Leprosy control in the Northern Territory.

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.

Leprosy in the tropics and Australia.

Leprosy is no longer the feared disease of the past, but it still causes significant morbidity in countries where it is endemic, and it is estimated that up to 2500 million people are at risk of contracting the disease. Control with dapsone monotherapy over the past 20-30 years has been effective in some countries but secondary and, more recently, primary drug resistance is now widespread. This situation prompted the development of multidrug therapy regimens which are proving highly effective. Here the natural history and clinical features are described, as well as the history and impact of leprosy in Australia. Early diagnosis and the current multidrug regimens offer hope for long-term control of the disease.

The fate of the left kidney after end renosplenic shunt in experimentally induced extrahepatic portal hypertension.

Extrahepatic portal hypertension was induced in the rabbit by a one-stage complete ligation of the portal vein. End renal vein to side splenic vein shunts (renosplenic) were performed with haemorrhagic necrosis of the left kidney occurring after ligation of the left renal vein lateral to the adrenolumbar tributary. Thus the ureteric, lumbar, and pericapsular collaterals cannot adequately drain the left kidney. Ligation of the left renal vein on the medial side of the adrenolumbar tributary maintained a patent left renal vein in all cases with 60% of left kidney biopsies showing no histological evidence of changes to glomeruli or tubules, and the remainder showing early acute tubular necrosis.

Freeze-dried microarterial allografts.

Rehydrated freeze-dried microarterial allografts were implanted to bridge arterial defects using New Zealand White rabbits as the experimental model. Segments of artery from the rabbit ear and thigh were harvested and preserved for a minimum of 2 weeks after freeze-drying. These allografts, approximately 1 mm in diameter and ranging from 1.5 to 2.5 cm in length, were rehydrated and then implanted in low-pressure and high-pressure arterial systems. Poor patency was noted in low-pressure systems in both allografts and autografts, tested in 12 rabbits. In the high-pressure arterial systems, allografts that were freeze-dried and reconstituted failed in a group of 10 rabbits with an 8-week patency rate of 30 percent. Gamma irradiation in an effort to reduce infection and antigenicity of grafts after freeze-drying was associated with a patency rate of 10 percent at 8 weeks in this system in another group of 10 rabbits. Postoperative cyclosporin A therapy was associated with a patency rate of 22.2 percent in the high-pressure arterial system in a 9-rabbit group. Control autografts in this system in a group of 10 rabbits showed a 100 percent patency at 8 weeks. Microarterial grafts depend on perfusion pressure of the vascular bed for long-term patency. Rehydrated freeze-dried microarterial allografts do not seem to function well in lengths of 1 to 2.5 cm when implanted in a high-pressure arterial system. Freeze-dried arterial allografts are probably not antigenic.

Clinical significance of changes in serum proteins, immunoglobulins, and autoantibodies in leprosy.

Changes in the level of acute phase reactants such as C-reactive protein (CRP), serum globulins, and autoantibodies have been reported previously in patients with leprosy, particularly at the lepromatous end of the spectrum. The clinical significance of these findings was investigated by comparing the same parameters of humoral immune function in populations of Australian Aboriginals with stable treated leprosy and relevant contact groups including a) noninfected European sporadic contacts and b) healthy Aboriginal relatives of patients with confirmed leprosy. Raised levels of CRP and immunoglobulins and the higher frequency of autoantibodies seen in leprosy patients compared with sporadic contacts are probably related to differences in the incidence of nonleprous infection rather than to leprosy per se. Comparable results were obtained in the leprosy patients and their family contacts. The data highlight the need to use antigen-specific assays for determining the significance of changes in acute phase reactants and for distinguishing between the primary and secondary effects of Mycobacterium leprae infection.

Nerve calcification caused by leprosy in northern territory aboriginals.

Three cases of nerve calcification caused by leprosy (Hansen's disease) in Aboriginal patients from the Northern Territory of Australia are reported. This is a rare manifestation of the disease and is the result of direct involvement of peripheral nerves with abscess formation and is usually seen in tuberculoid or borderline types of leprosy.

Peripheral nerve biopsies in the diagnosis of leprosy in Aboriginal patients from the Northern Territory of Australia.

In the 12 years from 1964 to 1976, 171 peripheral nerve biopsies were taken from 81 Aboriginal patients in the Northern Territory of Australia, in whom a diagnosis of leprosy was either known or strongly suspected. Sixty-eight biopsy samples were from 19 patients known to have leprosy, and who were under assessment for nerve grafting, results of which have already been published. We describe here the histopathological findings in the remaining 62 patients, in whom a diagnosis of leprosy was suspected on clinical grounds, backed in many cases by abnormalities of nerve conduction. Forty-one patients (66%) had abnormal histopathological findings in the nerve biopsy sample, 19 (31%) showing definite evidence of leprosy. Several patients with enlarged peripheral nerves, in whom the biopsy findings did not confine leprosy, remain under observation; their future investigation will include lymphocyte transformation tests and testing with refined lepromin, together with repeat nerve biopsy, where ethical and feasible. The clinical and epidemiological data suggest that a previous, and perhaps self-healing, form of leprosy may account for the neurological findings.

Nerve grafting in leprosy

SIR, - Dr Crawford says that nerve grafting should not be doe in leprosy, because the sensory loss leading to burns, trophic ulcers, cellulitis, osteomyelitis, and bone resorption is due to a generalised peripheral neuropathy rather than a localised lesion of peripheral nerves.

Nerve conduction studies in leprosy.

Motor and sensory nerve conduction studies have been performed on the peripheral nerves in the upper and lower limbs of 30 control subjects, and 36 subjects with leprosy from the Aboriginal population of the Northern Territory of Australia. Impairment of conduction was demonstrated in the vast majority of clinically abnormal nerves, and a large proportion of nerves which appeared clinically to be uninvolved. In a third group of subjects, abnormal conduction was demonstrated in a significant number of nerves which were considered to be clinically enlarged but in whom the diagnosis was initially in doubt. The majority of these patients were subsequently proven to have leprosy. It is concluded that nerve conduction studies are of considerable value in the diagnosis and management of leprosy.

Nerve grafting in leprosy / Nerve grafting in leprosy

The most serious disability from which patients with leprosy suffer is sensory