The effect on orchestia hurleyi (Amphipoda: Talitridae) of a whitey disease caused by bacillus subtilis

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 progressingsouthwards 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. Inthe vicinity of Dunedin and further south the amphipods are still disease-free. Signs of thedisease are a progressive weakening and wasting. The animal cannot jump, and its speed ofwalking 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 wasisolated, and healthy amphipods were re-infected from the isolate. Signs of the disease wereapparent within 7 days of inoculation. The presence of the disease-causing organism in thehaemoooel 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 theanimal’s defences are overcome, and haemocyte counts fall to an average of 784 mm-3during the later stages of disease. The blood of terminally diseased amphipods is thick andcreamy white, packed with motile bacterial cells, and few (if any) haemocytes are presentin the circulation. Two populations were studied, one disease-free (at Dunedin) and theother heavily diseased (at Christchurch). The incidence of disease (as measured by aperformance test) was about 3091 in Christchurch adults. The disease-causing strain of B.subtilis was found on the body surface of almost all adults in the diseased population. Itis possible that the bacterium gains entry to the haemocoel through wounds suffered duringecdysis, conflict, or predator attack. The main differences shown by the diseased populationrelative to the disease-free population were: lower average density (992 m-3, cf. 1677 m-3);lower maximum density (3104 m-3, cf. 9971 m-3); smaller average size, with fewer adultinstars; a smaller proportion of females brooding in each instar, and much lower eggproduction. 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 thediseased population only healthy females breed. Lower egg production in the diseasedpopulation reflects the smaller proportion of healthy females, and the number of broodsper female is lower since life expectancy is much less. A computer model based on Lesliematrices was used to simulate the ecological ettects of the disease. It gave predictions whichconformed with the observed population features with respect to age structure and density. © 1981 Taylor & Francis Group, LLC.