第19巻第3号

1991年9月15日

内
原

容

著

熱帯地域における各種急断障害の肝細胞病変を主とした病理組織学的特異性：
妊娠中毒症，肝炎ウイルス性劇症肝炎，黄熱，アフラトキシン中毒症の比較検討

一楠部

國泰，箕山

博夫，神田実喜男，江藤

守屋泰一郎，渡辺 正実，許田明，鐘千馬 正敬，鳥山寛，板倉 英音，中上気道におけるpyogenic

秀顕，

雪雲，

英男 22卜237

granulomaの血管増生性病変：・・箕山博夫，楠部 國泰，神田実喜男，江藤

守家泰一郎，許田

中

英男，板倉

秀

明，千馬 正敬，鳥山英卉

頭寛

東アフリカ・ケニアにおける異型血管組織を示した症例を中心として

239−250

西部ケニアにおける小児の風土病型リンパ節型カポシ肉腫（英文）

…小室

哲，鳥山

寛

251−263一高岡宏行

265−273

琉球列島においてS伽％伽郷（Oo吻hos∫づ」ゐ勿）64孟08％s6Edwardsと同定されていたブユ種の分類学的再検討（英文）ガーナ南部の農村2地区における5歳未満児の急性呼吸器感染症（英文）一E．A．Afari，酒徳浩之，中野貴司，F．Binka，
A．Assoku，E．Kwarteng Amaining，G．Mensah
andJ．Fenteng（裏面に続く）日本熱帯医学会

275−280

会報・記録他

平成3年度第1回幹事会記録・…

281−283

第3回熱帯医学と医療を語る会のお知らせ……
日本医学会だより…

・284

285−286

日本衛生動物学会創立50周年記念大会のご案内

287

投稿規定・

288−289

平成3年度会員・役員名簿…一…

291−315

編集部だより317−320

日本熱帯医学会雑誌

発行所

第19巻

編集者

第3号

平成3年9月15日

印刷

平成3年9月15日

発行

日本熱帯医学会板

倉英喜

印刷所昭和堂印刷
諌早市長野町1007−2（⑰854）
費0957−22−6000

本雑誌の刊行にあたりその費用の一部を文部省科学研究費補助金（研究成果公開促進費）によった。

日熱医会誌．，第19巻

第3号

229

1991年，229−237頁

熱帯地域における各種急性肝障害の肝細胞病変を主とした病理組織学的特異性：

妊娠中毒症，肝炎ウイルス性劇症肝炎，黄熱，

アフラトキシン中毒症の比較検討
楠部 國泰1・箕山 博夫1・神田実喜男1・江藤
守家泰一郎2・渡辺 正美2・許田明2・鐘千馬 正敬2・鳥山
寛2・板倉 英音2・中
平成3年1月14日受付／平成3年5月27日受理

秀顕2・

雪雲2・

英男3

その修復像に病理学的な差異が見られる。本研究

はじめにでは，赤道東アフリカ・ケニアにおける子痛の症

熱帯地域の住民にはさまざまな感染症，中毒性例を中心として，熱帯における上記の各種疾患の疾患，栄養障害などがあるが，それらの多くは肝病理解剖材料について，急性肝障害像および残存にも特徴ある病変をきたすことが多い（板倉ら，

肝細胞の動態像を病理組織学に把握し，病変の発1984）。それらの中には，急性肝病変を呈する特異生機序を推察した。

的な肝障害がある。本研究では，熱帯地域における妊娠中毒症（および子痴）を主とし，肝炎ウイ
ルス

材料と方法

幽劇症肝炎，黄熱，アフラトキシン中毒症の各疾患の急性肝障害像を，病理組織学的に比較検材料：以下の疾患の病理解剖材料を検索した。疾討した。

患は妊娠中毒症もしくは子痛（7例），亜広範性肝妊娠中毒症は熱帯地域，特に発展途上国におい壊死を示すB型肝炎ウイルス性劇症肝炎（19例），ていまだに散見される重要な疾患であり，また各

および同じく非A非B型ウイルス惚剰症肝炎（4型の肝炎ウイルスによるウイルス

断炎は熱帯地例），黄熱（3例），アフラトキシン中毒症（3例）

域では広く高頻度に見られる。黄熱はウイルスにである。これらは赤道東アフリカ・ケニア，およ

よるウイルス性出血熱の代表的疾患で，蚊によっび西アフリカ・ガーナの国立総合病院，国立大学て媒介される黄熱ウイルスによる疾患である。ア

病院などにおける症例である。妊娠中毒症およびフラトキシン中毒症は，食品寄生真菌類毒性代謝ウイルス

産物（マイコトキシン）によるマイコトキシン中立駒込病院，昭和大学医学部第一病理学教室，長毒症のなかで，最も障害をもたらす疾患の1つで崎大学熱帯医学研究所病理学部門など，各施設にあり，ときに熱帯地の食中毒として発生する。

幽劇症肝炎の材料については，旧東京都

おける病理解剖材料を補助的に加えて検索した。

これらの疾患は，何れも病理学的に特徴ある肝方法：病理組織学的ならびに組織化学的検索：

障害像を呈する。すなわち肝に急激な障害をきた

肝の組織片をホルマリン固定後，パラフィン包埋す場合，肝の主要な実質である肝細胞の障害像と，切片を用い，hematoxylin−eosin染色を全般的な昭和大学医学部第一病理学教室 〒142東京都品川区旗の台1−5−8
長崎大学熱帯医学研究所病理学部門 〒852長崎市坂本町12−4
北里大学東病院病理部 〒228相模原市麻溝台863−1

230

病理組織学的観察に，鍍銀染色，Malloryの膠原sue）などである。

線維染色，弾力線維染色の各染色を組織構造の観察に，periodic

acid−Schiff（PAS）反応を肝細胞の個々の病変の観察に用いた。

これらの指標に基づいた各疾患の病変は，下記のごとくである。また各疾患について比較した結果を表1に示す。

妊娠中毒症および子痛：肝小葉中間帯および結周辺部における肝細胞の変性，および壊死が見ら果れる。肝小葉中心部には壊死はほとんど見られな

急性肝障害を呈する各疾患の肝病変の病理組織

い。ときには肝小葉全葉にわたって変性・壊死が学的所見をもとに，以下の点を病理形態学的指標

およぶことがあるが，その場合でも門脈域周辺のとして比較検討した。すなわち，1）肝小葉にお肝細胞のいわゆる限界板は保たれている。壊死病

ける障害部位（site of lesion in hepatic巣の形状は帯状のこともあるが，不規則で地図状

lobule），2）肝小葉における肝実質の壊死の形状のことが多い。肝実質内各所に比較的新鮮な出血（shapeoflesions），3）出血性病変の部位と強が見られるが，症例によって軽度から強度までそ弱（hemorrhage），4）肝細胞の個々の病変：肝の程度はまちまちである。肝細胞の腫大が著しい細胞の変性・壊死（1ivercell

andこともある。肝細胞の大小不同性が見られる。肝necrosis）と多形性および大小不同性，5）肝構築

細胞索は萎縮性で，不規則な配列を示す。肝細網像：肝細胞索の配列の乱れ，6）残存肝細胞の動線維を鍍銀染色で見ると，壊死による肝実質構造

態像：結節性の再生・増殖像（nodularlivercellの部分的な破壊が見られる。残存肝細胞の結節性

regeneration），7）肝細胞の異型度：核の多形再生像は，ほとんど見られない。肝細胞核の大小性と大小不同性，核の異常染色性，異常あるいは不同性が見られる。肝細胞の異型性はほとんどな

degeneration

高頻度の核分裂像など，8）肝組織内の血栓形成い。ごく小さなフィブリン様あるいは血栓様形成（intrahepatic

fomation），9）炎物が部分的に見られたが，全般的には明らかなも症性細胞浸潤（innammatorycellinmtration），のは見られなかった。肝全体に浮腫が見られる。

10）間質における線維組織の増生（飾rous

肝類洞が全般的に拡張し，Kupffer細胞の動員とthrombus

Table
Site

of

lesionDiseaseinhepatic

lobuleeclampsia

Liver

l

ti＄

Histopathology of acute liver diseases

cell

Nodulardegeneration Hemorrhage
and necrosis

intermediate
and perilobular

十十Shape ofliver celllesions

regeneratiOnirregular notclear
and十十Intrahepatic

lnflammatory

thrombus

cellformation

in且1tration

一〜十十partiallyzonal

fulminantpanlobularviralandpartial＋＋＋＋＋＋〜＋＋＋ irregular＋＋＋＋＋ 一〜＋＋

十十十

hepatitis

yellow

intermediate

fever

and

十十十

十〜十十十十十

zonal

not

clear

not

clear

not

clear

十十

periportal（viralhemorrahgic
fever）

aflatoxicosis

centrilobular

十十十（一）；negative〜（＋＋＋＋＋）；StrOngeSt

一

〇r

十

regular

一〇r十

231

軽度のび漫性炎症性細胞浸潤が見られる。肝小葉症例2（ODKOM1711）：の門脈域の炎症性細胞浸潤は，比較的軽度である。

妊娠中毒症，

大白腎，心肥大，両側肺浮腫，全身陸皮下

線維組織の形成は，ほとんど見られなかった（図浮腫，腹水

症例3（ODKOM1870）：

1−7）。

33F

28F

妊娠中毒症，

大白腎，心筋混濁変性，胎盤剥離，肝腫大
妊娠中毒症および子痴の各症例と，剖検所見をおよび混濁腫張症例4（ODKOM1904）：示すと以下のようである。

28F

妊娠中毒症，

症例1（ODKOM1641）： 40F 妊娠中毒症，
妊娠腎，心嚢液多量，肺浮腫，肺炎，全身肝混濁腫張，両腎灰白色混濁，心筋混濁腫

貧血，内臓欝血，肝小葉周辺性壊死

性傾向，肝病変として肝小葉周辺性変性お灘§、張，両側副腎皮質出血，全身性浮腫，出血

譲麟。難Figurel Eclampsla． Edema Q董liver tlssue． Si血usQida重dilat＆tion andi浦ammatory exudate wi愉K叩働r celi mGわilization are seen、Livercell cords＆re＆troph量c an（i曲ow irregu茎ar structures a瞠d pleomorph童sm
Iiver cell nuclei． （Case6） （Hematoxylin and eos圭n sta量n， Originalof

燃a朗iHcation；XlOO〉

Figure2

Ecl覆r臓pis段．
Sin疑soid獄1 dilatation and in紐amr雁atory exudate w圭th
Kupffer cell mobilization蹴re seen．At鉛phic and irregu1＆r structureswith pleomorph捻m of Iiver cell nu￠lei are marked．Centriiobular areas（onrigぬtlowerp＆rt）are至ntact、（Case6）（Hematoxyま1na良deosin
stain．Ori蕊inaima墓ni丘￠atio駕×100）

232

Flgure3Eclampsia．Complicatednecrotic

Fi暮ure4liver

parεnchyma

andir紀gularinin七er工口ediate zones o圭

pattem（Case4）（Hematoxyli勲鋤deosin

st翫in、OriginalEclampsia． De霧enerat圭on

and

of

necrosis

liv奪r

oまde暮enerative
hepatic

orlobuies．

ma鯉迅￠駐tiGnl×100〉

ce董1呂are圭rregularandzonal i鏡intermediat（き20aes ofぬepatic k）b登1es、工葺a段mmatory㊤xudate isr＆ther sparse i血peripoyt盆1areas（on le赴＄id曝）． （C薮se農） （Hematoxylin

andeosinsta墨a．Ori蜘獄1magni負catio鷺；×10G）

よび壌死，肝内の軽度の出血ウイルスによる劇症肝炎の症例群を検索した。何子痛，大白腎，心点れも亜広範性肝壊死を示す症例である。本研究で状出血，肺欝血および部分出血，子宮拡張，は，両症例群の聞で肝障害像に明確な差異を見る

肝のび漫性出血壊死，脂肪変性ことができなかったので，全例をまとめて記載す

症例5（NAK130）：

24F

子痛，心肥大，両下る。肝小葉の部分的，あるいは全葉にわたる肝細肢浮腫，両側気管支肺炎，両側腎腫大，腹胞の変性・壊死が基本的組織像である。肝小葉周水，肝小葉周辺性の欝血と出血，肝実質黄辺領域の肝細胞の限界板が，破壊されている。病痕

変は不整形である。出血は部分的で軽度，時には症例6（NAK150）1

30F

症例7（SHO1428）： 26F 子痛中程度である。肝細胞には軽度ではあるが，結節性の再生性変化が見られる，しかしそれらの肝細肝炎ウイルス性劇症肝炎：B型肝炎ウイルス

胞には，異型性はほとんどない。門脈域周辺部にによる劇症肝炎の症例群，および非A非B型肝炎

偽胆管の増生が見られる。血栓の形成は症例によ233

Figure 5 Eclampsia. Silver impregnation of liver parenchyma. Liver cell cords
in intermediate zone and periportal area (on left side) of hepatic lobule
are irregular and collapsed, while centrilobular area (on right side) ls
intact. (Case 4) (Original magnification; x 100)

Figure 6 Eclampsia, Lobular necrosis and degeneration of hepatic parenchyma.
(Case 5) (Hematoxylin and eosin stain. Original magnification; x 100)

s"
*

+;

{=="

'･'･,'t ;^ ･ "Figure 7 Eclampsia. Higher magnification of the same case of Figure 6. Rela‑
tively intact liver cells at the periphery portion of hepatic lobule areobserved. (Case 5) (Hematoxylin and eosin stain. Original
magnification; x 400)

234

錘

Figu艶8Fulminant viral hepatiti銭Irregular necrosis o∫liver paでenchyma withinnammatoごy exud駁t琶船d rεgeΩerative nodular proli圭eration with scat・
teredbile stasis of live影導e雛s are seen、In contrast to edampsia，lobular
re3enerative arrangements o｛liver cell cords surro紋nded by necrotic or

co1圭apsedpare魏chym＆arech段racteristic、（He漁toxylina無deosins捻i艮、Originalmagni丘cation；×40），灘慧FiguregYello麟ev礁r．Zonalnecros墨s・ぞhep＆tiεP裁縢ch脚a圭sseenini捻t磁騰
4iat奪慧one80董hepatic lobules．C礁ntr量lobul訟r
Sc畿tt倉蓄εd

addophilic bo（玉ie80f

are段8寂reu魚i（二eUular貸融cr｛》＄isrε捻tiv砲1y麺t温ct・o董葺v（きr

cells

are

also

s醜r生i慧inconspicuo斌ssinuso圭ds．In且a瓢騰t剛r愈aζtio葺⑪fpolymor・凶㈱d鰹董eukocytesisrelativelysli蝉．（H翰matoxylin農篇deo＄in
st段i貸．Orig圭nalmagni負cation；x200）

り異なり，軽度からないものまでさまざまである。

る。症例によって異なるが，軽度から強度の不規

炎症性細胞浸潤が強度で，リンパ球，形質細胞を則な出血が見られる。単一肝細胞の特徴的な好酸

主とし，一部好中球が見られる。門脈域周辺部か性壊死が見られる。残存肝細胞の脂肪変性が見ら

ら肝細胞の壊死，脱落部分へ膠原線維の増生が見れることもある。肝小葉周辺部の肝細胞の限界板

られる

（図8）。

の破壊が見られる症例もあるが，これは壊死性病

黄熱：肝小葉中間帯から周辺部にかけて，肝細変の波及による二次的な変化であると思われる。

胞の強度の変性，壊死が見られる。病変は肝小葉

通常，肝細胞の結節性の再生性変化は見られない。

中闇帯で帯状を呈する場合もあるが，不整形もあまた残存肝細胞の異型性はない。血栓形成につい235

Figure10Afl＆toxicosis、Centri童obular誼ecrosおofliver cells showiロg clear zo血eof hepatocd圭貰laごpareれchyma ls prominenも．Inflammatory exudate i＄slighし （H￠matoxyl量n a登d eos圭n st寂in．Origin撮magni負catioa；×40）ては，肝の壊死性の変化が強く，ほとんど確認で胞の老若，肝細胞の酵素活性の差異などが考えらきなかった。リンパ球好中球，形質細胞などかれる。しかし実際には，これら多くの要素が組みらタる，軽度のび漫性炎症性細胞の浸潤が見られ合わさって，それぞれの疾患に特徴的な病態像がた。線維組織の増生はない（図9）。

表われるのであろう。

アフラトキシン中毒症：肝小葉中心性壊死が，妊娠中毒症は，妊娠後半期に高血圧，salt

中等度から強度に見られる。形状は不規則ながら

retent沁n，蛋白尿，および浮腫などの症状が発生も，概して肝小葉中心部を中心とした同心円状でする疾患である（鈴木，1975；本多，石井，ある。境界は鮮明である。肝小葉の他の部位は，

1983）。胎児発育遅延や胎児死亡をきたし，ときに組織学的には変化は軽度である。出血はほとんど

は母体死亡をもきたす，産科学上重要な疾患であ見られない。肝細胞の壊死は凝固壊死である。肝る。この重症型として，痙攣を伴う子痛が見られ細胞の再生像も，また異型性もない。血栓形成はる。妊娠中毒症は病態論的には全身性の血管攣縮見られない。炎症性細胞浸潤はほとんどない。線と，子宮と胎盤との問の血流量の減少という，2

維組織の増生はない（図10）。

つの異常を塁する疾患であるが，その発生原因は
まだ完全には明らかではない。妊娠中毒症では電考案と総括

解質の不均衡により，浮腫が生じることもあり，

血液が濃縮して血液粘度が高値を示すこともある。

各種の病因により，肝小葉単位における肝実質子痛ではフィプリン血栓によって肝，腎，脳など細胞の障害像のあり方として，1）巣薯却嚢死，2）各臓器の巣状壊死をきたす。子癒における肝壊死

帯状壊死，3）広範性壊死などがある、これらのの発生機序としては，全身や局所の循環障害によ障害の発生機序として，病原体や毒物などの原因

る血流の不均衡アレルギー，毒性障害などが考が，肝細胞を直接侵襲して障害する，免疫学的機えられる。

序が働く，循環障害による，栄養や内分泌障害を子痴における肝障害像としては，肝小葉周辺部

含む代謝障害などが考えられる。また肝障害像のの壊死像が知られているが，本研究では病変は必修飾要素として，標的細胞の種類，すなわち肝細

ずしも小葉周辺部だけではなかった。肝小葉中心胞か，胆管上皮細胞か，Kup晩r細胞か，または部の障害が強いわけではないので，単に全身性の間葉系組織かにより，また肝小葉内における位置

循環障害によるものだけではない。血栓等による的条件，すなわち肝内循環系における部位，肝細局所の循環障害も考えられるが，それに対応する

236

明確な所見は得られなかった。肝に毒性に働く，塩化炭素による実験的障害に類似している。検索

何らかの要因の存在も考えられた。結論として，

症例が剖検材料だけであるので，その後の推移が上記のごとくいくつかの要因が，病変発生の機序把握できないが，回復すればおそらく肝小葉中心として関与することが推定される。肝細胞の結節性の線維症と，癩痕化をきたすことであろう。肝性の再生性の変化は見られないので，肝病変は一小葉中心性の壊死は，循環障害よりも代謝毒性機

次的な障害によると思われる。

序の問題であることも考えられる。肝小葉中心静断炎では，急性障害像として肝細胞脈の拡張が軽度で，しかも炎症性細胞浸潤が軽度の壊死，ならびに再生像と胆管増生像が特徴的でであることは，間接的ではあるがこのことの推定ある（宇津田，1991）。これはB型肝炎ウイルスにの根拠となる。

ウイルスよる劇症肝炎でも，非A非B型ウイルス性劇症肝本研究のまとめは以下のようである。1）熱帯炎でも同様であった。肝炎ウイルスによる劇症肝地域に多い妊娠中毒症をはじめとした，急性肝障炎における肝細胞の壊死の機序を考えるに，肝細害をきたす各疾患の肝病変を病理形態学的に比較

胞の一様な変性と壊死およびリンパ球の著しい浸検討し，それらの特徴を把握した。2）特に妊娠

潤などにより，肝炎ウイルスの個々の肝細胞への中毒症は，熱帯地における発展途上国において，直接の攻撃だけではなく，免疫学的機序もあるこ

肝障害を惹起する重要な疾患であると考えられた。

とが推定される。このように残存肝細胞の再生結3）子痴では肝細胞の不規則な変性・壊死，ウイ

節が強い場合は，肝細胞は部分によって異なった

ルス性肝炎では肝細胞の壊死と再生，黄熱では肝異型度を示しながら，増殖しうることを示唆して細胞の肝小葉における帯状壊死，アフラトキシンいる。また肝細胞の結節性再生が強く長引くと，中毒症では肝小葉中心部の肝細胞の壊死という，線維組織の増生と相まって，肝硬変になる可能性

それぞれ特徴ある肝障害像が見られた。すなわち，がある。

それらの惹起された肝小葉単位における障害像が，黄熱では，肝は主要な病変の場で，発症後数日

各種の病因によってそれぞれ特徴があることを明は広範な肝細胞の脂肪変性をきたし，それ以後は確にした。4）それら各種の急性の肝障害の形態

肝細胞は，び漫1生好酸1生の変性および壊死に陥る

像を病理学的に考察することにより，これらおの（宇津田，1984）。肝細胞の障害が，ウイルスの直おのの急性肝障害をきたす要因は，病原体の直接接的攻撃によることが推定される。ただし帯状のの攻撃，免疫学的機序，毒性代謝障害，全身およ

壊死が何を意味するのか，その発生機序は不明で

び肝内局所の循環障害など諸要因の単独，またはある。肝構築の破壊が見られるが，肝細胞の再生

組合せによるものであることを推定した。5）急性の変化は見られない。やはり一次的障害機序に性肝疾患の発生状況として，地理病理学的には興よるものと考えられる。熱帯性食中毒の1つとし味ある点である。熱帯地におけるそれらの肝障害て，アフラトキシンに代表されるマイコトキシンの直接的原因はそれぞれ存在するが，疾患発症のが，ヒト肝癌の原因となりうるか否かについて従背景として多くの感染症，栄養状態，社会経済状

来から論議されているが，その実態は不明である態などの関与も考えられる。熱帯地域住民のこれ（Itakura， 1982）。

らの諸条件が，肝障害の発生にどのように関与しアフラトキシン中毒症では病変が特徴的で，四ているかは，今後の問題である。

献

文

1）本多

洋，石井明治（1983）： 重症妊娠中毒症，産婦人科の実際，32（12），1761−1769

2）Itakura，H．（1982）：Etiology
patocellular

carcinoma

1（2），309−316

causedof human primarybyhepatitis

viruses

hepatocellularor

carcinoma：Is

mycotoxins〜J、ToxicoLprimary he−

Toxin

Reviews，

2373）板倉英喜，宇津田 含，鳥山 寛，井上長三，入船賢司，戸田ゆみ子，千馬正敬（1984）： 熱帯地
域における肝疾患，病理と臨床，2（9），1208−1213
4〉鈴木雅洲（1975）： 産科婦人科用語問題委員会妊娠中毒症小委員会報，日産婦誌，27，1339−1345
5）宇津田 含（1984）： ウイルス性出血熱：黄熱，病理と臨床，2，1044−1048
6）宇津田 含（1991）： 劇症肝炎の経過に対応する肝実質細胞の再生像と胆管上皮化生，長崎医会誌．，66（1），11−19

LIVER

LESIONS AND

STRUCTUALARRANGEMENTOFREMAINING HEPATIC CELL CORDS IN ECLAMPSIA AND
OTHER ACUTE LIVER LESIONS IN THE TROPICS
KuNIYAsu NANBu1，HIROO MINOYAMA2，MIKlo KANDA1，HIDEAKI ETo2，
TAI−lcHIRo MoRIYA2，MAsAMI WATANABE2，AKIRA MoToDA2，ZHoNG XuE YuN2，

MAsAcHIKA

Histopathological

SENBA2，KAN

ToRIYAMA2，HIDEYo

Received

January141991／Accepted

findings

viral hepatitis，yellowoftropicalfever，and

tissue，sinusoidal

dilatation

andseen．Liver

cell

cords

atrophic

liver

cell

nuclei．Complicatedchyma

in intermediate

were
and

areas

were

with

inflammatory exudate

and

outer

intact、Fulminantdiseases，lobularorcollapsed

necrosisinScattered

acidophilicintermediate

tropics．

to

cause

Regenerative

parenchymal

lesions

such

with

Kupfferirregular

irregular

pattem of degenerative

hepatic

hepatitis

lobulescellstructures

zones

of

as

eclampsia，fulminant

were

showed irregularmobilization

and

of

remainingwere

pleomorphismofor necrotic liver parerト

observed，whilecentrilobular

necrosis of liver parenchyma

bile duct proliferation．In contrast to

arrangements

ofliverliver

other three

cell

cords

surroundedfeature．Yellow

fever

showedbyzones

lobules．Centrilobular areas were relatively intact．

bodies of

was slight．Thesediseasescharacteristic．Ineclampsia，edema

exudateshowedATARI3

distinctive

ous sinusoids．Inflammatory

and mechanism

liver
are

EIo

May271991

parenchyma wereof hepatic

reactionofnecrotic

resultsispolymorphonuclear leukocyteschangessuggest thatcharacteristicchangezonal

unicellular necrosis of liver cell were also seen in inconspicu−

In aflatoxicosis，centrilobular
exudateandperiportal

regenerative

necrotic

inflammatory

viral

and

acute

aflatoxicosis

ITAKuRA2AND

of liver cells

in

relatively slight．

there are different kinds of etiological factors

histological

specific

waswere prominent．Inflammatory

viralfeatures

of

acute

hepatitis，while

in

liver

lesionsotherthree diseases

are primary changes．

1 1st Department of Pathology，Showa University School of Medicine
2 Department of Pathology，Institute of Tropical Medicine，Nagasaki University
3 Department of Pathology，Higashi Hospita1，Kitasato University School of Medicine

in

the

日熱医会誌．，第19巻

第3号

239

1991年，239−250頁

上気道におけるpyogenic

granulomaの血管増生性病変東アフリカ・ケニアにおける異型血管組織を示した症例を中心として
箕山 博夫1・楠部 國泰1・神田実喜男1・江藤
守家泰一郎2・許田明2・千馬 正敬2・鳥山
中
英男3・板倉 英古2
平成3年2月15日受付／平成3年5月24日受理

で散見される風土病の1つである，Kaposi肉腫

granuloma （granuloma

pyogenicum，hemangioma

of

寛2・

tissue）などと比較検討した。さらに赤道アフリカ

はじめに

Pyogenic

秀顕2・

granulation

tis・（Kaposis sarcoma）の血管増生性の病変も予備的に参考症例として用いた。

suetype）（PG）は，皮膚や粘膜の毛細血管腫のポリープ状の病変であると考えられており，径数

材料と方法㎜から数cmに達する。PGは歯銀，指，口
唇，願，舌などに多く，しばしぱ潰瘍を形成し，

症例：東アフリカ・ケニアにおいて見られた咽頭

炎症性細胞浸潤や基質の浮腫を伴う肉芽組織を生部に生じた限局的血管増生性の病変の2例（Case

じる。PGを構成する血管内皮細胞や，基質の線

1およびCase2）（何れも中年男性），および比較

維芽細胞のmitosisが見られることがある。また

検討材料としておのおの約10例のPG（上気道，PGの毛細血管の増生像は，それに伴う感染性病

口腔粘膜，一部頸部および指の皮膚），血管肉腫（頭変によって修飾され，しばしば複雑な組織像を呈部および躯幹の皮膚），Kaposi肉腫（四肢の皮することがある。さらに増生する血管組織が，多膚），および非特異的肉芽組織（四肢の皮膚および少の異型性を帯びることもある。

口腔粘膜）を用いた。PG以下の各症例の患者は本研究では，口腔および上気道におけるPGの何れも中〜高年男子で，病理組織材料はアメリカ

血管組織増生像に着目し，増生した血管成分の異合衆国および日本において収集したものであるが，型性について病理組織学的に検討した。特に赤道Kaposi肉腫はケニア人の症例である。

東アフリカで見られた上気道のPG類似の病変で，病理組織学的ならびに組織化学的検索：ヘマトキ

病巣の表層部における炎症による肉芽性毛細血管の増生と，深層部における異型性を帯びた血管組

シリン・エオジン染色，鍍銀染色，Mallory膠原
線維染色，periodic acid』Sch雌（PAS）反応を

織の増生を併せ持った症例を中心に検索した。ま用いた。

た参考症例として，軟部組織におけるほかの血管増生性病変，すなわち血管肉腫（angiosarcoma）

や非特異的肉芽組織（non−specinc

granulation

昭和大学医学部第一病理学教室 〒142東京都品川区旗の台1−5−8
長崎大学熱帯医学研究所病理学部門 〒852長崎市坂本町12−4
北里大学東病院病理部 〒228相模原市麻溝台863−1

240

結

管組織は，感染に伴う炎症性の肉芽性毛細血管で果あると考えられる（図1，2）。病巣の中層部で各疾患の病理組織学的所見，すなわち増殖細胞

は，通常のPGとほぼ同じ程度の異型度を示す血の増生像（growingpattem），内皮細胞の異型度

管組織が増生している（図3−5）。病巣の基底部（atypia），血管組織像の強弱（vascular（深層部）では内皮細胞の腫大と増生が著しく，

proliferation），間質における線維組織（nbrous

血管内腔に詰まったように増生し，内腔をかなり

tissue），炎症性細胞浸潤（inHammatory

閉塞したような組織像を呈していることが特徴的

exudate）は表1に示した。

である。この部分の血管組織は腫瘍性の毛細血管

Case1およびCase2：この2例は以下の所見により，結果的にはPGの1型と考えられた症例である。病巣は何れも径5mm〜10mmである。

と考えられる（図6−10）。すなわち本症例群では，血管組織は異型度の点から見て3層に分かれており，表層部は非特異的な肉芽組織における毛不同性，核の多形性，核の異常染色性，異常ある細血管より成り，中間層はいわゆるPGと同程度の細胞異型性，ならびに構造異型性を示す血管組

いは高頻度の核分裂像など）について注目し，以織より成り，深層部は細胞異型性および構造異型

下のごとくの結果を得た。病巣の表層部は潰瘍化

性がやや強い組織より成り立っていた。

増生する血管組織の異型度（細胞の多形性，大小しており，著しい炎症性細胞浸潤とともに，毛細PG：毛細血管腫が基本的組織像であるが，血血管の新生や増生が見られる。これらの毛細血管管内皮細胞にはごく軽度の異型性が見られる（図の細胞の異型性はほとんどない。すなわちこの血11−13）。PGの表層部に感染が起これば非特異的

Table

l

Comparative

histologicalAtypia ofendothelial

Growing

Diseasepattern

granuloma
pyogenicum

findings

cellS

of

vascularandProliferationof vascular

tissuerelatedsoft

Fibroustissuediseases
Inflam−matorytissueexudate
十十十

十

十十十十

十十

十十十十十

十十十十十

十

十十

十十十

十十

十

十十

十十十十

十十十十十

十十

十十

十十

十十十

十

十十

十十

十

capillaryhemangioma−
tOUS，

lobulararrangement
angiosarcoma

highlyirregular

vascularspaces
Kaposissarcoma

irregular

vascularspacesnon−specificregulargranulation
tissueinregular

Case1

and

moderately
irregular，lobulararrangement

Case2

moderately
irregular（一）；negative〜（十十十十十）；StrOngeSt

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242

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243

離購懸灘鵜灘鶴麟鞭灘灘1、難灘羅灘
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244

Figure 7 Case 1. Silver impregnation of same area as Figure 4. Glomerular=1ike
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magnification; x 100)

Figure 12 Granuloma pyogenicum. Vascular cavities are relatively sparse.
Collagen fibers are admixed with infiammatory elements. (Hemato‑
xylin and eosin stain. Original magnification; x 200)

247

Figure 13 Granuloma pyogenicum. Vascular endothelial cells are plump. How‑ever, cellular atypia is less marked than Case 1. Number of mitosis isquite small, (Hematoxylin and eosin stain. Original magnification;
x 400)

Figure 14 Granuloma pyogenicum. Dilatation of lymphatic vessels adjacent tofoci of granuloma pyogenicum suggests lymphosta8is in surrounding
tissue. (Hematoxylin and eosin stain. Original magnification; X 100)

248

な肉芽組織が生じるが，その毛細血管には異型性については，本研究の範囲では十分に考察できなは見られない。周囲組織にはリンパの欝滞が見らかった。なお関連病変として毛細血管腫（単純血れた（図14）。

管腫）の場合は増生する血管組織が，一ないし数

皮膚の血管肉腫：本研究において検索した疾患

層の血管内皮細胞によって覆われている。異型度群のうちもっとも高度で，しかも種々の異型度をはきわめて軽度で，また基底膜は部分的に肥厚し示す血管内皮細胞から成っていた。増殖した腫瘍ているが概して非薄である。ケニアにおける上気細胞は結合組織を貫き，不規則な管腔を形成しな道のPGの症例では，増生した血管組織を観察す

がら周囲へ浸潤していた。頭皮に生じた症例ではると，同一の病巣の中でも部分によってかなり異肺に転移していた。

型度において相異（軽重）が見られた。地理病理

皮膚のKaposi肉腫：典型例では，毛細血管組
織と紡錐形細胞の増生が見られた。血管内皮細胞学的に地方病として存在するKaposi肉腫との鑑の異型度は，血管肉腫よりは軽度であるが，PGとと，介在する紡錐形細胞の増生が見られないこよりは強かった。

とから，同疾患とは異なるものであった。本症例別が必要であったが，血管組織の異型度が軽いこ

非特異的肉芽組織：肉芽性毛細血管の増生が，の位置付けとしては，基本的にはPG様の病変で主体である。血管組織の構造は通常，一層の血管あり，一方ではより異型性を示す腫瘍病変となり，内皮細胞によって成り立っており，また異型性はまた一方では感染による非特異的肉芽組織へと生ない。

長した病変であると思われた。なおKaposi肉腫
でも何らかの非特異的感染を起こすと，肉芽組織が生じる可能性もある。

考案と総括

一般に血管肉腫では，腫瘍細胞の異型度は多彩

軟部組織における，各種血管増殖性病変におけである。脾臓原発の血管内皮腫では，組織学的にる毛細血管増生のあり方，特に細胞異型性ならび増生細胞の異型度が軽く，良性か悪性か不明のこに構造異型性について，病理組織学的に比較検討ともある（北条ら，1967）。またhemangioendo・

theliomaは異型度が比較的低く，良性と悪性の中した。

PGにおける血管内皮細胞は軽度の異型性を示

間に存在すると考えられている（Weiss

and

En・

したが，基本的には毛細血管腫であった。上気道

zinger，1986；EnzingerandWeiss，1988）。鼻腔の非上皮性腫瘍に関して臨床病理学的に研究されているが（FuandPerzin，1974），上気道におけ

内血管関連腫瘍では，hemangiopericytomaに類似した腫瘍も報告されている（Compagnoand

るP

Hyams，1976）。本研究における検索例では，血管Gの基礎病変としては10bular

capillaryhemangiomaであり，また再発率は低いとされて肉腫が他の疾患に比べ最も強い異型度を示した。

いる。しかしPGはよく切除しなかったり，また通常の感染『生肉芽組織すなわち非特異的肉芽保存療法後の一部の症例では再発する。ただし浸組織では異型性がない毛細血管を生じるので，他

潤性の病変は見られないので，血管肉腫とは異なの血管増生性病変を見る上での対照群として用いる。一方，妊娠中に本病変の1型である

ることができる。

gravidarumが主として歯齪に発生以上のことは，1）軟部組織における血管増生することが知られている。多くは出産とともに消病変は，それぞれその疾患に応じた特徴ある異型

退するので，ホルモン感受性を示唆する。つまり自律1生の病変の証拠を欠いているので，腫瘍性の性を示すものであること，2）上気道におけるP
Gの病変にも見られるように炎症など繰り返され性格がやや希薄である。PGの発生状況として地る刺激によって，血管内皮細胞は同一病巣内でも理病理学的には興味ある点であるが，感染を生じ部分によって異なった異型度を示しながら，増殖やすい熱帯地域では多いものと思われる。原因論

しうることを示唆している。

granuloma

249

t

5t

1) Compagno, J. and Hyams, V.J. (1976) : Hemangiopericytoma‑like intranasal tumors: aclinicopathologic study of 23 cases, Am. J. Clin. Pathol., 66, 672‑683

2) Enzinger, F.M. and Weiss, S.W. (1988): Soft tissue tumors. 2nd ed., 533‑544, C.V. Mosby Co.,

Washington
3) Fu, Y.S. and Perzin, K.H. (1974) : Nonepithelial tumors of the nasal cavity, paranasal sinuses,
and nasopharynx: a clinicopathologic study. I. General features and vascular tumors, Cancer,
33, 1275‑1288

4)

t :

:,

# fEi. EE141 ) ,I : rtl ;p L

) I

lJ

i

!J.

i

: L,

:v L Cl ifl, 8(5), 597‑605:, 4 F lf ', l ,F i i, ( {;IE: ;(1967) : E :5) Weiss, S.W. and Enzinger, F.M. (1986): Spindle cell hemangioendothelioma: a low‑grade
angiosarcoma resembling a cavernous hemangioma and Kaposi's sarcoma, Am. J. Surg.
Pathol., lO(8), 521‑530

250

HISTOPATHOLOGY OF ATYPICAL VASULAR PROLIFERATION OF
PYOGENIC GRANULOMA OF THE UPPER RESPIRATORY TRACT：KENYAN

AND

OTHER

CASES

HIRoo MINoYAMA1，KuNIYAsu NANBu1，MIKIo KANDA1，HIDEAKI ETo2，
TAHcHIRo MoRIYA2，AKIRA MoToDA2，MAsAcHIKA SENBA2，KAN ToRIYAMA2，
Elo ATAR13AND HIDEYo ITAKuRA2
Received February151991／Accepted May241991

Pyogenic
lobularface

granuloma（PG）圭s polypoid lesion ofcutaneous or mucosal

capillaryandAlthoughcellularconservative

cells

of

with

other

sarcomahemangioma．Affected

tongue in descending

PG

and

The

results

cells

of

could

occur．

PG

atypiatreatmentofthevascular

is

is

not

perfect．In

upper

of

the lesion should befrequency，Not rarelynotremarkable，it

respiratory

this

tract

recur

that

granulation
there

ulcerous

studiedofpatients，andKenyantissueastissue．A wide variety ofcellular

could

be

of the upper respiratory tractwhen

cellularsuchatypia

areas

such

the

PG、

surgicalorcomparedangiosarcoma，Kaposi

ofin

accompany

histologicallyofpatientsofatypia of endothelial

atypical transformation
thecomposedgingiva，fingers，1ips2
lesions

occasionallywork，weproliferative lesions of soft

non−speci丘csuggestedsites

order oftissuewas observed．

proliferativeassendothelial

repeated

1 1st Department of Pathology，Showa University School of Medicine
2 Department of Pathology，Institute of Tropical Medicine，Nagasaki University
3 Department of Pathology，Higashi Hospita1，Kitasato University School of Medicine

infection

Jpn. J. Trop. Med. Hyg., Vol. 19 No. 3 1991, pp. 251 263

251

GEOPATHOLOGY OF ENDEMIC PEDIATRIC LYMPHNODE KAPOSI'S SARCOMA IN WESTERN KENYASATORU KOMURO AND KAN TORlYAMA
Received April 15 1991/Accepted May 15 1991

Abstract: We conducted an epidemiological and histological analysis of the endemic

lymph node‑type Kaposi's sarcoma (KS) in African children (under 16 years old) in
Western Kenya in order to determine the ethno‑geographical distribution of the disease
and to clarify its histological features and histogenesis during the 12‑year period between

1979 to 1990. The age distribution of all endemic type KS in Western Kenya showed two
age peaks; one in early childhood and the other in middle to advanced age. Most endemic
KS in children initially occurred in the lymph nodes, while that of people of middle toadvanced age showed a primary lesion in the skin. The male to female ratio of theendemic KS was 3.1 to I (in all pediatric types) , 3.4 to I (in the pediatric lymph node‑type)and 10.8 to I (in all adult types) . A high incidence of the lymph node‑type KS in children

was observed in the Luo group ethnically and in Nyanza Province around Lake Victoria

geographically. The lymph node‑type KS originated at the paracortical areas andgradually grew along the reticulin network originating from the trabeculae. The lesion of

KS histologically consisted of several types of cells, especially spindle‑shaped cells,
macrophage‑like cells and immature endothelial cell‑like cells and was accompanied byalmost normal small blood vessels, Iymphatic vessels and postcapillary venules. No
abnormal mitoses were observed in any of the cells. There were no primary necroses due
to tumor proliferation and also no extracapsular invasions. Immunohistochemically,
spindle‑shaped cells, immature endothelial cell‑like cells and mature endothelial cells
were positive for Vimentin, but only mature endothelial cells were positive for Factor‑

VIIIRa and UEA‑1. Macrophage‑like cells were positive for Factor‑XIIIRa. Thesefindings suggested that: I ) there are certain differences in the etiological co‑factors of

KS between the etidemic lymph node‑type KS in children and the endemic cutaneous type
KS in adults, 2 ) KS cells originate from pluripotent mesenchymal cells and 3 ) KS might
not be a malignant tumor, but rather a benign neoplasm, tumor‑like lesion or reactive
hyper plasia.

INTRODUCTION
Kaposi's sarcoma (KS) was first described by Kaposi in 1872 as an "Idiopathic multiple
pigmented sarcoma of the skin". Since then, it has been considered a specific neoplasm which

occurs in the skin of elderly men, mainly among people of Jewish origins in Eastern Europe

and the inhabitants of the Mediterranean basin. The first patient with KS in African
continent was reported by Jojot and Laigret (1922) from Cameroon. It is now a wellDepartment of Pathology, Institute of Tropical Medicine, Nagasaki University,

12‑4 Sakamoto‑machi, Nagasaki 852, Japan
Research permit number by office of the President, Republic of Kenya: No. OP. 13/001/8C224/12,
36.

252

recognized fact that KS is more prevalent in Equatorial Africa than in any other part of theworld (Oettle, 1962).

KS can be divided broadly into four types; the classical (European) type, the endemic(African) type, the epidemic (Acquired immunodeficieny syndrome‑related) type and thetype associated with immunosuppressive therapy. However, there are certain differencesamong the four types of KS with regard to sex ratio, age distribution, macroscopic findings,
histologic findings and biological behavior (Safai, 1985; Gottlieb and Ackerman, 1988) .

Pediatric cases of KS are uncommon, except in the African endemic type. According to
the published literatures, the majority of pediatric cases of KS in Equatorial Africa initiallyoccurred in the lymph node and often showed a generalized lymphadenopathy (Dutz andStout, 1960; Davies and Lothe, 1962; Slavin et al.. 1970; Olweny et al.. 1976; Owor, 1977;

Molyneux, 1979; Toriyama et al.. 1987a, b). However, no epidemiological and histologicalanalysis of the lymph node‑type KS in African children has ever been published.
Previous reports stated that KS is derived from vascular endothelial cell (Rutgers et al..
1986; Hashimoto et al., 1987) , Iymphatic endothelial cell (Russelljones et al.. 1986; Beckstead

et al.. 1985; Dictor, 1986) , Schwann cell (Pepler, 1959), mesenchymal cell (Harrison andKahn, 1978) or fibroblast (Mottaz and Zelickson, 1966; Nickoloff and Griffiths, 1989).
However, the cell origin of KS remains unknown.
Many hypotheses have been raised about the nature of KS, for example that it is amalignant tumor (Master et al.. 1970; Taylor et al.. 1971) , tumor with low‑grade malignancy,
tumor‑like lesion or reversible hyperplasia (Brooks, 1986; Mirra, 1986) , but no conclusion has

been reached.
We studied the lymph node‑type KS in children in Western Kenya to elucidate its ethno‑
geographical distribution and to determine its histological features and histogenesis.

Table 1 Dilution ratio of primary antibodies
Primary antibodies Animal

Dilution

rabbit/ poly

l :200rabbitlpoly

1:150
1:25

Desminmouse/monomouse/monomouse/monoACTrabbit/poly

l:300

CD35

mouse/mono

1:20

S‑100

rabbit/polyl:400

Factor‑VIIIRa
Factor‑XIIIRa
Vimentin
Actin

1:100

Pre‑digestiont

Sources+DAKO

BEHRING

DAKO
+

1:100

+
+

S.K.

DAKO
DAKO
DAKO
DAKO

rabbit/poly
1:200
E‑Y
UEA‑1*
DAKO: DAKOPATTS. Copenhagen, Denmark. Behring: Behringwerke AG,

Marburg. Gerrnany. S.K: Seikagaku Kogyo Co. Ltd., Tokyo, Japan. E‑Y: E‑Y
Laboratories, Inc.. San Mateo. CA, USA. Avidin‑biotin peroxidase complex
were obtained from Vector Laboratories: Vectastain ABC Kit, Burlingame, CA,

USA.
* Peroxidase‑conjugated rabbit immunoglobulins to UEA‑1.
t Incubated with trypsin in phosphate‑buffered saline at 37'C for 5 min.

253

MATERIALS AND METHODS
Twenty‑two cases of the lymph node‑type KS in children under 16 years old wereselected from 185 cases histologically diagnosed as KS. This study was carried out in threeprovinces, that is, Western, Nyanza and Rift Valley Province, in the Western part of the
Republic of Kenya, East Africa during the 12‑year period between 1979 and 1990. Clinicaldata and epidemiological information were recorded as accurately as possible with reference
to age, sex, ethnic group and habitant place. The specimens were examined histologicallyand immunohistochemically. Specimens of the cutaneous type KS and the lymph node‑type
KS in adults were used as controls.
After fixation in formalin and embedding in paraffin, the specimens were cut in 4 pm‑
thick slices. In addition to routine staining with hematoxylin and eosin (HE) , they were
subjected to periodic acid‑Schiff (PAS) , Azan‑Mallory, reticulin, elastica van Gieson (EVG) ,and mucicarmine stains. For immunohistochemical staining, twelve selected cases ofpediatric lymph node‑type KS were used and Factor‑VIIIRa, Factor‑XIIIRa, Vimentin,
Actin, Desmin, Alpha‑1‑antichymotrypsin (ACT) , CD‑35 and S‑100 were used as primary
antibodies at the dilution ratio shown in Table I and by the avidin biotin peroxidase complex(ABO technique (Hsu et al., 1981) . Lectin binding with Ulex europaeus agglutinin I (UEA‑l) was also performed.

RESULTS
Epidemiological results:

Figure I and Table 2 describe the age distribution of the lymph node‑type KS and the
cutaneous type KS in Western Kenya. There‑were two peaks in the age distribution of KS;

30

15

eo
cl3

V
O

I

Lymph node Type KS

Cl

Cutaneous Type KS

lO

Z
5

4 8 12 16 20 24 28 32 36 40 44 48 52 56 60 64 68 72 76 80

Age (Years)

CAU

C: Child, exact age is unknown, A: Adult, exact age is 'unknown.

U: Exact age is unknown.

Figure I Age distribution of endemic lymph node‑type and cutaneous type Kaposi's sarcoma.

254

Table 2 Lymph node‑type Kaposi's sarcoma in children

Age

Sex

7

ly6m
ly6m
ly8m
ly9m
ly9m
2y6m

8

3

lymph node
M Inguinal
M Generalized lymph nodes
M Unknown lymph node
M Generalized lymph nodes
lymph nodes
M Generalized
Generalized lymph nodes
M
M Generalized lymph nodes
M Generalized lymph nodes

Case
2
3
4

5
6

9

10

4

ll

F

Unknown lymph node

M
M

Generalized lymph nodes
Generalized lymph nodes
Generalized lymph nodes
Generalized lymph nodes
Generalized lymph nodes

F

12

5

13

6

14

7

15

8

16

10

17

12

18

12

19

Child*

20

Child*

21

Child*

22

Child*

Site of lesion

M
M
M
M
M
M
M
F

Ethnic group District

Province

Luhya
Luo
Luo
Luo

Busia

WestemSouth Nyanza

KisumuKisumuNyanzaNyanzaNyanzaLuhy aKakamega

Western

Luo
Luhya
Luhya
Luo
Luo
Luo

Siaya

KisumuNyanzaNyanzaKakamega

WestemSouth Nyanza

NyanzaNakuruRift Valley

Lu oSouth Nyanza
KisumuNyanzaNyanzaElbow lymph nodeUnknown lymph node
Generalized lymph nodes
Cervical lymph node
Generalized lymph nodes

Unknown lymph nodeUnknown lymph nodeUnknown lymph node

?.

Luo
Luo

Kakamega

Western

Kisii

Kisii

Nyanza

Luhya
Luo
Luo

Kakamega

Western

KisumuKisumuKisumuKisumuKisumuKisumuNyanzaNyanza

Lu o

Luo
Luo
Luo

N yanzaNyanzaNyanzaNyanza* Exact age is unknown (under 16 years old) .

Table 3 Age and sex distribution of 185 cases of Kaposi's sarcoma

Age group

Other lesions

In lymph node

Male Female Unknown

Male

Female Unknown

Total

0‑15
Child*
subtotal

15

3

o

5

2

o

25

2

2

o

o

o

o

4

17

5

o

5

2

O

29

Over 16
Adultt

3

o

o

98

7

o

108

4

o

O

24

5

2

35

subtotal

7

O

O

122

12

2

143

Unknownf

2

l

o

9

1

o

13

Total

26

6

o

136

15

2

185

* Exact age is unknown (under 16 years old) .
t Exact age is unknown (over 16 years old) .
$ Age is unknown.

255

childhood and middle to advanced age. Although 17% (32/185) of all KS patients had lymph
node lesions, 76% (22/29) of the pediatric type KS showed primary lesions in the lymph nodes

and 59% (13/22) of the lymph node‑type KS in children showed generalized lymph node
involvement without any skin lesions.
Table 3 describes the sex distribution of the endemic KS in Western Kenya. The maleto female ratio of KS was 3.1 to I (in all pediatric types) , 10.8 to I (in all adult types) and3.4 to I (in the pediatric lymph node‑type) .

A high incidence of the lymph node‑type KS in children was observed in the Luo group
ethnically and Nyanza province around Lake Victoria geographically.
Histological results :The early stage of KS, that is, initialocus localized in an infinitesimally small part ofthe lymph node, revealed that KS originated at a site near the paracortical area, gradually

growing toward the subcapsular sinus along the reticulin hetwork from the trabeculae(Photo. D. The center of the lesion consisted mainly of spindle‑shaped cells, while themarginal sites consisted of immature blood or lymphatic vessel‑like structures. Until the latestage when KS occupied most of the lymph node, Iymph follicles remained at the marginalsites and were slightly compressed and atrophic (Photo. 2). Finally, the lymph node wascompletely replaced by KS cells, but there were no extracapsular invasions. In the medullary

area of lymph node, there was only a small number of spindle‑shaped cells with marked
dilatation of blood and lymphatic vessels. Infiltration of plasma cell was slight (Photo. 3).
Histologically the KS Iesions consisted of several types of cells, especially spindle‑shaped

cells, macrophage‑like cells and immature endothelial cell‑like cells and were accompaniedby almost normal small blood vessels, Iymphatic vessels and postcapillary venules.
The spindle‑shaped cells in the lymph node‑type KS had more round nuclei than thosein the cutaneous type KS, and had long, thin, eosinophilic and slightly wavy cytoplasm. They

showed an interlacing bundle pattern. There were slit‑like structures containing eryth‑rocytes among some spindle‑shaped cells, which were indicative of an immature vascular
structure. However, the distinct formation of vascular basement membrane and communica‑tion with other vascular spaces were obscure. These spindle‑shaped cells showed various
sized compact nodules, and argyrophil fibers developed extensively around them (Photo. 4) .
These spindle‑shaped cells might have the ability to produce collagen fiber thereafter.

The macrophage‑like cells with relatively clear and abundant cytoplasm and roundnuclei showed phagocytic ‑activity because of cell, debris in the cytoplasm. There werenumerous macrophage‑like cells interposed among the spindle‑shaped cells, creating a starry
sky appearance (Photo. 5).
Immature endothelial cell‑like cells with hyperchromatic and slightly small plump nuclei
showed a hob‑nail structure in the slit‑like lumens. In several fields, some of the immature
endothelial cell‑like cells showed a transformation to spindle‑shaped cells.

In marginal sites of the lesion, there was a proliferation of blood vessels, Iymphatic
vessels and postcapillary venules with relatively tall endothelial cells (Photo. 6) .

Mitotic figures were observed only in spindle‑shaped cells and macrophage‑like cells; thenumber of mitotic figures was 2‑5 per each high power field ( x 200) . No abnormal mitoses
were observed in any of the KS cells.
Although there were secondary necroses due to hemorrhage from the thin‑walled dilated
blood vessels in several cases, there were no primary necroses due to tumor proliferation.

256
:;i?

' . '･*",‑.‑,･ ; ･･ il{ .

̲.

Photo. 1 KS cells proliferate along the reticulin network which originatedfrom the trabeculae of lymph node (H.E, original magnification,x 40) .

Photo. 2 KS cells proliferate in the paracortical area (in center) and lymph
follicles are compres8ed by KS eells (in left side) . (H.E. Original
magnification, x 40).

Photo. 3 A small number of spindle‑shaped cells in the medullary area withmarked dilatation of blood and lymphatic vessels (H.E. original
magnification, x 40).

257

Photo. 4 Argyrophil fibers prolong around spindleshaped cells, without

distinct formation of vascular basement membrane and communi‑

cation with other vascular spaces (Reticulin stain, original
magnification, x 100) .

*"** =* * ̲*"' '*"++'*='*;+'*=**""'*'*'* '<'**"**' *"'** '*=<='**'+'*= ' ‑*'= ""': i ' '* ** *"' *' '*. *Photo.. 5

M*c*'ph*g'‑hk* '*n* *hi*h ha'i*g de** a d abundant cyto‑
Pl*sm* +ith Ph*g"yti' **ti+ity i t**P'se " ' g spindle‑shaped'*n* (H'E"*igi**1 **g"ifi'*ti *' x loo) '*̲*,'.*',':' ' < >'Photo. 6 Postcapillary venules which having relatively tall endothelial cells
interpose among spindle‑shaped cells (H.E. original magnification,
x 100) .

258

Photo, 7 Marked proliferation of endothelial cells in blood and/or lymphatic
vessels adjacent to a lymph node, resembles intravascular papillary
endothelial hyperplasia (H.E, original magnificatiQn, x 40) .

Photo

8 Vimentin is strongly positive in spindleshaped cells and endothelial

cells but is negative in macrophage‑1ike cells (ABC technique.
original magnification, x 100).

The characteristic findings were papillary proliferation of KS cells in the blood vessels
aad/or lymphatic vessels adjacent to the lymph node (Photo. 7) . In the proliferative cells of
this lesion, there were no cellular atypia or mitotic figures.

In the immunohistochemical examination, spindle‑shaped cells, immature endothelial
cell‑1ike cells and mature endothelial cells were positive for Vimentin (Photo. 8), but only

mature endothelial cells were positive for FactorVIIIRa and UEA‑1. Macrophagelike cells
were positive for Factor‑VIIIRa. All types of KS cells were negative for Desmin, Actin,

S‑100, CD35 and ACT (Table 4).
DISCUSSION
Our epidemiological results and several reports showed that the African endemic‑type
KS is characterized by its occurrence in two age peaks; one in early childhood and the other259

Table 4 Immunohistochemical results

Pnmary antibodies SC
F‑VIIIRa
F‑XIIIRa
Vimentin

Cell types

M LC

IEC

PcV
+

LV
+

BV
+

+

+

+

+

+

+

+

+
+

Actin

Desmin

ACT
CD35
S‑lOO

UEA‑l

SC: Spindle‑shaped cell. MLC: Macrophage‑like cell. IEC: Immature endothelial
cell‑like cell. PCV: Post‑capillary venule. LV: Mature lymphatic vessel. BV:
Mature blood vessel.

in middle to advanced age (Oettle, 1962; Lulat, 1989) . Most endemic KS cases in children
initially occurred in the lymph node, while those of people of middle to advanced age showedprimary lesions in the skin. In addition, over half of pediatric cases showed generalized
lymphadenopathy. With regard to the male to female ratio, the adult type KS showed a muchhigher incidence in males than in females. On the other hand, the pediatric type KS showeda higher female incidence than the adult type KS. These findings suggest that there arecertain etiological differences between the pediatric type and adult type KS in Western
Kenya. It has been postu]ated that some infections with a transmissible agent in young non‑
immune children lead to proliferation of KS in the lymph node (Slavin et al.. 1969). Bothpediatric and adult type KS showed similar ethnic and geographic distribution (Taylor et al..
1971; Schmid, 1973; Toriyama et al.. 1987a, b) . A high incidence of KS was observed in the
Luo ethnic group living around Lake Victoria, which is a relatively moist tropical savanna.
However, there were only a few cases in dry areas where other ethnic groups including theLuo group reside. These findings are consistent with those of previous reports (Davies, 1959;
Davies and Lothe, 1962) and suggest that climatic conditions such as high temperature andhumidity play an important role in the causation of KS. In Colombia, South America, where
KS showed histological patterns similar to those of African endemic type KS, there were nopediatric patients with KS and the lymph node‑type KS (Garcia et al.. 1989) . In classicaltype KS, there were very few pediatric cases and lymph node cases (Bluefarb, 1957; Bisceglia
et al.. 1988) . These reports indicate that genetic factors and environmental factors such as
life style, Iiving conditions and aging differ among the various types of KS.
KS cells developed at the paracortical area of the lymph nodes and gradually proliferated

along the reticulin network originating from the trabeculae. KS cells were composed ofseveral elements, that is, spindle‑shaped cells without any differentiation, spindle‑shaped
cells with slit‑like structures and immature endothelial cell‑like cells. Immunohistochemical‑
ly these cells were only positive for Vimentin, which is a marker for mesenchymal cells, whileother markers for differentiated cells were negative. These results suggest that KS cells

260

originated from pluripotential cells near the reticulin network, that is, mesenchymal cells

which become immature and mature endothelial cells, and showed the features ofundifferentiated spindle‑shaped cells. Although previous reports have expressed different
opinions about the histogenesis of KS, such as vascular endothelial cell (Rutgers et al., 1986;

Hashimoto et al.. 1987), Iymphatic endothelial cell (Bechstead et al.. 1985; Dictor, 1986;
Russelljones et al.. 1986) , Schwann cell (Pepler, 1959) and fibroblast (Mottaz and Zelickson,1966) , there may be no contradiction if the stage of differentiation from mesenchymal cell toeach of the components is regarded as a spectrum of differentiation. It is thought thatmacrophage‑1ike cells are one of the components of KS Iesions, but it is still obscure whether

the macrophage‑like cells are part of the spectrum of mesenchymal cells, or of the stromal
reaction around KS tissues.
From the histological findings of the lymph node‑type KS in children, that is, coexistenceof spindle‑shaped cells, immature endothelial cell‑like cells, macrophage‑like cells, andrelatively well differentiated small blood and lymphatic vessels, KS seems to be an indepen‑
dent disease with histological features differing from those of I ) Castleman's disease, whichshows marked hyperplasia and hyalinization of intra‑ and extrafollicular blood vessels intumor tissue (Kessler and Beer, 1983); 2 ) angioimmunoblastic lymphadenopathy withdysproteinemia, which is characterized by bifurcated hyperplasia of PAS‑positive, thick‑walled small blood vessels and proliferation of immunoblasts and plasma cells (Frizzera etal.. 1974); and 3 ) vascular transformation of lymph node sinuses, which is characterized byhyperplasia of small blood vessels localized in the sinus or trabeculae without any associationof spindle‑shaped cells (Michal and Koza, 1989) .

The histological features of KS also differ from those of I ) spindle cell hemangioen‑
dothelioma, which shows the coexistence of cavernous hemangioma with spindle cells (Weiss
and Enzinger, 1986) ; 2 ) angiosarcoma, which is composed of Factor‑VIIIRa positive endoth‑elial cells with atypia (Enzinger and Weiss, 1988a); and 3 ) fibrosarcoma, which is surround‑
ed by enormous collagen fibers with a herring‑bone pattern of spindle cells but no slit‑likelumens (Enzinger and Weiss, 1988b) .
Several reports have suggested that the pediatric type KS is a malignant or low‑grademalignant tumor (Master et al.. 1970; Taylor et al.. 1971) because of its clinical andhistological features, that is, rapid growth and short period leading to death, generalized

invasion to organs, necroses, some abnormal mitoses and atypism of proliferating cells. In
our histological results, however, there are no abnormal mitoses, primary necroses, cellularatypia or invasive growth. Some cases with poor prognosis showed a potential for mis‑diagnosis as malignant tumors such as angiosarcoma. In classical KS, KS associated withimmunosuppressive therapy and Acquired immunodeficiency syndrome‑related KS, somecases showed spontaneous remission, and lesions of the patients who had been treated withsteroid therapy appeared or disappeared depending on variation in immunosuppressive status(Zisbrod et al., 1980; Real and Krown, 1985). These results indicate that KS might not be amalignant tumor, but rather a benign neoplasm, tumor‑1ike lesion or reactive hyperplasia.
Our findings indicate that: I ) there are certain differences in the etiological co‑factorsof KS between the endemic lymph node‑type KS in children and the endemic cutaneous type
KS in adults, 2 ) KS cells originate from pluripotent mesenchymal cells, and 3 ) KS might

not be a malignant tumor, but rather a benigu neoplasm, tumor‑like lesion or reactive
hyperpl asia.

261

ACKNOWLEDGEMENTS
The authors are indebted to Prof. Hideyo Itakura and all the members of the Departmentof Pathology, Institute of Tropical Medicine, Nagasaki University for their critical discussion

and kind advice during the course of this study. We would also like to thank Dr. Noah O.
Kamidigo and his staff in the Histology Department, Rift Valley Provincial General Hospital,
Nakuru, Kenya, for their kind permission to study the Kenyan materials.

REFERENCES
1 ) ' Beckstead, J.H.. Wood, 'G.s:;., hd Fletcher, F. (1985): Evidence for the origin of Kaposi's

sarcoma from lymphatic endothelium, Am. J. Pathol., 119, 294‑300
2 ) Bisceglia, M.. Mostafa:, A. nd Bosman, C. (1988) : Primary Kaposi's sarcoma of the lymph
node in children. Cancer, 61, 1715‑1718
3 ) Bluefarb, S.M. (1957): Kaposi's sarcoma, multiple idiopathic hemorrhagic sarcoma., pp 171.
Charles. C. Thomas, Springfield. Illinois, U.S.A.
4 ) Brooks, J.J. (1986): Kaposi's sarcoma: A revetsible hyperplasia. Lancet, 6, 1309‑1310

5 ) Davies, J.N.P. nd Lothe. F. (1962): Kaposi･'s sarcoma in African children, Acta Un. Int.
Cancer, 18, 372‑375
6 ) Dictor. M. (1986) : Kaposi's sarcoma. Origin and significance of lymphaticovenous connec‑

tions, Virchows Arch[Pathol Anat], 409, 23‑25 .
7 ) Dutz, W. and Stout, A.P. (1960): Kaposi's sarcoma in infants and children, Cancer, 13, 684‑694

8 ) Enzinger, F.M. and Weiss, S.W. (1988a): Malignant vascular tumor, Soft"Tissue Tumor, 2nded., 545‑561, St. Louis, Missouri9 ) Enzinger, F.M. and Weiss, S.W. (1988b): Fibrosarcoma, Soft Tissue Tumor, 2nd ed., 201‑222,
St. Louis, Missouri10) Frizzera, G., Moran, E.M. and Rappaport, H. (1974): Angioimmunoblastic lymphadenopathy
with disproteinemia, Lancet, 1, 1070‑1073
11) Garcia, A., Olivella, F., Valderrama, F. and Rodriguez, G. (1989): Kaposi's sarcoma in
Colombia, Cancer, 64, 2393‑2398
12) Harrison. A.C. and Kahn, L.B. (1978): Myogenic cells in Kaposi's sarcoma: An ultrastructural
study. J. Pati., 124, 157‑166

13) Hashimoto, H., Muller, H.. Falk, S. and Stutte, H.J. (1987) : Histogenesis of Kaposi's sarcoma

associated with AIDS: A histologic, immunohistochemical and enzyme histochemical study,
Path. Res. Pract., 182, 658‑668

14) Haverkos, H.W.. Friedman‑Kien, A.E.,J)rotman, D.P. and Morgan. W.M. (1990) : The chang‑ing incidence of Kaposi's sarcoma among patients with AIDS, J. Am. Acad. Dermatol., 22,1250‑1253
15) Hsu, S.M., Raine, L. and Fanger, H. (198D: Use of avidin‑biotin‑peroxidase complex (ABO
in immunoperoxidase techniques: A comparison between ABC and unlabeled antibody (PAP)
procedures. J. Histochem. Cytochem., 29, 577‑580
16) Jojot and Laigret, J. (1922): Un cas de tumeurs superficielles multiples observe au Cameroum,
Bull. Soc. Path. exot., 15, 956‑95

17) Kaposi. M. (1872): Idiopathisches multiples pigmented Sarkom der Haut. Arch. Derm. Syph.,4, 265‑273
18) Kessler, E. and Beer, R. (1983): Multicentric giant lymph node hyperplasia clinically simulat‑

ing Angioimmunoblastic lymphadenopaty. associated Kaposi's sarcoma in two of three cases,
Isr. J. Med. Sci., 19, 230‑234

26219) Kyalwazi, S.K. (1976): Histological classification of Kaposi's sarcoma. A basis forchemother‑apy, East Af. Med. J., 53(12) , 670‑677

20) Lulat, A.G.M.1. (1989): African Kaposi's sarcoma. Tran . Roy. Trop. Med. Hyg., 83, 1‑421) Master, S.P., Taylor, J.F., Kyalwazi, S.K. and Ziegler. J.1 .,(1 70): Immunological studies in

Kaposi's sarcoma in Uganda, Brit. Med. J., 1, 600‑60222) Michal, M. and Koza, V. (1989) : Vascular transformation pf lymph node sinuses ‑A diagnostic
pitfall. Histopathologic and immunohisto‑chemical study;' ath. Res. Pract., 185, 441‑444
23) Mirra. J.M. (1986): Kaposi's "sarcoma" ‑It is a Sarcoma at all?, Trop. Med., 28 (Suppl.), 49‑62

24) Molyneux, E.M. (1979): Childhood malignancies in Malawi 1967‑76., East Af. Med. J., 56(1),15‑2225) Mottaz, J.H. and Zelickson, A.S. (1966): Electron microscope observations of Kaposi's
sarcoma, Acta Derm. Venereol. 46, 195‑20026) Nickoloff, B.J. and Griffiths, C.E.M. (1989): The Spindle‑shaped cells in cutaneous Kaposi's
sarcoma. Histologic simulators include Factor XIIIRa dermal dendrocytes, Am. J. Pathol., 135,

793‑800
27) Oettle. A.G. (1962): Geographical and racial differenceS in the frequency of Kaposi's sarcoma
as evidence of enviromental or genetic causes. Acta. Un. Int. Cancer, 18, 330‑363･28) Olweny, C.L.M., Kaddumukasa, A.. Atine, I., Ower, R., Magrath, I. and Ziegler, J.L. (1976):
Childhood Kaposi's sarcoma: Clinical features and therapy. Br. J. Cancer, 33, 555‑560
29) Owor, R. (1977): Malignant neoplasms in African infants, East Af. Med. J., 54(1), 9‑1330) Pepler, W.J. (1959): The origin of Kaposi's hemangiosarcoma: Hitochemical study, J. Path.
Bact., 78, 553‑557

31) Real, F, and Krown, S. (1985): Spontaneous regression of Kaposi's sarcoma in patients with
AIDS, New Engl. J. Med., 313, 1659
32) Russelljones, R., Spaull, J., Spry, C. and Jones, E.W. (1986): Histogenesis of Kaposi's sarcoma
in patients with and without acquired immunodeficiency syndrome (AIDS) , J. Clin. Pathol., 39,

742‑749
33) Rutgers, J.L.. Wieczorek, R., Bonetti. F.. Kaplan, K.L., Posnett, D.N.. Friedman‑Kien, A.E. andKnowles II, D.M. (1986) : The expression of endothelial cell surface antigens by AIDS‑
associated Kaposi's sarcoma, Am. J. Pathol., 122, 493‑499

34) Safai. B. (1985): Kaposi's sarcoma and other neoplasms in Aquired Immunodeficency Syn‑drome: Advances in Host Defense Mechanisms, 5, 59‑73, Raven Press, New York35) Schmid, H. (1973): Kaposi's sarcoma in Tanzania. A statistical study of 220 cases, Trop.
Geogr. Med., 25, 266‑276
36) Slavin, G., Cameron, H.M., Forbes. C. and Mitchell, R.M. (1970) : Kaposi's sarcoma in East
African children: A report of 51 cases, J. Pathol., 100, 189‑199
37) Slavin, G., Cameron, H.M. and Singh, H. (1969): Kaposi's sarcoma in mainland Tanzania: areport of 117 cases, Br. J. Cancer, 23, 349‑357
38) Taylor, J.F., Templeton, A.C., Vogel. C.L., Ziegler, J.L. and Kyalwazi, S.K. (1971): Kaposi's

sarcoma in Uganda: A clinico‑pathological study. Int. J. Cancer, 8, 122‑135

39) Toriyama, K., Uzuta. F. and Itakura, H. (1987a): Kaposi's sarcoma of lymph node(s) in
Westem Kenya, Trop. Med., 29(2), 101‑l0640) Toriyama. K., Uzuta, F. and Itakura, H. (1987b) : Geopathological study on endemic Kaposi's
sarcoma in Western Kenya, Trop. Med., 29(2) , 87‑10041) Weiss, S.W. and Enzinger, F.M. (1986) : Spindle cell hemangio‑endothelioma. a Low‑grade

angiosarcoma resembling a cavernous hemangioma and Kaposi's sarcoma. Am. J. Surg.
Pathol., 10(8), 521‑53042) Zisbrod. Z., Haimov, M., Schanzer. H., Ambinder, E. and Burrows, L. (1980) : Kaposi's sarcoma
after kidney transplantation. Report of complete remission of cutaneous and viceral involve‑

ment, Transplantation, 30, 383

263

西部ケニアにおける小児の風土病型リンパ節型カポシ肉腫
小室

哲・鳥山

寛

風土病型カポシ肉腫（KS）は赤道アフリカに多く見られ，比較的小児にも好発し，また，リンパ節に発生するものも多く認められてきた。今までの我々の調査でも，小児に発生するKSは，主にリンパ節に初発していた。しかし，これらのKSに関する組織学的検討は，ほとんどなされていない。今回我々は，小児KSのうちリンパ節に初発した症例22例を用いて，地理病理学的，組織学

的，免疫組織学的な検索を行い，その民族，地理的分布，組織学的形態像，細胞の由来1発生機

序に関して検討した。その結果1）風土病型KSの好発年齢には，小児期と中高年齢期の二峰性が見られ，初発部位は小児では主にリンパ節で，多発する傾向が見られ，中高年齢期では四肢の皮膚に多く見られた。2）小児リンパ節型KSは，成人皮膚型KSと同様にLuo族に多く見られ，
高温で多湿なビクトリア湖周辺に多く，乾燥した地域にはまれであった。3）KSはリンパ節のpara−cortical

areaより発生し，reticulin

spindle−shaped

cel1，macrophage−likenetworkに沿って増生していた。4）KSの病変部は

ce11，immature endothelial

celHikecel1，mature bloodvessel，1ymphatic vesse1，postcapillaryvenuleなどの細胞からなっていた。5）悪性を示唆す

る細胞異型，異型核分裂像，腫瘍による増殖性懐死，リンパ節被膜外への浸潤像などは認められなかった。6）免疫染色およびレクチン染色では，内皮細胞のマーカーであるFactor−VIIIRa，
UEA−1はmature

blood

vesselなどのendothelial

cellに陽性で，spindle−shaped

cell，macro・

phage−likecell，immatureendothelialcell−1ikecellは陰性であった。間葉系細胞のマーカーであるVimentinは，spindle−shaped

cell，immature

endothelial

cel1−like

cell，mature bloodvesselなどのendothelialcellに陽性であった。macrophage−likecellはFactor−XIIIRaのみ陽性で，KSの病変部に多く見られたが，KSの構成成分の一種であるか，反応性の増生であるかは不明であった。これらの結果より，KSの発生には自然環境，生活様式などの因子とともに遺伝因子など，いくつかの因子が強い影響を与えていると考えられた。また，KSはparacorticalareaのreticulinnetwork近傍の多潜能なmesenchymalce11より発生し，悪性腫瘍というよりは良性腫瘍，あるいは反応性疾患と考えられたp

長崎大学熱帯医学研究所病理学部門

Jpn. J. Trop. Med. Hyg., Vol. 19 No.

1991, pp. 265‑273

265

A REVISIONARY NOTE ON THE BLACKFLY, HITHERTOCALLED "SIMULIUM ( GOMPHOSTILBIA)BATOENSE EDWARDS, 1934" FROM THE RYUKYUISLANDS, JAPAN (DIPTERA: SIMULIIDAE)
HIROYUKI TAKAOKA
Received May 1 1991/Accepted June 4 1991

Abstract: A new species name. Simulium ( Gomphostilbia) yaeyamaense sp. nov. is
proposed for the blackfly species in the Ryukyu Islands which has been hitherto regarded
as S. (G.) batoense Edwards, 1934, originally described from Java. The new species isreadily distinguished from S. (G.) batoense by the large basal tooth on the female claws,
the characteristic pruinose pattern on the male scutum, and the branching of the pupal gill

filaments. Revised descriptions are given for female, male, pupa and mature larva of thisnew species, and discussed are also taxonomic afiinities with related species.

INTRODUCTION
Edwards (1934) described Simulium ( Gomphostilbia) batoense from adult and immature
specimens collected from East Java. This species has not, since then, been recorded fromanywhere else until Ogata (1956) reported it from Ishigaki Island, Yaeyama‑island group,
situated in the southern part of Ryukyu Islands. This species was also found from lriomote
Island, close to Ishigaki Island (Takaoka, 1972, 1976). However, Iater surveys on blackfiy
fauna in Taiwan and the Philippines failed to discover S. ( G.) batoense, although several
other Gomphostilbia species were collected (Takaoka, 1979, 1983) .

Recently, the author had an opportunity to examine the lectotype male, two para‑
lectotype females, six pupae and three larvae of S. ( G.) batoense preserved in British Museum(Natural History) , London (BMNH) , and found the clear morphological differences at allstages between specimens from Java and Ryukyu Islands, which are considered to be
sufficient for species separation. Most striking is the observation that the Javanese females

bear a small subbasal tooth on the claws (Fig. 3e) whereas Ryukyu's specimens show a large
basal tooth (Fig. 2d) , as in most Gomphostilbia species. These differences have been also
confirmed by the materials newly collected from Java 'by the author.
In this paper, a new species name is proposed for the blackfly so far regarded as S. ( G.)batoense in Ryukyu Islands. Here given are revised descriptions of this new species althoughdescriptions wer previously given under the name of S. ( G.) batoense for the adults and pupa
by Ogata (1956) ahd for the larva by Takaoka (1976) . The taxonomic affinities with related
species including S. ( G. ) batoense are also discussed.

Dmsron of Medical Zoology, Medical College of Oita, Idaigaoka 1‑1, Hazama, Oita 879‑55, Japan

266

C

,

e

o

o
t

9

2d
(' '¥e3"

Figs. 1, 2, 4 and 5 S. ( G.) yaeyamaense sp. nov.: 1, hind leg of female (a, femur; b, tibia;

c, basitarsus) ; 2, female claw with a large basal tooth (d) ; 4 and 5, dorsal andfront views of male scutum.
Figs. 3, 8 and 9, S. (G.) batoense: 3, female claw with a small subbasal tooth (e) ; 8,enlargement of basal portion of pupal gill showing branching method; 9, ventral

view of larval head capsule showing deep postgenal cleft.
6
and 7, S. (G.) friederichsi: 6 and 7, dorsal and front view of male scutum.
Figs.

DESCRIPTION

Simulium ( Gomphostilbia) yaeyamaense sp . nov.
Simulium (Nevermannia) batoense (nec by Edwards) : Ogata (1956)

J pn. J.
,

M. Sc. Biol,,9, 59‑61 (female, male and pupa)
Simulium ( Gomphostilbia) batoense ( nec by Edwards) :Takaoka (1976),

Jpn. J. Sanit.

Zool., 27, 389 (larva)

Female. A small, blackish species (body length 2.0 mm) . Head slightly narrower than widthof thorax. Frons black, whitish grey pruinose, moderately covered with whitish yellow
pubescence as well as a few dark hairs, except middle longitudinal portion narrowly bare;frons shiny and brightly iridescent when viewed in light; frontal ratio (i.e., ratio of thegreatest width at vertex, the narrowest neai antennal base, and the height of the frons)
1.5:1.0:1.65. Frons‑head ratio (i.e., ratio of the greatest width against that of head) 1.0:4.6.

267
f

C ¥t "' ;!("‑ ̲‑ lrt I "¥fJ ‑‑ '.)1

̲‑ T; / ̲"‑

I I ' L *' L ‑1/// //J' /// //,,'// ';,;j //": : }: J J il; ?:' " i"}': ::':' ff::{i"':':I r: "15

s:' :1"'rF:F:!tr' i:I :t'F:'

' L 'i :'w": :'1:':'"f' ' 1;"5'i
'i: "
" 1L"

i

!I

18

e ･
11

i= ･ d
12

',

16

r

Figs. 10‑18 Female and male genitalia of S. (G.) yaeyamaense sp. nov.: 10, ventral
view of 8th sternite (a) , anterior gonapophyses (b) and genital fork (c) ; Il and12, ventral and side views of paraproct (d) and cercus (e) ; 13, spermatheca; 14,

ventral view of coxite (f) , style (g) and ventral plate (h) ; 15, dorsal view of
coxite and style; 16, end view of ventral plate; 17, paramere; 18, median sclerite.

Clypeus black, whitish grey pruinose, and densely covered with whitish yellow pubescenceinterspersed with several dark hairs. Antenna composed of 2 + 9 segments, black except
scape, pedicel and basal 1/2 of Ist flagellar segment yellow. Maxillary palp black, com osedof 5 segments with proportional length of 3rd, 4th and 5th segments being 1.0:1.2:2.2; 3rdsegment not enlarged, and sensory vesicle of moderate size, 1.8 x as long as its width and0.36 x length of 3rd segment, and with small round opening distally, its diameter 0.4 x as longas width of sensory vesicle. Maxilla with 12 teeth on each side. Mandible with about 22 small

inner teeth and 10 outer ones. Cibarium with heavily sclerotized arms but without any
denticles medially. Thorax. Scutum black in ground colour, thinly whitish gre,y pruinose,with three dark longitudinal lines which are distinct when viewed anterodors lly;= pruinose
areas brightly iridescent when illuminated; scuttim densely covered with whitish yellow andbrassy recumbent pubescence as well as several dark long hairs on p̲re, ctitellar area.
Scutellum black with dark pubescence as well as long upstanding dark hairs along posterior
margin. Postscutellum black, whitish grey pruinose , and bare. Pleural membrane bare.
Katepisternum black, whitish grey pruinose, with pale and dark hairs, and longer than deep;
sulcus distinct. Legs. All legs almost black except hind trochanter, base of mid tibia andbasitarsus, base of hind tibia, basal 3/5 of hind basitarsus, and basal 1/2 of hind 2nd tarsal
segment whitish yellow; whitish yellow hairs largely on outer surface of fore tibia, basal 1/2of mid tibia and basitarsus and basal 2/3 of hind tibia and basitarsus‑ these are brightly
iridescent when viewed in certain angles of light. Fore basitarsus not delated, ca. 5.9 x as
long as its greatest width. Hind tibia swollen on distal 1/4 and to lesser extent on basal l/3,

and about 0.8x awide as hind femur (Fig. Ib) . Hind basitarsus slender, parallel‑sided (Fig.

lc) . Calcipala moderately developed, 1.2 x as long as wide, and ca. 0.76x width of basitarsal

268

24

26

22
a

25

;f

,) 21

c

'‑'‑ 23

20

5
19
Figs. 19‑26 Pupal gill filaments of S. (G.) yaeyamaense sp. nov.: 19, whole gill
filaments; 20‑26, basal parts of gill filaments showing various branching
methods (20, normal form; 21‑26, other forms less frequently seen) (a, b and cindicating upper and middle triplets and lower pair groups, respectively) .

tip (Fig. Ic) . Pedisulcus also distinct at basal 1/3 of 2nd tarsal segment. Claws each withlarge basal tooth which is l/2 x as long as claw (Fig. 2). Wing. Length 1.6 mm. Costa with
spinules as well as hairs. Subcosta haired. Tuft hairs at base of stem vein dark brown. Basal
portion of radius fully haired. Abdomen. Basal scale black, with a fringe of pale hairs. Allsegments almost black dorsally, Iaterally and even ventrally, and with dark hairs; 2ndsegment with whitish grey pruinose band on basal l/2 of dorsal surface; tergites of 6th, 7th

and 8th segments shiny. Genitalia. Sternite 8 (Fig. 10a) bare medially, and with 18‑22 dark

macrosetae on each side. Anterior gonapophyses (Fig. 10b) thin, membraneous, rounded
posteriorly, covered densely with microsetae except posterior margins narrowly bare, andwith a few short setae near anterior border; inner margins well sclerotized. Genital fork (Fig.

10c) of usual inverted‑Y form, with somewhat flattened tip; arms each produced inwards tosome extent but lacking any projection directed forwards. Paraproct (Figs. 11 and 12d) of
usual form, short, 1/2 x as long as wide when viewed laterally, ahd with about 20 macrosetae
ventrally and laterally. Cercus (Fig. 12e) short, 1/2 x as long as wide, rounded posteriorly,

when viewed laterally, and covered with about 20 macrosetae on outside surface. Spermath‑

269

Hs+･:

','27' '

+
o

o

o

,,

ot

29

/‑'

/ / 1 28

: ,: r.

"E*31:*'*'‑'
r::" "::i. ! I :'i': I ''=;;4.* "

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:=: ̲': ': ::'!"" " {,: :]'{Sii ;i{:., t ' ' . ;;i.::::'t:";fi! :;=;t:,' 1',{{ :; x; ;,:: :'‑ ;:i.' ?:"iis"=':: t :: .: :;":': ' Li ;" eb::"'{i:::":::". ;:'=":.

i'"';:; ,iii{"'i'

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. : L**:"""' "' ;." ' """""'i$:" "'* s:{':;*,:

Figs. 27‑34 S' ( G') yaeyamaense sp' nov': 27 a'nd 28, terminal hookS of pupal abdomen;

29, cocoon; 30, cephalic apotome of larval head; 31' Iarval hypostomium; 32, tiPof larval mandible; 33, ventral View of larval head capsule shOWing deep
postgenal cleft; 34, Simple and branched black SPines on larval abdominal
cuticle'eca (Fig. 13) oblong, well sclerotized except small area near tubal juncture unscle‑rotized.
Male. Body length 2.0 mm. Head slightly wider than width of thorax. Upper eye consistingof about 14 vertical colums and 14 horizontal rows of large facets. Clypeus black, whitish

grey pruinose, and covered with dark hairs interspersed with pale yellow hairs. Antennacomposed of 2 + 9 segments, dark brown except scape, pedicel and base of Ist fiagellar
segment pale yellow; Ist flagellar segment somewhat elongated, 1.5 x as long as wide.
Maxillary palp with 5 segments; proportional length of 3rd, 4th and 5th segment 1.0:1.2:3.0; 3rdsegment of normal size, with sensory vesicle small, almost globose in shape. Thorax. Scutum
black, with semishiny, whitish grey pruinosity laterally and posteriorly and in 2 submedian
10ngitudinal bands extending from anterlateral corners so as to enclose a black, non‑pruinose

spot on each side and to leave middle of scutum black widely, as shown in Figs. 4 and 5;
middle black band narrowed towards anterior margin, appearing as a flat‑bottomed fiask;
pruinose areas brightly iridescent in certain angles of light; scutum densely covered withbright brassy recumbent pubescence, although these are replaced by bright yellow pubescenceon shoulders and also intermixed with yellow pubescence and upstanding long dark hairs onprescutellar region. Scutellum black, covered densely with dark pubescence as well as
several marginal long hairs. Postscutellum black, grey pruinose and bare. Pleural membranebare. Katepisternum shaped as in female, and with many dark hairs. Legs. Coloration andcovering of bright yellowish hairs as in female. Fore basitarsus slender, not delated, about

270

7.7x as long as its greatest width. Hind tibia of similar shape to that of female except its

greatest width subequal to that of hind femur. Hind basitarsus slender, parallel‑sided.
Calcipala as long as wide and ca. 0.66 x as long as width of basitarsal tip. Pedisulcus wellmarked. Wing. Length 1.5 mm. Other features as in female except subcosta bare. Abdomen.
Basal scale black with a fringe of dark hairs. All segments almost black, not shiny andsparsely covered with dark hairs; 2nd tergite with broad whitish greyish pruinose transverseband which is brightly iridescent when seen in light, and tergites 5‑7 each with a pair of thinly

greyish pruinose patches dorsolaterally which are shiny when viewed in certain angles oflight. Genitalia. Coxite (Fig. 14f) nearly rectangular in ventral view, much longer than wide.

Style (Fig. 14g) small, shorter than coxite, curved inwards ahd with a single apical spine.
Ventral plate (Figs. 14h and 16) fiat, rectangular in ventral view, about 0.6 x as long as wide,slightly concave on posterior margin, slightly produced ventrally forming low posteromedial
process, and densely covered with microsetae ventrally, posteriorly and dorsomedially; basalarms of moderate size, directed forwardly and slightly inwardly. Paramere (Fig. 17) ofmoderate size, with 3 Iong hooks and several shorter ones. Median sclerite (Fig. 18) broad,plate‑like, somewhat broadened distally and ended roundly.

Pupa. Body length (excluding gill filaments) 2.0‑2.3 mm. Head and thorax. Integument
yellowish brown, covered moderately with tubercles. Head with I facial and 3 frontal pairsof simple long trichomes. Thorax with 5 pairs of simple long trichomes. Gill (Fig. 19) with
8 slender filaments arranged in 3 groups, i.e., upper and middle triplets and I Iower pair;common stalk short, usually divided on the vertical plane into 3 subsequent stalks of which

lower one is longest (Fig. 20), but occasionally stalk of upper triplet arising somewhat
outwardly (Fig. 21) , and also stalk of middle triplet rarely arising a little distally from lower

stalk (Fig. 22) or a little upwardly from upper 'stalk (Fig. 23) ; stalk of lower pair stoutest of

all and usually much longer than primary and secondary stalks of middle group put together,but it is rarely subequal to or even shorter than the latter (Figs. 22 and 24); Iower paired
filaments (3.0‑3.5 mm long) much longer and stouter than 6 other filaments (1.5‑1.8 mm long) ;stalks of upper and middle groups each usually branched into I individual filament and paired

2 filaments but sometimes divided into 3 filaments at the same level (Figs. 25 and 26); allfilaments with numerous transverse ridges becoming less distinct towards apex, and covered

with minute tubercles. Abdomen. Terga I and 2 darkened, without tubercles; tergum I witha long simple seta on each side, and tergum 2 on each side with 5 short simple setae and along simple seta. Terga 3 and 4 each with 4 hooked spines directed forwards along posterior
margin, and a short set medially on each side. Tergum 5 with 5 very minute setae and withor without spine combs numbering I or 2, if present. Terga 6‑9 each with spine combs intransverse row, and comb‑like groups of very minute spines on each side of spine combs;
terga 6‑8 each also with a pair of minute setae on each side; tergum 9 with a pair of marked
terminal hooks, of which outer ridges smooth (Fig. 27) or somewhat undulated (Fig. 28).
Sterna 4‑8 each with comb‑like groups of minute spines scattered all over. Sternum 4 withl simple or bifid hook on each side. Sternum 5 with a pair of bifid hooks situated close
together on each side. Sterna 6 and 7 each with a pair of inner bifid and outer simple or bifid

hooks widely spaced on each side. Sternum 9 with 3 grapnel‑shaped hooks on each side.
Cocoon (Fig. 29) simple, slipper‑shaped, moderately woven, extending ventrolaterally, andwith thick anterior margin which has no anterior projection.

271

Mature larva. Body length 4.0‑4.5 mm. Body colour yellowish with greyish brown transverseband on each abdominal segment. Head with pale or somewhat darkened cephalic apotome
with positive head spots (Fig. 30) . Antenna longer than cephalic fan stem, 'with 4 segments

in proportion of 16:15:15:1. Cephalic fan with 34‑38 main rays. Mandible with 2 mandibular
serrations; comb teeth decreasing in length and thickness from Ist to 3rd tooth (Fig. 32) .
Hypostomium (Fig. 31) with a row of 9 apical teeth, of which corner and median teeth aremoderately developed; Iateral serration absent; 3 or 4 hypostomial setae lying parallel tolateral margin on each side. Postgenal cleft deep, about 6 x as long as postgenal bridge, andmuch constricted at base (Fig. 33). Thoracic cuticle bare. Abdominal cuticle bare on
segments I and 2, but dorsally covered with minute black spines very spatsely on segments
3 and 4, and moderately on the remaining posterior segments; most of these spines are split
into 2 or 3 branches apically, although there are some simple and quadrifid spines (Fig. 34) .

Rectal gill lobes compound, each lobe with 6‑8 finger‑like lobules. Anal sclerite of usual X‑
form, posterior arms a little longer than anterior ones; basal portion of arms widely sclerot‑

ized. Ventral papillae well developed. Posterior circlet with about 78 rows of about 12 hooks
each.

Type specimens: Holotype, slide‑mounted together with pupal skin and cocoon, taken asa pupa from a small stream at Inoda, Ishigaki Island, Yaeyama‑island group, Ryukyu Islands,
Japan, 12.V.1988, H. Takaoka. Allotype c71, slide‑mounted together with pupal skin andcocoon, same data as holotype. Paratypes, 9, 4 c71 cfl , reared from pupae and pinned, 10

pupal skins and cocoons, 5 mature larvae in alcohol, same data as holotype. Holotype,allotype and some paratypes will be deposited in BMNH, and other paratypes in Bishop

Museum, Hawaii.
Distribution: Ryukyus (Ishigaki Island and lriomote Island) .

DrscUssroN
Simulium ( G.) yaeyamaense sp. nov. is similar to S. ( G. ) batoense in having the darkcoloration of legs of both adult sexes, the slender, parallel‑sided male hind basitarsus and thepupal gill filaments of which lower paired filaments have a long stalk and are about twice aslong as the other six filaments. The female of this species is readily distinguished from thatof S. ( G. ) batoense by the large basal tooth on the claws (Fig. 2d) , as already mentioned. The
male of this species is also separable from that of the latter species by the difference in thepruinose pattern on the scutum which is, in S. ( G.) batoense, of usual form having pruinose

areas only on shoulders, along lateral margins and on prescutellar region. The pupal gill of
this new species seemed very similar to that of S. ( G. ) batoense originally illustrated by

Edwards (1934) . However, a close examination indicates that the middle group of the gill
filaments is, in S. ( G. ) batoense, composed of paired two filaments and two individual
filaments arising inwardly from its stalk near the base (Fig. 8) . The larva of S. ( G. ) batoenseshows similarities to this new species in having the dark branched spines dorsally on posterior

abdominal segments, but seems to differ by a much deeper postgenal cleft (Fig. 9) .
This new species appears to be most closely related to S. ( G. ) friederichsi Edwards, 1934
from East Java in having the similar pruinose pattern on the male scutum, as well as parallel‑

272

sided, male hind basitarsus; and dark legs. The pruinose scutal pattern of the holotype maleof S. ( G.) friederithsi preserved in BMNH shows that sublateral black spots are much larger

and the medial vita is shaped like a round‑bottomed bottle, as shown in Figs. 6 and 7. The
female, pupa and larva of this species are not known yet.

The male of S. (G.) siamense Takaoka and Suzuki, 1984 from Thailand posesses asimilar but different pruinose pattern ori the scutum which exhibits the medial vita with theposterior half much narrowed (Takaoka and Suzuki, 1984, cf. Fig. 17) . The female, pupa andlarva of ,this species also resemble S. ( G.) yaeyamaense sp. nov. in many features including thedark coloration of legs, the large basal tooth on the claws, the branching of the pupal gill
filaments, the simple slipper‑shaped cocoon, and the deep postgenal cleft. However, there aredifferences in the following features: in the female, frontal ratio 1.4:1.0:1.9, and macrosetae on

the 8th sternite, the paraproct and the cercus fewer in number (about half the number of thisnew species) ; pupal gill filaments as long as pupal body; black spines on the dorsal surfaceof larval abdomen split into many more branches.
This new species shows some similarities with S. ( G. ) torautense Takaoka and Roberts,
1988 from North Sulawesi and S. ( G. ) hrombeini Davies and Gy6rk6s, 1987 from Sri Lanka
in the dark coloration of legs, and male hind basitarsus parallel sided. The characteristic
pruinose pattern on the scutum separates the male of this new species from the latter two
known species which do not bear such a scutal pattern. The female of the new species isbarely distinguished from S. (G.) torautense by the wider frons (i.e., frontal ratio 1.5:1.0:1.65
vs. 1.3:1.0:2.5) and also from S. (G.) krombeini by the size of claw tooth (i.e., Iength of tooth/claw l/2 vs. 2/3) as well as the frontal ratio (1.4:1.0:2.9 in the latter) . The pupal gill with very

short stalks and the cocoon with an anterodorsal projection in S. ( G. ) torautense, and thepupal gill filaments shorter than the pupal body in S. ( G. ) krombeini easily separate themfrom the present species, respectively. In the lafval stage, S. ( G. ) yaeyamaense sp. nov. differsfrom S. ( G.) torautense by the branched spines on the abdominal cuticle rather than simple
spines as in the latter, and also from S. ( G.) hrombeini by the compound anal gill lobes anddeep postgenal cleft (simple anal gill lobes and medium‑sized cleft in the latter) .

AcKN OWLEDGEMEN TS
I thank Dr. R.W. Crosskey, Dr. A.J. Shelley, Ms. C. A. Lowry and Ms. T. M. Howard,
Department of Entomology, British Museum (Natural History) , London for their kind help
during my stay at their laboratory in 1990. My appreciation goes to Dr. D.M. Davies,
Professor Emeritus, MdMaster University, Ontario, and Dr. H. Takahashi, Tokyo for theirencouragement and advice.
This work was supported by "the grant‑in‑aid of Ministry of Education, Science andCulture, Japan for studying abroad,

REFERENCES
1 ) Davies, D.M. and Gydrkds, H. (1987): The Simuliidae of Sri Lanka. Descriptions of species
in the subgenera Eusimulium and Gomphostilbia of the genus Simulium. Can. J. Zool., 65,
1483‑1502
2 ) Edwards, F.W. (1934): Deutsche Limnologische Sunda‑Expedition. The Simuliidae (Diptera)

273

of

Java

and

Sumatra，Arch．F，HydrobioL，SuppL，13，92−138

3）Ogata，K．（1956）：Notes

on Simuliidae

of

the

RyukyunewofSimuliidae

lslands（Diptera），Jpn．J．M．Sc．Bio1．，

9，59−69

4）Takaoka，H．（1972）：A

speciesfrom

YonakmiIsland，Ryukyu

Islands，Japan（Diptera：Simuliidae），J．Med．Entomol．，9，521−523
5）Takaoka，H．（1976）：Studies

ofEnderleinRubzov，with

and

G

寓s

the

on

II．On six species

black flies

subgenera
theof

the Nansei Islands，Japan（Simuliidae；Diptera）．

Oo ψhosガ必∫descriptionofzEnderlein，掘o名oゆs

Enderlein，04㎎窺勿

S伽％伽吻（Oo解ρhosあ必血）o為

ηαωθ％s召sp．

nov．，JPn．」．Sanit．ZooL，27，385−398

6）Takaoka，H．（1979）：The

blackniesof Taiwan（Diptera：Simuliidae），Pacific Insects，20，

365−403
7）Takaoka，H．（1983）：The blacknies（Diptera：Simuliidae）of theScocietyforthe8）Takaoka，H．and

Philippines，pp．212，Japan

Promotion of Science，Tokyo

Roberts，D．M．（1988）：Notesonblacknies（Diptera：Simuliidae）from

Sulawesi，Indonesia，Japan．J．Trop．Med．Hyg．，16，191−219
9）Takaoka，H、and Suzuki，H．（1984）：The blacknies（Diptera：Simuliidae）fromThailand，Jpn．

」．Sanit．ZooL，35，7−45

琉球列島においてS伽御1勉卿（Go，％ρho語16毎）6α孟08ns6Edwardsと同定されていたブユ種の分類学的再検討
高岡宏行

吸血性双翅目昆虫ブユ科のなかで，S珈鹿伽吻属のGo吻ρhos観伽亜属に含まれる種は，一般に地理的分布が狭い。そこで，ジャワ島および琉球列島の石垣島と西表島から報告されている，ブユ種S（σ）加如㎝s召が両地域間で同一かどうかを明らかにする目的で，大英自然史博物館に保管されている本種の模式標本（ジャワ産雌雄成虫，蠕，幼虫）を観察し，琉球列島で採集された標本との比較を行った。その結果，琉球列島のブユ標本は，雌成虫の脚の爪の形態，雄成虫背胸部の斑紋，婦の呼吸糸の分岐方法などで，ジャワ産の模式標本と明らかに異なることが分かった。

この結果は，最近新たにジャワ島で採集された標本でも確認された。これらの結果をもとに，これまでS（G）δσ孟o飢s召とされていた琉球列島のブユに，新種名S（G）夘8翼耀召nsθ（和名，

ヤエヤマナンヨウブユ）を与え，記載を行った。さらに，ジャワ，タイ，スラウェシ，およびス
リランカからそれぞれ報告されている，4類似種との形態的相違についても論じた。

大分医科大学医動物学教室

Jpn. J. Trop. Med. Hyg., Vol. 19 No. 3 1991, pp. 275 280

275

ACUTE RESPIRATORY INFECTIONS IN
CHILDREN UNDER FIVE IN TWO RURALCOMMUNITIES IN SOUTHERN GHANA
E.A. AFARll, HIROYUKI SAKATOKU2, TAKASHI NAKAN03
F. BINKA4, A. AsSOKUl, E. KWARTENG AMANING1
G. MENSAHI AND J. FENTENGl
Received May 7 1991/Accepted June 10 1991

Abstract: A historical prospective study based on data collected on acute respiratory

infections (ARD from children aged 1‑4 years at Gomoa Fetteh and Gomoa Onyadze/Otsew Jukwa, two rural communities in the central region of Ghana from January 1987 to
December 1989 indicated that a child on average would have 5.3 to 7.0 episodes of ARI
annually. Acute upper respiratory infections (AURD constituted 99.4 and 99.7 per cent of
all ARI in the two communities, and acute lower respiratory infections (ALRD 0.3 and 0.6
per cent respectively. Incidence of ARI generally peaked in September/October in the two
communities. The under five mortality rates due to ARI were 4.5/1,000 and ll.511,000
representing 23.3 and 33.3 per cent of all under five deaths respectively at the beginning of

the programme in 1987 but these were reduced to nil in 1988 and 1989. Regular outreachservices including EPI and curative services delivered to the two communities within thecontext of PHC in Ghana may have contributed to the decline in mortality rates due to

ARI.

INTRODUCTION
The complex group of acute respiratory infections (ARD constitutes one of the principal
causes of morbidity and mortality in many developing countries. In many countries of Africa,
about 50 per cent of all deaths are in children under five years old. ARI is generally estimatedto be the cause in one fourth to one third of these deaths (Pio et al.. 1984). Accurate dataon the incidence of ARI in the general population is scarce but the limited data available
indicate that a child in an urban area has an average of five to eight attacks annually witha mean duration of 7‑9 days (Pio et al., 1984; WHO, 1986) . The situation may not be muchdifferent in Ghana but there had not been any longitudinal studies as yet to provide data inthe magnitude of childhood ARI although ARI for all age groups constitute 3.4‑8.0 per centl Epidemiology Unit, Noguchi Memorial Institute for Medical Research, Universify of Ghana,
P.O.Box 25, Legon, Ghana
2 Department of Pediatrics, Yamada Red Cross Hospital, 810 Takabuku Misono, Vatarai, Mie
3516, Japan
Department of Pediatrics, Mie University, 174 Edobashi, Tsu. Mie 514. Japan

4
Ghana‑Vast, P.O.Box ll4, Navrongo, Ghana
This study was performed as part of Noguchi Memorial Institute for Medical Research Project
supported by Japan International Cooperation Agency ( JICA) .

* Request for reprints should be sent to Dr. E.A. Afari through Dr. Hiroyuki SAKATOKU.

276

of new outpatients attendances in some clinics in Ghana (Ashitey et al.. 1972; Ashitey andNettey‑Marbje!1, 1988). The objective of the present study was to determine morbidity andmortality associated with ARI in children under five years of age in two rural communities

in Southern Ghana:

POPULATION AND METHODSThis historical prospective study was based on data collected on ARI from children underfive years of age in two rural communities ‑Gomoa Fetteh and Gomoa Onyadze/Otsew
Jukwa‑ in the central regio,n of Ghana, from January 1987 to December 1989. These twovillages are approximately 82 km from Accra, the capital of Ghana. Gomoa Fetteh is acoastal village with a population of 2,316 of whom 19% (440) is under five years of age.
Gomoa Onyadze/Otsew Jukwa, a twin village is few kilometers inland with a population ofl,300; 20% (260) are under five years. The people of these villages, are mainly farmers andpetty traders. These two villages like the rest of Ghana, experience two major seasons in a

year; a dry season from October/November to March, and a wet one from April to Septem‑
ber.

The Noguchi Memorial Institute for Medical Research (NMIMR) of the University of
Ghana maintains health research field stations in the villages mentioned above and provides

PHC including maternal and child care services to them. Population censuses were conductedby the NMIMR in the two villages in 1986, and in 1988, and all children under five years old

were registered for a weekly follow‑up at community clinics in the villages. There were 350
children under five on the register at Gomoa Fetteh in January 1987; 358 and 300 at the same

period in 1988 and 1989 respectively. During the same period the number of children underfive years of age for Gomoa Onyadze/Otsew Jukwa were 220, 218 and 188 respectively.
A team of three doctors, two senior nursing officers and field technicians visited thevillages and conducted clinics once every week on non‑farming days. Services provided atthe villages included growth monitoring, immunization, health educatiori and health careincluding diagnosis and treatment. Morbidity data and health status of the children wererecorded on a disease register. The data was then entered into a computer at the Institute.
Table l Incidence of acute respiratory infections in two rural communities

in southem Ghana 1987‑1989
Acute respiratory infections

VillageYear

Number of

Gomoa Fetteh

1987

266
258

1

1988

1989

260

Gomoa Onya‑

1987

dze/Otsew

1988

Jukwa

1989

children

AURI

ALRI
54

l 851 (7. o)lO(o . 04)

1651(6 . 4)

02)

1

410

(5 . 4)

1 04 7(5 . 3)216(6 . 3)934(5 . 4)797

1 64 1

(6.4)

1

406

(5 . 4)

4

199

1

046

(5 . 3)(o . O1)

193

1

207

(6 . 3)9 (o. 05)931

(5 . 4)

3

174

Total

(o . 2)(6 . 8)(.o .

(O . 02)

AURI: Acute upper respiratory infections
ALRI: Acute lower respiratory infections
Episodes of acute respiratory infections/child/year in brackects.

l

277

Any child who failed to attend clinic was visited at home and the health status assessed.
Nasal discharge, red throat (pharyngitis) , red tonsils (tonsillitis) , ear che and ear discharge(otitis media) constituted acute upper respiratory ,infections (AURD ,･whilst wheeze, cough,chest indrawing and or fast breathing (respriatory rate over 50 per m'mute) were classified

as acute lower respiratory infections (ALRD. These diagnoses were made clinically.
Criteria for, other diseases like malaria, diarrhoea diseases were also defined and children
found to be ill were managed accordingly. All seriously ill children were referred to a district

hospital for inpatient management. Two community health workers in each village weretrained to record all deaths which were followed by verbal autopsy by the three doctors on

the team. If a child had any of the above symptoms of ALRI immediately preceding death,then the death was associated with ALRI.
Data collected on children on the register for at least sixty per cent of the visit in eachyear from 1987 to 1989 in each village was included in the analysis of morbidity due to ARI.
All deaths associated with ARI for the same period were also included in the data analysis.

RESULTSIn Gomoa Fetteh 266 (76.0%), 258 (72.1%) and 260 (86.7%) of registered children underfive years of age were seen at least sixty per cent of clinic visits in 1987, 1988 and 1989

respectively. The figures for the same period for Gomoa Onyadze/Otsew Jukwa were 199(90.5%), 193 (88.5%) and 174 (92.6%). The Table I presents incidence of ARI in the twovillages for the period 1987 to 1989. AURI constituted about 99.4 and 99.7 per cent of all ARI
and mean episodes of ARI per child per year in the two villages were 5.3 and 7.0 respectively.

Incidence of ARI generally peaked in September/October (end of wet season) in the two
240
220
200
180

160

140
(u
"
v 120
o
d 100
c:l

;

80
60

40
20
O

J FMA M J J A S OND J FMAM J J AS OND J FMAM J J A S OND

1987

1988 1989

Figure 1 Acute respiratory infections in under five in Gomoa Fetteh 1987‑1989.

278

communities (Figs. I and 2).

Gomoa Fetteh recorded six under five deaths in 1987, four in 1988 and two in 1989.
Gomoa Onyadze/Otsew Jukwa also recorded eleven under five deaths in 1987, six on 1988 andfour in 1989. Two (if the deaths at Gomoa Fetteh (4.5/1,000 under five population) an:d threeat Gomoa Onyadze (11.5/1,000 under five population) in 1987 were due to ARI and could beclassified as post measles pneumonia. None of the under five deaths recorded in 1988 and in
1989 in the two communities were attributed to ARI. None of the children seen for at least
sixty per cent of clinic visits in the villages by the staff of NMIMR during the period underreview died from ARI.

DISCUSSION
Acute respiratory infections rank among the most common diseases of children the world
over. Available data on the incidence of ARI indicates that on the average a child in an urban
area has from five to eight attacks annually. Most of these are the less serious AURI. In rural

areas the incidence may be lower (Pio et al., 1984; WHO, 1986) .
The results of this rural community based study also show that children under five yearsof age had an average of 5.3 to 7.0 attacks of ARI annually for the three years study period,and most of these were due to AURI (99.4% to 99.7%). Indications are that the incidence of
ARI in children in a rural area may not be different from that in an urban area.
The incidence of ARI generally peaked in September/October (end of wet season) in thetwo communities. The seasonal variation in ARI may help formulate hypotheses in relation
to risk factors in the environment and changes in human behaviour which determine thechanges in incidence in ARI during the year. These hypotheses may form the basis for further

240
220
200
180
160

e) 140u'g.

cl$c) 120
,

o

100
80
60
40
20
o

J FMAM J J ASOND J1988FMAM J J AS OND 1989
J FMAMJ J ASOND

1987

Figure 2 Acute respiratory infections in under five in Onyadze/Otsew Jukwa 1987‑1989.

279

studies in ARI in the study area.
Data from 88 countries in five continents, with a total population of nearly 1,200 million,

showed that deaths due to ARI in 1972 amounted to 660,000 and this represents 6.3 per centof deaths from all causes (Bulla and Hitze, 1978) .
Of the estimated 15 million deaths occurring each year in children under five years of age,

25‑30 per cent are due to ARI, and the vast majority of these are caused by pneumonia(WHO, 1988) . The under five mortality rates due to ARI recorded in this study (4.5/1,000 andll.5/1,000 under five population) represent 23.3 and 33.3 per cent of all under five deaths in1987 in the two communities studied respectively at the initial stages of the Institute's
activities in the two villages. These deaths were mainly caused by post‑measles pneumonia,
and the children aged 1‑4 years who died from pneumonia were those who for one reason or
the other did not benefit fully from the Institute's outreach services especially the EPI.
Proportion of deaths due to ARI recorded in the study does not differ much from what isreported world‑wide (WHO, 1988) . However, deaths due to ARI in the two communities
were reduced to nil in 1988 and 1989. None of the children seen at least for sixty per cent of

the visits to the villages by the staff of the NMIMR from 1987 to 1989 died from ARI. The
results of this study indicate that an active health services out‑reach programme within thecontext of the PHC can efficiently reduce high child mortality from ARI and other diseases.

ACKNOWLEDGEMENT
We thank the mothers and children of the Gomoa Fetteh and Gomoa Onyadze/Otsew
Jukwa who participated in this survey. We also wish to thank Professor F.K. Nkrumah, thedirector of Noguchi Memorial Institute for Medical Research for useful suggestions in the
preparation of the manuscript.
This study was supported in part by Japan International Cooperation Agency (JICA) and

the Ghana Government.

REFERENCESl ) Ashitey, G.A. and Nettey‑Marbell (1988) : Momtormg disease patterns at the distnct level"The Suhum expenence 1982 1987" (1) General trends and patterns Ghana Med. J., 22, 49‑57
2 ) Ashitey, G.A., Wurapa, F.K. and Belcer, D.W. (1972): Rural health centre. It's patients
services 1970‑1971, Ghana Med. J. Il, 266‑273
3 ) Bulla, A. and Hitze, K.L. (1978): Acute respiratory infections: a review, Bull. WHO, 56, 481‑

4984 ) Pio, A., Leowski, J. and Ten, D. (1984): Acute respiratory infections in childhood, Proceedingsof an International Workshop in Sydney, Australia, 3‑65 ) Noguchi Memorial Institute for Medical Research Epidemiology Unit. June 1986 and 1988
Census Reports
6 ) WHO (1986) : WHO/UNICEF Basic Principles for Control of Acute Respiratory Infections inChildren in Developing Countries. A joint WHO/UNICEF statement, WHO Geneva Publica‑tion, 7‑87 ) WHO (1988) : WHO Programme for the Control of Acute Respiratory Infections. Programme
Report 1988, WHO/ARI/89.3, 1‑2

280

ガーナ南部の農村2地区忙おける5歳未満児の急性呼吸器感染症
E．A．Afari1・酒徳 浩之2・中野貴司3・F．Binka4・A．Assoku1・E．Kwarteng Amaning1・
G．Mensah1、・J．Fenteng1

1987年1月から1989年12月までの2年間，ガーナ共和国のセントラル地区の農村，フェテ村およびオンヤディ・オチュウジュクワ村の野口記念医学研究所のフィールドステーションを受診した，5歳未満の小児の急性呼吸器感染症について，追跡調査を実施した。それぞれの村では1人の小児に対して，年平均5．3回および7．0回の急性呼吸器感染が見られた。
急性呼吸器感染症のうち，急性上気道感染症の占める割合は，それぞれ9914％および99．7％で，下気道感染症は0．4％，0．3％であった。

急性呼吸器感染症の罹患率は9月，10月にピークを示した。1987年調査開始時の，急性呼吸器
感染症による1，000人あたりの5歳未満児の死亡率はそれぞれ4．5，11．5で，5歳未満小児の全死
亡数の23．3％，33．3％を占めていたが，1988年および1989年には急性呼吸器感染による死亡は見られなかった。ガーナにおけるPrimary HealthCare（PHC）に関連した拡大予防接種計画，および医療サービスを含む我々の診療活動により，急性呼吸器感染症による死亡率の減少に貢献したものと思われた。

野口記念医学研究所疫学ユニット
山田赤十字病院小児科
三重大学医学部小児科

ガーナビタミンA研究チーム

ISSN 0304‑2 J 46

JAPANESE JOURNAL OF
TROPICAL MEDIClNE AND HYGIENE
Vol. 19 No. 3

September 1991

CONTENTS
Original article

Nanbu, K., Minoyama, H., Kanda, M., Eto, H., Moriya, T., Watanabe, M., Motoda, A.,
Yun, Z.X., Senba, M., Toriyama, K., Itakura, H. and Atari, E.
Liver Lesions and Structural Arrangement of Remaining Hepatic Cell Cords inEclampsia and Other Acute Liver Lesions in the Tropics(in Japanese)

229‑237

Minoyama, H., Nanbu, K., Kanda, M., Eto, H., Moriya, T., Motoda, A., Senba, M.,
Toriyama. K., Atari, E. and Itakura, H.

Histopathology of Atypical Vascular Proliferation of Pyogenic Granuloma of

the Upper Respiratory Tract: Kenyan and Other Cases (in Japanese)

Komuro, S. and Toriyama, K.
Geopathology of Endemic Pediaric Lymph Node Kaposi's Sarcoma
in Western Kenya ""'Takaoka, H.

239‑250251‑263

A Revisionary Note on the Blackfly, Hitherto Called "Simulium (Gomphostilbia)
batoense Edwards, 1934" from the Ryukyu Islands, Japan (Diptera: Simuliidae)
265‑273

Afari, E.A., Sakatoku, H., Nakano, T., Binka, F., Assoku, A.,

Amaning, E.K., Mensah, G. and Fenteng, J.

Acute Respiratory Infections in Children Under Five in Two Rural Communities

in Southern Ghana""" """""" """ """ """ "'Jpn. J. Tro p.

Med. Hyg.

JAPANESE SOCIETY OF TROPICAL MEDIClNE

275‑280