The Norway rat as a reservoir host of Cryptosporidium parvum.

The potential of Norway rats (Rattus norvegicus) to spread the parasite Cryptosporidium parvum was investigated by examining parasite prevalence in relation to the structure and movements of three permanent rat populations living on farmland in Warwickshire (UK) from October 1994 to March 1997. One population lived among a group of farm buildings housing cattle, while the other two had no contact with livestock, one living around a pond and its outflowing stream and the other on a rubbish tip. Overall, parasite occurrence was 24% (n = 438), but it varied according to body weight (age) with 40% of juveniles (< or =100 g) infected decreasing to 12% for adults >400 g, suggesting that actively breeding populations are potentially more likely to spread the parasite than non-breeding populations. There was no difference in prevalence between the three populations. The parasite was detected in more males (29%) than females (19%). Seasonally, on the livestock farm, prevalence was significantly lower in autumn (10%), but varied little (31-36%) from winter to summer. In contrast, on the arable farm, prevalence peaked in summer (50%) with a trough in winter (6%). Infection in rats appeared to last <67 days. Rats living on the livestock farm had home ranges largely confined to the cattle sheds, thereby maintaining a potential source of infection for livestock if rodent control was not part of a decontamination program. Equally, rats living around the pond on the arable farm provided a source of oocysts to contaminate the pond water, as well as being able to carry the parasite to nearby farm buildings or even to neighboring farms.

Field trials of second-generation anticoagulants against difenacoum-resistant Norway rat populations.

Trials of rodenticidal baits containing 50 p.p.m. difenacoum, 50 p.p.m. bromadiolone or 20 p.p.m. brodifacoum were carried out on farmsteads against populations of Rattus norvegicus containing difenacoum-resistant individuals. Six difenacoum treatments failed in 14--42 days of baiting. Two treatments with bromadiolone succeeded in 23 and 33 days, but four further treatments lasting 35--56 days failed to eradicate the populations. Brodifacoum gave virtually complete control of six populations in 21--73 days and of the ten residual populations left behind by the other two compounds, after baiting for a further 11--85 days. The performance of both bromadiolone and brodifacoum was well below that reported by previous investigators, indicating the possibility of low-grade resistance to these compounds in the difenacoum-resistant strain.

High-speed automatic analysis of eeg spike and wave activity using an analogue detection and microcomputer plotting system.

Spike and wave activity is detected by analogue circuitry which separately filters the spike and the slow wave components from the EEG. The filter outputs are converted to DC voltages, which are then compared with individually adjusted threshold voltages. A detector output pulse is produced when both the spike and the wave threshold levels are exceeded. A graph of the incidence of spike and wave activity per 15 min intervals over 24 h is plotted by a microcomputer and modified impact printer. The analysis is carried out at 60 times real time on EEG recordings obtained from unrestrained patients using a portable cassette-tape recorder.

Sensorimotor rhythm feedback training and epilepsy: some methodological and conceptual issues.

This study examined the hypothesis that the enhancement of a 12-16 Hz sensorimotor rhythm in the EEG is inhibitory to epileptic seizure activity. The effects of training to enhance 12-16 Hz central EEG, to enhance 8-10 Hz central EEG, to suppress high voltage EEG activity, and of random feedback were compared over a period of 12 months in three adult patients suffering from chronic, drug-refractory epilepsy. All three patients experienced a significant reduction in seizure rate by the end of the study, but this was not related to any one particular training condition. It is suggested that the therapeutic mechanism might involve placebo effects, relaxation training, or a facilitation of EEG desynchronization, the effect being idiosyncratic to the individual patient.