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NEMATHELMINTHES
1. ASCARIS OVA
1. ASCARIS LUMBRICOIDES
1.ASCARIS LUMBRICOIDES
• Common name: Giant Intestinal roundworm
• Definitive host: Man (No intermediate host)
• Habitat: Small intestine
• Diagnostic stage: ova (fertilized or unfertilized)
• Infective stage: Embryonated ova
• SOI: soil-transmitted, eggs remain viable in the soil for month-10 years
• MOT: Ingestion, hand to mouth; fingers contaminated by soil contact
• Adult worm : “erratic ascaris” brain, liver , lungs
• Cause: Loeffler’s syndrome
• Treatment: Mebendazole or pyrantel pamoate
• Control: education and chemotherapy
• Ectopic sites: appendicitis, biliary tract duct of pancreas
• Children cause mental retardation
Ascaris worm
Toxocara cati, T. canis
• Cause: visceral larva migrans or Toxocariasis
• Eggs are threat to human
• Children more prone to infect because of a contact
• Migration produces hemorrhage, necrosis, granulomas
• Eosinophillia, liver damage, pulmonary inflammation,
ocular problem will be observed.
• Take note: they do not develop further than larva stage
2. Hookworm Ova
ascaris lumbricoides ova
Trichuris trichiura ova
hook worm ova
2. Hookworm Rhabditiform
Diagnostic stage
2. Hookworm filariform
Infective stage
Hookworm in human
• Ancylostoma duodenale and Necator
americanus
• Infection occurs when filariform (LARVAE)
penetrates the skin of man
• Causing “ground itch” or “dewy itch”
maculopapular lesion
• Iron deficiency anemia, hypoalbuminemia
Hookworm in Human
• Common name: Old world hookworm( Ancylostoma
duodenale), New world hookworm (Necator americanus)
• Definitive host: Human (no intermediate host)
• Body curvature: “C” shaped and “S” shaped
• Dental pattern: 2 pairs of teeth, semilunar-cutting plate
• Habitat: Small intestine
• Diagnostic stage: Ova
• Infective stage: L3 (filariform)
• Mode of transmission: skin penetration, transmammary and
purely percutaneous
• Disease: Hookworm infection, Ancylostomiasis
Animal Hookworm
• Ancylostoma caninum and Ancylostoma
braziliense
• Causing Cutaneous Larva Migrans (CLM)
produces linear, pruritic, papulovesicular lesions
• Condition referred to serpiginous dermatitis or
creeping eruption
2. Hookworm
• Infective stage: filariform larva(L3)
• Skin: site of entry of filariform
• Lung: Larva migration- bronchitis, pneumonitis
• Small intestine: habitat of adult worm-
steatorrhea, diarrhea w/ blood and mucus
• Eosinophil 30-60%
• Treatment: mebendazole (DOC) and pyrantel
pamoate
Characteristic of hookworm dentition
• A: Necator americanus, semi-luna cutting plate
• B: Ancylostoma braziliense: 2 pair of teeth
• C: Ancylostoma caninum: 3 pairs of teeth
• D: Ancylostoma duodenale: 2 pair of teeth
A B C D
Hookworm
No acute symptom
Chronic secondary
• Microcytic hypochromic anemia (iron
deficiency/loss blood)
• Hypoalbuminemia (loss blood, lymp, protein)
• Other symptom dyspnea, weakness, dizziness,
lassitude, signs include rapid pulse edema,
albuminuria
• In children: heavy infection-stunting growth &
mental retardation
Hookworm
• Laboratory diagnosis: based on the identification
of eggs
1. DFS (only in heavy infection)
2. Kato technique or Kato-katz method: detection
rate, quantitative diagnosis
3. Concentration method like ZnSO4 contrifugal
floatation& formalin-ether concentration
method, increase positive finding many folds
4. Harada-Mori culture allow hatching larva from
eggs on strips of filter paper with one end
immersed in water.
3. ENTEROBIUS VERMICULARIS or
PINWORM OVA
D-shape
3. ENTEROBIUS VERMICULARIS
or PINWORM FEMALE
3. Enterobius vermicularis
• Common name: Pinworm, seatworm, society worm
• Final host: man (without intermediate host and reservoir
host)
• Habitat: large intestine (caecum and colon)
• Diagnostic stage: ova
• Infective stage: Embryonated ova
• Source of infection: contact borne
• Mode of transmission: ingestion, inhalation
 Take note: Larva develop and the eggs become infected
within 4-6 hours
 Newly hatched larva migrate back to anus- Retroinfection
3. Enterobius vermicularis or Pinworm
• Causing enterobiasis, oxyuriasis or seatworm infection
• Lab: scotch tape method early in the morning before taking
a bath
• Familial disease
• Treatment:
1. pyrantel pamoate 10mg/kg w/ a second dose 2-4 wks later
2. Albendazole(400mg) mebendazole (500mg) single dose
4.TRICHINELLA SPIRALIS LARVA
4. Trichinella spiralis
• Common name: Trichinia worm
• Infective stage: Encysted larvae
• Habitat: Striated muscle tissue
• MOT: ingestion of raw/ uncooked
contaminated meat
• Diagnostic specimen- skeletal muscle, biopsy/
blood (LDH adolase, CPK, eosinoplil etc.)
4. TRICHINELLA SPIRALIS
• Infective stage: encysted larva (viable for 10
years)
• Impregnated female penetrates the duodenal
wall start to produce lava after a week
• Favorite sites: heart & systematic circulation,
striated muscle(heaviest infection), CNS,
serous cavities
• Treatment: Thiabendazole(intestinal phase),
corticosteroid (inflammation), salicylates(pain)
5. TRICHURIS TRICHIURA or
WHIPWORM
bipolar plug
5. TRICHURIS TRICHIURA OVA
5. Trichuris trichiura
• Common name: whip worm
• Final host: human
• Habitat: Large intestine-attached
• Diagnostic stage: Ova
• Infective stage: Embryonated ova
• Source of infection: Soil-transmitted helminthes
• Mode of transmission: Ingestion
• Portal of entry: mouth
5. Trichuris trichiura
• Egg Morphology; hatched in Large intestine
Trichuris trichiura eggs are 'football' or 'barrel'
shaped with clear, mucoid-appearing polar
plugs at each end.
5. Trichuris trichiura
Whipworm
• Infective stage: fully embryonated egg found in
brackish
• Stool exam: reveals bile-stained eggs w/ polar
plugs
• Pathology: Rectal prolapsed in children,
appendicitis, Iron deficiency anemia, diarrhea and
eosinophilia (seen in severe infection)
• Treatment : mebendazole(DOC)
To declare free from
Ascaris lumbricoides and Trichuris trichiura
• Three specimen- negative
• Stool examination negative for eggs-
interpreted as
1. All male parasites
2. Female worms are immature(migration
stage)
3. Unfertilized eggs (all females and males-
immature)
6. Capillaria philippinensis or
Pudoc worm
Peanut shaped
Flattened bipolar plug
Striated shells
• Common name: Pudoc worm
• Final host: man/other vertebrate; fish-eating birds
• Intermediate host(IH): glass fish, fresh brackish-water fish
• Diagnostic stage: Ova in stool;peanut-shaped(unembryonated
egg)
• Infective stage: encysted larva (larva in IH)
• Habitat: small intestine
• Source of infection: food borne
• Mode of transmission: eat raw brackish water fish/
contaminated fish
• Portal of entry: mouth
6. Capillaria philippinensis or
Pudoc worm
6. Capillaria philippinensis
Autoinfection and hyperinfection
Ova(diagnostic stage):
 Produced by typical female
 Moderately thick striated egg sheath with
flattened bipolar plug
6. Capillaria philppinensis or
Pudoc worm
 Pathology
 Decrease secretion of xylose, low e’lyte(K+)
 Cause micro ulceration, depression of intestinal villi (cause
malabsorption of fluid, protein and electrolytes)
 Borborygmi (Gurgling stomach)
 Malabsorption syndrome(Fat&sugar)
 Laboratory test
 DFS (direct fecal stool exam)
 Concentration technique(FECT)
 Examination of duodenal aspirate
6. Capillaria philippinensis or
Pudoc worm
• Treatment:
1. Albendazole(DOC) 400 mg once daily for 10 days
2. Mebendazole 200 mg 2 tab once daily for 20 days
 Relapse may occur if the treatment regimen is not
followed. If dis. Not treated soon after severe
manifestation – die
 Parasites can be found in small intestine by:
“duodenal aspiration”
7. Strongyloides stercularis
• Common name: Threadworm, smallest nematode of
man
• Final host: man
• Diagnostic stage: Rhabditiform Larva
• Infective stage: Filarliform Larva(L3)
• Mode of transmission: Skin penetration of infective
larva; AUTOINFECTION
• Causative agent of : Cochin China Diarrhea,
malabsorption syndrome
Take note: Hyperinfection are limited to Lungs and GIT
Rhabditiform larva of S. stercoralris can be mistaken from of
that the hookworm Rhabditiform
8. Wuchereria bancrofti
• Common name: Bancroft’s firalial worm
• Vectors: Anopheles, Culex, Aedes
• Host-adult: Lower lymphatic
• NO ANIMAL RESERVOIR
• Diagnostic stage: Microfilariae
• Infective stage: L3 filariform larva
• MOT: Skin penetration
• Periodicity: Nocturnal (Blood smear 10pm-4am)
• Habitat: Lymphatic and blood (disappear at day time)
• Pathology: BANCROFTIAN FILARIASIS
8. Wuchereria bancrofti
 Diagnosis:
• Blood smear examination between 10 pm -4am.
• Knott’s concentration technique
• RDT-ICT antigen detection (CFA)
• Both W. bancrofti & Burgia malayi demonstrates a
sheath on microfilariae
 Treatment
• Bancroftian filariasis 6 mg/kg/day DEC for 12 days
• Burgian filariasis 3-5 mg/kg/day up to 36-72 mg/kg
Diethylcarbamazine(DEC) and Ivermectin
9. Burgia malayi
• Common name: Malayan filarial worm
• Final host: Mansonia bonneae, M. uniformis
• Host-adult: upper limbs lymphatic
• Diagnostic stage: Microfilarial
• Infective stage: L3 filariform larva
• MOT: skin penetration
• Periodicity: nocturnal subperiodic
• Pathology: MALAYAN FILARIASIS
• Reservoir: Cats & monkeys
9.Loa Loa
• Common name: African eye worm
• Vector: a biting fly- CHRYSOPS
• Reservoir host: monkeys
• Blood smear between 10pm.-2am.
• Causing agent of subcutaneous nodules or ONCHOCERCOMATA
contain adult worms-painless
• Ocular disease: RIVER BLINDNESS
• Migratory lesion: CALABAR SWELLING- result of allergic reaction or
metabolic production, transients, painful & pruritus
10. Onchocerca volvulus
• Habitat: Laymphatic & subcutaneous tissues
• Causes: Onchocerciasis( River blindness)
• Vector: Black fly (Genus Simulium damnosum)-majority
• Human is a natural host
• Diagnostic stage: unsheathed microfilariae
• Infective stage: Microfilariae
 Pathology
• Onchocerciasis(river blindness), the least pathogenic-
causing ONCHOCERCOMATA(subcutaneous nodules)
11. Dirofilaria immitis
• Common name: Dog heartworm
• Intermediate host: mosquitoes
• Host: dogs, cats, raccoons, bobcats in nature,
occasionally man
• Cause: Man-subcutaneous nodules or so-called
“coin-lesion” in lungs
• Dogs- dog heartworm, rare in human’s heart
• Transmission- by mosquitoes controlled, treating
dogs with Ivermectin
12. Dracunculus medinensis
• “Little dragon of Medina”- ancient worm infection; “fiery serpant”
noted by moses with the Isralites at the Red Sea
• Reservoir host: dogs, fur-bearing animals drink contaminated water
containing infective Cyclops
• Human infection- result of ingestion of water from so-called
“stepwell” where people stand or bathe in the water , at which gravid
female worm discharges lava from lesion on the arms, legs, feet,
ankles to infect cyclops in the water.
• Take note: a filarial worm but a tissue invading nematodes. They are
not appeared in the blood
• Immediate host: fresh water microcutaneous(copped) of genus
Cyclops
12. Dracunculus medinensis
• Laboratory diagnosis: observation of typical ulcer
& flooding the ulcer with water to recover&
discharge the larval form
• Occasionally, x-ray examination reveals worms in
various part of the body
• Treatment: Surgical removal, wrapping the worm
on a twig
• Tiridazole(DOC), alternative drug:metronidazole,
thiabendazole
Take Note
• Filariform larva:-infective stage of hookworm ,
ascaris and other nematodes, long, thread-like
often “designed” for penetration
• Filarial worm: any of a group of parasitic
worms of family Filariaidae (Phylum
Nematodes) requires 2 hosts, an
arthropod(Intermediate host) and a vertebrae
(primary host) to complete the life cycle

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Nemathelminthes review

  • 4. 1.ASCARIS LUMBRICOIDES • Common name: Giant Intestinal roundworm • Definitive host: Man (No intermediate host) • Habitat: Small intestine • Diagnostic stage: ova (fertilized or unfertilized) • Infective stage: Embryonated ova • SOI: soil-transmitted, eggs remain viable in the soil for month-10 years • MOT: Ingestion, hand to mouth; fingers contaminated by soil contact • Adult worm : “erratic ascaris” brain, liver , lungs • Cause: Loeffler’s syndrome • Treatment: Mebendazole or pyrantel pamoate • Control: education and chemotherapy • Ectopic sites: appendicitis, biliary tract duct of pancreas • Children cause mental retardation
  • 5. Ascaris worm Toxocara cati, T. canis • Cause: visceral larva migrans or Toxocariasis • Eggs are threat to human • Children more prone to infect because of a contact • Migration produces hemorrhage, necrosis, granulomas • Eosinophillia, liver damage, pulmonary inflammation, ocular problem will be observed. • Take note: they do not develop further than larva stage
  • 7. ascaris lumbricoides ova Trichuris trichiura ova hook worm ova
  • 10. Hookworm in human • Ancylostoma duodenale and Necator americanus • Infection occurs when filariform (LARVAE) penetrates the skin of man • Causing “ground itch” or “dewy itch” maculopapular lesion • Iron deficiency anemia, hypoalbuminemia
  • 11. Hookworm in Human • Common name: Old world hookworm( Ancylostoma duodenale), New world hookworm (Necator americanus) • Definitive host: Human (no intermediate host) • Body curvature: “C” shaped and “S” shaped • Dental pattern: 2 pairs of teeth, semilunar-cutting plate • Habitat: Small intestine • Diagnostic stage: Ova • Infective stage: L3 (filariform) • Mode of transmission: skin penetration, transmammary and purely percutaneous • Disease: Hookworm infection, Ancylostomiasis
  • 12. Animal Hookworm • Ancylostoma caninum and Ancylostoma braziliense • Causing Cutaneous Larva Migrans (CLM) produces linear, pruritic, papulovesicular lesions • Condition referred to serpiginous dermatitis or creeping eruption
  • 13. 2. Hookworm • Infective stage: filariform larva(L3) • Skin: site of entry of filariform • Lung: Larva migration- bronchitis, pneumonitis • Small intestine: habitat of adult worm- steatorrhea, diarrhea w/ blood and mucus • Eosinophil 30-60% • Treatment: mebendazole (DOC) and pyrantel pamoate
  • 14. Characteristic of hookworm dentition • A: Necator americanus, semi-luna cutting plate • B: Ancylostoma braziliense: 2 pair of teeth • C: Ancylostoma caninum: 3 pairs of teeth • D: Ancylostoma duodenale: 2 pair of teeth A B C D
  • 15. Hookworm No acute symptom Chronic secondary • Microcytic hypochromic anemia (iron deficiency/loss blood) • Hypoalbuminemia (loss blood, lymp, protein) • Other symptom dyspnea, weakness, dizziness, lassitude, signs include rapid pulse edema, albuminuria • In children: heavy infection-stunting growth & mental retardation
  • 16. Hookworm • Laboratory diagnosis: based on the identification of eggs 1. DFS (only in heavy infection) 2. Kato technique or Kato-katz method: detection rate, quantitative diagnosis 3. Concentration method like ZnSO4 contrifugal floatation& formalin-ether concentration method, increase positive finding many folds 4. Harada-Mori culture allow hatching larva from eggs on strips of filter paper with one end immersed in water.
  • 17. 3. ENTEROBIUS VERMICULARIS or PINWORM OVA D-shape
  • 19. 3. Enterobius vermicularis • Common name: Pinworm, seatworm, society worm • Final host: man (without intermediate host and reservoir host) • Habitat: large intestine (caecum and colon) • Diagnostic stage: ova • Infective stage: Embryonated ova • Source of infection: contact borne • Mode of transmission: ingestion, inhalation  Take note: Larva develop and the eggs become infected within 4-6 hours  Newly hatched larva migrate back to anus- Retroinfection
  • 20. 3. Enterobius vermicularis or Pinworm • Causing enterobiasis, oxyuriasis or seatworm infection • Lab: scotch tape method early in the morning before taking a bath • Familial disease • Treatment: 1. pyrantel pamoate 10mg/kg w/ a second dose 2-4 wks later 2. Albendazole(400mg) mebendazole (500mg) single dose
  • 22. 4. Trichinella spiralis • Common name: Trichinia worm • Infective stage: Encysted larvae • Habitat: Striated muscle tissue • MOT: ingestion of raw/ uncooked contaminated meat • Diagnostic specimen- skeletal muscle, biopsy/ blood (LDH adolase, CPK, eosinoplil etc.)
  • 23. 4. TRICHINELLA SPIRALIS • Infective stage: encysted larva (viable for 10 years) • Impregnated female penetrates the duodenal wall start to produce lava after a week • Favorite sites: heart & systematic circulation, striated muscle(heaviest infection), CNS, serous cavities • Treatment: Thiabendazole(intestinal phase), corticosteroid (inflammation), salicylates(pain)
  • 24. 5. TRICHURIS TRICHIURA or WHIPWORM bipolar plug
  • 26. 5. Trichuris trichiura • Common name: whip worm • Final host: human • Habitat: Large intestine-attached • Diagnostic stage: Ova • Infective stage: Embryonated ova • Source of infection: Soil-transmitted helminthes • Mode of transmission: Ingestion • Portal of entry: mouth
  • 27. 5. Trichuris trichiura • Egg Morphology; hatched in Large intestine Trichuris trichiura eggs are 'football' or 'barrel' shaped with clear, mucoid-appearing polar plugs at each end.
  • 28. 5. Trichuris trichiura Whipworm • Infective stage: fully embryonated egg found in brackish • Stool exam: reveals bile-stained eggs w/ polar plugs • Pathology: Rectal prolapsed in children, appendicitis, Iron deficiency anemia, diarrhea and eosinophilia (seen in severe infection) • Treatment : mebendazole(DOC)
  • 29. To declare free from Ascaris lumbricoides and Trichuris trichiura • Three specimen- negative • Stool examination negative for eggs- interpreted as 1. All male parasites 2. Female worms are immature(migration stage) 3. Unfertilized eggs (all females and males- immature)
  • 30. 6. Capillaria philippinensis or Pudoc worm Peanut shaped Flattened bipolar plug Striated shells
  • 31. • Common name: Pudoc worm • Final host: man/other vertebrate; fish-eating birds • Intermediate host(IH): glass fish, fresh brackish-water fish • Diagnostic stage: Ova in stool;peanut-shaped(unembryonated egg) • Infective stage: encysted larva (larva in IH) • Habitat: small intestine • Source of infection: food borne • Mode of transmission: eat raw brackish water fish/ contaminated fish • Portal of entry: mouth 6. Capillaria philippinensis or Pudoc worm
  • 32. 6. Capillaria philippinensis Autoinfection and hyperinfection Ova(diagnostic stage):  Produced by typical female  Moderately thick striated egg sheath with flattened bipolar plug
  • 33. 6. Capillaria philppinensis or Pudoc worm  Pathology  Decrease secretion of xylose, low e’lyte(K+)  Cause micro ulceration, depression of intestinal villi (cause malabsorption of fluid, protein and electrolytes)  Borborygmi (Gurgling stomach)  Malabsorption syndrome(Fat&sugar)  Laboratory test  DFS (direct fecal stool exam)  Concentration technique(FECT)  Examination of duodenal aspirate
  • 34. 6. Capillaria philippinensis or Pudoc worm • Treatment: 1. Albendazole(DOC) 400 mg once daily for 10 days 2. Mebendazole 200 mg 2 tab once daily for 20 days  Relapse may occur if the treatment regimen is not followed. If dis. Not treated soon after severe manifestation – die  Parasites can be found in small intestine by: “duodenal aspiration”
  • 35. 7. Strongyloides stercularis • Common name: Threadworm, smallest nematode of man • Final host: man • Diagnostic stage: Rhabditiform Larva • Infective stage: Filarliform Larva(L3) • Mode of transmission: Skin penetration of infective larva; AUTOINFECTION • Causative agent of : Cochin China Diarrhea, malabsorption syndrome Take note: Hyperinfection are limited to Lungs and GIT
  • 36. Rhabditiform larva of S. stercoralris can be mistaken from of that the hookworm Rhabditiform
  • 37.
  • 38. 8. Wuchereria bancrofti • Common name: Bancroft’s firalial worm • Vectors: Anopheles, Culex, Aedes • Host-adult: Lower lymphatic • NO ANIMAL RESERVOIR • Diagnostic stage: Microfilariae • Infective stage: L3 filariform larva • MOT: Skin penetration • Periodicity: Nocturnal (Blood smear 10pm-4am) • Habitat: Lymphatic and blood (disappear at day time) • Pathology: BANCROFTIAN FILARIASIS
  • 39. 8. Wuchereria bancrofti  Diagnosis: • Blood smear examination between 10 pm -4am. • Knott’s concentration technique • RDT-ICT antigen detection (CFA) • Both W. bancrofti & Burgia malayi demonstrates a sheath on microfilariae  Treatment • Bancroftian filariasis 6 mg/kg/day DEC for 12 days • Burgian filariasis 3-5 mg/kg/day up to 36-72 mg/kg Diethylcarbamazine(DEC) and Ivermectin
  • 40. 9. Burgia malayi • Common name: Malayan filarial worm • Final host: Mansonia bonneae, M. uniformis • Host-adult: upper limbs lymphatic • Diagnostic stage: Microfilarial • Infective stage: L3 filariform larva • MOT: skin penetration • Periodicity: nocturnal subperiodic • Pathology: MALAYAN FILARIASIS • Reservoir: Cats & monkeys
  • 41. 9.Loa Loa • Common name: African eye worm • Vector: a biting fly- CHRYSOPS • Reservoir host: monkeys • Blood smear between 10pm.-2am. • Causing agent of subcutaneous nodules or ONCHOCERCOMATA contain adult worms-painless • Ocular disease: RIVER BLINDNESS • Migratory lesion: CALABAR SWELLING- result of allergic reaction or metabolic production, transients, painful & pruritus
  • 42. 10. Onchocerca volvulus • Habitat: Laymphatic & subcutaneous tissues • Causes: Onchocerciasis( River blindness) • Vector: Black fly (Genus Simulium damnosum)-majority • Human is a natural host • Diagnostic stage: unsheathed microfilariae • Infective stage: Microfilariae  Pathology • Onchocerciasis(river blindness), the least pathogenic- causing ONCHOCERCOMATA(subcutaneous nodules)
  • 43. 11. Dirofilaria immitis • Common name: Dog heartworm • Intermediate host: mosquitoes • Host: dogs, cats, raccoons, bobcats in nature, occasionally man • Cause: Man-subcutaneous nodules or so-called “coin-lesion” in lungs • Dogs- dog heartworm, rare in human’s heart • Transmission- by mosquitoes controlled, treating dogs with Ivermectin
  • 44. 12. Dracunculus medinensis • “Little dragon of Medina”- ancient worm infection; “fiery serpant” noted by moses with the Isralites at the Red Sea • Reservoir host: dogs, fur-bearing animals drink contaminated water containing infective Cyclops • Human infection- result of ingestion of water from so-called “stepwell” where people stand or bathe in the water , at which gravid female worm discharges lava from lesion on the arms, legs, feet, ankles to infect cyclops in the water. • Take note: a filarial worm but a tissue invading nematodes. They are not appeared in the blood • Immediate host: fresh water microcutaneous(copped) of genus Cyclops
  • 45. 12. Dracunculus medinensis • Laboratory diagnosis: observation of typical ulcer & flooding the ulcer with water to recover& discharge the larval form • Occasionally, x-ray examination reveals worms in various part of the body • Treatment: Surgical removal, wrapping the worm on a twig • Tiridazole(DOC), alternative drug:metronidazole, thiabendazole
  • 46. Take Note • Filariform larva:-infective stage of hookworm , ascaris and other nematodes, long, thread-like often “designed” for penetration • Filarial worm: any of a group of parasitic worms of family Filariaidae (Phylum Nematodes) requires 2 hosts, an arthropod(Intermediate host) and a vertebrae (primary host) to complete the life cycle