Association of simian virus 40 with a central nervous system lesion distinct from progressive multifocal leukoencephalopathy in macaques with AIDS. (1/429)

The primate polyomavirus SV40 is known to cause interstitial nephritis in primary infections and progressive multifocal leukoencephalopathy (PML) upon reactivation of a latent infection in SIV-infected macaques. We now describe a second central nervous system manifestation of SV40: a meningoencephalitis affecting cerebral gray matter, without demyelination, distinct from PML. Meningoencephalitis appears also to be a primary manifestation of SV40 infection and can be seen in conjunction with SV40-induced interstitial nephritis and pneumonitis. The difference in the lesions of meningoencephalitis and PML does not appear to be due to cellular tropism, as both oligodendrocytes and astrocytes are infected in PML and meningoencephalitis, as determined by in situ hybridization or immunohistochemistry for SV40 coupled with immunohistochemistry for cellular determinants. This is further supported by examination of SV40 nucleic acid sequences from the ori-enhancer and large-T-antigen regions, which reveals no tissue-or lesion-specific variation in SV40 sequences.  (+info)

Listeria monocytogenes and Escherichia coli septicemia and meningoencephalitis in a 7-day-old llama. (2/429)

Listeria monocytogenes and Escherichia coli were isolated from blood collected on presentation and tissues samples taken postmortem. Listeria monocytogenes was isolated from cerebrospinal fluid collected antemortem. The importance of passive transfer of immunity, the subtlety of neurologic signs in early meningitis, and considering blood-CSF penetration in antimicrobial selection are discussed.  (+info)

Non-purulent meningoencephalomyelitis of a Pacific striped dolphin (Lagenorhynchus obliquidens). The first evidence of morbillivirus infection in a dolphin at the Pacific Ocean around Japan. (3/429)

On March 22, 1998, a mature, male, hyposthenic Pacific striped dolphin (Lagenorhynchus obliquidens) was stranded at Aoshima Beach in Miyazaki prefecture, Japan. A necropsy performed 14 hr after death revealed mild diffuse congestion and edema of the leptomeninges and mild pulmonary atelectasis. Histopathologically, non-purulent inflammatory were observed throughout the cerebrum, thalamus, midbrain, pons, medulla oblongata, and spinal cord. Hematoxylin and eosin stain revealed no viral inclusion bodies. Immunohistochemistry using a monoclonal antibody against nucleoprotein of canine distemper virus (CDV-NP) revealed a number of CDV-NP-positive granular deposits in the cytoplasm and cell processes of the degenerating or intact neurons. The present paper is a first report of spontaneously occurred morbillivirus infection in a dolphin at the Pacific Ocean around Japan.  (+info)

Comparative efficacies of antibiotics in a rat model of meningoencephalitis due to Listeria monocytogenes. (4/429)

The antibacterial activities of amoxicillin-gentamicin, trovafloxacin, trimethoprim-sulfamethoxazole (TMP-SMX) and the combination of trovafloxacin with TMP-SMX were compared in a model of meningoencephalitis due to Listeria monocytogenes in infant rats. At 22 h after intracisternal infection, the cerebrospinal fluid was cultured to document meningitis, and the treatment was started. Treatment was instituted for 48 h, and efficacy was evaluated 24 h after administration of the last dose. All tested treatment regimens exhibited significant activities in brain, liver, and blood compared to infected rats receiving saline (P < 0.001). In the brain, amoxicillin plus gentamicin was more active than all of the other regimens, and trovafloxacin was more active than TMP-SMX (bacterial titers of 4.1 +/- 0.5 log10 CFU/ml for amoxicillin-gentamicin, 5.0 +/- 0.4 log10 CFU/ml for trovafloxacin, and 5.8 +/- 0.5 log10 CFU/ml for TMP-SMX; P < 0.05). In liver, amoxicillin-gentamicin and trovafloxacin were similarly active (2.8 +/- 0.8 and 2.7 +/- 0.8 log10 CFU/ml, respectively) but more active than TMP-SMX (4.4 +/- 0. 6 log10 CFU/ml; P < 0.05). The combination of trovafloxacin with TMP-SMX did not alter the antibacterial effect in the brain, but it did reduce the effect of trovafloxacin in the liver. Amoxicillin-gentamicin was the most active therapy in this study, but the activity of trovafloxacin suggests that further studies with this drug for the treatment of Listeria infections may be warranted.  (+info)

A diagnostic rule for tuberculous meningitis. (5/429)

Diagnostic confusion often exists between tuberculous meningitis and other meningoencephalitides. Newer diagnostic tests are unlikely to be available in many countries for some time. This study examines which clinical features and simple laboratory tests can differentiate tuberculous meningitis from other infections. Two hundred and thirty two children (110 tuberculous meningitis, 94 non-tuberculous meningitis, 28 indeterminate) with suspected meningitis and cerebrospinal fluid (CSF) pleocytosis were enrolled. Tuberculous meningitis was defined as positive CSF mycobacterial culture or acid fast bacilli stain, or basal enhancement or tuberculoma on computed tomography (CT) scan with clinical response to antituberculous treatment. Non-tuberculous meningitis was defined as positive CSF bacterial culture or Gram stain, or clinical response without antituberculous treatment. Thirty clinical/laboratory features of patients with tuberculous meningitis and non-tuberculous meningitis were compared by univariate and multiple logistic regression analysis. Five features were independently predictive of the diagnosis of tuberculous meningitis (p < 0.007): prodromal stage >/= 7 days, optic atrophy on fundal examination, focal deficit, abnormal movements, and CSF leucocytes < 50% polymorphs. When validated on another set of 128 patients, if at least one feature was present, sensitivity was 98.4% and, if three or more were present, specificity was 98.3%. This simple rule would be useful to physicians working in regions where tuberculosis is prevalent.  (+info)

Detection of antibodies to Brucella cytoplasmic proteins in the cerebrospinal fluid of patients with neurobrucellosis. (6/429)

The diagnosis of human neurobrucellosis usually relies on the detection of antibodies to Brucella lipopolysaccharide (LPS) in cerebrospinal fluid (CSF) by agglutination tests or enzyme-linked immunosorbent assay (ELISA). Here we describe the detection of immunoglobulin G (IgG) to cytoplasmic proteins (CP) of Brucella spp. by ELISA and Western blotting in seven CSF samples from five patients with neurobrucellosis. While IgG to CP (titers of 200 to 12, 800) and IgG to LPS (800 to 6,400) were found in the CSF of these patients, these antibodies were not detected in CSF samples from two patients who had systemic brucellosis without neurological involvement. The latter, however, had serum IgG and IgM to both LPS and CP. No reactivity to these antigens was found in CSF samples from 14 and 20 patients suffering from nonbrucellar meningitis and noninfectious diseases, respectively. These findings suggest that, in addition to its usefulness in the serological diagnosis of human systemic brucellosis, the ELISA with CP antigen can be used for the specific diagnosis of human neurobrucellosis.  (+info)

The clinical and epidemiological profile of tick-borne encephalitis in southern Germany 1994-98: a prospective study of 656 patients. (7/429)

Seven hundred and nine patients fell ill in southern Germany (Baden-Wurttemberg) after infection with the tick-borne encephalitis (TBE) virus between 1994 and 1998. Detailed clinical and epidemiological data on TBE were available for 656 patients. A biphasic course of the disease occurred in 485 patients (74%). TBE presented as meningitis in 320 patients (49%), as meningoencephalitis in 270 (41%) and as meningoencephalomyelitis in 66 (10%). Eight of the patients (1.2%) died from TBE. Four hundred and forty-five patients (68%) had noticed a tick bite and the first symptoms occurred, on average, 7 days later. The most frequent neurological symptoms were impairment of consciousness (31%), ataxia (18%) and paresis of the extremities (15%) and cranial nerves (11%). Laboratory investigations revealed leucocytosis in the peripheral blood in 224 out of 392 patients (74%), elevation of the erythrocyte sedimentation rate in 223 out of 245 (91%), increased C-reactive protein in 127 out of 155 (82%), pleocytosis in the CSF of all patients tested, damage of the blood-CSF barrier in 255 out of 322 (79%), abnormalities in EEG in 165 out of 214 (77%) and abnormalities in MRI in 18 out of 102 (18%). In general, adolescents up to 14 years of age had a more favourable course of the disease than adults. Of 230 patients who were re-examined at a later time, 53 (23%) had moderate or severe sequelae. Patients with sequelae presented more frequently (P < 0.001) with impaired consciousness (Glasgow Coma Scale < 7), ataxia, pareses of the extremities or cranial nerves, a need for assisted ventilation, abnormal findings in MRI, pleocytosis > 300 cells/microl and impairment of the blood-CSF barrier (total protein > 600 mg/l). In view of the severity of the illness and the high frequency of sequelae, active immunization against TBE is recommended for all subjects living in and travelling to areas of risk. Prevention of TBE by post-exposure prophylaxis with hyperimmunoglobulins is less effective and therefore should be performed only when absolutely necessary.  (+info)

Erythrocyte-aggregating relapsing fever spirochete Borrelia crocidurae induces formation of microemboli. (8/429)

The African relapsing fever spirochete Borrelia crocidurae forms aggregates with erythrocytes, resulting in a delayed immune response. Mice were infected with B. crocidurae and monitored during 50 days after infection. Spirochetes were observed extravascularly at day 2 after infection. Two days later, inflammatory responses, cell death, and tissue damage were evident. The pathologic responses in lungs and kidneys were similar, whereas the symptoms in the brains were delayed, with a less pronounced inflammatory response. Microemboli were found in the blood vessels, possibly a result of the erythrocyte aggregation. The B. crocidurae invasion emerged more rapidly than has been described for Lyme disease-causing Borrelia species. In addition to erythrocyte rosetting, the presence of extravascular B. crocidurae indicates a novel route for these bacteria to propagate and cause damage in the mammalian host. The histopathologic findings in this study may explain the clinical manifestations of human relapsing fever.  (+info)