The spread of Angiostrongylus cantonensis

Abstract. Until the recent establishment of Angiostrongylus cantonensis in North America, Australia was the only developed region endemic for this parasite. Almost 50 years ago the life cycle was elucidated there, in the city of Brisbane, and the first human infections probably occurred in 1959. From the 1970s, increasing numbers of autochthonous infections have been reported along the central east coast of the continent (southeast Queensland and northern New South Wales), involving humans, rats, dogs, horses, flying foxes and marsupials. Ten years ago, the parasite was discovered in Sydney, almost 1,000 km to the south, in dogs. In that city, it has since been diagnosed as a cause of neurological disease in increasing numbers of dogs, flying foxes, marsupials and zoo primates. Presumably, these infections resulted from the ingestion of snails or slugs, and it seems that virtually all species of native and exotic terrestrial molluscs can serve as intermediate hosts. It is not known how the parasite was introduced to this continent, or how it has spread over such an extensive territory, although eventually its range could encompass the entire east coast, and potentially other regions. It is also not known if the almost identical, native species, A. mackerrasae, is able to infect people (or other nonrodent hosts). All worms recovered to date, from one fatal human case, and from many animal infections, have been confirmed as A. cantonensis

Medical management

Apart from those infections transmitted by arthropod vectors, virtually all human parasitoses may be acquired orally. Even organisms that normally penetrate skin, such as schistosome cercariae and hookworm larvae, can establish infection after being ingested in drinking water or on contaminated food, although for them this portal hardly constitutes a significant route of transmission. Other fecally dispersed parasites, including the cysts of Giardia and Entamoeba, oocysts of Cryptosporidium, Cyclospora and other less common coccidia, and the eggs of geohelminths, may be transported mechanically on food or in drinking water, but they do not occur within the substance of unprocessed food

Health aspects of antarctic tourism

Increasing numbers of seaborne tourists are visiting Antarctica, with most coming from the United States (3503 in 1996-97), Germany (777), and Australia (680; cf. 356 in 1994-95 and 410 in 1995-96). The impression among travel medicine clinicians is that, each year, more prospective travelers seek advice about the health demands of this type of adventure, mostly relating to fitness for travel, exposure to extreme cold, hazards in ice and snow, and other potential health risks. This is a recent phenomenon. While a regular shipping service had been established between the Falklands and the subantarctic islands of South Georgia and the South Shetlands by 1924, the first documented tourists accompanied an Argentine expedition to the South Orkneys in 1933.1 Commercial airline flights over these islands and the Antarctic Peninsula began in 1956, from Chile, and recreational cruises to the Peninsula began in 1958. Tourist numbers subsequently grew slowly, for what was clearly an exclusive and very expensive undertaking, with few ships available for these hazardous voyages. From 1957 to 1993, 37,000 tourists visited by sea, most seeing only the Peninsula.2 The dramatic recent growth in numbers is a consequence of the collapse of the Soviet Union. The small fleet of ice-strengthened research vessels and working icebreakers, which was made redundant by withdrawal of central government support from isolated communities and military activities along the northern coast of Siberia (and from Antarctic research bases), now accounts for the bulk of charter-cruise tourism to Antarctica, at competitive prices. According to the International Association of Antarctica Tour Operators,3 7322 people traveled to Antarctica on commercially organized voyages in the 1996-97 season, and a record 10,000 shipborne visitors were expected for the 1997-98 season (November-March), traveling mainly from South America to the Peninsula on 15 ice-reinforced vessels, each carrying between 36 and 180 passengers. Most tours embark from Ushuaia in southern Argentina, or Punta Arenas in Chile, although occasional cruises leave from Australia, New Zealand, or even South Africa

Observations on the morphology of Toxocara pteropodis eggs

Fertile eggs of Toxocara pteropodis, passed in the faeces of juvenile flying-foxes, were ovoid to spheroid in shape with a diameter range of 80–110 μm. The shell was often seen to comprise 4 layers: a fine inner lipid layer, a thicker clear chitinous layer, an equally thick outer vitelline layer and a pitted outermost, proteinaceous uterine layer of variable thickness. Infertile eggs were less uniform in shape and generally did not have well-defined shell layers, the formation of which is triggered by sperm penetration of the oocyte. The eggs of this species are bulkier than those of related ascaridoids, apparently because of a thicker external coat which, while not providing mechanical strength, is thought to protect against desiccation. Scanning electron microscopical findings suggest that the outer layer is not applied directly by uterine cells, but forms by the gradual deposition of secretions in the uterine lumen, regardless of whether the oocyte has been fertilized

Intraovular development and moulting of Toxocara pteropodis

Observations of Toxocara pteropodis eggs removed from an adult worm and embryonated in 0.05 m-sulphuric acid showed the first moult to occur on the sixth day followed by the second moult over days 8-11, as indicated by the finding of a transient, loose, double-layered sheath over the definitive cuticle. Infectivity to mice first developed on day 11, reached a maximum at 36 days and then waned over the next 6 months. Details of larval development are described and the significance of loose sheaths on larvae recovered from tissues is discussed