02162nas a2200421 4500000000100000008004100001260001300042653001200055653002600067653002400093653001100117653002700128653001100155653001600166653002300182653001300205653001200218653002400230653000900254653002000263653002500283100001300308700001100321700001300332700001000345700001500355700001900370700001500389700001500404700001300419700001700432700001300449245014100462300001100603490000700614520110500621022001401726 2012 d c2012 Aug10aAnimals10aAntibodies, Bacterial10aAntigens, Bacterial10aBiopsy10aDisease Models, Animal10aFemale10aGlycolipids10aHistocytochemistry10aLepromin10aleprosy10aMacaca fascicularis10aMale10aMonkey Diseases10aMycobacterium leprae1 aWalsh GP1 aCruz E1 aAbalos R1 aTan E1 aFajardo TT1 aVillahermosa L1 aCellona RV1 aBalagon MV1 aWhite VA1 aSaunderson P1 aWalsh DS00aLimited susceptibility of cynomolgus monkeys (Macaca fascicularis) to leprosy after experimental administration of Mycobacterium leprae. a327-360 v873 a
Cynomolgus monkeys are a useful model for human tuberculosis, but susceptibility to M. leprae is unknown. A cynomolgus model of leprosy could increase understanding of pathogenesis-importantly, neuritis and nerve-damaging reactions. We administered viable Mycobacterium leprae to 24 cynomolgus monkeys by three routes, with a median follow-up period of 6 years (range = 1-19 years) involving biopsies, nasal smears, antiphenolic glycolipid-1 (PGL-1) antibody serology, and lepromin skin testing. Most developed evanescent papules at intradermal M. leprae inoculation sites that, on biopsy, showed a robust cellular immune response akin to a lepromin skin test reaction; many produced PGL-1 antibodies. At necropsy, four monkeys, without cutaneous or gross neurological signs of leprosy but with elevated PGL-1 antibodies, including three with nasal smears (+) for acid fast bacilli (AFB), showed histological features, including AFB, suggestive of leprosy at several sites. Overall, however, cynomolgus monkeys seem minimally susceptible to leprosy after experimental M. leprae administration.
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