2. Intestinal Nematodes
• Systemic classification :
Based on Anderson et al. (1974).
Two classes – 1. Adenophorea.
2. Secernentea.
• Classification based on habitat :
1. Intestinal : i) small intestine – A. lumbricoides
A. duodenale
Necator americana
ii) large intestine – Enterobius vermicularis
Trichuris trichura
7. • History & Epidemiology :
It is first described by Leuckart, in 1865.
Globally around 209 million people are infected each
year.
Prevalence is maximum among the school going
children.
Temperate climate, over crowding, impaired hygiene,
poor personal care are factors promoting infection.
• Habitat :
The adult worm remains attached to the large intestine
(caecum, appendix, adjacent portion of colon) by their
mouth end.
8. • Morphology :
Adult worm :
1. Apearance : small, white, tread like.
2. Size : male – 2-5mm x 0.1-0.2mm
female – 8-13mm x 0.3-0.5mm.
3. Cervical alae : a wing like expansion of
the cuticle near the
anterior end.
4. Double bulb esophagus : posterior
dilated end of esophagus which
forms the globular bulb.
5. Male : posterior end is tightly curved,
bearing a copulatory bursa with
spicules at the posterior end.
9. 6. Female : posterior one third is tapering, straight, thin
and pointed.
Eggs :
1. Shape : oval, planoconvex.
2. Size : 50-60µm x 20-30µm.
3. Surrounded by double layered egg shell.
4. Embryonated when passed fresh; contains a tadpole
larva inside.
5. Survives some weeks in fairly
high humidity and moderate
temperaure, few days in dry
dust.
12. • Pathogenicity :
Host : only human.
Infective form : embryonated eggs.
Mode of transmission :
1. Ingestion of eggs by contaminated hands (nail
biting, inadequate hand washing).
2. Exogenous autoinfection : scrapping of perianal
region due to intense itching, thus contaminating the
finger.
3. Endogenous autoinfection/ retroinfection : retrograte
migration of larvae those have hatched at perianal
region into rectum and large intestine.
13. • Pathogenesis :
A. Nocturnal migration of gravid female, fully filled
with eggs, from large intestine to perianal region and
start laying eggs.
Human with hypersensitivity to the secretion and
excretion of the worms
Rectal pruritus at night
Continuous scratching of skin
Excoriation of perianal skin
14. B. Migration of the worm
1. Invade female genital tract – vulvovaginitis.
2. Entrance into peritonial cavity – formation of
granuloma around eggs or worm which may lead to
chronic pelvic peritonitis.
3. Invade appendix – appendicitis.
4. Others : liver, lungs.
16. Microscopy :
detect eggs (planoconvex, 50-60µm x 20-
30µm), with a translucent shell of moderate
thickness, containing a larva inside.
17. • Treatment :
One of the followings –
1. Mebendazole 100mg once.
2. Albendazole 400mg once.
3. Pyrantal pamoate 11mg/kg once (max 1gm).
** the same treatment should be repeated after 2 weeks.
** all the family members, including asymptomatic
reserviors should be treated simultanously.
18. • Prevention :
1. By improving personal hygiene.
2. Proper washing of bed cloths.
3. Hand washing.
20. • It is the largest nematode parasitizing the human
intestine.
• ‘Askaris’ means intestinal worm, ‘Lumbricus’ means
resembling with common earth worm.
Epidemiology :
1. Cosmopolitan in distribution, mainly affecting
temperate and tropical countries.
2. 1430 million people are infected each year globally,
of which 120-150 millions are symptomatic.
3. Intestinal obstruction due to Ascaris infection is in a
range of 0-0.25 in 1000 population in endemic
regions; children under 10 years are susceptible with
fatality rate of 5.4%.
21. • Morphology :
Adult worm :
1. Appearance : pinkish
creamy.
2. Size : females – 20-30cm, male 15-31cm.
3. Shape : cylindrical with tapering end.
4. Life span : 1-2 years.
5. Mouth part : bears 3 characteristic toothed lips (1 dorsal,
2 ventral).
6. Body cavity : filled with ascaron or ascarase.
22. 7. Alimentary canal : well developed;
Mouth at anterior end, muscular and
glandular esophagus, intestine and
rectum, a subterminal anus.
- intestine or midgut is lined by
a single layer of columner cells.
8. Nervous system : rudimentary
and consists of circular nerve
ring; six longitudinal nerve trunk –
i) dorsal nerve – motor control.
ii) lateral nerve – sensory control.
iii) ventral nerve – control both.
9. Killed at excessive heat and dryness; remains viable in
moist soil for long period.
23. Male :
- slender, incurved tail bearing two
spicules at posterior end .
- rectum and genital duct open together
at cloaca near the posterior end.
Female :
- straight and pointed posterior end.
- anus : subterminal; situated posteriorly.
- vulvar waist : narrower portion at the junction of
anterior and middle third of the body on the ventral
surface bearing vulva.
24. Eggs :
1. Two types : i) fertilized (45-75µm x 35-50µm).
ii) unfertilized (90µm x 40µm).
- Clay soils are the most favourable for development
of eggs.
- ascaroside, a lipoprotein present in egg shell, protect
it from disinfectants, and allow it to survive for 15
years.
** Decorticated eggs : when fertilized eggs lose the
thick mamilated albuminous coat.
26. • Life cycle :
Host : only human.
Infective stage : embryonated eggs containing L₂ larvae.
Mode of transmission : ingestion of embryonated eggs
from the contaminated soil, food, water.
Phases : 1. Migratory phase.
2. Intestinal phase.
3. Development in soil.
27.
28. • Pathogenesis :
1. Affect due to migrating larva :
2nd week, after ingestion of eggs
Larva migrate into lungs
i) Pneumonitis :
Provoke immune mediated hypersensitivity
- Non productive cough,
- Chest discomfort,
- Fever.
29. ii) Eosiniphilic pneumonia / Loeffler’s syndrome :
- In severe cases, sensitive persons develop dyspnea
and asthmatic attack.
iii) Minor hemorrhage
- 20µm larvae get trapped in 10µm alveolar capillaries
Break out with consequent hemorrhage.
2. Affect due to Adult worm :
i) Asymptomatic.
30. ii) Symptomatic :
In the intestine
it liberates antienzymes- antitryptic, antipeptic
Protection from digestion by host intestinal ferments
1. Robbing of nutrients-
a) malnutrition and growth retardation,
b) vit.-A deficiency,
c) PEM (in hyperinfected children),
d) lactose maldigestion/ intolarance.
31. 2. Intestinal complication –
a) bowel obstruction (by forming tangled mass),
- abdominal distantion, rebound tenderness, vomiting.
b) perforation,
c) intussusception.
32. 3. Extraintestinal complication -
a) wandering ascariasis : migrate through ampulla of
vater into-
- appendix : appendicitis.
- pancrease : pancreatitis.
- biliary tree : biliary colic, cholecystitis.
- liver : abcess.
- esophagus : coming out though mouth and nose.
b) ectopic ascariasis : migrate to pharynx and
block eustachian tube/ rima glottidis causing suffocation.
33. 4. Allergic menifestation :
release of body fluid ascaron/ ascarase
- Typhoid like fever.
- Urticaria.
- Angioneuratic edema.
- Conjunctivitis
- Irritation in upper respiratory tract.
34. • Laboratory diagnosis :
A. Detection of the parasite :
1. Egg detection :
Sample : stool.
Microscopy : 1. saline wet mount.
2. iodine wet mount.
- both fertilized and unfertilized eggs can be detected.
35. 2. Adult worm detection :
i) occasionally found in stool or sputum by naked eye.
ii) Barrium meal X-ray of GIT : ‘trolley car lines’
appearance.
iii) USG and cholengiopancreatography : detect adult
worm in extraintestinal sites.
Giant roundworm
in CBD in ERCP.
Barrium meal X-ray
showing filling
defect
36. 3. Larva detection : during early pulmonary migration.
Sample : sputum, gastric aspirate.
Microscopy : hatching out larva.
37. B. Serology : antibody detection-
1. ELISA.
2. IFA.
3. IHT.
4. Micro precipitation test using larva serology :
- in pulmonary phase.
- seroepidemiological purpose.
C. Others
1. Eiosinophilia : prominent in early lungs
stage, disappears later.
2. Presence of charcot layden crystals
in stool and sputum.
38. • Treatment :
A. Antiparasitic drugs : any one of the followings-
1. Albendazole 400mg once (200mg in children
<2years).
2. Mebendazole 100gm twice daily for 3days, or
500mg once.
3. Ivermectine 150-200mg/kg once.
4. Nitazoxanide.
5. Pyrantel pamoate – in pregnancy.
39. B. Symptomatic :
1. Intestinal obstruction : nasogastric suction until
vomiting is controlled.
Administration of Piperazine 150mg/kg then
65mg/kg
twice per day for 3days.
2. Complete obstruction/ intussusception : immediate
surgical intervention.
41. • It is so named because the anterior end of adult worm is
bent.
• Ankylos – hooked, Stoma – mouth.
• Classification :
Family : Ankylostomatidae
Subfamily : Ankylostomatinae Subfamily : Uncinariinae
Tooth like process Cutting plates
Necator americana
2 pairs of teeth 1 pair of teeth 3 pair of teeth
Ankylostoma duodenale A. braziliense A. caninum
42. • History :
- A. duodenale 1st detected by an Italian physician
Dublini in 1843 and life cycle and pathogenesis was
described by Arthur Loss in 1898.
- N. americanus was first described by Stites in1902 in
Texas,USA, hence called American hookworm.
43. • Epidemiology :
- Globally 900 million people are infected.
- N. americana infection is more common (835
million).
- A. duodenale is prevalent in southern Europe, North
america, northern Asia.
- N. americana is prominent in Western world.
- Both coexist in South east Asia.
- Males and young adults are commonly affected.
44. • Morphology :
Adult Worm :
- Size : A.duodenale – male 5-11mm, female 9-13mm.
N. americana – male 5-9mm, female 1cm.
- Shape : straight except anterior end (bent dorsally).
- Colour : pink or grayish white; reddish due to
ingested blood.
45. - Mouth : present anteriorly directed dorsally;
contains-
• A.duodenale : buccal capsule, lined by a hard
substance bearing 6 teeth (4 hook like on ventral surface,
2 knob like dorsally).
• N. americana : 4 chitinious cutting plates (2 ventrally, 2
dorsally).
46. - Glands : digestive system is attached with 5 glands.
- Vulva : A.duodenale- behind the middle of the body;
N. americana – in front of middle of the body.
- Copulatory bursa :
A.duodenale : bifercation is tripartite.
rays – 13
dorsal ray splits at the tip.
two spicules present freely.
N. americana : bifercation is bipartite.
rays -14.
dorsal ray splits from the base.
spicules are fused at the tip.
47. Eggs :
- Size : 60µm x 40µm.
- Shape : oval.
- Not bile stained, colourless.
- Surrounded by thin, hyaline, translucent egg shell.
- Ovum (embryo) is segmented (4 or more
blastomeres).
- Floats on saturated salt solution.
48. Larva :
- 4 stages : L₁-L₄.
- L₁ : rhabditiform larva (100-150µm).
- L₃ : filariform larva (660-720µm)- infective stage.
Characteristics A. duodenale N. Americana
1. Size (µm) 720 660
2. Shape Head blunt, tail pointed. Same
3. Cuticle Faint transverse striation. Bears prominent striation.
4. Buccal capsule Shorter, lumen larger,
bounded by 2 thin chitinous
wall.
Larger, lumen short,
bounded by 2 thick chitinous
wall.
5. esophago-intestinal junc. No gap. Gap present.
6. Intestine Posterior end has a refractile
body.
Absent.
49.
50. • Life cycle :
Host : only human.
Infective stage : 3rd stage larvae (filariform).
Mode of transmission :
1. penetration of skin (most common).
i) thin skin between toes.
ii) dorsam of the feet.
iii) inner side of the sole.
2. percutanous, oral, transmammary,
transplacental (in case of A. duodenale).
51. Phases : 1. migratory phase (10 days).
2. intestinal phase (3- 4 weeks).
3. development in soil (8-10 days).
Life span : A. duodenale 1-5 years.
N. americana 18 years.
52.
53. • Clinical feature :
Due to larva :
1. Ground itch and serpiginous tracks.
2. Pneumonitis.
3. Nausea, vomiting, diarrhoea, flatulance.
4. Eiosinophilia : 1350- 3828 cells/ µl.
54. Due to adult worm :
1. Acute infection : rare.
2. Chronic infection :
i) Iron deficiency anaemia : cardiac decompansation
characterized by intercurrent infection.
ii) Hypoproteinaemia : facial and peripheral edema.
3. Others : Weakness, shortness of breath,
impaired intellectual power, behavioural
change.
55. • Pathogenicity :
A. Penetration is facilitated by :
i) proteolytic enzymes (aspartyl protease).
ii) hyaluronidase.
B. Ability to suck blood by :
i. attaching and making cuts by buccal capsule and
teeth.
ii. sucking the blood by muscular esophagus.
iii. hydrolytic enzymes.
iv. releasing anticoagulants like factor VIIa/ tissue
factor inhibitor.
v. ingestion of extravasated blood.
56. • Pathogenesis :
A. Affect due to migrating larva :
1. local lesion (in previously sensitized persons) :
i) At the site of entry
Provoke pruritic maculopapular dermatitis and rashes.
Ground itch.
ii) If after penetration, can not proceed to normal
development
Do not penetrate below stratum germinativum
Subcutaneous migration
Serpentine tracks.
57. 2. Mild transient pneumonitis :
During migration through lungs
Larvae break through the pulmonary capillaries
Enter into alveolar spaces
Bronchitis, broncho-pneumonia.
58. B. Affect due to Adultworm :
1. Asymptomatic.
2. Anaemia :
i) Heavy worm load
1. Attach and cut intestinal wall by buccal capsule and teeth.
2. Suck blood through contraction of their muscular
esophagus.
3. Release factor VIIa/ tissue factor inhibitor.
4. Ingestion of extravasated blood.
chronic hemorrhage from punctured sites
0.03-0.2 ml blood/ day and 1% Hb per 12 worms are lost .
59. ii) Nutritional defects
1. If associated with iron deficiency – hypochromic
microcytic anaemia.
2. If associated with folic acid and vit. B-12
deficiency- macrocytic anaemia.
3. If associated with both – dimorphic anaemia.
60. • Laboratory diagnosis :
Sample : stool.
Microscopy :
1. If sample is fresh : eggs are detected by saline wet
mount and iodine mount.
- oval, 60µm x 40µm, thin and colourless shell.
2. If sample is kept in room temp. larva may be seen
within egg shell.
61. Culture :
eggs may hatch out to develop to L₃ in 5-7 days.
Methods :
1. Herada Mori filter paper tube.
2. Petridish (slant culture technique).
3. Baermann funnel technique.
4. Charcoal culture method.
5. Agar plate technique (more sensitive).
63. • Treatment :
A. Antiparasitic : any one of the followings-
1. Albendazole 400mg once.
2. Mebendazole 500mg once.
3. Pyrantel pamoate 11mg/kg for 3 days.
Symptomatic :
1. Oral iron suppliment.
2. Proper nutritional support with protein.
64. • Prevention :
1. Personal care.
2. School based deworming.
3. Improved nutrition status.
4. Treatment of infected persons.
5. Vaccine :
- experimental immunization of animals with
vaccines using larva or adult stage antigen was found to
be effective.
- human trials are going on targeting molecules
like Ankylostoma secreted protein (ASP)
