Clinically mild encephalitis/encephalopathy with a reversible splenial lesion associated with febrile urinary tract infection.

UNLABELLED: Common pathogens of clinically mild encephalitis/encephalopathy with a reversible splenial lesion (MERS) are viruses, such as influenza virus. However, bacteria are rare pathogens for MERS. We report the first patient with MERS associated with febrile urinary tract infection. A 16-year-old lupus patient was admitted to our hospital. She had fever, headache, vomiting, and right back pain. Urinary analysis showed leukocyturia, and urinary culture identified Klebsiella pneumoniae. Cerebrospinal fluid examination and brain single-photon emission computed tomography showed no abnormalities. Therefore, she was diagnosed with febrile urinary tract infection. For further examinations, 99mTc-dimercaptosuccinic acid renal scintigraphy showed right cortical defects, and a voiding cystourethrogram demonstrated right vesicoureteral reflux (grade II). Therefore, she was diagnosed with right pyelonephritis. Although treatment with antibiotics administered intravenously improved the fever, laboratory findings, and right back pain, she had prolonged headaches, nausea, and vomiting. T2-weighted, diffusion-weighted, and fluid attenuated inversion recovery images in brain magnetic resonance imaging showed high intensity lesions in the splenium of the corpus callosum, which completely disappeared 1 week later. These results were compatible with MERS. To the best of our knowledge, our patient is the first patient who showed clinical features of MERS associated with febrile urinary tract infection. CONCLUSION: In patients with pyelonephritis and an atypical clinical course, such as prolonged headache, nausea, vomiting, and neurological disorders, the possibility of MERS should be considered.

Intraventricular polymyxin B for the treatment of neonatal meningo-ventriculitis caused by multi-resistant Acinetobacter baumannii--case report and review of literature.

Central nervous system infections due to multi- and pan-drug resistant Acinetobacter baumannii are an emerging problem in intensive care patients. A high mortality rate is seen in neonatal and central nervous system infections. Treatment can be prolonged and challenging. Polypeptide antibiotics remain one of the options but have poor cerebrospinal fluid (CSF) penetration. We present our experience of successfully treating pan-drug resistant A. baumannii neonatal meningitis and ventriculitis with intraventricular polymyxin B. This was administered by repeated ventricular punctures due to lack of consent for insertion of a ventricular reservoir.

Tuberculous meningoencephalomyelitis and coinfection with HTLV-I + HTLV-II: case report

Os vírus HTLV-I e HTLV-II são endêmicos em algumas regiões do Brasil, onde uma das doenças associadas, a paraparesia espástica tropical/mielopatia associada ao HTLV (PET/MAH), tem sido diagnosticada em significativo número de pacientes infectados. Nesses indivíduos, a prevalência de tuberculose é maior que na população geral, sugerindo que possa haver um maior risco para esta comorbidade. Relatamos o caso de um homem de 44 anos coinfectado HTLV-I + HTLV-II que desenvolveu meningoencefalomielite por Mycobacterium tuberculosis. O paciente apresentou recuperação clínica parcial, correção da disfunção de barreira hemato-liquórica e negativação no PCR, mediante o tratamento com corticoesteróides e tuberculostáticos.

[Subacute meningoradiculomyeloencephalitis due to cryptococcosis infection]. / Méningoradiculomyéloencéphalite subaiguë liée à une infection par Cryptococcus neoformans.

INTRODUCTION: If meningoencephalitis with or without mass lesion (granuloma or abscess) is the most common pattern of CNS cryptococcal infection, intramedullary involvement is very uncommon. EXEGESIS: The authors report an 70-year-old male with Hodgkin's disease treated by chemotherapy then corticosteroids because of pulmonary fibrosis who was presenting for eight days ago, an ataxia, pyramidal syndrome, and bradypsychy. Spinal MRI revealed a gadolinium T1 weighted homogeneous enhancing T4 level intramedullary lesion. CSF had showed 190 GB/mm3 of lymphomonocytes, increased protein level (2.28 g/l), decreased glucose level (1.5 mmol/l) and positivity for crytococcal antigen. Treatment by amphotericine B and flucytosine then fluconazole for six months was instituted and symptoms gradually improved. CONCLUSION: A cryptococcus infection must be searched by antigen in CSF in case of myelopathy isolated or associated with meningoradiculoencephalomyelopathy, specially in patients with a cellular immunodeficience. Antimycotic agents must be firstly used, surgery would be restricted to decompression if aggravation of disease and compressive effect on the adjacent structures radiologically (MRI) became evident. Prolonged treatment is necessary in case of immunodeficience.

Brucellosis and polyneuroradiculomyeloencephalitis. A case report.

Reports on simultaneous central and peripheral nervous system involvement in a patient with brucellosis are very rare. We report of one young female patient with a long history of consumption of non-pasteurized dairy products in which clinical and laboratory findings confirmed the existence of an active brucellosis with nervous system impairment. Cerebrospinal fluid (CSF) analyses were negative. Electrophysiology and positive findings on sural nerve biopsy complemented the diagnosis of polyneuroradiculomyeloencephalitis. Treatment with a combination of doxycycline and rifampin for 2 months was successfully applied. No relapse or sequelae occurred in the patient after 12 months of follow up.

[Encephalomyelitis due to Epstein-Barr virus]. / Encefalomielitis por el virus de Epstein-Barr.

We present a 28-year-old woman with encephalomyelitis and concomitant central nervous system infection by Epstein-Barr virus. Progression took place in 2 phases, with myelitis at the beginning and encephalitis developing later. Despite great functional impairment, recovery was good and the patient was left suffering only from urinary retention that was presumably caused by spinal lesions. The etiology of the case is unusual, particularly in adults.

Generalised Listeria monocytogenes infection in a dog.

A 6-year-old Doberman bitch was presented for an acute onset of circling, hemiparesis and depression. Clinical examination revealed conjunctivitis, abdominal pain, anaemia, decreased facial sensation, decreased jaw, tongue and pharyngeal tone, decreased conscious proprioception, decreased flexor withdrawal reflexes, and abnormal hemiwalking and hemistanding. Pancytopaenia was evident on haematological evaluation. Bone marrow cytology revealed a bacterial infection. Cerebrospinal fluid analysis was normal. Despite antibiotic treatment, the dog died. On autopsy, widespread multifocal inflammatory lesions were found to be present in the lungs, liver, spleen, meninges, lymph nodes, adrenal glands and kidneys. Listeria monocytogenes was isolated in pure culture from these organs and tissues. Histopathological examination showed numerous gram-positive intracellular rod-shaped bacteria seen in all the above-mentioned organs.

Coronavirus induced encephalomyelitis: an immunodominant CD4(+)-T cell site on the nucleocapsid protein contributes to protection.

In this communication we present clear evidence, that the N-protein of MHV-JHM contains immunodominant CD4+ T-cell sites. These sites were recognized by the immune system of virus infected Lewis rats. In previous investigations we have shown, that CD4+ T-cell lines with specificity for defined viral proteins can be selected from diseased Lewis rats and mediate protection, if transferred to otherwise lethally infected animals. To define regions of the N-protein, which are immunodominant for the T-cell response, we employed bacterially expressed N-protein and truncated subfragments of N as an antigen. We demonstrate, that T-cells from MHV-JHM infected, diseased Lewis rats recognized with high prevalence the carboxyterminal subfragment C4-N (95 aa) and to some extent the adjacent C3-N protein. The same results were obtained with T-cells derived from rats immunized with bacterially expressed N-protein or from animals vaccinated by a stable N-protein expressing vaccinia recombinant. Finally, transfer of CD4+ line T-cells to MHV-JHM infected rats specific for C4-N mediated protection against acute disease.

Postinfectious myelitis, encephalitis and encephalomyelitis.

Six cases of post-infectious encephalomyelitis are described. A preceding non-specific viral-like illness occurred 4 to 20 days before the onset of the neurological deficits. The clinical syndromes included transverse myelitis, focal encephalitis and encephalomyelitis (each in one case) and diffuse encephalitis in 3. Magnetic resonance imaging appeared to be the investigation of choice. High dose corticosteroids were given to 4 patients who recovered partially or fully. The patient with focal encephalitis had a spontaneous and complete recovery. The remaining patient with diffuse encephalitis died 3 days after the onset; autopsy showed prominent lymphocytic perivascular cuffing in the white matter and lymphocytic infiltration of the meninges.

Antibody-mediated clearance of alphavirus infection from neurons.

Humoral immunity is important for protection against viral infection and neutralization of extracellular virus, but clearance of virus from infected tissues is thought to be mediated solely by cellular immunity. However, in a SCID mouse model of persistent alphavirus encephalomyelitis, adoptive transfer of hyperimmune serum resulted in clearance of infectious virus and viral RNA from the nervous system, whereas adoptive transfer of sensitized T lymphocytes had no effect on viral replication. Three monoclonal antibodies to two different epitopes on the E2 envelope glycoprotein mediated viral clearance. Treatment of alphavirus-infected primary cultured rat neurons with these monoclonal antibodies to E2 resulted in decreased viral protein synthesis, followed by gradual termination of mature infectious virion production. Thus, antibody can mediate clearance of alphavirus infection from neurons by restricting viral gene expression.

Relapsing encephalomyelitis following transfer of partial immunity to JHM virus.

Mice infected with the JHM strain mouse hepatitis virus (JHMV) develop a fatal encephalomyelitis with evidence of demyelination. It has previously been shown that the adoptive transfer of 5 x 10(7) nylon wool adherent (NWA) spleen cells from immunized donors to lethally infected recipients clears virus from the central nervous system (CNS) and prevents demyelination. Adoptive transfer of a smaller number (1 x 10(7] of NWA spleen cells from immunized donors also protects from death but does not significantly alter virus replication in the CNS during the acute phase of the infection. Moreover, these mice develop a transient non-fatal encephalomyelitis which occurs approximately 3 weeks post-infection. This delayed encephalomyelitis is associated with a mononuclear cell infiltration into the CNS but little or no evidence of virus replication or increased viral antigen. A virus-specific delayed-type hypersensitivity (DTH) response precedes this delayed onset of disease by 24 to 48 h. Resolution of disease correlates with a selective and permanent suppression of the JHMV-specific DTH reactivity. In addition, no virus-specific DTH is detected following adoptive transfer of viral-specific DTH effectors derived from immunized donors. In contrast, these mice respond to a heterologous antigen, KLH, suggesting that the resolution of the encephalitis is accompanied by a profound suppression in viral-specific DTH response.

Pathogenesis of caprine arthritis encephalitis virus. Cellular localization of viral transcripts in tissues of infected goats.

Pathologic specimens of 18 goats with classical lesions of caprine arthritis-encephalitis (CAE) virus infection were examined morphologically and by in situ hybridization using molecularly cloned CAEV deoxyribonucleic acid (DNA) to determine which tissues and cells of naturally infected goats supported virus replication. Large numbers of cells with viral transcripts were detected in inflamed brain, spinal cord, lung, joints, and mammary gland. These cells were morphologically compatible with macrophages. Fewer cells with viral transcripts were seen in noninflamed tissues. Viral RNA was identified in macrophagelike cells in lung, liver, spleen, and lymph nodes, in cells lining the vessels of brain and synovium, and in epithelial cells of intestinal crypts, renal tubules, and thyroid follicles. These data suggest that the cell tropism of lentiviruses may extend beyond the narrow boundaries of lymphocytes and macrophages.

Insights into Theiler's virus neurovirulence based on a genomic comparison of the neurovirulent GDVII and less virulent BeAn strains.

Theiler's murine encephalomyelitis viruses (TMEV) are naturally occurring enteric pathogens of mice which can be divided into two subgroups based primarily on their neurovirulence after intracerebral inoculation: the highly virulent GDVII group and the less virulent TO strains. To begin to elucidate the molecular basis of neurovirulence of the two TMEV subgroups, we have cloned and sequenced the entire 8105 nucleotide RNA genome of the highly virulent GDVII virus and compared it to the less virulent BeAn 8386 virus (D. C. Pevear, M. Calenoff, E. Rozhon, and H. L. Lipton (1987) J. Virol. 61, 1507-1516). The viruses are 90.4% identical at the nucleotide level. The highest level of nucleotide identity is in the 5' and 3' noncoding regions of the RNAs (95.5 and 99.2%, respectively): regions believed to be important for control of viral RNA synthesis, initiation of translation, encapsidation, and virion uncoating. The 2303 amino acid polyproteins of BeAn and GDVII viruses are 95.7% identical at the amino acid level (99 of 2303 residues differed). Thirty-nine of these amino acid differences occur in the three surface coat proteins, VP1 (20 differences), VP2 (10 differences), and VP3 (9 differences), while the remainder of the changes are distributed throughout the polyprotein. Although these levels of identity are too low to determine where neurovirulence maps based solely on nucleotide sequence analysis, having the complete sequence will facilitate construction of recombinant BeAn-GDVII viruses to be used for this purpose.

Postviral fatigue syndrome: persistence of enterovirus RNA in muscle and elevated creatine kinase.

Enterovirus-specific probes have been prepared by reverse transcription of conserved sequences in purified Coxsackie B2 virus genomic RNA and molecular cloning techniques. These probes were used in quantitative slot blot hybridizations to test for the presence of enterovirus-specific RNA in skeletal muscle biopsy specimens from 96 patients who had suffered from the postviral fatigue syndrome myalgic encephalomyelitis for up to 20 years. Biopsy specimens from 20 patients were positive for the presence of virus-specific RNA with hybridization signals more than three standard deviations greater than the mean of the normal muscle controls. Biopsies from the remaining 76 patients were indistinguishable from the controls. These data show that enterovirus RNA is present in skeletal muscle of some patients with postviral fatigue syndrome up to 20 years after onset of disease and suggest that a persistent virus infection has an aetiological role.