Hookworms

1. Hookworms Associated prof. Tian

2. Background 1. Hookworms are thevoracious blood feedersof the nematode world Hookworms parasitize more than 900 million people worldwide. 2. Ancylostomiasis is second only to ascariasis in infections by parasitic worms.

3. 3. There are two species of hookworms of medical importance Ancylostoma duodenale: - Africa, India, China and South East Asia (Asia hookworms) Necator americanus: - First reported in Brazil, then Texas, but since found in Africa, India and South East Asia. (American hookworms)

4. Morphology Adult: The adult parasites are small cylindrical worms, 0.5 - 1.5cm long (Ancylostoma duodenale being slightly larger than Necator americanus ). A.duodenale N. americanus

5. Curved teeth buccal capsule(mouth capsule) The anterior end of the parasites are formed into a buccal capsule Ancylostoma duodenale

6. cutting plates (semilunar) Necator americanus

7. The posterior end of the male worm is equip with a characteristic copulatory bursa

8. (umbrella-shaped bursa) Copulatory bursa of male of A.duodenale

9. Copulatory bursa of male of N.americanus

10. Comparison of Hookworms N. americanesA.duodenale Size (lenth) about 10 mm slight larger Shape “ S ” “ C ” buccal capsule a pair of two pair of cutting plates curved teeth

11. Eggs: shell Morula(4-8cell) Size 57-76 µm by 35-47 µm  Oval or ellipsoidal shape Thin shell, colorless. The eggs usually contain 4-8 cells in feces

12. A: Hookworm egg, advanced cleavage (iodine).B: Embryonated hookworm egg.

13. adult Are passed in the stool Life cycles warm moist shaded soil Rhabditiform larvae egg Intestinallumen hatching 24-48h, Contact host and penetrate the skin into the body 5-8days adult Filariform larvae Migrant by lungs

14. The route of larvae migrant Skin lungs trachea Oesophagus stomach intestine

15. Life Cycle

16. Soil polluted with human excreta is commonly responsible for exposure to infection with human hookworms Individuals become infected, usually by walking bare footed across contaminated soil

17. Penetration of the intact skin by filariform larvae of hookworm, on coming in contact with fecal polluted soil.

18. A, B: Hookworm rhabditiform larva (wet preparation). A, B: Hookworm filariform larva (wet preparation).

19. A, B, C: Hookworm filariform larva (A and B, wet preparations; C, iodine). Larva tail is depicted in Figures B and C.

20. Pathogenesis and clinical manifestation • Cutaneous or invasive phase: • by hookworm larvae • Dermatitis(ground itch): • irritation and itching

21. The larva of a hookworm is visible in the center of this photograph

22. (2) Pulmonary phase:by hookworm larvae Local haemorrhaging, pneumonitis Symptoms in respiratory system cause a cough and a sore throat.

23. (3) Intestinal phase:By adult worm A)the intestinal mucosa are damaged B)Anemia: Protein and iron in-take is insufficient Blood loss Hypochromic microcytic anemia

24. Blood loss a)Ingestion of the blood by the worm b)Seepage of the blood around the site of attachment of the worm c)Oozing of the blood from the burrowed site previously attached by the worm d)Anticoagulants

25. This is a photograph of the hookworm's appearance against the lining of the intestine (intestinal mucosa).

26. Clinical features of hookworm disease Site Symptoms Pathogenesis Dermal Local erythema, macules, papules (ground itch) Cutaneous invasion and subcutaneous migration of larva Pulmonary Bronchitis, pneumonitis and, sometimes, eosinophilia Migration of larvae through lung, bronchi, and trachea Gastro- intestinal Anorexia, epigastric pain and gastro-intestinal hemorrhage Attachment of adult worms and injury to upper intestinal mucosa Hematologic Iron deficiency, anemia, hypoproteinemia, edema, cardiac failure Intestinal blood loss

27. Diagnosis Laboratory diagnosis It includes parasitic diagnosis and immunodiagnosis l) Microscopy Direct smear examination of feces is adequate to detect moderate or severe infections.

28. 2) Concentration Concentration of stool by formalin-ether or simple salt floatation stool is essential to detect light hookworm infection. 3) Third-stage larvae in the fecal culture

29. Epidemiology Distribution Hookworm diseases is widely epidemic parasitic disease in the world. Hookworm distribute these areas between northern latitude 45○ to southern latitude 30○. A.duodenale is chiefly found in tropic areas and subtropic areas, N.americanus is commonly found in warm zone.

30. Distribution of Hookworm in china

31. Hookworm: World Distribution

32. Reservoir, source and transimission of infection Human is the only reservoir of infection Human feces is the only source of infection

33. Prevention and control l ) Sanitary disposal of human feces; 2) Treatment of infected persons; 3) Health education with improved use of sanitary latrines and use of foot wears

34. Treatment of hookworm infection consists of a) treatment of worm infection by anthelmintics such as mebendazole; b)treatment of anemia.

36. TRICHINELLA SPIRALIS

37. Trichinosis is related to the quality of pork and consumption of poorly cooked meat. Autopsy surveys indicate about 2 percent of the population is infected.

38. female Morphology Adult worm The adult worms are very small and slender with slightly tapered anterior ends, white and just to the naked eye. female 2.2 mm in length, males 1.2 mm; male

39. male papilla

40. pharynx female Its pharynx is one third or half of worm body long, and posterior part of pharynx consists of a column of cells called of stichocytes. juveniles

41. Cyst (larvae) The cyst are found in skeletal muscle commonly, its size is about 0.25~0.5

42. Larvae in Muscle Section Larvae in Muscle Press

43. Larvae of Trichinella, freed from their cysts, typically coiled; length: 0.8 to 1.0 mm.

44. Trichinella spiralis: Electron microscopy

45. Life cycles Into skeletal via bloodstream dischargeing adult cycst larvae ( 1 month) Intestine of the humans、pigs、rats、cats、dogs Swallowed by another host adult larvae

47. cyst cyst adult lavae

48. Trichinellosis is acquired by ingesting meat containing cysts (encysted larvae) of Trichinella. After exposure to gastric acid and pepsin, the larvae are released from the cysts and invade the small bowel mucosa where they develop into adult worms (life span in the small bowel: 4 weeks).

49. After 1 week, the females release larvae that migrate to the striated muscles where they encyst

50. Life Cycle < Infection occurs by ingesting encysted larvae in undercooked meat. < Larvae penetrate the intestinal wall and move to muscle tissue where they encyst in individual cells (nurse cells).  Active muscles, such as the diaphragm and tongue, often have the greatest numbers of larvae. < Adults attach to the intestinal mucosa and being to release larvae in one week.  The adults live for about 4 weeks and may release more than 1000 larvae.