Neomycin is not administered via injection, as it is extremely nephrotoxic (damaging to kidney function) even when compared to other aminoglycosides. The exception is when neomycin is included, in small quantities, as a preservative in some vaccines – typically 25 μg per dose. Spectrum
Similar to other aminoglycosides, neomycin has excellent activity against gram-negative bacteria and is partially effective against gram-positive bacteria. It is relatively toxic to humans, with allergic reactions noted as a common adverse reaction (see: hypersensitivity). Physicians sometimes recommend using antibiotic ointments without neomycin, such as Polysporin. The following represents minimum inhibitory concentration (MIC) susceptibility data for a few medically significant gram-negative bacteria. Enterobacter cloacae: >16 μg/ml
Escherichia coli: 1 μg/ml
Proteus vulgaris: 0.25 μg/ml

Side effects
In 2005–06, Neomycin was the fifth-most-prevalent allergen in patch test results (10.0%). It is also a known GABA gamma-Aminobutyric acid antagonist and can be responsible for seizures and psychosis. Like other aminoglycosides, neomycin has been shown to be ototoxic, causing tinnitus, hearing loss, and vestibular problems in a small number of patients. Patients with existing tinnitus or sensorineural hearing loss are advised to speak with a healthcare practitioner about the risks and side effects prior to taking this medication. Molecular biology
Activity
Neomycins antibacterial activity stems from its binding to the 30S subunit of the prokaryotic ribosome, where it inhibits prokaryotic translation of mRNA.Neomycin also exhibits a high binding affinity for phosphatidylinositol 4,5-bisphosphate (PIP2), a phospholipid component of cell membranes. Resistance
Neomycin resistance is conferred by either one of two kanamycin kinase genes.
Patients report an ongoing battle to distinguish themselves from those with psychiatric disorders, such as delusions of parasitosis and other psychiatric conditions. Pathophysiology
Chronic and repetitive scratching, picking, or rubbing of the nodules may result in permanent changes to the skin, including nodular lichenification, hyperkeratosis, hyperpigmentation, and skin thickening. Unhealed, excoriated lesions are often scaly, crusted or scabbed. Many patients report a lack of wound healing even when medications relieve the itching and subsequent scratching.Patients often:
seek treatment during middle-age, although PN can occur at any age. have a history of chronic severe pruritus. have a significant medical history for unrelated conditions. develop liver or kidney dysfunctions. develop secondary skin infections. have a personal or family history of atopic dermatitis. have other autoimmune disorders. have low vitamin D levels. Diagnosis
Diagnosis is based on visual examination and the presence of itching. A skin biopsy is often performed to exclude other diseases. Lesion biopsies usually show light inflammation, sometimes with increased numbers of eosinophils. A culture of at least one lesion will rule out staphylococcus infection, which has been significantly linked to atopic dermatitis. Treatment
Prurigo nodularis is very hard to treat, but current therapies include steroids, vitamins, cryosurgery, thalidomide and UVB light. In the event that staphylococcus or other infection is present, antibiotics have proven effective, but tend to cause more harm than good for this particular disease. A physician may administer a strong dose of prednisone, which will almost immediately stop the itch/scratch cycle. However, cessation of steroids allows relapse to occur, usually within a few weeks.