Effects of aggregation and sample size on composite faecal egg counts in sheep

Composite faecal egg counts (FEC) are increasingly used to support strategic anthelmintic treatment decisions in grazing livestock. However, their accuracy as estimators of group mean FEC is affected by the number of individual samples included, how thoroughly they are mixed, and the underlying degree of parasite aggregation between individual hosts. This paper uses a Negative Binomial model for parasite aggregation, and a Poisson model for egg distribution within faecal suspensions, in order to optimise composite FEC protocol for commercial sheep flocks. Our results suggest that faecal egg density in a well-mixed composite sample from 10 sheep (3g of faeces from each), estimated by examination of four independently filled McMaster chambers, is likely to provide an adequate estimate of group mean FEC in the majority of situations. However, extra care is needed in groups of sheep for which high levels of FEC aggregation might be expected. The implications of statistical error in FEC estimates depend on how they are used. The simulation-based approach presented here is a powerful tool for investigating the risks of error in FEC-driven treatment decisions in different situations, as well as for the statistical analysis of parasitological data in general.     

Microgemma vivaresi (Microsporidia: Tetramicridae): host reaction to xenomas induced in sea scorpions, Taurulus bubalis (Osteichthyes: Cottidae)

Xenomas caused by Microgemma vivaresi Canning, Feist, Longshaw, Okamura, Anderson, Tsuey Tse et Curry, 2005 were found in liver and skeletal muscle of sea scorpions, Taurulus bubalis (Euphrasen). All muscle xenomas examined were in an advanced stage of destruction. In developing xenomas found in liver, parasites were restricted to the centre of the cell, separated from a parasite-free zone by a nuclear network formed by branching of the host cell nucleus. Although xenomas were able to reach a size of several hundred microns, the surface remained a simple plasma membrane. Host reactions took the form of penetration by phagocytes and isolation by fibroblasts. Once the xenoma had been attacked, the nuclear profiles became pycnotic and the barrier between parasitized and parasite-free zones was lost. Parasite antigens cannot be exposed at the surface of intact xenomas, as the host does not recognise the enlarging cell as foreign. Breaches in the plasma membrane of the xenoma and leakage of parasite antigens are thought to be the stimuli for phagocyte entry into the cell, its isolation by fibroblasts and eventual granuloma formation.