Essay: ARBOVIRAL ENCEPHALITIS

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  • Subject area(s): Health essays
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  • Published on: November 9, 2015
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  • ARBOVIRAL ENCEPHALITIS
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Introduction
Encephalopathy is a term used to describe general brain dysfunction due to edema and neural degeneration. This disease can result from alcohol hepatitis, an alteration in blood chemistry, particularly electrolyte imbalance, and an increase in toxic chemicals that affect the central nervous system (CNS). A category of viruses, the arboviruses, can also cause encephalitis.
The term arboviruses is defined as arthropod-borne viruses [2]. There are three families of arboviruses: the Bunyaviridae, Flaviviridae, and Togaviridae. These viruses require amplifying hosts, such as birds, and dead-end hosts, such as horses and humans. As a virus amplifies in birds, they are incidentally transmitted to horses and humans through arthropods, such as mosquitoes and ticks. In the arthropods, the virus live in a symbiotic relationship. Upon transmission to horses and humans, it is unable to cope due to immune responses and causes encephalitis. [3].
In this section, we will be focusing on the complexity of arboviral encephalitis in humans in terms of its pathophysiology, clinical manifestations, and medical management.
Pathophysiology
Initial arboviral infection in humans results in amplification of the viral genome, an RNA strand, in either the skin or the muscle. As a result of the amplification, primary viremia occurs. Viremia is the term that describes the presence of viral particles in the blood [4].
Different viruses have different mechanisms for invading the CNS. Some do so by attacking the lymphatic system, after which macrophages and monocytes initiate an immune response that is carried out by the body. Following the immune response, secondary viremia arises [4]. The virus then travels from the lymph and thoracic ducts into the blood and it may travel to the bone marrow for further replication. Following replication, it will continue circulating in the blood before reaching the CNS [2].
Other viruses enter the CNS through the olfactory pathway, the cerebral epithelial cells surrounding the blood-brain barrier (BBB), or by budding off the parenchymal cells at the BBB [2].
The BBB is responsible for protecting the CNS from foreign objects but the arboviral particles are able to infiltrate the barrier. The microglial cells of the CNS, which are responsible for recognizing the viral penetration, mediate an immune response through both pro- and anti-inflammatory cytokines. However, the immune response results in inflammation of the endothelial cells which results in vascular congestion and can eventually lead to hemorrhage, demyelination of the neurons, and apoptosis of the glial cells [4]
Clinical Manifestations
The manifestations of arboviral infection varies from one individual to the next because of age, environment, the type of arthropod that delivers the infection, and the individual’s genes and immune status. The early symptoms of arboviral infection includes those common to many other diseases: a fever and a headache. Severe manifestations include muscle pain, muscular incoordination, coma [2], and seizures [4].
Clinical tests can be performed to confirm the presence of an arbovirus. Such tests include blood samples, cerebral spinal fluid analysis, and MRI and CT scan of the brain and spine [4].
Advances in Medical Management
The immune system is responsible for fighting and destroying foreign objects, however because there are different classifications of the viruses, a single immune response cannot provide protection against all the arboviral strains. Furthermore, the number of available vaccines are very limited and are confined to the United States military and the laboratories because of the infection risk associated with testing and the high production cost [4].
Different vaccination approaches are being analyzed to determine which approach seems most effective in suppressing the arboviruses. Several approaches include subunit vaccines, chimeric recombinants, and gene deleted live mutants. [3]. Subunit vaccines do not include the entire virus but only the antigen. Live chimeric recombinants are a mixture of the genomes of two viruses that may or may not display the biological properties of both viruses. The gene deleted live mutants involve the deletion of the E2 protein, an essential protein of some arboviruses that is involved in allowing the virus to attach to endosomes to be engulfed into human cells [5]. There are advantages and disadvantages in the various vaccination techniques but regardless, these vaccines need to be tested on animal models, such as horses with encephalitis, to provide promising results before human use to treat arboviral encephalitis [4].
If proper measures are taken, it is possible to control outbreaks. Such measurements include insecticide spraying, utilizing insect repellent, and remaining indoors during the hot seasons when mosquitoes are likely to be outdoors [2].
Conclusion
Easily transmitted from amplifying hosts to dead-end host through arthropods, they are also capable of disrupting the blood-brain barrier and infiltrating the central nervous system. Once inside, they can cause hemorrhage, demyelination, and apoptosis of the glial cells, eventually leading to encephalitis.
Because they exist with various RNA genomes, it is difficult to vaccinate an individual against all species but different vaccinations are being studied and a suitable animal model is being searched for before the vaccines can be put into human practice.
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