Subject(s)
Antiviral Agents/therapeutic use , Encephalitis/diagnosis , Epilepsy, Tonic-Clonic/virology , Fever/virology , Ganciclovir/therapeutic use , Herpesvirus 6, Human/pathogenicity , Encephalitis/drug therapy , Encephalitis/physiopathology , Epilepsy, Tonic-Clonic/drug therapy , Epilepsy, Tonic-Clonic/physiopathology , Fever/drug therapy , Fever/physiopathology , Humans , Infant , Male , Treatment OutcomeABSTRACT
Abnormal manifestations of central nervous system in system lupus erythematosus (SLE) patients are mainly caused by primary neuropsychiatric SLE (NP-SLE). We reported a new onset SLE patient who had secondary neuropsychiatric manifestations caused by Epstein-Barr virus (EBV) encephalitis. Although EBV has an uncertain association with SLE, Epstein-Barr virus encephalitis occurred in active SLE patients was not reported previously. Our report may be the first case about EBV encephalitis occurred in active SLE.
Subject(s)
Encephalitis, Viral/virology , Epstein-Barr Virus Infections/complications , Herpesvirus 4, Human/pathogenicity , Lupus Erythematosus, Systemic/complications , Anticonvulsants/administration & dosage , Antiviral Agents/administration & dosage , Depression/virology , Drug Administration Schedule , Encephalitis, Viral/diagnosis , Encephalitis, Viral/drug therapy , Epilepsy, Tonic-Clonic/virology , Epstein-Barr Virus Infections/diagnosis , Epstein-Barr Virus Infections/drug therapy , Glucocorticoids/administration & dosage , Headache/virology , Humans , Lupus Erythematosus, Systemic/diagnosis , Lupus Erythematosus, Systemic/drug therapy , Lupus Vasculitis, Central Nervous System/etiology , Male , Treatment Outcome , Young AdultABSTRACT
An 18-year-old woman presented with coma, hemicomvulsions, and transient periodic lateralized epileptiform discharges (PLEDs). Serological tests were positive for influenza B, and cerebrospinal fluid PCR for herpes simplex virus DNA was negative. Magnetic resonance imaging later showed abnormal signal intensity in the temporal lobe ipsilateral to the PLEDs. Influenza-associated encephalopathy may cause hemiconvulsions and PLEDs, and can mimic herpes simplex encephalitis.
Subject(s)
Encephalitis, Viral/complications , Epilepsy, Partial, Motor/virology , Epilepsy, Tonic-Clonic/virology , Influenza B virus , Influenza, Human/complications , Adolescent , Electroencephalography , Encephalitis, Viral/diagnosis , Encephalitis, Viral/physiopathology , Encephalitis, Viral/virology , Epilepsy, Partial, Motor/physiopathology , Epilepsy, Tonic-Clonic/physiopathology , Female , Functional Laterality , Humans , Influenza B virus/isolation & purification , Influenza, Human/diagnosis , Influenza, Human/virology , Periodicity , Tomography, X-Ray ComputedABSTRACT
The clinical features of infection with human herpesvirus 7 (HHV-7) are not well described. Exanthem subitum is the only illness that is confirmed to be caused by HHV-7. We report two children who had exanthem subitum associated with central nervous system manifestations. Two strains of HHV-7 were isolated sequentially from peripheral blood mononuclear cells and saliva of the some child who had exanthem subitum complicated with acute hemiplegia in childhood. Two strains were confirmed to be HHV-7 by means of monoclonal antibodies to human herpesvirus 6 (HHV-6) and HHV-7, polymerase chain reaction, and DNA analysis. During the convalescent period, the antibody titer to HHV-7 rose from less than 1:10 to 1:320, whereas the antibody titer to HHV-6 remained less than 1:10. Another child with exanthem subitum complicated by acute hemiplegia had serologic evidence of primary HHV-7 infection. These two cases demonstrate a new relationship between HHV-7 and central nervous system symptoms.
Subject(s)
Brain Diseases/virology , Herpesviridae Infections/pathology , Herpesvirus 7, Human , Antibodies, Viral/analysis , Brain Diseases/pathology , DNA, Viral/analysis , Epilepsy, Generalized/virology , Epilepsy, Tonic-Clonic/virology , Exanthema Subitum/pathology , Exanthema Subitum/virology , Female , Hemiplegia/virology , Herpesvirus 6, Human/genetics , Herpesvirus 6, Human/immunology , Herpesvirus 6, Human/isolation & purification , Herpesvirus 7, Human/genetics , Herpesvirus 7, Human/immunology , Herpesvirus 7, Human/isolation & purification , Humans , Infant , Leukocytes, Mononuclear/virology , Polymerase Chain Reaction , Saliva/virologyABSTRACT
Canine distemper virus (CDV) is thought to have caused several fatal epidemics in canids within the Serengeti-Mara ecosystem of East Africa, affecting silver-backed jackals (Canis mesomelas) and bat-eared foxes (Otocyon megalotis) in 1978 (ref. 1), and African wild dogs (Lycaon pictus) in 1991 (refs 2, 3). The large, closely monitored Serengeti lion population was not affected in these epidemics. However, an epidemic caused by a morbillivirus closely related to CDV emerged abruptly in the lion population of the Serengeti National Park, Tanzania, in early 1994, resulting in fatal neurological disease characterized by grand mal seizures and myoclonus; the lions that died had encephalitis and pneumonia. Here we report the identification of CDV from these lions, and the close phylogenetic relationship between CDV isolates from lions and domestic dogs. By August 1994, 85% of the Serengeti lion population had anti-CDV antibodies, and the epidemic spread north to lions in the Maasai Mara National reserve, Kenya, and uncounted hyaenas, bat-eared foxes, and leopards were also affected.
Subject(s)
Disease Outbreaks/veterinary , Distemper Virus, Canine , Distemper/virology , Lions/virology , Amino Acid Sequence , Animals , Animals, Domestic , Animals, Wild , Antibodies, Viral/analysis , Carnivora/virology , Distemper/epidemiology , Distemper/mortality , Distemper/pathology , Distemper Virus, Canine/isolation & purification , Dogs/virology , Epilepsy, Tonic-Clonic/pathology , Epilepsy, Tonic-Clonic/veterinary , Epilepsy, Tonic-Clonic/virology , Female , Kenya/epidemiology , Male , Molecular Sequence Data , Tanzania/epidemiologyABSTRACT
A patient presenting with a severe subacute encephalopathy was shown to be infected with a stealth virus. Although the patient partially recovered, he remained lethargic with cognitive impairment and worsening headaches. Ten months after the onset of his illness, his clinical condition further deteriorated with seizures, coma and death. A brain biopsy revealed vacuolated degenerate neural cells consistent with a stealth viral encephalopathy. Focal perivascular lymphocytic inflammation was present within the leptomeninges and to a lesser extent within the parenchyma of the brain. Vasculitis may occasionally contribute to the complex symptomatology of stealth viral encephalopathy.
