Encephalitis is an acute inflammation of the brain. Encephalitis with meningitis is known as meningo encephalitis. Symptoms include headache, fever, confusion, drowsiness, and fatigue. Further symptoms include seizures or convulsions, tremors, hallucinations, stroke, and memory problems. In 2013 encephalitis was estimated to have resulted in 77,000 deaths, down from 92,000 in 1990. Adult patients with encephalitis present with acute onset of fever, headache, confusion, and sometimes seizures. Younger children or infants may present irritability, poor appetite and fever. Neurological examinations usually reveal a drowsy or confused patient. Stiff neck, due to the irritation of the meninges covering the brain, indicates that the patient has either meningitis or meningo encephalitis. The signs and symptoms of tick born encephalitis are: The virus can infect the brain (encephalitis), the meninges (meningitis) or both (meningoencephalitis). In general, mortality is 1% to 2%, with deaths occurring 5 to 7 days after the onset of neurologic signs. In dogs, the disease also manifests as a neurological disorder with signs varying from tremors to seizures and death. In ruminants, neurological disease is also present, and animals may refuse to eat, appear lethargic, and also develop respiratory signs.
Epidemiological and occurrence of potential arthropod-borne encephalitis viruses circulating in the Amazon Region of Brazil are discussed. These viruses are the Eastern Equine Encephalitis (EEE), Western Equine Encephalitis (WEE), St. Louis Encephalitis (SLE), Mucambo (MUC) and Pixuna (PIX). These last two are subtypes (III and IV) of Venezuelan Equine Encephalitis virus. The areas of study were the highways and projects of development, as well as places where outbreaks of human diseases caused by arboviruses had been detected. These viruses are widespread in all Amazonia, and at least four of them, EEE, WEE, SLE and MUC are pathogenic to man. EEE and WEE infections were detected by serology, while SLE and MUC by either serology and virus isolation. The PIX virus has the lowest prevalence and, it was isolated in only a few cases, one being from a laboratory infection. Wild birds are the main hosts for all these viruses, except MUC, whose major hosts are rodents. The symptoms presented by infected people were generally a mild febrile illness. Although, jaundice was observed in two individuals from whom SLE was isolated. A comparison of the clinical symptoms presented by the patients in the Amazon Region and other areas of America, especially in the USA is made. In Brazilian Amazon region epidemics have not been detected although, at least, one EEE epizootic was recorded in Bragança, Para State, in 1960. At that time, of 500 horses that were examined 61% were positive to EEE by HI and of them 8.2% died. On the other hand, SLE has caused four epizootics in a forest near Belem. Wild birds and sentinel monkeys were infected, but no human cases were reported. Overall, 415 (55.1%) of the 753 horses that were screened were seropositive for fl avivirus and, among them, monotypic reactions were observed to SLEV in 93 (12.3%) and to ROCV in 46 (6.1%).
These results suggested that these viruses, or other closely related viruses, are infecting horses in Brazil. None of the studied horses presented infected symptoms of central nervous system. 4. Advanced Treatment Methods: Advanced treatment is as follows: Antiviral medications, Antibiotics, Steroids are used to reduce brain swell, Sedatives for restlessness, Acetaminophen for fever, Physical therapy. The disease is incurable once manifested, so there is no specific drug therapy for TBE. Symptomatic brain damage requires hospitalization and supportive care based on syndrome severity. Anti-inflammatory drugs, such as corticosteroids, may be considered under specific circumstances for symptomatic relief. Tracheal intubation and respiratory support may be necessary. Prevention includes non-specific (tick-bite prevention, tick checks) and specific prophylaxis in the form of a vaccine. TBE immunoglobulin is no longer used. Tick-borne encephalitis vaccine is very effective and available in many disease endemic areas and in travel clinics. There is no specific treatment for Japanese encephalitis and treatment is supportive, with assistance given for feeding, breathing or seizure control as required. Raised intracranial pressure may be managed with mannitol. There is no transmission from person to person and therefore patients do not need to be isolated. A breakthrough in the field of Japanese encephalitis therapeutics is the identification of macrophage receptor involvement in the disease severity. A recent report of an Indian group demonstrates the involvement of monocyte and macrophage receptor CLEC5A in severe inflammatory response in Japanese Encephalitis infection of the brain. This transcriptomic study provides a hypothesis of neuro inflammation and a new lead in development of appropriate therapeutic against Japanese encephalitis. Anti-viral medications are effective for treating herpes encephalitis. However, they have not yet been shown to work for other forms. Instead, treatment often focuses on relieving symptoms, using: pain killers, corticosteroids (to reduce brain inflammation), mechanical, ventilation, or breathing treatments, lukewarm sponge baths, anticonvulsants, sedatives (for seizures, restlessness, aggressiveness, and irritability), rest and fluids.