Stephanurus dentatusの寄生によるイノシシ肝臓の病理学的所見

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　宮崎県下で捕獲した体重10kg内外の幼イノシシ9頭を剖検したところ, うち4頭の肝臓に S. dentatus(幼若型)の寄生とそれに伴う病変を認めた. 肝臓の病変は血管系(門脈枝･動脈枝)の病変と肝実質のそれとに大別される.これらの病変は各肝葉に発現するが,とりわけ肝門部に多発の傾向がみられた.　血管病変としては,虫体の血管内侵入に基因する血栓形成と,虫体の刺激に基づく血管内膜の増生(増殖性血管内膜炎)であるが, 発生の頻度は前者がはるかに多い. 血栓はその大きさ･形状が区々であるが,大部分は既に器質化する. 器質化血栓の内部には未熟な虫体を含み,それを取りまく変性壊死層,小膿瘍等を認め,更にその周囲の肉芽組織には細胞浸潤が著しい.肉芽組織層は周辺部から漸次内部に向って線維化する. 血管病変に伴い管壁周囲の結合織は増生するが,その程度は一般に軽く,隣接肝組織に波及して肝硬変を起こすには至らない.　肝実質の病変は,血管を脱出した虫体が肝組織内を穿行･遊走することにより生じる.これら虫道性の病変としては,出血,壊死,小膿瘍の形成(好酸球及びその他細胞の集族より成る)などであるが,穿入虫体の周囲には帯状の変性壊死層が囲み,上記の病変を含めてその外側を細胞浸潤の著しい肉芽組織層が包囲する.ただし供試イノシシが幼獣のため,肉芽組織の線維化は軽度であり,かつそれが広く増殖して周囲の肝組織に拡延することは,肝門部を除いては見られなかった.　宮崎県下のイノシシは成獣はもとより幼獣までも, かなり濃厚に S. dentatus に感染することが判明した.イノシシの本症は豚への感染源になることも考えられるので,単に野獣の寄生虫症として無視するわけにはいかない.Autopsy was performed on nine young wild boars, Sus scrofa leucomystax, weighing about 10kg and caught in Miyazaki Prefecture in the hunting season in 1975, 1976, and 1977. As a result, immature worms of Stephanurus dentatus were parasitized in the liver and caused lesions of this organ in four of these animals. These lesions were roughly divided into two groups: those induced in the parenchyma of the organ and those in the vascular system (arterial and portal vein branches). They were found in every hepatic lobe (lateral and medial left lobe, lateral and medial right lobe, quadrate and caudate lobes). They occurred rather frequently in a region around the hepatic hilus. The vascular lesions consisted of thrombosis caused by worms invading blood vessels and hyperplasia of the vascular intima caused by the stimulation with worms. The thrombi formed were variable in size and shape. Most of them were organized, while some retained residual blood. Organized thrombi contained very immature worms and small abscesses. On the other hand, the mechanical and chemical stimulation of worms caused proliferous endoangiitis. The site of proliferation of connective tissue in the intima was projected into the lumen and collicular or tubercular in shape. Concurrently with these vascular changes, connective tissue proliferated around the vascular wall, generally to a small extent. Accordingly, it did not extend to any neighboring hepatic tissue or induce hepatic cirrhosis. Furthermore, worms penetrated through the vascular wall into Glisson's sheath outside this wall. They formed eosinophilic abscess and necrotic foci in the sheath. Worms penetrated through the vascular wall into the hepatic tissue, in which they perforated and wandered. Therefore, migrating worms induced lesions in the hepatic parenchyma. They were in more advanced stage of development than those having invaded blood vessels, but were still immature. They migrated gradually toward the surface of the capsule of the liver. Eventually, they penetrated through the capsule into the peritoneal cavity. The migration of worms in the hepatic tissue induced hemorrhage and the formation of small abscesses (composed mainly of aggregated eosinophils). The worm body was surrounded by two zones. The internal zone was a layer of degeneration and necrosis, and the external zone a layer of granulation tissue affected intensely with cellular infiltration. Only mild fibrosis was noticed in the granulation tissue, since the wild boars examined were young.
宮崎大学農学部の論文

著者

芦沢広三
宮崎大学農学部家畜病理学教室

Stephanurus dentatusの寄生によるイノシシ肝臓の病理学的所見

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