Cases reported "Encephalitis"

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1/14. Chromosomal rearrangements affecting biofilm production and antibiotic resistance in a staphylococcus epidermidis strain causing shunt-associated ventriculitis.

    During two clinical courses of shunt-associated meningitis in a 3-month-old child, five multiresistant S. epidermidis isolates were obtained and analyzed with regard to biofilm production and antibiotic susceptibility. Three S. epidermidis strains, which were initially isolated from the cerebrospinal fluid, produced biofilms on polystyrene tissue culture plates. Following antibiotic treatment and subsequent exchange of the shunt system, sterilization of the CSF was achieved. However, after three weeks a relapse of the infection occurred. The two S. epidermidis isolates obtained now were biofilm negative, but showed an identical resistance pattern as those from the previous infection, except that resistance to rifampicin and increased mininal inhibitory concentrations of aminoglycoside antibiotics had emerged. dna fingerprinting by PFGE indicated the clonal origin of all isolates. However, some DNA rearrangements and differences in the IS256-specific hybridization patterns could be identified in the isolates from the second infection period that led to altered biofilm formation and increased expression of aminoglycoside resistance traits. The data evidence that variation of biofilm expression occurs in vivo during an infection and highlight the extraordinary genome flexibility of pathogenic S. epidermidis.
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2/14. early diagnosis and successful treatment of acute cytomegalovirus encephalitis in a renal transplant recipient.

    We report the case of a 40-year-old male hiv-negative renal transplant patient with allograft rejection and immunosuppressive therapy who presented with acute cytomegalovirus (CMV) encephalitis. CT and MRI of the brain were normal but EEG showed diffuse slowing and dysrhythmia. In cerebrospinal fluid (CSF) initially 81 cells/microliters were found and immunocytochemistry showed a decreased CD4/CD8 ratio and increased values of activated lymphocytes, natural killer cells and immunoglobulin-containing cells. CMV-specific IgM antibodies in CSF and serum, immunostaining of CMV antigen in CSF cells and virus culture from CSF and urine were negative. During the first 3 weeks of illness no intrathecal production of immunoglobulins could be detected. early diagnosis of CMV encephalitis was made by in situ hybridization (ISH) on CSF cell preparations and the polymerase chain reaction (PCR) which was positive in CSF and blood. On day 26 diagnosis was confirmed by detection of CMV-specific intrathecal IgG production. The patient was treated with ganciclovir, anti-CMV immunoglobulins and intrathecal beta interferon. He recovered completely after 2 months. Our data demonstrate the usefulness of ISH and PCR in the early diagnosis of CMV encephalitis and perhaps may encourage the use of intrathecal beta interferon in other patients with this disease.
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3/14. Presence, distribution and spread of productive varicella zoster virus infection in nervous tissues.

    Nervous tissue lesions were retrospectively studied for detection of productive varicella zoster virus (VZV) infection in 33 autopsied cases, including 19 herpes zoster (HZ) (10 trigeminal, nine spinal) and 14 cases of nodular brainstem encephalitis without HZ. Immunocytochemistry for VZV antigens and in situ hybridization with a biotinylated VZV DNA probe were used on formol-fixed paraffin sections. Peripheral and central nervous system, skin and striated muscle were investigated in serial sections; available tissue blocks, however, varied between cases. Varicella zoster virus production (both antigen and DNA) in nervous tissue was found in HZ cases but only of short survival after a rash of up to 7 wks (eight out of 12 patients). Varicella zoster virus was visualized in nerve cells, glial cells, schwann cells and blood vessels. In the central nervous system (CNS), VZV was detected in trigeminal nuclei (one out of 10 brains) or disseminated nodular brainstem lesions (one out of 10 brains), in subependymal microvessels (one out of 10 brains) or vasculitic arteries (two out of 19 brains or spinal cords). In the peripheral nervous system (PNS), VZV (DNA and antigen) was found in neurons and satellite cells of sensory ganglia (four out of seven cases with sampling of ganglia), and in damaged nerve fibres including a muscle nerve in one case; myositis with VZV in affected muscle fibres was found in the latter case. In nodular brainstem encephalitis, one case contained VZV within nodular lesions. We conclude that (i) VZV neural spread is suggested by detectable virus in ganglia, nerve fibres and CNS target nuclei; (ii) haematogenous spread of VZV is suggested by detection of virus in CNS microvessels and in disseminated brainstem encephalitis; (iii) VZV myositis may occur in zosteric myotomes; and (iv) VZV is a possible agent in nodular brainstem encephalitis.
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4/14. cytomegalovirus encephalitis in a non-immunocompromised patient: CSF diagnosis by in situ hybridization cells.

    cytomegalovirus (CMV) encephalitis in immunologically normal patients is rarely reported in the literature. CMV infection was diagnosed by viral DNA probe techniques on CSF cells in a 32-year-old, immunologically normal male presenting with a severe clinical picture due to encephalitis. Administration of ganciclovir was followed by an immediate improvement in the patient's condition. More sensitive techniques for CMV detection could allow to discover more cases of CMV encephalitis in non-immunocompromised patients than previously recognized.
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5/14. Evolution of post-natal herpes simplex virus encephalitis to multicystic encephalopathy.

    A 3-week-old, previously healthy infant developed biopsy-proven Herpes virus type 2 (HSV-2) encephalitis. The encephalitis was characterized by cells having intranuclear inclusions and was without evidence of inflammation or hemorrhage. neuroimaging studies did not show any destructive lesions in the brain. In spite of antiviral therapy, the infant's neurological conditions deteriorated, and the patient died at the age of 18 weeks. Post-mortem examination showed that most of the cerebral hemispheres were replaced by multiloculated cystic cavities of various sizes, typical of multicystic encephalopathy (MCE). The cystic lesions were randomly distributed and were not confined to any vascular territory. By light microscopy, there were no features of viral infection in the brain. Although in situ hybridization of the biopsy specimen taken during the acute phase of the disease demonstrated abundant HSV genome, this same method failed to detect HSV on the post-mortem specimen. These findings suggest that HSV-2 can induce MCE. Furthermore, the absence of histological features of viral encephalitis and the failure to demonstrate viral genome in the brain at autopsy does not exclude an infectious etiology in certain cases of MCE.
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6/14. Adenovirus encephalitis and widespread ependymitis in a child with AIDS.

    A 4-year-old child with AIDS developed encephalitis 2 months prior to death. Adenovirus was cultured from the cerebrospinal fluid. At autopsy, sections of the brain revealed complete sloughing of the intracranial ependyma, with marked gliosis and edema of the periventricular white matter. Cells with large, dark, smudgy intranuclear inclusions, consistent with adenovirus inclusions, were also seen in subependymal locations. in situ hybridization studies confirmed the presence of adenovirus DNA in these cells. This represents a case of morphologically proven adenovirus encephalitis in a pediatric AIDS patient.
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7/14. Pathologic features of AIDS encephalopathy in children: evidence for LAV/HTLV-III infection of brain.

    The neuropathologic findings in 11 children with a new CNS disorder that occurs in children with the acquired immunodeficiency syndrome (AIDS) and is postulated to be due to LAV/HTLV-III, the virus that causes AIDS, are reported. The children, who ranged in age from 4 months to 11 years, died of AIDS complicated by progressive encephalopathy. Ten of the children either had positive serum antibody for LAV/HTLV-III or had received blood products from donors later found to be antibody-positive. Examination of the brains of these children at autopsy revealed a unique constellation of findings, including varying degrees of diminished brain weight in all cases, inflammatory cell infiltrates in nine brains, multinucleated cells in eight, three of which also contained multinucleated giant cells, vascular calcification in ten, vascular and perivascular inflammation in five, and white matter changes in nine. Inflammatory and vascular lesions were most prominent in basal ganglia and pons. LAV/HTLV-III retroviral particles, associated with multinucleated giant cells, were observed in two brains on electron microscopic examination. These two and one additional brain had evidence of the LAV/HTLV-III genome by hybridization studies. Only one brain had a recognizable opportunistic infection.
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8/14. Human T-cell lymphotropic virus type III infection of the central nervous system. A preliminary in situ analysis.

    patients with the acquired immunodeficiency syndrome (AIDS) are subject to a spectrum of central nervous system (CNS) disorders. Recent evidence implicates the human T-cell lymphotropic virus type III (HTLV-III) in the pathogenesis of some of these illnesses, although, the cells infected by the virus have yet to be identified. Using in situ hybridization, we examined brain tissue from two patients with AIDS encephalopathy for the presence of HTLV-III rna. In both cases, viral rna was detected and concentrated in, though not limited to, the white matter. The CNS cells most frequently infected included macrophages, pleomorphic microglia, and multinucleated giant cells. Less frequently, cells morphologically consistent with astrocytes, oligodendroglia, and rarely neurons were also infected. The findings strengthen the association of HTLV-III with the pathogenesis of AIDS encephalopathy. in situ hybridization can be applied to routinely prepared biopsy tissue in the diagnosis of HTLV-III infection of the CNS.
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9/14. Concurrent herpes simplex type 1 necrotizing encephalitis, cytomegalovirus ventriculoencephalitis and cerebral lymphoma in an AIDS patient.

    Unlike cytomegalovirus (CMV) ventriculoencephalitis, herpes simplex virus type 1 necrotizing encephalitis has only rarely been observed in AIDS patients. A 40-year-old bisexual man was followed for an HIV1 infection from 1987 onwards. In June 1993 he was referred for sudden confusion, left hemiparesia and fever. The blood contained less than 10 CD4 lymphocytes/mm3. The patient remained comatose and febrile, and died 4 weeks later. In coronal sections of the brain there was necrosis of the internal parts of the left temporal lobe, necrosis of certain areas of the ventricular walls and a small tumor at the top of the right frontal lobe, which proved to be a polymorphic high-grade lymphoma. CMV ventriculoencephalitis lesions were prominent in the ventricular walls of the occipital lobes and there was a strong nuclear signal for CMV using in situ hybridization. herpes simplex virus type 1 was shown in the nuclei and cytoplasm of certain neurons and astrocytes in the borders of the necrotized temporal lobe areas by immunohistochemistry, in situ hybridization and electron microscopy, whereas in situ hybridization and immunohistochemistry for CMV were negative in such areas. Necrotizing type 1 encephalitis must not be overlooked in immunodeficient patients.
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10/14. Life-threatening infectious mononucleosis: is it correlated with virus-induced T cell proliferation?

    infectious mononucleosis is a well-established clinical entity characterized by the proliferation of B lymphocytes that are infected with Epstein-Barr virus (EBV). These lymphocytes give rise to an increase in specifically reacting cytotoxic T cells, which leads to self-limitation of the lympho-proliferative process. We describe the case of a 1-year-old boy who developed life-threatening EBV infection in association with liver failure, depletion of bone marrow, and severe encephalitis. The fact that clinical cure was achieved when acyclovir (50 mg/[kg.d]) and prednisolone (1 mg/[kg.d]) were administered indicates a correlation between antiviral therapy and clinical improvement. Hypogammaglobulinemia--which had not been present at the onset of disease--persisted after clinical recovery. During the acute phase of the illness, the patient's blood lymphocytes were predominantly T cells, most of which contained the EBV genome, as shown by in situ hybridization; some of these cells stained positive for EBV-specific latent membrane protein. Examination of peripheral blood mononuclear cells in vitro revealed an exceedingly high histocompatibility antigen-unrestricted cytotoxicity against the K562 cell line, which is normally not an immunogenic target of cytotoxic cells in patients infected with EBV. This anomalous natural killer cell-like T cell function suggests that EBV infection of T cells might cause auto-aggressive activity, which was probably responsible for the severity of the infection in our patient.
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