Pathophysiology and pharmacology Introduction Encephalitis and Meningitis are similar and related though different highly fatal infections of the central nervous system (CNS) resulting from blood-borne pathogens which cause inflammation within the system. The virus lies dormant in the ganglion of the trigeminal cranial nerve, but the reason for reactivation, and its pathway to gain access to the brain, remains unclear, though changes in the immune system caused by stress clearly play a role in animal models of the disease. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. The herpes simplex virus causes inflammation on the temporal lobe of the brain, and if not treated, half to three quarters of the patients succumb. The incidence of encephalitis in EV infection is reported to be about 3% and is associated with high mortality and morbidity. A widely accepted view of MS is that it is an inflammatory disease with autoimmune characteristics influenced by environmental or infectious factors in genetically susceptible individuals. However, much of our current understanding of HSV-1 encephalitis pathogenesis comes from rodent models in which intranasal HSV-1 administration results in an acute necrotizing encephalitis that closely resembles human disease [41–45].
EV encephalitis and meningo-encephalitis cases were first reported in late 1950s (most cases in 1959) and they were of non-polio EV and ECV.17,18 Since then many serotypes have been recognized as the causative agent for encephalitis. Encephalitis was considered typical or atypical based on published criteria. Certain arboviruses have a predilection for different geographic areas of the US depending on the climate, mosquito vector and the virus itself. clinical presentation and epidemiology (~10 min) physiological and pathophysiological mechanisms, including biological mechanisms in common with other diseases/ disorders/ conditions (40-45 min) current therapies AND/OR strategies for developing future therapies: the role of “translational research”; design and conduct of patient-oriented research AND/OR any relevant ethical issues in clinical research, and/or ethics of particular clinical trial designs in specific patient populations (~10 min) patient visits (when possible) Class format “Typical” class format: 60 min: faculty lecture 30 min: informal discussion by students of assigned review paper with course directors leading discussion. Louis, MO: Elsevier. Between 1,500 and 3,000 cases of viral encephalitis are reported to the Centers for Disease Control and Prevention (CDC) each year, but most doctors think that the actual number of cases is higher. Many other viruses are capable of causing acute encephalitis including other members of the Herpes virus family, enteroviruses, mumps, LCM, adenovirus, and postvaccinal.
1.3. Clinical Manifestations Meningoencephalitis usually begins with the acute onset of fever, headache, vomiting and stiff neck. Earlier treatment improves the chances of a good recovery. Thus, a single amino acid change in WNV has led to rapid geographic expansion and increased intensity of transmission. The CSF may vary between several hundred and several thousand white blood cells. Generally there is a lymphocyte predominance but Eastern Equine Encephalitis may have a polymorphonuclear predominance, especially in the early stages. Secondary progressive MS is marked by a gradual progression of symptoms with or without occasional relapses and minor remissions.
Such upregulation was not specific to this neurotropic alphaherpesvirus as the leukotropic gammaherpesvirus, MHV-68, was also capable of elevating DAI expression by both cell types. simplex). Herpes simplex encephalitis frequently has a temporal lobe focus on EEG, brain scan, CAT scan, MRI or arteriogram. The CSF frequently shows several thousand red blood cells in addition to a mildly elevated WBC. The glucose may be slightly depressed. Because viral encephalitis involves the brain diffusely, such processes like secretion of inappropriate ADH may occur with resultant hyponatremia. These types of encephalitis include West Nile virus, Japanese encephalitis, equine encephalitis, La Crosse encephalitis, and St.
Diagnosis Presence of HSV DNA in CSF detected by PCR is best means to make a diagnosis of HSV encephalitis. Arboviral infection detected by serum antibody of CSF, culture of CSF or serum antibody. Enteroviruses can be cultured from CSF, stool, and throat wash. 1.5. Furthermore, NS1, a non-structural glycoprotein that is absent from the virion but expressed on the surface of infected cells, elicits non-neutralizing protective antibodies that inhibit infection through both Fc-γ receptor–dependent and -independent mechanisms . 1.6. Prognosis In contrast to aseptic meningitis the morbidity and mortality for encephalitis is considerable.
The recent detection of different patterns of demyelination (48, 95, 96) suggests a possible heterogeneity in the mechanisms involved in lesion development. For example, the overall mortality for arboviral encephalitis in the United States between 1955 and 1971 was 50% for Eastern Equine Encephalitis (EEE), 8% for St. Louis Encephalitis (SLE), 2.9% for Western Equine (WE) and 0.4% for California (CE). include source? The mortality for untreated Herpes simplex encephalitis is 70%.With current therapy, acyclovir, the mortality can be reduced to about 15-20% but there may be considerable morbidity with long term neurologic sequelae, especially if the onset of treatment is delayed. In children with WEE who were < 1 year of age at the onset of infection, 57% developed either mental retardation, paralysis, seizures, spasticity, speech difficulties, hearing defects. The most treatable form of viral encephalitis is Herpes simplex. An EEG is a test that measures patterns of electrical activity in the brain. It is a flavivious like St. Louis Encephalitis, Japanese Encephalitis and Dengue. Clinical manifestations similar to other viral encephalitides except profound weakness, lower motor neuron symptoms common. Most severe illness in elderly. This may explain the relatively narrow therapeutic window for IFN administration that has been observed in animal models or humans infected with WNV . Rabies can present as a form of encephalitis.The virus is transmitted from animals to humans by salivary contamination of a bite or wound.Dogs, cats, bats and other animals may transmit the disease. The virus is neurotropic. MS has been typically considered a Th1-driven disease. The incubation period can be weeks to months, and rarely even longer. Diagnosis can be made by antibody determination, or immunofluorescence staining of impression smear of cornea, nerve biopsy or brain Bx. Pathognomonic Negri bodies may be present. Clinical findings may be an encephalitis, personality change, agitation and eventually coma. It is uniformly fatal. Spasms on feeding or water exposure (hydrophobia) are classic findings, but are not always present and may be late findings. • Patients who are having seizures are given anticonvulsants (antiseizure drugs). It is uniformly fatal. Spasms on feeding or water exposure (hydrophobia) are classic findings, but are not always present and may be late findings.laxis of wound exposure with wound washing, rabies vaccine and human rabies immunoglobulin should be given when appropriate. Creutzfeldt-Jakob disease (CJD) is a spongiform encephalopathy related to scrapie of sheep, bovine spongiform encephalopathy (BSE) and kuru. The disease appears to be due to an infectious fibrillar protein called prion protein. Mechanisms of evasion by WNV include the following: (a) reduction in IFN-β gene transcription by the viral NS2A protein; (b) impairment of RIP-1 signaling by high mannose carbohydrates on the structural E protein and attenuation of TLR3 signaling by NS1; and (c) a delay in recognition of WNV RNA by RIG-I. Infectivity associated with abnormal variant prion protein (PrPsc). Genes for normal prion protein (prp) found in all animals. Moreover, focal BBB breakdown seems to precede the development of most lesions (94). Presumed that infectious prpsc initiates irreversible conversion of host PRP to abnormal form. Transmission is thought to be due to contaminated food. Nosocomial cases have occurred due to contaminated instruments, contaminated human growth hormone. The incubation period is years. New variant CJD diagnosed in 1995, 10 years after BSE. Disease is manifest by rapid onset of presenile dementia. People planning a trip to Japan or eastern Asia may want to consider being vaccinated before departure. Clumsiness, ataxia, tremor are followed by intellectual and motoryoung adults. There is no therapy. The only effective means of disinfection is autoclaving infected material (brain or CSF). Other form of chronic encephalitis may rarely occur in association with infection or vaccine administration. Thus, CCR5 functions as an essential host factor to resist neuroinvasive WNV infection, which may have implications for the use of CCR5 antagonists in HIV therapy. There are also rare chronic encephalitides associated with varicella-zoster infection, and rubella.