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Staphylococcus aureus causes an extremely broad range of diseases in human being and animals from superficial skin lesions
such as boils to deep seated infections such as osteomyelitis, endocarditis, and septicaemia.
S. aureus also causes the majority of hospital acquired (nosocomial) bacteraemia infections of contaminated surgical wounds
such as bone and joint infections. S. aureus has become resistant to many commonly used antibiotics such as the penicillin?s,
tetracycline and chloramphenicol and the possibility which increase the seriousness is that the pipeline of novel antibiotics is
poor and there are no vaccines available. Host innate and acquired defences are crucially important in human resistance to
this opportunist pathogen. Such defences are multi-fold and include antimicrobial lipids, enzymes (lipases), complement and
immunoglobulins.
We discovered multi-component factor in serum able to kill S. aureusin vetro with remarkable efficiency 3 log degrees less
(106-103 CFU/ml) within 2 hours. In addition we identify it is likely Staphylococcal receptor as well as putative host effectors of
this activity and use this to isolate serum protein that putatively mediate the activity.
In this study we used electron micrograph imaging (TEM and SEM) to show the morphology of S. aureus during the NRS
killing assay at different time points in an attempt to identify the potential killing mechanism.
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