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[Correlation between CT findings and clinical course in viral and bacterial meningoencephalitis].

The computed axial tomograms (CAT) of 50 patients with viral or bacterial meningoencephalitis are correlated with the clinical course, the laboratory data, and the EEG changes. The diagnostic value of CAT in the early diagnosis of herpes simplex encephalitis is of specific importance. Hypodense regions are demonstrated after the fifth day of illness in the temporal lobe. All other viral or bacterial meningoencephalitis cases have no specific changes on CAT examination compared with clinical or laboratory data. However, in localised encephalitis CAT may reveal hypodense regions. For follow-up studies of meningoencephalitis CAT is of important diagnostic value in demonstrating complications such as abscess or occlusive hydrocephalus.

Aged↗

[Acute meningoencephalitis and the problem of viral persistence in complicated rubella].

The results of combined clinico-virological and immunological examinations of 25 children with rubellar meningoencephalitis are presented. The meningoencephalitis was preceded by typical rubella in 24, and by rubellar infection without eruptions in 1 child. In 6 children the rubella virus was isolated from the cerebrospinal fluid in the acute period of the disease (5th to 19th days), and in 2 children it was re-isolated on the acute period of the disease (5th to 19th days), and in 2 children it was re-isolated on the 17th-19th days. A persistence of the immunoglobulins M specific to the rubella virus was revealed both in the acute period of the disease and long time after the disease onset (the observation period was 409 days). The data obtained confirm the etiological role of the rubella virus in the development of rubellar meningoencephalitis, suggesting that the rubella virus may persist in complicated post-natal rubella.

Acute Disease↗

[A case of toxoplasmic chorioretinitis and meningoencephalitis in an immunocompetent adult].

A 71-year-old man who presented with toxoplasmic chorioretinitis and meningoencephalitis is reported. He had been healthy and immunologically normal. Initially, he complained of blurring of vision without headache, nor fever. Neurological examinations revealed papilledema, nuchal rigidity, and disorientation. Fluorescent angiography of the ocular fundi disclosed hyperfluorescent leaks suggesting chrioretinitis. His EEG had dysrhythmic slow alpha wave with some theta slowing. CSF studies showed pleocytosis up to 80/mm3; the cells were predominantly lymphocytes. The titers of toxoplasma antibody in the serum and CSF were prominently increased. Toxoplasmosis was highly suspected and he was treated with predinsolone, acetylspiramycin, and pyrimethamine. After the treatment, ophthalmologic and neurological symptoms improved, and the laboratory findings including the titers of toxoplasma antibody in the serum and CSF were also improved. Recently, toxoplasmosis associated with neurological complications as an opportunistic infection is a serious problem in the immunocompromised hosts, especially in AIDS, but this infection is rare in immunologically normal adults. Our case and some other reports may suggest a chance of developing toxoplasmic meningoencephalitis even in healthy individuals. We have to think of the possibility of toxoplasmosis in the immunocompetent hosts when they are presenting with chorioretinitis and meningoencephalitis.

Aged↗

[Acute meningoencephalitis--diagnosis and therapy].

Meningoencephalitis is still associated with a mortality rate of up to 30% and early selective treatment is extremely important. Whenever the disease is suspected, lumbar puncture should be performed immediately with the aim of differentiating on the basis of the cell count and cell picture between the various forms of inflammation namely bacterial, viral, and other special forms (tuberculous, leptospiral, spirochaete-associated or fungus-associated infections). Bacterial meningoencephalitis requires immediate antibiotic treatment. The present article discusses the choice of suitable medication. When herpes encephalitis is suspected, acyclovir should be administered immediately. The diagnosis and treatment of tuberculous meningoencephalitis are also briefly discussed. Infections with less common pathogens are not considered in the present article.

Acute Disease↗

[Herpes simplex meningoencephalitis in an infant observed during an epidemic of enteroviral infections of the nervous system].

An infant with Herpes simplex meningoencephalitis which occurred during an epidemic of enteroviral neuroinfections is described. Clinical and laboratory signs of meningitis as well as preceding aphtous oropharyngeal inflammation, initially suggested an enteroviral etiology. The appearance of signs of encephalitis with focal neurologic disturbances and the results of brain imaging by computed tomography, primarily the detection of temporoparietal areas of hypodensity, raised the possibility of HSV infection. Thanks to early specific treatment with acyclovir, the infant recovered from meningoencephalitis and 4 months later presented only minor neurological sequelae (slight left hemiparesis). The diagnosis of Herpes simples meningoencephalitis was confirmed by detecting IgM and IgG anti-HSV antibodies in the serum and cerebrospinal fluid both at the beginning and after 10 days of treatment and also by a eightfold rise of the anti-HSV-1 antibody level in serum. The authors emphasize the role of brain imaging (computed tomography and magnetic resonance) in the differential diagnosis of viral nervous system infections and suggest early treatment with acyclovir in case of suspicion of HSV-encephalitis.

Humans↗

[Viral meningoencephalitis caused by enterovirus in Cuba from 1990-1995].

The results of a study on enterovirus as causal agents of viral meningoencephalitis from 1990 to 1995 are described. From the 1458 samples of patients studied, 586 were from feces, 108 from cerebrospinal fluid and 1095 were paired sera. The samples for viral isolation were inoculated in two different cellular systems. A total of 225 samples (32.42%) were found to be positive; the highest number of isolations (n = 217) was found in feces and in diploid human lung fibroblast cells (PHuE-1). Antibody determination were carried out using neutralization by micromethod test with 10 enterovirus antigens (Echovirus 4, 6, 9, 11 and Coxsackievirus B1-6). The isolated virus was also used as antigen during epidemic periods. There were 3 epidemic outbreaks: Coxsackievirus A9 (1990-1991), Echovirus 30 (1994), and Coxsackievirus B5 (1995). Coxsackievirus A9 and Echovirus 30 have been related to viral meningoencephalitis epidemics in Cuba since 1970. In paired sera 66.84% were positive, Echovirus 6 and 11 exhibited higher positivity. When positive results by isolation and serology were considered together, more than 80% of the studied cases were associated to enterovirus infection. These results show the importance of enteroviruses as cause of viral meningoencephalitis in our country.

Animals↗

[The clinical use of Amoxiclav in patients with suppurative meningoencephalitis].

Clinical use of Amoxiclav showed high therapeutic efficacy in patients with purulent meningoencephalitis both alone and in combination with cefalosporinum of the first generation. Against the background of treatment of patients with overt manifestations of meningoencephalitis and neurotoxicosis meningeal and encephalitic manifestations got attenuated during the first week, with liquorodynamics being stabilized, cerebrospinal fluid ameliorating by day 8-10 of the disease course. Bacteriologic assays showed that up to 83.4% of bacterial flora most common in Ukraine are sensitive to Amoxiclav, with such pathogenic organisms as Pneumococcus, Meningococcus, hemophilia bacillus that are actually main pathogens implicated in acute meningoencephalitis in Ukraine being sensitive to the above drug preparation in 100% of cases.

Acute Disease↗

A fatal case of coxsackievirus B4 meningoencephalitis.

BACKGROUND: Coxsackieviruses and echoviruses are common causes of aseptic meningitis, but they rarely cause life-threatening illness. We report a fatal case of coxsackievirus B4 meningoencephalitis in a woman who developed extrapyramidal symptoms suggestive of encephalitis lethargica. The exact causative agent of encephalitis lethargica has rarely been found, but most cases of the syndrome are assumed to be of viral origin. CASE DESCRIPTION: A 33-year-old woman previously treated with methylprednisolone and cyclophosphamide for Henoch-Schönlein purpura was transferred from a referring hospital because of sore throat, fever, and chills. Her neurologic findings progressed from headache with mild photophobia to lethargy, cogwheeling, increased tone in all 4 limbs, and brisk reflexes. The patient was diagnosed as having coxsackievirus B4 meningoencephalitis and, despite treatment with the experimental antiviral agent pleconaril, died of an overwhelming central nervous system infection and myocarditis. Magnetic resonance imaging showed focal hyperintense lesions in the substantia nigra that corresponded to the location of pathological changes seen at autopsy. CONCLUSIONS: This patient had a fulminant coxsackievirus B4 viral meningoencephalitis with a clinical pattern reminiscent of encephalitis lethargica and striking focal abnormalities in the substantia nigra identified on magnetic resonance imaging. The magnetic resonance imaging findings correlated with pathological changes identified at autopsy that were similar to the pathological findings observed in patients with encephalitis lethargica and postencephalitic parkinsonism. It is likely that the patient's immunocompromised state led to an overwhelming infection from an otherwise relatively innocuous viral infection.

Adult↗

An autopsy case of amebic meningoencephalitis. The first Japanese case caused by Balamuthia mandrillaris.

We report here the first case of amebic meningoencephalitis caused by Balamuthia mandrillaris in a 78-year-old Japanese woman with Sjögren's syndrome. Fourteen days before her death, she presented with high fever and lost consciousness and later developed neck stiffness and abducens palsy. Computed tomography scans of the brain demonstrated multiple low-density areas throughout the brain. Neuropathologically, hemorrhagic and necrotic lesions with many amebic trophozoites were scattered in the brain and spinal cord. Granulomatous lesions were only rarely found. The amebas were identified as Balamuthia mandrillaris based on immunofluorescence assay. Clinicopathologically, our case was thought to be an intermediate between primary amebic meningoencephalitis due to Negleria fowleri and granulomatous amebic encephalitis due to Acanthameba species. Essentially, the case was one of an elderly person with suspected immunodeficiency with fulminant necrotic meningoencephalitis and scanty granulomatous lesions of 14 days course.

Aged↗

Human herpesvirus-6 meningoencephalitis in a recipient of an unrelated allogeneic bone marrow transplantation.

BACKGROUND: Human herpesvirus-6 (HHV-6) has been implicated in bone marrow suppression, interstitial pneumonitis, and fatal meningoencephalitis in bone marrow transplant (BMT) recipients. METHODS: We describe the case of a woman with acute myeloid leukemia in second remission who developed febrile meningoencephalitis 8 months after a second unrelated BMT. RESULTS: Computed tomography and magnetic resonance images of the brain were nonspecific. Analysis of cerebrospinal fluid (CSF) revealed lymphocytosis and an increased protein level. Using polymerase chain reaction methods, HHV-6 was the only pathogen detected in CSF, peripheral blood mononuclear cells, and bone marrow. The patient was treated with ganciclovir and foscarnet for 3 months. All clinical manifestations resolved and HHV-6 polymerase chain reaction analysis of CSF became negative 40 days after the beginning of antiviral treatment. CONCLUSIONS: This observation strongly suggests that HHV-6 should be sought in BMT patients with neurological complications and that HHV-6 meningoencephalitis may respond to ganciclovir and foscarnet therapy.

Acute Disease↗

West Nile virus meningoencephalitis in a Suri alpaca and Suffolk ewe.

The first confirmed cases of West Nile virus (WNV) in the Western Hemisphere were reported in the state of New York in 1999. Since then, the virus has spread throughout the eastern and central United States and continues to extend westward. This report describes clinical signs and microscopic lesions associated with WNV infection in a Suffolk ewe and an alpaca, 2 species in which the disease has not been reported previously. In late August 2002, a 4.5-year-old female alpaca developed an acute onset of clinical signs characterized by torticollis, hyperesthesia, ataxia, recumbency, and altered mentation. The animal died 3.5 days after the onset of clinical signs. Microscopic examination of the brain revealed a mild to moderate, diffuse, lymphoplasmacytic meningoencephalitis. In early September 2002, a 3-year-old Suffolk ewe developed a rapidly progressive illness characterized by ataxia and convulsions. The apparent duration from onset of clinical signs until death was less than 8 hours. The ewe had a moderate, diffuse, lymphoplasmacytic meningoencephalitis with focal gliosis. Reverse transcription-polymerase chain reaction assays and immunohistochemistry on the brain were positive for WNV in both animals. These cases demonstrate that WNV is capable of causing sporadic, fatal, nonsuppurative meningoencephalitis in alpacas and sheep.

Animals↗

[Coxsackie B2 virus fatal meningoencephalitis in a student]

OBJECTIVE: To present the case of a girl who was previously healthy but had fatal evolution due to Coxsackie B2 viral meningoencephalitis.METHODS: The authors describe the case of a female child with fatal meningoencephalitis caused by Coxsackie B2 virus and present a review of the literature (Medline and Lilacs).RESULTS: The girl was eight years old when she presented meningoencephalitis with bad evolution, leading to death on the 32nd day of internation. The exams showed positive serologic reaction to Coxsackie B2. The virus taken from two stool samples was isolated. The CRF exam showed an increase four times higher on Coxsackie B2 titulation.CONCLUSION: The death of healthy patients with enteroviral encephalitis, as described here, is rarely dealt with in the medical literature, perhaps because of lack of clinic suspicion. This case tries to drive attention to the importance of an early etiologic diagnosis in the meningoencephalities and the search for specific etiological treatment.

Journal Article↗

[Effect of splenectomy on development of primary amoebic meningoencephalitis]

To elucidate the effect of splenectomy on the development of experimental primary amoebic meningoencephalitis in mice, the death rate and survival time of mice infected intranasally with Naegleria fowleri trophozoites 5 x 10(4) cultivated in CGVS medium were compared according to the age when splenectomy was done, and post-operation until experimental infection. Immunodiffusion was undergone to detect the presence of serum antibody due to N. fowleri infection in mice. Polyacrylamide gel electrophoresis was done to compare the protein fractions of mouse serum in each experimental groups. In experiment I, splenectomy was done 3 weeks and infection 4 weeks after birth, the death rate of control, sham operated and splenectomized group were 100 percent, 85 percent and 95 percent, and the mean survival time after infection 7.3 days, 7.5 days and 7.8 days, respectively. In experiment II, splenectomy was undergone 3 weeks and infection 6 weeks after birth, the death rate of control, sham operated and splenectomized group were 95 percent, 95 percent and 95 percent, and the mean survival time after infection 12.1 days, 11.5 days and 11.5 days, respectively. In experiment III, splenectomy was done 5 weeks and infection 6 weeks after birth, the death rate of control, sham operated and splenectomized group were 95 percent, 90 percent and 95 percent, and the mean survival time after infection 8.1 days, 8.3 days and 8.5 days, respectively. By Ouchterlony immunodiffusion, anti-N. fowleri antibody in the serum of mouse with primary amoebic meningoencephalitis was detected against a N. fowleri antigen, which was prepared by ultrasonication of N. fowleri trophozoites, each reacting two lines of precipitation. The patterns of serum fractions by polyacrylamide gel electrophoresis were different between control and sham operated groups from splenectomized group in fraction II, III and V, the sera of which were collected after N. fowleri infection. This results may be summarized as that splenectomy has no effect on the development of primary amoebic meningoencephalitis in mice.

Journal Article↗

[Protective immunity against Naegleria meningoencephalitis in mice]

This study is to verify the protective ability against experimental Naegleria meningoencephalitis by immunization with Naegleria fowleri in mice. Naegleria fowleri, strain 0359, and Naegleria gruberi, strain EGB, were used in this study, and cultured in CGVS medium axenically. Inbred BALB/c mice, weighing about 20g, were immunized by three intraperitoneal injection of 1 x 10(6) N. fowleri trophozoites at the interval of one week. This N. fowleri trophozoites antigen was fixed with 5 percent formaldehyde. N. fowleri trophozoites from culture were homogenized with sonicator at 4 degrees C as monitored by phase contrast microscopy, and their membrane and cell content preparations were made for the immunization of mice. Their inoculation dose in volume was equivalent to the 1 x 10(6) trophozoites in each injection for immunization. And N. gruberi trophozoites, which was fixed with 5 percent formaldehyde, were also used for immunization. Mice were inoculated intranasally with 5 x 10(4) N. fowleri trophozoites in a 5 microliter suspension under anesthesia by as intraperitoneal injection of about l mg secobarbiturate. Nervousness, rotation or sluggish behaviour were observed in the mice which were infected with N. fowleri. Necrotic lesion was demonstrated in the anterior portion of brain, especially in the olfactory lobe. The inflammatory cell infiltration with numerous N. fowleri trophozoites was noticed. This pathological changes were more extensive in the control than in the experimental groups. Mice were dead due to experimental primary amoebic meningoencephalitis that developed between 8 days and 23 days after inoculation. Mortality rate of the mice was low in the immunized experimental group. Mean survival time, which is the survival duration of mice from the infection to death, was prolonged significantly in the immunized mice except in the mice immunized with N. fowleri membrane. Even in the mice immunized with N. gruberi, survival time was delayed. In summary, the effectiveness of immunization is demonstrated in terms of protective immunity against Naegleria meningoencephalitis in mice.

Journal Article↗

Listeria meningoencephalitis: two cases and a review of the literature.

INTRODUCTION: Although presently uncommon locally, Listeria is increasing an important cause of central nervous system (CNS) infection worldwide. It differs from the common meningitis pathogens in its clinical features and treatment. CLINICAL PICTURE: We present 2 recently encountered cases of Listeria meningoencephalitis. In case 1, a previously healthy 42-year-old man presented with clinical features of meningoencephalitis. In case 2, a 64-year-old woman had clinical features of pneumonia and meningoencephalitis. Both had a predominantly lymphocytic picture in their cerebrospinal fluid (CSF) samples. Listeria grew in blood cultures of both patients and the CSF culture of the first. TREATMENT: In both cases, Listeria was resistant to the empirical antibiotics used. Intravenous ampicillin was eventually used in both patients, with gentamicin, added for synergistic action in the first. OUTCOME: The first patient developed complications of hydrocephalus, subdural collection and extensive cerebritis and ventriculitis. The second patient had focal seizures and a pontine infarct. Both did not survive. CONCLUSION: These 2 recent cases with different presentations of intracranial listerosis highlight the increasing importance of listerial infections in Singapore. Clinicians need to be familiar with the features of this lethal disease in order to recognize and manage it successfully.

Adult↗

Adenoviral meningoencephalitis in a patient with lead toxicity.

Adenovirus type 12 was recovered from the CSF of a 36-year-old woman with adenoviral meningoencephalitis and lead toxicity. The serum level of lead was 199 micrograms/dL and the CSF level was 7 micrograms/dL. After therapy with edetate disodium calcium (Calcium Disodium Versenate), she had an uneventful recovery. The possibility of exacerbation of lead poisoning with encephalopathy due to adenovirus type 12 meningoencephalitis is raised.

Acute Disease↗

A case of Balamuthia mandrillaris meningoencephalitis.

Balamuthia mandrillaris is a newly described pathogen that causes granulomatous amebic encephalitis, an extremely rare clinical entity that usually occurs in immunosuppressed individuals. We report a case of pathologically proven Balamuthia encephalitis with unusual laboratory and radiologic findings. A 52-year-old woman with idiopathic seizures and a 2-year history of chronic neutropenia of unknown cause had a subacute illness with progressive lethargy, headaches, and coma and died 3 months after the onset of symptoms. Cerebrospinal fluid (CSF) glucose concentrations were extremely low or unmeasurable, a feature not previously described (to our knowledge). Cranial magnetic resonance imaging scans showed a single large temporal lobe nodule, followed 6 weeks later by the appearance of 18 ring-enhancing lesions in the cerebral hemispheres that disappeared after treatment with antibiotics and high-dose corticosteroids. The initial brain biopsy specimen and analysis of CSF samples did not demonstate amebae, but a second biopsy specimen and the postmortem pathologic examination showed Balamuthia trophozoites surrounded by widespread granulomatous inflammation and vasculitis. The patient's neutropenia and antibiotic use may have caused susceptibility to this organism. Amebic meningoencephalitis should be considered in cases of subacute meningoencephalitis with greatly depressed CSF glucose concentrations and multiple nodular lesions on cerebral imaging. Arch Neurol. 2000;57:1210-1212

Amebiasis↗

Simian immunodeficiency virus-induced meningoencephalitis: natural history and retrospective study.

Simian immunodeficiency virus (SIV) is a lentivirus with morphological and antigenic similarities to human immunodeficiency virus, the causative agent of acquired immunodeficiency syndrome (AIDS) of humans. Macaque monkeys infected with SIV show profound immunological impairment, clinically characterized by multiple opportunistic infections and neoplasms. Retrospective examination of autopsy tissue from 27 SIV-infected animals demonstrated that approximately 60% of the experimentally inoculated animals had a meningoencephalitis characterized by perivascular infiltrates of macrophages and multinucleate giant cells in the white and gray matter and leptomeninges. Ultrastructurally, these macrophages contained typical lentiviral particles within membrane-bound intracytoplasmic vacuoles. Other findings in the central nervous system included discrete randomly located neuroglial nodules, endothelial hypertrophy, and leptomeningeal thickening. The results indicate tha the meningoencephalitis induced by SIV in monkeys is similar to the lesions of the central nervous system in patients with AIDS and that SIV infection in the macaque is a useful animal model to study the pathogenesis of human immunodeficiency virus--related subacute encephalitis or AIDS encephalopathy.

Animals↗