Since the discovery of Borrelia recurrentis as a cause of relapsing fever (1), biologists have been intrigued by the ability of the organism to cause repeated attacks of disease in man. Early investigators attempted to elucidate the relapse phenomenon by comparing the serologic responses of recovered animals with original and relapse populations of spirochetes. Most found that peak antibody titers to relapse spirochetes subsequently appeared in the order in which the spirochete populations were isolated (2). This finding suggested that the surface antigens of the organism had been changed and that growth of a modified population was responsible for each relapse. However, this concept was not uniformly accepted. Some investigators could not detect an immune response with any serologic test then in use. As explained in a review by Schuhardt (3), there were many reasons for controversy about early theories on the mechanisms of relapse. Many strains studied had been grown by repeated passage in animals without a complete record of factors that affected the relapse phenomenon. A variety of tests were used to measure serologic responses, and there was serious disagreement about which tests gave valid results. In addition, the phenomenon was different in the many animal hosts used to study the process.In recent years, little progress has been made in elucidating the true nature of the phenomenon. According to one popular concept (3, 4), new serotypes arise from borreliae that escape the specific antibody response and retreat into organs where new antigens are unmasked. These changed organisms penetrate the blood stream and cause a relapse that, in turn, is terminated when the host produces a specific serologic response to that relapse population. This process is repeated until death intervenes or a complete immunity is established.The development of a medium for cultivating borreliae (5, 6) and the demonstration by Coffey and Eveland (7,8) that individual organisms in a relapse population can be identified by specific fluoresceinated antiserum could have enabled new approaches to a study of the phenomenon. Investigating the relapse phenomenon in rats, they identified four serotypes of B. hermsii with rabbit and rat antisera conjugated with fluorescein-isothiocyanate (FITC) 1 according to a modification of the method of Gordon et al. (9). Initially, we attempted to repeat their work with antisera prepared in rabbits against the original and three relapse populations of B. hermsii obtained from a single mouse. Borreliae in smears of mouse blood were stained with these antisera by indirect immunofluorescence, but organisms from one population could not be clearly distinguished from those of the other three. Furthermore, the variability *

This is the first epidemiological study of Australian biopsy-proven GCA patients. Age at onset and gender associations were similar to other Western populations. There was a high burden of steroid use in these patients.

Adrenal nodules, suppressed ACTH and increased VP sensitivity may represent preclinical disease, allowing early detection, and treatment, of affected individuals. In AIMAH-01, increased VP sensitivity may be due to adrenal VP receptor overexpression. In these kindreds, VPs-AIMAH is familial, and autosomal dominant inheritance is most likely.

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SC should always be considered in the histological differential diagnosis of any eyelid lesion which resembles BD, particularly if the upper eyelid is involved or if multivacuolated cytoplasmic clear cell changes are seen.