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  1. 1. Nematodes
  2. 2. ► Nematodes are vermiform, cylindrical and taper towards their anterior and posterior ends. The body has a complete digestive tract and covered with a thick cuticle. ► Adult Nematodes are dioecious and male worms are typically smaller than the females and have a typically coiled tail.
  3. 3. ► Almost all nematode parasites, humans serve as the optimum host where they pass their entire life cycles. For some, however, an intermediate host is required. ► Humans may serve as the definitive host to the adult males(Ascaris) or as both an intermediate and definitive host ( Trichinella). ► Despite their diversity and complexity, all nematodes generally have 3 stages in their lifecycle: egg, larva and adult.
  4. 4. ► ► ► ► Eggs may hatch either within the host or external environment, where the first stage develops inside the egg and hatches under suitable conditions and the larva emerge. During the larval stage , the nematodes undergo a series of four molts, thus referred to as the first, second, third and the fourth stage, called the Rhabditiform larva, filariform larva or microfilaria. The infective stage can be the filariform stage (Hookworm) or the very first stage of the egg itself containing the larva (Ascaris). As adults, these live within the human body, but can exist in the soil as well (Strongyloides).
  5. 5. ► Unlike protozoan parasites, the adult helminthes are incapable of increasing their numbers within their definitive host. Thus the severity of the clinical illness is related to the total number of worms acquired over a period of time. ► Adult nematodes cause damage by mechanical disruption and toxicity. These may involve erosion, bleeding, inflammatory reaction and proliferation of tissues. ► The primary pathogenic mechanism for a larva appears to be the invasion and subsequent migration in tissues of the host causing immunological reactions with allergic or anaphylactic reactions to fever, lymphadenopathy and transient pneumonias and nocturnal paroxysms of asthma..
  6. 6. ► Ascaris lumbricoides: ► Largest and most common of the intestinal heminthes parasitizing humans. ► Reside in the Intestinal tract and cause Ascariasis, producing embarrasment, discomfort, malnutrition, anemia and occassional death. ► Cylindrical, fusiform body, light brown to pink.
  7. 7. ► Mouth opening at the anterior end with three lips with fine teeth at the lumen edge. ► Male slightly smaller than female with a curved tail. Matured female can pass upto 200,000 eggs daily. ► Fertilized eggs enclose a embryo cell and elleptical in shape with a rough, albuminous coating over their chitinous shells. Unfertilized eggs have a thinner outer proteinic membrane.
  8. 8. ► Definitive hosts: Humans. Intermediate hosts: None. ► Life cycle: ► Adults live in small intestine and absorb nutrition from semi-digested food – intense muscular activity – copulate – unsegmented ovum deposited into intestinal lumen – passed in the feces – eggs embryonate in the soil for 3 weeks – become infectious – enters human body on the ingestion of eggs – larva hatch – penetrate the intestinal mucosa – invade portal veinules – carried to the liver – as still small can squeeze through capillaries and exit to the hepatic vein – to the heart – to the lungs – as the larva have increased in size become too big to wriggle out of the pulmonary capillaries rupture into the alveolar spaces – coughed up and subsequently swallowed – regain their position in the upper small intestines. ►
  9. 9. ► Pathogenicity and clinical manifestations: ► Both migrating larva and adult worms can cause pathological changes and symptoms due to mechanical damage and toxicity.
  10. 10. ► Migrating Larva: ► Larval migration of A.lumbricoides through the lungs lead to vasrying degrees of pneumonitis and bronchospasm. ► The migrating larva continuously produce immunogenic substances that cause immune and allergic reactions to develop, including bronchial asthma, transient eosinophillic pulmonary infiltrates (Loeffler’s syndrome) and angioneurotic edema.
  11. 11. ► II) Adult worm: ► Worm burden small : asymptomatic. ► Heavier worm load : Clinical manifestations result… A) Malnutrition and growth retardation: presence of Ascaris hinders absorption of fat, protein and carbohydrates and deficiencies of Vitamins A, B2 and C. Children frequently infected and show growth retardation and severe malnutrition. ►
  12. 12. ► B) Allergic reaction: Ascaris allergen (a glycoprotein) most potent allergen of parasitic origin. Clinical manifestations include urticaria, itch, conjunctivitis and angioneurotic edema. ► C): Ascariasis: Symptoms of Ascariasis may be severe due to the characteristic migratory activities of the adult worm – accelerated by peppery food, rise in temperature (fever), anaesthesia, improper drugs etc… - can migrate to bile duct, appendix, pancreatic duct causing obstruction and inflammation of the organ. Biliary ascariasis most common – abdominal pain, gall-stones, gallbladder rupture, peritonitis or liver abscess. Can cause mechanical obstruction of the ileum ( entangled worm forming a bolus). Ascaris may, unusually, crawl out of the patients mouth, nose, ear or genitourinary organ. ► ► ► ►
  13. 13. ► Lab diagnosis: ► Characteristic eggs ( oval to ellipsoidal with irregular surface) in the stool specimen. Occasional adult worm can also be seen. ► Larva and eosinophils in the sputum, during the pulmonary phase.
  14. 14. ► Treatment and prevention: ► Treatment effective: Mebendazole, Albendazole and pyrantel pamoate. ► Prevention: Proper disposal of feces.
  15. 15. ► Trichuris trichiura: ► Also known as Whipworm. Habitats human cecum causes Trichuriasis. Anterior part of the body thin and thread like and constitute a single column of secretory cells (serves as the oesophagus) and the posterior part is bulbous and fleshy containing the intestines and reproductory organs – giving a whiplike appearance. Male little smaller and shorter than female, with a tightly coiled tail. ► ► ►
  16. 16. ► Eggs: Females lay 3,000-10,000 eggs – characteristic barrel shaped – distinctive brown shell with a translucent knob at each pole.
  17. 17. ► Life cycle: ► Only one host : Man. The adults reside in the colon attached to the colonic mucosa – gravid female releases eggs – pass out with the feces – reach soil – mature in 3-5weeks – become embryonated and infectious- transmission is fecal-oral route by playing children especially – or food contaminated ( grown in sewage water) – ingested eggs hatch in the duodenum – grow and mature for a month and then move to the cecum as adults. ►
  18. 18. ► Pathogenesis and clinical symptoms: ► Attachment of the adult worms to the colonic mucosa and subsequent feeding produce localized ulcerations and hemorrhage (0,005 ml blood/worm/day). ► Ulcers provide enteric bacteria with a portal of entry- results in sustained bacteremia. ► IgE mediated immunity present but ineffective to cause appreciable worm expulsion.
  19. 19. ► Light worm load : Asymptomatic. ► Moderate worm loads : damages the intestinal mucosa, induces nausea, abdominal pain, diarrhea and stunted growth. ► Children with >800 worm load – entire colonic mucosa parasitized – significant mucosal damage – blood loss and anemia. ► Prolapse of the colonic or rectal mucosa through the anus, particularly with strain at defecation or during childbirth.
  20. 20. ► Lab diagnosis: ► Characteristic eggs in feces. ► Treatment and Prevention: ► Treatment of choice: Albendazole, Mebendazole. ► Prevention: Improvement of sanitary facilities and health education.
  21. 21. ► ► ► ► ► Ancylostoma duodenale (old world hookworm) and Necator americanus (new world hookworm): Both are hookworms. Cause Hookworm infection. Indistinguishable from eggs and larval stages. Eggs are small, may show a visible embryonic cleavage ( 2-,4-, or 8-celled stage). Difference in adult worms for morphological differences. Ancylostoma attach to the walls of the small intestine with their teeth and Necator with their cutting plates.
  22. 22. ► ► ► ► ► Rhabdititform larva : immature, newly hatched hookworm – actively feeding – presence of a long buccal cavity. Filariform larva: non-feeding, infective larva emerges from the rhabditiform larva – completes second molt – hookworm filariform larva has a distinctly pointed tail. Adult: pinkish, with head turned opposite to their curved body, giving appearance of hook. Males typically smaller. Buccal capsule of A.duodenale has actual teeth, N.americanus has a pair of cutting plates.
  23. 23. ► Life cycle: Both life cycles are similar. ► Eggs passed out in feces at 4-, 8-cell stage development – reach soil – hatch within 48 hours – release rhabditiform larva – feeds on debris and bacteria - molt to become infective filariform larva – penetrate skin through unprotected feet – migrates to the lymphatics and blood system – larva reaches lungs via blood – penetrate capillaries and enter alveoli – migration continues into bronchioles – coughed up to the pharynx – swallowed and deposited in the intestines – mature to adulthood. Females lay 10,000 – 20,000 eggs per day, passed out through feces – reach soil. ►
  24. 24. ► Pathogenesis and clinical manifestations: ► Adult worms live for years within the intestines, leaving bleeding points at old sites of attachment. Adult A.duodenale extracts 0.2 ml blood/worm/day and N.americanus 0.03ml/worm/day. The accumulated blood loss is enormous. Humoral antibody response and immediate hypersensitivity (IgE mediated eosinophilia) reactions but may not be effective. ► ►
  25. 25. ► Worm burden small: Asymptomatic. A diet rich in iron, protein and vitamins help maintain asymptomatic state. ► Hookworm disease: ► Repeatedly infected individuals may develop intense allergic itching at the site of hookworm penetration, known as Ground-itch. ► Larval migration manifests various symptoms like sore throat, bloody sputum, wheezing, headache, mild pneumonia with cough.
  26. 26. ► ► ► ► ► Intestinal phase symptoms depend on the number of worms present: A) Chronic infections ( <500 eggs/gram of feces) : light worm burden – vague GI symptoms, slight anemia and weight loss or weakness. B) Acute infection ( >5000 eggs/gram of feces): diarrhea, anorexia, edema, pain, enteritis and epigastric discomfort. Feeding hookworms may also lead to microcytic hypochromic iron deficiency, weakness and hypoproteinemia. In children, may lead to heart failure or Kwashiorkar. Mental, sexual, physical retardation can also result with even death.
  27. 27. ► Lab diagnosis: ► Characteristic eggs in stool specimen. ► Occult blood is frequent and with eosinophilia. ► Treatment of choice: Mebendazole, Albendazole, pyrantel pamoate. ► Prevention: Proper disposal of sewage and proper footwear.
  28. 28. ► Enterobius vermicularis: ► Also known as Pinworm or seatworm. ► Parasitic only to humans. ► Causes pinworm infection or Enterobiasis.
  29. 29. ► Adults are small, white, spindle-shaped and threadlike. Females have a wing like expansion of the body wall, at the anterior end called Alae. Males are smaller and possess a curved tail. ► Eggs are ovoid with a colorless, thick shell covering the larva. Embyonated eggs infective to humans.
  30. 30. ► Life cycle: ► Only one host: Man. Sexually mature worms inhabit the intestines and can spread to adjacent regions of both small and large intestines like cecum, appendix, rectum, colon etc…- adhere to the mucosa and feed on epithelial cells and bacteria. Males die on copulation and the gravid females migrate to the perianal regions. Lower temperature and aerobic conditions stimulate the laying of eggs and they perish as well. Each egg contains an immature larva and the third stage larva completes development inside the egg. Infection and reinfection occur – picked up from the bed-clothes, or finger nails after scratching perianal region – or even inhaled. Retroinfections can also occur when third stage larva hatch from peri-anally located eggs and enter the hosts intestine through the anus. Ingested eggs hatch shortly after reaching the duodenum – escape – molt and reach adulthood before residing in the colon. ► ► ► ► ► ►
  31. 31. ► Pathogenesis and clinical symptoms: ► Not highly pathogenic as does not cause significant damage to the colonic mucosa and the allergic toxicity of pinworms is yet to be confirmed. Itching and irritation due to the gravid females migration around the perianal areas. Usually asymptomatic. Heavy infections in children may cause sleeplessness, weight loss, hyperactivity, teeth grinding, abdominal pain and vomiting. Gravid females may migrate up the female genital tract causing vaginitis, endometritis and granuloma in the uterus and fallopian tubes – may also reach appendix, peritoneal cavity or urinary bladder. ► ► ► ►
  32. 32. ► Lab diagnosis: ► Demonstration of small white thread-like worms in the under garments of children. ► Eggs rarely found in feces – strip of cellophane around the perianal area touching the skin and observe under microscope. Negative results for 7 days consecutively indicates infection free.
  33. 33. ► Treatment of choice: Mebendazole or pyrantel pamoate kills worms in the colon, but not the eggs. Hence, retreatment in 2 weeks time may be necessary. Reinfec tion is common. ► Prevention: No definite prevention known.