:
Aminoglycosides that are derived from bacteria of the Streptomyces genus are named with
the suffix mycin, whereas those that are derived from Micromonospora are named with the
suffix micin.
SPECTRUM OF ACTIVITY:
These antibiotics are most often used to treat infections involving aerobic, gram-negative
bacteria, such as Acinetobacter, Pseudomonas, and Enterobacter. In some cases, certain
microbacteria, like the bacteria responsible for causing tuberculosis, are vulnerable to this
type of antibiotic. Aminoglycosides are most often used as empiric therapy for serious
infections, including complicated intra-abdominal infections, nosocomial respiratory tract
infections, septicemia, and complicated urinary tract infections. This type of antibiotic is
mostly unable to treat fungi, anaerobic bacteria, and viruses.
GENTAMYCIN AS AN ANTIBIOFILM.
COMMONLY USED BRAND NAME(S):
(1)Alcomicin(2) Garamycin(3)Genoptic Liquifilm(4) Genoptic S.O.P.(5) Gentacidin(6)
Gentafair(7) Gentak(8) Ocu-Mycin(9) Spectro-Genta.
STRUCTUREOF GENTAMYCIN:
CHEMICAL GROUP
aminoglycosides
METHODS:
Using Staphylococcus aureus, Pseudomonas aeruginosa and Escherichia coli bioluminescent strains, we studied the
combination of L-arginine and gentamicin against planktonic persisters through time-kill curves of late stationaryphase cultures. In vitro biofilm tolerance towards gentamicin was assessed using PVC 96 well-plates assays.
Efficacy of gentamicin as antibiotic lock treatment (ALT) at 5 mg/mL at different pH was evaluated in vivo using a
model of totally implantable venous access port (TIVAP) surgically implanted in rats.
Amikacin as an antibiofilm:
PRESCRIBED FOR: Amikacin is used for serious bacterial infections like bacterial meningitis, infected burns,
cystic fibrosis, and severe urinary tract infections. It used when the infecting organism is resistant to tobramycin and
gentamicin.
Generic Name: Amikacin sulfate
BRAND NAME: Amikin
CHEMICAL GROUP
aminoglycosides
STRUCTURE:
cation chelator EDTA on the bacterial killing of in vitro biofilms formed by an array of clinical
strains responsible for CRBSI and representative of epidemiologically relevant bacterial
species.
METHOD:
we focused on the most antibiotic-tolerant strains including CoNS (n=4), Staphylococcus
aureus (n=4), Enterococcus faecalis (n=2), Pseudomonas aeruginosa (n=4) and
Enterobacteriaceae (n=4). We used an in vitro biofilm model (96-well plate assay) to study
biofilm tolerance and tested various combinations of antibiotics and non-antibiotic
adjuvants. Gentamicin, amikacin or vancomycin was combined with disodium EDTA or larginine for 24 h to reproduce the antibiotic lock therapy (ALT) approach. Killing of biofilm
bacteria was measured by cfu quantification after a vigorous step of pipetting up and
down in order to detach all biofilm bacteria from the surface of the wells.
The aim of this study was to determine the effect of subinhibitory concentrations (sub-MICs)
of ciprofloxacin, amikacin and colistin on biofilm formation, motility, curli fimbriae formation
by planktonic and biofilm cells of E. coli strains isolated from the urine of patients with
various urinary system infections. Quantification of biofilm formation was carried out using a
microtiter plate assay and a spectrophotometric method. Bacterial enumeration was used to
assess the viability of bacteria in the biofilm. Curli expression was determined by using
YESCA agar supplemented with congo red. Using motility agar the ability to move was
examined. All the antibiotics used at sub-MICs reduced biofilm formation in vitro, decreased
the survival of bacteria, but had no effect on the motility of planktonic as well as biofilm
cells. The inhibitory effect of sub-MICs of antimicrobial agents on curli fimbriae formation
was dependent on the form in which the bacteria occurred, incubation time and antibiotic
used. Our results clearly show that all the three antibiotics tested reduce biofilm production,
interfere with curli expression but do not influence motility. This study suggests that
ciprofloxacin, amikacin and colistin may be useful in the treatment of biofilmassociated infections caused by E. coli strains.
2011: http://www.ncbi.nlm.nih.gov/pubmed/21333405
OBJECTIVES:
To study the resistance of biofilms developed by non-pigmented rapidly growing
mycobacteria (NPRGM) against amikacin, ciprofloxacin and clarithromycin in an in vitro
model using clinical strains of different species.
DESIGN:
Antimicrobial susceptibilities of different clinical strains of Mycobacterium abscessus,
Mycobacterium chelonae, Mycobacterium fortuitum, Mycobacterium peregrinum,
Mycobacterium mucogenicum and Mycobacterium mageritense using conventional
techniques were measured. Biofilm resistance was measured by using the sandwich
technique developed by Anderl et al. using a concentration of antibiotic of 50mg/L.
Penetration of antibiotics through biofilm was measured using the same technique with
minimal modifications.