Lujan R, Chapman W L, Hanson W L, Dennis V A
Exp Parasitol. 1986 Jun;61(3):348-58. doi: 10.1016/0014-4894(86)90190-6.
Twelve male and 8 female feral owl monkeys, Aotus trivirgatus, were inoculated intradermally at the dorsal base of the tail with 2 X 10(7) promastigotes (strains WR 128 or WR 539) or 5 X 10(5) amastigotes (strain WR 128) of Leishmania braziliensis panamensis, and the progression and regression of subsequent lesions were examined for up to 13 or 54 weeks after inoculation. Three of these monkeys had been infected previously with L. donovani, had been treated with meglumine antimoniate, and had recovered clinically from visceral leishmaniasis. All monkeys developed a cutaneous nodule at the inoculation site, but the size of the nodule varied (maximum 78 to 326 mm2 between 4 and 16 weeks after inoculation.) The initial nodule became ulcerated after 4 to 8 weeks in 17 of the 20 monkeys, and the ulcers persisted for 4 to 16 weeks until covered by a crust. Primary lesions disappeared by 17 to 52 weeks after inoculation, but satellite lesions, of similar morphology to the primary lesions but smaller, developed after 4 to 21 weeks in 14 of the monkeys. The primary nodule was excised in 4 monkeys at 6 weeks and did not recur nor did satellite lesions subsequently develop. The satellite lesions (median total number of 4, range 1 to 25) were adjacent to or at a maximum distance of 6 cm from the primary lesion, varied in size from 3 to 117 mm2, and persisted for 10 to 37 weeks. At 6 and 8 weeks after inoculation, tissue from the cutaneous leishmanial lesions from five monkeys was excised and examined. The granulomatous leishmanial lesions, located primarily in the dermis and subcutis, consisted of macrophages containing parasites, lymphocytes, plasma cells, and occasionally eosinophils. Satellite lesions at 14 weeks after inoculation were similar grossly and microscopically to the initial nodule. No significant differences were observed between promastigote or amastigote derived infections, between the two strains of L. b. panamensis, or between the course of infection based on the sex, age, karyotype, or country of origin of the owl monkeys. Cutaneous lesions developed when 5 X 10(5) amastigotes of L. b. panamensis (strain WR 128) were inoculated intradermally into the dorsal base of the tail, the upper eyelid, and the thorax of three monkeys. Leishmanial nodules which developed on the thorax regressed rapidly (after 2 to 5 weeks) whereas those on the upper eyelid and at the dorsal base of the tail persisted for 5 to 45 weeks after inoculation.(ABSTRACT TRUNCATED AT 400 WORDS)
将2×10⁷前鞭毛体（WR 128或WR 539株）或5×10⁵无鞭毛体（WR 128株）的巴拿马利什曼原虫皮内接种于12只雄性和8只雌性野生夜猴（Aotus trivirgatus）的尾背基部，接种后长达13或54周观察后续病变的进展和消退情况。其中3只猴子先前感染过杜氏利什曼原虫，接受过葡甲胺锑酸盐治疗，且已从内脏利什曼病临床康复。所有猴子在接种部位均出现皮肤结节，但结节大小各异（接种后4至16周最大为78至326平方毫米）。20只猴子中有17只在接种后4至8周初始结节发生溃疡，溃疡持续4至16周直至结痂覆盖。原发性病变在接种后17至52周消失，但14只猴子在接种后4至21周出现了与原发性病变形态相似但较小的卫星病变。4只猴子在6周时切除原发性结节，结节未复发，卫星病变也未随后出现。卫星病变（中位数总数为4个，范围为1至25个）与原发性病变相邻或距其最大距离为6厘米，大小从3至117平方毫米不等，持续10至37周。在接种后6周和8周，切除5只猴子皮肤利什曼病损组织进行检查。肉芽肿性利什曼病损主要位于真皮和皮下组织，由含有寄生虫的巨噬细胞、淋巴细胞、浆细胞以及偶尔的嗜酸性粒细胞组成。接种后14周的卫星病变在大体和显微镜下与初始结节相似。在由前鞭毛体或无鞭毛体引起的感染之间、巴拿马利什曼原虫的两个菌株之间，或根据夜猴的性别、年龄、核型或原产国的感染过程之间，均未观察到显著差异。将5×10⁵无鞭毛体的巴拿马利什曼原虫（WR 128株）皮内接种于3只猴子的尾背基部、上眼睑和胸部时，出现了皮肤病变。胸部出现的利什曼结节迅速消退（2至5周后），而上眼睑和尾背基部的结节在接种后持续5至45周。（摘要截于400字）
