encephalitis(redirected from toxoplasma encephalitis)
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encephalitis(ĕnsĕf'əlī`təs), general term used to describe a diffuse inflammation of the brain and spinal cord, usually of viral origin, often transmitted by mosquitoes, in contrast to a bacterial infection of the meninges (membrane surrounding the brain and spinal cord), known as meningitismeningitis
or cerebrospinal meningitis
, acute inflammation of the meninges, the membranes that cover and protect the brain and spinal cord. It can be caused by bacteria, viruses, fungi, or other organisms, usually introduced via the bloodstream from infections
..... Click the link for more information. . Diagnostic symptoms include capillary congestion, small hemorrhages into perivascular spaces, accumulation of plasma cells and lymphocytes, and increased pressure and protein content of cerebrospinal fluid.
Among the several forms of viral brain inflammation are rabies, polio, and two types transmitted by the mosquito: equine encephalitisequine encephalitis
, infectious disease of horses caused by any of several viruses, three of which—the Eastern, Western, and Venezuelan viruses—can also infect humans.
..... Click the link for more information. in its various forms and St. Louis encephalitis. The latter two have appeared in epidemic form in the United States and are characterized by high fever, prolonged coma (which is responsible for the disease being known as a "sleeping sickness"), and convulsions sometimes followed by death. Encephalitis that results as a complication of another systemic infection is known as parainfectious encephalitis and can follow such diseases as measles (rubeola), influenza, and scarlet fever. The AIDS virus also infects the brain and produces dementia in a predictably progressive pattern. Although no specific treatment can destroy the virus once the disease has become established, many types of encephalitis can be prevented by immunization.
any one of a group of inflammatory diseases of the human and animal brains caused mainly by viruses, bacteria, protozoans, and other pathogenic microorganisms.
A distinction is made between primary and secondary encephalitides. Primary encephalitides include diseases that develop after penetration of the brain by neurotropic viruses (epidemic encephalitis, Russian spring-summer encephalitis, Semliki forest encephalitis, herpes encephalitis, and zoster encephalitis). The existence of a natural reservoir of virus (usually rodents and birds), virus transmitters (mosquitoes and ticks), and associated natural focality and seasonality are characteristic of most primary encephalitides. The causative agents of primary encephalitides penetrate the brain through the blood and, less commonly, the nerve fibers.
Secondary encephalitides result from brain lesions caused by local or systemic infection, for example, rheumatism, influenza, measles, rubella, and chicken pox. Sensitization to the particular antigen produced by some infections seems to be the decisive factor in the development of secondary encephalitides. The inflammatory process may involve chiefly the white or gray matter of the brain (cranial nerves and subcortical ganglia), as in epidemic lethargic and Russian spring-summer encephalitides.
The course of most encephalitides is acute. The most common symptoms are elevated body temperature, headache, nausea, and vomiting; blackouts, convulsions, and other neurological disturbances (paresis and loss of sensitivity and cranial nerve function) frequently occur. Injury to the oculomotor nerves and drowsiness are characteristic of lethargic encephalitis (also called von Economo’s disease after C. von Economo, who described it). Hyperkinesia and other disorders are associated with rheumatic encephalitis. The acute stage is sometimes followed by the appearance of new or the intensification of existing neurological symptoms, for example, the development of postencephalic parkinsonism in epidemic encephalitis. The prognosis is unfavorable for sclerotic encephalitis, which occurs in young children and teen-agers and is characterized by loss of memory, mental retardation, epileptic seizures, and other symptoms. Purulent and necrotizing encephalitides, in which large portions of the brain die, also have an unfavorable prognosis.
Muscular weakness, numbness, and elevated body temperature persisting for several days usually appear in Russian spring-summer encephalitis ten to 12 days after the bite of an infected tick in a natural focus of the disease. Paresis or paralysis of the neck and shoulder muscles, involvement of cranial nerves, and symptoms of meningeal irritation are characteristic. The course of the disease is often mild.
Drugs with anti-inflammatory, antimicrobial, and desensitizing action (hormones, salicylates, antibiotics, sulfanilamides, dimedrol) are used to treat encephalitides. The prevention of encephalitides characterized by natural focality requires control of transmitters of the disease, immunization, and individual protection against ticks and mosquitoes (repellents, protective clothing).
REFERENCESNeirovirusnye infektsii. Leningrad, 1954.
Panov, A. G. Kleshchevoi entsefalit. Leningrad, 1956.
Petrishcheva, P. A., E. N. Levkovich, and S. T. Boldyrev. laponskii entsefalit. Moscow, 1963.
Tsuker, M. B. Meningity i entsefality u detei. Moscow, 1975.
Encephalitides. Edited by L. van Bogaert. Amsterdam, 1961.
V. A. KARLOV