No abstract

Background Pre-Delta, vaccination reduced transmission of SARS-CoV-2 from individuals infected despite vaccination, potentially via reducing viral loads. While vaccination still lowers the risk of infection, similar viral loads in vaccinated and unvaccinated individuals infected with Delta question how much vaccination prevents onward transmission. Methods We performed a retrospective observational cohort study of contacts of SARS-CoV-2-infected index cases using contact testing data from England. We used multivariable logistic regression to investigate the impact of index case and contact vaccination on transmission, and how this varies with Alpha and Delta variants (classified using S-gene detection/calendar trends) and time since second vaccination. Results 51,798/139,164(37.2%) contacts tested were PCR-positive. Two doses of BNT162b2 or ChAdOx1 vaccines in Alpha variant index cases independently reduced PCR-positivity in contacts (aOR, adjusted odds ratio vs. unvaccinated=0.18[95%CI 0.12-0.29] and 0.37[0.22-0.63] respectively). The Delta variant attenuated vaccine-associated reductions in transmission: two BNT162b2 doses reduced Delta transmission (aOR=0.35[0.26-0.48]), more than ChAdOx1 (aOR=0.64[0.57-0.72]; heterogeneity p<0.001). Variation in viral load (Ct values) explained only a modest proportion of vaccine-associated transmission reductions. Transmission reductions declined over time since second vaccination, for Delta reaching similar levels to unvaccinated individuals by 12 weeks for ChAdOx1 and attenuating substantially for BNT162b2. Protection from vaccination in contacts also declined in the 3 months after second vaccination. Conclusions Vaccination reduces transmission of Delta, but by less than the Alpha variant. The impact of vaccination decreased over time. Factors other than PCR-measured viral load are important in vaccine-associated transmission reductions. Booster vaccinations may help control transmission together with preventing infections.

No abstract

SUMMARY Analyses of the ontogeny of temporal lobe epilepsy have been made using differential neuropathology as the internal control system; using differential aetiology as the internal control system; using laterality of lesion, onset‐age and gender. These analyses concur in suggesting: Severe convulsions of any provenance early in life tend to damage mesial temporal structures by convulsive hypoxia. The laterality of subsequent mesial temporal sclerosis is crucially dependent on age and sex. A re‐examination of 438 unselected children with febrile convulsions by age, sex, outcome and family history is presented. The patterns elicited suggest that there are two systems potentiating febrile seizures: A general propensity of infants to convulsive to cerebral insult. This propensity declines rapidly from birth onwards; the decline is more rapid in females. A specific propensity to convulsive in response to fever. This propensity is specifically gene‐dependent. The expression of the gene begins at about 6 months, rises rapidly to a peak at about 18 months, and thereafter declines to the population level. The effect is, again, gender‐dependent. RÉSUMÉ On a analysé différents facteurs dans 'ontogénèse de 'épilepsie du lobe temporal utilisant les différentes formes de lésions neuropathologiques comme système de con‐trôle interne; es différentes variétés étiologiques comme système de contrôle interne; la latéralité de la lésion, 'âge du début et le sexe. Cette analyse nous amène aux conclusions suivantes: Les convulsions graves de la première enfance tendent à produire des lésions dans les structures mesiales du lobe temporal par 'hypoxie consécutive aux convulsions. La latéralisation de cette sclérose mesiale temporale est en relation étroite avec 'âge et le sexe. De 'étude de 438 enfants non selectionnes ayant eu des convulsions fiébriles en tenant compte de 'âge, du sexe, de 'évolution et de 'histoire familiale, il semble que deux facteurs facilitent les crises convulsives: Une prédisposition générate des nourrissons à faire des crises convulsives lors 'une atteinte cérébrale. Cette prédisposition diminue rapidement à partir de la naissance et 'autant plus rapidement qu'il s'agit du sexe féminin. Une prédisposition spécifique à faire des convulsions, en réaction à la fièvre. Cette tendance est spécifiquement dépendante 'un gene. 'expressivité du gene commence autour de 6 mois, atteint son maximum vers 18 mois et redescend ensuite au niveau moyen de la population. Cet effet est, lui aussi, en relation avec le sexe.

Five of eight bears died during an outbreak of Aujeszky's disease in a travelling circus in the north of Spain. The bears had been fed on a diet which included raw pigs' heads. One of three Himalayan bears and a Kodiak bear died acutely with signs of the disease. One of four polar bears died acutely without signs, another died with signs of Aujeszky's disease while it was being treated, and a third died with enteritis and disseminated intestinal coagulation some time later without showing signs of the disease. A fourth polar bear recovered from the same gastrointestinal problem without showing signs of the disease. Although one of the two surviving Himalayan bears showed some signs referrable to Aujeszky's disease, the results of tests for neutralising antibodies were negative. Two of the polar bears, the Himalayan bear and the Kodiak bear were examined postmortem and three of them were examined histologically. No lesions referable to Aujeszky's disease were found. The tissues from one female polar bear were examined and shown to be positive for Aujeszky's disease virus by virus isolation, polymerase chain reaction, electron microscopy and fluorescent antibody tests. The DNA of the isolate was shown to be similar to that of the strains of the virus circulating in pigs in northern Spain some years earlier.