The current trend, in the investigation of staphylococcal infections is to concentrate attention on the bacterium and. its products. Not only does the bacterium receive most attention, but also the prevalent tendency is to experiment in vitro. This thesis presents an attempt to approach the question as a problem in host resistance, rather than one simply of bacterial virulence. Furthermore, partly as a result of inclination, and partly because of the nature of the facilities available, I have limited the study, to the morbid anatomy of the host response, and not its immuno-chemical aspects. The problem has not so much been sought after, but has rather presented itself, in the course of my routine work as a hospital pathologist. The scope of this thesis falls into three main sections: 1. A study of the type of patient who contracts staphylococcal septicaemia; 2. A study of the morbid anatomical changes observed in fatal cases; 3. A, study of the response of the experimental animal to staphylococcal septicaemia. Whilst the importance and complexity of bacterial variations in the production of disease are realised, this thesis is that host resistance is a major factor in the response to, and outcome of, severe staphylococcal infections. Whilst this may appear to be a truism, the staphylococcus does nevertheless claim, perhaps, more than its share of attention. It may be the "villain of the piece", hut that is no reason for neglecting the "piece". Early in the course of this work it became apparent that fatal cases, both in their clinical course, and pathological picture, showed features suggestive of a state of hypersensitivity to the bacterium or its products. The kidneys, and to a lesser degree the lungs, were found to be indices of such a state of hypersensitivity. Therefore, this thesis argues that in staphylococcal septicaemia there may arise a state of hypersensitivity to the bacterium or its products, and that this state, mediated principally by its effect on the kidneys and lungs, is often the decisive factor in a fatal outcome. In presenting this thesis, I am all too well aware of the many questions that have been left unanswered, or questions that have not even been asked. Many new techniques could, with advantage, be utilised in the investigation of this problem. The animal experiments are described, not because they give irrefutable proof of the argument of the thesis, but the findings do provide some comparative and corroborative evidence. I regret the relatively small number of animals that could be used, and the limited scope of the experiments, but I believe that sufficient evidence of structural damage is presented to indicate, and justify, further experimentation - particularly of the serological aspects. Staphylococcal infections are an example of a field of research, where the "climate of opinion", conditions the direction of such research in an almost exclusive fashion. Judging from current medical literature, more people are concerned about the staphylococci present in hospital dust, than are concerned with the pathogen in the human body. I trust that it is not too presumptuous to hope that this thesis will, in some small measure, contribute to a re-orientation of thought, and a different emphasis, concerning staphylococcal infections.