ABSTRACT
BACKGROUND: Staphylococcus aureas bacteraemia can spread to cause endocartitis, spondylodiscitis or infection of vascular or joint prostheses. Endogenous endophtalmitis is a serious complication which may result in permanent visual loss of the affected eye. Treatment consists of intra-ocular injection of antibiotics or a vitrectomy. CASE DESCRIPTION: A 79-year-old man attended the emergency department because of septic arthritis. Blood cultures were positive for a S. aureus bacteraemia. On the second day of admission he developed a blurred vision and he was diagnosed with an endophtalmitis. The patient was referred to an academic hospital for treatment with intra-ocular antibiotics. After treatment his vision improved again. CONCLUSION: Visual complaints should be taken seriously when a patient has a proven S. aureus bacteraemia. Infectious disease consultation may accelerate early recognition, referral and treatment. When endophtalmitis is suspected, it is essential to refer the patient to a treatment centre where intra-ocular antibiotics can be administered.
Subject(s)
Bacteremia/microbiology , Eye Infections, Bacterial/microbiology , Staphylococcal Infections/microbiology , Staphylococcus aureus , Vision Disorders/microbiology , Aged , Anti-Bacterial Agents/therapeutic use , Arthritis, Infectious/drug therapy , Arthritis, Infectious/microbiology , Bacteremia/drug therapy , Eye Infections, Bacterial/drug therapy , Humans , Male , Staphylococcal Infections/drug therapy , Vision Disorders/drug therapyABSTRACT
In mice, the deletion of either Mdm2 or Mdm4 results in a p53-dependent embryonic lethality. We used zinc-finger nucleases to construct mutations in the mdm2 and mdm4 genes of zebrafish. Although the loss of mdm2 results in a p53-dependent early embryonic lethality, mdm4 mutant fish are viable and grow to adulthood. We also found that an in-frame five-amino acid deletion in mdm2 creates a novel hypomorphic allele. The lethal phenotype observed in the mdm2 mutant fish could be partially rescued by injecting mRNA encoding functional Mdm2, and this required the E3 ligase activity of the protein. Complete rescue was obtained by crossing the mdm2 mutant fish onto a p53M214K mutant background. Although p53 mutant fish on a wild-type mdm2 background were shown to accumulate high levels of p53 protein specifically in tumor tissues, we detected extensive staining of p53 in many normal tissues of the mdm2-p53M214K double-mutant fish. Our results are suggestive of the hypothesis that p53 protein accumulates during tumor formation as a result of tumor-specific inactivation of the Mdm2 pathway.
