Novel in vitro pharmacodynamic model simulating ofloxacin pharmacokinetics in the treatment of Pseudomonas aeruginosa biofilm-associated infections

The conventional in vitro models simulate pharmacodynamics of antibiotics in the treatment of planktonic Pseudomonas aeruginosa. In this study, we propose a novel pharmacodynamic model of ofloxacin activity in the treatment of P. aeruginosa biofilm. P. aeruginosa biofilm carrying coupons were suspended in a continuous flow central compartment bioreactor [CCB]. In the CCB, the pharmacokinetics of different ofloxacin dosing regimens were simulated. Samples from the coupons and the CCB were assessed for viability of the biofilm and the shedding planktonic cells, respectively, over 24 h. In addition, ofloxacin concentrations were assessed in each sample withdrawn for the CCB using bioassay method. The microbiological outcomes on P. aeruginosa biofilm and the shedding planktonic cells in response to different ofloxacin dosing regimens were not parallel and this may explain the non-coincidence of microbiological and clinical outcomes with biofilm associated infections. The current study has introduced unprecedented novel dynamic model for the assessment of the microbiological outcome on both biofilm and shedding planktonic cells of P. aeruginosa in response to different dosing regimens of ofloxacin which in turn can simulate the clinical outcomes in biofilm associated infections of P. aeruginosa, e.g. cystic fibrosis. Furthermore, different scenarios of antibiotic dosing regimens against biofilm related infections can be mimicked using such model

Unexpected induction of resistant Pseudomonas aeruginosa biofilm to fluoroquinolones by diltiazem: a new perspective of microbiological drug-drug interaction

The increase of multi-drug resistant Pseudomonas aeruginosa infections is a worldwide dilemma. At the heart of the problem is the inability to treat established P. aeruginosa biofilms with standard antibiotic therapy, including fluoroquinolones. We address a previously unstudied question as to the effect of a commonly prescribed calcium channel blocker [CCB] diltiazem on the biofilm growth. Real-time monitoring of the overall growth and killing of P. aeruginosa biofilm during fluoroquinolones therapy in the presence and absence of diltiazem was performed. In this study, we demonstrate that for P. aeruginosa biofilms, resistance to the first-line fluoroquinolones may be induced by the commonly prescribed calcium channel blocker diltiazem

Effectiveness of intranasal sodium cromoglycate 2 in catarrhal children / in catarrhal children

Clinical and laboratory evaluation of the effectiveness of using intranasal sodium cromoglycate [SCG] 2% in 48 children during their catarrhal stage was studied. The diagnosis of catarrhal reaction was confirmed through proper history taking, clinical examination, x-ray and allergelogical tests. Patients were maintained on sodium cromoglycate 2% spray 4 times daily for 4 weeks. The response to the therapy was evaluated every 2 weeks for the successive 2 months. From the start of therapy. Clinical and laboratory assessment was done according to the degree of the severity of nasal symptoms, mean levels of IGE, eosinophilic count in the sera and mean of positive nasal smears for eosinophils. The results before and after the treatment were presented. This study showed that application of intranasal sodium cromoglycate 2% is effective in decreasing the incidence of recurrent upper respiratory tract infections and controlling the nasal symptoms in catarrhal children. Consequently, this effect helped in avoiding unnecessary surgery. The drug was well tolerated with no side effects throughout the study period

Vitiligo: an added risk factor to aminoglycosides ototoxicity

Hearing assessment in 30 vitiligo patients revealed the presence of mild to moderate subclinical high tone sensorineural deafness in 11 patients [36.7%]. Auditory brain stem response [ABR] was done for patients with moderate affection. In these patients, there was a significant decrease of the latency of the peak of wave 1 indicating a numerical decrease of melanocytes in the inner ear which may result in cochlear sensorineural hearing loss. There was also a significant increase of the interpeak latency of waves I-III. This can be explained by the presence of abnormal synaptic activity from the auditory nerve to the superior olivary nucleus. The present work suggests that destruction of the melanocytes in the inner ear of vitiligo patients is responsible for disturbance of the auditory function. This finding might warrant tagging vitiligo patients against further auditory damage by the use of ototoxic drugs like aminoglycosides