The effect onOrchestia hurleyi(Amphipoda: Talitridae) of a whitey disease caused byBacillus subtilis

Publisher Website
Google Scholar
Abstract
Field observations made over 10 years suggested that a bacterial disease of adults of the terrestrial amphipod Orchestia hurleyi Duncan, caused by Bacillus subtilis, is progressing southwards down the eastern side of New Zealand's South Island. As the disease spread, amphipod density appeared to decline and population age structure became truncated. In the vicinity of Dunedin and further south the amphipods are still disease-free. Signs of the disease are a progressive weakening and wasting. The animal cannot jump, and its speed of walking is reduced. Its body becomes opaque white instead of the normal translucent reddish-brown. Diseased females do not brood. There is no evidence that diseased animals moult. Death is caused by general wasting or by predators. The disease-causing organism was isolated, and healthy amphipods were re-infected from the isolate. Signs of the disease were apparent within 7 days of inoculation. The presence of the disease-causing organism in the haemocoel causes host defences to be mobilised, as shown by elevated haemocyte counts (4512 mm−3, cf. 300 mm−3 in healthy, disease-free adults), but as the disease progresses the animal's defences are overcome, and haemocyte counts fall to an average of 784 mm−3 during the later stages of disease. The blood of terminally diseased amphipods is thick and creamy white, packed with motile bacterial cells, and few (if any) haemocytes are present in the circulation. Two populations were studied, one disease-free (at Dunedin) and the other heavily diseased (at Christchurch). The incidence of disease (as measured by a performance test) was about 30%r in Christchurch adults. The disease-causing strain of B. subtilis was found on the body surface of almost all adults in the diseased population. It is possible that the bacterium gains entry to the haemocoel through wounds suffered during ecdysis, conflict, or predator attack. The main differences shown by the diseased population relative to the disease-free population were: lower average density (992 m−2, cf. 1677 m−2); lower maximum density (3104 m−2, cf. 9971 m−2); smaller average size, with fewer adult instars; a smaller proportion of females brooding in each instar; and much lower egg production. The brood size/mother age relationship was the same for both populations — number of eggs in brood = -4.9 + 0.64(instar number of mother)—because in the diseased population only healthy females breed. Lower egg production in the diseased population reflects the smaller proportion of healthy females, and the number of broods per female is lower since life expectancy is much less. A computer model based on Leslie matrices was used to simulate the ecological effects of the disease. It gave predictions which conformed with the observed population features with respect to age structure and density.