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1 NEMATODES Faculty: SAMUEL AGUAZIM, M.D. Lange Chapter 56Lange Chapter 56.

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Presentation on theme: "1 NEMATODES Faculty: SAMUEL AGUAZIM, M.D. Lange Chapter 56Lange Chapter 56."— Presentation transcript:

1 1 NEMATODES Faculty: SAMUEL AGUAZIM, M.D. Lange Chapter 56Lange Chapter 56

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4 case 4 year old female with constant scratching of her buttocks for 1 week. The mother says that the child has been very irritable, uncomfortable at night. On examination of her anal area: numerous scratch marks, erythematous and swollen. 4

5 Pyrantel pamoate 2 doses Recovered Impression: Pinworm infection, secondary to Enterobius vermicularis 5

6 6 Nematodes are roundworms with a cylindrical body and complete digestive tract, including a mouth and an anus. The body is covered with a noncellular, highly resistant coating called a cuticle. Nematodes have separate sexes; the female is usually larger than the male

7 7 Nematodes The medical important nematodes can be divided into two categories according to their primary location in the body to: Intestinal Nematodes Tissue Nematodes

8 8 Intestinal Nematodes Enterobius vermicularis most common helminthic infection in the United States Disease: Pinworm infection. Characteristics: Intestinal nematode.

9 9 Enterobius vermicularis Life cycle: confined to humans. The infection is acquired by ingesting the worm eggs. The eggs hatch in the small intestine, where the larvae differentiate into adults and migrate to the colon. The adult male and female worms live in the colon, where mating occurs. At night, females migrate from the anus and lay many thousands of fertilized eggs on perianal skin and in environment. Embryo within egg becomes an infective larva within 4—6 hours. Reinfection can occur if they are carried to the mouth by fingers after scratching the itching skin.

10 10 Life cycle of Enterobius Life cycle of Enterobius

11 11 Enterobius vermicularis adult male and female

12 12 Enterobius egg(flattened side with larvae inside) Enterobius egg(flattened side with larvae inside)

13 13 Females lay eggs in the perianal area at night MOT: ingestion of eggs

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15 15 Enterobius vermicularis Transmission: Transmitted by ingesting eggs. Humans are the only hosts. Occurs worldwide. Pathogenesis: Worms and eggs cause perianal itching. Scratching predisposed to Secondary bacterial infection Laboratory Diagnosis:Eggs visible by “Scotch tape” technique. Eggs are not found in stool. Adult worms found in stool or near anus. Treatment: Mebendazole

16 16 Memory Tool On the bus (Enterobius), you sit on a pin (pinworm), and get an itchy bottom and use scotch tape to make it feel better.

17 17 Trichuris trichiura Disease: Whipworm infection Characteristics: Intestinal nematode. The characteristic of “whiplike” apperance of the adult worm. Life cycle: Humans ingest eggs, which develop into adults in gut. Eggs are passed in feces into soil, where they embryonate, ie, become infectious.

18 18 The characteristic of “whiplike” apperance of the adult worm. The characteristic of “whiplike” apperance of the adult worm.

19 19 Trichuris trichiura Transmission: More than 500 million infected. Transmitted by food or water contaminated with soil containing eggs. Humans are the only hosts. Occurs worldwide, especially in the tropics. Pathogenesis: Worm in gut usually causes little damage. The whipworm infects about 2 million children in the U.S. Causes rectal pruritis and tenesmus, which often results in rectal prolapse.

20 20 Infectious Diseases Whipworm – Rectal Prolapse

21 21 Infectious Diseases Whipworm – Rectal Prolapse

22 22 Trichuris trichiura Laboratory Diagnosis: Eggs visible in feces. The egg is barrel-shape with a plug at each end, in the stool. Treatment: Mebendazole. Prevention: Proper disposal of human waste

23 23 Trichuris trichiura eggs, a typical barrel shape two polar plugs, that are unstained

24 24 Trichuris trichiura Tricksy (Trichuris) carries a whip and ate eggs which gave her rectal prolapse. Poor Tricksy!!!

25 25 Ascaris Disease: Ascariasis. Characteristics: Intestinal nematode. Life cycle: Humans ingest eggs, which form larvae in gut. Larvae migrate through the blood to the lungs, where they enter the alveoli, pass up the trachea, and are swallowed. In the gut, they become adults and lay eggs that are passed in the feces. They embryonate, ie, become infective in soil. The adult worms are the largest intestinal nematodes (25 cm or more).

26 26 Ascaris Life Cycle

27 27 Ascaris adult male and female

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29 Erratic ascariasis 29

30 30 Ascaris Transmission: food contaminated with soil containing eggs. Humans are the only hosts. Endemic in the tropics. Pathogenesis: Larvae in lung can cause pneumonia. Heavy worm burden can cause intestinal obstruction or malnutrition. Laboratory Diagnosis: Eggs visible in feces. Eggs are oval with irregular surface. Eosinophilia occurs. Treatment: Mebendazole Prevention: Proper disposal of human waste

31 31 Eggs are oval with irregular surface

32 32 Billy (biliary obstruction) drives his car (Ascaris) while eating eggs and gets short of breath. Poor Billy!!! Add intestinal obstruction

33 33 Strongyloides Disease: Strongyloidiasis Characteristics: Intestinal nematode. Life cycle: Larvae penetrate skin, enter the blood, and migrate to the lungs. They move into alveoli and up the trachea and are swallowed. become adults and enter the mucosa, where females produce eggs that hatch in the colon into noninfectious, rhabditiform larvae that are usually passed in feces. NOTE: the only helminth to secrete larvae (and not eggs) in feces

34 34 Strongyloides Occasionally, rhabditiform larvae molt in the gut to form infectious, filariform larvae that can enter the blood and migrate to the lung (autoinfection). The noninfectious larvae passed in feces form infectious filariform larvae in the soil. These larvae can either penetrate the skin or form adults. Adults in soil can undergo several entire life cycles there. This free-living cycle can be interrupted when filariform larvae contact the skin.

35 35 Strongyloides Transmission: Filariform larvae in soil penetrate skin. Endemic in the tropics. Pathogenesis: Little effect in immunocompetent persons. In immunocompromised persons, massive superinfection can occur accompanied by secondary bacterial infections. Laboratory Diagnosis: Larvae visible in stool. Eosinophilia occurs. Treatment: Thiabendazole. Prevention: Proper disposal of human waste. Use of footwear

36 36 Memory Tool The strongman (Strongyloides) is brought down by a larvae penetrating his skin causing pulmonary distress and superinfection. Poor strongman!

37 37 Ancylostoma duodenale Necator Americanus Disease:Hookworm. Characteristics:Intestinal nematode.

38 38 Ancylostoma duodenale Filariform larvae in soil penetrate skin of feet, enter the blood, and migrate to the lungs. enter alveoli, pass up the trachea, then are swallowed. become adults in small intestine and attach to walls via teeth (Ancylostoma) or cutting plates (Necator). Eggs are passed in feces and form noninfectious rhabditiform larvae and then infectious filariform larvae.

39 39 Ancylostoma duodenale adult male and female

40 40 Ancylostoma duodenale Transmission: Filariform larvae in soil penetrate skin of feet. Humans are the only hosts. Pathogenesis:Anemia due to blood loss from gastrointestinal tract. Laboratory Diagnosis: Eggs visible in feces. Eosinophilia occurs. Treatment:Mebendazole AND Iron therapy Prevention:Use of footwear. Proper disposal of human waste.

41 ANCYLOSTOMA BRAZILIENSE ANCYLOSTOMA CANINUM DOG and CAT Hook worm Forms/ Transmission. Filariform larvae penetrate intact skin but cannot mature in humans Disease/organ most affected Cutaneous larvae migrans: intense itching Tunnels through tissue Diagnosis: clinical signs Treatment- ivermectin 41

42 Ancylostoma braziliensis (cutaneous larva migrans/creeping eruption) 42 Pathognomonic: serpiginous tunnels Lacks hydrolytic enzymes to penetrate into the dermis; remains localized in the epidermis

43 Ancylostoma braziliensis (cutaneous larva migrans/creeping eruption ) 43 freezing with liquid nitrogen/ethyl chloride; Mebendazole Dog, cat hookworm Gulf states, South US

44 44 Trichinella Disease : Trichinosis. Characteristics: Intestinal nematode that encysts in tissue.

45 45 Trichinella Life cycle: Humans ingest under cooked pork and other meat containing encysted larvae, which mature into adults in small intestine. Female worms release larvae that enter blood and migrate to skeletal muscle or brain, where they encyst. Pigs:most important reservoirs of human disease in USA, except Alaska where bears are the ones. Reservoir hosts are primarily pigs and rats. Humans are dead end hosts. Occurs worldwide but endemic in eastern Europe and west Africa

46 46 Trichinella life cycle Trichinella life cycle

47 47 Encysted larvae of Trichinella in pressed muscle tissue. The coiled larvae can be seen inside the cysts. CDC

48 48 Trichinella Pathogenesis: Inflammation of muscle Laboratory Diagnosis: Encysted larvae visible in muscle biopsy Eosinophilia Serologic tests positive. Treatment: Thiabendazole effective early against adults. None for established disease Prevention: Adequate cooking of pork

49 49 Memory Tool A tricky (Trichinella) pig caused cysts in his owners muscles.

50 50 Tissue nematode Dracunculus Disease: Dracunculiasis. Characteristics: Tissue nematode.

51 51 Dracunculus Life cycle: Humans ingest copepods containing infective larvae in drinking water. Larvae are released in gut, migrate to body cavity, mature, and mate. Fertilized female migrates to subcutaneous tissue and forms a papule, which ulcerates. Motile larvae are released into water, where they are eaten by copepods and form infective larvae.

52 52 Dracunculus Transmission: copepods in drinking water. Humans are definitive hosts. Many domestic animals are reservoir hosts. Endemic in tropical Africa, Middle East, and India Pathogenesis: Adult worms in skin cause inflammation and ulceration. Treatment: Niridazole. Extraction of worm from skin ulcer. Prevention: Purification of drinking water

53 Dracunculiasis 53

54 54 Dracunculus: posterior end

55 55 Dracula ate an infected crustacean and got an ulcer with protruding worm. He removed the worm by winding it around a stick.

56 56 Loa Loa (eye worm) Disease: Loiasis. Characteristics: Tissue nematode.

57 57 Loa Loa Life cycle: Bite of deer fly (mango fly) deposits infective larvae, which crawl into the skin and develop into adults that migrate subcutaneously. Females produce microfilariae, which enter the blood. These are ingested by deer flies, in which the infective larvae are formed.

58 58 Loa Transmission: Transmitted by deer flies. Humans are the only definitive hosts. No animal reservoir. Endemic in central and west Africa. Pathogenesis:Hypersensitivity to adult worms causes “swelling” in skin. Adult worm seen crawling across conjunctivas Laboratory Diagnosis: Microfilariae visible on blood smear. Treatment: Diethylcarbamazine. Prevention: Deer fly control.

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60 60 Memory Tool Her name was Loa she was an eye worm …….

61 61 Onchocerca Disease: Onchocerciasis (river blindness). Characteristics: Tissue nematodes.

62 62 Onchocerca Life cycle: Bite of female black fly deposits infective larvae, which mature in body cavity. Worms enter subcutaneous tissue, where they mature within skin nodules. Females produce microfilariae, which migrate in interstitial fluids and are ingested by black flies, in which the infective larvae are formed.

63 RIVER BLINDNESS/SOWDA 63 trapped microfilaria in the cornea, choroid, iris and anterior chambers, leading to photophobia, lacrimation and blindness

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65 65 Onchocerca Transmission: Transmitted by female black flies. Humans are the only definitive hosts. No animal reservoir. Endemic along rivers of tropical Africa and Central America. Pathogenesis:Microfilariae in eye ultimately can cause blindness. Adults induce inflammatory nodules in skin. Laboratory Diagnosis: Microfilariae visible in skin biopsy, not in blood. Treatment: Ivermectin affects microfilariae, not adult worms. Suramin for adult worms. Prevention: Black fly control and ivermectin

66 66 Toxocara canis Disease:Visceral larva migrans. Characteristics: Nematode larvae cause disease.

67 67 Toxocara canis Life cycle: Toxocara eggs are passed in dog feces Ingested by humans. Hatch into larvae in small intestine Larvae enter the blood and migrate to organs, especially liver, brain, and eyes, where they are trapped and die. Transmission: ingestion of eggs in food or water contaminated with dog feces. Dogs are definitive hosts. Humans are dead end hosts. Pathogenesis: Granulomas form around dead larvae. Granulomas in the retina can cause blindness

68 68 Toxocara canis Laboratory Diagnosis: Larvae visible in tissue. Serologic tests useful. Treatment: Diethylcarbamazine Prevention: Dogs should be dewormed

69 69 Wuchereria Disease: Filanasis. Characteristics:Tissue nematodes.

70 70 Wuchereria Life cycle: Bite of female mosquito Deposits infective larvae that penetrate bite wound, form adults, and produce microfilariae. These circulate in the blood, chiefly at night, and are ingested by mosquitoes, in which the infective larvae are formed. Transmission: Female mosquitoes of several genera. Humans are the only definitive hosts. Endemic in many tropical areas.

71 71 Here are microfilaria. These tiny worms circulate in the bloodstream. There are several species with slightly different clinical characteristics, but they are spread by mosquitos. These microfilaria happen to be Wuchereria bancrofti.

72 72 Wuchereria Pathogenesis: Adult worms cause inflammation that blocks lymphatic vessels (elephantiasis). Chronic, repeated infection required for symptoms to occur. Laboratory Diagnosis: Microfilariae visible on blood smear. Treatment: Diethylcarbamazine affects microfllariae. No treatment for adult worms. Prevention: Mosquito control

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74 74 hydrocele: most common manifestation of chronic W bancrofti infection ELEPHANTIASIS

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