➨  ᅇ⏕⏘ᆅ࡟࠾ࡅࡿ㍍✀㤿ࡢ⑌⑓࡟㛵ࡍࡿࢩ࣏ࣥࢪ࣒࢘㸦  ᖺ ᗘ 㸧ㅮ ₇ ᢒ 㘓᪥᫬ ᖺ᭶᪥㸦ᮌ㸧఍ሙ 㟼ෆ࢚ࢡࣜࣉࢫ࣍ࢸࣝ)࢚ࢡࣜࣉࢫ࣮࣍ࣝ

᪥ᮏ୰ኸ➇㤿఍㤿஦㒊 㜵␿ㄢ➨ 㻡 㻝 ᅇ 䚷 ⏕ ⏘ᆅ 䛻 䛚 䛡 䜛 ㍍ ✀ 㤿䛾 ⑌ ⑓ 䛻 㛵䛩 䜛 䝅 䞁 䝫 䝆 䜴 䝮䝍䜲䝮䝔䞊䝤䝹
㛤఍ᘧ㻌㻝㻜䠖㻜㻜䡚

≉ูㅮ₇㻌㻝㻜䠖㻝㻜䡚

䛂㻭㼎㼛㼞㼠㼕㼛㼚㻌㼍㼚㼐㻌㻼㼑㼞㼕㼚㼍㼠㼍㼘㻌㻰㼑㼍㼠㼔㻌㼕㼚㻌㻴㼛㼞㼟㼑㼟㻛㻌㻼㼍㼠㼔㼛㼘㼛㼓㼥㻌㼛㼒㻌㻲㼛㼍㼘䛃
Fabio Del Piero (䝹䜲䝆䜰䝘ᕞ❧኱Ꮫ䚷⋇་Ꮫ㒊䚷⋇་⑓⌮Ꮫᢸᙜᩍᤵ)ఇ᠁㻌㻝㻝䠖㻝㻜䡚䝅 䞁 䝫䝆 䜴 䝮䛂⏕⏘ᆅ䛷㐼㐝䛩䜛⑌⑓䛻ᑐ䛩䜛⑓⌮デ᩿䛃㻌㻝㻝䠖㻞㻜䡚
ᗙ㛗䠖ୖ㔝䚷Ꮥ⠊

䚷䚷䞉₇㢟䚷㻝䠅䚷䡚䚷㻠䠅㻌㻝㻞䠖㻞㻜䡚

᫨㣗㻌㻝㻟䠖㻞㻜䡚

䛂㻶㻾㻭䛛䜙䛾䛚▱䜙䛫䛃୍⯡ㅮ₇㻌㻝㻟䠖㻠㻜䡚

ᗙ㛗䠖㛵䚷୍ὒ

䚷䚷䞉₇㢟䚷㻝䠅䚷䡚䚷㻠䠅

㛢఍ᘧ
㻝㻡㻦㻜㻜

⤊஢䞉ゎᩓ

22

第 51 回 生産地における軽種馬の疾病に関するシンポジウム
プログラムおよび抄録目次

主催：日本中央競馬会（JRA）
開催日時：2023 年 7 月 13 日 (木) 10 時 00 分～15 時 00 分
開催場所：静内エクリプスホテル 2Ｆ エクリプスホール（日高郡新ひだか町静内吉野町 3-1-1）＜開  会＞
＜開会の辞＞  栗本 慎二郎（JRA 馬事部防疫課）＜開会挨拶＞  菊田 淳  （JRA 馬事担当理事）＜演  題＞
● 特別講演

10：00

10：10～

座長：上野 孝範（JRA 競走馬総合研究所）「Abortion and Perinatal Death in Horses/ Pathology of Foal」------------------------------------------------------------------------------------------------------------------------- 1           〇Fabio Del Piero(ルイジアナ州立大学 獣医学部 獣医病理学担当教授)


休憩（11 時 10 分～11 時 20 分）● シンポジウム 各 15 分（質疑応答含む）

11：20～

座長：上野 孝範（JRA 競走馬総合研究所）「生産地で遭遇する疾病に対する病理診断」
１）2014 年度以降の日高管内における馬異常産について～病理学的所見～ -------------------- 12                ○佐藤 陽輔（北海道日高家畜保健所）
２）周産期および仔馬の肺病理 ------------------------------------------------------------------------------ 13○松田 一哉（酪農学園大学）
３）当歳馬の急性間質性肺炎：超音波、X 線画像と病理所見の対比 ------------------------------- 14○水口 悠也（NOSAI 北海道）
４）ウマの腸炎--------------------------------------------------------------------------------------------------- 15○越智 章仁（JRA 競走馬総合研究所）

昼食（12 時 20 分～13 時 20 分）「JRA からのお知らせ」

13：20～

日本中央競馬会における新たな薬物規制制度について------------------------------------------------------- 16   ○石川 裕博（JRA 馬事部アンチドーピング課）

23

● 一般講演 各 15 分（質疑応答含む）

13：40～

座長：関 一洋（日本軽種馬協会）
１）全身麻酔下での難産介助方法の評価 ～４つの術式の成績比較～ ---------------------------- 17○鈴木 吏（社台ホースクリニック）２）繁殖牝馬の子宮頸管裂創に対する経直腸超音波検査による診断の試み ---------------------- 18○水口 悠也（NOSAI 北海道）
３）馬のジノプロスト（PGF2α）による発情回帰成績 ---------------------------------------------- 19○小笠原 慶（NOSAI 北海道）
４）心房細動における体表心電図を用いた f 波の FFT 周波数解析の検討および
心房細動停止との関連性 --------------------------------------------------------------------------------- 20○井上 佳織（JRA 栗東トレーニング・センター）＜閉会の辞＞  笠嶋 快周（JRA 競走馬総合研究所）＜閉  会＞

24

15：00

Abortion and Perinatal Death in Horses
Pathology of Foal
‫ ۑ‬Fabio Del Piero, DVM, PhD, Dipl. ACVPLouisiana State University, School of Veterinary Medicine
and Louisiana Animal Disease Diagnostic Laboratory࠙₇⪅␎Ṕࠚ
1990 ᖺ University of Milano ࢆ༞ᴗᚋ㸪࢔࢖ࣝࣛࣥࢻࢆ⤒࡚࢔࣓ࣜ࢝ ࢥ࣮ࢿࣝ኱Ꮫ࡛⋇་ゎ๗Ꮫࡢࣞࢪࢹࣥࢺࢆಟ஢ࡋ㸪࢔࣓ࣜ࢝⋇་⑓⌮Ꮫ఍ㄆᐃ་࡜࡞ࡿࠋࡑࡢᚋ㸪࣌ࣥࢩࣝࣂࢽ࢔኱Ꮫ࡛༤ኈྕࢆྲྀᚓᚋ㸪ྠ኱Ꮫ࡟࡚ᩍ㠴ࢆྲྀࡿࠋ2012 ᖺ㸪ࣝ࢖ࢪ࢔ࢼᕞ❧኱Ꮫ⋇་Ꮫ㒊ࡢᩍᤵ࡟ᑵ௵ࡍࡿ࡜࡜ࡶ࡟㸪ྠ኱ᏛLouisiana Animal Disease Diagnostic Lab ⑓⌮㒊㛛࡟╔௵ࡍࡿࠋ⣙ 30 ᖺ࡟ࢃࡓࡗ࡚⑓⌮デ᩿ᴗົ࡟ᦠࢃ
ࡗ࡚࠾ࡾ㸪≉࡟࢘ࢩࡸ࣐࢘࡞࡝ࡢ኱ື≀ࡢ⑓⌮Ꮫࡢᶒጾ࡜ࡋ࡚▱ࡽࢀࡿࠋ
࠙Abortion and Perinatal Death in Horses (࣐࢘ࡢὶ⏘࡞ࡽࡧ࡟࿘⏘ᮇ)ࠚ
㤿ࡢὶṚ⏘ࡣ㸪㠀ឤᰁᛶ㸦⮖ᖏ᤬㌿㸪⫾┙ኚᛶࡸ཮⫾࡞࡝㸧࡜ឤᰁᛶ࡟኱ูࡉࢀࡿࠋឤᰁᛶὶṚ⏘ࡣ㸪ᵝࠎ࡞⑓ཎయ࡟ࡼࡗ࡚ᘬࡁ㉳ࡇࡉࢀࡿࠋឤᰁᛶṚὶ⏘ࡢሙྜ㸪ឤᰁ⑕ࡢண㜵࣭⟶⌮࡞࡝ࡀᚲせ࡛࠶ࡾ㸪ឤᰁ⑕ࡢ㐺ษ࡞デ᩿ࡀࡑࡢ➨୍Ṍ࡜࡞ࡿࠋᮏㅮ₇࡛ࡣ㸪㤿㰯⫵⅖࢘࢖ࣝࢫ㸪㤿ື⬦⅖࢘࢖ࣝࢫ㸪⣽⳦㸦Streptococcus equi zooepidemicus, Escherichia coli, Klebsiella spp.࡞࡝㸧࠾ࡼࡧ┿⳦㸦Aspergillus spp.
࡞࡝㸧࡟ࡼࡿὶṚ⏘࡟ࡘ࠸࡚ࡑࡢ⑓⌮Ꮫⓗ࣭⑓ཎᏛⓗ≉ᚩ㸪࡞ࡽࡧ࡟⑓⌮デ᩿ୖࡢ࣏࢖ࣥࢺ࡟ࡘ࠸࡚ゐࢀࡓ࠸ࠋࡲࡓ㸪⡿ᅜࢣࣥࢱࢵ࣮࢟ᕞ࡛Ⓨ⏕ࡋࡓὶ⏘㸪ࡪ࡝࠺⭷⅖㸪ᚰ⭷⅖㸪⬻⅖࡞࡝ࢆ୺ッ࡜ࡍࡿ Mare
Reproductive Loss Syndrome㸦eastern tent caterpillars ࢆཎᅉ࡜ࡍࡿ⑌ᝈ㸧࡞࡝ࡢ⑕౛࡟ࡘ࠸࡚ࡶྜࢃࡏ
࡚ㄝ᫂ࡋࡓ࠸ࠋ
࠙Pathology of Foal㸦Ꮚ࣐࢘ࡢ⑓⌮㸧ࠚᏊ࣐࢘ࡢ⑌⑓࡟ࡣ㸪ඛኳᛶ⑌ᝈ㸪ឤᰁᛶ⑌⑓㸦࢘࢖ࣝࢫ㸪⣽⳦㸪┿⳦࠶ࡿ࠸ࡣᐤ⏕⹸ᛶ⑌ᝈ㸧㸪ᰤ㣴ᛶ⑌⑓㸪୰ẘ㸪እയࡑࡋ࡚⭘⒆ࡀ࠶ࡿࠋ⑌⑓ࢆ≉ᐃࡋ㸪ࡑࡢ⑓ᅉࢆ▱ࡿࡇ࡜࡛㸪⮫ᗋ⋇་ᖌࡣࡇࢀࡽ᝟ሗࢆࡶ࡜
࡟⌮᝿ⓗ࡞἞⒪ࡸண㜵ࢆ㑅ᢥࡍࡿࡇ࡜ࡀ࡛ࡁࡿࡼ࠺࡟࡞ࡿࠋᏊ࣐࢘ࡢ⑌⑓ࢆ⛉ྍ⬟࡞㝈ࡾ⤂௓ࡋ㸪ࡑࡢ⑓⌮Ꮫⓗ≉ᚩ࡜⑓⌮デ᩿ࡢ࣏࢖ࣥࢺ࡟ࡘ࠸࡚ゐࢀࡓ࠸ࠋ࠙᭱ᚋ࡟…ࠚ
⑌⑓ࢆṇࡋࡃㄆ㆑ࡋゎ㔘࡛ࡁࡿ⮫ᗋ⋇་ᖌࡣ㸪๗᳨࡟࠾࠸࡚ほᐹࡉࢀࡿ⑓ⓗ࣭㠀⑓ⓗኚ໬ࢆṇࡋࡃ⌮ゎࡋゎ㔘ࡍࡿࡇ࡜ࡶ࡛ࡁࡿࡔࢁ࠺ࠋ⑓ኚࢆṇࡋࡃㄆ㆑ࡍࡿࡇ࡜࡛㸪㐺ษ࡞᳨యࡢ᥇ྲྀࢆ⾜࠺ࡇ࡜ࡀྍ⬟࡜࡞ࡾ㸪㎿㏿࠿ࡘ㐺ษ࡞⑓ཎᏛⓗ᳨ᰝ࡟ࡘ࡞ࡀࡿࠋࡼ࠸⋇་་⒪࡟ࡣ㸪⮫ᗋ⋇་ᖌ࡜⋇་⑓⌮་࡜ࡢ㛫ࡢⰋዲ࡞┦஫స⏝࡜⤯࠼㛫࡞࠸ࢥ࣑ࣗࢽࢣ࣮ࢩࣙࣥࡀ᭱ࡶ㔜せ࡛࠶ࡿࠋ1

Abortion and Perinatal Death in Horses
Fabio Del Piero, DVM, PhD, Dipl. ACVP

Professor of Pathology
Louisiana State University
School of Veterinary Medicine
Department of Pathobiology
andLouisiana Animal Disease Diagnostic Laboratory (LADDL)
Baton Rouge – LA -70803
fdelpiero@lsu.edu

horses.

Numerous and frequent are the etiologic agents able to cause abortion, stillbirth in

EHV-1 causes epidemic abortion, stillbirth, respiratory disease andmyeloencephalopathy with paralysis in Equidae and Camelidae, whereas EHV-4 induces
sporadic abortion and mainly respiratory disease. Considering the value of some foals, it
is clear that both sporadic and epidemic abortions are of great economic importance tothe horse industry. Rapid diagnosis is paramount. Often the mares abort in the last few
months of pregnancy with no particular premonitory signs. The fetus is often contained
within the fetal membranes with the red chorion on the external part. The fetus may show
the following suggestive, but non specific, features and lesions: meconium staining on the
body surfaces, mucosal petechiae, straw color fluid in the serosal cavities, edematous
atelectatic lungs with rib impressions and thymic necrosis. Unfortunately, thepathognomonic macroscopic gray foci representing hepatic necrosis are not always
present. Histologically, if lung, liver and thymus are collected, is always possible toobserve the suggestive multifocal coagulative necrosis associated with the intranuclear
acidophilic pathognomonic viral inclusions. It is also possible to examine frozen sections
and detect lesions shortly after post mortem examination. EHV-1 antigen (EHV-1 Ag)
can be detected in fixed tissues using peroxidase immunohistochemistry, which allows
the simultaneous evaluation of lesions and EHV-1 Ag localization. EHV-1 Ag can also
be abundant in areas where lesions are mild or absent. EHV-1 Ag is intranuclear andintracytoplasmic and can be mainly detected in endothelium, epithelium and monocytemacrophages, but also in myocytes and pericytes. Target organs are mainly lung, liver,
reticular cells of lymphoid tissue and cortices of adrenal gland, but also intestine, kidney,pancreas and fetal membranes. EHV-1 grows well in RK-13 cells where it produces acytopathic effect, generally within 24 hours. EHV-4 is a slow growing herpesvirus, which
replicates in a few days on equine lung cells. Virus identification can also be obtainedwith immunohistochemistry using fluorescent antibodies. Considering the latency ofherpesviruses, PCR techniques may be able to identify the infection, but without thecontemporary evaluation of the presence of the lesions it is not possible to differentiate
between latency, productive infection and disease. Fetal and maternal serology may be of
benefit. However, vaccinated dams may not have a representative humoral immune
response and fetal death can be very rapid, with insignificant fetal serological response,even in immunocompetent fetuses.
Equine arteritis virus is an arterivirus, which is also able to induce respiratory
disease, stillbirth foal mortality and abortion. The aborted fetus can be fresh or2

moderately autolyzed and pathognomonic lesions are not observed. Occasionally there ismild interstitial pneumonia and vasculitis. Although with immunoperoxidase
histochemistry it may be possible to identify EAV Ag in fetuses and the allantochorion,
serological evaluation of the dam and virus isolation are, at the moment, the mostpowerful tools used to diagnose EAV abortion. On the other hand, lesions are highlysuggestive in fatal cases involving adults and foals: interstitial pneumonia, systemic
vasculitis, and, in terminal phases of the disease, tubular necrosis. Getah virus and equine
influenza are also potential causes of abortion. Perhaps a vesivirus is able to cause equine
abortion, but additional studies are needed to verify this.
Other rather common infectious etiologic agents of abortion in horses are bacteria
and fungi. Streptococcus equi var. zooepidemicus induces severe progressive cervicalchorionic necrosis and thickening with neovascularization and allantoic hyperplasia
lesions progress from the cervical area toward the placental body inducing progressive
placental insufficiency. Sometimes this is not followed by fetal septicemia. Similar grossand histologic findings are observed in cases of Aspergillus spp. mitotic placentitis.
Gram-negative bacteria like Escherichia coli, Klebsiella spp and others are often able toinduce fetal septicemia with dissemination of bacterial emboli in various organs.
Leptospira interrogans serogroup pomona, serovar kennewicki and gryppotyphosa havebeen identified as a cause of abortion and neonatal sepsis in horses in Kentucky. In thiscase, placentitis does not ascend from the cervical area, but is most likely hematogenic in
origin. Examination of the placenta may reveal edema and necrosis of the chorion,
enlarged liver and swollen kidneys with pale streaks. Histologically there is placental
thrombosis, vasculitis and villitis with necrosis followed by hepatocellular dissociation,
giant cell hepatopathy, nephritis, pneumonia and myocarditis. It is possible to identify thespiraliform bacteria using Steiner and Whartin Starry silver stains and or
immunoperoxidase histochemistry, which allow to simultaneous evaluation of the lesions
and bacterial antigens. This technique has made the use of fluorescent antibodies to detect
Leptospira in the placenta obsolete, where the specificity of the staining is difficult tointerpret. Higher bacteria may cause equine placentitis and other bacteria have been
identified as sporadic causes of abortions in mares. Neorickettsia risticii, the etiologic
agent of Potomac horse fever induces enteritis, splenitis and hepatitis in the fetus. In
addition to the relatively common Aspergillus, other causes of mycotic abortion include
Mucor spp., Histoplasma capsulatum, Candida spp., whereas Allescheria boydii and
Coccidioides immitis are rare.
Amongst the noninfectious causes of abortion there are umbilical cordabnormalities, which may induce fetal hypoxia and death. Umbilical cord torsion ispredisposed by an abnormal increase of his length. Acute and recurrent chronic torsions
have been observed. The first is associated with severe segmental to diffuse edema andhemorrhage of the cord, whereas the latter may be characterized by urinary bladderdistention, urachal dilatations, chorionic vessel thrombosis and intraluminal
mineralization. Twinning often ends in abortion. Fetal loss appears to be caused by a
combination of factors including inadequate nutrition, interfetal incompatibility andimmunologic reactions. A sharp line of demarcation can readily identify the placentae
from twins where the chorioallantois of the two fetuses comes in contact with each other.
Other non infectious causes of abortion include: early placenta separation, placenta
edema, contracted foal syndrome, congenital anomalies, atrophy of placenta’s villi, body3

pregnancy, fetal diarrhea syndrome. Fescue toxicosis is an important cause of perinatal
death of foals. It is associated with the endophyte Neotyphodium (previously Acremonium
spp.). In these cases placenta membranes are congested and very edematous.
It is proposed that the Mare Reproductive Loss Syndrome observed in Kentucky
USA, which includes early fetal loss, late fetal loss, uveitis, pericarditis, and encephalitis,
is associated to tissue penetration by septic barbed setal fragments (septic penetrating
setae) from Eastern tent caterpillars (Malacosoma americanum). Once ingested, thesebarbed setal fragments migrate through moving tissues, followed by rapid hematogenous
spread of bacteria, bacterial emboli, and/or septic fragments of setae (septic penetrating
setal emboli).
There are others suggested but unproven causes of equine abortion.
The dissection of the aborted fetus and placenta and the following ancillary
procedures including histopathology, immunohistochemistry, virology, bacteriology, andserology will allow us to obtain a rapid diagnosis and to prevent other fetal and neonatal
losses.
Several control measures are required for the management of an epizootic
situation, but of primary importance is the proper diagnosis of the disease involved. Oncethe offending agent is identified, control measure must be implemented. Control
measures include isolation of affected animals, isolation and examination of any newly
introduced animals, maintaining separate implements for sick and healthy animals andseparating farm workers into those working with sick animals and those working withhealthy animals. Depending on the infectious agent, vaccination in the face of an
outbreak may be warranted, particularly in previously unvaccinated animals considered atrisk. Transport of any animals to and from the farm should be prevented during thedisease outbreak and for several weeks after the last affected animals is normal.

4

Pathology of the Foal
Fabio Del Piero, DVM, PhD, Dipl. ACVP

Professor of Pathology
Louisiana State University
School of Veterinary Medicine
Department of Pathobiology
andLouisiana Animal Disease Diagnostic Laboratory (LADDL)
Baton Rouge – LA -70803
fdelpiero@lsu.edu

Several are the pathologic processes affecting foals. The identification of thelesions and knowledge of their pathogenesis will allow the veterinarian to correlate
clinical signs with this information being able to choose ideal treatment and or
prevention. The foal’s pathological conditions can be congenital, infectious (viral,bacterial, mycotic, parasitic), nutritional, toxic, traumatic and, but not frequently,
neoplastic.
Congenital lesions
Congenital pathological conditions include malformations, which can be related
to malpositioning in utero such as tendon contraction with deviation of the limbs anddeformity of facial bones or most likely associated to genetic defects. Cheiloschisis andpalatoschisis are occasionally observed, and may predispose to inhalation of milk withexogenous foreign body pneumonia. Other defects include “parrot mouth” (prognatism),
vertebral malformations and instabilities, which can predispose to stenotic compressive
cervical myelopathy in the yearling, soft palate abnormalities, microopthalmia and otherminor ocular malformations, hydrocephalus. Occasional cardiac anomalies are also
observed. The homozygote Overo foal may present with hypopigmentation andhypogenesis or agenesis of large intestinal intramural ganglia. This is a condition rather
similar to the colon aganglionosis of humans (Hirschprung disease). The Overo foal will
suffer large intestine constipation and bacterial intestinal overgrowth and death due toseptic shock. Arab foals may present with cerebellar abiotrophy with decrease of
cerebellar size because of diminished numbers of cerebellar and neural cells and fibers.
Combined Immunodeficiency (CID) is occasionally observed in the Arab foal. This
inherited condition is characterized by severe atrophy of the lymphoid tissue: thymus andspleen are rather small. The CID foal soon dies because of secondary infections (e.g.
adenovirus systemic infection with bronchopneumonia.
Lesions caused by infectious agentsSome of the infections afflicting foals can originate in utero (viral infections,some bacterial septicemias) or develop during the first period of life. The Equine5Herpesvirus 1 (EHV-1) in utero infected foal is weak and shortly after birth develops asevere bronchointerstitial pneumonia, which leads to hypoxia and respiratory distress.
Other tissues and organs may be affected, but the lung lesions are the most severe and areassociated with a large quantity of virus. The Equine Arteritis Virus (EAV) infected foal
soon develops severe interstitial pneumonia with pneumocyte hypertrophy andhyperplasia and hyaline membranes inducing severe hypoxia. Later vasculitis and renal
tubular necrosis develop. Influenza orthomyxoviruses are also able to induce
bronchointerstitial pneumonia with life threatening secondary bacterial infection, but thiscondition is now rarely fatal in horses, because of vaccination. Bacterial placentitis may
result in the birth of a septicemic foal. This may occur with Streptococcus equi spp.,
Escherichia coli, and Salmonella spp among others. Although Actinobacillus equuli
infection is thought arise from placentitis by some, this author believes that
Actinobacillus equuli infection occurs postpartum and, as demonstrated for othersepticemic agents, is associated with unsuccessful establishing of passive immunity.
Foals with low colostrum IgG may die with Actinobacillus equuli septicemia in thesecond day of life. Lesions associated with Actinobacillus equuli septicemia include
distribution of bacteria in each anatomical system, and within the kidneys multifocal
suppurative glomerulitis and progressive formation of microabscesses occur.
Microabscesses may be also identified within other organs and meningitis can develop.
Multisystemic bacterial distribution, microabscesses and meningitis can also occur withother bacterial infections, particularly with Escherichia coli. Ascending omphalitis,
caused by aerobic and anaerobic bacteria, may also result in hepatic microabscesses andterminal septicemia. Osteomyelitis may be a serious sequela of septicemia. Streptococcus
equi equi is able to cause purpura haemorrhagica in foals as well.
The lung can be affected by several infectious agents, mainly viruses and bacteria.
EHV-1 and EHV-4, and also non velogenic EAV isolates induce upper and lower
respiratory infections in weanlings, generally with no serious consequences, althoughinfection may predispose them to bacterial suppurative cranioventral bronchopneumonia.
EAV isolates similar to the Bucyrus strain are able to induce severe broncho-interstitial
pneumonia, which may be often fatal. If the foal survives the early pneumonic phase,
which characterizes EAV infection, vasculitis and tubular nephritis occur. Between 2 and6 months of age the foal is susceptible to Rhodococcus equi bronchopneumonia, which
can be characterized by necrosis and abscess formation. Rhodococcus equi may be also
cause of septicemia, lymphadenitis and lymphangitis, enteritis, typhlitis, colitis,
polyarthritis. Occasionally the foal is affected by bacterial pleuropneumonia withempyema, resulting from chronic cranioventral suppurative bronchopneumonia withformation of apical areas of necrosis comprised of sequestrum (necrotic tissue) andinvolucrum (perinecrotic fibrous capsule). Leakage of septic necrotic exudates within thepleural cavity leads to formation of empyema. Shipping and other distressing situations
predispose the onset of bronchopneumonia in several species.
Virus and bacteria may induce enteritis and colitis and typhlitis in the foal. Mild
to moderate, generally nonfatal, enteritis can be associated with rotavirus infection.
Escherichia coli, Salmonella spp., Clostridium may all induce severe fatal enteritis andtyphlocolitis. Necrotic cells, blood, fibrin and bacteria are the constituents of themalodorous exudates and dyphteroid membranes, which, with multifocal hepatic
microabscesses, generally characterize intestinal salmonellosis. Clostridia produce

6powerful toxins rapidly inducing coagulative necrosis of the intestinal mucosa. The
intestine will be severely congested, containing reddish material, sometimes with asegmental distribution mimicking the strangulation of an intestinal volvulus.
Dermatitis due to Dermatophilus congolensis (sporothrichosis) may be observedin some foals.
Eastern equine encephalitis alphavirus is able to cause a polioencephalomyelitis
in foals with perivascular lymphocytic cuffs, neuronal necrosis and neuronophagia andneutrophilic infiltrates. So far we did not observed cases of West Nile flavivirus
encephalomyelitis in foals, but in adults only.
Occasionally, multifocal mycotic pneumonias predisposed by leukopenic diseases(e.g. salmonellosis) and candidiasis of the tongue may occur. Antibiotic treatment may
predispose to opportunistic mycotic infections.
Parasites, and in particular the ascarid Parascaris equorum, may be present inlarge numbers within the small intestine of foals which did not received proper treatment
and can cause malnutrition. Ascarids can cause intestinal obstruction. The tapeworm
Anoplocephala perfoliata may be also present and is localized around the ileocecal
orifice. The precocious and frequent antihelminthic treatment dramatically reduced these
infestations. For the same reason, Oxyuris equi infestation is a rare finding now.
Traumatic lesions
Traumatic injuries are not uncommon and lead to limb and vertebral fractures,
skeletal muscle, tendon and ligament injuries, rupture of organs and blood vessels, andcan be rapidly fatal. Rib fractures are particularly common in newborn foals and may
result in fatal hemorrhage secondary to lung or heart lacerations.
Lesions caused by toxic substances and malnutrition
Natural and artificial toxic substances can occasionally produce severe disease infoals. A compound containing iron and probiotics was withdrawn from the market
because it was responsible of multifocal necrosis of the liver. Non steroidal
antiinflammatory drugs (NSAID’s) can cause gastric and duodenal ulcers which may leadto duodenal stenosis, ascending colangiohepatitis and pancreatitis, ascending ulcerativeesophagitis, additional gastric ulceration with possible perforation. Upper intestinal
obstructions may also lead to gastric ruptures. Toxic tubular necrosis due toaminoglycosides and ischemic medullary crest ischemic necrosis caused by NSAIDs are
relatively common iatrogenic nephropathies of foals.Nephropathy caused by these toxic
drugs can be associated with anemia due to decreased renal erythropoietin production andmultisystemic vascular mineralization.
White muscle disease is an enzootic, and sometimes epizootic, myopathy
responsive to administration of vitamin E and selenium. The affected skeletal muscles
may present with mild to prominent whitish chalky changes corresponding to necrotic
and mineralized muscular areas. This condition can be also observed in the fetus if thedam is deficient. Vitamin D toxicity, which can be iatrogenic or associated with theingestion of plants (Cestrun diurnum, Solanum malacoxilon, others) containing Vitamin7

D-like substances is associated with mineralization of vessels and several parenchymousorgans.
Neoplastic lesions
Hepatoblastoma is a hepatic neoplasm, which rarely occurs in foals. It leads tohepatic failure and death. Occcasional, benign, neoplasms of the skin include capillaryhemangiomas and viral papillomas.
There are numerous pathological conditions affecting the foal. The practicing
veterinarian able to recognize and interpret them will be also able to correlate clinicalsigns with the possible lesions and correctly interpret the pathological changes observed
during the field necropsies. Rapid and thorough identification of lesions during a
postmortem examination allows collection of proper specimens for ancillary laboratory
evaluations and consequent prevention of epizootics. A good interaction an constantcommunication between the equine practitioner and pathologist is paramount to achieve
good results.
References are available upon request.

8

Post mortem diagnosis of the 3 fatal forms of Equine herpesvirus 1 and 4 infections in horses.
Fabio Del Piero, DVM, PhD, Dipl. ACVP - Professor
fdelpiero@lsu.edu

INTRODUCTION
Equine herpesvirus 1 (EHV-1) causes acute respiratory disease in foals and yearlings, and is the most importantviral cause of equine abortion. Some EHV-1 isolates also cause encephalomyelopathy, which may precede or accompany
abortion epizootics. The economic impact of EHV-1 can be devastating. Other equine herpesviruses include EHV-2, EHV-3,
EHV-4, and EHV-5. EHV-6-7-8 are asinine viruses. EHV-2 has been associated with conjunctivitis and EHV-5 has beenclearly associated with multinodular fibrosis in horses where intranuclear herpesviral particles and EHV-5 DNA have been
identified in intralveolar macrophages of affected lungs. EHV-3 causes equine coital exanthema, a self-limiting infection
characterized by vesicles and ulcers on the external genitalia of mares and stallions, leaving areas of depigmented epithelium
after 10-15 days. EHV-4 is an important cause of acute respiratory disease in horses and is able to induce sporadic abortion inmares. Whitwell reported that in England, between 1987 and 1993, EHV-4 represented up to 16% of virus abortions. Reports
from Kentucky indicate that this virus causes just the 1% of the viral abortions. Various laboratory techniques are available toidentify EHV-1 and other equine herpesviruses in samples.
LABORATORY TECHNIQUESVirus isolation is generally performed on RK-13 for EHV-1. For its in vitro growth EHV-4 requires equine lungcells. Following identification of the cytopathic effect characterized by ballooning and plaque formation, EHV infected cells
are examined using monoclonal antibodies for further virus characterization.
Polymerase chain reaction (PCR) can be performed following DNA extraction from fresh and fixed tissues.
Primers amplifying a 369bp product from bp numbers 1025 -1393 of the EHV-1 glycoprotein 13 (gp13) gene can be used.
Other primer sets may include three primers that amplify both EHV-1 and EHV-4 simultaneously, with the EHV-1
amplification generating an 188bp band and EHV-4 generating a 677bp band. Here is possible to amplify a sequence fromposition 2699-2886 of the EHV-1 glycoprotein B (gB) gene.
Histology using conventional hematoxylin and eosin stain allows identification of lesions and pathognomonic
intranuclear Cowdry type A viral inclusions.
The identification of EHV-1 antigen in selected tissue sections from aborted fetuses, stillborn foals, young
horses with the fulminant pulmonary vasculotropic form, and adult horses with myeloencephalopathy using specific murine
monoclonal recognizing the EHV-1 envelope glycoprotein C with the indirect immunoperoxidase technique is a very reliable
tool. Polyclonal antibodies recognizing multiple EHV epitopes can be also used. This allows simultaneous identification ofviral antigen within nucleus and cytoplasm of infected cells, fine histological details and lesions. This immunohistochemical
technique is also very appropriate for pathogenetical studies, where precise viral distribution in tissues needs to be assessed.
Serum neutralization can be diagnostic for the respiratory and neurological form, particularly if acute andconvalescent titers are available. The practice frequent vaccination for this disease, and frequent natural exposure, results inmost vaccinated horses having positive titers for the virus.
RESPIRATORY FORM
Respiratory disease due to EHV-1 and EHV-4 infection is common, particularly in young horses. In general,
respiratory disease due to this virus is mild. Horses may experience a short period of fever, lethargy and anorexia. They may
cough and have serous nasal and ocular discharge. In foals, this syndrome is colloquially known as having the ‘snots’ and thenasal discharge may take on a whitish yellow mucoid character. Horses can develop secondary bacterial infections andshould be monitored for this complication. The available vaccines are aimed at preventing or reducing the incidence of thisform of the disease. However, protection is short-lived and horses may need to be re-vaccinated frequently depending on
their management and potential for exposure. Epidemics can occur, particularly in naïve populations and the respiratory formof the disease may preceed abortions or cases of the neurologic form of the disease. Horses with respiratory EHV-1 andEHV-4 infection shed a large amount of virus within the environment, because EHV-1 and 4 can replicate in any part of therespiratory tract, particularly the epithelium, macrophages and endothelial cells. The epithelium of the nasal turbinates is ahighly productive virus factory. Diagnosis is based on demonstration of virus from the blood or nasopharyngeal swab.
Affected neonates have been reported to survive following treatment with the antiviral drug acyclovir at high doses.
Treatment of adults is primarily symptomatic and supportive.
Rarely, non-neurological systemic fatal systemic infection, characterized by severe vasculitis with pulmonary
edema, occurs in equine young adults. This form resembles African Horse Sickness, Equine viral arteritis and shock.

9ABORTION and STILLBIRTH
The large majority of abortions occur in the last third of pregnancy. The increased susceptibility of the latepregnant mare to abortigenic infection can, perhaps, be generally related to anatomical and endocrine changes in the placental
barrier, which may facilitate cotyledonary infarction as pregnancy proceeds. It is also possible that the areas of Arcadian
hematophagic trophoblasts, located at the base of the villi and maturing late in pregnancy, play a role in the passage of thevirus, as observed in equine arterivirus infection. Prostaglandin release may also give a substantial contribution. The
incubation period for EHV-1 abortion is variable and premonitory clinical signs are rare in the mare. A mare that aborts does
not become immune to other EHV-1 infections, but abortions in successive pregnancies are rare. Rapid diagnosis andisolation of the aborting mare are paramount to minimize the spread of the infection. The aborted fetus is generally fresh andenclosed within the fetal membranes. The following pathological changes, suggestive of EHV-1 abortion, may be seen but
fetuses with no gross lesions are often observed: mucosal petechiae, meconium staining, yellowish-orange fluid within the
body cavities, splenomegaly, perirenal edema, pulmonary edema, friable thymus. Pathognomonic changes are gray foci ofhepatic necrosis within the liver, but they are present just in a small percentage of cases. Histological examination allows
identification of coagulative necrosis in liver, lung, thymus, spleen and other lymphoid organs, lung, and small intestine. The
necrotic foci are generally associated with peripheral intranuclear viral eosinophilic inclusions with margination of nuclear
chromatin, which are always identified if the organs mentioned above are examined. If fetal infection occurs close topregnancy term, the infected foal may be born weak and die shortly after because of severe necrotizing bronchointerstitial
pneumonia and multifocal visceral necrosis. Pulmonary lesions are predominant in these foals and the lung should always
carefully examined. In addition to gross examination, followed by histopathology, which always lead to a diagnosis if lung,
liver and thymus are examined, the virus can be detected in multiple tissues with fluorescent antibodies andimmunoperoxidase histochemistry. EHV-1 antigen will be identified in multiple visceral organs, localized withinendothelium, epithelium, macrophages, and myocytes. Although slightly less reliable, virus isolation or application ofpolymerase chain reaction (PCR) using a pooled sample of fetal lung, liver, thymus and spleen can be performed.
Immunoperoxidase histochemistry, virus isolation and PCR are particularly useful when the aborted fetus is not available andonly allantochorion is present. Fetal and maternal serologies are not a reliable diagnostic aid for the diagnosis of EHV-1
abortion. Differential diagnoses include equine viral arteritis, and all the infectious and non-infectious causes of equine
abortion and stillbirth.
ENCEPHALOMYELOPATHY
The neurological syndrome associated with EHV-1 infection affects young horses and adults. It is characterized
by encephalomyelopathy secondary to vasculitis. The virus localizes within endothelium, vascular myocytes and pericytes,
and induces cytopathic effect, perhaps emphasized by the cytotoxic action of the T lymphocytes forming the perivascular
cuffing. Multifocal endothelial necrosis is followed by thrombosis, ischemia and segmental hemorrhagic necrosis of the
spinal cord. These changes induce clinical signs of variable intensity such as ataxia, paraparesis, tetraparesis and urinary
bladder paralysis. The diagnosis in vivo can be achieved with virus isolation from the patient buffy coat and nasopharyngeal
swab in addition to evaluation for seroconversion. Virus isolation attempts from the affected central nervous tissue,
immunohistochemical examination of tissue sections and PCR are not always rewarding: often the distribution of the virus
within the central nervous system is segmental and small quantities of virions are present. Histological examination of tissue
sections for the identification of the highly suggestive lesions is the most reliable technique for post mortem diagnosis of
EHV-1 encephalomyelopathy.
There is debate regarding whether the pathogenesis of the neurologic form of the disease is directly virally
induced or secondary to antigen antibody complex interaction resulting in an Arthus type 3 reaction. It seems clear from
immunohistochemical studies that the pathogenesis is virally mediated. Antigen-antibodies complexes have never been
demonstrated within affected blood vessels and the EHV-1 vasculitis is morphologically different from an Arthus type 3
reaction.
Treatments include intravenous DMSO, corticosteroids, anti-inflammatory agents, fluid support, broadspectrum antimicrobial therapy and good nursing care. Treatment of this form has been attempted using anti-viral drugs. The
efficacy of this treatment remains unclear. The long-term outcome is determined by whether the patient remains on his feet,as recumbent horses are much more likely to die or be euthanized.
This condition may also occur in Southern American Camelidae. Differential diagnoses include rabies,
arboviral protozoal encephalomyelitides, compressive cervical myelopathy, among other ischemic and toxic lesions.
LATENCY
Latency and reactivation are important features of EHV-1 biology, developed as an evolutionary strategy.
Through latency the virus persists in previously infected horses and, following reactivation, may result in nasopharyngeal
shedding and infection of susceptible animals. Latently infected horses do not present with clinical signs of disease during theperiod of latency and are virologically negative until reactivation. Following reactivation, the virus is shed from therespiratory tract, and clinical signs of disease may be present. Latently infected cells may harbor EHV-1 DNA, and infectious
virus can be detected by prolonged cocultivation, which induces in vitro reactivation of latent virus to a productive form. As

10herpes virus infections in other species, reactivation of latent EHV-1 can be triggered by stressful events or corticosteroid
administration. EHV-1 demonstrates tropism for endothelium, epithelium, macrophages, and dendritic-like cells of lymphoidorgans during the productive infection, but neurons have not been identified containing the virus during productive infection
in any form of disease in horses. This is a substantial difference from other neuronotropic herpesviruses such as porcine
herpesvirus, and bovine herpesvirus 1 and 5. The circulating monocyte is, in this authors opinion, the most important cell fortransport of the virus during viremia and it may also transport EHV-1 to latency sites, although other studies tend to attribute
this role mainly to CD8+ T lymphocytes with some involvement of CD4+ T lymphocytes. EHV-1could potentially become
latent in all these cell types. The majority of the studies attempting to identify the cell type(s) necessary for the latency do not
involve visualization of viral DNA in tissues but rely on DNA extraction from tissues and PCR detection. Latency associatedtranscripts of EHV-1 in ganglionic neurons using in situ hybridization is illustrated in one study. Still other cell types may be
involved in EHV-1 latency and may be more involved than gangliar neurons.
PREVENTION
Prevention of EHV-1 infection is difficult, as the virus is ubiquitous. Strategies for decreasing morbidity andmortality include isolation of new animals from the main herd for a period of 2 to 4 weeks, avoiding exposure of pregnant
mares to young animals or new animals, and rigid vaccination schedules. No vaccine is labeled as preventative for theneurologic form of EHV-1 infection. Vaccination of pregnant mares at 5, 7 and 9 months of gestation has been show to beprotective against the abortigenic form, although EHV-1 abortions have been documented in well-vaccinated mares.
CONCLUSION
It appears that EHV-1 is forever. Latency in the host will always be the secret weapon of this virus. However,preventative measures have dramatically decreased the frequency of abortion storms attributed to this virus and the incidenceof epidemics of respiratory disease. Both the neurologic and neonatal forms of the disease remain sporadic. As treatment
modalities for viral infections emerge more specific treatments may emerge with improved survival from the more severe
forms of disease.
References are available upon request

11

2014 ᖺᗘ௨㝆ࡢ᪥㧗⟶ෆ࡟࠾ࡅࡿ㤿␗ᖖ⏘࡟ࡘ࠸࡚㹼⑓⌮Ꮫⓗᡤぢ㹼‫ ۑ‬బ⸨㝧㍜᪥㧗ᐙ␆ಖ೺⾨⏕ᡤ࠙⫼ᬒ࡜┠ⓗࠚ㤿ࡢ␗ᖖ⏘㸦ὶ⏘ཬࡧ⏕ᚋ┤Ṛ㸧ࡣ⏕⏘∾ሙࡢ⤒ႠࡸᏳᐃⓗ࡞㍍✀㤿౪⤥࡟኱ࡁ࡞ᦆኻ࡜࡞ࡿࠋឤᰁᛶࡢ
␗ᖖ⏘࡛࠶ࡗࡓሙྜࠊⓗ☜࡞デ᩿ࡸ㜵␿ᑐ⟇ࡀ⾜ࢃࢀ࡞ࡅࢀࡤࠊ∾ሙෆ࡛ࡢ⥅⥆Ⓨ⏕ࡸ௚∾ሙ࡬ࡢឤᰁᣑ኱
࡟ࡘ࡞ࡀࡿࡓࡵࠊ⟶ෆ࡛ࡣᆅᇦ࡜ࡋ࡚␗ᖖ⏘ࡢཎᅉ✲᫂࡜ᑐ⟇࡟ྲྀࡾ⤌ࢇ࡛࠸ࡿࠋᙜᡤ࡛ࡣ㤿␗ᖖ⏘ࡢ⑓ᛶ㚷ᐃࢆᖺ㛫⣙250௳ᐇ᪋ࡋࠊ10ᖺࢆ┠ฎ࡟ᡂ⦼ࢆྲྀࡾࡲ࡜ࡵ࡚ࡁࡓࠋ௒ᅇࠊ2014ᖺᗘ௨㝆ࡢ᪥㧗⟶ෆ࡟࠾ࡅࡿ␗ᖖ⏘ࡢ⑓ᛶ㚷ᐃᡂ⦼࡟ࡘ࠸࡚㞟ィ᳨࣭ウࡋࡓࡢ࡛ࠊ⑓⌮Ꮫⓗᡤぢࢆ஺࠼࡚⤂௓ࡍࡿࠋ࠙ᮦᩱ࡜᪉ἲࠚ
 2014 ᖺᗘ௨㝆࡟ᙜᡤ࡛⑓ᛶ㚷ᐃࢆᐇ᪋ࡋࡓࠊὶ⏘ 1,798 ᳨యࠊ⏕ᚋ┤Ṛ 485 ᳨యࠊィ 2,283 ᳨యࡢ㤿␗ᖖ⏘ࢆᮦᩱ࡜ࡋࡓࠋ๗᳨ᚋࠊ㤿㰯⫵⅖ࡢ㑇ఏᏊ᳨ᰝཬࡧ⣽⳦ᇵ㣴ࢆᐇ᪋ࡋࠊᚲせ࡟ᛂࡌ࡚┿⳦ᇵ㣴ࡸ⑓⌮⤌⧊Ꮫⓗ᳨ᰝ➼ࢆᐇ᪋ࡋࡓࠋ
࠙␗ᖖ⏘ཎᅉࡢෆヂࠚὶ⏘ཎᅉࡣࠊឤᰁᛶࡀ 15.1%(272/1,798)ࠊ㠀ឤᰁᛶࡀ 35.9%(646/1,798)ࠊཎᅉ୙᫂ࡀ 48.9%(880/1,798)࡛
࠶ ࡗ ࡓ ࠋ ឤ ᰁ ᛶ ࡢ ࠺ ࡕ ࠊ ࢘ ࢖ ࣝ ࢫ ᛶ ࡀ 61.4%(167/272) ࡛ ࠶ ࡾ ࠊ ඲ ࡚ 㤿 㰯 ⫵ ⅖ ࡛ ࠶ ࡗ ࡓ ࠋ ⣽ ⳦ ᛶ ࡣ
32.0%(87/272)࡛࠶ࡾࠊStreptococcus equi subsp. zooepidemicus ࡀ᭱ࡶከࡃศ㞳ࡉࢀࡓ(26/87)ࠋ┿⳦ᛶࡣ
6.6%(18/272)࡛࠶ࡾࠊAspergillus ᒓࡀ᭱ࡶከࡃศ㞳ࡉࢀࡓ(11/18)ࠋ⣽⳦ᛶཬࡧ┿⳦ᛶ࡛ࡣ⫾┙⅖ࡀከࡃࡳࡽࢀࡓࠋ㠀ឤᰁᛶ࡛ࡣ⮖ᖏ᤬㌿➼ࡢ⮖ᖏ␗ᖖࡀ᭱ࡶከࡃࠊ89.0%(575/646)ࢆ༨ࡵࡓࠋ⏕ᚋ┤Ṛཎᅉࡣࠊឤᰁ
ᛶࡀ 18.4%(89/485)ࠊ㠀ឤᰁᛶࡀ 13.8%(67/485)ࠊཎᅉ୙᫂ࡀ 67.8%(329/485)࡛࠶ࡗࡓࠋឤᰁᛶࡢ࠺ࡕࠊ࢘
࢖ࣝࢫᛶࡀ 36.0%(32/89)࡛࠶ࡾࠊ඲࡚㤿㰯⫵⅖࡛࠶ࡗࡓࠋ⣽⳦ᛶࡣ 61.8%(55/89)࡛࠶ࡾࠊ Actinobacillus

equuli (A. equuli) ࡀ᭱ࡶከࡃศ㞳ࡉࢀࡓ(42/55)ࠋ┿⳦ᛶࡣ 2.2%(2/89)࡛࠶ࡗࡓࠋ㠀ឤᰁᛶࡣከ⫾ࡸወᙧࠊ⭘⒆➼࡛࠶ࡗࡓࠋ
࠙୺࡞⑕౛ࡢ⑓⌮Ꮫⓗᡤぢࠚ㤿㰯⫵⅖࡜デ᩿ࡉࢀࡓ⑕౛࡛ࡣࠊ๗᳨᫬࡟ῐ㯤Ⰽ⬚Ỉࡢቑ㔞ࠊ⫵ࡢỈ⭘ࡸ◳⤖ឤࠊ⫢⮚ࡢᚤᑠⓑᩬࠊ⭁⮚ࡢℐ⬊᫂░ࡀࡳࡽࢀࡓࠋ⤌⧊᳨ᰝ࡛ࡣࠊ⫵ࠊ⫢⮚ࠊ⭁⮚ཬࡧ๪⭈➼࡟ቯṚᕢࡀከⓎᛶ࡟ࡳࡽࢀࠊ᰾ෆᑒධయ
ࡀẼ⟶ᨭࡸ⫵⬊ࡢୖ⓶⣽⬊ࠊ⫢⣽⬊ཬࡧ⣽⥙⣽⬊➼࡟ࡳࡽࢀࡓࠋ⣽⳦ᛶཬࡧ┿⳦ᛶ⫾┙⅖ࡣࠊᏊᐑ㢕⟶ࢆ௓ࡋ࡚ࡢୖ⾜ឤᰁࡀ୍⯡ⓗ࡛࠶ࡿࡓࡵࠊ◚⭷㒊࡟⑓ኚࡀࡳࡽࢀࡿࡇ࡜ࡀከࡃࠊⁱฟ≀ࡢ௜╔ࡸ⫾┙ࡢ⫧ཌ➼ࡀࡳࡽࢀࡓࠋ⤌⧊᳨ᰝ࡛ࡣ⤧ẟ⭷ࡢቯṚࡸ⅖⑕⣽⬊ᾐ₶ࠊ⳦యࡀࡳࡽࢀࠊ⮖ᖏࡸ⫵ࠊ⓶⭵➼࡟⑓ኚࡀࡳࡽࢀࡿ
ࡇ࡜ࡶ࠶ࡗࡓࠋA. equuli ࡣ๗᳨᫬࡟⭈⮚࡟ᚤᑠⓑᩬࡀࡳࡽࢀࡿࡇ࡜ࡀከࡃࠊ᫬࡟⫵࡟ᬯ㉥Ⰽ◳⤖㒊ࡸ⫢⮚࡟ᚤᑠⓑᩬࡀࡳࡽࢀࡓࠋ⤌⧊᳨ᰝ࡛ࡣ⫗║⑓ኚ࡟୍⮴ࡋ࡚ࠊᚤᑠ⮋⒆ࡸቯṚᕢࠊ⅖⑕⣽⬊ᾐ₶ࡸ⣽⳦ሢࡀࡳࡽࢀࡓࠋ⮖ᖏ᤬㌿ࡣ㐣㛗⮖ᖏࡢ㝿࡟ዲⓎࡋࠊ⾑ᵝ⭡Ỉࡢ㈓␃ࡸ⮚ჾࡢ⼥ゎ➼ࠊᚠ⎔㞀ᐖࡢᡤぢࡀࡳࡽࢀࡓࠋ
12࿘⏘ᮇ࠾ࡼࡧ௘㤿ࡢ⫵⑓⌮‫ ۑ‬ᯇ⏣୍ဢ㓗㎰Ꮫᅬ኱Ꮫ ⋇་Ꮫ⩌ ⋇་Ꮫ㢮 ⋇་⑓⌮Ꮫࣘࢽࢵࢺ࠙┠ⓗࠚ⫵ࡣฟ⏕࡟కࡗ࡚ࡑࡢᶵ⬟ࡀ኱ࡁࡃኚ໬ࡍࡿ⮚ჾ࡛࠶ࡾࠊฟ⏕ᚋࡣ⏕࿨⥔ᣢ࡟┤⤖ࡍࡿ㠀ᖖ࡟㔜せ࡞⮚ჾ࡛࠶ࡿࠋ⫵ࡢ⫾ඣᮇࡢჾᐁᙧᡂࡣ⬇ᮇࠊ⭢ᵝᮇࠊ⟶≧ᮇࠊ⤊ᮎᄞᮇࠊ⫵⬊ᮇࡢ㡰࡟㐍⾜ࡍࡿࠋ⫾ඣࡢ⫵ࡣ㛫㉁࡛⏘⏕ࡉࢀࡿ⫵ᾮ࡛‶ࡓࡉࢀ࡚࠾ࡾࠊฟ⏕᫬ࡢ྾Ẽ࡜࡜ࡶ࡟㛫㉁㸦⾑⟶࣭ࣜࣥࣃ⟶㸧࡬྾཰ࡉࢀࡿࠋࡲࡓࠊ
⫵⬊ࡢᣑᙇ࡟ࡣࢡࣛࣛ⣽⬊ࠊϩᆺ⫵⬊ୖ⓶⣽⬊࠿ࡽ⏘⏕ࡉࢀࡿ⫵ࢧ࣮ࣇ࢓ࢡࢱࣥࢺ࡟ࡼࡿ⏺㠃άᛶస⏝㸦⾲㠃ᙇຊపୗస⏝㸧ࡀ୙ྍḞ࡛࠶ࡿࠋ᪂⏕ඣ㸦࠾ࡼࡧ᪂⏕௘㤿㸧ࡢ࿧྾㞀ᐖࡢཎᅉ࡜ࡋ࡚ࡣࠊ⫵⤌⧊ࡢⓎ⫱୙඲ࠊ⫵ᾮ྾཰㐜ᘏࠊ⫵ࢧ࣮ࣇ࢓ࢡࢱࣥࢺࡢ୙㊊࣭␗ᖖࠊప㓟⣲⑕࣭❅ᜥࠊ࢘࢖ࣝࢫ࣭⣽⳦ឤᰁࠊ⬚㒊࣭ୖ㒊Ẽ㐨ࡢඛኳ␗ᖖࡀᣲࡆࡽࢀࡿࠋᮏ◊✲࡛ࡣࠊ㤿࡟࠾ࡅࡿ࿘⏘ᮇ࡞ࡽࡧ࡟௘㤿ࡢ⫵⑓ኚ࡬ࡢ⌮ゎࢆ῝ࡵࡿࡓࡵࠊ
⮬㦂౛࡟㛵ࡋ࡚௨ୗࡢ᳨⣴ࢆᐇ᪋ࡋࡓࠋ
࠙ᮦᩱ࡜᪉ἲࠚ
ᙜ◊✲ᐊ୍࡛ᐃᮇ㛫࡟⑓⌮᳨ᰝࢆᐇ᪋ࡋࡓࢧࣛࣈࣞࢵࢻ✀㤿ࡢὶ⏘⫾௘ 16 ౛ࠊṚ⏘⫾௘ 18 ౛㸦㞴⏘࡟ࡼࡿ⏘㐨Ṛ㸧ࠊ᪂⏕௘Ṛ 8 ౛㸦㹼3 ᪥㱋ࠊᏳᴦṚ 2 ౛ྵࡴ㸧ࠊ⫵⅖⨯ᝈ௘㤿 10 ౛㸦㹼5 ࠿᭶㱋㸧ࡢྜィ 52౛࡟ࡘ࠸࡚ࠊ⫵ࡢ⤌⧊Ꮫⓗኚ໬࡟╔┠ࡋࡓ⑓ែࡢホ౯᳨࣭ウࢆᐇ᪋ࡋࡓࠋ
࠙⤖ᯝ࡜⪃ᐹࠚ
ὶ⏘⫾௘ࡢ⫵࡛ࡣ⭢ᵝᮇ࠿ࡽ⫵⬊ᮇ࡟࠿ࡅ࡚ࡢ⤌⧊ᵓ㐀ࡀ☜ㄆࡉࢀࠊ␗ᖖᡤぢࡣㄆࡵࡽࢀ࡞࠿ࡗࡓࠋ⫾┙࣭⮖ᖏࡢ␗ᖖࡀ 6/16 ౛࡛ㄆࡵࡽࢀࡓࠋṚ⏘⫾௘࡛ࡣ኱㒊ศ㸦15/18㸧ࡢ⑕౛ࡢ⣽Ẽ⟶ᨭ࠿ࡽ⫵⬊ෆ⭍࡟⫾౽ࠊゅ㉁࣭ẟࠊዲ㓟ᛶ₢ᾮࡢᏑᅾࢆㄆࡵࡓ㸦㔞ࡣ⑕౛࡟ࡼࡾᵝࠎ㸧ࠋ࠸ࡎࢀࡶ⅖⑕⣽⬊཯ᛂࡸ㈎㣗཯ᛂࢆḞ࠸࡚࠾ࡾࠊ㞴⏘࡟క࠺⫵࡬ࡢ⨺Ỉ྾ᘬࡲࡓࡣὶධ࡜⪃࠼ࡽࢀࡓࠋࡇࡢ௚࡟⫵࡟␗ᖖᡤぢࡣㄆࡵࡽࢀ࡞࠿ࡗࡓࠋ
᪂⏕௘Ṛ࡛ࡣࠊฟ⏕ᚋᩘ᫬㛫௨ୖ⤒㐣ࡋࡓ 6 ⑕౛࡟࠾࠸࡚ࠊ◪Ꮚ⭷ᙧᡂࢆక࠺ࡧࡲࢇᛶ⫵⬊യᐖ 2 ౛ࠊ⫾౽྾ᘬᛶ⫵⅖ 1 ౛ࠊㄗᄟᛶ㸭⣽⳦ᛶ⫵⅖ 3 ౛ࢆㄆࡵࡓࠋࡇࢀࡽࡢ⫵⑓ኚࡣ⫵ࢧ࣮ࣇ࢓ࢡࢱࣥࢺ㞀ᐖ㸦⨺Ỉ྾ᘬᡤぢࢆḞࡁࠊ⫵⬊യᐖ࣭◪Ꮚ⭷ᙧᡂࢆㄆࡵࡿ㸧࡞ࡽࡧ࡟⫾౽ࡸ⣽⳦ࢆྵࡴ⨺Ỉ྾ᘬ࡟㉳ᅉࡍࡿ࡜⪃࠼ࡽࢀࠊ᪂⏕௘Ṛࡢཎᅉ࡜ࡋ࡚㔜せ࡞⑓ែ࡛࠶ࡿࡇ࡜ࡀ☜ㄆࡉࢀࡓࠋ⫵⅖⨯ᝈ௘㤿࡛ࡣ 10 ౛୰ 8 ౛࡟ࣟࢻࢥࢵ࢝ࢫ
⑕ࢆ␲࠺໬⮋ᛶ⫗ⱆ⭘ᛶ⫵⅖ࠊ2 ౛࡟ࡧࡲࢇᛶࡢ㛫㉁ᛶ⫵⅖㸦ෆ 1 ౛࡛ࡣ㝈ᒁᛶ໬⮋ᛶ⫗ⱆ⭘ᛶ⫵⅖ࢆక࠺㸧ࢆㄆࡵࡓࠋ௒ᅇࡢ⤖ᯝ࠿ࡽࠊ≉࡟᪂⏕௘ṚࡢṚᅉ࣭⑓ែホ౯࡟࠾࠸࡚ࠊ⫵ࡢ᳨ᰝࡀ㔜せ࡛࠶ࡿࡇ࡜ࡀ☜ㄆࡉࢀࡓࠋ௒ᚋࠊ⑕౛ᩘࡢ⵳✚࡜ࠊ⮫ᗋ⤒㐣࣭἞⒪Ṕ➼࡜ࡢ㛵㐃ᛶࢆྵࡵࡓゎᯒࡀ㤿ࡢ࿘⏘ᮇ࠾ࡼࡧ௘㤿ࡢ
⫵⅖ࡢ⑓ែᢕᥱ࡟᭷⏝࡜⪃࠼ࡽࢀࡓࠋ

13ᙜṓ㤿ࡢᛴᛶ㛫㉁ᛶ⫵⅖㸸㉸㡢ἼࠊX ⥺⏬ീ࡜⑓⌮ᡤぢࡢᑐẚࠐ Ỉཱྀᝆஓ 1 బ⸨ṇே 1 ᐑ㉺኱㍜ 1 ᾏ㐨☻㔛 1 ᵽཱྀᚭ 1 㒔⠏┤ 2
1NOSAI ໭ᾏ㐨᪥㧗ᨭᡤ ᐙ␆㧗ᗘ་⒪ࢭࣥࢱ࣮ 2 㓗㎰Ꮫᅬ኱Ꮫ⮫ᗋ⑓⌮࠙ࡣࡌࡵ࡟ࠚ
ᙜṓ㤿ࡢᛴᛶ㛫㉁ᛶ⫵⅖㸦AIP㸧ࡣᛴᛶ࠿ࡘ๻⑕ᆺࡢ⫵⅖ࢆ࿊ࡋࠊึᮇ἞⒪ࡢ㐜ࢀࡣቯ⁛ⓗ࡞㌿ᖐ࡟࠸ࡓࡿࠋ⏕⏘ᆅ࡟࠾ࡅࡿ AIP ࡢⓎ⏕ࡣᩓⓎⓗ࡛࠶ࡿ࡜ᛮࢃࢀࡿࡀࠊᐇែࡣ༑ศ࡟ᢕᥱࡉࢀ࡚࠾ࡽࡎࠊ⏕๓デ᩿࠾ࡼࡧ㐺ษ࡞἞⒪ࡀ࡞ࡉࢀ࡚࠸࡞࠸ࢣ࣮ࢫࡶᩓぢࡉࢀࡿࠋᮏⓎ⾲࡛ࡣࠊᐇ㝿ࡢ AIP Ⓨ⑕౛࡟࠾ࡅࡿ⏬ീデ᩿ᡤぢ࡜⑓⌮ᡤぢࡢᑐẚࢆ⾜࠺ࡇ࡜࡛ࠊAIP ࡬ࡢ⌮ゎ࡜ㄆ㆑ࢆ῝ࡵࡿࡇ࡜ࢆ┠ⓗ࡜ࡋࡓࠋ
࠙⑕౛ࠚ
2015-2022 ᖺࠊ⮫ᗋ᳨ᰝ࠾ࡼࡧ⫵㉸㡢Ἴ᳨ᰝ㸦LUE㸧࡟ࡼࡾᙜṓ㤿 17 ౛㸦7-97 ᪥㱋㸹୰ኸ್ 50ࠊᅄศ఩⠊ᅖ 46-57㸧ࢆ AIP ࡜デ᩿ࡋࡓࠋ5 ౛ࡣ἞⒵࣭⏕Ꮡࠊ12 ౛ࡣ἞⒪ࡢ⏥ᩫ࡞ࡃṚஸࡋࡓࠋ
࠙㉸㡢ἼࠊX ⥺᳨ᰝࠚⓎ⑕᫬ࠊLUE ࡛ࡣᗈ⠊ᅖ࡟ྵẼ㔞ῶᑡ㸦B-line ࡢከⓎ࣭⼥ྜ㸧ࢆㄆࡵࡓࠋ἞⒪࡟ࡼࡾ୍ᐃࡢྵẼ㔞ᨵၿࡀㄆࡵࡽࢀࡓࡀࠊ⑓ែࡢ៏ᛶ໬࡟క࠸㠀ྵẼ㡿ᇦ㸦consolidation㸧ࡢᒁᅾ໬ࡀほᐹࡉࢀࡓࠋഃ᪉ X ⥺᳨ᰝ㸦LR㸧
࡛ࡣึᮇ࡟ X ⥺୙㏱㐣ᛶஹ㐍㸦㛫㉁ࣃࢱ࣮ࣥ㸧ࢆㄆࡵࡓࡀࠊ⑓ໃᝏ໬࡟క࠸⫵⬊ࣃࢱ࣮ࣥࡢΰᅾࠊ⤖⠇⑓ኚࡢฟ⌧ࢆㄆࡵࡓࠋ
࠙⑓⌮ゎ๗࣭⤌⧊ᡤぢࠚ⑓⌮ゎ๗᫬ࡢ୺⑓ኚࡣ⫵ࡢ㏥⦰୙඲࠾ࡼࡧ◳⤖໬࡛࠶ࡾࠊከࡃࡢ⑕౛࡛ࡣ Rhodococcus equi ࡀ㛵㐃ࡋࡓ⮚ഃ⬚⭷ୗ࡟⮳ࡿᕧ኱⮋⒆ᙧᡂࡲࡓࡣᏙᅾᛶ⮋⒆ࡢᩓᅾࢆㄆࡵࡓࠋ⑓⌮⤌⧊Ꮫⓗ᳨ᰝ࡟࠾࠸࡚ࡣ⤊ᮎ࣭࿧྾⣽Ẽ⟶ᨭ࡟࠿ࡅ࡚⣽ⴥ㛫⤖ྜ⤌⧊ࡢỈ⭘ᛶ⫧ཌ࠾ࡼࡧ⅖⑕⣽⬊ᾐ₶ࢆㄆࡵࠊ⫵⬊⭍ෆ࡬ࡢዲ୰⌫ࢆ୺࡜ࡋ
ࡓ⅖⑕⣽⬊ᾐ₶ࠊ⫵⬊ቨ◚⥢ࠊϩᆺ⫵⬊ୖ⓶໬⏕ࠊ◪Ꮚ⭷ᙧᡂ࡞࡝ࠊỗ⫵⬊㞀ᐖࢆ♧၀ࡍࡿᡤぢࢆㄆࡵࡓࠋ࠙⪃ᐹࠚ
LUE ࡛ࡣ⮚ഃ⬚⭷ୗ⫵⬊ࡲࡓࡣ㛫㉁࡟⏕ࡌࡓᚤᑠ⑓ኚ࡟ࡼࡾࠊᮏ᮶ࡣ୍ᵝ࡟ྵẼࡍ࡭ࡁ⫵⤌⧊࡟㡢㡪࢖ࣥࣆ࣮ࢲࣥࢫࡢኚ໬ࡀ⏕ࡌࠊB-line ࡜ࡋ࡚ㄆ㆑ࡉࢀࡿࠋ⑓ኚࡢ⛬ᗘ࡟ᛂࡌ࡚ྵẼ㔞ࡣῶᑡࡋࠊB-line ࡢⓎฟ㛫㝸⊃ᑠ໬ࠊ⼥ྜࠊconsolidation ࡬࡜ᡤぢࡀ㐍⾜ࡍࡿࠋ୍᪉ࠊLR ࡛ࡣ⫵Ỉศ㔞ቑຍ࡟క࠸ X ⥺୙㏱㐣ᛶࡀஹ㐍ࡍࡿࠋ⑓⌮⤌⧊Ꮫⓗ࡟ AIP ࡣỗ⫵⬊㞀ᐖࢆ≉ᚩ࡜ࡍࡿࡀࠊ୍⯡ⓗ࡟ࡣ 3 ࣇ࢙࣮ࢬ㸦ⁱฟᮇ࣭ቑṪᮇ࣭⥺⥔໬ᮇ㸧࡛㐍⾜ࡋࠊ㛫㉁⑓ኚࡀ⫵⬊⑓ኚ࡟ඛ⾜ࡍࡿࠋࡋࡓࡀࡗ࡚ࡇࢀࡽ୍㐃ࡢኚ໬ࡣ LUE/LR ࡟࠾࠸࡚ࡑࢀࡒࢀ B-line Ⓨฟ࣭⼥ྜ㛫㉁ࣃࢱ࣮ࣥࠊࡑࡋ࡚ consolidation⫵⬊ࣃࢱ࣮࣭ࣥ⤖⠇⑓ኚࡢฟ⌧࡬࡜₞ḟ㐍⾜ࡍࡿ࡜⪃࠼ࡽࢀࡿࠋ௒ᅇࡢ⮫ᗋ౛࡟࠾࠸࡚ࡣ㉸㡢ἼࠊX ⥺⏬ീ࠿ࡽ᝿ᐃࡉࢀࡿ⑓ែ࡜ᐇ㝿ࡢ⑓⌮᳨ᰝᡤぢ࡟୍⮴ࡀぢࡽࢀࡓࡇ࡜࠿ࡽࠊAIP Ⓨ⑕㤿࡟࠾ࡅࡿ LUE/LR ࡣ⫵⑓ኚࡢ㐣⛬ࢆ༑ศ࡟ᤊ࠼࡚࠸ࡿ࡜⪃࠼ࡿࠋࡋ࠿ࡋࠊLUE/LR ࡑࢀࡒࢀࡢ฼Ⅼ࣭ḞⅬࢆ⪃៖ࡍࡿ࡜ఱࢀࡶ༢⊂࡛ࡣ༑ศ࡞᳨ᰝ࡛ࡣ࡞࠸࡜⪃࠼ࡿࡀࠊ┦⿵ⓗ࡟ᐇ᪋ࡍࡿࡇ࡜࡛࣐ࢡࣟ࡜࣑ࢡࣟ┦஫࠿ࡽ⑓ែࢆ㢮᥎ࡍࡿࡇ࡜ࡀྍ⬟࡛࠶ࡿ࡜⪃࠼ࡿࠋ14࣐࢘ࡢ⭠⅖‫ ۑ‬㉺ᬛ❶ோ㸪ᓊ኱㈗㸪ୖ㔝Ꮥ⠊᪥ᮏ୰ኸ➇㤿఍ ➇㉮㤿⥲ྜ◊✲ᡤ ᚤ⏕≀◊✲ᐊ࣐࢘࡟࠾࠸࡚㸪⭠⅖ࡣ㔜せ࡞⑌⑓ࡢ୍ࡘ࡛࠶ࡿࠋ⭠⅖ࡣ㸪ឤᰁᛶ࠾ࡼࡧ㠀ឤᰁᛶ࡟኱ูࡉࢀࡿࠋࡑࡢཎᅉ
ࡣከ✀ከᵝ࡛࠶ࡿࡀ㸪ཎᅉࡀ≉ᐃ࡛ࡁ࡞࠸஦ࡶከࡃ㸪ࡑࢀࡽࡣ X ኱⭠⅖࡜ࡋ࡚ᢅࢃࢀ࡚ࡁࡓࠋࡋ࠿ࡋ㸪᳨ᰝ࣭デ᩿ᢏ⾡ࡢྥୖ࡞࡝࡟ࡼࡗ࡚ཎᅉࡀ☜ᐃࡍࡿ⑕౛ࡶቑ࠼࡚࠸ࡿࠋᮏ₇㢟࡛ࡣ㸪㤿ࡢ⭠⅖ࡢ୺࡞ཎᅉ
㸦Salmonella spp.㸪Clostridioides difficile㸪Clostridium perfringens㸪Lawsonia intracellularis㸪

Rhodococcus equi㸪ࣟࢱ࢘࢖ࣝࢫ㸪ࢥࣟࢼ࢘࢖ࣝࢫࡸ NSAIDs ࡞࡝㸧࡟ࡘ࠸࡚⑓⌮Ꮫⓗ࡞ࡽࡧ࡟⑓ཎᏛⓗ≉ᚩ࡞࡝࡟ࡘ࠸࡚㏙࡭ࡓ࠸ࠋ

15

᪥ᮏ୰ኸ➇㤿఍࡟࠾ࡅࡿ᪂ࡓ࡞⸆≀つไไᗘ࡟ࡘ࠸࡚
‫▼ ۑ‬ᕝ ⿱༤᪥ᮏ୰ኸ➇㤿఍ 㤿஦㒊 ࢔ࣥࢳࢻ࣮ࣆࣥࢢㄢ

࠙ࡣࡌࡵ࡟ࠚ
㏆ᖺࠊ➇㉮㤿⌮໬Ꮫ◊✲ᡤࡀᅜ㝿ࣜࣇ࢓ࣞࣥࢫࣛ࣎㸦ᅜ㝿ㄆドࢆཷࡅࡓ᳨ᰝᶵ㛵㸧ᣦᐃࢆཷࡅࡓࡇ࡜࡛ࠊ
㧗ᗘ࡞᳨ᰝฎ⌮⬟ຊࢆഛ࠼ࡓ᳨ᰝᶵ㛵ࡀᅜෆ࡟ᩚഛࡉࢀࠊᅜ㝿ᶆ‽࡜࡞ࡿ᪂ࡓ࡞⸆≀᳨ᰝయไࢆ㛤ጞࡍࡿ‽ഛࡀᩚࡗࡓࠋᮏㅮ₇࡛ࡣࠊࡇࡢ᳨ᰝయไࢆᇶ┙࡜ࡋ࡚᪂ࡓ࡟ᑟධࡉࢀࡿ⸆≀つไไᗘࡢᴫせࢆ⤂௓ࡍࡿࠋ࠙ᴫせࠚ⚗Ṇ⸆≀㸦⌧⾜ 114 ⸆≀㸧࠾ࡼࡧつไ⸆≀㸦⌧⾜ 85 ⸆≀㸧ࢆ㏣ຍࡋࠊࡑࢀࡒࢀ 351 ⸆≀ࠊ230 ⸆≀࡜ࡍࡿ᪥ᮏ୰ኸ➇㤿఍➇㤿᪋⾜つ⣙➼ࡢㅖつᐃࡢᨵṇࢆ⾜ࡗࡓ㸦2023 ᖺ 1 ᭶ 1 ᪥බᕸࠊ2024 ᖺ 4 ᭶ 1 ᪥᪋⾜㸧ࠋㅮ₇࡛ࡣࠊලయⓗ࡞⸆≀ྡ࡞ࡽࡧ࡟⸆ຠࢆᴫㄝࡍࡿࠋㅖつᐃࡀ᪋⾜࡜࡞ࡿࡲ࡛ࡢ㛫㸦࿘▱ᮇ㛫㸧࡟ࡘ࠸࡚ࡣࠊ
㏣ຍࡉࢀࡿ⸆≀ࡀ➇㤿᳨య࠿ࡽ᳨ฟࡉࢀࡓ࡜ࡋ࡚ࡶ⨩๎➼ࡢ㐺⏝ࡣకࢃ࡞࠸ࠋ୍᪉࡛࿘▱ᮇ㛫୰ࡢ᳨ฟࡸ౑
⏝≧ἣࡢ☜ㄆ࡞࡝ࠊヲ⣽࡞ཎᅉㄪᰝࢆ⾜࠺ࡇ࡜࡛ࠊ࿘▱ᮇ㛫⤊஢ᚋࡢ⸆≀㝧ᛶ஦᱌ࡢ㜵Ṇᑐ⟇ࢆ᳨ウࡍࡿࠋḟ࡟ࠊ⸆≀ࡢྲྀ⥾ࡾࡢ୍⎔࡜ࡋ࡚ࠊつไ⸆≀ࡀ౑⏝ࡉࢀࡓሙྜ࡟㤿ࢆฟ㉮ࡉࡏࡿࡇ࡜ࡀ㐺ษ࡛࡞࠸࡜ㄆࡵ
ࡽࢀࡿᮇ㛫࡜ࡋ࡚ฟ㉮ࢆไ㝈ࡍࡿᮇ㛫㸦ฟ㉮ไ㝈ᮇ㛫㸧ࢆタᐃࡋࡓࠋ㛵ಀ⪅࡟ᑐࡋ࡚ࡣ⸆≀࠾ࡼࡧᢞ୚⤒㊰ࡈ࡜࡟᪥ᩘࢆつᐃࡋࡓࠕฟ㉮ไ㝈ᮇ㛫୍ぴ⾲ࠖࢆ♧ࡋࠊᮇ㛫ෆ࡟ᐇ᪋ࡉࢀࡿ➇㉮࡬ࡢฟ㉮ཪࡣฟ㤿ᢞ⚊ࢆไ㝈ࡍࡿࡇ࡜࡜ࡋࡓࠋࡇࡢࠕฟ㉮ไ㝈ᮇ㛫୍ぴ⾲ࠖ࡟ࡣࠊJRA ᪋タෆ࡛౑⏝ࡉࢀ࡚࠸ࡿつไ⸆≀࡟ຍ࠼ࠊ⸆
≀ືែ࡟㛵ࡍࡿ⛉Ꮫⓗ▱ぢ࡟ᇶ࡙ࡁࠊᢞ୚ᚋ㛗ᮇ㛫యෆ࡟Ꮡᅾࡍࡿྍ⬟ᛶࡢ࠶ࡿつไ⸆≀ࢆྵࡵࡓࠋ
᭱ᚋ࡟ࠊୡ⏺ⓗ࡟ㄢ㢟࡜࡞ࡗ࡚࠸ࡿ㑇ఏᏊࢻ࣮ࣆࣥࢢ㸦㑇ఏᏊ἞⒪ࢆ➇㉮⬟ຊྥୖࡢࡓࡵ࡟୙ṇ฼⏝ࡍࡿ⾜Ⅽ㸧࡟ᑐࡋࠊࡇࢀࢆ JRA ᪋タࡢෆእࢆၥࢃࡎ⚗Ṇࡍࡿ⾜Ⅽ࡜ࡋ࡚ 2022 ᖺ 4 ᭶࡟つᐃ໬ࡋࡓࠋຍ࠼࡚
2023 ᖺࡼࡾ᪂ࡓ࡞ྲྀ⥾ࡾࡢ୍⎔࡜ࡋ࡚ࠊධཕ᫬ࡢ➇㉮እ᳨ᰝ࡟࠾ࡅࡿ⸆≀᳨ᰝ࡟ຍ࠼࡚㑇ఏᏊࢻ࣮ࣆࣥࢢ
᳨ᰝࢆྠ᫬࡟ᐇ᪋ࡍࡿࡇ࡜࡜ࡋࡓࠋࡲࡓࠊᚑ๓࠿ࡽ➇㉮እ᳨ᰝ࡟࠾࠸࡚ᐇ᪋ࡋ࡚ࡁࡓ⸆≀᳨ᰝ࡟ࡘ࠸࡚ࡶࠊ
࢔ࢼ࣎ࣜࢵࢡࢫࢸࣟ࢖ࢻ࡟␃ࡲࡽࡎࠊᅜ㝿ⓗ࡟ၥ㢟࡜࡞ࡗ࡚࠸ࡿ⸆≀࡟ࡘ࠸࡚ࡶᑐ㇟ࢆᣑ኱ࡋ࡚ᐇ᪋ࡍࡿࡇ
࡜࡜ࡋࡓࠋ
࠙ࡲ࡜ࡵࠚ
JRA ࡛ࡣㅖつ⛬ࢆᩚഛࡋࠊ⚗Ṇ⸆≀࣭つไ⸆≀ࢆ㏣ຍࡍࡿ࡜࡜ࡶ࡟ࠊつไ⸆≀౑⏝ᚋ࡟ฟ㉮ࢆ᥍࠼ࡿ࡭
ࡁᮇ㛫࡜ࡋ࡚᪂ࡓ࡟ฟ㉮ไ㝈ᮇ㛫ࢆタᐃࡋࡓࠋࡲࡓࠊබṇ☜ಖࡢほⅬ࠿ࡽᮏ఍᪋タࡢෆእࢆၥࢃࡎ⚗Ṇࡍࡿ
⾜Ⅽ࡛࠶ࡿ㑇ఏᏊࢻ࣮ࣆࣥࢢ࡟ᑐࡋࠊ᪂ࡓ࡟᳨ᰝࢆ㛤ጞࡋࡓࠋࡇࢀࡽࡣ JRA ࡟㝈ࡽࡎࠊᆅ᪉➇㤿ࠊ⏕⏘࣭⫱ᡂ∾ሙࡸᨺ∾ඛ࡛ࡢ⟶⌮࡟ࡶ㛵ࢃࡿෆᐜ࡜࡞ࡿࡓࡵࠊᮏࢩ࣏ࣥࢪ࣒࢘ࢆྵࡵࡓྛ㞟఍ࡸ㤿㛵㐃㞧ㄅ➼࡛ࡢ
ᗈሗࢆ㏻ࡌࠊ௒ᚋࡶ㛵ಀ⪅࡟ᗈࡃ࿘▱ࢆᅗࡗ࡚࠸ࡃᡤᏑ࡛࠶ࡿࠋ

16

඲㌟㯞㓉ୗ࡛ࡢ㞴⏘௓ຓ᪉ἲࡢホ౯ 㹼4 ࡘࡢ⾡ᘧࡢᡂ⦼ẚ㍑㹼
‫ ۑ‬㕥ᮌ ྣ ຍ⸨ྐᶞ ᒣᐙᓫྐ ⏣ୖṇᖾ ᳃ᮏ⣧⳯ ᐑୗᜨ㔛 ⏣ୖṇ᫂♫ྎ࣮࣍ࢫࢡࣜࢽࢵࢡ
࠙⫼ᬒ࡜┠ⓗࠚ㤿ࡢ㞴⏘ࡀⓎ⏕ࡋࡓ㝿ࠊ⌧ሙ࡛ࡢ௓ຓศፔࡀᅔ㞴࡜ุ᩿ࡉࢀࡿ࡜ࠊࡑࡢከࡃࡣ඲㌟㯞㓉ࡀྍ⬟࡞⑓㝔࡬࡜
ᦙ㏦ࡉࢀࡿࠋ㏻ᖖࡣࠊ㯞㓉ୗ࡟࡚ᚋ⫥ࢆྞࡾୖࡆࡓ≧ែ࡛⫾఩ࢆᩚ᚟ࡋࠊ⏘㐨࠿ࡽࡢ≌ᘬࡀヨࡳࡽࢀࡿࠋ⫾ඣࡢṚஸࡀ☜ㄆ࡛ࡁࢀࡤษ⫾⾡ࡶ㑅ᢥ⫥࡜࡞ࡿࠋྞࡾୖࡆ࡟ࡼࡿፔฟࡀ୙ྍ⬟࡞⑕౛࡛ࡣᖇ⋤ษ㛤ࡀᐇ᪋ࡉࢀࡿࡀࠊ࠸ࡎࢀࡢ᪉ἲ࡟࠾࠸࡚ࡶࠊᏊᐑ㢁㒊ࡸ⏘㐨ࡢᦆയࡣ⾡ᚋࡢ⦾Ṫᡂ⦼࡟ᙳ㡪ࢆ୚࠼ᚓࡿࠋ௒ᅇࡣࠊ௓
ຓࡉࢀࡓ⦾Ṫ㞤㤿ࡢ⾡ᚋྜే⑕ࡸ⾡ᚋ⦾Ṫᡂ⦼࡟ࡘ࠸࡚ㄪᰝࡋࡓࠋ
࠙ᮦᩱ࡜᪉ἲࠚ
ㄪᰝᑐ㇟ࡣ 2000 ᖺ࠿ࡽ 2023 ᖺࡲ࡛࡟ࠊ඲㌟㯞㓉ୗ࡛㞴⏘௓ຓࢆᐇ᪋ࡋࡓ 133 ౛㸦131 㢌㸧࡜ࡋࠊ2021ᖺ௨๓࡟ᡭ⾡ࡋࡓ⑕౛࡛⾡ᚋ⦾Ṫᡂ⦼ࢆㄪᰝࡋࡓࠋྛ⑕౛ࡢデ⒪グ㘓ࢆᅇ㢳ࡋ࡚἞⒪ෆᐜࢆࠊ⪺ࡁྲྀࡾࡸJBIS-Search ࡟ࡼࡗ࡚⦾Ṫᡂ⦼ࢆㄪᰝࡋࡓࠋ
࠙⤖ᯝࠚᖹᆒᖺ㱋ࡣ 10.8 ṓ㸦4㹼21 ṓ㸹୰ኸ್ 10 ṓ㸧ࠊ๓ᖺࡲ࡛ࡢ⏘Ṕࡣᖹᆒ 3.9 ᅇ㸦0㹼11 ᅇ㸹୰ኸ್ 3 ᅇ㸧ࠊึ⏘ࡀ 23 ౛(17.3%)ྵࡲࢀ࡚࠸ࡓࠋ㞴⏘ࡢཎᅉࡣࠊኻ఩㸦ᅄ⫥ఙᒎ␗ᖖࢆྵࡴ㸧ࡀ 116 ౛(87.2㸣)࡛᭱ࡶከ
ࡃࠊᅄ⫥௨እࡢወᙧࡀ 11 ౛(8.3%)࡛ㄆࡵࡽࢀࡓࠋ㸳౛ࡣ∾ሙ࡟࡚ษ⫾⾡ࢆᐇ᪋ࡋࡓ࡟ࡶ㛵ࢃࡽࡎፔฟ࡛ࡁ
ࡎ࡟᮶㝔ࡋࡓࠋᡭ⾡ࡣࠊᚋ⫥ࢆྞࡾୖࡆ࡚⫾఩ࢆᩚ᚟ࡋ≌ᘬ࣭ፔฟ (A ἲ㸧73 ౛ࠊᏊᐑࢆษ㛤ࡋ࡚⫾఩ࢆᩚ᚟ࡋ⤒⭐࡛ፔฟ㸦B ἲ㸧12 ౛ࠊᏊᐑษ㛤㒊࠿ࡽ⫾ඣࢆፔฟ㸦C ἲ㸧43 ౛ࠊ㛤⭡ࡋᏊᐑࢆษ㛤ࡏࡎ࡟Ꮚᐑእ
࠿ࡽᩚ᚟ࡋ࡚⤒⭐࡛ፔฟ㸦D ἲ㸧3 ౛࡛࠶ࡗࡓࠋፔฟ࡛ࡁࡎ࡟⾡୰ᏳᴦṚ࡜࡞ࡗࡓ⑕౛ 2 ౛(1.5%)ࠊ㯞㓉࠿
ࡽぬ㓰࡛ࡁ࡞࠿ࡗࡓ⑕౛㸳౛ࠊ⾡ᚋྜే⑕࡟ࡼࡾ㏥㝔࡛ࡁ࡞࠿ࡗࡓ⑕౛ 13 ౛࡛ࠊ㏥㝔⋡ࡣ 85.0㸣(113/133౛)࠶ࡗࡓࠋྛ⩌ࡢ㏥㝔⋡ࡣ A ⩌ 94.5%ࠊB ⩌ 91.7%ࠊC ⩌ 69.8%ࠊD ⩌ 100%࡛࠶ࡗࡓࠋ㏥㝔㤿࡟࠾ࡅࡿᡭ
⾡ᖺ஺㓄⋡࡜⩣ᖺศፔ⋡࠾ࡼࡧࠊ⩣ᖺ஺㓄⋡ࡣ A ⩌ 79.0-38.6-93.0%ࠊB ⩌ 80.0-40.0-100%ࠊC ⩌ 77.336.4-100%ࠊD ⩌ 100-66.7-100%࡛࠶ࡗࡓࠋፔฟ᫬࡟ 25 ౛ࡢ⫾ඣ⏕Ꮡࢆ☜ㄆࡋࡓࡀࠊከࡃࡣᅄ⫥ఙᒎ␗ᖖࡢࡓࡵᏳᴦṚ࡜࡞ࡾࠊ㏥㝔࡛ࡁࡓ௘㤿ࡣ 6 ౛(4.5%:඲౛ A ⩌)࡛࠶ࡗࡓࠋ
࠙ࡲ࡜ࡵ࡜⪃ᐹࠚ⾡ᚋࡢṚஸ⌮⏤ࡣฟ⾑࡟ࡼࡿࡶࡢࡀ᭱ࡶከࡃ㸦7 ౛㸧ࠊC ⩌ࡢ㏥㝔⋡పୗࡢ୍ᅉ࡛࠶ࡗࡓࠋA ⩌ࡢ 1 㢌ࡣࠊ↓⌮࡞≌ᘬ࡟ࡼࡿᏊᐑ⿣๰ࡀ⏕ࡌࠊ❧఩࡛Ꮚᐑ⿣๰㒊ࡢ⦭ྜࡀᚲせ࡛࠶ࡗࡓࠋA ⩌࡛ࡣࠊ⾡ᚋ࡟Ꮚᐑ㢕㒊ࡸ⭼࡟࠾ࡅࡿᦆയࡀࡼࡃࡳࡽࢀࡿࡀࠊࡑࢀࡽࡢᦆയࡀ⦾Ṫᡂ⦼࡬୚࠼ࡓᙳ㡪ࢆ⪃ᐹࡋᚓࡿࡔࡅࡢヲ⣽࡞グ㘓ࢆᢕᥱࡍࡿࡇ࡜ࡣ࡛ࡁ࡞࠿ࡗࡓࠋࡋ࠿ࡋ࡞ࡀࡽࠊA ⩌ࡢᡭ⾡⩣ᖺࡲ࡛ࡢ஺㓄⋡ࡀ௚⩌ࡼࡾࡶప࠿ࡗࡓࡇ࡜ࡣࠊ
ࡇࢀࡽࡢ஦㇟ࢆ཯ᫎࡋ࡚࠸ࡿࡢ࠿ࡶࡋࢀ࡞࠸ࠋB ἲࡣࠊA ࡜ C ࡢᢡ⾺ἲ࡛࠶ࡾࠊ㏥㝔⋡ࡶ஺㓄⋡ࡶඃࢀ࡚࠸
ࡓࠋD ἲࡣ㐺ᛂ⑕౛ࡀ㝈ࡽࢀࡿࡀࠊᐇ᪋ࡉࢀࡓ⑕౛ࡣ࠸ࡎࢀࡶ⤒㐣Ⰻዲ࡛࠶ࡗࡓࠋ௨ୖࡢ஦࠿ࡽࠊA ἲ࡟ࡼࡿፔฟࡀᅔ㞴࡞ሙྜࡣࠊ㐜⁫࡞ࡃ㛤⭡ᡭ⾡ࢆ⾜࠸ࠊD࣭B࣭C ࡢ㡰࡟⾡ᘧ㑅ᢥࡍࡿࡢࡀⰋ࠸࡜⪃࠼ࡿࠋ17⦾Ṫ∷㤿ࡢᏊᐑ㢕⟶⿣๰࡟ᑐࡍࡿ⤒┤⭠㉸㡢Ἴ᳨ᰝ࡟ࡼࡿデ᩿ࡢヨࡳࠐỈཱྀᝆஓ బ⸨ṇே ᐑ㉺኱㍜ ᾏ㐨☻㔛 ᵽཱྀᚭNOSAI ໭ᾏ㐨 ᪥㧗ᨭᡤ ᐙ␆㧗ᗘ་⒪ࢭࣥࢱ࣮
࠙ࡣࡌࡵ࡟ࠚ
㤿ࡢᏊᐑ㢕⟶⿣๰ࡣศፔ᫬ࡢയᐖ࡜ࡋ࡚᫬࡟ほᐹࡉࢀࠊឤᰁᛶᏊᐑෆ⭷⅖ࡸᩓⓎⓗὶ⏘ࡢせᅉ࡟࡞ࡾᚓࡿࠋ
Ꮚᐑ㢕⟶⿣๰ࡢデ᩿࡟ࡣゐデ᳨ᰝࡀࢦ࣮ࣝࢻࢫࢱࣥࢲ࣮ࢻ࡛࠶ࡿࡀࠊ᳨ᰝ⪅㛫࡛ホ౯࡟ᕪࡀ⏕ࡌᚓࡿⅬࠊⓎ᝟ࢫࢸ࣮ࢪ࡟ࡼࡾゐデᡤぢࡀࢲ࢖ࢼ࣑ࢵࢡ࡟ኚ໬ࡋᚓࡿⅬ࡟ຍ࠼ࠊ⦾ᛁᮇ࡟㏣ຍࡍࡿ୍ᡭ㛫ࡣ↓どࡋ㞴࠸ࠋᮏㄪᰝ࡛ࡣ⤒┤⭠㉸㡢Ἴ᳨ᰝࢆ⏝࠸ࡓᏊᐑ㢕⟶⿣๰ࡢデ᩿ࢆヨࡳࠊࡑࡢᐇ⏝ᛶ࡟ࡘ࠸᳨࡚ウࡋࡓࠋ࠙⑕౛࡜᪉ἲࠚ
௨ୗࡢఱࢀ࠿࡟ヱᙜࡍࡿሙྜ࡟ problem mare ࡜ᐃ⩏ࡋㄪᰝ࡟౪ࡋࡓ㸦2020-2022 ᖺ㸧ࠋ㸦1㸧1 ᖺ௨ୖ୙ཷ⫾ࠊ
㸦2㸧」ᩘᅇࡢ஺㓄࡟ࡶ࠿࠿ࢃࡽࡎ୙ཷ⫾ࠊ
㸦3㸧Ꮚᐑෆ⭷⅖ࢆ᭷ࡍࡿࠊ
㸦4㸧⫾Ꮚ႙ኻ᪤ Ṕࢆ᭷ࡍࡿࠋᑐ㇟㤿ࡣᏊᐑ㢕⟶⿣๰ࡢ᭷↓ࢆ⤒⭐ゐデ᳨ᰝ࡟ࡼࡾ☜ㄆࡋࠊ⿣๰ࢆ᭷ࡍࡿሙྜ࡟ࡣ㒊఩㸦⫼ഃ⭡ഃ㸧ࠊ῝ᗘ㸦⿣๰㒊▮≧㍈㛗ࠊmm㸧࡟ࡘ࠸ุ࡚᩿ࡋࡓࠋࡲࡓࠊᏊᐑ㢕⟶ゐデ࡟ඛࢇࡌ࡚⤒┤⭠㉸㡢Ἴ᳨ᰝ࡟ࡼࡾᏊᐑ㢕⟶⦪᩿ീ࠾ࡼࡧᶓ᩿ീࢆᥥฟࡋࠊ⿣๰㒊ࡢホ౯ࢆヨࡳࡓࠋࡉࡽ࡟ࠊヱᙜ㤿ࡢ⦾Ṫᡂ⦼ࢆేࡏ࡚㏣㊧ࡋࡓࠋ࠙⤖ᯝࠚ59 㢌ࡀㄪᰝᑐ㇟࡟ヱᙜ㸦୰ኸ್㸹ᖺ㱋 12ࠊ⏘ḟᩘ 5㸧ࡋࠊ࠺ࡕ 46 㢌࡛Ꮚᐑ㢕⟶⿣๰ࢆㄆࡵࡓ㸦⫼ഃ㸸1ࠊ
⭡ഃ㸸45ࠊ῝ᗘ㸸5-25 mm㸧ࠋᏊᐑ㢁⟶⿣๰ࢆ᭷ࡍࡿ 46 㢌୰ 44 㢌࡛ࡣ㉸㡢Ἴ᳨ᰝୗ࡛Ꮚᐑ㢕⟶⿣๰ࡀᏑࡍ
ࡿ㒊఩࡟୍⮴ࡋ࡚ᒁᡤⓗ࡞ echotexture ࡢኚ໬ࢆㄆࡵࡓ୍᪉ࠊᏊᐑ㢁⟶⿣๰ࢆ᭷ࡉ࡞࠸ 13 㢌୰ 9 㢌࡛ࡶྠᵝࡢ㉸㡢Ἴᡤぢࢆᚓࡓࠋ᳨ᰝ࡟せࡋࡓ᫬㛫ࡣᩘ༑⛊ࠊᚓࡽࢀࡓ㉸㡢ἼᡤぢࡣⓎ᝟ࢫࢸ࣮ࢪࢆ㏻ࡌ࡚ほᐹࡉࢀࡓࠋ
ࡲࡓࠊ⦾Ṫᡂ⦼ࡀ㏣㊧࡛ࡁࡓ㤿ࡢཷ⫾⋡ࡣ 72.9㸣㸦35/48㸧ࠊ⫾Ꮚ႙ኻ⋡ࡣ 33.3㸣㸦13/39㸧࡛࠶ࡗࡓࠋ
࠙⪃ᐹࠚ
Problem mare ࡢከࡃࡣᏊᐑ㢕⟶⿣๰ࢆ᭷ࡋ࡚࠸ࡿࡇ࡜ࡀ☜ㄆࡉࢀࡓࠋ㉸㡢Ἴ᳨ᰝࢆ⏝࠸ࡓᏊᐑ㢕⟶⿣๰ࡢ
ホ౯ࡣ㎿㏿࠿ࡘⓎ᝟࿘ᮇࢆၥࢃࡎ⑓ኚࢆデ᩿࡛ࡁࡿྍ⬟ᛶࡀ࠶ࡿࠋࡋ࠿ࡋ࡞ࡀࡽࠊゐデ᳨ᰝ࡛Ꮚᐑ㢁⟶⿣๰ࢆ᭷ࡉ࡞࠸࡜ุ᩿ࡋࡓ㤿࡟࠾࠸࡚ࡶྠᵝࡢ㉸㡢Ἴᡤぢࢆᚓࡓࡇ࡜࠿ࡽ⏬ീࡢゎ㔘࡟ࡣὀពࢆせࡍࡿ୍᪉࡛ࠊ
㉸㡢Ἴ᳨ᰝࡣゐデࡢࡳ࡛ࡣุ᩿࡛ࡁ࡞࠸ᚤᑠ⑓ኚࢆ཯ᫎࡋ࡚࠸ࡿࡇ࡜ࡶ⪃࠼ᚓࡿࠋᏊᐑ㢕⟶⿣๰ࡢ἞⒪࡟㛵ࡋ࡚ࡣእ⛉ⓗಟ᚟ࡀ᥎ዡࡉࢀࡿࡀࠊࡑࡢᑐ㇟㤿࡟ࡘ࠸࡚ࡢゝཬࡣᩥ⊩࡟ࡼࡾ␗࡞ࡾ୍ᐃࡢࢥࣥࢭࣥࢧࢫࢆᚓ
࡚࠸࡞࠸ࠋᮏㄪᰝ࡛ࡣᏊᐑ㢁⟶⿣๰ࡢ㒊఩࡞ࡽࡧ࡟῝ᗘ࡜⦾Ṫᡂ⦼࡜ࡢ㛵㐃ࡣุ↛࡜ࡋ࡞࠿ࡗࡓࡀࠊཷ⫾⋡ࡣ 72.9㸣ࠊ⫾Ꮚ႙ኻ⋡ࡣ 33.3࡛࠶ࡾࠊ⫾Ꮚ႙ኻ⋡ࡢ㧗ࡉࡀ㝿❧ࡘࠋࡼࡗ࡚ࠊᏊᐑ㢕⟶⿣๰࡟ᑐࡍࡿ✚ᴟⓗ࡞እ⛉ⓗಟ᚟ࡣ᥎ዡࡉࢀࡿ࡜⪃࠼ࡽࢀࠊࡑࡢࡼ࠺࡞どⅬ࠿ࡽࡳࡿ࡜ᮏἲࡣᚑ᮶ࡢゐデἲࡢ⿵ຓⓗᡭẁ࡜ࡋ࡚ࠊ⑓ኚࡢ᭷↓ࢆ㎿㏿࠿ࡘᐈほⓗ࡟ࢫࢡ࣮ࣜࢽࣥࢢホ౯࡛ࡁࡿ࡜࠸࠺Ⅼ࡛ỗ⏝ᛶࡀ㧗࠸࡜ᛮࢃࢀࡿࠋᚓࡽࢀࡓ㉸㡢Ἴᡤぢࡣ⿣๰㒊ࡢ⒕⑞໬ᇦࢆ཯ᫎࡋ࡚࠸ࡿ࡜⪃࠼ࡽࢀࡿࡀࠊ௒ᚋ⑕౛ࢆ⵳✚ࡍࡿࡇ࡜࡛᭦࡞ࡿ▱ぢࡀᚓࡽࢀࡿ࡜⪃࠼ࡿࠋ
18㤿ࡢࢪࣀࣉࣟࢫࢺ㸦PGF2α㸧࡟ࡼࡿⓎ᝟ᅇᖐᡂ⦼ࠐ ᑠ➟ཎ៞NOSAI ໭ᾏ㐨᪥㧗ᨭᡤ᪥㧗す㒊ᐙ␆デ⒪ࢭࣥࢱ࣮࠙ࡣࡌࡵ࡟ࠚ ࢧࣛࣈࣞࢵࢻ⏕⏘࡟࠾࠸࡚ࠊ⏕⏘⋡ࡢప࠸ Foal Heat Breeding ࢆᅇ㑊ࡋ Short Cycling ࢆࡍࡿࡇ࡜ࡀ୍⯡ⓗ࡟࡞ࡗࡓࡇ࡜࡛ࠊࣉࣟࢫࢱࢢࣛࣥࢪࣥ F2α㸦PGF2α㸧ࡸ㢮⦕యࡢᢞ୚ᶵ఍ࡀቑຍࡋࡓࠋࡋ࠿ࡋ࡞ࡀࡽࠊ㯤య⼥ゎ࠾ࡼࡧࡑࡢᚋࡢⓎ᝟ᅇᖐࢆ┠ⓗ࡜ࡋࡓ PGF2α ࡸ㢮⦕యࡢ⏝㔞⏝ἲࡣ⋇་ᖌ࡟ࡼࡾᵝࠎ࡛࠶ࡿࠋࡑࡇ
࡛௒ᅇࠊኳ↛ᆺ PGF2α 〇๣࡛࠶ࡿࢪࣀࣉࣟࢫࢺ࡟ࡼࡿ⏝㔞⏝ἲูࡢⓎ᝟ᅇᖐ࠾ࡼࡧ஺㓄ᡂ⦼ࢆሗ࿌ࡍࡿࠋ
࠙ᑐ㇟㤿ࠊヨ㦂᪉ἲࠚ2018 ᖺ࠿ࡽ 2023 ᖺ࡟⤒┤⭠㉸㡢Ἴ᳨ᰝ࡟ࡼࡾ㯤యࡢᏑᅾࢆ☜ㄆࠊࡲࡓࡣ᤼༸ࢆ☜ㄆ࠶ࡿ࠸ࡣண

ࡋࡓ᪥

࠿ࡽ 7 ᪥⤒㐣ࡋࡓ✵⫾ࡢ⦾Ṫ∷㤿㸦n=491㸧࡟ᑐࡋࠊ1 ᅇ࠶ࡿ࠸ࡣ 24 ᫬㛫㛫㝸࡛ 2 ᅇࢪࣀࣉࣟࢫࢺ㸦PGF2α㸧ࢆᢞ୚ࡋࡓࠋPGF2α ᢞ୚ᚋ࡟⤒┤⭠㉸㡢Ἴ᳨ᰝࢆ㐺ᐅᐇ᪋ࡋࠊ஺㓄ࡋࡓಶయࠊ஺㓄๓࡟᤼༸ࡋࡓಶయࢆⓎ᝟ᅇᖐࡋࡓ࡜ุ᩿ࡋࡓࠋ஺㓄ᚋ 14~21 ᪥࡟⤒┤⭠㉸㡢Ἴ᳨ᰝࢆ」ᩘᅇᐇ᪋ࡋࠊዷፎࡢ᭷↓ࢆ☜ㄆࡋࡓࠋPGF2αࢆᢞ୚ࡋࡓ㢌ᩘࢆ࣮࣋ࢫ࡟Ⓨ᝟ᅇᖐ⋡ࠊዷፎ⋡ࢆ⟬ฟࡋࠊᒣୗࡽࡢሗ࿌㸦ࢪࣀࣉࣟࢫࢺ 10mg 1 ᅇࠊ2019 ᖺ㸧࡜ẚ㍑ࡋࡓࠋྛᢞ୚⩌㛫࡛ Fisher’s exact test ࡟ࡼࡾ⤫ィศᯒࢆ⾜ࡗࡓࠋ࠙⏝㔞⏝ἲ࠾ࡼࡧ⤖ᯝࠚ⏝㔞⏝ἲࡣࠊ6.0mg 1 ᅇ㸦n=225㸧ࠊ7.5mg 1 ᅇ㸦n=110㸧ࠊ5.0mg 2 ᅇ㸦n=52㸧ࠊ2.5mg 2 ᅇ㸦n=57㸧ࠊ0.5mg
2 ᅇ㸦n=47㸧࡜ࡋࠊࡍ࡭࡚➽⫗ෆ࡟ᢞ୚ࡋࡓࠋⓎ᝟ᅇᖐ⋡࣭ዷፎ⋡ࡣࠊ6.0mg 1 ᅇ࡛ 90.7%࣭46.7%ࠊ7.5mg
1 ᅇ࡛ 92.7%࣭51.8%ࠊ5.0mg 2 ᅇ࡛ 98.1%࣭59.6%ࠊ2.5mg 2 ᅇ࡛ 96.5%࣭59.6%ࠊ0.5mg 2 ᅇ࡛ 100%࣭
71.1%࡛࠶ࡗࡓࠋ⤫ィᏛⓗ᭷ពᕪࡣࠊⓎ᝟ᅇᖐ⋡ࡢ 6.0mg 1 ᅇ࡜ 0.5mg 2 ᅇࡢ㛫ࠊዷፎ⋡ࡢ 6.0mg 1 ᅇ࠾ࡼࡧ 7.5mg 1 ᅇ࡜ 0.5mg 2 ᅇࡢ㛫࡛ㄆࡵࡓ(p<0.05)ࠋ
࠙⪃ᐹࠚ ᒣୗࡽࡢሗ࿌࡛ࡣ 10mg 1 ᅇࡢⓎ᝟ᅇᖐ⋡࣭ዷፎ⋡ࡣ 95.7%࣭55.8%࡛࠶ࡗࡓࠋ௒ᅇࡢ⤖ᯝ࡜ᒣୗࡽࡢሗ࿌
ࢆẚ㍑ࡍࡿ࡜ࠊPGF2α ࡢ 1 ᅇᢞ୚࡛ࡣⓎ᝟ᅇᖐ⋡ࠊዷፎ⋡࡜ࡶ࡟⏝㔞౫Ꮡⓗ࡞ຠᯝࢆ♧ࡋࠊ10mg ᮍ‶࡛ࡣ⦾Ṫ∷㤿ࡢཷ⫾ᛶࢆ᭱኱㝈࡟ᘬࡁฟࡍࡇ࡜ࡀ࡛ࡁ࡞࠸ࡇ࡜ࡀ♧၀ࡉࢀࡓࠋ࢔࣓࡛ࣜ࢝ᕷ㈍ࡉࢀ࡚࠸ࡿࢪࣀࣉࣟࢫࢺ〇๣ࡢῧ௜ᩥ᭩࡟ࡣ 100lbs(Ҹ45.5kg)࠶ࡓࡾ 1mg ᢞ୚࡜ࡢグ㍕ࡀ࠶ࡾࠊࢧࣛࣈࣞࢵࢻ✀⦾Ṫ∷㤿࡛ࡣ
10mg ࢆ㉸࠼ࡿᢞ୚㔞࡛᭦࡞ࡿᡂ⦼ࡢྥୖࡀᮇᚅ࡛ࡁࡿࡀࠊྠ᫬࡟⏝㔞౫Ꮡᛶࡢ๪స⏝ࡢቑຍࡀᠱᛕࡉࢀࡿࠋ
୍᪉࡛ࠊ2 ᅇᢞ୚࡛ࡣᑡ࡞࠸⏝㔞࡛ࡶ 1 ᅇᢞ୚ࡼࡾⰋዲ࡞ᡂ⦼ࢆ♧ࡋࠊ⤖ᯝ࡜ࡋ࡚๪స⏝ࡢฟ⌧ࢆᢚ࠼ࡿࡇ
࡜࡟ࡘ࡞ࡀࡗࡓࠋPGF2α ࡢ 2 ᅇᢞ୚ࡣ☜ᐇ࡟㯤య⼥ゎࡉࡏࡿ⏝ἲ࡛࠶ࡿ࡜ࡢ᪤ሗࡀ࠶ࡿࡀࠊᮏⓎ⾲࡛ࡣ㧗࠸
Ⓨ᝟ᅇᖐ⋡࡟ຍ࠼ࠊ⦾Ṫ∷㤿ࡢཷ⫾ᛶࢆ༑ศ࡟ᘬࡁฟࡍ⏝ἲ࡛࠶ࡿࡇ࡜ࡀ♧၀ࡉࢀࡓࠋ

19ᚰᡣ⣽ື࡟࠾ࡅࡿయ⾲ᚰ㟁ᅗࢆ⏝࠸ࡓ f Ἴࡢ FFT ࿘Ἴᩘゎᯒࡢ᳨ウ࠾ࡼࡧᚰᡣ⣽ື೵Ṇ࡜ࡢ㛵㐃ᛶ‫ ۑ‬஭ୖె⧊
᪥ᮏ୰ኸ➇㤿఍ ᰩᮾࢺ࣮ࣞࢽࣥࢢ࣭ࢭࣥࢱ࣮ ➇㉮㤿デ⒪ᡤ

࠙⫼ᬒ࡜┠ⓗࠚᚰᡣ⣽ືࡣ➇㉮㤿࡛ࡋࡤࡋࡤㄆࡵࡽࢀࡿ⑌ᝈ࡛ࠊయ⾲ᚰ㟁ᅗ࡛☜ᐃデ᩿ࡉࢀࡿࡶࡢࡢࠊ⌧≧࡛ࡣᐈほⓗᩘ್ࢆ⏝࠸࡚⑓ែࢆヲ⣽࡟ᢕᥱࡍࡿࡇ࡜ࡣᅔ㞴࡛࠶ࡿࠋf ἼࡢἼᙧࢆ࿘Ἴᩘゎᯒࡍࡿࡇ࡜࡟ࡼࡾᚓࡽࢀࡿ
Dominant Frequency㸦DF㸧ࡣᚰᡣࡢ㟁Ẽⓗ⯆ዧࡢᣦᶆ࡜ࡉࢀ࡚࠾ࡾࠊࣄࢺ་⒪࡛ࡣᚰᡣ⣽ືࡢ⮬↛೵Ṇࡸ἞⒪ຠᯝุᐃࡢᣦᶆ࡜ࡋ࡚ᮇᚅࡉࢀࠊయ⾲ᚰ㟁ᅗ࠿ࡽᚓࡽࢀࡿἼᙧࢆゎᯒࡋ࡚࠸ࡿࠋ୍᪉ࠊ㤿ࡢ⮫ᗋ⌧ሙ࡛㢖⏝ࡉࢀࡿ༳Ꮠࡉࢀࡓయ⾲ᚰ㟁ᅗࢆ⏝࠸ࡓゎᯒἲࡣ☜❧ࡉࢀ࡚࠾ࡽࡎࠊ➇㉮㤿࡛ࡣయ⾲ᚰ㟁ᅗ࠿ࡽ࿘Ἴᩘ
ゎᯒࢆ⾜ࡗࡓሗ࿌ࡣ࡞࠸ࠋᮏ◊✲࡛ࡣࠊ༳Ꮠࡉࢀࡓయ⾲ᚰ㟁ᅗ࡟࠾ࡅࡿ f Ἴࡢ࿘Ἴᩘゎᯒἲࢆ☜❧ࡋࠊDF
࡜㤿ࡢᚰᡣ⣽ື೵Ṇ࡜ࡢ㛵㐃ᛶࢆ᳨ウࡍࡿࡇ࡜ࢆ┠ⓗ࡜ࡋࡓࠋ
࠙ᮦᩱ࡜᪉ἲࠚ ゎᯒ᪉ἲࡢ᳨ウ࡜ࡋ࡚ࠊᐇ㦂ⓗ࡟ᚰᡣ⣽ືࢆⓎ⑕ࡉࡏࡓࢧࣛࣈࣞࢵࢻ✀ 8 ౛࠿ࡽయ⾲࠾ࡼࡧᚰᡣෆࡢᚰ㟁ᅗἼᙧࢆྠ᫬࡟ィࡋ ࠊ ༳ Ꮠ ࡉ ࢀ ࡓ ᚰ 㟁 ᅗ Ἴ ᙧ 㸦 10-50 mm/sec 㸧 ࢆ ⏝ ࠸ ࡚ FFT 㸦 Fast Fourier

Transform㸧ゎᯒࢆᐇ᪋ࡋࡓࠋゎᯒ࡛ᚓࡽࢀࡓయ⾲ᚰ㟁ᅗ f Ἴࡢ DF ࡜ᚰᡣෆᚰ㟁ᅗἼᙧࡢ DF ࡟ࡘ࠸࡚ࣆ
࢔ࢯࣥࡢ✚⋡┦㛵ಀᩘࢆ⟬ฟࡋ 2 ⪅ࡢ㛵㐃ᛶࢆㄪ࡭ࡓࠋ୍᪉ࠊf Ἴࡢ DF ࡜ᚰᡣ⣽ື೵Ṇ࡜ࡢ㛵㐃ᛶ࡟ࡘ࠸
࡚ࡣࠊ2015 ᖺ㸫2022 ᖺ࡟ᮏ఍࡛ᚰᡣ⣽ື࡜デ᩿ࡉࢀࡓ 18 ⑕౛ࢆᑐ㇟࡜ࡋࡓࠋⓎ⑕᪥࠿ࡽ 2 ᪥௨ෆ࡟Ὕㄪ
ᚊ࡬᚟ࡋࡓ 12 ⑕౛ࢆ⮬↛೵Ṇ⩌ࠊ4 ᪥௨ୖᚰᡣ⣽ືࡀᣢ⥆ࡋ㝖⣽ືࢆᐇ᪋ࡋࡓ 6 ⑕౛ࢆ㝖⣽ື⩌࡜ศ㢮ࡋࠊ
2 ⩌ࡢⓎ⑕ࡲࡶ࡞࠸᫬ᮇࡢ DF ࢆẚ㍑ࡋࡓࠋ࡞࠾ࠊ⤫ィゎᯒࡣ p <0.05 ࡛᭷ពᕪ࠶ࡾ࡜ࡋࡓࠋ࠙⤖ᯝࠚ ゎᯒ᪉ἲࡢ᳨ウ࡛ࡣࠊゎᯒ࡟⏝࠸ࡿ f Ἴࡢࣆ࣮ࢡࡢᩘࡀ 3 ࡘ௨ୖࡢሙྜࡣ f Ἴࡢ DF ࡜ᚰᡣෆᚰ㟁ᅗἼᙧ
ࡢ DF ࡀⰋዲ࡞┦㛵㸦r =0.870, p <0.05㸧ࢆ♧ࡋࡓࡀࠊࣆ࣮ࢡࡢᩘࡀ 3 ࡘᮍ‶ࡢሙྜࡣ┦㛵ࡀㄆࡵࡽࢀ࡞࠿
ࡗࡓ㸦r =0.156, p Ӎ0.05㸧ࠋᚰᡣ⣽ື೵Ṇࡢ㛵㐃ᛶㄪᰝ࡟ࡘ࠸࡚ࡣࠊ⮬↛೵Ṇ⩌ࡢⓎ⑕᫬ DF ࡢᖹᆒ್㸦±ᶆ‽೫ᕪ㸧ࡣ 4.8㸦±0.5㸧Hzࠊ㝖⣽ື⩌ࡣ 5.7㸦±0.6㸧Hz ࡛࠶ࡾࠊ㝖⣽ື⩌ࡢⓎ⑕᫬ DF ࡣ᭷ព࡟㧗್ࢆ♧ࡋࡓࠋ࠙⪃ᐹࠚ
f Ἴࡢࣆ࣮ࢡࡀ 3 ࡘ௨ୖࡢ᮲௳ୗ࡞ࡽࡤయ⾲ᚰ㟁ᅗࡢ f Ἴࡢ DF ࡣᚰᡣෆᚰ㟁ᅗἼᙧࡢ DF ࢆⰋዲ࡟཯ᫎ
ࡋ࡚࠾ࡾࠊᚰᡣ⯆ዧࡢ࿘Ἴᩘ≉ᛶࢆ㠀౵くⓗ࠿ࡘẚ㍑ⓗ⡆౽࡟᥎ᐃྍ⬟࡛࠶ࡗࡓࠋf Ἴࡢ DF ࡣ 2 ᪥௨ෆ࡟⮬↛೵Ṇࡍࡿ⑕౛࡜ 4 ᪥௨ୖᣢ⥆ࡍࡿ⑕౛࡛ᕪࡀࡳࡽࢀࠊ⮬↛Ⓨ⑕౛ࡢⓎ⑕᫬ࡢ f Ἴ࠿ࡽᚓࡽࢀࡓ DF ࡣⓎసᛶ࠿ᣢ⥆ᛶ࠿ࢆุูࡍࡿᣦᶆ࡜࡞ࡿྍ⬟ᛶࡀ♧၀ࡉࢀࡓࠋ௒ᚋࡣࠊᚰᡣ⣽ືࡢ⑓ែࣔࢽࢱࣜࣥࢢ࡟࠾ࡅࡿ
DF ࡢ᭷⏝ᛶࢆ᳨ウࡍࡿࡓࡵࠊ៏ᛶ⑕౛ࡸ㝖⣽ື᫬ࡢኚ໬ࢆㄪᰝࡋࡓ࠸ࠋ
20

➨ 51 ᅇ⏕⏘ᆅࢩ࣏ࣥࢪ࣒࢘ ㅮ₇ື⏬㜀ぴ᪉ἲ ᮏᖺࡢ⏕⏘ᆅࢩ࣏ࣥࢪ࣒࡛࢘ࡣㅮ₇ື⏬ࢆ᧜ᙳࡋࠊᚋ᪥ JRA ➇㉮㤿⥲ྜ◊✲ᡤࡢ࣮࣒࣮࣍࣌ࢪ࡟࢔ࢵࣉ࣮ࣟࢻࢆ⾜࠸ࡲࡍࠋື⏬ࡢ㜀ぴࢆࡈᕼᮃࡉࢀࡿ᪉ࡣࠊ
௨ୗࡢ URL㸦QR ࢥ࣮ࢻ㸧࠿ࡽ࢔ࢡࢭࢫࢆ࠾㢪࠸࠸ࡓࡋࡲࡍࠋ

https://company.jra.jp/equinst/other/2023keibokyo.html
QR ࢥ࣮ࢻЎͤୖグࢧ࢖ࢺࡣ≉タ࣮࣌ࢪ࡜࡞ࡾࠊ㏻ᖖࡢ᳨⣴࢚ࣥࢪࣥ࠿ࡽࡣ࢔ࢡࢭࢫ࡛ࡁࡲ
ࡏࢇࡢ࡛ࠊࡈὀពࡃࡔࡉ࠸

࡞࠾ࠊㅮ₇ື⏬ࡢබ㛤ࡣ 7/21㸦㔠㸧㡭ࢆணᐃࡋ࡚࠾ࡾࡲࡍࠋබ㛤๓ࡣୖグࡢㅮ₇ື⏬ᑓ⏝࣮࣌ࢪ࡬࢔ࢡࢭࢫࢆࡋ࡚ࡶࠊື⏬ࡣᥖ㍕ࡉࢀ࡚࠾ࡾࡲࡏࢇࡢ࡛ࡈ
ὀពୗࡉ࠸ࠋ
බ㛤ᮇ㛫ࡣᮏᖺ 10 ᭶ᮎࡲ࡛ࢆணᐃࡋ࡚࠾ࡾࡲࡍࠋࡑࢀ௨㝆ࡣㅮ₇ື⏬ࢆࡈぴ࠸ࡓࡔࡅ࡞ࡃ࡞ࡾࡲࡍࡢ࡛ࠊࡈ஢ᢎࡃࡔࡉ࠸ࠋ

ࡈ୙᫂࡞Ⅼࡀࡈࡊ࠸ࡲࡋࡓࡽ⏕⏘ᆅࢩ࣏ࣥࢪ࣒࢘஦ົᒁࡲ࡛࠾ၥ࠸ྜࢃࡏࡃࡔࡉ࠸ࠋ
⏕⏘ᆅࢩ࣏ࣥࢪ࣒࢘஦ົᒁ JRA 㤿஦㒊㜵␿ㄢ
TEL㸸050-3139-9535

21

第 51 回「生産地における軽種馬の疾病に関するシンポジウム」講演抄録

編集〒 105-0003

東京都港区西新橋 1-1-1

日本中央競馬会TEL

馬事部防疫課050-3139-9535