Introduction

The nematodes ( /ˈnɛmətoʊdz/) or roundworms are traditionally regarded as the phylum Nematoda or Nemathelminthes. As such, they would be the most diverse phylum of pseudocoelomates, and one of the most diverse of all animal phyla, but discussion is in progress to determine whether the phylum is to be split or not.

Nematode species are very difficult to distinguish; over 28,000 have been described, of which over 16,000 are parasitic. The total number of nematode species has been estimated to be about 1 million. Unlike cnidarians and flatworms, nematodes have tubular digestive systems with openings at both ends.

Habitat :-

Nematodes have successfully adapted to nearly every ecosystem from marine to fresh water, to soils, and from the polar regions to the tropics, as well as the highest to the lowest of elevations. They are ubiquitous in freshwater, marine, and terrestrial environments.

Anatomy :-

Digestive system

The oral cavity is lined with cuticle, which is often strengthened with ridges or other structures, and, especially in carnivorous species, may bear a number of teeth. The mouth often includes a sharp stylet, which the animal can thrust into its prey. In some species, the stylet is hollow, and can be used to suck liquids from plants or animals.The oral cavity opens into a muscular, sucking pharynx, also lined with cuticle. Digestive glands are found in this region of the gut, producing enzymes that start to break down the food. In stylet-bearing species, these may even be injected into the prey.There is no stomach, with the pharynx connecting directly to the intestine that forms the main length of the gut. This produces further enzymes, and also

absorbs nutrients through its lining. The last portion of the intestine is lined by cuticle, forming a rectum, which expels waste through the anus just below and in front of the tip of the tail. The intestine also has valves or sphincters at either end to help control the movement of food through the body.

Excretory system:-Nitrogenous waste is excreted in the form of ammonia through the body wall, and is not associated with any specific organs. However, the structures for excreting salt to maintain osmoregulation are typically more complex.In many marine nematodes, one or two unicellular 'renette glands' excrete salt through a pore on the underside of the animal, close to the pharynx. In most other nematodes, these specialised cells have been replaced by an organ consisting of two parallel ducts connected by a single transverse duct. This transverse duct opens into a common canal that runs to the excretory pore.

Nervous system:-

Four peripheral nerves run the length of the body on the dorsal, ventral, and lateral surfaces. Each nerve lies within a cord of connective tissue lying beneath the cuticle and between the muscle cells. The ventral nerve is the largest, and has a double structure forward of the excretory pore. The dorsal nerve is responsible for motor control, while the lateral nerves are sensory, and the ventral combines both functions.

At the anterior end of the animal, the nerves branch from a dense, circular nerve ring surrounding the pharynx, and serving as the brain. Smaller nerves run forward from the ring to supply the sensory organs of the head.

The bodies of nematodes are covered in numerous sensory bristles and papillae[disambiguation needed] that together provide a sense of touch. Behind the sensory bristles on the head lie two small pits, or 'amphids'. These are well supplied with nerve cells, and are probably chemoreception organs. A few aquatic nematodes possess what appear to be pigmented eye-spots, but is unclear whether or not these are actually sensory in nature.

History of Discovery :-

Nematodes suspected to be A. cantonensis were first identified in the cerebrospinal fluid of a patient with eosiniphilic meningitis by Nomura and Lim in Taiwan in 1944. They called the parasite Haemostrongylus ratti, and noted that raw food eaten by the patient may have been contaminated by rats. This paper, however, was not translated from Japanese to English until 1964, just a few years after the parasite had been defined, so their discovery was not widely recognized.

In 1955, Mackerass and Sanders identified the life cycle of the worm in rats, defining snails and slugs as the intermediate host and noting the path of transmission through the blood, brain, and lungs in rats.

In 1961, an epidemiological study of eosiniphilc meningitis in humans was conducted by Rosen, Laigret, and Bories, who hypothesized that the parasite causing these infections was carried by fish. However Alicata noted that raw fish was consumed by large numbers of people in Hawaii without apparent consequences, and patients presenting with mengitis symptoms had a history of eating raw snails or prawns in the weeks before presenting with symptoms. This observation along with epidemiology and autopsy of infected brains confirmed A. cantonensis infection in humans as the cause of the majority of eosiniphilic meningitis cases in Southeast Asia and the Pacific Islands [4]

Scientific classification

Kingdom: Animalia

Phylum: Nematoda

Class: Secernentea

Order: Strongylida

Family: Metastrongylidae

Genus: Angiostrongylus

Species: A. cantonensis

Angiostrongylus cantonensis

Epidemiology

Nematodes suspected to be Angiostrongylus cantonensis were first identified in the cerebrospinal fluid of a patient with eosinophilic meningitis by Nomura and Lim in Taiwan in 1944. They called the parasite Haemostrongylus ratti, and noted that raw food eaten by the patient may have been contaminated by rats. Their paper, however, was not translated from the original Japanese into English until just after the parasite had been recognized in 1964, so their discovery was not widely recognized.

In 1955, Mackerass and Sanders identified the life cycle of the worm in rats, defining snails and slugs as the intermediate host and noting the path of transmission through the blood, brain, and lungs in rats.

Following World War II, A. cantonensis spread throughout Southeast Asia and Western Pacific Islands including Australia, Melanesia, Micronesia, and Polynesia. Cases were soon reported in the following nations: New Caledonia, the Philippines, Rarotonga, Saipan, Sumatra, Taiwan and Tahiti. In the 1960s even more cases were reported from

the region from locations such as: Cambodia, Guam, Hawaii, Java, Thailand, Sarawak, Vietnam and the New Hebrides (Vanuatu).[4]

In 1961, an epidemiological study of eosinophilic meningitis in humans was conducted by Rosen, Laigret, and Bories, who hypothesized that the parasite causing these infections was carried by fish. However Alicata noted that raw fish was consumed by large numbers of people in Hawaii without apparent consequences, and patients presenting with meningitis symptoms had a history of eating raw snails or prawns in the weeks before presenting with symptoms. This observation along with epidemiology and autopsy of infected brains confirmed A. cantonensis infection in humans as the cause of the majority of eosinophilic meningitis cases in Southeast Asia and the Pacific Islands.[5]

Since then, cases of A. cantonensis infestations have appeared in American Samoa, Australia, Hong Kong, Bombay, Fiji, Hawaii, Honshu, India, Kyushu, New Britain, Okinawa, Ryukyu Islands, Western Samoa and most recently mainland China. Other sporadic occurrences of the parasite in its rat hosts have been reported in Cuba, Egypt, Louisiana, Madagascar, Nigeria, New Orleans and Puerto Rico[4]

In recent years, the parasite has been shown to be proliferating at an alarming rate due to modern food consumption trends and global transportation of food products. Scientists are calling for a more thorough study of the epidemiology of A. cantonensis, stricter food safety policies, and the increase of knowledge on how to properly consume products commonly infested by the parasite.[6]

Morphology

A. cantonensis is a nematode roundworm with 3 outer protective collagen layers, and a simple stomal opening with no lips or buccal cavity leading to a fully developed gastrointestinal tract [1]. Males have a small copulatory bursa at the posterior. Females have a “barber pole” shape down the middle of the body, which is created by the twisting together of the intestine and uterine tubules. The worms are long and slender - males are 15.9-19 mm in length, and females are 21-25 mm in length [7].

Adult male (top) and female (bottom) A. cantonensis worms. Note copulatory bursa at posterior of male, and characteristic “barber pole” spiral in female.

Adult female worm of Angiostrongylus cantonensis with characteristic barber-pole appearance (anterior end of worm is to the top). Scale bar is 1 mm.

Tail of adult male of Angiostrongylus cantonensis, showing copulatory bursa and long spicules (arrows). Scale bar is 85 µm.

Life Cycle :-

The adult form of A. cantonensis resides in the pulmonary arteries of rodents, where it reproduces. After the eggs hatch in the arteries, larvae migrate up the pharynx and are then swallowed again by the rodent and passed in the stool. These first stage larvae then penetrate or are swallowed by snail intermediate hosts, where they transform into second stage larvae and then into third stage infective larvae. Humans and rats acquire the infection when they ingest contaminated snails or paratenic (transport) hosts including prawns, crabs, and frogs, or raw vegetables containing material from these intermediate and paratenic hosts. After passing through the gastrointestinal tract, the worms enter circulation [6]. In rats, the larvae then migrate to the meninges and develop for about a month before migrating to the pulmonary arteries, where they fully develop into adults [5].

Humans are incidental hosts; the larvae cannot reproduce in humans and therefore humans do not contribute to the A. cantonensis life cycle. In humans, the circulating larvae migrate to the meninges, but do not move on to the lungs. Sometimes the larvae will develop into the adult form in the brain and CSF, but they quickly die, inciting the inflammatory reaction that causes symptoms of infection.

Transmission :-

Transmission of the parasite is usually from eating raw or undercooked snails or other vectors [2]. Infection also occurs from ingestion of contaminated water or unwashed salad that may contain small snail and slugs, or have been contaminated by them. Therefore it is very important to avoid raw snails, wash and cook vegetables thoroughly, and avoid open water sources that may be contaminated.

Third stage (infective) larvae taken from snail host

Pathology & symptoms:-

The presence of parasitic worms burrowed in the neural tissue of the human CNS will cause obvious complications. All of the following will result in damage to the CNS:

1. Direct mechanical damage to neural tissue from the worms' motion.2. Toxic by-products such as nitrogenous waste.3. Antigens released by dead and living parasites.

Symptoms :-The clinical symptoms of Eosinophilic Meningitis are as follows:

fever is often minor or absent but the presence of high fever suggests severe disease.

headaches- a bitemporal character in the frontal or occipital lobe. meningismus - neck stiffness. photophobia - sensitivity to light. nausea with or without vomiting. paresthesias - tingling, prickling, or numbing of skin. hyperesthesia - severe sensitivity to touch. bladder dysfunction with urinary retention.

vertigo. blindness. paralysis localized to one area. general paralysis often ascending in nature starting with the feet and progressing

upwards to involve the entire body. Coma. death.

Diagnosis:-

The diagnosis of disease caused by Angiostrongylus cantonensis infestation is often difficult and relies heavily on the history of a likely ingestion of a commonly infested host and the presence of typical features of the disease. The presumptive diagnosis is particularly strong when eospinophilic meningoencephalitis can be confirmed. The diagnosis of Eosinophilic Meningitis can be arrived at through detection of elevated cranial pressure and increased numbers of eosinophils. The diagnosis of the cause of eosinophilic meningitis and the presence of A. cantonensis is remarkably more difficult. A spinal tap, or a sample of CSF, must be taken to search for A. cantonensis worms or larvae. A. cantonensis is undetectable in the CSF of more than half of the infected individuals. Current methods of detecting specific antigens associated with A. cantonensis are also unreliable. Consequently, alternative approaches to detect antigen-antibody reactions are being explored, such as Immuno-PCR.

Host-parasite relationship:-

Intermediate hosts of larvae of for Angiostrongylus cantonensis include:land snails: Thelidomus aspera from Jamaica,[7] Achatina fulica,[6][8][9][10] Satsuma mercatoria,[9][10] Acusta despecta,[9][10] Bradybaena brevispira,[6] Bradybaena circulus[9] Bradybaena ravida,[6] Bradybaena similaris,[6] Plectotropis appanata[6] and Parmarion martensi from Okinawa[9] and from Hawaii,[11] Camaena cicatricosa,[6] Trichochloritis rufopila,[6] Trichochloritis hungerfordianusand Cyclophorus spp.[10]freshwater snails: Pila spp.,[8] Pomacea canaliculata,[6][8] Cipangopaludina chinensis, Bellamya aeruginosaand Bellamya quadrata[6]slugs: Limax maximus, Limax flavus[6] Deroceras laeve, Deroceras reticulatum, Veronicella alte, =? Laevicaulis alte, Sarasinula plebeia, Vaginulus yuxjsjs, Lehmannia valentiana,[9] Phiolomycus bilineatus, Macrochlamys loana, Meghimatium bilineatum[6] and probably other species of slugs.

Definitive host of Angiostrongylus cantonensis include wild rodents, especially Rattus norvegicus, Rattus rattus.

Paratenic hosts of Angiostrongylus cantonensis include: predatory land flatworm Platydemus manokwari[9] and amphibians Bufo asiaticus,[9] Rana catesbeiana,[9] Rhacophorus leucomystax[9] and Rana limnocharis.[9]

In 2004, a captive Yellow-tailed Black Cockatoo (Calyptorhynchus funereus) and 2 free-living Tawny Frogmouths (Podargus strigoides) suffering neurological symptoms were shown to have the parasite. They were the first non-mammalian hosts discovered for the organism

Treatment:-

The severity and clinical course of Angiostrongylus disease depends significantly on the ingested load of third stage larvae [15] creating great variability from case to case making it difficult to design clinical trials and to judge the effectiveness of treatments. Typical conservative medical management including analgesics and sedatives provide minimal relief the headaches and hyperthesias. Removing Cerebrospinal fluid at regular 3 to 7-day intervals is the only proven method of significantly reducing intracranial pressure and can be used for symptomatic treatment of headaches. This process may be repeated until improvement is shown.[4] Recent studies have shown that treatment with an antihelminthic such as mebendazole or albendazole combined with prednisone or prednisolone can reduce the severity and duration of headaches but have not been shown to improve long term neurologic outcomes.

References:-1. ^ Baheti, N. N.; Sreedharan, M.; Krishnamoorthy, T.; Nair, M. D.;

Radhakrishnan, K. (2008). "Eosinophilic meningitis and an ocular worm in a patient from Kerala, south India". Journal of Neurology, Neurosurgery & Psychiatry 79 (3): 271. doi:10.1136/jnnp.2007.122093. edit

2. ^ Li, H.; Xu, F.; Gu, J. B.; Chen, X. G. (2008). "A severe eosinophilic meningoencephalitis caused by infection of Angiostrongylus cantonensis". The American journal of tropical medicine and hygiene 79 (4): 568–570. PMID 18840746. edit

3. ^ "Helminth Taxonomy - Phylum Nematoda", Schistosomiasis Research Group, accessed 26 February 2009.

4. ^ a b c d e "EOSINOPHILIC MENINGITIS". Revised 28 February 2006, accessed 1 June 2011.

5. ^ Alicata J. E. (1991). "The Discovery of Angiostrongylus cantonensis as a Cause of Human Eosinophilic Meningitis". Parasitology Today 7(6): 151-153.

6. ^ a b c d e f g h i j k l m n o p q r s t Lv S., Zhang Y., Steinmann P. &, Zhou X.-N. (2008). "Emerging angiostrongyliasis in mainland China". Emerging Infectious Diseases 14(1): 161-164. HTM.

7. ^ a b c Lindo J. F., Waugh C., Hall J., Cunningham-Myrie C., Ashley D., Eberhard M. L., Sullivan J. J., Bishop H. S., Robinson D. G., Holtz T. & Robinson R. D. (2002). "Enzootic Angiostrongylus cantonensis in Rats and Snails after an Outbreak of Human Eosinophilic Meningitis, Jamaica". Emerging Infectious Diseases 8(3): 324-326. HTM.

8. ^ a b c Lv, S.; Zhang, Y.; Chen, S. R.; Wang, L. B.; Fang, W.; Chen, F.; Jiang, J. Y.; Li, Y. L. et al. (2009). Graeff-Teixeira, Carlos. ed. "Human Angiostrongyliasis Outbreak in Dali, China". PLoS Neglected Tropical Diseases 3 (9): e520. doi:10.1371/journal.pntd.0000520. PMC 2739427. PMID 19771154. edit

9. ^ a b c d e f g h i j k l Asato R., Taira K., Nakamura M., Kudaka J., Itokazu K. & Kawanaka M. (2004) "Changing Epidemiology of Angiostrongyliasis Cantonensis in Okinawa Prefecture, Japan". Japanese Journal of Infectious Diseases 57: 184-186. article [1]

10.^ a b c d (20 June 2001). "Land snail infection rates for the human parasitic nematode, Angiostrongylus cantonensis (rat lung worm) with notes on snail and parasite biology and distribution on Kadena AB, Okinawa Japan. Consultative Letter, IERA-DO-BR-CL-2001-0049." MEMORANDUM FOR 18 MDG/SGPM, Department of the Air Force, 11 pp. PDF.

11.^ Hollingsworth, R. G.; Kaneta, R.; Sullivan, J. J.; Bishop, H. S.; Qvarnstrom, Y.; Da Silva, A. J.; Robinson, D. G. (2007). "Distribution of Parmarion cf. Martensi (Pulmonata: Helicarionidae), a New Semi-Slug Pest on Hawai'i Island, and Its Potential as a Vector for Human Angiostrongyliasis1". Pacific Science 61 (4): 457. doi:10.2984/1534-6188(2007)61[457:DOPCMP]2.0.CO;2. edit.

12.^ Senanayake, S. N.; Pryor, D. S.; Walker, J.; Konecny, P. (2003). "First report of human angiostrongyliasis acquired in Sydney". The Medical journal of Australia 179 (8): 430–431. PMID 14558868. edit

13.^ a b c d Högger C. H. (update 25 March 2003). "Antagonists of Slugs and Snails. A Bibliography of Sources and a List of Citations grouped according to Taxon of the Antagonists". in web Archive.

14.^ Monks, D. J.; Carlisle, M. S.; Carrigan, M.; Rose, K.; Spratt, D.; Gallagher, A.; Prociv, P. (2005). "Angiostrongylus cantonensis as a Cause of Cerebrospinal Disease in a Yellow-tailed Black Cockatoo (Calyptorhynchus funereus) and Two Tawny Frogmouths (Podargus strigoides)". Journal of Avian Medicine and Surgery 19 (4): 289. doi:10.1647/2004-024.1. edit

15.^ Tsai, H. C.; Liu, Y. C.; Kunin, C. M.; Lee, S. S.; Chen, Y. S.; Lin, H. H.; Tsai, T. H.; Lin, W. R. et al. (2001). "Eosinophilic meningitis caused by Angiostrongylus cantonensis: Report of 17 cases". The American journal of medicine 111 (2): 109–114. doi:10.1016/S0002-9343(01)00766-5. PMID 11498063. edit

16.^ Chye, S. -M.; Lin, S. R.; Chen, Y. L.; Chung, L. Y.; Yen, C. M. (2004). "Immuno-PCR for Detection of Antigen to Angiostrongylus cantonensis Circulating Fifth-Stage Worms". Clinical Chemistry 50 (1): 51–57