Baiting intervals and duration of control of the small fox tapeworm: a simulation study

Field trials to control the small fox tapeworm Echinococcus multilocularis failed to reduce the prevalence of the parasite persistently. With the experience from this empirical work, a simulation model for the population dynamics of the small fox tapeworm was developed. This model is used to examine the effect of different control strategies. Sufficient control duration is able to eradicate the parasite in simulation experiments. Baiting intervals of 4 or 6 weeks were found to be more efficient than shorter or longer intervals. The strategy used in field trials showed no sustainable effect in any of the simulation experiments. The applicability of simulation models for the planning of control measures for wildlife diseases is discussed.     

Controlling Echinococcus multilocularis-ecological implications of field trials

Two field trials to reduce the prevalence of Echinococcus multilocularis in foxes have been conducted in recent years. Although both trials reduced prevalence considerably, they failed to eradicate the parasite in the study region. Following the control trial in northern Germany, prevalence recovered unexpectedly and rapidly, reaching pre-control levels five quarters (15 months) after the end of control. To understand the internal dynamics of the parasite-host system's reaction to control, we developed a spatially explicit simulation model, Echi. The simulation model incorporates the information available concerning fox tapeworm population dynamics.Using epidemiological parameters to adjust pre-control prevalence, the model predicts the temporal evolution of the prevalence of E. multilocularis in controlled foxes without departing from the range of uncertainty of the field data. However, the model does not predict the rapid pre-control recovery observed in the field trial.The deviation of the model's prediction from field data indicates the involvement of processes not yet taken into account. We modified the model step by step to mimic processes with the potential to cause the rapid post-control recovery of the prevalence of E. multilocularis in foxes.Neither the longevity of tapeworm eggs nor the migratory behaviour of foxes showed any influence on the post-control reaction of the parasite-host system. However, landscape structures leading to a heterogeneous distribution of infected foxes have the potential to alter the system's reaction to control. If infected foxes are concentrated in multiple clusters in the landscape, the model prediction tallied with the range of uncertainty of the field data. Such spatial distribution of infected foxes may be caused by differential abiotic conditions influencing the survival of tapeworm eggs.The model was found to comply best with field data if the foxes acquire partial immunity by being exposed to the fox tapeworm.Both hypotheses explaining the rapid post-control recovery of the prevalence of E. multilocularis observed in the fox population were supported by field data.Both hypotheses have far-reaching consequences for future control trials. The spatial aggregation of infected foxes would enable control efforts to be concentrated on these highly infected areas. However, the acquisition of immunity acts as a buffer to control, necessitating intensified control measures.     

Formation of wall openings in root cells of Arabidopsis thaliana following infection by the plant-parasitic nematode Heterodera schachtii

The induction and differentiation of feeding structures (syncytia) of the cyst nematode Heterodera schachtii in roots of Arabidopsis thaliana is accompanied by drastic cellular modifications. We investigated the formation of cell wall openings which occurred during syncytium differentiation. At the beginning of syncytium induction, a callose-like layer was deposited inside of the wall of the initial syncytial cell (ISC). First wall dissolutions developed by gradual widening of plasmodesmata between the ISC and neighbouring cells. As a general thickening of syncytial cell walls blocked existing plasmodesmata, other large openings were formed by enzymatic dissolution of intact walls by putative cellulase activity.