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hypodermis b. muscle layer The cuticle not only acts as outer covering but also has significance in performing many roles in functional activity. 3. The cuticle of the parasite may be expanded at the anterior part of the parasite which is called as the cervical alae. 4. Cuticle may be expanded at the posterior part of the of the nematode which is called the caudal alae. 5. At the anterior part of the body, cuticle may form cervical papillae. 6. Cuticle may form the pre-cloacal and post cloacal papillae. 7. Cuticle from different types of thickenings which have got taxonomic importance. In Gongylonema there are many cuticular thickenings. In the Acuaria and Dispharynx there are presence of cordons which are recurring or non-recurring types. In some nematodes cuticles forms some ridges or in others, forms epaulletes ( Stephanurus ) or dentigerous structures. In some nematodes there may be formation of leaf crown ( Strongylus) or cutting plates or teeth (Ancylostoma). The cuticle also forms one important structure which is called bursa which is the posterior expansion of the cuticle (Haemonchus). Spicule is another structure formed by the cuticle. Some sensory organs are also formed by the cuticle, like phasmid (present in the posterior part of the nematode) and amphids (present in the anterior part of the nematode) 8. Moderately digestive system is found in the nematodes. The digestive system starts in the mouth. The mouth may be surrounded by lips. Structure and arrangements of lips varied. 9. Other structures found in the digestive system are pharynx, oesophagus, intestines, anus etc. Esophagus is very important in respect of taxonomic identification. The different types are: Bulbus- presence of posterior bulb ( eg. Heterakis gallinarum). Some roundworms is double bulbed ( Oxyuroids) Rhabditiform- shows anterior pyriform and posterior bulbous appearance ( Strongyloides ) Ventriculus- anterior part of the esophagus is muscular and posterior part of the same is glandular (all spirurid worm ) Filariform- esophagus is tubular ( filarial worm) Trichuroid- esophagus is composed of cells arranged in a row ( Trichinella spp) 10. Flame cells are absent. In most nematodes excretion is performed by a ventral pore and a pair of lateral longitudinal vessels 11. The nervous system includes oesophageal nerve ring, nerve ganglia, nerve fibers connecting nerve ganglia, sense organs (phasmids, amphids, cervical papillae and genital papillae ) General biological development of nematodes 1. The eggs are expelled out. The eggs do not hatch in the environment. Within the eggs the larvae develop. The larvae hatch after being ingested by the host. ( Ascarid worm) 2. The eggs are expelled out of the host and the eggs hatch in the presence of different environmental factors. The larvae develop to a certain limit to reach to the infective stage. Final host gets the infection by ingestion of infective larvae ( Strongyle ) 3. The eggs are expelled out of the host and the eggs when these eggs are ingested by the intermediate hosts. In the Intermediate host the larvae reached to the infective stage. (Spiruroidea )
4. The eggs are hatched and the larvae developed to the infective stage after being ingested by the intermediate host. ( Metastrongyloidea) 5. The worms are viviparous and the larvae mix up in the blood or lymph of the host. These larvae reach to the infective stage in the IH (Filarid worms ) FAMILY ASCARIDIDAE Characteristics: 1. Three lips are present. One dorsal and two subventral. Each lips bears two papillae. 2. In between the lips there maybe small intermediate lips which are called interlabia. 3. Teeth or cutting plates are absent 4. Pharynx and oesophageal bulb are absent. 5. Usually two spicules are present. Bursa is absent. 6. Eggs are typically round or subglobular and outer wall is pitted. Genus Ascaris Ascaris suum Host- pig Site/location- small intestine Developmental stages: Eggs are expelled out. Larvae developed within the egg shell. Second larvae (L2) within the egg shell are the infective stage. The host gets the infection by ingestion of the infective eggs. Hatching occurs in the intestine and the larvae reach the liver either by active penetration by active penetration via peritoneal cavity or hepatoportal circulation. The larvae are transported to heart and then to lungs where these are found as 3rd larvae. Then the larvae follow the tracheal migration. The larvae are coughed up and develop to the fourth stage in the intestine and to adult stage subsequently. Pathogenesis: 1. Migration of larvae causes hemorrhagic lesions in liver and creates a “milk spot” appearance. 2. The migrating larvae also creates lesions in the bronchiole and a;veoli which results in pneumonia Genus Toxocara Species: T. canis- dangerous to the puppies T. cati T. vitolorum- causes calf-hood mortality in buffaloes in India Toxocara canis ( also known as Arrow-headed worm or arrow worm) Life cycle: Egg> larva 1 in the egg shell> larva 2 in the egg shell (infective stage)> larva 3>larva 4 >adult Routes of Infection a. oral infection or ingestion of infective stage of eggs i. tracheal route of migration -when the pups are below 3 months of age, the tracheal route of migration occurs. After ingestion of the eggs, hatching occurs due to the presence of different biochemical factors present in the host. The larvae come out and start migration. The larvae penetrate into the wall of the intestine and enter into the general circulation. By the hepatoportal circulation the larvae are
transported to the liver and it penetrates the liver capsule. Then the larvae are transported to the lungs through the pulmonary circulation. The larvae are found first in the lower lung and then migrate to the upper part of the respiratory tract. They reach the bronchi, trachea etc. In the lung one moulting occurs and the second stage larvae are transformed into the third stage larvae. Then the larvae reached the GI tract when the cough containing the larvae is ingested and the larvae developed furthewr to become adult. ii. somatic route of migration -occurs when the dog is pregnant. The larvae migrate to different organs and remain in dormant stage. The activity and mobility are seized. The reason of this dormancy is not clearly but it is supposed to be due to the alternation of hormonal status of the blood during pregnancy stage. After about 1.5 months of the infection the larvae mobilize from the dormant stage and reach the general circulation. Through the blood the larvae enter the different organs of the fetus. In the liver of the fetus the larvae perform one month moulting again. In this way the transuterine or congenital infection occurs. b. transuterine infection (congenital infection) c. Transmammary infection ( lactogenic infection) -the offspring gets the infection when it sucks the colostrums from its mother. Through the colostrums the larvae enter the GI tract and they directly develop into the adult stage. d. Paratenic host transmission - rodents acts as the paratenic host for transmission of the parasite. Pathogenesis and clinical signs: 1. hepatic damage due to migrating larvae 2. alveolar destruction 3. pneumonia ( ascarid pneumonia) 4. vomiting 5. pendulous pot bellied abdomen Visceral Larva Mirgrans (VLM) This occurs in children due to migration of ascarid larvae in the different vital organs of the abnormal host ( means not the definitive host which is the dog). The habit of dirt eating predispose to this condition. Mainly the liver is affected but some organs maybe affected too. Eosinophilia occurs in the organs affected. It is caused by Toxocara canis, T. cati, T. leonine , Capillaria hepatica and Lagochilascaris minor. Family Oxyuridae: -whip like, non-bursate nematodes. Genus Oxyuris Oxyuris equi ( pin worm or seat worm of horses) -causes rat tailed appearance due to the irritation caused by the crawling female worms in the anus Life cycle: The female parasites crawl out of the anus and lay a number of eggs. Wirthin the eggs the larvae develop. The eggs fall on the ground and the host gets the infection by ingestion of the eggs along with the feed materials. After ingestion the eggs hatch and the larvae come out of the egg. The larvae develop to the adult stage in the intestine. ( egg>larva1 in the egg shell>larva2 in the egg shell (infective stage)>larva3>larva4>adult)
Family Heterakidae Genus Ascaridia Ascaridia galli -non-bursate nematode of birds. The incidence or the manifestation of this parasitic infection does not apparently cause significant damage to the host Life cycle: The eggs are expelled out of the host. In the environment the eggs develop to reach to the infective stage (L2). The birds get the infection when the eggs are ingested along with the food material. After ingestion the eggs hatch and the larvae come out and develop to adulthood. No migration occurs. Genus Heterakis Heterakis gallinarum Life cycle: The eggs are expelled out the host .The eggs develop in the environment. Within the eggs, the second stage larvae are formed. The second stage larva within the shell is the infect5ive stage. The birds gert the infection when the eggs are ingested. After ingestion the eggs hatch and the larvae come out. The larvae develop very simply in the GI tract. No migration of the larvae occurs Heterakis gallinarum 1. occurs in the ceca of fowl 2. oesophagus has strong posterior bulb 3. earth worm may act as the transport host 4. The eggs of Heterakis gallinarum transmit Histomonas melagridis Genus Subulura Subulura brumpti- pinmorm of fowl Family Strongyloididae Strongyloides spp discovered by Bavay in the year 1876 Species: S.papillosus- Si of sheep, goat, cattle S. cati- cat S. westeri- pigs and horse S. ransomi- pigs S. stercoralis human being Disease/pathological condition caused- Strongyloidosis, Foot rot, Larva migrans, Larva currens Salient morphology: 1. parasites show free living and parasitic life cycle 2. oesophagus is rhabditiform in free living generation and filariform in parasitic generation. 3. the adult parasite has noticeably long esophagus 4. the female worm is parthenogenetic Ascaridia galli 1. occurs in the small intestine 2. oesophagus has no posterior bulb 3. there is no evidence of transport host 4. does not transmit any protozoan parasite
Life cycle: a. Homogonic The eggs are expelled out of the host and hatch and larvae come out. The larvae reach the infective stage. The final host get the infection by skin penetration or orally. The larvae get entry into the blood circulation and transported to the lungs. They penetrate the lung alveoli and gradually ascend up the respiratory tract. Then they dome down to the esophagus and finally reach the intestine. b. Heterogonic The eggs are expelled out of the host and hatch in the environment and larvae cone out. The larvae directly develop to adult male and female. This free living male and female parasite copulate and the gravid female lay the eggs. The eggs hatch in the environment and the larvae come out. The larvae directly develop to become infective stage parasite. The final host gets the infection by skin penetration performed by the infective larvae or by ingestion. Further development occurs as that mentioned in homogenic life cycle. Pathogenesis: The larvae cause formation of lesion when they penetrate the skin. Foot rot condition is commonly found in the sheep and goat. The cutaneous lesion is called larva migrans. The lesions are circular or straight in appearance as linear urticarial lesion called as larva currens Control: Biological control is applied by nematode-trapping fungi, Arthrobotrys oligospora Family Trichuridae: Salient morphology: 1. appearance is like a whip 2. parasite is slender anteriorly and thick posteriorly 3. the anterior part contains the GI tract and the posterior part contains the reproductive system 4. The posterior end of the male parasite is slightly spiral and one spicule is protruded out of the hind end. The spicule remains within a spicule sheath.
*guys kindly check your manual regarding this, sorry coz I consulted a picture regarding the parts of trichuris and it showed that the posterior part bears the whip.. * Life cycle:
The host gets the infection by ingestion of infective stage of eggs. After hatching the larva comes out and then the parasite reaches the adult stage after several moultings. Capillaridae: -known as hair worms -egg barrel shaped and with sides nearly parallel and with polar plugs. Family Trichinellidae: Morphology 1. spicules are absent 2. the parasite is posteriorly thicker than the anterior part. 3. the male parasite has two lateral flaps on either side at the posterior end. Life cycle: The seat of predilection site of the parasite is small intestine. After copulation the male parasite dies and the female parasite burrows the wall of the intestine. During this activity the larvae get entrance in the blood circulation via lymphatic vessel and the larvae enter the different musculatures like subcostal muscles, tongue and diaphragm. The affected muscle is called nurse cell. The larvae get maturity in the striated muscle fiber and the larvae remain there forming a coil.
The whole coil remains encapsulated. The final host gets infection by ingestion of the muscles containing the larva. ( egg>L1 the infective stage>L2>L3>L4 >adult) PICTURES 1. Trichuris trichura a. female, b. male
ova of Toxocara canis
Ova of Toxocara cati
Ova of capillaria
ova of trichuris
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