What Is Japanese B Encephalitis;Treatment,Symptoms,Diagnosis

Japanese B encephalitis is one of the most serious of the arbovirus encephalitides. It occurs in eastern Asia from Siberia to southeast India and on the offshore islands, including Japan, Okinawa, Guam, Taiwan, the Philippines, and the East Indies. Two cases have occurred in the United States in persons returning from Korea and Japan.

Etiology.

The causative agent, a group B arbo­virus, is closely related to Murray Valley, West Nile, and St. Louis viruses. At least two distinct genotypes have been recognized. These differ from St. Louis virus antigenically and in behavior in various hosts. Infection of porcine kidney cell cultures results in clear cytopathic effect. Cere­bral infection of rhesus or cynomolgus monkeys usually induces fatal encephalitis. Naturally infected horses often develop encephalitis, and infection of sows early in pregnancy results in abnormal or stillborn offspring. Swine and many birds including waterfowl experience silent in­fections with viremia sufficient to infect feeding mosquitoes.

Epidemiology.

The designation “Japanese B encephalitis” dates from an epidemic of more than 6000 cases in 1924, which were recognized as different from encephalitis A or Von Economo’s disease. However, the disease probably has existed in Japan at least since 1871. The virus was first recovered in monkeys from a fatal case in 1934.

In temperate zones disease occurs only in the warmer months, and large epidemics with high case fatality may occur at irregular intervals; in tropical areas cases are sporadic and unrelated to season. In Japan some 10 per cent of children are infected annually, but only about one in 500 develops disease (in Korea, one case develops among 25 infected U.S. troops). Because of this extensive early immunization, disease is largely restricted to children, adults recently entering the country (U.S. military included), and native adults 60 years or older. The incidence is unrelated to sex.

Present epidemiologic knowledge derives largely from the long-continued efforts of Japanese workers and American teams working with U.S. military support. The basic cycle is mosquito- lower vertebrate-mosquito, the particular species differing with, locale. Principal vectors are C. annulirostris on Guam, C. gelidus in Malaya, and C. tritaeniorhynchus in most other areas including Japan. Important amplifying hosts are herons and egrets in Japan and swine throughout the Far East, where pork is popular and pig populations turn over rapidly. Thus, as noted in Japan, a high prevalence of antibody in pigs coming to slaughter portends an epidemic in man. Human infection occurs only after a high density of infected mosquitoes is attained. Overwintering mechanisms for the virus in temperate zones remain to be deter­mined.

Pathogenesis and Pathology.

Pathogenesis pre­sumably is similar to that described previously for St. Louis encephalitis. Incubation time is un­determined. The morbid anatomy also resembles that of St. Louis encephalitis but involves a gen­erally greater neuronal destruction in many vital areas and extensive destruction of the Purkinje cells in the cerebellum.

Clinical Manifestations of Japanese B Encephalitis.

Japanese B infection of man parallels that with St. Louis virus in the high frequency of inapparent infection or abortive illness and in the general nature of the onset, signs, and symptoms of true central nervous sys­tem disease. However, such disease resulting from Japanese B infection is of much greater over­all severity. Facial paralysis or paralysis of extremities is common in children, whereas symmetrical paresis without corresponding sen­sory changes occurs in adults. Other findings may include signs of cerebellar involvement, sen­sorial changes, general spastic rigidity, and coma. Fever, with a relative bradycardia, reaches its peak in two to four days and then subsides grad­ually. Duration of the acute illness is variable and is usually followed by prolonged convales­cence. A transient leukocytosis, averaging about 14,000 leukocytes per cubic millimeter, occurs early. The cerebrospinal fluid shows some increase in pressure, a pleocytosis ranging up to 400 or more, an elevated protein, and normal sugar.

Diagnosis.

Although time, place, and clinical picture may strongly suggest it, . the specific diagnosis of Japanese B encephalitis requires virologic procedures similar to those described for St. Louis encephalitis. Virus can be recovered, rarely, from early blood specimens and from brains of rapidly fatal cases. However, viral antigen can be demonstrated by fluorescent antibody methods in a high proportion of brains .examined post mortem. Early (IgG) antibody possesses neutral­izing and hemagglutination-inhibiting KL reactivity, but only the later (IgM) antibody fixes complement. Hence, the HI test is useful when the acute phase serum is taken very early; other­wise, the complement-fixation (CF) test is  reliable.

Use of both HI and CF tests yields 15 :c 25 per cent more diagnoses than either alone, and when both are negative the neutralization test may still prove positive. Where other group 3 arboviruses abound, as in India, use of a of group B antigens may be necessary.

Japanese B Encephalitis Treatment.

Although no specific treatment  exists, control of hyperpyrexia is spartaaa (tepid sponges, ice packs, artificial.For severe convulsions anticonvulsants may be necessary. Intensive supportive and nursing care with prolonged hospitalization are required with severe disease.

Prognosis.

The mortality rate for encephalitis varies with age from 30 per cent for those under age 20 to 80 per cent in older age groups. Progno­sis in nonfatal cases must be guarded, because slow improvement is possible over a lengthy period. Permanent sequelae are most common under age ten and most severe in infants. They include, in approximate order of frequency, mental deteriora­tion and personality changes, upper or lower motor neuron types of paralysis, aphasia, cere­bellar syndromes, organic psychoses, and decere­brate rigidity.

Prevention.

Vector control is not usually practicable because of the habits and extensive breeding area of the vector. Vaccine prepared from formalinized* mouse brain is widely used with children in Japan and is credited with signifi­cant effect, but it is not available in the United States. Formol-inactivated vaccines produced from virus grown in cell culture have given promising results in pilot studies. Because proved potential vectors and vertebrate hosts abound on the West Coast, prevention of importation of the virus into the U.S. is vitally important.

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