St Louis Encephalitis

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St Louis encephalitis virus is the principal cause of viral encephalitis in the USA and the outbreak in New York City in 1999 brought viral encephalitis into international prominence once again. The virus is related antigenically to the Japanese encephalitis complex of the flaviviruses. It should be noted that the virus which caused the outbreak

Figure 6.8 Geographical distribution of St Louis encephalitis virus

in New York City in 1999 has now been identified as Kunjin/West Nile-like virus.

Epidemiology and Geographical Distribution

The virus is distributed throughout the USA, but it has been found in southern Canada, Central and South America and the Caribbean Islands (Figure 6.8). It is transmitted by the bite of an infected mosquito, and birds, particularly domesticated sparrows, are the principal amplifying hosts. Small mammals such as rodents and domesticated animals may also be infected; however, the virus is maintained in nature in an avian cycle and is transmitted by Culex mosquitoes which feed readily on birds.

St Louis encephalitis virus is disseminated widely throughout the USA and causes periodic outbreaks, usually at intervals of several years, in urban settings in California, Texas, the southeast and in the Ohio Mississippi valley.

Clinical Features and Diagnosis

More than 99% of infections with this virus are without symptoms. In clinical cases, the disease is characterised by fever, malaise, nausea and vomiting and headache. Aseptic meningitis or focal encephalitis, and cranial nerve palsies in about 20% of cases, indicate involvement of the central nervous system. Coma may ensue. The case fatality rate is approximately 7% in symptomatic cases but may be higher, particularly in the elderly, when the fatality rate may be 30%.

Rapid diagnosis is based on IgM antibody capture ELISA using serum or cerebrospinal fluid. Immunofluorescence test on cells infected with the virus is also a useful rapid diagnostic technique.

Prevention and Control

A licensed vaccine is not available. The infection is controlled in the USA by vector control, including water drainage and aerial low volume spraying of insecticides in populated areas. Secondary control measures to protect against mosquito bites should be deployed during reported outbreaks.

TICK-BORNE ENCEPHALITIS Introduction and Definitions

The tick-borne flaviviruses are maintained by tick-mammal cycles and by transovarian transmission in ticks. Humans are infected by virus transmitted by the bite of an infected tick or, less commonly, by drinking unpas-teurised milk from infected goats or other mammals. The disease is endemic in forested parts of western, central and eastern Europe and Scandinavia, caused by Central European encephalitis virus, and the Far Eastern subtype or Russian Spring-Summer encephalitis virus.

Other viruses within the subgroup of tick-borne flaviviruses include Omsk haemorrhagic fever virus, Kyasanur Forest disease virus (India) and Powassan virus, which causes sporadic encephalitis in eastern parts of Canada (Ontario) and the USA. These viruses are not considered further in this text.

Nature of the Infectious Agent

The tick-borne encephalitis viruses are a closely related subgroup of flaviviruses.

Epidemiology and Geographical Distribution

The geographical distribution of the Central European encephalitis virus extends to the forested areas of western, central and eastern Europe, Scandinavia, Italy, Yugoslavia and Greece and follows closely the distribution of its arthropod vector, Ixodes ricinus (Figure 6.9). Russian Spring-Summer encephalitis virus is found in the forest belt and taiga of Russia and Siberia following the distribution of I. persulcatus (Figure 6.10). Infection is transmitted by the bite of an infected tick. Domestic animals,

Figure 6.9 Geographical distribution of Central European encephalitis virus. Reproduced from Zuckerman et al, 2000

such as sheep, goats and cows, excrete virus in their milk, and ingestion of unpasteurised milk or unpasteurised milk products may transmit the infection.

The infection is endemic, with increased incidence in the summer months in relation to temperature and humidity which affect tick activity. The infection is common in rural populations, especially in farmers and forest workers, with seroprevalence of 5-20% or even greater.

The incubation period is 8-14 days.

Pathology

The virus replicates in the liver before a significant vir-aemia occurs. Vascular permeability is altered and the virus crosses the blood-brain barrier. Severe neuronal damage may occur, affecting the cervical segments of the spinal cord, medulla, midbrain and pons. There is glial proliferation and lymphoid proliferation around vessels.

Clinical Features and Diagnosis

The onset of illness is sudden with a nonspecific febrile illness including headache and lassitude. Visual disturbances may occur such as blurring of vision and diplopia. In the majority the illness lasts 4-7 days. A biphasic

Figure 6.10 Geographical distribution of Russian Spring-Summer encephalitis virus. Reproduced from Zuckerman et al., 2000

illness may follow after a short remission, with fever and signs of meningoencephalitis. Extrapyramidal and cere-bellar syndromes may persist for months, and residual paralysis involving the upper limbs and the shoulder girdle is common. Mortality in different outbreaks varies from 1 to 5%.

Serological diagnosis is based on an IgM antibody-capture ELISA on serum or cerebrospinal fluid. Haem-agglutination-inhibition or neutralisation tests are useful. Virus can be isolated early after the onset of symptoms.

Prevention and Protective Measures

Forests in some areas of the former Soviet Union are closed to visitors.

Tick repellents are useful on outer clothes and socks, and the arms, legs and ankles must be covered. Travellers who plan to walk, camp or work in late spring and summer in the heavily forested areas listed above, especially where there is heavy undergrowth, should be immunised with a formalin-inactivated vaccine. Two doses of 0.5ml given intramuscularly 4-12 weeks apart will provide protection for 1 year. An immunoglobulin preparation is also available for postexposure prophylaxis.

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