SUMMARYAn analysis was made of the spread of foot-and-mouth disease during the epidemic in Hampshire in January and February 1967. To explain the pattern of spread, it had to be postulated that virus was present seven days before the first outbreak was reported. It is suggested that the disease occurred initially in pigs fed on infected meat and that the virus was subsequently disseminated from the local abattoir, where the pigs were killed, to four farms by movement of animals, slaughterhouse waste, people or vehicles, and to fifteen by the airborne route. Subsequent spread from these farms was by movement in two instances and by the airborne route in five. The source and route of infection of the last farm in the outbreak were not determined.The risk of spread through movement was associated more with carriage of infected slaughterhouse waste, movement of animals, people or vehicles carrying animals than through collection of milk, artificial insemination or movement of other types of vehicles. Outbreaks of disease among pigs gave rise to more secondary spread than outbreaks in cattle. Secondary outbreaks attributed to airborne spread occurred only in ruminants. Most airborne spread was into areas of high livestock density and cattle in the larger herds became infected. Airborne spread could be correlated with wind direction and speed but not with rain. The reduction in the number of outbreaks at the end of the epidemic could be attributed to the elimination of the largest sources of virus, the control of movements and the fact that in all instances except two the wind was blowing virus over towns and out to sea, to areas of low stock density and to areas where animals had been killed.

Three adults with progressive cognitive decline and extrapyramidal dysfunction were studied. They were all mentally retarded women without known chromosomal abnormalities, ranging in age at the time of onset from 31 to 42 yrs with an average duration of illness of 6 yrs. Neurological signs were stereotyped and consisted of a unilateral equinovarus foot posture followed by progressive dementia, rigidity and quadriparesis. Identical pathological findings were noted in all cases. There was marked deposition of iron-containing pigments in the globus pallidus and reticulate zone of the substantia nigra. Numerous axonal spheroids were noted in these areas and in the gracile and cuneate nuclei. In addition to these typical changes of Hallervorden-Spatz disease (HSD), abundant neurofibrillary tangles (NFTs) were found within the hippocampus, neocortex, nuclei of basal forebrain, subthalamic nucleus and brainstem reticular formation. Rare Hirano bodies and granulovacuolar degeneration were noted within the hippocampus; neuritic plaques and amyloid deposits were absent. Ultrastructurally the NFTs were mostly paired helical filaments (PHFs) with a diameter of 20 to 25 nm and a half-periodicity of 80 nm. Straight filaments and incompletely twisted forms were also seen. Immunocytochemistry with polyclonal antibodies to PHFs was positive in a distribution identical to that of Bodian-positive NFTs. Biochemical analysis of frozen frontal cortex from 1 case revealed a 94% depletion of the cholinergic marker enzyme choline acetyltransferase. Somatostatin-like immunoreactivity was within normal range. Study of 1 case with laser microprobe mass analysis revealed evidence of aluminium accumulation in tangle-bearing hippocampal neurons. Adjacent tangle-free neurons failed to show comparable accumulations. These findings indicate that adult onset HSD occurring in mentally retarded individuals may represent a distinct clinicopathological entity associated with neurofibrillary pathology without amyloid deposition.

Pigs vaccinated with glutaraldehyde-fixed alveolar macrophages (AM) infected with African swine fever virus (ASFV) had an accelerated serological response after subsequent challenge and a slight reduction in levels of viraemia. Vaccination of pigs with detergent-treated infected AM produced no detectable serological response and no protection against homologous challenge. Guinea pigs were vaccinated with glutaraldehyde-fixed ASFV-infected cells, detergent-treated infected cells, detergent-treated infected spleen homogenate, purified ASFV or sonicated infected cells. Antibody was detectable by ELISA after vaccination with all preparations except the detergent-treated infected spleen vaccine. However, vaccination with purified ASFV or sonicated infected cells induced antibodies that were also strongly reactive in antibody-dependent cell-mediated cytotoxicity and complement-mediated lysis assays. If such antibodies are protective, immunization of pigs with purified ASFV or sonicated infected cells may induce a protective immunity.