Viral encephalitis pathophysiology and symptoms PDF

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Encephalitis-A range of viruses can cause encephalitis.Mainly Herpes simplex,Varicella zoster etc.The infection provokes an inflammatory response that involves the cortex, white matter, basal ganglia and brain stem....

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ENCEPHALITIS Viral Encephalitis A range of viruses can cause encephalitis. In Europe, most serious cause of viral encephalitis is Herpes simplex, which probably reaches the brain via the olfactory nerves. Varicella zoster is also an important cause. The development of effective therapy for some forms of encephalitis has increased the importance of clinical diagnosis and virological examination of the CSF. In some parts of the world, viruses transmitted by mosquitoes and ticks (arboviruses) are an important cause of encephalitis. Pathophysiology The infection provokes an inflammatory response that involves the cortex, white matter, basal ganglia and brainstem. The distribution of lesions varies with the type of virus. For eg; in Herpes simplex encephalitis, the temporal lobes are usually primarily affected, whereas CMV (Cyto Megalo Virus) can involve the areas adjacent to the ventricles (Ventriculitis). There is neural degeneration and diffuse glial proliferation, often associated with cerebral oedema. Clinical features: Viral encephalitis presents with acute onset of head ache, fever, focal neurological signs (aphasia and/ or hemiplegia, visual field defects) and seizures. Disturbance of consciousness ranging from drowsiness to deep coma supervenes early and may advance dramatically. Meningism occurs in many patients. Investigations: Imaging by CT scan may show low-density lesions in the temporal lobes, but MRI is more sensitive in detecting early abnormalities. Lumbar puncture should be performed once imaging has excludes a mass lesion. The CSF usually contains excess lymphocytes, but polymorphonuclear cells may predominate in the early stages. The CSF may be normal in upto 10% of cases. Some viruses, including the ‘West Nile virus’ may cause a sustained neutrophilic CSF. The protein content may be elevated but the glucose is normal. EEG is usually abnormal in the early stages, especially in Herpes simplex encephalitis, with characteristic periodic slowwave activity in the temporal lobes. Virological investigations of the CSF, including PCR for viral DNA, may reveal the causative organism, but treatment initiation should not await this. Management: Optimum treatment for Herpes simplex encephalitis (Aciclovir 10mg/kg IV 3 times daily for 2-3 weeks) has reduced mortality from 70% to around 10%. This should be given early to all patients suspected of suffering from viral encephalitis.

Brainstem Encephalitis This presents with ataxia,dysarthria,diplopia or other cranial nerve palsies. The CSF is lymphocytic, with a normal glucose. The causative agent is presumed to be viral. However Listeria monocytogenes may cause a similar syndrome with meningitis and requires specific treatment with ampicillin 500mg 4 times daily.

Japanese B Encephalitis This flavivirus is an important cause of endemic encephalitis in Japan, China, Russia, South-East Asia, India, and Pakistan; outbreak also occur elsewhere. Pigs and Aquatic birds are the virus reservoirs and transmission is by mosquitoes. Exposure to rice paddies is a recognized factor. Incubation period: 4-21 days Clinical features: Most infections are subclinical in childhoods and 1% or less of infections lead to encephalitis. Initial systemic illness with fever, malaise and anorexia is followed by photophobia, vomiting, head ache and changes in brainstem function. Mortality with neurological disease is 25%. Most children die from respiratory failure with infection of brainstem nuclei. Approximately 50% of survivors are left with neurological sequelae. Investigations: Other infectious causes of encephalitis should be excluded. There is neutrophilia and often hyponatraemia. CSF analysis reveals lumphocytosis and elevated protein. Serological testing may be helpful and there is a CSF antigen test. Management: Treatment is supportive, anticipating and treating complications. Vaccination for travelers to endemic areas during the monsoon period is effective prophylaxis. Some endemic countries include this vaccination in their childhood schedule.

Nipah Virus Encephalitis: In 1999, a newly discovered paramyxovirus in the Hendra group, the Nipah virus caused an epidemic of encephalitis amongst Malaysian pig farmers. Natural reservoir: Pteropus bat species

Incubation period: 4-14 days. However an incubation period as long as 45 days has been reported. Symptoms: Human infection range from asymptomatic infection to acute respiratory infection (mild, severe) and fatal encephalitis. Infected people initially develop symptoms including fever, head ache, myalgia, vomiting and sore throat. This can be followed by dizziness, drowsiness, altered consciousness and neurological signs that indicate acute encephalitis. Some people can also experience atypical pneumonia and severe respiratory problems, including acute respiratory distress. Encephalitis and seizures occur in severe cases, progressing to coma within 24 to 48 hours. Most people who survive acute encephalitis make a full recovery, but long term neurologic conditions have been reported in survivors. Approximately 20% of the patients are left with residual neurological consequences such as seizure disorder and personality changes. A small number of people who recover subsequently relapse or develop delayed onset encephalitis. The case fatality rate is 40% to 75%. This rate can vary by outbreak depending on local capabilities for epidemiological surveillance and clinical management. Diagnosis: Nipah virus infection can be diagnosed with clinical history during the acute and convalescent phase of the disease. The main tests used are Real Time Polymerase Chain Reaction (RT-PCR) from bodily fluids and antibody detection via Enzyme Linked Immuno Sorbent Assey (ELISA) test. Other tests include Polymerase Chain Reaction (PCR) assay and virus isolation by cell culture Management: There are currently no drugs or vaccines specific for Nipah virus infection. Intensive supportive care is recommended to treat severe respiratory and neurologic complications.

West Nile Virus Encephalitis The flavivirus has emerged as an important cause of neurological disease in an area that extends from Australia, India and Russia through Africa and Southern Europe and across North America. The disease has an avian reservoir and a mosquito vector. The elderly are at risk of neurological disease. Incubation period: 2-6 days. A prolonged incubation may be seen in immunocompromised individuals.

Clinical features: Most infections are asymptomatic. A mild febrile illness and arthralgia constitute the most common clinical presentation. Children may develop a macula-papular rash. Neurological disease is seen in 1% and is characterized by encephalitis, meningitis or asymmetric flaccid paralysis with 10% mortality. Diagnosis: Diagnosis is by serology or detection of viral RNA in blood or CSF. Serological tests may show cross-reactivity with other flavivirus, including vaccine strains. Management: Supportive.

CMV Encephalitis (CMV= Cyto Megalo Virus) This presents with behavioural disturbance, cognitive impairment and a reduced level of consciousness. Focal signs may also occur. Detection of CMV DNA in the CSF supports the diagnosis. Response to anti-CMV therapy is poor....