Spectrum of activity
Linezolid is effective against all clinically important Gram-positive bacteria—those whose cell wall contains a thick layer of peptidoglycan and no outer membrane—notably Enterococcus faecium and Enterococcus faecalis (including vancomycin-resistant enterococci), Staphylococcus aureus (including methicillin-resistant Staphylococcus aureus, MRSA), Streptococcus agalactiae, Streptococcus pneumoniae, Streptococcus pyogenes, the viridans group streptococci, Listeria monocytogenes, and Corynebacterium species (the latter being among the most susceptible to linezolid, with minimum inhibitory concentrations routinely below 0.5 mg/L). Linezolid is also highly active in vitro against several mycobacteria. It appears to be very effective against Nocardia, but because of high cost and potentially serious adverse effects, authors have recommended that it be combined with other antibiotics or reserved for cases that have failed traditional treatment.Linezolid is considered bacteriostatic against most organisms—that is, it stops their growth and reproduction without actually killing them—but has some bactericidal (killing) activity against streptococci. Some authors have noted that, despite its bacteriostatic effect in vitro, linezolid "behaves" as a bactericidal antibiotic in vivo because it inhibits the production of toxins by staphylococci and streptococci. It also has a post-antibiotic effect lasting one to four hours for most bacteria, meaning that bacterial growth is temporarily suppressed even after the drug is discontinued. Gram-negative bacteria
Linezolid has no clinically significant effect on most Gram-negative bacteria. Pseudomonas and the Enterobacteriaceae, for instance, are not susceptible. In vitro, it is active against Pasteurella multocida, Fusobacterium, Moraxella catarrhalis, Legionella, Bordetella, and Elizabethkingia meningoseptica, and moderately active (having a minimum inhibitory concentration for 90% of strains of 8 mg/L) against Haemophilus influenzae.
Bladder outlet obstruction (or obstructive uropathy) occurs when urine is unable to flow from the kidneys through the ureters and out of the bladder through the urethra. Decreased flow of urine leads to swelling of the urinary tract, called hydronephrosis. This process of decreased flow of urine through the urinary tract can begin as early as during intrauterine life and it prevents normal development of fetal kidneys and fetal urine. Low levels of fetal urine leads to low amniotic fluid levels and incomplete lung maturation. Older children and adults can also experience bladder outlet obstruction; however, this process is usually reversible and isnt associated with as many poor outcomes as in infants with congenital bladder outlet obstruction. Causes
Bladder outlet obstruction is classified based on where along the urinary tract the obstruction occurs, including upper urinary tract obstruction and lower urinary tract obstruction. Depending on the location of the obstruction, one or both sides of the urinary tract will be involved. In approximately 50% of cases of congenital hydronephrosis, there is no known cause. In many cases, obstruction along the urinary tract in utero leads to some form of CAKUT mentioned above. Upper urinary tract obstruction
Upper urinary tract obstruction includes the renal pelvis and upper ureters. Ureteropelvic junction obstruction
Ureteropelvic junction obstruction (UPJ obstruction) is an obstruction at the level of the ureter and renal pelvis. It is the most common cause of hydronephrosis detected in utero and is the most common anomaly detected on prenatal ultrasounds.