IgM serum antibodies to phenolic glycolipid-I and clinical leprosy: two years' observation in a community with hyperendemic leprosy.

A village population with hyperendemic leprosy in Papua New Guinea was repeatedly examined for clinical leprosy and for serum IgM antibodies to phenolic glycolipid-I (APGL-I) over 2 years between 1984 and 1986. In 1984, serum APGL-I was elevated in 15% of the subjects without clinical leprosy, and the prevalence of seropositivity was not significantly different in subjects from households with or without leprosy. In 1986, the prevalence of elevated serum APGL-I in leprosy-free subjects had risen to 23%. The incidence of seroconversion from APGL-I negative to APGL-I positive was 9.5% per year (95/1000 person years) in 253 subjects tested in 1984 and 1986. During the same period, 27 of 40 (67%) leprosy-free subjects reverted from positive to negative. The positive seroconversion rate in the community was higher than the incidence of clinical leprosy (11.2/1000 person years) over the same period. However, elevated serum APGL-I was not associated with clinical disease and failed to predict the development of disease over 2 years. The significance of persistent seropositivity found in 14 (5%) leprosy-free subjects is uncertain.

The epidemiology of leprosy in a high prevalence village in Papua New Guinea.

In a village of about 1000 people in Papua New Guinea the prevalence of clinical leprosy was 8.6% compared to about 3% in surrounding villages. This exceptionally high prevalence could not be explained by recent introduction of the disease or by social factors. Dapsone-resistant disease and faulty compliance with treatment are considered to be contributory to persistent infectivity of old cases which, together with the presence of 20 previously undiagnosed cases, comprised a large infective source. Social ostracism of cases was not observed and the extensive social mixing of all ages would facilitate widespread dissemination of infection. A high prevalence, particularly in children, of elevated levels of IgM antibody to phenolic glycolipid-1 Mycobacterium leprae specific antigen suggests frequent subclinical infection. The greater prevalence of clinical leprosy following childhood in the village favours altered susceptibility following exposure in childhood. There was a higher prevalence of leprosy in close relatives of cases when compared with the same relatives of age and sex matched leprosy-free controls. The occurrence of familial clustering of leprosy in a hyperendemic area with intense transmission suggests that unidentified inherited factors influence susceptibility to clinical leprosy. It is suggested that the clustering of adverse inherited traits through intermarriage may explain this hyperendemic focus on leprosy.

BCG vaccination in leprosy: final results of the trial in Karimui, Papua New Guinea, 1963-79.

The efficacy of BCG vaccine in preventing the clinical manifestations of leprosy in a tuberculosis-free area of Papua New Guinea is reported. Between 1963 and 1966 a total of 5356 subjects, randomized to receive BCG or saline inoculations, were examined for leprosy before the vaccination and surveillance was continued until 1979. BCG afforded 48% protection against clinical leprosy, being most effective against borderline tuberculoid leprosy and in children vaccinated when under 15 years old. Protection was evident within 12 months in those vaccinated between the ages of 10 and 15 years but was delayed in other age groups. There was evidence for accelerated manifestations of tuberculoid leprosy in children vaccinated when under 5 years of age. Tuberculin sensitivity was more likely to be sustained following multiple BCG inoculations; vaccinees with sustained tuberculin sensitivity had the lowest incidence of leprosy, but protection was also evident in tuberculin-negative vaccinees. These results may have implications for ongoing trials of leprosy vaccine incorporating BCG.

BCG vaccination in leprosy: Final results of the trial in Karimui, Papua New Guinea, 1963-79

The efficacy of BCG vaccine in preventing the clinical manifestations of leprosy in a tuberculosis-free area of Papua New Guinea is reported. Between 1963 and 1966 a total of 5356 subjects, randomized to receive BCG or saline inoculations. were examined for leprosy before the vaccination and surveillance was continued until 1979

BCG afforded 48 per cent protection against clinical leprosy, being most effective against borderline tuberculoid leprosy and in children vaccinated when under 15 years old. Protection was evident within 12 months in those vaccinated between the ages of 10 and 15 years but was delayed in other age groups. There was evidence for accelerated manifestations of tuberculoid leprosy in children vaccinated when under 5 years of age. Tuberculin sensitivity was more likely to be sustained following multiple BCG inoculations; vaccines with sustained tuberculin sensitivity had the lowest incidence of leprosy, but protection was also evident in tuberculin-negative vaccinees. These results may have implications for ongoing trials of leprosy vaccine incorporating BCG(AU)

Use of phenolic glycolipid 1 for serodiagnosis of leprosy in a high prevalence village in Papua New Guinea.

This study reports on the usefulness of an IgM phenolic glycolipid 1 (PGL-1) ELISA for serodiagnosis of leprosy in the first year of a prospective longitudinal community survey in a high (8.8%) prevalence village in Papua New Guinea. The IgM PGL-1 ELISA had limited value as a screening method for detection of new cases. Many normal persons, particularly children, had elevated IgM anti-PGL-1 antibodies, presumably a consequence of early subclinical infection.