance ◽  
Host Immunity ◽  
High Definition ◽  
Loss Of Resistance ◽  
Pseudomonas Aeruginosa Infection ◽  
Second Wave

AbstractIt is well established that antibiotic treatment selects for resistance, but the dynamics of this process during infections are poorly understood. Here we map the responses of Pseudomonas aeruginosa to treatment in high definition during a lung infection of a single ICU patient. Host immunity and antibiotic therapy with meropenem suppressed P. aeruginosa, but a second wave of infection emerged due to the growth of oprD and wbpM meropenem resistant mutants that evolved in situ. Selection then led to a loss of resistance by decreasing the prevalence of low fitness oprD mutants, increasing the frequency of high fitness mutants lacking the MexAB-OprM efflux pump, and decreasing the copy number of a multidrug resistance plasmid. Ultimately, host immunity suppressed wbpM mutants with high meropenem resistance and fitness. Our study highlights how natural selection and host immunity interact to drive both the rapid rise, and fall, of resistance during infection.

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