Chlamydia trachomatis detected in human placenta.

AIMS: To evaluate the relation between Chlamydia trachomatis infection and stillbirth, placental tissue was studied for the presence of C trachomatis. METHODS: Paraffin wax embedded placental tissue of a stillbirth fetus, born at the 36th week of gestation to a 21 year old mother with high serum antibody titres to C trachomatis immunotypes during pregnancy and who was culture positive to C trachomatis three years previously, was studied by in situ hybridisation, polymerase chain reaction, and immunohistochemistry for the presence of C trachomatis. RESULTS: C trachomatis was detected in placental specimens by in situ hybridisation and alkaline phosphatase antialkaline phosphatase staining in several sections, whereas control tissues were uniformly negative, indicating the presence of C trachomatis nucleic acid and antigen in the placenta. CONCLUSION: This is the first reported case in which C trachomatis has been demonstrated in the human placenta.

Culturing of acoustic neuroma--methodological aspects.

We have been able to culture acoustic neuroma (AN) tissues by taking small tumor pieces during surgery from the cisternal or, preferably, metal part of the tumor where macroscopic tissue degeneration is not prominent. The AN pieces were transported in culture tubes to our cell laboratory where they were sliced and transferred to culture medium. The AN tissue demands a crude culture suspension containing laminin. We have been successful in culturing 15 successive ANs. The cells have different morphological features with characteristics of type Anthony A and B. Four main cell types were recognized: ameboid microglia-like cells, spindle-shaped cells, racket-shaped cells, and kite-shaped cells. However, no immortal cell line could be established. Some of the cultures were viable for up to 4 months.

Baltic myoclonus.

It has been found that PME without Lafora bodies is more common in Finland than elsewhere. The incidence is 1:20,000. The mode of inheritance is autosomal recessive. At first the children are healthy. Stimulus-sensitive myoclonic jerks and grand mal seizures appear at the age of 6 to 15 years. The EEG shows a generalized disturbance with spike-wave or polyspike-wave paroxysms which increase during photic stimulation. Myoclonic jerks incapacitate the patient. Within 5 years after the onset of the first symptoms, many patients have a disorder of gait and may become confined to bed. Sodium valproate alone or combined with clonazepam is the most effective therapy. However, the course of the disease is progressive. The mean age at death has been 24 years but appears to be increasing. The etiology and pathogenesis of PME without Lafora bodies are unknown. Increased excretion of indican has been noted, suggesting deficient intestinal absorption of L-tryptophan. A loss of Purkinje cells is the most prominent neuropathological feature. No inclusion bodies are present. Finnish PME patients are similar to the patients described by Unverricht from Estonia and by Lundborg from Sweden. Neuropathological data from these patients are not available. Clinically, these patients could form an entity with Finnish patients defined as a Baltic or Nordic type of PME. The gene is enriched in Finland, but elsewhere it is rare.

Altered white cell count, protein concentration and oligoclonal IgG bands in the cerebrospinal fluid of many patients with acute psychiatric disorders.

In a prospective study, an abnormal white cell count and/or elevated protein concentration in the cerebrospinal fluid (CSF) was observed in 14/54 patients (26%) with acute psychiatric disorders, but in none of the 46 control subjects (p less than 0.001). In addition, electrophoretic analysis of immunoglobulin G (IgG) showed an oligoclonal pattern in the CSF of 22 psychiatric patients (41%). No such pattern could be detected in the control group (p less than 0.001). These findings reinforce the value of lumbar puncture and CSF analysis in acute psychiatric disorders.

Herpes simplex virus encephalitis. Prolonged intrathecal IgG synthesis and cellular activity in the cerebrospinal fluid with transient impairment of blood-brain barrier.

Alterations of cerebrospinal fluid (CFS) proteins and cells and blood-brain barrier impairment were determined in 4 patients with proven and 2 patients with presumptive herpes simplex virus encephalitis ( HSVE ) using simultaneous nephelometric measurements of CSF and serum albumin and immunoglobulins and combined MilliporeR filtration-cytocentrifuge cytologic techniques. The follow-up period ranged from 17 to 855 days. All patients showed intrathecal IgG synthesis which in 1 case continued for 28.5 months (855 days). The daily production of IgG in the central nervous system ranged up to 1157 mg. CSF-IgA and -IgM were also elevated in the early phase of the disease. The impairment of the blood-brain barrier was variable being apt to develop during the first 2 months of the disease and diminishing thereafter. Pleocytosis, mainly due to lymphoid cells, varied from slight to severe (325 X 10(3) cells/ml) and was observed in the CSF of all cases during the first 2 months. Lymphoid reaction (increase of enlarged stimulated lymphoid cells) was persistent and was the most pronounced cellular alteration. The lymphoid reaction and intrathecal IgG synthesis indicated continuous immunoactivation of the CNS, which was most intensive during the first 2 months and appeared to persist for at least 16-28.5 months.

Gyriform calcification after herpes simplex virus encephalitis.

Intracranial calcification simulating Sturge-Weber syndrome is rare in association with intracranial infection. A case of bilateral gyriform calcification after herpes simplex virus encephalitis evaluated by repeat computed tomography (CT) scans is presented. To our knowledge this is the first published report of CT findings in this entity.

Simultaneous determination of tryptophan and its 5-hydroxy metabolites in human cerebrospinal fluid by reversed phase liquid chromatography with electrochemical detection.

A sensitive ion-pair reversed phase liquid chromatographic method for determining tryptophan, 5-hydroxytryptophan, 5-hydroxytryptamine (serotonin) and 5-hydroxyindole acetic acid has been developed. To separate these indoles in cerebrospinal fluid both octadecyl- and phenyl-bonded columns were tested. The effect of an ion-pair reagent (n-heptyl sulphonate) and pH of the mobile phase on the separation was examined. With the method described the concentrations of the four indoles can be determined within 45 min without sample pretreatment. The sensitivity obtained with electrochemical detection is 0.45 mumol/l for tryptophan and 2-4 nmol/l for 5-hydroxyindoles in human cerebrospinal fluid samples.

Cerebrospinal fluid IgG bands and virus-specific IgG, IgM, and IgA antibodies in herpes simplex virus encephalitis.

To characterize the immune response of the central nervous system in herpes simplex virus (HSV) encephalitis, cerebrospinal fluid (CSF) specimens of 7 biopsy proven and 7 presumptive herpes simplex virus (HSV) encephalitis patients were studied, using sodium dodecyl sulfate polyacrylamide gel electrophoresis for the presence of CSF IgG bands, and solid-phase enzyme immunoassays for HSV-specific antibodies. IgG bands were detected in all CSF specimens of the patients, as early as day 6 and up to day 1088. A novel, unidentified, 120 000 dalton polypeptide was found in the CSF of most of the patients, in a total of 25/50 specimens, but not in the controls. This polypeptide was evident by day 6, its intensity fluctuated and it was present in specimens collected as late as day 855. HSV-specific antibodies, of either IgG, IgM, or IgA class, were not detected in the CSF during the first week of illness. IgG antibodies appeared later in all patients and persisted to the end of the follow-up of 3 years. The fact that CSF IgG bands were present in some patients before the appearance of HSV antibodies, and also persisted longer, suggests that the IgG response is not restricted to HSV-specific antigenic determinants.

Chronic encephalomyelitis with specific increase in intrathecal mumps antibodies.

Symptoms of severe encephalomyelitis developed in a 31-year-old man in 1967. He had a high serum antibody titre to mumps virus associated with a polymorphic cell reaction and an increased protein concentration in cerebrospinal fluid (CSF). He recovered considerably within a year and was able to resume work. In 1975 his condition deteriorated again; it improved during the following few years, but a further deterioration then occurred. In March, 1981, the complement-fixing antibody titre to mumps virus was 1/32 in the serum and 1/4 in the CSF. In November, 1981, the CSF IgG index was increased and the altered serum/CSF antibody ratio persisted. The specificity of the altered antibody ratio was confirmed by the single radial haemolysis test and an immunoassay specific for mumps virus. Antibodies against the mumps virus envelope glycoprotein, M-protein, and nucleoprotein could be demonstrated by immunoprecipitation and the antibody patterns in serum and CSF were similar. Antibodies against other microorganisms were not detected in the patient's CSF, and mumps antibodies were not found in the CSF specimens of 57 control patients. This case may be an example of a new disease-chronic mumps virus infection in the central nervous system.

Diagnostic value of cerebrospinal fluid antibodies in herpes simplex virus encephalitis.

Antibodies to different viruses and bacteria were measured in the cerebrospinal fluid (CSF) of six patients with herpes simplex virus encephalitis proven by brain biopsy and in five others with a presumptive diagnosis. Antibodies to herpes simplex virus but not to other organisms appeared in the CSF of all patients after the first weeks of the illness. Herpes simplex virus antibodies were not found in control CSF. The antibodies persisted in the CSF and the serum/CSF antibody ratio remained altered, 32:1 to less than 1:1, in all cases during the follow-up to 29 months or until death. The CSF albumin level was normal and the IgG index (formula: see text) elevated in four proven and three presumptive cases indicating a local antibody production; in four patients the findings were inconsistent. These results suggest that prolonged antigen stimulation is present in the central nervous system after acute herpes simplex encephalitis and that serological measurements combined with immunoglobulin and albumin determinations may provide a tentative but not definite diagnosis in some cases after the acute phase of encephalitis together with a method for follow-up of patients.

Acute encephalitis of viral origin.

75 patients with acute encephalitis of confirmed or suggestive viral or virus-like etiology showed a predominance of herpes simplex virus (HSV) as an etiological agent (13.3-32.0%) in all age groups without seasonal variation and increasing in number during years. Mumps, occurring mainly in female patients, was next in order and thereafter coxsackievirus B, varicella-zoster, and adenoviruses, followed by multiple coincident infections, and a large number of occasional agents. HSV seems to have displaced tick-borne encephalitis virus as the major cause of acute encephalitis in Finland. Pregnancy appeared to increase susceptibility to HSV encephalitis. The outcome was associated with the etiological agent in the first hand, HSV and nonviral microbes appeared unfavourable, but also with the clinical symptomatology, particularly altered consciousness, mental symptoms and focal neurological signs. The need for exact and rapid diagnosis in all cases of acute encephalitis is underlined in view of the possibility of specific therapy.

Trial with human leucocyte interferon and vidarabine in herpes simplex virus encephalitis: diagnostic and therapeutic problems.

A combination therapy of human interferon, vidarabine, and dexamethasone was administered to six patients with proven (Patients I-III) or presumed (Patients IV-VI) herpes simplex virus encephalitis (HSVE). Interferon combined with dexamethasone was given to one patient with presumed HSVE (Patient VII). Leucopenia and elevated serum transaminase levels appeared in all patients and a diffuse bleeding in one of them. Patients II, III and IV died, 26, 43, and 209 days after the onset of encephalitis, respectively. Patients I, V, VI, and VII were left with moderate brain damage although their physical condition was good. HSV encephalitis presents diagnostic difficulties, complementary diagnostic methods are needed, and current therapeutic trials must be considered as preliminary.

Deficient intestinal absorption of L-tryptophan in progressive myoclonus epilepsy without Lafora bodies.

L-Tryptophan was administered orally to 7 patients with progressive myoclonus epilepsy (PME) without Lafora bodies and 7 controls. Total and free plasma tryptophan wre subsequently measured at intervals. Concentration of free tryptophan was equal in the two groups. Total tryptophan was significantly lower in PME patients and the difference became marked at 120 and 240 min after the oral dose. At the same time urinary excretion of indican rose in PME patients but not in controls but the change was not statistically significant. Urinary 5-HIAA excretion was a little lower in PME patients. The increase of 5-HIAA after administration of L-tryptophan was equal in both groups. Intravenous administration of L-tryptophan produced an equal increase of plasma concentrations in PME patients as in controls, measured at 2-h intervals. These findings suggest incomplete absorption of L-tryptophan through the intestinal tract in PME patients.

Computed tomography appearance of Herpes Simplex encephalitis.

The eight computed tomography (CT) scans in five patients with proven herpes simplex encephalitis (HSVE) showed a low density lesion in the deep temporal lobe. In one patient the deep frontal and occipital lobes were also involved. Contrast enhancement was present in all patients examined within 78 days of the onset of symptoms. CT is valuable in the investigation of patients suspected of having HSVE and for whom it is vital to exclude a temporal lobe tumour or abscess. A CT examination may indicate the site for a brain biopsy to confirm the diagnosis.