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.
BT - Transactions of the Royal Society of Tropical Medicine and Hygiene C1 - http://www.ncbi.nlm.nih.gov/pubmed/2603189?dopt=Abstract DA - 1989 Jan-Feb DO - 10.1016/0035-9203(89)90735-9 IS - 1 J2 - Trans. R. Soc. Trop. Med. Hyg. LA - eng N2 -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.
PY - 1989 SP - 121 EP - 7 T2 - Transactions of the Royal Society of Tropical Medicine and Hygiene TI - The epidemiology of leprosy in a high prevalence village in Papua New Guinea. VL - 83 SN - 0035-9203 ER -