Western equine encephalitis

Introduction to Western equine encephalitis Western equine encephalitis (WEE) is a human-to-human viral disease caused by Western equine encephalitis virus. In 1930, Meger isolated the virus from the equine encephalitis. In 1937, the virus was isolated from the brain tissue of a child who died of encephalitis. It was first discovered in the western United States and was called western equine encephalitis. The main clinical manifestations are similar to those of oriental equine encephalitis, but they are lighter than Eastern equine encephalitis and have a low mortality rate. basic knowledge Sickness ratio: 0.05% Susceptible people: no specific population Mode of transmission: insect vector transmission Complications: coma

Western equine encephalitis

(1) Causes of the disease

Like the Eastern equine encephalitis virus, Western equine encephalitis belongs to the arbovirus group A. There are two representative strains: one is Mc Millan strain, which is isolated from the western population; one strain is Highland strain, which is isolated from birds, and the two antigenicity are significantly different, and the antigenicity between the virus strains There are also regional differences.

(two) pathogenesis

After being bitten by an infected arthropod, the virus replicates in local tissues and local lymph nodes. The occurrence and persistence of viremia depends on the stage of viral replication in local tissues outside the nervous system, the speed at which the mononuclear-macrophage system clears the virus, and the specificity. The emergence of sexual antibodies, and thus the clinical manifestations of large differences.

The brain is filled with blood and water, and has extensive neuronal degeneration. There are multiple hemorrhagic foci in the brain tissue. Microscopic examination shows degeneration and necrosis of nerve cells, lymphocytes around the blood vessels, monocytes and polymorphonuclear leukocytes infiltrate, forming " Perivascular sleeves, some glial cell hyperplasia and polymorphonuclear leukocyte accumulation form nodules, lesions mainly found in the basal ganglia of the brain, brain gray matter and white matter, can also invade the cerebellum and spinal cord.

Western equine encephalitis prevention

The main measures are anti-mosquito and vaccination. It is especially important for infants and pregnant women. This disease is prevalent in the horse population before it is prevalent in the world. Livestock poultry can be injected with inactivated monovalent or bivalent, trivalent vaccine to reduce Animals are poisoned, which has reduced the prevalence of the population. The inactivated vaccine for human use is still under development.

Western equine encephalitis complications Complications

Coming in a coma and dying.

Western equine encephalitis symptoms common symptoms behavior and emotional abnormalities personality changes mental disorders emotional ups and downs, intelligent decline, quadriplegia

The course of western equine encephalitis is 3 to 5 days, mostly in 8 to 14 days. Adults have no sequelae. The sequelae of infants and young children often have low intelligence, emotional instability, toughness of limbs, and elderly patients with mental disorders and personality. change.

Western examination of equine encephalitis

Blood picture

The number of white blood cells decreased at the beginning of the disease, and the total number of white blood cells increased after entering the extreme stage, (1.0 ~ 2.0) × 10 ⁹ / L, neutrophils more than 0.80, and then converted to lymphocytes.

2. Cerebrospinal fluid

Colorless and clear, about half of the pressure is slightly higher, the number of cells is mostly below 200×10 ⁶ /L, and the individual can reach 500×10 ⁶ /L or more. The number of cells is the highest in the first week of the disease course, and then gradually decreases, and the early stage is neutral. Granulocytes are predominant, and they turn to lymphocytes, with slightly higher protein and normal sugar and chloride.

In recent years, RT-PCR has been used to detect viral RNA with high sensitivity and specificity, which can rapidly diagnose this disease early.

Diagnosis and identification of western equine encephalitis

The disease is the same as Eastern equine encephalitis. The diagnosis mainly depends on epidemiological data and serological examination. The clinical symptoms and signs of this disease cannot be distinguished from St. Louis encephalitis. The diagnosis depends mainly on double serum complement binding test or hemagglutination inhibition test. Whether it is 4 times higher or not, in recent years, the enzyme-specific IgM is detected by enzyme-linked immunosorbent assay. The antibody can be detected 1 day after the disease and lasts for 3 months. This method is often used as an early rapid diagnosis from the patient's serum and cerebrospinal fluid. The isolation of Western equine encephalitis virus is rarely successful. If the patient dies, the brain tissue can be used for virus isolation. If positive, the diagnosis can be confirmed. In 1956, the western equine encephalitis virus was isolated from the brain tissue of patients with similar encephalitis. In 1957, the virus antibody was detected from bovine serum, but no case report was reported. Whether there is an infection of group A arbovirus in nature and in the population needs further confirmation.

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