Buruli ulcer is a skin disease caused by Mycobacterium ulcerans (M. ulcerans). In this review, we introduce our recent studies and other important works. Lesions of Buruli ulcer are usually painless, despite the extensive tissue necrosis. We have reported that mice inoculated with M. ulcerans show nerve degeneration and absence of pain, but the mechanism evoking the nerve damage have not been clarified. In order to define whether mycolactone, a toxic lipid produced by M. ulcerans, can induce nerve damages, we have injected mycolactone A/B to BALB/c mouse footpads. Mycolactone induced footpad swelling, and sensory test showed hyperesthesia on day 7 and 14, recovery on day 21, and hypoesthesia on days 28 and 42. Histologically, nerve bundles showed hemorrhage, neutrophilic infiltration, and loss of Schwann cell nuclei on days 7 and 14. Semithin section studies revealed vacuolar change of Schwann cells started on day 14, which subsided by day 42, but myelinated fiber density remained low. This study suggests that mycolactone directly damages nerves and is responsible for the absence of pain characteristic of Buruli ulcer. In the human lesions, presence of neuritis is reported (Rondini S, 2006), and murine studies showed "autoamputation" (Addo P, 2005). In order to prevent the serious deformities evoked by Buruli ulcer, further studies are necessary.
We aimed to elucidate the patterns and trends of autochthonous leprosy in Japan from 1964 to 2009, to compare them with the findings from other studies of leprosy in decline. Data on registered leprosy cases in Japan in the period 1964-2009 were analysed with reference to trends in case detection, geographical distribution, age at diagnosis, sex, classification and family history. A consistent decline in leprosy case detection was observed in all areas of the country over the period 1964-2009. Highest incidence was consistently in Okinawa. Autochthonous leprosy has not been reported in anyone born in Japan since 1980. Increasing average age and a shift towards lower latitudes were demonstrated throughout the period. Analyses of data on autochthonous cases revealed patterns similar to those reported in other countries with declining leprosy. Okinawa has had the highest incidence of leprosy in all of Japan since the first national survey in 1900. Several possible explanations include the difference of leprosy control history between Okinawa and the rest of Japan, Okinawa's unique geographical condition, large-scale problem of stigma and discrimination against leprosy patients and delayed improvement of socio-economic conditions.
Leprosy is suspected to develop after a long period of latency following infection with Mycobacterium leprae (M. leprae) during infancy, but definitive proof has been lacking. We found a rare case of leprosy in a chimpanzee (Pan troglodytes) born in West Africa (Sierra Leone) and brought to Japan around 2 years of age. At 31, the ape started exhibiting pathognomic signs of leprosy. Pathological diagnosis, skin smear, serum anti-phenolic glycolipid-I (PGL-I) antibody, and by PCR analysis demonstrated lepromatous leprosy. Single-nucleotide polymorphism (SNP) analysis verified the West African origin of the bacilli. This occurrence suggests the possibility of leprosy being endemic among wild chimpanzees in West Africa, potentially posing a zoonotic risk.
平成22年11月9日、10日の両日、国立感染症研究所、戸山庁舎において WHO, South-East Asia Region Office (SEARO), Global Leprosy Programme (GLP)による第3回 Meeting on Sentinel Surveillance for Drug Resistance in Leprosy が開催された。事業の概要と今回の会議について報告する。