Viral Diseases - ST. LOUIS ENCEPHALITIS

SYNONYMS:

Type C lethargic encephalitis.

ETIOLOGY:

RNA virus belonging to the genus Flavivirus (formerly group B of the arboviruses) of the family Togaviridae; forms part of the virus complex including Murray Valley, West Nile, and Japanese B encephalitides. There are indications that strains of the virus isolated in different zones differ in their capacity to produce viremia in birds, virulence in 3-week-old mice, and neurovirulence in rhesus monkeys. By the technique of nucleotide mapping, considerable genetic variation among the strains of the virus was demonstrated, and it was proposed to name these geographic variants as topotypes.

GEOGRAPHIC DISTRIBUTION:

The agent is distributed from Argentina to Canada. The disease is unknown outside the Americas.

THE DISEASE IN MAN:

The clinical infection presents a wide spectrum, from an undifferentiated febrile disease similar to influenza to severe encephalitis. Three syndromes can be distinguished: febrile disease, aseptic meningitis, and encephalitis. The febrile syndrome usually has a benign course, with fever and intense cephalalgia lasting several days, followed by complete recovery. The aseptic meningitis has a sudden onset, with fever, stiffness of the neck, and positive Kemig and Brudzinski signs, but without neurologic dysfunction. Pleocytosis is common. The disease characterized by encephalitis also begins suddenly, with fever and one or more signs of brain inflammation, such as personality changes, confusion. delirium, lethargy, paresis, convulsions, and others. The encephalitis syndrome is more frequent in elderly persons; its frequency increases from 56% in patients up to 20 years old to 87% in those over 60. Convalescence in these cases lasts several weeks. The incubation period is estimated at 4 to 21 days. In the United States, the case fatality rate in 2,261 confirmed clinical cases between 1955 and 1968 was 5 to 10%. The majority of deaths were in persons over 50 years old, among whom the fatality rate can be as high as 30% or more. During the 1962 epidemic in Tampa Bay, Florida, the highest fatality rate (36.3%) was recorded in patients 65 years of age and older in Pinellas County, where a large number of retired persons live. In that county the general mortality rate was 22.2%, while the rate was 9.8% in the remaining three counties in that area. In Central and South America, most of the small number of recorded patients did not exhibit impairment of the central nervous system.

THE DISEASE IN ANIMALS:

The infection is subclinical in animals. Experimental peripheral inoculation of the virus produces viremia without clinical symptoms in domestic and wild fowl and in various species of insectivorous bats. When the disease occurs in man, antibodies for SLE are generally found in horses and in some other mammals. In contrast to western, eastern, and Venezuelan equine encephalitides, St. Louis encephalitis does not cause clinical illness in equines. Some equines inoculated experimentally develop viremia.

SOURCE OF INFECTION AND MODE OF TRANSMISSION:

The basic cycle of the infection involves wild birds and omithophilic mosquitoes. Culex salinarius, from which the SLE virus has been isolated, could be the vector in the wild enzootic cycle. In the United States, two different epidemiologic situations are known, depending on the habits of the primary vector and other ecologic conditions. West of the Rocky Mountains the disease is rural and sporadic because the vector, C. tarsalis, is sparse and the widely scattered human population has a high rate of subclinical infection, protecting it against reinfection. Though the vector and birds reach high concentrations in areas flooded by irrigation water, human cases are not numerous for the reasons given. In the south-central and north-central states of the country, by contrast, the disease is urban-suburban in character, primarily because the vectors are the peridomestic and domestic mosquitoes C. quinquefasciatus and C. pipiens. These vectors proliferate where water contaminated with organic wastes collects, that is, in poorer urban and suburban areas deficient in environmental sanitation. The same conditions favor the proliferation of sparrows, pigeons, and other birds that feed among household wastes. Peridomestic birds and domestic fowl serve as amplifiers of the virus: that fact, together with the increased density of the human population, creates the conditions necessary for epidemics. During the 1964 epidemic in Houston, the virus was isolated from geese, domestic pigeons, and various other species of birds. In addition, antibodies were found in 20% of the birds, especially house sparrows (Passer domesticus), and in almost all poultry examined. How the virus gets into urban areas is not yet established, but it is suspected that migratory wild birds may introduce it. As is true for many other arboviruses, the mechanism that allows the virus to overwinter in temperate climates is not fully known. The virus has been isolated from hibernating adult female C. pipiens, which indicates that the virus can persist in the vector during the winter in temperate climates. It also has been proven experimentally that low-level transovarial transmission occurs in C. pipiens.

ROLE OF ANIMALS IN THE EPIDEMIOLOGY OF THE DISEASE:

Man is an accidental host of the virus and does not play any role in the natural maintenance cycle. The basic reservoir is wild birds and perhaps the vector mosquitoes; poultry and peridomestic and domestic birds act as amplifiers of the virus, which circulates from one host to another by means of mosquitoes. Wild and domestic mammals are not thought to play a role in the virus cycle because their viremia is low-level and transitory and virus strains isolated from them possess low virulence. In Panama, sloths inoculated with the SLE virus developed prolonged high-titer viremia, but the role of these animals under natural conditions has not been determined. Likewise, bats may be involved in the virus's overwintering within enzootic foci in temperate climates, as well as in its dissemination to epizootic foci, a subject that requires further study.

DIAGNOSIS:

SLE may be confused clinically with other febrile diseases or with encephalitides and aseptic meningitis caused by different agents. Laboratory confirmation is essential. Laboratory diagnosis is based primarily on serology. Only on a few occasions has it been possible to isolate the etiologic agent from the blood of viremic patients. Most successful isolations have been made from the brain of patients who died a short time after contracting the disease.

DIAGNOSIS:

Is based on demonstrating serologic conversion in the patient by comparing titers of serum samples taken during the acute phase with those taken during convalescence. The most widely used tests are complement fixation, neutralization (which is the most specific), and hemagglutination inhibition. Antibodies can be detected during the first week of the disease by the hemagglutination inhibition and neutralization tests, while the complement fixation antibodies appear during the second or third week. In Latin American and Caribbean countries, where infections due to several flaviviruses occur, tests must include all of the other viruses of the group known to be present in the area.

TREATMENT:

Vigorous supportive therapy. Such measures include reduction of intracranial pressure (mannitol), monitoring of intraventricular pressure, the control of convulsions, maintenance of the airway, administration of oxygen, and attention to adequate nutrition during periods of prolonged coma. No antiviral agent is effective for arboviral encephalitis.

CONTROL:

The only preventive measure available is control of the vector. Programs of epidemiologic surveillance and vector control have given satisfactory results in California against C. tarsalis, in Florida against C. nigripalpus, and in Texas against C. quinquefasciatus. An effective vaccine is not yet available.