Introduction

Hydatid disease is caused by accidental infection with the intermediate stages of tapeworms of Echinococcus species, principally Echinococcus granulosus and E.multilocularis. The adult worm parasitises the small intestine of carnivores, usually Canidae, and sheds proglottids containing eggs which pass with the host's faeces. If the eggs are then ingested by a herbivore they develop into a larval stage (cyst) within the liver or other viscera. The cycle is completed when the carnivore consumes the herbivore, ingesting a mature cyst. Echinococcus granulosus originated in a wolf-deer life-cycle, and has evolved in dogs and sheep and other domesticated and wild animals. The definitive hosts of E.multilocularis are foxes, and the intermediate hosts small rodents such as voles and lemmings. Echinococcus granulosus is ubiquitous but E.multilocularis is confined to the Northern Hemisphere. Cystic hydatid disease in man is caused by the larval form of E.granulosus. Surgery provides a cure in 50–90% of cases, but recurrence is common. Alveolar hydatid disease caused by E.multilocularis results in metastases throughout the soft organs. Until recently it was invariably fatal, but chemotherapy may retard the proliferation of cysts. For further information on the epidemiology of echinococcosis and hydatid disease see Roberts and Gemmell (1994). This paper presents two examples where models of the dynamics of Echinococcus species have been used to investigate control policies.

Echinococcus granulosusin farmed animals in New Zealand.

The first case of cystic hydatid disease in New Zealand was recorded in 1862. The annual number of cases peaked at 7.2 per 100,000 in 1946, and then declined to 0.37 per 100,000 in 1987, largely due to the control programme that was initiated in 1959. From that time all dogs were subjected to regular chemotherapy to remove tapeworms.