肝および肺の病変について (豚腎虫症の病理学的所見-1〜3-)

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　南九州のと畜場で採取した豚腎虫自然感染肝5例, 同肺2例について病理学的検索を行ない, 以下の所見を得た.　1) 肝における豚腎虫性病変の基本は,泌尿器系の場合と同じく, 虫道性病変と虫性嚢胞に区別されるが,肝の虫道病巣は虫体の細菌汚染により膿瘍(虫性膿瘍)の型をとるものが多い. 典型的な嚢胞はむしろ少なく,膿瘍との中間移行型を示すのが普通. なお肝では, 虫体の穿孔遊走が活発に行なわれるためか,病巣の被包形成ないし器質化による結合織増生がすこぶる顕著. ただし, その形式に二様あり,一つは肝の広い範囲に部厚い瘢痕組織層を形成し,他は限局性の結節性肝硬変巣を形成する(これら瘢痕層や硬変巣中に膿瘍･嚢胞が埋在).　2) 鏡検上,肝の虫道性病巣には組織破壊に伴う出血,壊死並びに好酸球･好中球等の浸潤が見られ,とくに好中球の多数集族による膿場形成が目立つ. その際,膿瘍の被包層の内側には多数の大単核細胞(大食細胞) が集族, また被包性肉芽組織層には好酸球･リンパ球･プラスマ細胞が浸潤,巨細胞も発現する. 虫性嚢胞においては, 虫体に接する被嚢内壁に幅狭い壊死層が見られ,その外を肉芽組織が包む.膿瘍や嚢胞の外周の結合織増生巣では,好酸球･プラスマ細胞を主とする血管周囲性浸潤,水腫,ヘモジデリン沈着などを所見. また隣接肝組織では,間質増生と肝小葉の萎縮･荒廃が著明.それら増生間質においては細胞浸潤,小葉間胆管の増生,偽胆管の発現を認め, また間質中を走る小動脈の管壁は肥厚を里する.肝の被膜は一般に肥厚し線維素付着,横隔膜と癒着を示す部分もある.　3) 肝の血管系(主として門脈およびその分枝,一部は肝静脈･後大静脈) の内壁に肉芽性隆起物を認めたものが少なくない. 隆起物を鏡検すると,一部に出血,壊死,好中球集族などの虫道性病変像をとどめているが,大部分は器質化巣より成る. これは血管壁の虫道性病変により形成された血栓の器質化したものと解される. なおこれら血管の周囲組織にも虫体侵入や虫道性病変を所見.また鏡検上,病巣部付近を走る小静脈に,血栓の器質化･栓塞を認めたものが多い.　4) 肺の病変は肝と同じく虫道性病巣としての膿瘍形成と, 虫体寄生部位に形成される嚢胞に分けられるが,肺ではとくに前者が顕著である. なお血行を介して侵入した虫体は,主として間質を中心に病変を現わし, そのため間質の増厚を招く.時にはそれが限局性に拡大して結節性の肺線維症を呈する.一方,肺胸膜面からの迷入虫体により,肺胸膜面に絨毛性線維素ないしそれの器質化物が付着する.またかなり広い範囲の肺の表層部が厚さ3～4mm の瘢痕組織層に変化する(その内に膿瘍･嚢胞が埋在).　5) 肺病変の鏡検所見は,基本的に肝の場合と同じであるが, ただ組織内の虫卵散布が比較的著明.これは成熟に近い迷入虫体によるものであろう.病巣部の周囲若干範囲の肺組織は,増殖性間質性肺炎と滲出性(カタル性)肺炎の病像が種々の程度に混在する.　肺における血管系の虫性病変は,肝のそれに比し一般に軽少であるが,鏡検上,血管内壁に虫道性病巣並びにそれに対する被包性肉芽組織の増殖像を確認した.Livers and lungs were collected from 5 and 2 pigs affected with stephanuriasis, respectively, at slaughterhouses in the southern part of Kyushu over a period from 1965 to 1970. They were studied pathologically with the following findings. 1) The pathological changes of the liver caused by Stephanurus dentatus were divided into two basic types, as well as those of the uropoietic organs. Lesions caused by migratory worms belonged to one type and worm cysts to the other. Most of those lesions took a form of abscess (wrom abscess) on account of the bacterial contamination of the worm body. It was rather rare to encounter a typical cyst. Such cyst as usually observed was an intermediate transitional between cyst and abscess. In the liver, worms wandered by perforation in an active manner. Since lesions caused by worms were high in density, there was a marked hyperplasia of connective tissue on account of encapsulation and organization of lesions. The hyperplasia of connective tissue took place in two different manners. In one manner a thick layer of cicatricial tissue was formed over a wide area in the liver. In the other manner, a localized nodular cirrhotic focus was formed in the organ. In other words, abscesses and cysts were buried in the cicatricial tissue layer and cirrhotic foci and projected from the surface of the capsule. 2) Microscopical examination revealed destruction of tissues accompanied by hemorrhage and necrosis and infiltration with eosinophile and neutrophile leukocytes in lesions caused by migratory worms in the liver. Frequently seen were abscesses with an accumulation of many neutrophile leukocytes inclosed in a capsule made of granulation tissue. A number of mononuclear cells (macrophages) were present inside the granulation tissue. The layer of this tissue contained a few giant cells, in addition to infiltrating lymphocytes, plasma cells, and eosinophile leukocytes. When the worm cyst was examined, the inner wall of the capsule adjacent to the worm body had a narrow necrotic layer, the outside of which was surrounded by granulation tissue. This tissue presented the same findings as mentioned above. Perivascular cell infiltration with plasma cells was outstanding in proliferative foci of connective tissue around lesions caused by worms. Moreover, edematous changes and hemosiderin deposition were noticed. In the hepatic tissue adjacent to the proliferative foci of connective tissue, hyperplasia of interstitial tissue and atrophy and devastation of hepatic lobules were conspicuous. The hyperplastic interstitial tissue exhibited cell infiltration, proliferation of interlobular bile-ducts, and appearance of pseudo-bile-ducts. Hyperplasia occurred to the walls of arterioles running in the interstitial tissue. Organization of thrombi and development of embolism were observed in venules running in this tissue. The capsule of the liver was generally thickened, with fibrin attached to it. Some portions of it adhered to the diaphragm. 3) Projections consisting of granulation tissue were formed on the inner walls of blood vessels of the liver (mostly the portal vein and its branches and partly the hepatic veins and posterior vena cava) in not a few cases. Microscopical examination revealed that they were mostly composed of organized tissue, although they still had such changes caused by migratory worms as hemorrhage, necrosis, and accumulation of neutrophile leukocytes partially. These findings are interpreted that organization may have occurred to thrombi formed by worms having invaded the vascular wall or lesions caused by migratory worms. Furthermore, lesions caused by worms were also present in tissues around blood vessels in not a few cases. 4) In principle, the pathological changes of the lung caused by swine kidney worms were the same as those of the liver. They were divided into two types. To one type belonged the formation of abscesses as lesions caused by migratory worms. The cyst formation seen in an area parasitized by the worms belonged to the other type. The appearance of abscesses induced by the bacterial contamination of worms was very outstanding. Lesions caused by worms occurred most frequently in the interstitial tissue. As a result, this tissue was proliferated and thickened. Sometimes it was enlarged locally to form foci of pulmonary nodular fibrosis. Villose fibrin or its organized tissue attached to these foci as a result of stimulation by aberrant worms which had invaded the lung through the pulmonary pleura. Some areas on the surface of the pulmonary pleura changed into layers of cicatricial tissue 3 to 4 mm in thickness. Some foci caused by worms were buried in these layers, some parts of which were projected on the surface of the pulmonary pleura. In general, the pathological changes of the lung appeared more mildly and were less severe than those of the liver. This is probably because the worms having invaded the lung were very immature (except aberrant worms), and that they were fewer in number than the worms having entered the liver. 5) In principle, the histological findings of lesions caused by worms were the same in the lung as in the liver. In the lesions of the lung, however, the infiltration of eosinophile leukocytes was unexpectedly infrequent, the appearance of giant cells relatively frequent, and the dissemination of eggs in the tissue relatively outstanding, probably because the aberrant worms (worms close to maturity). In the pulmonary tissue around those lesions, the pictures of two types of pathological changes, i. e., productive interstitial pneumonia and exudative (catarrhal) pneumonia, were mixed to a varying extent. Lesions caused by worms in the blood vascular system were generally milder in the lung than in the liver. None of them in the lung were large enough to be seen by the naked eye. Microscopical examination revealed that there were lesions caused by migratory worms on the inner walls of blood vessels, and that these lesions were accompanied by the proliferation of granulation tissue forming a capsule.
宮崎大学農学部の論文
1972-10-00

宮崎大学農学部 | 論文

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