An epidemic of leprosy occurred among Aboriginal people of the Top End of the Northern Territory following its introduction towards the end of the 19th Century. The extent of this outbreak became apparent through community surveys conducted in the 1950s which revealed that one in 10 Aboriginal people in some areas were affected by leprosy. Initial control activities were outbreak‐focused, directed at case finding and management. Case finding was by systematic community survey. Case management included appropriate rehabilitation and reconstructive surgery. Regular review of treated patients ensured early detection of relapse and detection and treatment of sequelae. Education and full participation of Aboriginal health workers in the diagnosis and management of cases provided local expertise at the hospital and community level. The case detection rate fell from 270 per 100,000 in the Aboriginal population in 1951 to four per 100,000 in 1997. Elimination of transmission is now the objective of the control program. Combining of the tuberculosis and leprosy control activities of the Territory Health Service in 1996 resulted in increased efficiency of the mycobacterial services.

The peat fenlands, including areas where much of the original peat has disappeared, cover about 350,000 acres. At the present time, the land is almost wholly in arable cultivation, the main crops being potatoes, wheat and sugar beet. Potatoes have been the most important crop for more than 50 years and on most farms provide the largest cash return and receive the heaviest manuring.The first part of the paper describes the soils of the peat fenlands, gives a simple method of classification, and shows how the different kinds of soil are related to the maturity and progressive wastage of the peat. The remainder of the paper gives the results of a series of thirty-eight manurial experiments on potatoes on the three main kinds of soil and relates the effects of fertilizers to the manurial requirements of this crop as determined by chemical analysis of the soils.

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It is generally agreed that the metabolic pathway of a drug and its thera peutic activity are relatcd1 2. Some years ag03 metabolic studi e s on the two tuberculostatics 4-pyridyl-oxadiazolone5 and isoniazid, showed that both substances gave in the rat three identical metabolites. This fact was considered sufficient evidence to draw the conc1usion that 4-pyridyl oxadiazolone was metabolised in the body via isoniazid, which latter would be responsible for the tuberculostasis. The two drugs would be therefore clinically identical. Cross resistance studies using the two sub stances against various strains of Mycobacterium tuberculosis showed between 80-90 per cent cross resistance, confirming this view. Studies on 4-pyridyl oxadiazolone5 were therefore stopped, it being considered that it was simply another somewhat less active form of isoniazid.Yet codeine, morphine and heroine are chemically closely related and show similar metabolic pathways in the body. But no one would think of applying them as clinically interchangeable. Their clinicaI and pharma cological spectra are different and well defined, even though their chemistry and metabolic pathways are so similar. Knowledge of the meta bolic pathway is certainly useful, but a great deal of further data such as tissue and organ concentration, chemical stability towards enzymes, par tition coefficients, etc., are necessary before attempting to pronounce on the likely clinicaI spectrum of new substance.It is proposed here to describe one or two surprises we have experienced in research in the above field in the past few years. I.If one subcultures H37 Rv in the presence ofjust sub-liminal doses of isoniazid, resistance develops rapidly as shown in Table I. After six sub cultures the minimal inhibitory dose of isoniazid has risen from I : 40 million to I : 80 thousand.But if 4-pyridyl-oxadiazolone is cultured under the same conditions against H37 Rv resistance emergence is much slower (Table I). 2.It seemed, therefore, that the two substances INH and 4-pyridyl oxadiazolone were not absolutely biologically identical, at least in vitro, otherwise the resistance emergence rates would have been identical too.If their biological spectra are not absolutely identical, it was thought likely that, in the presence of 4-pyridyl-oxadiazolone, the resistance emergence rate towards INH would be modified. If the two substances possess exactly the same biological spectrum, a I : I mixture of INH and 4-pyridyl-oxadiazolone should show a resistance emergence rate'