The periventricular region was studied in the brains of 129 cases of multiple sclerosis, with the purpose of establishing the mechanism and order of events in the development of the periventricular plaque, and deciding whether there is any relationship between granular ependymitis and such plaques. Periventricular plaques were found in 82.2% of cases. Observation and computerized morphology showed that the early stage of the periventricular plaque is the formation of a lesion around a subependymal vein and that adjacent lesions later coalesce. These plaques do not appear to arise from the ependyma, which is against any role for the CSF in their initial development. Chronic or burnt-out periventricular lesions often show overlying granular ependymitis (10.9% of cases) and subependymal gliosis (17.8%), presumably as a result of the long-continued low-grade inflammatory process. This process, which is not specific for multiple sclerosis, is sometimes associated with transfer of IgG and C3, as shown with peroxidase methods, across the subependymal vein wall and the ependymal epithelium. Increased permeability of the inflamed ependyma constitutes a possible abnormal entry route from plaque to CSF or, in reverse, from CSF to brain.

We report the cloning and sequencing of vanA genes present in the high-level vancomycin- and teicoplanin-resistant clinical isolates Oerskovia turbata 892 and Arcanobacterium (Corynebacterium) haemolyticum 872. The presence of vanA was detected by Southern blotting and PCR and confirmed by DNA sequencing. vanA-like sequences were encoded on plasmids of 15 and 20 kb respectively. The A. haemolyticum 872 DNA sequence was identical to the published vanA sequence of vancomycin-resistant Enterococcus faecium BM4147, but the O. turbata 892 sequence showed three coding changes. Induction experiments indicated that vancomycin resistance in A. haemolyticum 872 and O. turbata 892 was constitutive. SDS-PAGE analysis of membrane proteins showed the presence of a c. 39 kD protein in both clinical isolates whose expression was unaltered in the presence of vancomycin, while a similar protein in E. faecium BM4147 was inducible. Since A. haemolyticum and O. turbata are naturally susceptible to vancomycin, the high-level constitutive resistance seen in these isolates appears to be mediated by vanA. This is the first report confirming the presence of vanA in genera other than Enterococcus.

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THE response of connective tissues to lipid deposition has been the subject of several investigations. Hass (1938) observed that cod-liver oil provokes an eosinophilic and giantcell response in subcutaneous tissue. Subsequently the injected material was converted into a lipofuscin-like substance. Hirsch (1938) found that intravenous injection of a cholesterol-fat mixture causes a giant-cell and fibroblastic reaction in the lungs and connective tissues; cholesterol acetate stimulates a similar giantcell response (Day and French, 1961). Spain (1961) observed that subcutaneous implantation of free cholesterol or desmosterol provokes an inflammatory response and fibrosis. Later it was noted that tripalmitin, tristearin and cholesterol esters are fibrogenic (Spain and Aristizabal, 1962). Hirsch and Weinhouse (1940) noted that emulsified cholesterol esters are inert and are resorbed by the reticuloendothelial system, but nonemulsified esters are intensely sclerogenic. A d a m et al. (1963) confirmed that cholesterol provokes a giantcell reaction and has a sclerogenic action on subcutaneous connective tissues, and found that these effects were prevented by adding phospholipids (lecithin or sphingomyelin) to the cholesterol implant. Later, Adams and Morgan (1967) confirmed with radioisotopes that phospholipid accelerates the resorption of 4-14C-cholesterol from subcutaneous implants; this effect depends upon both the surface active groups and the unsaturated fatty acids of phospholipids. METHODS Implantation of lipiak.Fifty-four male albino rats of weight 280-300 g. were used. The fur on the anterior abdominal wall was removed with a depilating cream and lipids were implanted aseptically under the skin of each quadrant. Solid lipids were inserted with a trocar and cannula (see Adams et af., 1963), whilst liquid lipids were injected with a 1-ml. syringe and widebore needle. The animals were killed so as to enable each lipid to be studied at intervals of 4 days, and 1,2,3,4+ and 6 wk after implantation; the lesions were exposed, measured, I. mni. BACT.-VOL. 94 rig69 63

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