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1. Soil- transmitted Helminths
Arvin Ray M. delos Santos, RMT
MPH – 1 | Lyceum Northwestern University

2. SOIL-TRANSMITTED HELMINTHS
• This remain a major public health concern in
developing countries like the Philippines, where
poverty, poor environmental hygiene and
impoverished health services exist.
• Open defecation outside latrines by infected persons
contributes significantly to the transmission of the
diseases via contamination of soil and water supply.

3. SOIL-TRANSMITTED HELMINTHS (STH)
• STH infections are caused by Ascaris lumbricoides,
Trichuris trichiura, and the hookworms Necator
americanus and Ancyclostoma duodenale.
• High risk groups for STH infections include children,
adolescent females, pregnant women and other
occupational groups such as farmers, soldiers and
indigenous groups.

4. SOIL-TRANSMITTED HELMINTHS (STH)
• Helminth infections often result in subtle morbidities
such as anemia, impaired physical and cognitive
development, as well as poor school performance.

5. STH EPIDEMIOLOGY
• Approximately 2 billion people worldwide are infected
with soil-transmitted helminths.
• It is estimated that 807 million individuals are infected
with Ascaris, 604 million with Trichuris and 576 million
with hookworms (Bethony et.al., 2006)
• The burden caused by STH infection remains high in the
Philippines according to results of studies supported by
the Department of Health and UNICEF.

6. STH EPIDEMIOLOGY
PARASITE LIGHT INTENSITY MODERATE
INTENSITY
HEAVY INTENSITY
eggs per gram eggs per gram eggs per gram
A. Lumbricoides 1 – 4,999 5,000 – 49,999 > 50,000
T. Trichiura 1 – 999 1,000 – 9,999 > 10,000
Hookworms 1 – 1,999 2,000 – 3,999 > 4,000
Threshold for the classification of intensity of STH infections in individuals

7. STH DIAGNOSIS
• Parasitologic diagnosis of STH infections is made by
analyzing stool samples for the presence of eggs.
• Direct Fecal Smear (DFS) alone is the routine method
for stool examination for the detection of motile
protozoan trophozoites in diarrheic stool
• DFS and Kato Thick method together are
recommended for use in routine stool exam for STH
infections and other helminths

8. Ascaris lumbricoides

9. Ascaris lumbricoides
• Common name: Giant Roundworms
• It is the most common intestinal roundworm
of man. (Habitat: small intestine)
• Causing the disease known as Ascariasis
• It occurs frequently in tropical and
subtropical regions of Asia, Central and
South America and Africa where sanitation is
lax.

10. Morphology
1. Ova
1.1. Fertilized egg: broadly oval, nearly spherical;
golden brown in color; 45-75 x 35-45 microns
3 layers of egg shell
a. albuminoid layer: outermost layer
b. glycogen layer: a thick transparent middle layer
c. lipoidal vitelline membrane: inner non-permeable
membrane; absent in infertile eggs

11. Morphology
2. Ova
1.2. Unfertilized egg: never undergo further
development; generally larger, narrower and
elongated; 88-94 microns
DECORTICATED EGG: an egg that has no albuminoid
layer; it has smooth shell and appears pale yellow or
colorless.

12. Morphology
DECORTICATED EGG

13. Morphology
2. Adult: white, creamy or pinkish yellow when
freshly expelled
– Male: curve posterior end, mouth have 3 oval lips,
usually shorter and slender, 15-30cm x 3 mm
– Female: longer/stouter than male,
30-24cm x 5mm, straight posterior end
– It lays 240,000 eggs per day
– Approximately 65 to 85 million eggs during its life
span of about 12 months

14. Adult A. lumbricoides

15. Adult A. lumbricoides

16. Pathology and Symptomatology
• Due to larval migration
 LUNGS – petechial hemorrhage (larvae break out
of the lung capillaries into the air sacs)
 Damage to the pulmonary tissues giving rise to
Ascaris pneumonitis
 Symptoms manifested: asthmatic type of
respitation; cough; bronchial rales (abnormall
respiratory sound); urticarial rash(hives, vascular
reaction of the upper dermis; eosinophilia in the
circulatory blood

17. Pathology and Symptomatology
• Due to adult worms
 Diarrhea, vague abdominal pain, nausea and loss
of appetite
 Fever may stimulate the worms to migrate upward
and be vomited and may pass through the nose
 Suffocation ( because vomited ascaris may pass
into the larynx
 Pulmonary gangrene
 Otitis media (Eustachian tube)

18. Pathology and Symptomatology
• Due to larval migration (con’t)
 Obstructive jaundice: due to obstruction of bile duct by the
worms.
 Liver abscess (hepatic ascariasis) when worm force its body
through gall bladder and enter the liver.
 The worms may enter the liver veins then carried to (brain,
heart, lungs) causing serious complications.
 Pancreatitis when the worms migrate up enter and block
the pancreatic duct.
 Appendicitis when the worm migrate down enter and block
the appendix.

19. Pathology and Symptomatology

20. Laboratory Diagnosis
• Direct Fecal Smear (DFS)
• Kato-Thick Smear
• Concentration Technique
• ELISA
• Indirect fluorescent antibody test (IFA)
• Indirect hemagglutination test (IHA)
• Eosinophilia is prominent during the early lung stage,
but disappears later
• Presence of Charcot Leyden crystals in sputum and
stool
Direct Fecal Smear

21. Transmission
Soil eating
Soil contaminated foodHuman manure as
fertilizer
Food handlers

22. Development of Ascaris Eggs

23. How man become infected?
Man become infected by
ingestion of infective
Ascaris eggs; contain
second stage larva L2
The larva hatch in the small
intestine, and penetrate the
wall of the intestine enter the
portal circulation, carried to
heart, then to lungs (Heart-
Lung migration)
Within 9-15 days in lungs, the
larva develop to L3, which
migrate through the
bronchial tree, reach the
throat the swallowed and
enter the intestine.
In the intestine the
Ascaris larva grow into L4
then L5 which then
mature into worm within
2-3 months
The mature female
will be fertilized by the
male worms (mating).
Each worm uteri may
contain up to 27 million
eggs at a time, but it
produces about 200,000
eggs per day which
deposit in feces

24. How life cycle continue?
The life cycle continue when the eggs reach the soil
When infected human defecate in soil, the
eggs will reach the soil
Under certain soil conditions: oxygen, shad,
moisture, temperature (22-30 C), the
fertilized egg develop into infective eggs.
Ingesting those infective eggs by others
(contamination of hands, foods, drinks
with soil containing the eggs.
While the infertile eggs
don’t develop; they
don’t have role in the life
cycle

25. Life Cycle of A. lumbricoides

26. Ascaris worm coming through
anus, nose and mouth

27. Obstruction of bowel by
Ascaris Worm

28. Treatment
• Albendazole
• Levamisole
• Mebendazole
• Piperazine salts
• Pyrantel pamoate
 Treatment is simple, effective and safe nowadays
 These drugs have neuromuscular blocking effect on
the parasite causing paralysis
 Community based chemotheraphy done at interval
of 4 months or 3x a year for 3 years appear to be
promising in the control of Ascaris.

29. Prevention
• Sanitary disposal of human excreta
• Good personal hygiene
• Avoid the use of fresh human feces as
fertilizers in vegetable gardens and rice
fields
• Thorough cooking of food particularly
vegetables
• Washing fruits before eating

30. Trichuris trichiura

31. Trichuris trichiura
• Common name: Whip Worm
• Inhabits the human large intestine (ceacum)
• Causing the disease known as trichiuriasis
• It is soil transmitted infection (eggs are
infective stage found in soil)
• The adult worm looks like a whip, that is why
it is called whip worm.

32. Trichuris trichiura

33. Trichuris trichiura
• The worm has thin anterior and
thick posterior part
• They attached to intestinal
mucosa by embedding the
anterior part.
• They feed on tissue fluid (not
blood)

34. Morphology
• Shape: Round; narrow long
anterior part end and shorter
and thicker posterior
• Color: pinkish-white
• Size: Female 35-50 mm long
Male 30-45 mm, with a
coiled posterior end

35. Eggs of Trichuris trichiura
• Shape: oval (barrel-shaped)
has polar hyaline mucoid blugs
• Size: 60 x 40 µm
• Color: honey brown
• Shell: thick
• Contents: mass of granules
(unembryonated)

36. Development of Trichuris Eggs

37. How man become infected?
Infection to man is by
ingestion of the infective
eggs (contain larva) that
may be in contaminated
food or drinks, hands
with soil
The larva hatch in the
human small intestine
then migrte to large
intestine
They attach to mucosa of
the large intestine
Then develop into
mature worms within 3
months
After mating, female
produces 2,000-10,000
single-celled eggs per
day which come out with
feces
Worms can live up to five
years.

38. Life Cycle of Trichuris trichuira

39. Pathology and Symptomatology
• People with light infections usually have no symptoms
• People with heavy infection show symptoms like:
Frequent defecation
Painful passage of stool
Stool appearance: contains a mixture of mucus and
blood (dysentery)
The clinical feature is identical to amebis dysentery.

40. Complications
 Colonic obstruction because of the tangled
worms
 Ulceration of large intestine which result in
blood loss
 Iron deficiency anemia
 Rectal prolapse

41. Complications: Rectal Prolapse

42. Laboratory Diagnosis
 Direct Fecal Smear
 Kato Thick Smear
 Concentration by sedimentation technique
 Floatation technique

43. Treatment
 Several antehelmintics drugs of choice:
 Albindazole
 Mebendazole
 Prognosis is good in light infection, but
poor in heavy chronic infection.

44. Prevention and Control
 Prevent contamination of soil with human
feces
 Construction of toilet or latrines
 Washing hands before eating (children, soil
workers)
 Washing of vegetables and fruits
 Do not use night soil as fertilizer

45. Hookworms

46. Hookworm
• Ancylostoma duodenale and Necator
americanus are nematode worms
• Habitat: found in human small intestine
• They are bloodsucking nematodes
• Causing the disease known as hookworm
infection, ground itch or tunnel disease
• It is a soil transmitted infection (infective
stage is larva found in soil)

47. Geographical distribution
Hookworms are the second most common
human worm after A. lumbricoides, mostly
found in tropical and subtropical climates
A. duodenale found in
the Middle East,
Southern Europe and
North Africa.
N. americanus
predominates in the
America (North, Central
and South America) and
Australia

48. The Worm: Morphology
• Shape: cylindrical
• Color: pink – red – brown
– Female pointed at
posterior end
– Male in both species
has broad posterior
end (copulatory bursa)

49. What is Copulatory Bursa?
• Is the cuticle expansion
at the posterior end of
the male worm
• Contains the male genital
organs (spicules)
• Helps in capturing female
worm during mating.

50. The Worm: Morphology
• Size of worms
 A. duodenale
Female: 10-13 x 0.6 mm
Male: 8-11 x 0.5 mm
 N. americanus
Female: 9-11 x 0.4 mm
Male 7-9 x 0.3 mm

51. The Worm: Morphology
• Buccal capsule (mouth) help differentiation of both species
A. duodenale N. americanus
Provided with teeth provided with cutting plates

52. The Worm: Morphology
• The hookworms feed on blood, they are well adapted to
suck blood from the capillaries of intestinal mucosa.
• They use the teeth and cutting plates to attach and make
wounds on the intestinal mucosa.
• Their mouth is also provided by amphidial glands which
secrete a potent anticoagulant on the wounds to ensure
continuous blood flowing.

53. Eggs of A. duodenale and N. americanus
Hookworms produce identical eggs
• Shape: oval
• Size: 60 x 40 µm
• Content: has brown colored 4-8
cells (plastomers)
• Surrounded by hyaline space
• Shell: thin

54. Development of hookworm egg

55. How man become infected
Man become infected
when the infective
larval stage (L3) which
found in soil penetrate
through the skin
The larva enter the
blood vessels in the
epidermis, reach the
heart then lungs
(heart-lung migration)
After 1 week the larva
migrate from the lungs
through the bronchial tree,
reach the throat then
swallowed and enter the
intestines
In the small intestine,
the larva attach to
intestinal mucosa,
make wound and feed
on blood.
The grow into
adult (male and
female) worm in
about 5 weeks.
The mature worms
mate. After mating
the female worm
start laying eggs.
N. americanus
produce up to
10,000 eggs
per day
A. duodenale
produce up to
30000 eggs
per day

56. Life cycle of Hookworm

57. Pathology and Symptomatology
1. Cutaneous Phase
1.1. Ground Itch
• First sign after exposure
to soil
• Allergic reaction of the
skin to penetrating larva
(L3)
• Characterized by itching,
redness and skin rash

58. Pathology and Symptomatology
1. Cutaneous Phase
1.2. Creeping Eruption
• An allergic reaction to the
motile larva under the skin
• Characterized by red
tunnels, itching, may
persists for weeks or
months.
• Usually caused by Necator
americanus

59. Pathology and Symptomatology
2. Lung Phase
• Inflammation due to
entrance of larva in
lungs (pneumonitis)
• Severity of lung phase
depends on the number
of larvae

60. Pathology and Symptomatology
3. Intestinal Phase
Presence of worms in small intestine will cause the following:
 Loss of apptite
 Nausea
 Stomach or abdominal pain
 Vomiting
 Weight loss
 Constipation / diarrhea
 Fatigue (tiredness)
 Black stool color

61. Complication of Hookworm Infection
• Usually hookworms in human host live for a few years but can
live up to 15 years
• The main complication of hookworm is iron deficiency anemia
(microcytic, hypochromic), the hemoglobin level may decrease
to 5 g/dL or less
• This occur in chronic infection or heavy infection, due to
continuous blood loss from the wounds made by the worms
on the intestines.

62. Laboratory Diagnosis
 Direct Fecal Smear
 Kato Thick Smear
 Brine flotation Technique
 Formalin-ether concentration technique (FECT)

63. Treatment
Several antehelmintics drugs of choice
 Pyrantel pamoate
 Mebendazole
 Tetrachloroethylene
 Thiabendazole
 In addition to iron containing supplements
Prognosis is good!

64. Prevention and Control
 Prevent direct contact with soil
 Prevent contamination of soil with human feces
 Construction of comfort rooms and
encouragement of their use
 Disinfect the soil using aqueous iodine solution
to kill the larva
 Disinfect the night soil before use as fertilizer.

65. Thank you…