Medical Helminthology Lecture 1 24 PDF

Medical Helminthology The term helminth derived from Greek language meaning worm. The helminthes are multicellular, bilaterally symmetrical parasites having three germ layers – ectoderm, mesoderm and endoderm. The characteristic features of helminthes are following: 1. The outer covering, known as c...

Medical Helminthology The term helminth derived from Greek language meaning worm. The helminthes are multicellular, bilaterally symmetrical parasites having three germ layers – ectoderm, mesoderm and endoderm. The characteristic features of helminthes are following: 1. The outer covering, known as cuticle is tough. It is resistant to intestinal digestion and may be armed with spines or hooks. 2. Digestive system is absent or underdeveloped. 3. Nervous system is primitive. 4. Reproductive system is well developed. The parasites may be monoecious (hermaphrodite) or dioecious (sexual dimorphism). 5. They produce eggs in great amounts to help them survive and infect a suitable host. 6. They do not possess organs of locomotion. They generally move by muscular contraction and relaxation. Classification of Helminthes The helminthes of medical importance are classified into two phylums: 1. Phylum Platyhelminthes (Flat worms) Classes: Cestoda (Tape worms( Trematoda (Fluke worms( 2. Phylum Nemathelminthes (Round worms) Class: Nematoda (Round worms) In regard to the life cycle there are mainly two types of helminthes: geohelminthes and biohelminthes. Geohelminthes start their life cycle in soil (geo - soil) and complete it in one host organism. Biohelminthes pass the life cycle only in living hosts (bios - life), two or more hosts are required for completion of whole cycle. All the flat worms are biohelminthes, and the round worms have both biohelminth and geohelminth species. A specific group of helminthes is defined, whose life cycle is completed in one host as with geohelminthes, however, their eggs do not require soil for maturation as with biohelminthes. Pathology of helminthiasis An important difference between infestation with helminthes and infection with bacterial, viral or protozoan parasites is that the helminthic parasites do not increase in numbers within their host after infection. That is, each larval helminthe that infects the definitive host will give rise to only one adult parasite. Exceptions are the cases of autoinfection (reinfection with egg or larvae produced by helminthes already in the body) which can increase the parasite burden. All of the helminthes are endoparasites. Pathology with infection of helminthes may be due to a number of reasons, including: 1. Mechanical infection. Obstruction of the gut (Ascaris). Some helminthes may also press surrounding tissues in their larval stage (e.g., hydatid cyst of Echinococcus). 2. Depletion of nutrients and vitamins. For example, undernourishment caused by intestinal helminthes that have large sizes reaching more than 10 m; vitamin B12 depletion, leading to anaemia with infection by Diphyllobothrium latum; hypovitaminosis A in Ascaris infection). 3. Anaemia caused by helminth-parasites feeding on blood (for example, infection with hookworms, Trichuris trichiura) 4. Allergic responses to adult, larval or egg stages of the helminth lifecycle (for example with the Echinococcus, Ascaris). Larval stages of human species of helminthes that migrate during their life cycle cause both local inflammatory alterations in the organs through which they pass (e.g., Ascaris causes lung inflammation - pneumonitis) and general allergic reactions. 5. Toxic effect is common for many helminthes, especially Ascaris, tapeworms.  Phylum Platyhelminthes (Flat worms) Class Trematoda (Fluke worms) The flat worms are identified in respect to dorso-ventrally flattened body, which is either leaf-shaped (Trematoda) or tape-shaped (Cestoda). Morphology of Trematoda Trematodes or fluke worms are members of phylum Platyhelminthes. Their body is flat, leaf- shaped, the size ranging between few millimeters and centimeters. Usually two muscular suckers (oral and ventral) are present. The alimentary tract is incomplete, starting with mouth and having no anus (intestines end up blind). Reproductive system is highly developed. Trematodes are hermaphrodites except for blood flukes (schistosomes). The eggs of most trematodes are operculated (have a lid) except for schistosomes. General Life Cycle of Trematoda All Trematode species are biohelminthes and develop by alternation of hosts and develop adult, egg and larval stages. Definitive hosts can be the humans and sometimes animals (mammals) which harbour the adult worm. The first or the only intermediate host is the freshwater snail. A second intermediate host (fish, crab or ant) in the life cycle of some flukes is sometimes required. The eggs liberated by the definitive host usually pass to water. A ciliated embryo called miracidium develops from the egg. It enters the intermediate host (snail), where larval stages of sporocyst, redia and cercaria. The cercaria escapes from the snail into the water and, depending on the species, may: encyst on aquatic vegetation transforming into metacercaria, enter the second intermediate host (if present) and transform into metacercaria,   directly infect definitive host in case of Schistosomes. Man is infected by one of these invasive stages depending on the species.On entering the definitive host, the young worms proceed to their sites of localization to grow into adult worm, become sexually mature and repeat the cycle. The trematodes are classified according to the habitat in the definitive host. They are as following: 1. Liver flukes (Fasciola hepatica, Clonorchis sinensis). 2. Lung fluke (Paragonimus westermani). 3. Blood flukes (Schistosoma mansoni, Schistosoma haematobium, Schistosoma japonicum).  Liver Flukes Fasciola hepatica Fasciolosis is an anthropozoonosic, non-endemic disease. Fasciola hepatica or sheep liver fluke is common parasite of herbivores, it is rare in humans. Geographical distribution. Worldwide. Habitat. The parasite lives in bile passages of liver. Morphology. The adult worm is a large leaf-shaped fluke, measuring 3-4 cm. Eggs are large (about 140 mkm), ovoid, and operculated. Life cycle of Fasciola hepatica The adult worms release eggs that pass with the bile into the duodenum and are then voided with the host’s faeces. If the eggs fall into freshwater they continue their development and under ideal circumstances they hatch after about 9–10 days to release the free-living but non-feeding miracidium stage. The miracidium is covered in cilia and actively searches for the intermediate host. The miracidium chemically and physically bores its way into the snail and then sheds its cilia and transforms into the sack-like mother sporocyst stage. The mother sporocyst lacks a mouth and gut and absorbs nutrients across its tegument. Within the mother sporocyst the next life cycle stage is the first generation redia that develops through asexual reproduction. The rediae are motile and after they are released from the mother sporocyst, they move through the snail host’s tissues. The rediae also have a mouth and gut and are able to ingest snail tissues although they can continue to absorb nutrients across their tegument. The rediae then undergo a complex pattern of reproduction in which they form second and sometimes third generation rediae. Each redia gives rise to several cercariae and these physically and chemically burrow out of the snail and swim away. The cercaria consists of two body regions: a globular body anda long, stoutly tail. The cercariae of Fasciola hepatica usually emerge from their snail host during the night and after swimming for a while they settle on blades of grass, or other plants. Here they lose their tails and transform into metacercariae. The definitive host becomes passively infected when it eats plants contaminated with the metacercariae. For example, human fascioliasis is relatively rare and usually associated with eating semi-aquatic plants such as water cress. After ingestion, the metacercariae hatch in the duodenum in response to specific physical (e.g. temperature) and chemical stimuli (e.g. bile composition). The young flukes then physically and chemically bore their way through the gut and enter the abdominal body cavity. They probably reach the liver and they then penetrate the liver capsule and begin migrating through the liver parenchyma. The young flukes take about 5– 6 weeks to reach the gall bladder. Once the flukes reach the gall bladder, they become sexually mature and start laying eggs.  Life cycle of Fasciola hepatica (A) adult stage of Fasciola hepatica (B) adult stage of F. gigantica (C) egg of F. hepatica (D) egg of F. gigantica Pathogenicity. Clinical symptoms. Nausea, vomiting, fever, pain, allergic reactions, diarrhea and hepatomegaly and eosinophilia.. If the flukes block the bile ducts then obstructive jaundice may develop. In complicated cases fasciola may lead to liver cirrhosis (replacement of destructed liver tissue with connective tissue) and hepatic failure. In chronic phase, the liver parenchyma is inflamed with formation of multiple subcapsular abscesses (called as liver rot). Diagnosis. Demonstration of eggs in stool or bile obtained by duodenal intubation. For confirmation or rejection of the suspected diagnosis of fasciolosis the person is asked to stop eating raw liver for about a week, and the stool is re-examined again. Prevention. Humans should avoid eating unwashed vegetables, fruits and drinking contaminated water. Eradication of the disease in the reservoir hosts, draining fields to prevent snails. Clonorchis sinensis The Chinese liver fluke, Clonorchis sinensis causes clonorchosis, which is endemic and anthropozoonosic. Geographical distribution.China, Japan. Habitat. Bile ducts. Morphology. The adult worm is about 1 cm, narrower than F. hepatica. The egg is operculated, measures 25-30 mkm. Life Cycle of Clonorchis sinensis Definitive host is man, in addition to humans it is also a parasite of dogs, cats, pigs, and a variety of other mammals. Consequently, there are a large number of reservoir hosts and this can make control problematic. First intermediate host is freshwater snail, the second intermediate host is fresh water fish. 1. In people, adult flukes release eggs through the bile ducts into the intestine. Fluke eggs are passed in stool (feces).  2. In the environment, the eggs are ingested by snails. Inside the snail, the eggs go through several stages to develop into an immature form of the fluke that has a tail and can swim (cercariae). 3. The cercariae penetrate the skin of a freshwater fish and form cysts in the tissues of the fish( metacercariae). 4. People are infected when they consume the cysts in raw, undercooked, salt-cured, or smoked freshwater fish, or sometimes freshwater shrimp. 5. In the intestine, the larvae leave the cysts. 6. The young flukes excyst in the duodenum from where they migrate to the bile ducts, where they develop into adults and produce eggs. Pathogenicity. Clinical features. Light infections are asymptomatic but numerous parasites in liver can lead to diarrhea, hepatomegaly, allergic reactions. Obstruction of bile passages may result in obstructive jaundice, cholecystitis (inflammation of gall bladder), formation of bilestones, pancreatitis. Diagnosis. Demonstration of eggs by microscopical examination of feces. Prophylaxis. Prevention of water pollution with feces of humans and reservoir hosts, eradication of snails, proper cooking of fish.  Lung Fluke Paragonimus westermani The disease caused is known as paragonimosis, which is endemic and anthropozoonosic( food- born zoonosis). Geographical distribution. India, China, Japan, Korea and South America.. Pigs and monkeys serve as reservoir hosts, as well as other animals whose diet includes crayfish and crabs. Also known to cause human disease. Adult worm resides in small bronchi (bronchioles) of human Life cycle. The definitive hosts are humans, cats, dogs and wild carnivores. First intermediate host is freshwater snail, second intermediate host is freshwater crab or crayfish. Eggs are passed either directly in the sputum when coughing, or may be swallowed then passed in the feces. The cercariae penetrate the crab or crayfish where they encyst as metacercaria, which is the invasive stage for human. Infection of the humans takes place by eating raw or pickled crabs or crayfish. The metacercaria excyst in the duodenum, young flukes penetrate through the intestinal wall into the abdominal cavity, from where they migrate to the diaphragm directly and enter the lungs. Eggs are discharged into bronchioles and are coughed out with the sputum. Pathogenicity. Clinical features. The adult worms are encysted in pairs and cause“burrows” in lungs. The eggs may retain in the lung tissue and along with adults cause lung inflammation – pneumonia. The initial symptoms include fever, cough, chest pain, shortness of breath, allergic reactions. The sputum is usually blood-stinged (hemoptysis), and this symptom may closely resemble pulmonary tuberculosis. In complicated cases the fluke may enter other parts of the body such as brain (cerebral paragonimosis), spinal cord, subcutaneous tissues, liver, and here eggs are discharged. Ectopic worms can be found in several different tissues.the most sever ectopic form occurs in brain Diagnosis. Identification of eggs in sputum or feces. The pulmonary paragonimosis should be differentiated from pulmonary tuberculosis. In the latter no eggs are found in sputum, and eosinophilia is absent. Prevention. Proper cooking of crabs and crayfish, diagnosis and treatment of infected individuals, destruction of freshwater snails as intermediate hosts.. Life cycle of Paragonimus westermani