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INF 1 10/11 batch INTESTINAL NEMATODES Objectives: 1. List the different groups of parasitic helminthes. 2.

. List the major characteristics of parasitic nematodes. 3. List the common intestinal nematodes in humans. 4. Outline the life cycles (LC) with stages and events. 5. State the stages that cause pathogenic effects and identify those stages of diagnostic importance. 6. Describe the pathogenesis and relate it to the clinical features 7. Describe laboratory methods of diagnosis. 8. Identify points in the life cycle where preventive measures are applicable. Helminths as a group Helminths are among the major parasites of humans and are classified under two phyla:Nemathelminthes and platyhelminthes. The majority of helminthes that infect humans belong to the following three classes 1. Nematoda: They are elongated, cylindrical worms. The sexes are separate. A complete alimentary canal is present with some species having well developed buccal capsules. They possess a body cavity ( pseudocoelome) 2. Cestoda They are flatten tape like segmented worms. Sexes are not separate, each segment having a setoff male and female reproductive organs. Alimentary canal is absent. The head end possesses suckers, often with hooks. The body cavity is absent. 3. Trematoda- They are flatten and leaf like. Each fluke has a set of male and female reproductive organs( except blood flukes). The alimentary canal is incomplete and there is no body cavity. They possess oral and ventral suckers. Nematodes The parasitic nematodes are remarkable in being similar to each other but vary widely in size. They are cylindrical with unsegmented bodies and have false body cavities. The outer multi-layered cuticle is non-nucleated and allows contraction and expansion of the body. Inner to the cuticle is muscle layer. Among the major organs are the alimentary, excretory and the reproductive systems, which are suspended in the body cavity. They have separate sexes. The cuticle is shed ( moulting) four times during development from egg to adult worm. Some species have direct life cycle while others need intermediate hosts. Nematodes do not multiply in humans (except in the form of auto infection with strongyloides). Parasitic nematodes are found in various tissues such as subcutaneous,muscle,lymphatic tissues and in organs such as the intestinal tract. Nematodes parasites of humans Intestinal nematodes Small intestine: Ascaris lumbricoides ( The large round worm) Necator americanus (Hook worm) Ancylostoma duodenale (Hook worm) Strongyloides stercoralis (threadworm) Large intestine: Trichuris trichiura (Whipworm) Enterobius vermicularis(Pin worm) Tissue nematodes Subcutaneous tissues: filarial worm sp. And animal hookworm larvae Lymphatics: Filarial worms ( Wuchereria and Brugia) Visceral organs : Toxocara (larvae) CNS:Angiostrongylus cantonensis (Larvae), Toxocara (larvae)

Soil Transmitted helmithes (STH)

Five intestinal parasite species, namely, Ascaris lumbricoides, Necator americanus, Ancylostoma duodenal, Strongyloides stercoralis and Trichuris trichiura are collectively classed as STH. The eggs or the larvae of these nematodes are not infective when they are passed in the faeces of infected persons but have to under go a further period of development in soil before becoming infective to others. Exception is Trichuris trichiura where it does not develop in the soil but it contaminates the soil as eggs pass through faeces. Ascaris lumbricoides (Round worm) Geographical distribution: Worm has worldwide distribution but the prevalence is high in warmer climates in the tropical region where personal and environmental sanitation is poor. It is also prevalent in Sri Lanka Morphology: Adult: Female worms are 20-40 cm long while male measures 15 -30cm. The tail end of the male is curved Egg: Fertilizes eggs are oval in shape (60 -70X 40 -50m), has thick outer mammilated, albuminous coat. Unfertilized eggs are longer and rectangular in shape with no embryo seen. Life cycle: . The female lays as many as 200,000 eggs a day. Adult worms live in the lumen of the small intestine. A female produce up to 240,000 eggs per day, which are passed with the faeces . Fertile eggs embryonate and become infective after 18 days to several weeks, depending on the environmental conditions (optimum: moist, warm, shaded soil). After infective eggs are swallowed with contaminated food, the larvae hatch from the egg, penetrate the intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs. The larvae mature further in the lungs (10-14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed. Upon reaching the small intestine, they develop into adult worms. Time taken for infective egg to become adult worm and oviposition is 2-3 months. Adult worms can live 1 to 2 years. Diagnosis: Demonstration of characteristic eggs in the faeces. Pathogenesis and clinical features: many infected patients remain asymptomatic. However presence of small number of worms may lead to complications. Pathological and clinical features can be categorized into, pulmonary ascariasis, intestinal ascariasis, complications of ascariasis and allergy to ascaris species. Pulmonary ascariasis: An intense reaction occurs in the lungs as a result of larval migration. Larval antigens released by moulting larvae elicit an inflammatory reaction associated with moderate eosinophilia, pneumonitis, bilateral pulmonary infiltration, cough, dyspnea, substernal pain, fever and often asthma. These symptoms collectively called the Lofflers syndrome. The severity of the host reaction depends on the number of larvae migrating and the previous infection history. Hypersensitive individuals show severe reaction with other allergic manifestations Intestinal ascariasis: Adult worm in the intestine may cause mild abdominal pain and restlessness. Clinical consequence of the infection generally depend on the worm load. infection precipitates severe malnutr4ition ( even kwashiorkor and marasmus) in undernourished children. Ascarasis also known to lead to Vit A deficiency. Ascariasis can also adversely affect normal growth and educational achievement Complications of ascariasis: commonest complication is intestinal obstruction. Particularly in persons with heavy worm loads. They also may cause intestinal perforations leading to peritonitis. Adult worm may wander into orifices such as the opening of the bile duct, pancreatic duct causing obstruction. Allergy to Ascaris species: Manifestations are common during the acute phase of larval migration and due to the presence of adult worms in the intestine. Many experience asthma. The passage of adult worms in sensitive persons may give rise to intense anal pruritus, vomiting of worms and oedema of the glottis Epidemiology: It is a common backyard infection in most developing countries in tropics including Sri Lanka because of warm and humid conditions that facilitate development and survival of eggs. Infection is commonest among children of preschool age group Children get re-infected when they play in contaminated soil. Pica or dirt eating habit promotes infection. Transmission of infective eggs to human take place by way of contaminated green vegetables, fruit fallen under trees on contaminated grounds. Eggs may also transmit via drinking water. Prevention: Vegetables that are usually eaten raw or under cooked should be thoroughly washed. Fruits fallen under trees should be washed before eating. Washing hands after working with soil is also a important preventive measure. Control: Prevention of indiscriminate defaecation, Provision of sanitary latrines, Elimination of parasite reservoir by worm treatment and health education Parasitic hookworms of humans Necator americanus Ancylostoma duodenale

Geographical distribution: the parasite is widely distributed in the tropics and sub-tropics. Two species infect humans. Necator americanus is the species found in Sri Lanka. It is also found in South Asia, Africa, Europe and South America. Ancylostoma is the main hook worm of Eastern Europe, North Africa, India, Northern China and Japan. Location in the host: Inhabit the small intestine of humans. Unlike Ascaris it is attached to the mucosa of the intestine with the buccal capsule Morphology: the worm measures1-2 cm in length. The head end of the worms are sharply bent backwards (hooklike). The buccal cavity of N. americanus bears a pair of ventral cutting plates used in biting the mucosa for feeding. A. duodenale has two pairs of curved teeth Eggs: oval in shape an have thin glass like egg shell .Embryo is usually divided when the eggs passed in faeces. Life cycle: Embryonated Eggs are passed in the faeces, and under favorable conditions (moisture, warmth, shade), larvae hatch in 1 to 2 days. The released rhabditiform larvae grow in the faeces and/or the soil, and after 5 to 10 days (and two molts) they become filariform (third-stage) larvae that are infective. These infective larvae can survive 3 to 4 weeks in favorable environmental conditions. On contact with the human host, the larvae penetrate the skin and are carried through the blood vessels to the heart and then to the lungs. They penetrate into the pulmonary alveoli, ascend the bronchial tree to the pharynx, and are swallowed. The larvae then reach the small intestine, where they inhabit and mature into adults. Adult worms live in the lumen of the small intestine, where they attach to the intestinal wall with resultant blood loss by the host. Most adult worms are eliminated in 1 to 2 years, but the longevity may reach several years. Some A. duodenale larvae, following penetration of the host skin, can become dormant (in the intestine or muscle). In addition, infection by A. duodenale may probably also occur by the oral and transmammary route. N. americanus, however, requires a transpulmonary migration phase. Pathogenesis and clinical features In the acute infection the initial signs and symptoms are due to the penetration and migration of larvae in the skin. At the site of entry, a transient dermatitis with intense pruritus results. This condition is called ground itch. The lesions may get secondarily infected. The ling migratory phase of hookworm is short and the pulmonary symptoms are either absent or minimal. The pathogenesis of hookworm disease is directly related to the attachment of the worms to mucosa. They attach the mucosa by biting in plug of mucosa (including 7-9 villi), which are stripped off the lamina propria. The pool of blood thus created is sucked in using muscular pharynx. Only a part of sucked blood is use for food and oxygen, a large part being excreted continuously. This lead to blood loss and result in hypochromic microcytic ( Iron deficiency) anaemia. Each N. americanus sucks about 0.03ml of blood per day while A. duodenale sucks about 0.26 ml per day. The degree of aneamia related to the worm load and nutritional status of the host. Hypoproteinaemia seen severe hookworm disease may be related to 1) poor food intake 2) impaired absorption, 3) Increase loss and 4) combination of all. All these collectively result in stunting ( growth retardation). The pathogenesis of impaired mental and physical development in hook worm disease is not clear. Diagnosis: by demonstrating characteristic eggs in faeces. Eggs can be cultured into infective larvae. Epidemiology: It is an infection of the adults in many parts of the world including Sri Lanka. The prevalence of hook worm disease in a population depends on the deposition of eggs on favourable locations for external development. This location should have proper environmental conditions such as optimal temperature, moisture, shade, sandy soil and opportunities for infective larva to penetrate human skin. Prevention: Avoidance of indiscriminate defaecation, use of footwear Control Provision of hygienic latrines, chemotherapy of infected people and health education are important in the control programmes. Strongyloides stercoralis Parasite has worldwide distribution. But this infection is more common in tropical and subtropical regions. It has been reported in Sri Lanka Habitat: It is found embedded in small intestinal mucosa Morphology: only females are seen in parasitic cycle. (i.e. In the intestine of infected persons) Male is there for only short duration of time S. stercoralis is the only nematode or helminth that multiplies in the human body. The process is known as internal autoinfection. It differs from the hook worm in that1) No males in parasitic life cycle, 2) No eggs are pass in the faeces but the L1 rhabditiform larva 3) Internal autoinfection occurs when L1 larvae undergo accelerated development in to second rhabditiform larva (L2) and then to L3 which is filariform/infective larva while moving

down the intestinal tract, 4) has a free living cycle in the soil, 5) Parasite can cause severe disseminated disease with larvae in vital organs in immunocompromised host. Life cycle: There are two life cycles Parasitic life cycle Free living cycle Female worm lay eggs in the mucosa of small intestine. Generally, eggs hatched in the mucosa and L1 (rhabditiform)larvae enter the lumen and excreted in the faeces. When external conditions are unfavourable L1 rapidly develop in to L2 and then to infective L3 larva. Infective larva penetrate human skin and they carried to the lung via blood stream or the lymphatics. They breakthrough alveoli, enter the bronchi and to trachea and swallowed on reaching the pharynx. They mature in the mucosa of the small intestine into adults. If the external conditions are favourable L1 larvae develop in to L2 and then to L3. Subsequently, Infective larvae (L3) larvae develop into freeliving males and females. The larvae produced by free living adults mature into free living L3 stages. These larvae penetrate the skin of humans and once again start a parasitic life cycle. Pathogenesis and clinical features: At the site of skin penetration ground itch may occur. Pulmonary migration of larvae can cause lung symptoms and pneumonitis. But severe lung symptoms are rare. In mild infection there can be increase mucous secretion in to the lumen. In heavy infection the vili become flattened and atrophied. Epigastric pain, nausea, anorexia, nausea and finally watery diarrhea results In the hyperinfection seen in immunocompromized patients L1 rapidly develop in to infective L3 stage, which penetrate the gut wall and enter the blood stream( Internal autoinfection) Larvae in large numbers can carried in to various organs resulting in serious damage to respective organs and systems that can be damaged by larvae include brain, heart, pancreas, hepatobilliary systems, lungs, genitourinary system and the skin If the L1 larvae develop into infective stage in soiled cloths, bed linen or around the anal verge the migrating larvae produce characteristic dermatitis starting in the per anal region extending rapidly to buttocks and lower abdomen This condition is called larva currens Diagnosis.: Diagnosis is difficult because , female produce only small numbers of larvae. In cases suspected of strongyloidiasis, negative report on a single wet smear of faeces does not exclude the infection. Several samples over a period of 3 -7 days may be necessary to exclude infection In the faeces, rhabditiform larvae are looked for. In old samples sometimes hookworm larvae may also found. Then, the larvae have to be distinguished from those of strongyloides (compare the morphology in practical class). Of L1 larvae of either species or culture by Harada-Mori technique to obtain L3 larvae which could be easily identified -see practical).Duodenal intubations or 'Entero test' may be used to obtain larvae directly from the small intestine. Epidemiology - True prevalence of the infection is not known, as many infected persons are asymptomatic. On the other hand infection can last for long periods(over 30-40years)due to a degree of internal autoinfection. The infection may be found in cold climates if suitable 'micro-environments' as in coal mines are present. Larvae and the free-living adults are destroyed by direct sunlight. Prevention and control - Same as those for hookworm. Special care should be taken in immunocompromized persons. Trichuris trichiura - Whipworm Geographical distribution -It is widely distributed in warm tropical climates including Sri Lanka. Morphology - Female worm is about 30-50mm in length while the male is about 20-30mm.The anterior 3/5th of the body is thin while the posterior 2/5 th is thick in both sexes. The posterior end of the male is curved. Location in host - The worms inhabit the large intestine. The entire thin anterior end is threaded into the mucosa while the thick, short posterior end project into the lumen of the intestine. Life cycle- The female lays 2000-10,000 eggs per day. The eggs have a characteristic 'paddy seed' shape.(50 x 20 um) with 'polar caps' (see practical).The eggs are passed in the faeces. They require a period of maturation in the soil. The optimal conditions are similar to those for Ascaris (see Ascaris).Because of this fact trichuriasis often coexist with ascariasis. When infective eggs are ingested by humans, the eggs hatch in the lower part of the small

intestine and the larvae pass down into the large intestine to mature into adults. The mode of transmission is similar to that of ascariasis.(check ascariasis). Note - There is no pulmonary migration of larvae in trichuriasis. Pathogenesis and clinical features: Light infection may be asymptomatic heavy infections lead to blood and mucous diarrhoea. In children tenesmus and constant straining may lead to rectal prolapse. In some heavily infected children the infection may result in trichuris dysentery syndrome(TDS) Trichuriasis and malnutrition: Both conditions co-exist and it is difficult to determine a cause and effect TDS is generally seen with worm load over 500 worms The symptom s lead to lowering of food intake, which worsen already existing malnutrition Anaemia of trichuriasis: Anaemia is a constant feature of heavy infection It is hypochronic and microcytic anaemia. Anaemia may be due to : a) Blood loss from colonic mucosa, b) blood loss due to ingestion by worms. It is not certain whether Trichuris is a blood sucker. Growth retardation: Growth retardation is a distinct association in trichuriasis This is seen even with mild infection. Finger clubbing: Clubbing of figure is another association of the severe infection (TDS). Diagnosis: Demonstration of characteristic eggs in faeces A simple wet smear with saline/iodine is often sufficient Concentration techniques such as formol-ether could be used For quantitative studies Kato-Katz technique is good. Epidemiology: Children (5-15 years) are mostly infected in endemic areas Epidemiological factors described for ascariasis are applicable to trichuriasis as well. Enterobius vermicularis - Pinworm Enterobiasis is not a soil transmitted helminthes infection Geographical distribution - The parasite has a worldwide distribution with a high prevalence in cold temperate climates. Morphology - The adult worms are small (1cm) with both ends pointed. Males have curved tail ends and are rarely seen. The 'cervical alae' extend right down the sides of the body so that in cut sections they are seen as two projections on either side of the body. Location in host - The worm is found attached to the mucosa of the large intestine particularly the caecal area. They are not blood suckers. Life cycle - A gravid female carry approximately 10,000 eggs in the uterus. The female migrate down the large intestine to reach the anus. This occurs during night. The female then lays eggs on the anal verge. Following egg deposition, the female dies. The eggs are plano-convex in shape and have double walls(50x25 um).The outer wall is albuminous and is sticky. The embryos develop into infective larvae inside the eggs in 6 hours. When these eggs are ingested via contaminated fingers or via fomites they hatch in the lower part of the small intestine. The larvae move down to the large intestine to mature into adult males and females. There is no pulmonary migration of the larvae as in trichuriasis. Some infective eggs may hatch on the anal area and the larvae can move into the large intestine through the anus (retro-infection, a type of autoinfection) Pathogenesis and clinical features Enterobiasis is frequently asymptomatic The most typical symptom is perianal pruritus, especially at night, which may lead to excoriations and bacterial superinfection. Damage caused by the worm is not extensive Sometimes they produce inflammation of colon leading to granulomatous conditions Complications include perforation of gut (rarely) and migration to ectopic sites, commonest being the female vagina The moving female and deposited eggs cause severe pruritus ani. This lead to loss of sleep causing irritability . Occasionally, invasion of the female genital tract with vulvovaginitis and pelvic or peritoneal granulomas can occur. Other symptoms include anorexia, irritability, and abdominal pain. Epidemiology - Wind and air currents due to their lightness carry the eggs. They are deposited on objects found in the environment such as tabletops, doorknobs, chairs and seats. The infection makes no exception to any social class. It is a household infection and is highly prevalent where there is overcrowding such as in refugee camps, armed forces camps, prisons, hostels, orphanages etc. Generally if one member of the family gets infected, soon all in the household acquire the infection. Modes of transmission - (a) Direct infection from the anal and perianal region by fingernail contamination (b) Exposure and ingestion of viable eggs on soiled night clothes and other contaminated objects in the environment (c) By way of contaminated dust from bed clothes ,toys, furniture and (d) Retroinfection (see above). Prevention and control - (a) Cut finger nails short (b) wash hands with soap and water regularly (c) avoid scratching the anal area (d) treat everyone in the household including boarders and helpers (in institutions all

intimates including staff have to be treated at the same time.(e) following treatment all bed linen and personal clothes washed and dried in the hot sun (f) mats and mattresses exposed to hot sun (g) wet mopping of floors and surfaces. Diagnosis: Old methods include NIH (National Institute of Health, USA)) swab and Grahams Scotch Tape method A simple cello-tae strip can be used. , especially in the morning before the patient's first bowel movement. Eggs will adhere to the tape and can be seen microscopically. Examination of faeces: Collection of faeces Collect faeces, in a dry, clean, leak proof container, using a wooden spatula. Make sure no urine, water, soil or other material gets in the container. Label all samples clearly with patients name, reference number, date and time of collection. All samples should be accompanied by a requisition form from the physician giving relevant clinical details .Any whole worms or segments passed should be placed in separate container. Delivery and transportation Formed faeces samples without evidence of blood or mucus should be examined during the day of passage. It is possible to store these samples overnight at 4 C The irregular release of helminth ova makes it necessary to examine three samples routinely from each patient, preferably on alternate days. Preservation method Preservation allow faecal samples to be examined after a delay in delivery or postage Various preservatives are available (see table), with the two most commonly used being 10% aqueous formalin and PVA (polyvinyl-alcohol). Exercise based on topic 1 Outline the life cycle of each intestinal nematode parasite studied and mark the points at which the lifecycle could be interrupted 3 Described the measures one could take to interrupt the life cycle at the points you marked 3 Write an essay on nutritional consequences of intestinal nematode parasitic infections 4.Write a comparative account of the different LSs(SGL)