Herpes simplex encephalitis. Immunohistological demonstration of spread of virus via olfactory and trigeminal pathways after infection of facial skin in mice.

An immunohistological study of viral antigen (VA) in the brain was carried out in mice which had been infected with herpes simplex type 1 virus (HSV) in the skin of the face. In 77% of the mice with VA in the brain the olfactory system as well as the trigeminal system/brainstem was affected. The remaining 23% had VA in the trigeminal system/brainstem only. Eye swab cultures yielded HSV from all mice with VA in the olfactory system. The ease of access of virus infecting the face to the olfactory system shown in this model may have implications for human infections.

Herpes simplex encephalitis. Immunohistological demonstration of spread of virus via olfactory pathways in mice.

Six-week-old Balb/c mice were inoculated intranasally with a suspension of HSV1 virus and the distribution of viral antigen in the brain 3-7 days later was surveyed using the immunoperoxidase technique. Virus was first detectable in the brain 4 days later at 2 distinct sites: the trigeminal root entry zone in the brain stem and the olfactory bulbs. On succeeding days virus spread from the trigeminal focus to many other brain stem nuclei and, in some mice, to the thalamus and the cerebellum. From the olfactory bulbs, in a proportion of mice, virus spread to anterior olfactory nucleus, lateral olfactory tract, septal nuclei, temporal lobe, hippocampus and cingulate cortex. Infection of olfactory bulbs was found to occur following intracorneal as well as intranasal inoculation of virus. The relevance of this model to human herpes simplex encephalitis is discussed.

Disinfection studies with two strains of mouse-passaged scrapie agent. Guidelines for Creutzfeldt-Jakob and related agents.

A variety of disinfection procedures were tested on two strains of scrapie agent, treated either as brain macerates (autoclaving) or as 10% homogenates (chemical treatments). It is suggested that a given treatment should produce a titre loss, of both strains of scrapie, of at least 10(4) units before it be regarded as useful for the disinfection of the agents of scrapie and Creutzfeldt-Jakob disease (CJD). By this criterion, treatment at room temperature with about 4% Hycolin (0.6% chlorinated phenols), 0.2% permanganate, 5% Tego (dodecyl-di(aminoethyl)-glycine) or 5% sodium dodecyl sulphate (SDS) are unsuitable. However, data indicate that SDS might be used to reduce the heat stability of scrapie agent. Hypochlorite (Sterilex) was the only satisfactory chemical reagent tested. At least 10(4)-10(5) units of infectivity were lost by treatment with hypochlorite containing 1,000 ppm available chlorine after a 4-16 h exposure, or containing 10,000 ppm available chlorine after a half-hour exposure. The latter result points to the use of concentrated hypochlorite (about 2% available chlorine; approximately 20% Sterilex) to decontaminate surfaces. We suggest that the cleaning action of SDS, or other strong detergents, might also help to decontaminate surfaces, but studies on this are needed. Autoclaving at 126 degrees C for 1-2 h reduced titres by 10(3)-10(7) units, depending on the strain of agent. However, total disinfection of brain containing high titres of infectivity was approached only at 136 degrees C when titre losses of about 10(6) units were obtained by autoclaving for 4-32 min. Further studies are needed before we can make simple, general recommendations for the disinfection of CJD agents in hospital practice.

Measles virus and subacute neurological disease: an unusual presentation of measles inclusion body encephalitis.

A 20-year-old girl developed a subacute neurological illness characterized by seizures and epilepsia partialis continua, which resulted in her death within 10 weeks of her first symptom. Although she had a history of unusual reactions to viral infections, there was no evidence of any underlying disorder resulting in immunosuppression. Histopathology demonstrated the presence of dense infection with measles virus. The unusual clinical features of this cases suggest that measles virus may be responsible for a wide spectrum of neurological disease ranging from measles inclusion body encephalitis on the one hand to subacute sclerosing panencephalitis on the other.

Reye's syndrome associated with respiratory syncytial virus infection.

An upper respiratory tract infection in a 22-month-old boy was followed by rapid loss of consciousness, hypoglycaemia, uraemia, and death. Necropsy examination showed fatty change of liver and kidneys, severe cerebral oedema, bronchiolitis, and endocardial fibroelastosis affecting the left ventricle. Immunofluorescence staining showed infection with respiratory syncytial virus (RSV). The clinical and pathological findings were those of Reye's syndrome, not previously reported accompanying RSV infection.

Measles inclusion-body encephalitis in a child with treated acute lymphoblastic leukaemia.

A child with acute lymphoblastic leukaemia, being treated in the UKALL II Trial, had while in remission an attack of measles and made a normal recovery. Four months later she developed an acute encephalopathy and died within two weeks. The brain showed mild inflammatory features and widespread inclusion bodies in neurones and glial cells. Immunofluorescence proved an infection with measles virus. Similar cases have been called SSPE; reasons are given for preferring the term "measles inclusion-body encephalitis".

Immunofluorescence staining for the diagnosis of herpes encephalitis.

Direct immunofluorescence staining for herpes simplex virus was applied to cryostat sections of 43 specimens removed at brain biopsy. Herpes antigen was found in 10 specimens and virus was isolated from them. Antigen was found in one specimen from which virus was not isolated. Two specimens from which virus was isolated gave equivocal fluorescence. Thirty specimens gave no fluorescence or live virus. Immunofluorescence provided a diagnosis in three hr compared with 24-42 hr for virus isolation. Indirect immunofluorescence staining was applied to sections of brain removed at necropsy and fixed in formalin. Herpes antigen was found in sections of six of the 12 brains examined.

The incidence of complement-fixing antibody to varicella-zoster virus in hospital patients and blood donors.

The sera of 308 patients, not suffering from varicella or zoster infections, and the sera of 183 blood donors were examined for complement-fixing antibody to varicella-zoster virus. In both groups about 70% of sera from persons aged 11-40 years had antibody titres >/= 1/4; the incidence was less in the age range 41-60 years and increased in later decades. Antibody titres of 1/16 or 1/32 were noticeably less frequent in those aged 41-60 years than in younger or older groups.It was concluded that an unchanging titre of 1/16 or 1/32 was of no diagnostic significance. The age distribution of antibody was consistent with the theory that zoster only occurs when antibody has declined.