Japanese encephalitis

Japanese: 日本脳炎 - にほんのうえん
Japanese encephalitis

It is an acute infectious disease caused by the Japanese encephalitis virus, and is classified as a Class 5 infectious disease under the Infectious Disease Prevention and Medical Care Act (Infectious Diseases Act). In the past, it was called by various names, such as type B encephalitis or summer encephalitis, because of its similarity to lethargic encephalitis, which is the same type of epidemic encephalitis. From 1948 (Showa 23) to 1967, the number of cases per year was over 1,000, and in 1950, there were over 5,000 cases. However, as vaccinations became effective, the number of cases dropped to under 100 since 1972, and has been in single digits since 1992 (Heisei 4). At the time, it was prevalent in various places except Hokkaido, and it was prevalent in children and people over 60 years old, but since 1992, the area of ​​occurrence has been limited to western Japan, mainly in the Kyushu, Chugoku, and Shikoku regions, and patients are almost exclusively elderly people.

The name Japanese encephalitis does not mean that the disease is found only in Japan. It was named after the fact that Japan was the first country to recognize the disease, and where it has been most thoroughly studied in terms of its pathogenesis, epidemiology, and clinical practice. Japanese encephalitis is also found, and epidemics are seen, in Korea, Taiwan, mainland China, Thailand, Myanmar, India, and also in the southwest Pacific region, including the Mariana Islands, the Philippines, and the Sunda Islands.

[Noriaki Yanagishita]

Symptoms

The patient develops a sudden fever of 38-39°C, accompanied by a strong headache, nausea and vomiting. In younger children, gastrointestinal symptoms such as abdominal pain and diarrhea are not uncommon. At first, it is similar to a summer cold or catching a cold, but the fever reaches around 40°C, and symptoms such as agitation, confusion, and occasional facial and limb convulsions appear, which are reminiscent of encephalitis. The most severe stage of the illness is 4-7 days after onset, after which the fever gradually subsides and the patient begins to recover, but complications such as pneumonia and myocarditis may occur. In addition, aftereffects are common, such as a low and monotonous voice for several weeks to several months, amnesia, and personality changes, but in severe cases, tonic paralysis of the limbs may remain for the rest of the patient's life, and mental disorders such as personality disorders and dementia may also occur. In general, aftereffects in young children are difficult to cure, and in adults, even if the symptoms are quite severe at first, recovery usually takes place within about six months.

[Noriaki Yanagishita]

diagnosis

In the early stages, it is easily misdiagnosed as various types of meningitis, cerebral hemorrhage, or the common cold. When symptoms are severe, the diagnosis can be made almost entirely from clinical symptoms and cerebrospinal fluid tests, but a definitive diagnosis, especially in cases where it is differentiated from other viral encephalitides or where the infection is mild or subclinical, must be made by serological reactions (complement fixation reaction and hemagglutination inhibition reaction). However, this reaction has the drawback that it does not appear until more than 10 days have passed since the onset of symptoms.

[Noriaki Yanagishita]

Treatment

There is no causal treatment, and in addition to symptomatic treatment, emphasis is placed on general nursing care, such as preventing complications and treating aftereffects. The use of ICUs (intensive care units) has made it possible to save lives, and rehabilitation for aftereffects is now carried out early in the recovery period, but recovery from aftereffects in young children is difficult.

[Noriaki Yanagishita]

prognosis

The prognosis is poor for infants and the elderly, and also for those with a fever of 41°C or higher. In general, about 20% of those who contract the disease die, about 20% suffer from severe aftereffects, and only 50-60% make a full recovery.

[Noriaki Yanagishita]

Infection and onset of disease

Infection occurs when a mosquito (usually a Culex tritaeniorhynchus) carrying the pathogenic virus bites the person, and it is not transmitted from person to person. Therefore, Japanese encephalitis is prevalent from July to October in association with the outbreak of mosquitoes, and is not seen in other seasons, and the epidemic areas are limited. Also, most people are asymptomatically infected and do not feel any sickness, and although it varies depending on the epidemic, usually only a few people out of 100,000 people become ill.

Japanese encephalitis is also a livestock disease that is prevalent among large mammals such as horses, cattle, pigs, and goats, but most infections are asymptomatic, and the incidence rate is highest in humans and horses.

[Noriaki Yanagishita]

Epidemic forecast

Since 1965, the Ministry of Health and Welfare (now the Ministry of Health, Labour and Welfare) has been predicting the spread of Japanese encephalitis, based on the fact that Japanese encephalitis occurs in humans three to five weeks after it has spread among pigs and horses. Every year from May to October, blood samples are collected weekly from one to three slaughterhouses in each prefecture from 20 pigs aged five to eight months that are not involved in a Japanese encephalitis epidemic the previous year, and the presence of antibodies against Japanese encephalitis is tested. If the antibody possession rate reaches 50% or more, it is determined that a Japanese encephalitis epidemic has occurred in pigs, and therefore it is assumed that there is a possibility of human cases occurring within two to three weeks. As such, an epidemic forecast (designation of epidemic areas) is published and the implementation of emergency vaccinations is considered.

[Noriaki Yanagishita]

prevention

Besides avoiding overwork and lack of sleep and eradicating mosquitoes, there are also routine vaccinations. Stage I of the vaccination, as stipulated by the Vaccination Act, involves two subcutaneous injections of the Japanese encephalitis vaccine at 1-4 week intervals to build up initial immunity, followed by one subcutaneous injection about a year later for booster immunity. Stage II of the vaccination is administered subcutaneously once at ages 9-13, while Stage III is administered subcutaneously once at ages 14-15. However, in Hokkaido and some parts of Tohoku where the disease is not prevalent, the vaccination is not administered in some places.

[Noriaki Yanagishita]

Japanese encephalitis virus

It is the causative agent of Japanese encephalitis, which was first transmitted to monkeys by intracerebral inoculation in 1934 (Showa 9), and in 1936, Taniguchi, Kasahara and others succeeded in isolating the virus from mice. It is an RNA virus belonging to group B of arboviruses (currently classified as Flaviviridae family, Flavivirus genus), and is similar to the viruses that cause St. Louis encephalitis and West Nile encephalitis, but can be distinguished by virus neutralization tests.

The Japanese encephalitis virus is transmitted by mosquitoes and infects humans and livestock, but if we could understand how it survives the winter when there are no mosquitoes and causes an epidemic again the following year, we could prevent the virus from spreading again, but this is still unknown. In temperate regions, it is possible that the virus survives inside the bodies of hibernating mosquitoes, but this has not yet been proven. Other theories include the possibility that the virus survives inside the bodies of lizards and geckos that eat mosquitoes, or that it is carried by wild birds, especially herons, that are unable to leave nests. Also, as the virus is distributed throughout the southwestern Pacific, some people are focusing on migratory birds. Infected horses and pigs may grow the virus that year, but are not thought to be carriers of the virus.

[Noriaki Yanagishita]

[References] | Arbovirus | Culex tritaeniorhynchus | Encephalitis lethargica | Encephalitis

Source: Shogakukan Encyclopedia Nipponica About Encyclopedia Nipponica Information | Legend

Japanese:

日本脳炎ウイルスによる急性感染症で、感染症予防・医療法(感染症法)では5類感染症に分類されている。かつては同じ流行性脳炎の嗜眠(しみん)性脳炎との異同からB型脳炎とか夏季脳炎などといろいろな名称でよばれていた。1948年(昭和23)から67年までは年間発生数が1000例以上、50年には5000例を超える発生もあったが、予防接種などの効果が現れて72年以来100例以下となり、92年(平成4)以降は一桁(けた)まで減少した。多発時には北海道を除く各地で流行し、小児と60歳以上に好発したが、1992年以降は発生地も九州、中国、四国地方を中心とする西日本地区に限局され、また、患者もほとんど高齢者に限られている。

 なお、日本脳炎という名称は、この病気が日本にだけあるという意味ではない。日本で最初に認識され、病原、疫学、臨床なども日本でもっともよく研究されたからという意味で命名されたものである。日本脳炎は、韓国、台湾、中国本土、タイ、ミャンマー、インド、さらにマリアナ諸島、フィリピン、スンダ列島に至る西南太平洋地域にも存在し、流行がみられる。

[柳下徳雄]

症状

急に38~39℃の発熱がおこり、かなり強い頭痛のほか、悪心(おしん)や嘔吐(おうと)を伴う。年少者では腹痛や下痢などの胃腸症状もおこることがまれでない。最初は夏かぜや寝冷えによく似ているが、熱はさらに40℃前後に達し、興奮、意識混濁、顔面や手足のけいれんがときどきおこったりして脳炎らしい症状が現れてくる。発病後4~7日が病気の峠で、この時期を過ぎれば熱もしだいに下がって回復に向かうが、肺炎や心筋炎などの合併症をおこすことがある。また、後遺症が高率に現れ、数週から数か月にわたって音声が低く単調になったり、健忘がみられ性格が変調したりするが、重症では手足の強直性麻痺(まひ)が一生残り、性格異常や認知症などの精神障害もおこる。一般に幼小児の後遺症は治りにくく、成人の場合は最初かなり重症でも半年くらいで回復することが多い。

[柳下徳雄]

診断

初期は各種の髄膜炎、脳出血、感冒などと誤診されやすい。症状が強く現れたときは臨床症状と髄液の検査でほぼ診断されるが、確実な診断、とくに他のウイルス性脳炎との鑑別や軽症あるいは不顕性感染であった場合の診断は、血清反応(補体結合反応および赤血球凝集抑制反応)によらなければならない。しかし、この反応は発病後10日以上経過してからでないと現れてこない難点がある。

[柳下徳雄]

治療

原因療法はなく、対症療法のほか、合併症の予防や後遺症の治療など一般的看護に重点が置かれる。ICU(集中治療室)の活用によって救命しうるようになり、後遺症のリハビリテーションも回復期の早期から実施されるようになったが、幼小児の後遺症の回復は困難である。

[柳下徳雄]

予後

乳幼児と高齢者の予後が悪く、また発熱が41℃以上になった場合も悪い。一般的には発病者の約20%が死亡、約20%には重い後遺症がみられ、完全に治癒するのは50~60%である。

[柳下徳雄]

感染と発病

病原ウイルスをもったカ(多くはコガタアカイエカ)に刺されることによって感染し、ヒトからヒトへの感染はない。したがって、日本脳炎はカの発生に関連して7~10月に流行し、ほかの季節にはみられず、流行地域も限定されてくる。また、大部分の人は不顕性感染で、なにも病感がおこらず、流行によって差もあるが、普通10万人について数人が発病するにすぎない。

 なお、日本脳炎は家畜伝染病でもあり、ウマ、ウシ、ブタ、ヤギなど大形の哺乳(ほにゅう)類にも流行するが、やはり不顕性感染が大部分で、発病率はヒトとウマがもっとも高い。

[柳下徳雄]

流行予測

1965年(昭和40)から厚生省(現厚生労働省)では日本脳炎の流行予測を行っているが、これは、日本脳炎がブタやウマの間に流行してから3~5週後にヒトに流行がおこるという事実に基づいて実施されている。毎年5月から10月にかけて各都道府県ごとに、1~3か所の食肉処理場から生後5~8か月のブタ、すなわち前年の日本脳炎の流行に関係のないブタ20頭の血液を毎週集めて日本脳炎に対する抗体の有無を調べる。抗体保有率が50%以上になればブタに日本脳炎の流行がおこったことがわかり、したがって2~3週後にはヒトにも患者発生が到来する可能性があるものとみて、流行予測(流行地指定)が公表され、臨時予防接種の実施が検討される。

[柳下徳雄]

予防

過労や睡眠不足を避け、カを駆除するほか、定期予防接種がある。予防接種法による第Ⅰ期定期接種は、初回免疫をつくるために1~4週間隔で2回日本脳炎ワクチンを皮下注射し、その後約1年を経過した時期に1回皮下注射して追加免疫する。第Ⅱ期定期接種は9~13歳未満に1回皮下注射、第Ⅲ期定期接種は14~15歳に1回皮下注射する。ただし、流行のない北海道と東北の一部の地域では行わない所もある。

[柳下徳雄]

日本脳炎ウイルス

日本脳炎の病原体で、1934年(昭和9)に林道倫(みちとも)(1885―1973)が脳内接種法によって初めてサルに伝播(でんぱ)させ、36年には谷口・笠原(かさはら)らがマウスを使ってウイルスの分離に成功した。アルボウイルスのB群(現在の分類法ではフラビウイルス科フラビウイルス属)に属するRNAウイルスで、セントルイス脳炎や西ナイル脳炎のウイルスと類似するが、病毒の中和試験によって区別される。

 なお、日本脳炎ウイルスはカに媒介されてヒトや家畜に感染をおこすが、カのいない冬季をどのようにして越年し翌年ふたたび流行をおこすのか、これがわかれば予防できるわけであるが、まだ不明である。温帯地方では冬眠したカの体内で越年する可能性もあるが、まだ実証されず、カを食べるトカゲやヤモリの体内で越年する可能性や巣立ちのできない野鳥とくにサギ類の体内に保有されるという考えなどもある。また、西南太平洋一帯に分布することから渡り鳥に注目する者もある。なお、感染したウマやブタはその年のウイルスを成育させることはあっても、ウイルスの保有者ではないとされている。

[柳下徳雄]

[参照項目] | アルボウイルス | コガタアカイエカ | 嗜眠性脳炎 | 脳炎

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