A 7-year-old intact male American cocker spaniel that had undergone removal of a nictitating gland was referred for severe ulcerative keratitis. Slit-lamp examination showed swelling of the eyelid, mucopurulent discharge, conjunctival
injection and chemosis, diffuse corneal edema and opacity, and a deep ulcer in central cornea. Gram staining of discharge from the eye demonstrated Gram-positive cocci. Despite topical ofloxacin, oxytetracycline and polymyxin B ophthalmic solution and intravenous cefazolin, there was no improvement. Cultures revealed MRSA that was sensitive only to chloramphenicol, vancomycin, lincomycin, and Selleckchem DAPT clindamycin. The antibiotic regimen was changed to topical and systemic chloramphenicol. After 9days of treatment, although inflammation started to be resolved, the dog developed nonregenerative anemia. The antimicrobial regimen was changed again to topical and systemic vancomycin. Inflammation continued to improve over the next week. MRSA should be considered a potential organism in infectious keratitis, especially when general antibiotics are not effective. Although topical and systemic CBL0137 cost chloramphenicol and/or vancomycin are effective for treating MRSA keratitis, vancomycin should
only be used when culture and susceptibility results indicate it is appropriate and no other options are available. To our knowledge, this is the first detailed case report of MRSA keratitis in a dog.”
“Rheumatoid arthritis (RA) is a chronic, disabling disease of the synovial joints, thought to be autoimmune in origin. The emergence of biologic therapies has proven to be highly successful in effectively treating RA in the
majority of cases. However, the cost of these agents is high and some patients do not respond to these drugs, or they suffer from adverse events. This article will review the currently available data on efficacy and the clinical, genetic, and biomarkers of response to these biologic therapies in RA.
The anti-tumour IWR-1-endo necrosis factor-alpha (anti-TNF alpha) agents, adalimumab, etanercept and infliximab, act to neutralize the pro-inflammatory cytokine. Response to these agents is higher in patients receiving concurrent disease modifying anti-rheumatic drugs or non-steroidal anti-inflammatory drugs, in those with lesser disability, and in non-smokers. Many genetic predictors of response have been investigated, such as the shared epitope, the TNF gene and its receptors, but none have been absolutely confirmed. Synovial expression of TNF alpha has been suggested as a biomarker of response, while anti-cyclic citrullinated peptide antibody and rheumatoid factor (RF)-positivity predict poor response. Newer biologic agents include the interleukin (IL)-1 receptor antagonist anakinra, the B-cell depleting agent rituximab, the selective costimulation modulator abatacept, and the anti-IL-6 receptor monoclonal antibody tocilizumab.
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