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Encephalitis is an acute inflammation of the brain, commonly caused by a viral infection. Sometimes, encephalitis can result from a bacterial infection, such as bacterial meningitis, or it may be a complication of other infectious diseases like rabies (viral) or syphilis (bacterial). Certain parasitic protozoal infestations, like by toxoplasma, can also cause encephalitis in people with compromised immune systems. more...

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Patients with encephalitis suffer from fever, headache, vomiting, confusion, drowsiness and photophobia. The patients could also suffer from weakness, seizure, and less commonly, stiffness of the neck. Rarely, the patients may have limb stiffness, slowness in movement and clumsiness, depending on the specific part of the brain involved. The symptoms of encephalitis are caused by the brain's defense mechanisms activating to get rid of the infection, including swelling, small bleedings and cell death.


Victims are usually exposed to viruses resulting in encephalitis by insect bites or food and drink. The most frequently encountered agents are arboviruses (carried by mosquitoes or ticks, see also tick-borne meningoencephalitis) and enteroviruses (coxsackievirus, poliovirus and echovirus). Some of the less frequent agents are measles, rabies, mumps, varicella and herpes simplex viruses. Incidentally type 3 Lyssavirus (Mokola virus), found in Australia, causes a lethal encephalitis which hardly resembles rabies. Numerically, the most important cause of encephalitis worldwide is probably Japanese encephalitis, as it causes up to 50 000 cases a year, with about 15 000 deaths. Japanese encephalitis affects East and Southeast China, Korea, Japan, Taiwan, Southeast Asia, Papua New Guinea, South Asia and even Northern Australia. The most widespread cause of encephalitis worldwide, however, is Herpes Simplex encephalitis. 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. In very young children, however, the virus could affect any part of the brain, even sparing the temporal lobe.

An interesting cause of viral encephalitis is the Nipah virus. It was first discovered in Malaysia among the pig farmers in 1998 - 1999. Since then it has been reported in Bangladesh. The virus probably originates from fruitbats, which is widespread in South and Southeast Asia.


Neurologic examination usually reveals a stiff neck due to the irritation of the meninges covering the brain. Examination of the cerebrospinal fluid obtained by a lumbar puncture procedure reveals increased amounts of proteins and white blood cells with normal glucose. A CT scan examination is performed to reveal possible complications of brain swelling, brain abscess or bleeding. Lumbar puncture procedure is performed only after the possibility of prominent brain swelling is excluded by a CT scan examination.


Treatment is usually symptomatic. Reliably tested specific antiviral agents are available only for a few viral agents (e.g. aciclovir for herpes encephalitis) and are used with limited success. In patients who are very sick, supportive treatment, such as mechanical ventilation, is equally important.


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Tick-borne encephalitis in Southern Norway
From Emerging Infectious Diseases, 3/1/04 by Peter A. Csango

The first five cases of human tick-borne encephalitis in Norway were reported from Tromoya, in Aust-Agder County. Serum specimens from 317 dogs in the same geographic area were collected. An enzyme immunoassay demonstrated antibody to human tick-borne encephalitis virus in 52 (16.4%) of the dogs, which supports the notion of an emerging disease.


First described in humans in Austria (1), tick-borne encephalitis (TBE) is rapidly becoming a growing public health problem in Europe (2). Although observations indicated antibody presence in humans in southern Norway (3), this country has been absent from maps visualizing TBE-endemic areas. This situation may be changing. The first case of clinically manifest TBE in humans in Norway was reported in 1998 (4). Four additional cases were described from 1998 to 2001; all five cases were from Tromoya in Aust-Agder County of southern Norway (5). Infected dogs indicate that TBE virus (TBEV) is present in different geographic areas. The first case of TBE in dogs was reported by Lindblad in Sweden (6), and later by others in Central Europe (7). We investigated and found TBEV immunoglobulin (Ig) G in dogs in southern Norway, an area where this virus was not previously considered endemic.

The Study

From 1992 to 2000, we collected serum samples from 317 (65 breeds, 146 male, 171 female) dogs seen at a veterinary clinic in Arendal, in southern Norway. The laboratory received 436 serum specimens. In case of multiple specimens from one dog, collected during several months or years, we controlled the results for possible changes in antibody levels.

We used two different enzyme-linked immunosorbent assay (ELISA) techniques. The presence and level of IgG antibodies to TBEV were tested by an enzyme immunoassay for the detection of IgG antibodies to TBEV (Enzygnost Anti-TBE virus IgG, Dade Behring Marburg GmbH, Marburg, Germany). Antibody levels [greater than or equal to]: 100 were considered positive. Controls were obtained from the laboratory InVitro (InVitro, Vienna, Austria). IgG to TBEV was detected by a specific sheep, anti-dog, heavy and light chain IgG antibody (A40-105P-7, Bethyl Laboratories, Montgomery, TX) in a dilution of 1:20,000. Positive specimens were confirmed by a second ELISA (Baxter-Immuno, Orth, Austria), as previously described (7). In this assay, titers [greater than or equal to] 100 were considered to be positive.


A total of 52 (16.4%) of 317 dogs had IgG antibodies to TBEV; 40 (12.6%) had IgG antibody titers to TBEV [greater than or equal to] 450, while 12 dogs (3.8%) had moderate levels ([greater than or equal to] 100-< 450) (Table 1). Positive serum specimens, including samples with 11 to < 100 U in the enzymeimmunoassay (EIA)-E test, were confirmed with the Baxter-Immuno (B-I) test (Table 2). The confirmatory test included five extra serum samples in instances where such blood samples were drawn; thus the number of positive specimens to be confirmed was 57.

We could not confirm one result (no. 287) with 116 U in the Enzygnost (EIA-E) by the Immuno ELISA. Of the low-positive specimens in the Enzygnost (<100 U), only four specimens had low-positive results in the B-I ELISA; all others were negative. Four low-positive EIA-E specimens gave positive results in the B-I test. On the other hand, 9 low-positive specimens in the EIA-E (20-37 U) were negative by the B-I test.

The codes were not broken until after the experiments were performed. Thus serum specimens sampled and coded at different times were in some cases collected from a single dog. Nevertheless, high positive antibody levels were reproducible even after several years. In five instances, we had two or more serum specimens from one dog with high positive results at our disposal. All these samples were tested by both ELISA techniques.

Only results of [greater than or equal to] 450 U in the Enzygnost test could be registered, which in two instances gave lower results in the new specimens. The Immuno ELISA was in agreement with the Enzygnost in case A, and it showed stable titers in case B. In cases C and D, one could observe an increase in titers by the B-I test. We observed seroconversion in three cases.

The average age of the dogs at the time of blood sampling was 6.6 years (0.5-15). The 52 dogs with [greater than or equal to] 100 U were 8.02 years versus dogs with < 100 U, which were younger, 6.29 years. The distribution of antibodies according to the size of the dogs is shown in Table 3. A total of 34 (21.8%) of 151 large dogs had antibodies to TBEV [greater than or equal to] 100 U versus 18 (10.8%) of 166 small and medium-sized dogs. Large dogs were defined as having a body weight of [greater than or equal to] 20 kg. This difference is statistically significant: with odds ratio = 2.39, [chi square] = 7.03, p = 0.008 with Yates' correction. Among dogs with [greater than or equal to] 450 U, 25 (62.5%) of 40 were large.


Antibodies to TBEV were detected in 16.4% of dogs in Aust-Agder County of southern Norway. This finding indicates that TBEV is present in this geographic region. Although the first human cases prove the existence of TBEV in southern Norway, the levels of seropositivity in dogs were still unanticipated in a region where TBE has previously not been seen.

TBE in dogs has been reported from several European countries (7), and the number of cases is growing. Searching for antibodies to TBEV in our canine population would be useful since dogs are suitable serologic indicators of TBEV in a geographic area, and canine serum has been used to reveal natural epidemic loci. Our data support the recent findings of human TBE cases in Norway and the notion of an emerging disease, especially because the serum samples were collected from the same geographic area where the first human cases were described. The changing epidemiologic situation suggests that better monitoring of TBE is needed in Norway.


(1.) Schneider H: On the epidemic acute serous meningitis. Wien Klin Wochenschr 1931;44:350-2. German.

(2.) Haglund M: Occurrence of TBE in areas previously considered being non-endemic. Int J Med Microbiol 2002;291(Suppl 33):50-4.

(3.) Skarpaas T, Csango PA, Pedersen J. Tick-borne encephalitis in southern Norway. MSIS-rapport 2000; No. 9. Oslo: The National Institute of Public Health; 2000. Norwegian.

(4.) Ormaasen V, Brantsaeter AB, Moen EW. Tick-borne encephalitis in Norway. Tidsskr Nor Laegeforen 2001;121:807-9. Norwegian.

(5.) Skarpaas T, Sundoy A, Vene S, Pedersen J, Eng PG, Csango PA. Tick-borne encephalitis in Norway. Tidsskr Nor Laegeforen 2002;122:30-2. Norwegian.

(6.) Lindblad G. A ease of tick-borne encephalitis in a dog. Medlemsblad for Sveriges veterinarforbund 1960;12:416-7. Swedish.

(7.) Kirtz G. Tick-borne encephalitis in Austrian dogs [Doctoral dissertation]. Vienna: University of Vienna; 1999.

Peter A. Csango, * Ellef Blakstad, ([dagger]) Georges C. Kirtz, ([double dagger]) Judith E. Pedersen, * Brigitte Czettel ([double dagger])

* Vest-Agder Hospital, Kristiansand, Norway; ([dagger]) Norwegian Veterinary Association, Oslo, Norway; and ([double dagger]) InVitro, Labor for Veterinamedizinische Diagnostik und Hygiene GmbH, Vienna, Austria

Dr. Csango is director of the Department of Microbiology, Sorlandet Hospital, Kristiansand, Norway. His areas of research interest are medical microbiology and infectious diseases.

Address for correspondence: Peter A. Csango, Department of Microbiology, Sorlandet Hospital, Kristiansand, NO-4604 Norway; fax: +47 38073491 ; email:

COPYRIGHT 2004 U.S. National Center for Infectious Diseases
COPYRIGHT 2004 Gale Group

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