Hypothalamic abnormalities and Parkinsonism associated with H1N1 influenza infection.

OBJECTIVE: To describe a case of a young adult with severe H1N1 influenza illness associated with hypothalamic abnormalities and post-influenza parkinsonism. DESIGN: Case report. PATIENT: A 22-year-old woman with H1N1 influenza infection developed encephalopathy followed by diverse hypothalamic dysfunction manifestations, sleeplessness, and persistent parkinsonian features. RESULTS: CSF analysis, brain imaging and EEG ruled out hypoxic brain injury or other illnesses. CONCLUSIONS: A number of viruses have been associated with both acute and chronic parkinsonism. A link between parkinsonism and influenza viruses is somewhat controversial. This is the first reported case of parkinsonism following an H1N1 influenza infection.

Acute meningoencephalitis due to human immunodeficiency virus type 1 infection in 13 patients: clinical description and follow-up.

The objective of this study is to describe a series of cases of severe meningitis caused by human immunodeficiency virus type 1 (HIV-1) occurring during primary infection or after antiretroviral treatment interruption. In an observational cohort study, 13 patients with clinical diagnosis of meningitis or meningoencephalitis were reviewed. Ten cases occurred during primary HIV-1 infection and 3 after antiretroviral therapy (ART) withdrawal. Demographic parameters, clinical presentation and outcome, and laboratory and cerebrospinal fluid (CSF) parameters were recorded. The risk factor for HIV-1 infection acquisition was sexual transmission in all cases. The most frequent systemic symptoms were fever (12/13) and headeache (9/13). Among neurologic symptoms, focal signs appeared in seven patients (53.8%), confusion in six (46.2%), and agitation in five (38.5%). The median CD4 cell count was 434 cells/mm3. In all cases, CSF was a clear lymphocytaire fluid with normal glucose levels. Cranial computerized tomography was performed in seven patients, with a normal result in all of them; brain magnetic resonance in eight patients was normal in five cases and showing cortical atrophy, limbic encephalitis, and leptomeningeal enhancement in one patient each. The electroencephalographs (EEG) just showed diffuse dysfunction in three cases. ART was started in 11 patients. HIV RNA load at 12 months was <50 copies/ml in all treated patients. The 13 patients recovered without neurologic sequela. Meningitis or meningoencephalitis during primary HIV-1 infection or after ART cessation are unusual but sometimes a life-threatening manifestation. Although all patients tend to recover and the necessity of ART is not well established, some data suggest its potential benefit in these patients.

West Nile virus encephalitis.

West Nile virus (WNV) is a mosquito-borne virus that has caused a large number of deaths in the United States since the first outbreak in New York City in 1998. The outbreak initially was limited to the northeast but has since spread across the entire continental United States. WNV causes a variety of clinical symptoms, but the most severe consequences result from central nervous system infection, resulting in meningitis, encephalitis, or meningoencephalitis. We present a case of a 62-year-old male with metastatic cancer, who died as a result of WNV encephalitis. This is followed by a discussion on the epidemiology of WNV and a detailed summary of the methods and resources available to make a diagnosis of WNV infection postmortem. The material presented in the discussion should provide the forensic pathologist with all the information necessary to make a diagnosis of WNV infection postmortem. If nothing else, the routine collection and storage of serum, cerebrospinal fluid, and tissue for every case can enable the forensic pathologist to make this diagnosis even in cases in which WNV is not suspected until after autopsy.

Properties of a calicivirus isolated from cats dying in an agitated state.

In June 1993, two of five pet cats kept in Yokohama city in Japan suddenly became agitated and died. Feline calicivirus (FCV) was isolated from them. One strain (FCV-S) was isolated from the spinal cord, lung and tonsil of cat 1, another (FCV-B) from the ileum, medulla oblongata and cervical spinal cord of cat 2, and a third (FCV-SAKURA) from the oral cavity of one of the three surviving cats which showed no clinical signs. These three strains were equally resistant to pH 3.0 and serologically similar to each other, but distinct from strain F9. A genetic analysis, using a 208 base pair fragment from region E of the capsid, showed that FCV-Ari had a 70.4 per cent nucleotide and 77.3 per cent amino acid homology and FCV-F9 had a 68.6 per cent nucleotide and 73.9 per cent amino acid homology with the three strains, indicating that these two strains were genetically distinct from the three new isolates. Unvaccinated cats and cats which had been vaccinated against FCV-F9 developed watery diarrhoea but did not become agitated after the administration of FCV-S. The FCV-S strain did not induce signs of excitability after it was administered orally to specific pathogen-free cats.

Effects of genetic background on neonatal Borna disease virus infection-induced neurodevelopmental damage. I. Brain pathology and behavioral deficits.

The pathogenic mechanisms of gene-environment interactions determining variability of human neurodevelopmental disorders remain unclear. In the two consecutive papers, we used the neonatal Borna disease virus (BDV) infection rat model of neurodevelopmental damage to evaluate brain pathology, monoamine alterations, behavioral deficits, and responses to pharmacological treatments in two inbred rat strains, Lewis and Fisher344. The first paper reports that despite comparable virus replication and distribution in the brain of both rat strains, neonatal BDV infection produced significantly greater thinning of the neocortex in BDV-infected Fisher344 rats compared to BDV-infected Lewis rats, while no strain-related differences were found in BDV-induced granule cell loss in the dentate gyrus of the hippocampus and cerebellar hypoplasia. Unlike BDV-infected Lewis rats, more severe BDV-induced brain pathology in Fisher344 rats was associated with (1) greater locomotor activity to novelty and (2) impairment of habituation and prepulse inhibition of the acoustic startle response. The present data demonstrate that the same environmental insult can produce differential neuroanatomical and behavioral abnormalities in genetically different inbred rat strains.