This information is taken from the Book “Understanding Encephalitis” by Elaine Dowell.  The book is available from Amazon Understanding Encephalitis.

More than 100 infectious agents are known to cause Infectious Encephalitis and this number could increase with emerging infections.   The most common global causes include herpes simplex virus (HSV), varicella zoster virus (VZV), enteroviruses, measles virus, mumps virus, Japanese encephalitis virus (JEV), influenza virus, adenovirus, echovirus and mycoplasma pneumonia.   However, vaccination against mumps and measles is substantially reducing the number of encephalitis cases associated with those diseases.

 There are several types of encephalitis in which the virus is transmitted by mosquitoes or ticks (these insects are also known as arthropods).  The viruses that are transmitted in this way are called arboviruses (Arbovirus is short for arthropod-borne virus.) The viruses are transmitted when the insect bites infected animals then people. The different types of encephalitis that result are usually named for the place the virus was discovered or the animal species that typically carries it.  Examples are West Nile Virus encephalitis, Tick borne encephalitis, Japanese encephalitis and Murray Valley encephalitis.

 Sometimes bacteria, parasites and fungi cause encephalitis, but these are very rare and usually only occur in people who are immunocompromised: that is people who have AIDS , people undergoing chemotherapy, people taking drugs to prevent rejection following transplantation and people who have certain diseases that significantly lower their ability to fight disease.

 Subacute infectious encephalitis is a rare chronic form of encephalitis.  It occurs years after an initial infection. Examples are progressive rubella panencephalitis, a rare condition that occurs some 8 to 19 years after congenital or perinatal rubella and subacute sclerosing panencephalitis (SSPE) that occurs some years after a measles infection.

 Perhaps the most challenging aspect of encephalitis for patients, families and clinicians is that, despite the many infectious organisms known to cause encephalitis, in many cases none is found.



In-Depth Report on the West Nile Virus and Encephalitis  ( from the New York Times, August 2012)

Research Paper links are to a pdf if the article is free and to the Pubmed page is the article is not free

The Long-term outcomes of Human West Nile Virus Infection Abstract: Since its introduction to North America in 1999, human infection with West Nile virus (WNV) has resulted in considerable acute morbidity and mortality. Although the ongoing epidemic has resulted in a great increase in our understanding of the acute clinical features of human illness and helped to define associated clinical syndromes, far less is known about potential long-term clinical and functional sequelae. Several recent assessments, however, suggest that patients–even those with apparently mild cases of acute disease–frequently have subjective, somatic complaints following WNV infection. Persistent movement disorders, cognitive complaints, and functional disability may occur after West Nileneuroinvasive disease. West Nile poliomyelitis may result in limb weakness and ongoing morbidity that is likely to be long term. Although further assessment is needed, the long-term neurological and functional sequelae of WNV infection are likely to represent a considerable source of morbidity in patients long after their recovery from acute illness.

Herpes simplex encephalitis in Iceland   Abstract – Herpes simplex encephalitis (HSE) is a serious disease with 10-20% mortality and high rate of neuropsychiatric sequelae. This study is a long-term, nationwide study in a single country, Iceland. Clinical data were obtained from patient records and from DNA PCR and antibody assays of CSF. Diagnosis of HSE was classified as definite, possible or rejected based on symptoms, as well as virological, laboratory and brain imaging criteria. A total of 30 definite cases of HSE were identified during the 25 year period 1987-2011 . Males were 57% of all patients, median age 50 years (range, 0-85). Fever (97%), cognitive deficits (79%), impaired consciousness (79% with GCS < 13), headache (55%) and seizures (55%) were the most common symptoms. Brain lesions were found in 24 patients (80%) by MRI or CT. All patients received intravenous acyclovir for a mean duration of 20 days. Three patients (10%) died within one year and 21/28 pts (75%) had a Karnofsky performance score of <70% with memory loss (59%), dysphasia (44%), frontal symptoms (44%) and seizures (30%) as the most frequent sequelae. Mean delay from onset of symptoms to treatment was 6 days; this was associated with adverse outcome. In conclusion, the incidence of `HSE is higher than recently reported in a national registry study from Sweden. Despite advances in rapid diagnosis and availability of treatment of HSE, approximately three of every four patients die or are left with serious neurological impairment. 

Tick-borne encephalitis: A review of epidemiology, clinical characteristics, and management.  Abstract – Tick-borne encephalitis is an infection of central nervous system caused by tick-borne encephalitis virus transmitted to humans predominantly by tick bites. During the last few decades the incidence of the disease has been increasing and poses a growing health problem in almost all endemic European and Asian countries. Most cases occur during the highest period of tick activity, in Central Europe mainly from April to November. Tick-borne encephalitis is more common in adults than in children. Clinical spectrum of the disease ranges from mild meningitis to severe meningoencephalitis with or without paralysis. Rare clinical manifestations are an abortive form of the disease and a chronic progressive form. A post-encephalitic syndrome, causing long-lasting morbidity that often affects the quality of life develops in up to 50% of patients after acute tick-borne encephalitis. Clinical course and outcome vary by subtype of tick-borne encephalitis virus (the disease caused by the European subtype has milder course and better outcome than the disease caused by Siberian and Far-Easter subtypes), age of patients (increasing age is associated with less favorable outcome), and host genetic factors. Since clinical features and laboratory results of blood and cerebrospinal fluid are nonspecific, the diagnosis must be confirmed by microbiologic findings. The routine laboratory confirmation of the tick-borne encephalitis virus infection is based mainly on the detection of specific IgM and IgG antibodies in serum (and cerebrospinal fluid), usually by enzyme-linked immunosorbent assay. There is no specific antiviral treatment for tick-borne encephalitis. Vaccination can effectively prevent the disease and is indicated for persons living in or visiting tick-borne encephalitis endemic areas.

Epidemiology of Japanese encephalitis past, present and future prospects  Abstract – Japanese encephalitis (JE) is one of severe viral encephalitis that affects individuals in Asia, western Pacific countries, and northern Australia. Although 67,900 JE cases have been estimated among 24 JE epidemic countries annually, only 10,426 have been reported in 2011. With the establishment of JE surveillance and vaccine use in some countries, the JE incidence rate has decreased; however, serious outbreaks still occur. Understanding JE epidemics and identifying the circulating JE virus genotypes will improve JE prevention and control. This review summarizes the current epidemiology data in these countries.