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LECTURE NOTES ON

LECTURE NOTES ON. MEDICAL HELMINTHOLOGY. Dept. of Parasitology FK Unpad. Introduction to Medical Helminthology. Medical helminthology : the study of parasitic worms (helminthes/ vermes/cacing) affecting man, which : Spend part or the entire life cycle in a human host or

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LECTURE NOTES ON

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  1. LECTURE NOTES ON MEDICAL HELMINTHOLOGY Dept. of Parasitology FK Unpad

  2. Introduction to Medical Helminthology • Medical helminthology : the study of parasitic worms (helminthes/ vermes/cacing) affecting man, which : • Spend part or the entire life cycle in a human hostor • Animal parasite causing disease in human

  3. NEMATHELMINTHES PLATYHELMINTHES NEMATODES TREMATODES CESTODES CLASSIFICATION HELMINTHES

  4. General characteristics of Nematodes • The species parasitic in man range in length from 2 mm (Strongyloides stercoralis) to over a meter (Dracunculus medinensis) • The adult is an elongate cylindrical worm, bilaterally symmetrical like a thread; also known as roundworm • Unsegmented • Body covered by fine and smooth cuticle, sometimes striated • Has inner body cavity (pseudocoelom)

  5. Nematodes Life cycle • Transmission to a new host : • Ingestion the mature infectious egg or larva • Penetration of the skin or mucous membranes by the larva • Some species have an intermediate host – usually an arthropod • The same animal both the definitive and intermediate host of Trichinella spiralis • Nematodes, do not multiply in man

  6. Nematodes Pathogenicity • The effect of parasitic nematodes upon the host depends upon : species, the intensity of the infection and the location of the parasite • Simultaneous infection with several species of intestinal nematodes is common in tropical and subtropical countries • Injury may be produced by adult and larval parasites • Intestinal parasites produce less local and systemic effect than tissue parasites

  7. Nematodes Pathogenicity • The local reaction from intestinal parasites result from irritation, invasion of the intestinal wall and occasionally penertation to extraneous site • The local reaction in the liver, lungs (and other) – may destroy or encapsulate the larvae • The degree of local reaction – depend upon the sensitivity of the host to the proteic product of the parasite • Intestinal mucosa is damaged by biting and bloodsucking, by lytic ferment secreted by the parasite and by mechanical irritation

  8. Pathogenicity • The general reaction are produced by loss of blood, absorption of toxin, nervous reflexes and proteic sensitization • The larvae of certain species, produce local and general reaction • In unatural host the larvae may be pass through their invasive stages, never become established as adult parasite – paratenic host • Immunity is acquired through the invasion of the tissues by the parasite and its larvae or through the absorption of its products • Immunity is both humoral and cellular

  9. INTESTINAL NEMATODES BLOOD AND TISSUE NEMATODES SOIL TRANSMITTED HELMINTHS (STH) OTHER (NON-STH) FILARIA and DRACUNCULUS NEMATODES Classification based on Habitat HABITAT

  10. NEMATODES • Soil Transmitted Helminthes • Ascaris lumbricoides • Trichuris trichiura • Hookworm (Necator americanus, Ancylostoma duodenale) • Strongyloides stercoralis Important • Non-Soil Transmitted Helminthes • Enterobius vermicularis • Trichinella spiralis • Filaria and Dracunculus • Wuchereria bancrofti • Brugia malayi • Brugia timori Important

  11. IMMATURE INFECTIVE INTO Disease caused by Soil transmitted helminthes DEFINITIONSoil transmittedhelminth : NEMATODE WORMS WHICH REQUIRE PERIOD OF DEVELOPMENT AND MATURATION DURING ITS LIFE CYCLE ON SOIL

  12. Non-acute and not fatal Occurs primarily in slum areas Children are commonly infected with : Ascaris lumbricoides Trichuris trichiura Young adults mostly infected with hookworms (in the plantations and mining area) : Necator americanus Ancylostoma duodenale SOIL TRANSMITTED HELMINTHS GENERAL CHARACTERISTICS OF STH INFECTION

  13. DISTRIBUTION Cosmopolitan Prevalence 70-90 % Primarily affects underfives and school children HABITAT Lumen of the intestine : Jejunum Media ileum Ascaris lumbricoides

  14. Mature eggs Ingested Migration of larva inside the circulatory system Adults Larva Source : Medical Parasitology in Plates Piekarski G. Infertile eggs Ascaris lumbricoides LIFE CYCLE • Ingestion of mature eggs • Hatched in the gaster, larva penetrates the wall of the intestine and enter into blood circulation • To the right heart chamber, into the lungs • Alveoli – bronchioles - bronchus - trachea - swallowed • Arrived in the intestine and becomes mature adult

  15. (1). Larva Allergic manifestation : urticaria, swollen lips, asthma attack Loffler Syndromes : Ascaris pneumonia (coughing) Hyper-eosinophilia Thorax X-ray : temporary white spots Larva migration Ascaris lumbricoides PATHOGENESIS AND CLINICAL SYMPTOMS Disease ; Ascariasis Complaints due to direct effect by

  16. DISTRIBUTION Cosmopolitan Prevalence 70-90 % Primarily affects underfives and school children HABITAT Lumen of the intestine : Jejunum Media ileum Source : Dept. of Parasitologi FKUP, 1999 Adult worms expelled after deworming Source : Color Atlas of Medicine and Parasitology. 1977 Peters W. & Gillers H.M. Ascaris lumbricoides

  17. (2). Adult worm Irritations of the mucosal folds Blocking of the intestine - ileus Erratic migration Competes in the absorption of food and vitamins Release of toxic metabolic products Ascaris lumbricoides PATHOGENESIS AND CLINICAL SYMPTOMS Complaints due to direct effect by

  18. Laboratory diagnosis Identify the eggs found in feces using following methods : Direct smear method Concentration method Identify larva found in sputum Identify adult worm found expelled from anus, mouth, nostril Do quantitative lab method to measure level of infection Additional : chest X-ray Ascaris lumbricoides Diagnosis

  19. Treatment Drug available Pyrantel pamoate Mebendazol Oxantel pamoate Piperazine Albendazole ? Ascaris lumbricoides Mass treatment Based on prevalence of A. lumbricoides in one area : • prevalence > 30 %, treatment 3x/year • prevalence (20-30) %, treatment 2x /year • prevalence (10-20) %, treatment 1x /year • prevalence < 10 %, individual treatment in positive cases only

  20. PREVENTION treatment of individual case Provision of sanitary public bath, wash and toilet facilities Media information and health education Routine health check up of children Ascaris lumbricoides

  21. Distribution Trichuriasis - cosmopolitan Primarily in hot and humid areas prevalence 80-90 %, especially among underfives and school children Infection byTrichuris trichiura Habitat Caecum, appendix, colon (proximal end) Mode of infection  oral Infective eggs embedded under fingernail (hand to mouth infection) Ingested with contaminated food/drinks (carried by insect vector: cockroach, flies)

  22. Trichuris trichiura LIFE CYCLE

  23. Trichuris trichiura PATHOLOGY AND CLINICAL SYMPTOMS Disease : Trichuriasis Heavy infectionworm migrate to colon, rectum • Prolapsus recti, worm found in mucosal lining (due to frequent defecation)

  24. Trichuris trichiura PATHOLOGY AND CLINICAL SYMPTOMS Chronic and heavy infection • Heavy anemia (Hb = 3 gr%) (1 worm absorb 0,005 cc blood/day) • Abdominal pain, nausea, weight loss, vomiting • Prolapsus recti • Headache, fever Mixed infection may occur with Ascaris lumbricoides, hookworm and Entamoeba histolytica

  25. Trichuris trichiura Diagnosis • Identify egg worm found in fecal sample • Identify adult worm from prolapsed anus and rectum (by proctoscopy) • Measure level of infection by counting : • Number of eggs per gram feces • Number of female worm expelled through deworming

  26. Drugs available: Oxantel pamoate Mebendazol (drug of choice) Treatment • Elimination of source of infection • Improved personal hygiene (hand washing, toilet training) • Through washing of sold vegetables • Health education • Provision of sanitary public toilet Trichuris trichiura PREVENTION

  27. Infection by Hookworm PREFERENTIAL HABITAT • Small intestine (jejunum) • In heavy infection : duodenum, colon GEOGRAPHIC DISTRIBUTION Cosmopolitan, especially : • Tropical equator • Coal/tin mines, coffee/rubber plantations • Ideal soil for egg development : • Sandy soil • Clay soil • Muddy soil hindered from excessive dryness or wetness

  28. HOOKWORM LIFE CYCLE

  29. HOOKWORM PATHOLOGY AND CLINICAL SYMPTOMS • Disease: Ancylostomiasis • Synonym: Uncinariasis, necatoriasis • infection by A. duodenale are more serious than N. americanus • Chronic infection rarely produce acute manifestation • Tissue damage and symptoms are caused by : • Larva stage • Adult worm

  30. HOOKWORM PATHOLOGY CAUSED BY LARVA STAGE • Larva penetrates the skin - maculopapules - erythema - heavy itching : ground itch/dew itch • In sensitive patient, larva carried in the circulation, may cause: • Bronchitis / Pneumonitis

  31. HOOKWORM PATHOLOGY CAUSED BY ADULT WORM • Hooked to the intestinal mucosal wall : abdominal pain, nausea, diarrhea • Absorbing 0,2-0,3 ml of blood/day/worm : progressive anemia, hypo chrome, microcytic type of Fe deficiency anemia • Heavy anemia (Hb may reach 2 gr %) : • Dyspnea, physical weakness, headache • Rapid pulse beat, cardiac weakness • Children : physical growth retardation, mental

  32. Blood smear of patient with heavy infection caused by hookworm indicating Fe deficiency anemia with low MCHC and low serum Fe concentration Source : Color Atlas of Medicine and Parasitology. 1977 Peters W. & Gillers H.M. HOOKWORM PATHOLOGY CAUSED BY ADULT WORM (Anemia by HOOKWORM)

  33. HOOKWORM PATHOLOGY CAUSED BY ADULT WORM (Anemia by hookworm) • Atrophic glossitis found with hypo chromic microcytic anemia, caused by heavy infection of hookworm • Tongue surface become smooth and lacking of papillae

  34. source : Atlas Parasitologi Kedokteran, Zaman P. Alih Bahasa : Anwar C.; Mursal Y. HOOKWORM PATHOLOGY CAUSED BY ADULT WORM (Anemia by hookworm) • Patient with atrophic glossitis also show fingernail deformity (koilonichia) • Fingernail becomes thin and concave with elevated ridge • Glositis atrofik pada anemi hipokrom mikrositer yang disebabkan infection berat HOOKWORM • Tampak lidah halus dan kurang papila

  35. HOOKWORM Diagnosis • Identify eggs from feces sample • Identify larva from : • Fecal culture • Old feces sample

  36. HOOKWORM ANTIHELMINTHICS • Tetrachlorethylen • Mebendazole • Albendazole • Pyrantel pamoate • Bitoskanate • Bephenium hidroxynaphtoate PREVENTION • Same as with Ascariasis but with the addition of : wearing shoes during work in plantation or mine area

  37. HOST, HABITAT AND DISTRIBUTION Man is the definitive Host Habitat of female worm, mucosal lining of : Duodenum Jejunum (proximal end) Found very cosmopolitan, especially in the tropical and subtropical region Infection byStrongyloides stercoralis

  38. Strongyloides stercoralis LIFE CYCLE

  39. Disease : Strongyloidiasis, Strongyloidosis, Cochin China diarrhea Level of infection : Mild - asymptomatic Moderate Heavy and chronic Strongyloides stercoralis CLINICAL FEATURES

  40. In moderate infection • Female worm embedded in the mucosal wall of duodenum • Burning sensation and stinging pain in the epigastrium • Nausea, vomiting, diarrhea and constipation

  41. In heavy and chronic infection • Loss of body weight; Anemia • Dysentery (chronic); Slight fever • May be accompanied by secondary bacterial infection where worm inhabits the entire intestinal epithelium up to the distal colon)

  42. Find and identify Rhabditiform larva : From fresh feces Gastric (duodenal) juice *Eggs : In heavy diarrhea After administration of laxative Strongyloides stercoralis Diagnosis

  43. Strongyloides stercoralis TREATMENT AND PREVENTION Drugs given • Thiabendazole • Mebendazole • Pyrvinium pamoate

  44. PREVENTION • Similar to the prevention of hookworm • Autoinfection is prevented by means of : • Avoid constipation • Anal hygiene

  45. NON-SOIL TRANSMITTED HELMINTHS = Members of intestinal nematode that have transmissions are not via soil. = It happens because egg or larva of non-soil transmitted helminths don’t do maturation process (to become infectious) in the soil.

  46. NON-SOIL TRANSMITTED HELMINTHS 1. Enterobius vermicularis 2. Trichinella spiralis

  47. Enterobius vermicularis A. MORPHOLOGY > Enterobius vermicularis = Oxyuris vermicularis = pinworm. > In its life, this worm (ovipar) develops from: egg larva worm. > Its egg is oval, assymetry, that contains embrio. > This worm has lateral ala cephalic in anterior tip. > One female worm can produce 11.000 eggs in one day. > The female worm will die after producing eggs. > The male worm will die after copulation.

  48. B. LIFE CYCLE of Enterobius vermicularis Female & male worms do copulation in cecum & around (appendix, ascending colon & ileum) Pregnant female worms migrate at night & produce eggs in anus & around (anal area) After several hours, eggs become mature & infectious, then come to host, via: air (person inhalates) food (person eats food with infectious hand after scartching anal area) Eggs crack in duodenum & larvas appear Larvas become mature (be worm) in ileum

  49. Enterobius vermicularis C. SPREADING > Cosmopolite (spread around the world), especially in children. D. PATHOLOGY & CLINIC > The worm causes disease, called enterobiasis. > This disease has clinical symptoms: - Ithcing in anal area (pruritus ani) at night. - In girl, this disease can make inflammation in fallopian tube (salpingitis). - Intestine is seldom disturbed, etc.

  50. Enterobius vermicularis E. DIAGNOSIS > Scotch adhesive tape swab method, is done before taking a bath or defecating. F. TREATMENT > Mebendazole, thiabendazole, etc. G. PREVENTION > Washing hand before eating > Cutting long fingernail, etc.

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