Angiostrongylus cantonensis

Angiostrongylus cantonensis was discovered in China. Since then it has been found in Australia, the southwestern Pacific including Hawaii, South and southeast Asia, Madagascar, Japan, Taiwan, Egypt, Ivory Coast of Africa, India, Samoa, Fiji, Cuba, the Caribbean, Puerto Rico, and Southeastern USA. Angiostrongylus cantonensis probably originated in eastern Asia, but because of its large dispersal as a result of human activity, there is no way to be sure. (Prociv, Spratt, and Carlisle, 2000)

Angiostrongylus cantonensis is not specific for either definitive or intermediate hosts. The requirement is that the intermediate host must be an invertebrate while the definitive is a terrestrial mammal. Paratenic hosts, where the parasites don't develop to the next stage, can be either invertebrate or vertebrate. The definitive hosts for Angiostrongylus cantonensis are usually rodents from the genus Rattus, with some main ones being Rattus norvegicus and Rattus rattus. Angiostrongylus cantonensis can survive in humans and monkeys as well. Two cases of monkeys dying from complications of eosinophilic meningoencephalitis in zoos were attributed to their contact with snails serving as intermediate hosts.

The main intermediate hosts include slugs and snails. Achatina fulica, or the African giant land snail, can contain thousands of third-stage larvae. Although it's not the major intermediate host, this particular snail is important because it may be a primary reason why Angiostrongylus cantonensis has spread. This snail is considered a delicacy in several regions and typically eaten raw. With the amount of larvae in one Achatina fulica, A. cantonensis can easily be dispersed to new areas.

Paratenic hosts include anything that eats the mollusks. Some main ones include terrestrial planarians and crabs, fresh-water shrimp and frogs, toads, marine fish, and sea snakes. However, recent evidence indicates it may be intolerant of salinity, so marine species may be questionable as hosts. (Anderson et al., 1990; Janovy and Roberts, 2000; Prociv, Spratt, and Carlisle, 2000)

As a nematode, A. cantonensis is cylindrical, and has a cuticle with three main outer layers made of collagen and other compounds. The outer layers are non-cellular and are secreted by the epidermis. The cuticle layer protects nematodes so they can invade digestive tracts of animals. The worms molt four times, the first two before hatching, and then before their adult stage.

As a member of the Secernentea, A. cantonensis has a specialized tubular excretory system system with three canals. The canals are arranged to from an "H".

Angiostrongylus cantonensis is a flimsy and slender worm with a simple mouth and no lips or buccal cavity. The bursa, a structure used to clasp females when copulating, is small and dorsal lobe is not present. The males have long and slender spicules which are almost equal in length and form. The gubernaculum, used to guide spicules when mating, is present but is not immediately noticeable.

There are obvious differences between male and female A. cantonensis. The males are 15.9 to 19 mm in length, while the females can grow 21 to 25 mm in length. Females are easily distinguished from males by the noticeable barber-pole appearance in their bodies. This is actually the interweaving of the intestine and uterine tubules. Females have a vulva, which is located 0.2 mm in front of the anus. (Barnes, 1987; Brusca and Brusca, 2003; Janovy and Roberts, 2000)

The worms molt before becoming adults, two molts occuring before they hatch from the eggs. Most all adult structures except certain reproductive parts are found in the young just after hatching. As adults, the worms will not molt, but can grow in size.

Angiostrongylus cantonensis has a complex life cycle that involves intermediate, paratenic, and definitive hosts as well as several larval stages before becoming an adult. Adults are found in the right ventricles of hearts and the pulmonary arteries. The females release their eggs in these arteries. They are carried to the lungs, and within the capillaries here they embryonate. The thin-shelled egg breaks open and the first larval stage hatches. The larvae break through the alveoli and move up the trachea, where they wait to be swallowed and then expelled in the feces.

The intermediate host starts eating the fecal matter, also ingesting the parasitic larvae. There is some development in the intermediate host, but not to sexual maturity. The larvae develop into the 3rd stage in the molluscan muscle tissue. A parantenic host such as a frog or fish may eat the intermediate host, where the larvae survive in their muscle but no development occurs. The larvae enters the definitive host either by ingestion of the intermediate host, ingestion of paratenic host, or ingestion of material that contains the slimy path that a slug or snail leaves behind. Larvae may escape the intermediate host and be present on that trail.

Once inside the intestine of the definitive host, the larvae go through obligatory migration through the central nervous system via bloodstream to the brain and spinal cord. They leave the capillaries and start wandering randomly through the tissues. At the same time, they reach the fifth stage larvae. When the larvae reach the surface of the brain or spinal cord, they penetrate the veins to reenter the circulatory system. The larvae end up at the pulmonary arteries where they mature into adults in about six weeks. However, some larvae wander to other places in the body and mature there. Common places are in the central nervous system, the meninges, and the eyes. (Barnes, 1987; Brusca and Brusca, 2003; Prociv, Spratt, and Carlisle, 2000)

Lifespan and growth to the next parasitic larval stage depends on what host is infected. In paratenic hosts, the larval may not develop to the next stage. (Janovy and Roberts, 2000)

Nematodes such as Angiostrongylus cationensis are able to swim intermittently. The worms are usually only able to move effectively when the pseudocoel is filled with fluid and hypertonic to the surrounding media. (Barnes, 1987; Brusca and Brusca, 2003)

Nematodes within the Secernentea have phasmids, which are unicellular glands. Phasmids likely function as chemoreceptors. Females may produce pheromones to attract males.

Nematodes in general have papillae, setae and amphids, which are the main sense organs. Setae detect motion (mechanoreceptors), while amphids detect chemicals (chemoreceptors). (Barnes, 1987; Brusca and Brusca, 2003)

Angiostrongylus cantonensis has a simple mouth and no buccal cavity. Pharyngeal glands and intestinal epithelium produce digestive enzymes, and feed on the body fluids of its hosts. Extracellular digestion begins within the intestine, and the digestive cycle is completed intracellularly.

As an endoparasite, Angiostrongylus cantonensis is usually found in the pulmonary arteries and in the right ventricle of the heart. The larvae are found circulating in the blood, spinal fluid, cerebrospinal fluid, or in the blood vessels of the brain and the meninges. Angiostrongylus cantonensis is mainly found in rodents, especially rats, which are the definitive hosts. The worm has also been able to survive and sexually mature in other mammals including humans and monkeys. (Anderson et al., 1990; Barnes, 1987; Brusca and Brusca, 2003; Prociv, Spratt, and Carlisle, 2000)

These parasites are usually not preyed on directly, but are ingested from host to host. Larval mortality is high as most of the parasites do not reach appropriate hosts. (Barnes, 1987; Brusca and Brusca, 2003)

Angiostrongylus cantonensis is not specific for either definitive or intermediate hosts. The requirement is that the intermediate host must be an invertebrate while the definitive is a terrestrial mammal. Paratenic hosts, where the parasites don't develop to the next stage, can be either invertebrate or vertebrate. The definitive hosts for Angiostrongylus cantonensis are usually rodents from the genus g. Rattus, with some main ones being Rattus norvegicus and Rattus rattus. Angiostrongylus cantonensis can survive in humans and monkeys as well.

The main intermediate hosts include slugs and snails. Paratenic hosts include anything that eats the mollusks. Some main ones include terrestrial planarians and crabs, fresh-water shrimp and frogs, toads, marine fish, and sea snakes. However, recent evidence indicates it may be intolerant of salinity, so marine species may be questionable as hosts. (Barnes, 1987; Brusca and Brusca, 2003; Janovy and Roberts, 2000)

Angiostrongylus cantonensis is the primary cause of human eosinophilic meningoencephalitis in many parts of the Indo-Pacific region. The hosts become infected when the third stage larva is ingested. Humans get severe headaches, stiff necks, clouded consciousness, meningeal irritations, and extensive tissue damage from wandering worms in the brain. Eosinophil counts are increased in peripheral blood and spinal fluid, and lymphocyte counts are increased in the cerebrospinal fluid. The final results of these symptoms lead to neural disorders, paralysis of 5th cranial nerve, comas, and even death.

Dead worms that are present in the blood stream can cause inflammatory responses. Immune responses are evoked by dead worms and cause the destruction of brain and spinal cord cells. However, symptoms are so vague that they can be mistaken for a variety of other parasitic diseases. With this delay in correct diagnosis, dead worms can be worse than live worms. (Ishih et al., 1998; Janovy and Roberts, 2000; Jitpimolmard et al., 2000)

Angiostrongylus cantonensis was initially found in the lungs of rodents in China. It was given little notice since it was not yet found in humans. In 1944, the first case of A. cantonensis in a human was found. A young adult worm was in the cerebrospinal fluid of a young boy in Taiwan who had come in for treatment for meningitis. Since then, many cases have been linked to eosinophilic meningoencephalitis. Even though its symptoms are similar to other diseases, if it shows up in an area that didn't have it before, research will be prompted to start to see if the worm has reached that area. If symptoms show up in an area that is known to have the worm, then the worm will be the first suspect. (Aguiar, Morera, and Pascual, 1981; Prociv, Spratt, and Carlisle, 2000)