1. Enterobius vermicularis Department of Medical Parasitology

2. Introduction Enterobius vermicularis, commonly known as pinworm or seatworm E. vermicularis is parasitic only to humans Adults inhabit the ileocecus, that is, cecum and adjacent ascending colon and distal ileum. The infection of E. vermicularis may cause Enterobiasis World-wide distribution, it is commonly found in kindergarten and primary school students

3. Phylum Nemathelminthes Class Nematoda Order Oxyurata Family Oxyuridae Classification

4. Morphology -- Adult Female -- fusiform body with a long, thin, tapering tail, 8 to 13mm Male -- “6” shape, curved tail, 2 to 5mm. Males die right after mating, thus are rarely seen White in color

5. Cephalic alae The anterior end tapers and is flanked on each side by cuticular extensions of head Pharyngeal bulb The esophagus is slender, terminating in a prominent posterior bulb

6. Morphology -- Egg Oval in shape, 50~60×25μm in average, a larva inside Clear, colorless and doubly refractive egg shell, flattened on one side

7. molt molt 3 times Adults Newly laid Infective Larvae Adults eggs 6h eggs Life cycle

8. Humans are the only host in nature No intermediate host (direct life cycle) No larval migration between organs Characteristics of life cycle

9. Infection Infective eggs Stage Type Self-infection: anus-hands-mouth route Cross-infection: contact transmission Inhalation Retroinfection

10. Adults Cecum and adjacent large and small intestines Adhering to intestinal mucosa Residence Site Stage Mode Feed Blood, tissue fluid, epithelial cells

11. Habitus 15000 eggs/ ♀ Fecundity Life span Female 1~2 months Gravid female crawl out of anus at night and deposit eggs on the perianal and perineal region (anal sphincter relaxed) Residence

12. Female release eggs on the perianal zone Discharge Eggs Stage Mode

13. Pathogenesis Enterobiasis is usually asymptomatic, the adults may cause slight irritation of the intestinal mucosa The most typical symptom is perianal pruritus (itching and irritation), which associates with the nocturnal migration of the gravid females from the anus and deposition of eggs in the perianal folds of the skin, may lead to excoriations and bacterial superinfection

14. Heavy infection in children may result in restlessness, sleeplessness, anorexia, weigh loss, grinding of teeth, nervousness, irritability, abdominal pain and vomiting Sometimes, pinworm may migrate up the female reproductive tract, cause vaginitis, endometritis and granuloma in uterus and fallopian tubes. Occasionally, invasion of the female to the appendix, the peritoneal cavity or the urinary bladder may occur Pathogenesis

15. Laboratory Diagnosis Microscopic identification of eggs collected in the perianal area by cellophane (Graham Scotch) tape method or anal swabs. This must be done in the morning, before defecation and washing Detection of adult on anal skin

16. Geographical distribution Epidemiology Geographical distribution—cosmopolitan in temperate zones with about 30~50% of the population infected, and more prevalent in children than adults. it is estimated that 500 million people are infected Worldwide Enterobiasis is most common where people live under crowded conditions such as orphanages, kindergartens, and large families

17. Distribution of pinworm in children under the age of 12 (23.6% in average, 71% in Fujian and Jiangsu )

18. Source of infection Prevalent features Patients and carriers Multiple ways of infection Reinfection

19. Treatment and prevention Albendazole/Mebendazole: 95% effective Repeated retreatment may be necessary for a radical cure Personal hygiene and eating habits Sanitary disposal of clothing, bed linen, and environment Health education

20. Trichinella spiralis

21. Introduction Trichinella spiralis is capable of infecting all mammals, cause parasitic zoonosis--trichinellosis Human beings acquire the food-borne trichinellosis by ingesting the raw or undercooked meat of pigs and other animals containing the Trichinella larvae Larvae which inhabit the striated skeletal muscles are the main pathogenic stage World-wide distribution

22. Phylum Nemathelminthes Class Nematoda Order Trichurata Family Trichinellidae Classification

23. Morphology -- Adult Thread like Male--1.5mm in length, female--3~4mm in length Ivory-white in color

24. Morphology -- Larva The newborn larvae--100µm long, the fully developed, encapsulated larvae--1 mm long Larvae encyst in skeletal muscle cells

25. Life cycle

26. Encapsulated larvae Digestive enzymes Larvae Penetrate mucosa Adults ♀, ♂ mate ♂ die right after mating ♀ 3~5 days Newborn larvae Blood stream skeletal muscle Molt 4 times ， 48h Encapsulated larvae

27. Infection Encapsulated larvae Stage Mode Oral infection

28. Adults, larvae Adults--duodenal and jejunal mucosa Larvae--skeletal muscles of the tongue, the deltoid, pectoral, and intercostal muscles, the diaphragm, and the gastrocnemius Residence Site Stage Life span Female adults--1~2 months Larvae--several to 30 years

29. Adults and larvae live in the same host (not only final host but also intermediate host), alternation of hosts is needed to complete the whole life cycle Ovoviviparity No discharge or free-living stages The only intracellular parasitic nematode Characteristics of life cycle

30. Pathogenesis Intestinal phase Muscular phase Convalescent phase Fever, myalgia, eosinophilia Stage Adults, encapsulated larvae (main) Symptomatology Clinical feature

31. Laboratory Diagnosis Parasitological examination --muscle biopsy Deltoid or gastrocnemius muscles are the best choice Immunodiagnosis --ELISA Detection of specific antibodies in serum

32. Geographical distribution Epidemiology Cosmopolitan The global prevalence of trichinellosis is estimated as many as 11 million people may be infected. More cases of human infection have been found in developed countries than in developing countries

33. Distribution of Trichinella spiralis in China

34. Source of infection Mode of infection Pigs and other wild animals containing the Trichinella larvae Ingesting the raw or improperly prepared pork products

35. Treatment and prevention Albendazole / Mebendazole Development of industrialized pig farms Improvement of pig feeding Inspection of meat Health education

36. Filaria

37. Introduction Filariasis is a widely spread disease caused by different species of filariae The adults of filariae inhabit the lymphatics, subcutaneous tissue, deep connective tissue, peritoneal or thoracic cavity There are eight species of filariae, namely, Wuchereria bancrofti, Brugia malayi, Brugia timori, Loa loa, Onchocerca volvulus, Mansonella ozzardi, Dipetalonema perstans and Dipetalonema streptocerca in humans

38. Larvae known as microfilariae appear in the circulating blood or tissue fluids W. bancrofti and B. malayi which lie coiled in the lymphatic vessels are most commonly responsible for lymphatic filariasis and of more medical importance Microfilariae circulate in peripheral blood once each day. Mosquito is essential vector and intermediate host

39. Phylum Nemathelminthes Class Nematoda Order Filariata Family Dipetalonematidae Classification

40. Wuchereria bancrofti and Brugia malayi

41. Morphology -- Adult Slender, thread-like White in color Male -- 2.5-4 cm long and has a curved tail, female -- 5-10 cm in length

42. Microfilaria--177~296 µm in length, encased in a sheath with free endings. Bluntly rounded anteriorly and tapers to a point posteriorly. A large number of nuclei seen in the body are arranged in a column from head to the posterior Wuchereria bancrofti Brugia malayi Morphology -- Larva

43. The morphological differentiation of bancroftian and malayan microfilariae W. bancroftiBrugia malayi SizeLarger, 244~296 by 5.3~7 µm Smaller, 177~230 by 5~6 µm ShapeCurves of body are natural, smooth Curves of body are rigid, the small in larger curve Cephalic spaceShorter (length is equal to or less than width) Longer (length is two times as long as width) Body nucleiEqual sized, clearly defined, countable Unequal sized, coalescing, uncountable Terminal nucleiNoTwo

44. Life cycle

45. Microfilariae Blood meal Microfilariae Take off sheath, migrate to thoracic muscles Sausage larvae Molt Infective larvae Adults Molt 2 times Lymphatics Molt Migrate to prosbocis Blood meal Infective larvae Peripheral blood Ovoviviparity Human stageMosquito stage

46. Host: mosquitoes as intermediate host, human as final host Location: lymphatic vessels and lymph nodes Infective stage: infective larvae Transmission stage: microfilariae Diagnostic stage: microfilariae Ovoviviparity Characteristics of life cycle

47. Different parasitic site between the two species of lymphatic filariae: W. bancrofti parasitizes in the superficial and deep lymphatic systems, including in the genitourinary lymphatic system; B. malayi parasitizes in the shallow lymphatic system only, especially in the lymphatics of limbs Characteristics of life cycle

48. Nocturnal periodicity: the numbers of microfilariae present in the peripheral blood during daytime is very low in density, usually undetectable, but gradually increase from evening to midnight and reach the greatest density at 10 p.m. to 2 a.m. The mechanism for this phenomenon is still not clear. It may be related to the change of oxygen tension in cerebral and the pulmonary vessels Characteristics of life cycle

49. Pathogenesis Results from a complex interplay of the pathogenic potential of parasite, the immune response of the host, and external bacterial and fungal infections Acute diseases--dilatation of the lymphatics / hyperplastic changes in the vessel endothelium / infiltration by lymphocytes, plasma cells and eosinophils / thrombus formation

50. Pathogenesis Chronic lesion--the changes include granuloma formation, fibrosis, and permanent lymphatic obstruction Repeated infections eventually result in massive lymphatic blockade The skin and subcutaneous tissues become edematous, thickened, and fibrotic Dilated vessels may rupture, spilling lymph into the tissue to cause lymphedema and elephantiasis

51. Asymptomatic amicrofilariaemic Asymptomatic microfilariaemic Acute manifestation Obstructive (Chronic) lesions Clinical manifestations

52. Asymptomatic amicrofilariaemic--in endemic areas, a proportion of population does not show microfilariae or clinical manifestation even though they have some degree of exposure to infective larva similar to those who become infected. Laboratory diagnostic techniques are not able to determine whether they are infected or free Clinical manifestations

53. Asymptomatic microfilariaemic-- considerable proportions are asymptomatic for months and years, though they have circulating microfilariae. They are an important source of infection. They can be detected by night blood survey and other suitable procedures Clinical manifestations

54. Acute manifestation--during initial months and years, there are recurrent episodes of acute inflammation in the lymph vessel/node of the limb & scrotum that are consisting of filarial fever, lymphangitis, lymphadinitis, epididymitis, orchitis Clinical manifestations

55. Lymphangitis Lymphoedema

56. Obstructive (Chronic) lesions--takes 10-15 years, main pathological change is lymph obstruction. The lymph circulation is disturbed and lymphedema occurs. The affected limb feels soft at first and becomes fibrotic after extensive growth of connective tissue as elephantiasis develops. e.g. hydrocoele (40~60%), elephantiasis of scrotum, penis, leg, arm, vulva, breast, and chyluria Clinical manifestations

57. Penis Scrotum Hydrocoele

58. Leg

59. Arm

60. Breast Vulva

61. Chyluria and haematuria

62. Laboratory Diagnosis Microfilariae: demonstration of microfilarae in the peripheral blood a. Thick blood smear: 2~3 drops of free flowing blood by finger prick method b. Membrane filtration method: 1~2 ml intravenous blood filtered through 3µm pore size membrane filter c. DEC provocative test (2mg/Kg): after consuming DEC, mf enters into the peripheral blood in day time within 30~45 minutes Adult: biopsy of the nodes or lymphatic vessels Immunological tests: antibody or circulating filarial antigen (CFA)

63. Geographical distribution Epidemiology W. bancrofti is widely distributed throughout the tropics and subtropics. It is prevalent in Africa, Asia, and certain islands in the Pacific Ocean B. malayi has a distribution centering around the Malay peninsula. In addition to Malaysia, it occurs in India, Indonesia, New Guinea, Thailand, Vietnam, Korea, Japan and China

65. Global scenario Epidemiology Population at risk: 1.2 Billion No. of countries: > 80 Mf carriers: 76 Million Diseased: 44 Million Hydrocele: 27 Million Lymphoedema: 16 Million

66. Treatment and prevention The source of infection should be eradicated by mass survey and treatment All person with microfilariae should be treated with diethylcarbamazine (DEC) which is the low toxicity but most effective drug. 200mg tid for seven days as one course. DEC added to table salt (3:1000) and distributed in endemic areas over a period of six months, results in great reduction of microfilaria in the blood stream Elimination of vectors and protection of the people from mosquito bites are important to control filariasis