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3.

01
January 6,
2017

INTESTINAL NEMATODES
Dr. Malijan

Department of Microbiology and Parasitology

TOPIC OUTLINE
I.
Introduction: Metazoan parasites
II.
Overview: Intestinal Nematodes
a. Ascaris lumbricoides
b. Hookworms
c. Strongyloides stercoralis
d. Capilaria philippinensis
e. Enterobius vermicularis

f.

Trichuris trichiura

Red italicized from Doc Malijan


Green italicized from Transer

METAZOAN PARASITES

Metazoan parasites are either helminths or


arthropods

Helminths. 3 groups causing infection to man:


o Annelids (leeches)
o Nematodes

Aka roundworms

Elongated and cylindrical in shape with


bilateral symmetry

Generally, with complete digestive tract


and muscular pharynx which is
characteristically triradiate

Separate sexes or parthenogenetic

with sensory organ in the anterior


(amphids) and posterior (phasmids) ends
(Amphids A Anterior; Phasmids P
posterior)
o Flatworms (*Platyhelminthes)
Phylum Nematoda (Round Worms)

Intestinal
o Acaris lumbricoides
o Hookworms
o Strongyloides stercoralis
o Capilaria philippinensis
o Enterobius vermicularis
o Trichuris trichiura

Extra-intestinal
o Angiostrongylus cantonensis
o Filarial worms
o Trichinella spiralis
Phylum Cestoidea (Tapeworms)

Order Cyclophyllidea
o Dipylidium caninum
o Echinococcus spp.
o Hymenolepis spp.
o Raillientina garrisoni
o Taenia spp.

Order Pseudophyllidea

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o Diphyllobothrium latum
o Spirometra
Phylum Trematoda (Flukes)
o Artyfechinostomum malayanum
o Clonorchis sinensis
o Echinostoma ilocanum
o Heterophyids
o Opistorchis spp.
o Paragonimus westermani
o Schistosoma spp.
Phylum Nematoda
Roundworms
Unsegmented, elongated and cylindrical
Sexes are separate females are larger than males
Posterior end of male usually curved
Class Aphasmidia lacking phasmids or caudal
receptor (Adenophorea)
o Trichuris
o Trichinella
o Capilaria
2. Class Phasmidia with phasmids or caudal
papillae (Secernentia)

1.

ORDER
Ascaridida
Strongylida
Rhabditida
Oxyurida
Spirurida

GENUS/ORGANISM
Ascaris
Angiostrongylus and
hookworms
Strongyloides
Enterobius
Filarial worms

INTESTINAL NEMATODES
Species which parasitize the small intestine
o Ascaris lumbricoides
o Necator americanus (hookworm)
o Ancylostoma duodenale (hookworm)
o Strongyloides stercoralis (threadworm)
o Capilaria philippinensis
Species which parasitize the large intestine
o Enterobius vermicularis (pinworm)
o Trichuris trichiura (whipworm)
Life cycle:
1. Egg stage
2. Four larval stages
3. Adult stage
Adult female may be:

Intestinal Nematodes
1.

Oviparous eggs are oviposited and


embryo develops outside the maternal
body (e.g. A. lumbricoides)
2. Viviparous female gives birth to
larvae (C. philippinensis)
3. Parthogenetic can produce visible
eggs without being fertilized by the male
worms (S. stercoralis)
Mode of infection:
o Auto-infection possible in:

Capilaria, Strongyloides, Enterobius


o Transmission through inhalation:
Enterobius, Ascaris
Ascaris lumbricoides

Figure 2. (L) to (R): Ascaris adult female, Ascaris Adult


Male. Notice the ventrally curved posterior end of
male.

Human Intestinal Giant Roundworm


Largest and most common parasitic worm
in humans
Found worldwide (1/6 of the population, >1
billion infected) but prevalent in tropical
countries
Two separate populations and reservations
o Adult ascaris parasitizing man
o Ascaris eggs environment
Ascariasis considered a disease of
poverty
o Contribute to impairment of cognitive
performances and growth of children
o Reduce work capacity and productivity of
adults
Parasite Biology
Adult
o Creamy white or pinkish yellow
o Polymyarian type of somatic muscle
arrangement:

Cells are numerous and project well


into the body longitudinally
o Covered by acid-resistant cuticle for
protection against hosts GIT
environment
o Terminal mouth with three lips and
sensory papillae anteriorly
o Reside in but do not attach to the
mucosa of small intestine

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Female
o Bigger and longer, tapered at both ends
o Large (22-35cm x 5mm) and may grow
up to 45 cm long
o Reproductive potential: 240,000
eggs/day
o With paired reproductive organs in
posterior 2/3
o Vulva in anterior end and comprises 1/3
of its whole length

Male
o Ventrally curved posterior end with two
spicules in tail
o 15-25cm x 3mm (10-31cm)
o Reproductive organ: single, long,
tortuous tubule

Fertilized egg
o Mostly oval or spherical, golden brown
o Capable of further development in soil
from single cell to embryonated eggs
o Shell (Corticated)

Inner highly impermeable lipoidal


vitelline membrane

Thick transparent middle glycogen


layer

Outermost coarsely mammilated


albuminoid layer
o Decorticated

absent mammillated albuminous


layer
o At oviposition, fertile eggs have an ovoid
mass of protoplasm -> larvae
development in 14 days
o 45-70m x 35-50m

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Intestinal Nematodes

Figure 3. (L): Corticated Fertilized egg.

(R): Decorticated Fertilized egg.

Unfertilized eggs
o 1st two layers absent; shell is thinner with
irregular mammilated coating (only one
layer) filled with refractile granules
o Generally larger, narrower, more
elongated
o Can never undergo development in soil
o 88-94m x 39-44m (longer and
narrower)

Figure 4. Unfertilized egg (longer and narrower


compared to fertilized egg)

Life Cycle

Figure 5. Life cycle of Ascaris lumbricoides.

1. Adult worms live in the lumen of the small


intestine. A female may produce
approximately 200,000 eggs per day, which
are passed with the feces
2. Unfertilized eggs may be ingested but are
not infective
3. Fertile eggs embryonated and become
infective after 18 days to several weeks,
depending on the environmental conditions
(optimum: moist, warm, shaded soil)
4. After infective eggs are swallowed, the
larvae hatch, invade the intestinal mucosa,
and are carried via the portal, then systemic
circulation to the lungs
5. The larvae mature further in the lungs (10 to
14 days), penetrate the alveolar walls,
ascend the bronchial tree to the throat, and
are swallowed
6. Upon reaching the small intestine, they
develop into adult worms
7. (Back to 1) Between 2 and 3 months are
required from ingestion of the infective eggs
to oviposition by the adult female.

Adult worms can live 1 to 2 years

Embryonated eggs can survive in moist


shaded soil for a few months to 2 years in
tropical and sub-tropical areas, much longer
in temperate regions

Mode of infection: ingestion of


embryonated eggs

Infective stage: embryonated egg (inside


is third-stage larva)

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Pathogenesis and Clinical Manifestations


Larval Stage
o Larval lung migration

Migratory larvae -> hemorrhages


and destruction of the lung

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Intestinal Nematodes

Larval migration to other organs

Lactose intolerance

Eosinophilia

Abdominal pain most common


complaint

parenchyma as the larvae breaks


through the capillaries
Asthmatic type of respiration
Cough with rales and chest pain
Ascaris pneumonitis
Loefflers syndrome:

Allergic

Eosinophilic infiltration of the


lungs

Adult Stage
o Intestinal

Bowel obstruction (heavy


infections)

Lactose intolerance (moderate


infections)
o Extraintestinal

Suffocation: passage in the larynx


of vomited Ascaris

Otitis media: enter Eustachian


tube
10-20 worms asymptomatic
Intestinal volvulus, intussusception and
obstruction
Continuous biting or pricking of intestinal
mucosa by a few adults may irritate nerve
endings in the mucosa and result in
intestinal spasm leading to intestinal
obstruction
Organ
May become entangled in
intestine
Appendix
Bile duct

Liver
Perforate the bowel and
into peritoneal cavity
Gallbladder

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Complication
Intestinal obstruction
Acute appendicitis
Biliary ascariasis
presenting with severe
colicky abdominal pain
Multiple abscesses
Peritonitis

Gall stones (Ascaris eggs)


Pancreatitis may be
caused by even just a
single Ascaris adult

Diagnosis
Direct fecal smear:
o 2mg stool used
Kato Technique of Cellophane Thick Smear:
o 20-60mg stool, purely qualitative
method recommended for mass
examination
Kato-Katz Technique:

modified Kato technique, 40-60mg stool


to quantify number of eggs in sample

Quantitative: count number of


eggs per gram of stool

Determine egg reduction rate


post-treatment

Determine intensity of infection


Kato technique and Kato-Katz method is
useful for individual and mass screening
than DFS
These techniques are more sensitive,
cheaper, and easier to maintain
Negative Stool Exam
o When patients are actually free from
infection (true negative)
o During larval migration via blood stream
o When worms are still sexually immature
o When only male worms are found in
intestines
Treatment
Broad spectrum antihelminthics:
neuromuscular blocking effect on parasite ->
paralysis of worms
o Albendazole

Drug of choice (DOC)

400mg single dose


o Mebendazole: 500mg single dose
o Pyrantel pamoate: 10mg/kg single
dose
o Ivermectin: effective as Albendazole at
200g/kg single dose
Community-based chemotherapy: 4-month
interval or thrice a year for 3 years
Among school children: twice a year of 4-6
months interval
Reinfection observed 4 months posttreatment and full reinfection at 6-7 months
Cure rates close to 100%, tolerance and
resistance not observed
Teratogenic: shouldnt be given to pregnant
women
o

Epidemiology
Occurs most frequently in tropical and
subtropical regions (Asia, Central and South
America, Africa)
Estimated to infect 1.2 billion individuals (1/5
of the worlds population)
Thrives in areas with lack of sanitation,
poverty, and ignorance
Most common source of infection soilcontaminated foods esp. raw vegetables
Cosmopolitan distribution
20,000 die annualy, mostly young children
Risk of infection exist wherever fecal
disposal is improper
Factors contributing to transmission:
o High density of human population

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Intestinal Nematodes
o
o
o

Involvement of agriculture (night-soil as


fertilizer)
Illiteracy
Poor sanitation

Prevention and Control


Mass Treatment
Selective Treatment
o treating only those found positive for
eggs on stool exam
Targeted group
o treating children alone
Sanitary disposal of human excreta
Health education and Personal hygiene
Avoiding use of human feces for fertilizer
Thorough cooking of food

1.
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3.
4.

Hookworms
Necator americanus: New world
hookworm/ American murderer
Ancylostoma duodenale: Old world
hookworm
Ancylostoma braziliense: Cat hookworm
Ancyclostoma caninum: Dog hookworm

Numbers 1 and 2

Soil-transmitted helminths that infect man

Blood-sucking nematodes that attach to


mucosa of small intestine (Ascaris do not
attach)

Most commonly found in sub/tropical


countries occurring as single or mixed
infections
Parasite Biology
Necator americanus

Adult
o Small, cylindrical, fusiform, gray-white
o Females > Males
o Males: posterior end broad
membranous caudal bursa with rib-like
rays used for copulation
o Hook-like head curved opposite to bodys
curvature
o Buccal capsule: ventral pair of
semilunar cutting plates

Figure 6. (L) adult with ventral pair of semilunar


cutting plates
(R top) Male with copulatory bursa. (R below) Female

Rhabditiform larva (1st stage)


o Resembles those of S. stercocoralis
o Somewhat larger, more attenuated
posteriorly
o Longer buccal cavity
o Smaller genital primordium

Filariform larva
o Buccal spears are conspicuous and
parallel to body
o Conspicuous transverse striations on
sheath of tail
o Infective stage to man

Egg
o 60-75m x 35-40m
o Bluntly rounded ends
o Single, thin, transparent, hyaline shell
o Unsegmented at oviposition
o Ovoidal, colorless, 4-8 cell stage
o Constipated stool: embryo inside shell
o Differentiation of N. americanus and A.
duodenale:

Difficult and impractical

Ancylostoma duodenale
Adult
o Larger than N. americanus
o Single-paired male and female
reproductive organs
o Head continues in same direction as
body
o Buccal capsule: 2 pairs of curved
ventral teeth

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Intestinal Nematodes

Figure 7. (L) Adult A. duodenale with 2 pairs


ofcurved ventral teeth. (R) Female and Male
respectively.

Rhabditiform larva (1st stage)


o Same as N. americanus

Figure 10. Hookworm egg in wet mount (L) unstained.

Life Cycle

Figure 8. Hookworm rhabditiform larva.

Filariform larva
o Same but with inconspicuous buccal
spears and transverse striations on tail
region

Figure 11. Life cycle of intestinal hookworm

1.

Figure 9. (L) Hookworm filariform larva in wet mount.


(R) Close up of posterior end of hookworm filariform
larva

Egg

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Eggs passed in stool under favorable


conditions (moisture, warmth, shade) ->
larvae hatch in 1 to 2 days -> rhabditiform
larvae released and grow in feces and/or soil
2. Becomes infective filariform (thirdstage) larvae after 5 to 10 days (and two
molts)

Survive 3-4 weeks in favorable


environments
3. Contact with human host -> larvae
penetrate skin and carried through
circulation to heart and lungs -> penetrate
into pulmonary alveoli, and ascend to
bronchial tree to pharynx, and swallowed
4. Larvae reside and mature into adults in small
intestine. Adults live in lumen of small

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Intestinal Nematodes

5.

intestine -> attach to intestinal wall ->


resultant blood lost by host
Most adult worm eliminated 1-2 years but
longetivity may reach several years
Some A. duodenale larvae after skin
penetration can become dormant in intestine
or muscle
N. americanus infection by transpulmonary
migration phase
A. duodenale infection by oral and
transmammary route

Figure 12. Cutaneous larval migrans

Cutaneous larval migrans (creeping


eruption) is zoonotic with hookworm species
using non-human as definitive hosts (A.
braziliense cats, and A. caninum dogs)
Cycle in definitive host is very similar
Humans may be infected when filariform
larvae penetrate skin
Pathogenesis and Clinical Manifestations
Larval Stage
o Ground Itch/Coolie Itch

Intense localized itching, edema,


erythema and papulovesicular
eruption

Lasts up to 2 weeks

Site of entrance of filariform (L3)


larvae:

Dermatitis

Dew itch related to contact with soil


(on a dewy morning)
o Creeping eruption/ Cutaneous Larva
Migrans

Due to exposure of skin to filariform


larvae of A. braziliense or A,
caninum

Occasional: N. americanus and A.


duodenale

Serpiginous tunnel in stratum


germinativum of skin

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x

Larvae move several mm to few cm


per fay

Pyogenic infection: pruritus


Pulmonary lesions

Petechial hemorrhages

Eosinophilic and leucocytic


infiltration

Bronchitis or pneumonitis
Intestine

Abdominal pain, steatorrhea,


diarrhea with blood and mucus

Eosinophilia 30-60%

Adult Stage
o Hookworm Anemia

Due to continuous mechanical


suction of blood from intestinal
mucosa attachment

Progressive, secondary, microcytic,


hypochromic anemia (irondeficiency type)

RBC loss in gut

N. americanus: 0.03-0.05mL
blood/day
A. duodenale: 0.16-0.34mL
blood/day
o Hypoalbuminemia
Combined loss of blood, lymph and
protein
o Other signs and symptoms
Exertional dyspnea, weakness,
dizziness and lassitude
Rapid pulse, edema, albuminuria
Diagnosis
Ground itch and creeping eruption:
characteristic lesion, history of contact with
soil
DFS: for heavy infection (cant detect <400
eggs/gm feces)
Kato/Kato-Katz
o Kato-Katz Technique (quantitative
method)
Concentration methods (ZnSO4
Centrifugal Floatation method or
Formalin Ether Concentration)
o Determining whether stool is positive or
negative of hookworm eggs
Culture method (Harada-Mori)
o Allowing hatching of larvae from eggs
on filter paper strips with one end
immersed in water
o Recommended for species
determination via filariform larvae
Concentration techniques improve likelihood
to find eggs
Culture methods help identify the species of
hookworm involved
N. americanus is of a more serious concern
in the Philippines

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Intestinal Nematodes
o

Treatment
Treat all infections, except in high reinfection
(because it is impractical)
Priority is given to:
o Pregnant women
o Children with malnutrition, pulmonary
tuberculosis, and anemia
Severe anemia (Hgb=7-8g/dL) before
dealing with worm infection
Iron-deficiency anemia
o
diet and iron supplementation therapy
Severe hypoalbuminemia
o quick deworming
Broad anti-helminthic
o Albendazole

Drug of Choice

Chewable or suspension

Not recommended for pregnant


o Mebendazole

Not for children < 2 years old


o Oxantel/Pyrantel
o Ferrous sulfate

200mg TID p.o. for 3 months


o Benzimidazole derivatives

Block uptake of glucose by most


intestinal and tissue nematodes
Adverse Effects:
o Epigastric pain, headache, nausea,
vomiting, and dizziness
Epidemiology
Hookworm infecitons: 96% N. americanus,
2% Ancyclostoma, 2% mixed
Over 900 million infections in sub/tropical
countries
50 thousand deaths annually associated with
anemia
Mode of infection:
o N. americanus

Percutaneous and oral

Tropical Africa and America


o A. duodenale

Percutaneous

Prevalent in Europe and


Southwestern Asia
Infection greater in agricultural areas;
farmers more prone
o Compostela valley province: >50% rates
in 1990
Factors contributing to transmission:
o Suitability of environment for eggs or
larvae: damp, sandy or friable soil with
decaying vegetation, temperature 2432C
o Mode and extent of fecal pollution
(unsanitary disposal of feces, night soil
as fertilizer)

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Mode and extent of contact between


infected soil and skin or mouth

Prevention and Control


Proper treatment of human excreta used as
fertilizer
Avoiding ingestion of raw vegetables not
washed properly
Sanitary disposal of feces
Wearing of shoes, slipper, or boots to avoid
skin contact with infected larvae
Health education
Treatment of infected individuals
Protection of susceptible individuals:
improve household, diet
Trichuris trichiura
Whipworm
Soil-Transmitted helminth
Frequently occurs together with Ascaris
Holymyarian
o Based on arrangement of somatic
muscles in cross section
o Small numerous and closely packed in
narrow zone
Parasite Biology
Adult
o Inhabit large intestine
o Entire whip-like portion embedded into
intestinal wall of cecum
o Eggs become embryonated within 2-3
weeks
o No heart-lung migration
o Female
35-50mm
Bluntly rounded posterior
Lays 3,000-10,000 eggs/day
o Male
30-45mm, shorter than female
Coiled posterior end with a single
spicule and retractile sheath

Figure 13. (L) Female and (R) Male T. trichiura

Egg
o 50-54m x 23m

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Intestinal Nematodes
o
o
o
o

Lemon-shaped/ barrel-shaped/ footballshaped/ like a Japanese lantern


With plug-like translucent polar
prominences
Yellowish outer and transparent inner
shell
Embryonic development when eggs
deposited in clayish soil

4cm long, live and fixed in cecum and


ascending colon, anterior whip-like
portions threaded into mucosa
Females oviposit 6-70 days after infection,
shed 3,000-20,000 eggs/day
Lifespan: 2 years

Pathogenesis and Clinical Manifestations


Worms embedded in mucosa cause petechial
hemorrhages
-> predisposed to amebic dysentery (ulcers
suitable for E. hystolitica
Mostly sa intestine kasi dun sila
nageembed

Figure 14. T. trichiura eggs

Life Cycle

Figure 16. Rectal Prolapse

Figure 15. Lifecycle of T. trichiura

1. Unembryonated eggs passed in stool


2. In soil:

Eggs develop to 2-cell stage (advanced


cleavage stage) then embryonated
3. Eggs become infective in 15-30 days
4. After ingestion

Eggs hatch in small intestine -> four


larval stages -> mature to adults in colon
5. Diretso na agad sa intestine, wala nang
lakwatsa
6. Adult worms

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Hyperemic and edematous mucosa


Enterorhagia
Trichuris dysentery syndrome:
o Chronic Dysentery
o Rectal Prolapse - kasi ire nang ire
Appendicitis or granulomas
5,000 eggs/g -> symptomatic
>20,000 eggs/g feces -> severe diarrhea or
dysenteric syndrome
Light infection
o Asymptomatic
Heavy parasitism
o Blood-streaked stools
o Abdominal pain
o Anemia
o Weight loss
Diagnosis
Heavy infections
o Relies upon clinical symptoms such as
rectal prolapse, blood streaked diarrhea,
abdominal pain, and tenderness
Light infections
o DFS, Kato Thick Smear Method,
Kato-Katz

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Intestinal Nematodes

Kato technique and Kato-Katz technique are


simpler and cheaper
o High sensitivity and specificity in
detecting Trichiura
One may see the adults in the intestinal
mucosa for those with rectal prolapse
Treatment
Mebendazole
o Drug of Choice
o 100 mg twice a day for 3 days
Albendazole
Contraindication to Mebendazole and
Albendazole:
o
Early pregnancy (within the 1st
trimester)
o Hypersensitivity
Adverse effects (mild and transient):
o Headache, nausea, vomiting, GI
discomfort, itchiness

Eggs deposited by single female:


4,672 16,888 (mean
11,105/day)
Male
2.5mm
Tail curves ventrad
Single copulatory spicule
Male dies after copulation
(awtsu.)

Epidemiology
Children 5-15 years old frequently infected
Philippines: 80-84% prevalence
Infection through ingestion of
embryonated eggs
Prevention and Control
Mass treatment if infection rate is >50%
Preventive measure
o Treatment of infected individuals
o Sanitary disposal of human feces by
constructing toilets and their proper
use
o Washing of hands with soap and
water before and after meals
o Health education on sanitation and
personal hygiene
o Thorough washing and scalding of
uncooked vegetables especially
those areas where night soil is used
as fertilizer
Enterobius vermicularis
Human pinworm
Causes Enterobiasis or Oxyuriasis
characterized by perianal itching or pruritus
ani
Parasite Biology
Adult
o Small, whitish, or brownish in color
o Anterior end: posterior cuticular alar
expansions (lateral wings or cephalic
alae)
o Posterior esophageal bulb
o Female
8-13mm x 0.4mm
Long pointed tail (pinworm)
Females die after oviposition

10
of x

Figure 17. Adult (L) Female and (R) Male E.


vermicularis

Egg
o 50-60m x 20-30m
o Elongated, ovoid, flattened on ventral
side
o Similar to letter D
o Translucent shell (two layers):
Outer, triple, thick hyaline
albuminous shell: mechanical
protection
Inner embryonic lipoidal membrane:
chemical protection
o Outside host, eggs become
infective/embryonated within 6 hours
o Ovum develops into tadpole-like embryo
o Resistant to putrefaction and
disinfectants but succumb to
dehydration in dry air within a day
o Cool and moist conditions: eggs
remain viable for several days

Figure 18. E. vermicularis eggs in wet mount. (R)


iodine-stained wet mount

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Intestinal Nematodes

Larvae
o Folded once within shell, creating a
visible line along eggs long axis
o Rhabditiform larvae
Characteristic esophageal bulb but
has no cuticular expansion on
anterior end

Life Cycle

Figure 19. Life cycle of E. vermicularis

1. Eggs deposited on perianal folds


2. Autoinfection
o Transferring infective eggs to mouth with
hands that have scratched perianal area
3. Person-to-person transmission
o Handling of contaminated clothes or bed
linens
o Contaminated clothes (e.g. underwear)
beddings -> fixing your bed -> ingestion
( tumatawa kasi habang pinapag-pag)
o Enterobiasis acquired through
ingestion of embryonated eggs and
contact with egg-contaminated
surfaces
o Some may become airborne and
inhaled
4. Ingestion of infective embryonated eggs ->
larva hatch in small intestine -> adults
establish themselves in colon
o Ingestion of infective eggs -> oviposition
of adult females is abouth 1 month
(lifespan: 2 months)
5. Gravid females migrate nocturnally outside
the anus and oviposit on perianal area
6. (Back to 1) Larvae in eggs develop and
become infective 4-6 hours under optimal
conditions

Retroinfection
o Migration of newly hatched larvae from
anal skin back to rectum
Pathogenesis and Clinical Manifestations

11
of x

1/3 asymptomatic
Forms:
o Pathology at the site of attachment
of worm
Mild catarrhal inflammation of the
mucosa due to attachment of the
worms
Mechanical irritations and secondary
bacterial infection
Minute ulceration or abscesses in
cecal mucosa
o Pathology due to egg deposition in
perianal area
Intense itching or pruritus in
perianal region -> scarified
Pruritus ani -> hemorrhage,
eczema, bacterial infection of
anal and perianal regions and
perineum
o Pathology caused by migrating
adults
Migrating worms lay eggs in genital
organs causing vulvovaginitis,
worms enter fallopian tube causing
salpingitis
Pregnant female is responsible for
signs and symptoms
Children suffer insomnia due to pruritus
Hinahanap ni female yung pinagmulan niya
kaya kung saan-saang butas pumasok
vaginitis, endometriasis, salpingitis,
peritonitis, appendicitis
Other s/sx: poor appetite, weight loss,
irritability, teeth grinding, abdominal pain
Diagnosis
History and physical exam
Direct Fecal Smear
o Eggs are found only in 5% of infected
persons
Perianal Cellulose Tape Swab or
Grahams Scotch Adhesive Tape Swab
o D-shaped ova
o Best time: soon after patient awakens
and before bathing
Worms seen migrating out of childs anus at
right
Treatment
Pyrantel pamoate
o Drug of Choice
o 10mg/kg with second dose 2-4 weeks
later
Albendazole
o 400 mg, single dose
Mebendazole
o 500mg, single dose
A second dose is necessary for heavy
infection

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Intestinal Nematodes

Egg reduction rate as a parameter for cure is


difficult because eggs are hardly found in
stools
Epidemiology
Mode of Transmission:
o Hand-to-mouth transmission: most
common
o Inhalation of airborne eggs in dust
o Retroinfection through anus
Enterobiasis is the only intestinal
nematode condition that cannot be
controlled through proper sanitary
disposal of feces because eggs are
deposited in perianal region
Local prevalence
o 29% among school children from
exclusive private schools
o 56% among those from public schools
Local prevalence higher in females than
males
Collected from fingertips and fingernails of
school children
Adult female worms migrate to perianal area
even during daytime but more migration
occurs at night

Femal
e

Prevention and Control


All members of household who are positive
should be treated
At least 7 consecutive post-treatment
perianal smears using scotch-tape swab
method should be negative to declare
negative infection
Personal hygiene
Cut fingernails short
Bed linens and clothing of infected persons
sterilized by boiling

2.2mm x
0.04mm
Colorless, semitransparent with
a finely striated
cuticle
Slender tapering
anterior end and
a short conical
pointed tail
Short buccal
cavity with four
indistinct lips
Uteri with single
file of 8-12 thinshelled,
transparent,
segmented ova
Long, slender
esophagus
extends to the
anterior fourth of
the body
Intestine is
continuous
Subterminal
anus
Vulva located
1/3 of body from
posterior end

Gubernaculu
m but no
caudal alae

1mm x
0.06mm
Smaller than
parasitic
female
With
muscular
doublebulbed
esophagus
Intestine is a
straight
cylindrical
tube

Strongyloides stercoralis
Causes Strongyloides, Cochin-China
Diarrhea, threadworm infection
Epidemiology: infections run parallel with
hookworm infection
Infective stage: filariform larvae via skin
penetration
Parasite Biology

Adults
Male

12
of x

PARASITIC

None

FREE LIVING

0.7mm x
0.04mm

Smaller than
female

With
ventrally
curved tail, 2
copulatory
spicules

Figure 20. (L) Free-living adult male S. stercoralis with


spicules (red arrow) (R) Free-living adult female with
row of eggs inside the body .

Rhabditiform larvae
o 225m x 16m

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Intestinal Nematodes
o
o
o

Elongated esophagus with a pyriform


posterior bulb
Differs from hookworm rhabditiform
larva in being slightly smaller and less
attenuated posteriorly
Also, shorter buccal capsule and a
larger genital primordium

Filariform larvae
o Infective stage
o Non-feeding, slender, 550m
o Usually smaller than hookworm
filariform larvae, with distinct cleft at
tip of tail

Figure 23. Life cycle of S. stercoralis

Figure 21. (L) Rhabditiform and (R) Filariform larva of


S. Stercoralis.

Egg
o Clear thin shell
o Similar to egg or hookworm but is only
50-58m x 30-34m

Figure 22. (L) Eggs of S. Stercoralis.

Life Cycle

13
of x

Free-living cycle
o The rhabditiform larvae passed in the
stool

Molt twice and become infective


filariform larvae (direct
development)

Molt four times and become free


living adult males and females
that mate and produce eggs from
which more rhabditiform larvae
hatch

Parasitic cycle
o Begins when filariform larvae in
contaminated soil penetrate the human
skin -> lungs -> alveolar spaces ->
bronchial tree -> pharynx -> swallowed
-> small intestine
o Duodenum: molt twice, become adult
female worms
o The females live threaded in the
epithelium of the small intestine and by
parthenogenesis produce eggs, which
yield rhabditiform larvae
o The rhabditiform larvae can either be

passed in the stool (free living),


or

cause autoinfection
o In autoinfection, the rhabditiform
larvae become infective filariform larvae,
which can penetrate either:

the intestinal mucosa (internal


autoinfection) or

the skin of the perianal area


(external autoinfection)
o Autoinfection in humans with
helminthic infections:

Strongyloides stercoralis

Capilaria philippinensis only


*Strong Capi (coffee)

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Intestinal Nematodes
o

Mode of infection: skin penetration


(filariform larvae)

Pathogenesis and Clinical Manifestations


Filariform larvae
o Skin penetration, petechial
hemorrhage, congestion and edema,
pruritus
o Lungs -> pneumonitis (cough), lobar
pneumonia, pleural effusion
Filariform and adult
o Intestine -> GIT disturbances
o Stool: watery mucous, diarrhea
depends on intensity of infection,
duration, host-tissue reaction
(encapsulate the worms)
Blood Picture
o Leukocytosis (WBC = 25,000)
o Eosinophilia (40%)
Three Phases of Infection
1. Invasion of the skin by filariform
larvae
o Erythema
o Pruritic elevated hemorrhagic
papules
2. Migration of larva through body
o Lungs are destroyed -> lobar
pneumonia with hemorrhage
3. Penetration of the intestinal mucosa
by adult female worms
o Pylorus to rectum
o Greatest number in duodenum and
jejunum
Intensity of infection
o Light infection

no intestinal symptoms; good


prognosis
o Moderate infection

diarrhea alternating constipation


o Heavy infection

Intractable, painless, intermittent


diarrhea (Cochin China diarrhea)
-> numerous episodes of watery
and bloody stool
o High mortality rates for moderate and
heavy infections
Diagnosis
Direct or Concentration Methods
o Finding rhabditiform larvae in feces or
duodenal aspirate

Eggs only obtained by drastic


purge/NGT duodenal aspirates

Eosinophilia as a clue
Harada mori culture
o For use in field
Baermann funnel, Bealess string Test,
Duodenal aspiration, Small bowerl
biopsy
Serology

14
of x

Not useful in endemic areas


Strongyloides cross react with filarial
worm antigens
Culture technique
o Practical, low cost, recommended for
mass screening and individual diagnosis
o
o

Epidemiology
Found throughout the world with same
distribution pattern as hookworms
More of a fecally-transmitted worm than
soil-transmitted helminth because it is
infective shortly after passage with the feces
Low local prevalence
More frequently found among male children
7-14 years old than among females and
adults
Prevention and Control
Proper waste disposal
Protection of the skin from contact with
contaminated soil
Early detection and treatment of cases
Capilaria philippinensis
Family Trichuroidea
o Thin filamentous anterior end and
slightly thicker and shorter posterior
end
Adults have subterminal anus
Parasite Biology
Adult
o Female
2.3-5.3mm
Esophagus has rows of secretory
cells (stichocytes)
Entire esophageal structure
(stichosome)
Vulva at the junction of anterior and
middle third
o Male
1.5-3.9mm
Spicule 230-300m long and has
unspined sheath
Chitinized spicule and a long spicule
Egg
o Peanut-shaped with striated shells,
flattened bipolar plugs
o 36-45m x 20m
o Passed in feces, embryonated in soil or
water
o In water, ingested by freshwater or
brackish water fish

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Intestinal Nematodes
Hyperinfection: massive number of
adult worms
7. Definitive natural hosts: migratory fisheating birds
Pathogenesis and Clinical Manifestations
Sypmtoms:
o abdominal pain,
o gurgling stomach (borborygmus)
o chronic diarrhea
o
weight loss, malaise
o anorexia
o
vomiting
o
edema
Lab findings:
o sever protein-losing enteropathy
o malabsorption of fats and sugars
o decreased excretion of xylose
o low electrolyte (K+) levels
o high IgE levels
Histology
o Flattened and denuded villi
o dilated mucosal glands
o lamina propria infiltrated with plasma
cells
o lymphocytes, macrophages, neutrophils
No invasion of intestinal tissue but with
micro-ulcers in epithelium and
compressive degeneration and
mechanical compression of cells

Figure 24. Egg of C. philippinensis in an unstained


wet mount of stool.

Life Cycle

Figure 23. Life cycle of C. philippinensis

1.-2. Unembryonated eggs passed in stool


become embryonated externally
3. Ingested freshwater fish -> larvae hatch ->
penetrate intestine -> migrate to tissues
4. Humans ingest raw or uncooked fish -<
infection by infective 3rd stage larvae
-> inhabit jejunum
5. Adults burrow in mucosa where females
deposit embryonated eggs
6. Autoinfection
o Some become embryonated and
releases larvae in the intestine ->

15
of x

Diagnosis
Finding rhabditiform larvae
o Feces or duodenal aspirate direct or
concentration methods
Eggs only obtained by drastic purge/NGY
duodenal aspirates
Treatment
Electrolyte replacement and high protein
diet
Anti-diarrheal agents
Antihelminthic drugs
o Albendazole

400mg once daily for 10 days

Preferred as it destroys larvae


more readily
o Mebendazole

200mg twice daily for 20 days


Epidemiology
1967-1968 epidemic: 1,000 cases with
almost 100 deaths
In Northern Luzon, Zambales, South Leyte,
Compostela Valley, Zamboanga del Norte
Compostela Valley Province (1998): mystery
disease that causes death of villagers due
to misdiagnosis

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Intestinal Nematodes

Only intestinal nematode with Bagsit


fish as intermediate host
Also found in Thailand, Iran, Japan, Egypt,
Korea, Taiwan, and India
Transmission by eating uncooked small
freshwater/brackish water fish
Prevention and Control
Discouraging people from rural areas to eat
raw fish
Good sanitary practices
Education
Infected people: treated quickly and feces
disposed properly

16
of x

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