Cases reported "Encephalomyelitis"

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1/9. Central nervous system infection caused by borrelia burgdorferi. Clinico-pathological correlation of three post-mortem cases.

    The spirochete borrelia burgdorferi (B. burgdorferi) may cause severe meningoencephalomyelitis as the sole manifestation of Lyme borreliosis. We would like to present three such cases, where definite neuroborreliosis was clinically diagnosed in two cases and possible neuroborreliosis was recognized in one case. Alive spirochetes were isolated and cultured from blood and cerebrospinal fluid (CSF) in both definite cases. B. burgdorferi as the causative agent of the infection was confirmed in CSF by polymerase chain reaction (PCR) in one definite case. In the possible case spirochetes were cultured from blood and CSF. Alive spirochetes were not isolated, however anti-B. burgdorferi antibody value in serum was significantly elevated. On necropsy gross examination brain edema without focal changes was detected in two cases. Cerebral atrophy was seen in Case 3. Microscopically, lymphocytic infiltrates, microglial diffuse and nodular activation, spongiform changes, diffuse demyelination of the cerebral and cerebellar white matter, and diffuse astrocytosis, were characteristic pathological features in all presented cases. Multifocal, perivascular degenerative changes in the cerebral and cerebellar white matter were observed in the first case. Inflammatory changes in the nuclei and roots of cranial nerves were present in the third case.
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2/9. Lethal encephalopathy complicating childhood shigellosis.

    A 6-year-old girl is described who died following rapid neurological deterioration, ending in lethal cerebral oedema. Despite the absence of severe intestinal and metabolic derangement, shigella was cultured from the stool. Toxic encephalopathy is responsible for death following this rare complication of childhood shigellosis in developed countries. The pathophysiology is unknown. CONCLUSION: Lethal toxic encephalopathy can be caused by shigella despite the absence of severe intestinal and metabolic derangement. If shigelllosis is suspected, headache may be a first significant sign for the development of toxic encephalopathy. Early recognition and rapid measures to prevent brain oedema may improve outcome.
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3/9. encephalomyelitis due to human parechovirus type 1.

    OBJECTIVES: The implication of a viral agent in encephalomyelitis has been reported for several years. In the present study we wanted to demonstrate the presence of human parechovirus type 1 (HPEV1) in a patient diagnosed with encephalomyelitis. STUDY DESIGN: Clinical samples (throat and rectal swabs, acute and convalescent sera, cerebrospinal fluid) were collected from a 10-month-old boy diagnosed with encephalomyelitis. The appropriated samples were tested for cytomegalovirus, varicella zona virus, mumps virus and enteroviruses with specific culture, and serological and molecular biological techniques. RESULTS: HPEV1 was isolated from the throat and its genome was additional detectable in the cerebrospinal fluid, throat swab and acute serum. The samples were negative for all other tested viruses. CONCLUSION: To our knowledge, this is the first reported case of HPEV1 infection related to encephalomyelitis. This emphasis that human parechoviruses can be responsible for severe central nervous system infections in children.
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4/9. Acute brucella meningomyeloencephalo-spondylosis in a teenage male.

    BACKGROUND: brucellosis has been known from the time of Hippocrates. In 1885 Sir David Bruce isolated the causative organism from the spleens of soldiers who had died from "malta disease" (now brucellosis). There are 4 species of brucella pathogenic to humans and each of them has a specific types of animal reservoir: B.arbotus (cattle, buffalo), B.melitensis (goats, sheep, camels), B.suis (pigs), B.canis (dogs). humans are infected when they are exposed to body fluids from an infected animal. The symptoms and signs of brucellosis are protean. diagnosis is usually dependent on clinical features and serology or culture. OBJECTIVES: To describe a case of neurobrucellosis, raise awareness about the existence of the disease in uganda and africa in general and share our experiences in its diagnosis and management. methods: A male teenager was admitted with symptoms and signs of an acute meningo-encephalitis. He underwent clinical, laboratory and basic radiological evaluation. RESULTS: The un-incubated brucella titer was significantly reactive(1:160).Oblique-view cervical x-rays showed early osteophyte formation with encroachment on the vertebral foramina on the left hand side. A diagnosis of acute brucella meningomyeloencephalo-spondylosis was made and the patient was successfully treated using conventional therapy for brucellosis (oral doxycycline for 6weeks and IM streptomycin for 2 weeks). CONCLUSIONS: Neurobrucellosis though said to be rare, is a reality in our health units should be considered in the differential diagnosis of neurological and psychiatric illnesses. The good news is that it is curable and is responsive to drugs used for other forms of brucellosis.
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5/9. Ocular histopathologic findings in a case of human herpes B virus infection.

    A 37-year-old male laboratory technician who sustained a cutaneous penetrating wound from a rhesus monkey developed a progressive ascending encephalomyelitis due to culture-proven herpes B virus (Herpesvirus simiae) infection. He died 6 weeks after his injury despite acyclovir and ganciclovir treatment that was initiated after central nervous system symptoms developed. Histopathological examination of the patient's left eye revealed a multifocal necrotizing retinitis associated with a vitritis, optic neuritis, and prominent panuveitis. Herpes-type virus was identified in the involved retina by electron microscopy. Postmortem vitreous cultures taken from both eyes and retinal cultures taken from the right eye were positive for herpes B virus. Herpes B virus produces infection and destruction of retinal tissues similar to other herpesviruses. To our knowledge, this case represents the first histopathologic demonstration of herpes B virus infection in a human eye.
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6/9. Chronic persistent nodular polioencephalomyelitis presenting with brain atrophy.

    A 61-year-old male had a recurrent fever (approx. 38 degrees C) and one month later, disorientation and forgetfullness became gradually apparent. His mental and somatic status deteriorated progressively with the recurrence of fever; 3 years later he was in a persistent vegetative state accompanied by status epilepticus, and died after 5 years. Mononuclear cytosis (8-20/microliters) and increased protein (20-70 mg/100 ml) were observed in the cerebro-spinal fluid (CSF) at each examination. There was no increase of antibody titers against various viruses, chlamydia, mycoplasma and toxoplasma in the serum and CSF. Neuropathologically, the prominent microscopic finding was patchy scarred foci consisting of neuronal loss replaced by glial tissue throughout the gray matter. A few gliomesenchymal nodules were found. In addition, rod-shaped macrophages were found to varying degrees in all areas of the brain and spinal cord. No viral inclusion bodies were identified. Electron microscopic examination revealed no viral particles in the affected areas. suspensions of the frozen brain and CSF were inoculated into primary neuron cultures derived from fetal mice and into mouse brains, but the results were negative. There had been five reported cases of chronic nodular encephalitis up until 1971; this case seems to differ from the others by the presence of persistent inflammation and by neuropathologic findings.
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7/9. Echovirus meningomyeloencephalitis with administration of intrathecal immunoglobulin.

    Echovirus meningomyeloencephalitis was treated with cerebral intraventricular immunoglobulin. This case includes a complete examination of the central nervous system (CNS) supported by viral culture studies, immunoperoxidase staining and electron microscopy. Neuronal loss was most severe in the cerebellum and spinal cord. This may lead to the ataxia and a poliomyelitis-like syndrome often seen in cases of echovirus meningomyeloencephalitis. Focal encephalitic lesions, antigen-antibody reactions and live virus were found at numerous levels of the CNS in spite of intrathecal and intravenous immunoglobulin therapy. This mode of therapy and the electron microscopic features noted in echovirus infections are discussed.
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8/9. encephalomyelitis in primary hypogammaglobulinaemia.

    The neurological features of 13 patients with primary hypogammaglobulinaemia are described. Seven patients had X-linked agammaglobulinaemia (XLA) and six had common variable immunodeficiency (CVID). Three clinical pictures emerged: (i) a progressive myelopathy (one case); (ii) a myelopathy progressing to an encephalopathy (four cases); (iii) a pure encephalopathy (eight cases). In four patients the encephalopathy was temporarily reversible; the relationship of this to immunoglobulin therapy is unclear. Additional features occurred in some patients. Three had retinopathy interpreted as retinitis pigmentosa, in one of whom the retinopathy resolved. Two patients had a sensori-neural hearing loss and three had features of dermatomyositis; a variable pleocytosis was found in the CSF of nine patients. Imaging revealed atrophic changes in the cerebral hemispheres in eight cases. Ten patients have died, 1-11 years after the onset of the CNS manifestations, and in four autopsies were obtained. Two patients had encephalopathy, one with XLA had evidence of end-stage encephalitis and the other with CVID had a multi-focal leucoencephalopathy. The other two with XLA had leptomeningitis without evidence of encephalitis. Enteroviral infection is probably an important cause of neurological disease in these patients as CSF from seven patients was either positive by polymerase chain reaction (PCR) or by culture for enteroviruses. Other possible mechanisms are discussed.
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9/9. Encephalomyeloradiculopathy associated with Epstein-Barr virus: primary infection or reactivation?

    INTRODUCTION: Encephalomyeloradiculopathy (EMR) is a new syndrome, characterized by extensive involvement of the nervous system at different levels, including brain, medulla and spinal roots. We describe a patient presenting with prodromal febrile illness, followed by a wide infection of the nervous system with transverse myelitis and less severe meningitis, encephalitis and polyradiculopathy. The patient was treated with high-dose corticosteroids, antibiotics and acyclovir; in spite of therapy his condition improved very slowly, with severe neurological sequelae. MATERIAL AND methods: Antiviral antibodies were searched for in serum and cerebrospinal fluid (CSF) by commercially available ELISA kits. Viral investigations were performed by cell culture isolation and search for viral antigens, and genomic nucleic acids were investigated by polymerase chain reaction (PCR). RESULTS: Virological and serological studies evidenced a primary infection by cytomegalovirus (CMV), possibly responsible for the prodromal illness, persisting in the course of the disease. PCR performed in the peripheral blood mononuclear cells (PBMCs), dna collected early and in the CSF drawn 30 days after the onset of the disease showed Epstein-Barr virus (EBV) dna. The serum panel of EBV antibodies was typical of an intercurrent virus reactivation, more than of a primary infection. CONCLUSION: EBV is known to be highly infectious for the nervous system, in this case of EMR the presence of dna sequences in the PBMCs and CSF suggests that EBV plays a role in the development of this newly described syndrome.
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