Encephalitis literally means brain infection. Strictly speaking, "-itis" means inflammation, which includes redness, swelling, pain, and warmth, and can be due to infection or other types of irritation. The brain can become infected with many different germs, including viruses, bacteria, fungi, and parasites. The symptoms of encephalitis include fever, chills, headache, altered mental status (confusion, delirium, and agitation), stiff neck, nausea, vomiting, seizures, coma (unconsciousness), and death. Viral brain infections are rarely as serious as other kinds of encephalitis.
Japanese encephalitis (JE), St. Louis encephalitis (SLE), and tick-borne encephalitis (TBE) are all caused by viruses in the flavivirus group. The viruses of these diseases are transmitted by mosquitoes or ticks. Each virus is particular to certain regions of the world. The following geographical distributions are typical for each disease: Japanese encephalitis is found in Asia and Australia; St. Louis encephalitis is found in North, Central, and South America. Tick-borne encephalitis is found in Europe and Asia.
JE can be a risk to travelers in rural areas of Japan, where there are 30,000 to 50,000 cases annually. Fewer than one case per year is reported in Americans traveling to or working in Asia. Birds and domestic pigs can carry the virus. Symptoms appear six to eight days after the mosquito bite. JE kills roughly 30% of its victims. Another 30% will have serious and permanent brain damage. A vaccine known as Japanese encephalitis virus vaccine is available, but it is expensive and occasionally causes significant side effects. Ten percent of patients report fever, headache, malaise, rash, and other reactions such as chills, dizziness, muscle pain, nausea, vomiting, and abdominal pain. Twenty percent report pain at the injection site. A few suffer generalized allergic reactions.
SLE is similar to West Nile virus, LaCrosse virus, and eastern and western equine encephalitis. Birds can carry the virus. Symptoms appear five to 15 days after the mosquito bite. It kills 5% to 30% of its victims. Between 1964 and 2005, 4651 cases were reported in the United States. It occurs most often in warmer weather, when mosquitoes abound.
TBE occurs in many parts of Europe and Asia. Several thousand cases are reported every year. The disease can also be acquired from raw cow, goat, and sheep milk, and from the air in infectious disease laboratories. Symptoms appear seven to 14 days after the tick bite. Permanent brain damage occurs in 10% to 20% of patients. Death occurs in only one percent to two percent of victims.
Arthropod, brain infection, chimera, dengue, Flavivirus, genome, Japanese encephalitis, JE, mosquitoes, protease inhibitors, reverse transcriptase inhibitors, St. Louis encephalitis, TBE, Tick-Born encephalitis, ticks.
types of the disease
Japanese encephalitis (JE), St. Louis encephalitis (SLE), and tick-borne encephalitis (TBE) are all caused by viruses in the flavivirus group. The viruses of these diseases are transmitted by mosquitoes or ticks. Each virus is particular to certain regions of the world. The following geographical distributions are typical for each disease: Japanese encephalitis is found in Asia and Australia; St. Louis encephalitis is found in North, Central, and South America; tick-borne encephalitis is found in Europe and Asia.
Vaccine development and improvement: Vaccination has been the primary means by which viral illnesses have been reduced over the past century. Vaccines traditionally have employed a killed or weakened virus that stimulates an immune reaction without causing the disease. Recently molecular biology techniques have been used to increase the safety and potency of vaccines by genetically altering the virus. For example, genes from a dengue virus were spliced into the genome of a harmless virus from the same flavivirus family. These combinations are called chimera. When this chimera was injected into a mouse, the mouse developed antibodies to the dengue virus.
Antiviral drugs: Antiviral drugs have been developed using genetic techniques. Once the gene structure of a virus in known, specific drugs can target the critical genes in the virus that cause it to be infectious. The AIDS virus, for example, has several enzymes (proteins that mediate chemical reactions) that allow it to multiply within human cells. Drugs such as reverse transcriptase inhibitors and protease inhibitors block the action of these enzymes.
Progress in virus research has made great advances in the past several decades. The ability to determine the exact structure of viral molecules is enabling scientists to develop chemicals that precisely target the viral molecules. Progress is also being made in identifying how diseases are spread, so that control of vectors (agents that spread disease like rats and mosquitoes) is becoming more effective. There is always an intricate and complex relationship between disease-causing agents and the hosts that harbor them. These relationships are mediated at the genetic and molecular level and each is very specific to the two organisms involved. Each must have a genetic structure that allows the other to coexist. The host's immune system must not attack the parasite. The parasite must be able to grow in the host's unique environment and must also be able to transfer from the host to a human or other animal where it causes disease.
Diagnostic tests: In the laboratory, many tests are being developed that can identify each virus, so that when treatments become available there will be no delay in using them. Many of these tests rely on identifying proteins or sequences of DNA (deoxyribonucleic acid) or RNA (ribonucleic acids) that are unique to a particular virus, creating a tag molecule that attaches to only that unique sequence and adding to the tag a label such as a fluorescent particle that can be seen. Often these tags are antibodies produced by laboratory animals when challenged with the virus product that has been isolated.
In addition to vaccine and drug development, increasing knowledge of the genetic determinants of viral and arthropod host behavior will inform efforts to eliminate these diseases before they attack humans. Genetic studies of humans will identify specific genetic profiles that are more likely to contract these diseases and more likely to have severe disease, such as those with HIV and other immune deficiencies.