9 CLINICAL

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MR. JOHN MARIO CALIGUIRAN,
RMT
NEMATODES

OUTLINE
I NEMATODES
A. Intestinal Nematodes (Soil Transmitted)
i. Ascaris lumbricoides
ii. Hookworms
a) Necator americanus
b) Ancylostoma duodenale
c) Ancylostoma braziliense
d) Ancylostoma caninum
iii. Trichuris trichiura
iv. Strongyloides stercoralis
B. Other Intestinal Nematodes (Non Soil Transmitted)
i. .Enterobius vermicularis
ii. Capillaria philippinensis
iii. UNCOMMON INTESTINAL NEMATODES
C. Tissue Nematodes
i. Parastrongylus cantonensis
ii. Trichinella spiralis
iii. Dracunculus medinensis

NEMATODES  Members of the class Nematoda (multicellular

parasites that appear round in cross section) may
assume three basic morphologic forms:
o Eggs (female sex cells after fertilization).
The eggs vary in size and shape. Diagnostic
stage
o Juvenile worms known as larvae.
Developing larvae located inside fertilized
eggs emerge and continue to mature. These
larvae are typically long and slender
o Adult worm: Sexes are separate. The adult
female worms are usually larger than adult
males.

o PATHOGENESIS AND CLINICAL SYMPTOMS

o In general terms, three possible factors may
contribute to the ultimate severity of a nematode
infection:
 (1) the number of worms present
 (2) the length of time the infection
persists
 (3) the overall health of the host
o Nematodes are round worms INTESTINAL NEMATODES (SOIL TRANSMITTED)
o GENERAL CHARACTERISTICS IN PLACES WITH POOR SANITATION
1. Elongated, cylindrical in shape with bilateral symmetry, equal 1. Ascaris lumbricoides
size 2. Hookworms
2. Complete digestive tract with muscular pharynx that is o Necator americanus
triradiate- three lips o Ancylostoma duodenale
3. Separate sexes, some are parthenogenetic, flukes or flatworms o Ancylostoma braziliense
they are hermaphrodite which means they can have two o Ancylostoma caninum
sexes 3. Trichuris trichiura
4. Non-segmented unlike cestode 4. Strongyloides stercoralis
5. Has sensory in anterior ends (amphids) and posterior end * Hookworms, Ascaris lumbricoides and Trichuris trichiura –
(phasmids) Unholy three because they are always together
o Aphasmids: Lacks phasmids or caudal chemoreceptors-
they are the primary interface of most organism to their
chemical environment
 Trichuris, Capillaria, Trichinella
o Phasmids: with caudal chemoreceptors –
 Hookworm, Strongyloides, Wuchereria, Brugia
malayi (FILARIAL WORMS)

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MR. JOHN MARIO CALIGUIRAN,
RMT
Importance in Nematodes
o Other names
o Appearance of eggs
o Natural habitat

*Man as the main host

ASCARIS LUMBRICOIDES
 Largest round worm, popular
 Other names: giant intestinal round worm, lumbricus
teres, eenworm
 Morphology:
o Eggs:
 1. Corticated
 2. Fertilized
 Normal appearance:
Decorticated (mammilated
albuminous coating)
 Outer mammilated
albuminous coating
 Thick glycogen middle layer
 Inner vitelline, lipoidal
membrane. o Mouth at the anterior end has 3 finely tooth lips,
 Has ovoid mass of triradiate
protoplasm, which develops  2 ventro lateral
into larvae into 14 days  1 dorsal
 3. Unfertilized o Spicule- 2 copulatory spicules, for copulation
 Longer and narrower than o Cuticle- form barrier for survival; it resists
fertile eggs extreme environmental condition
 Thin shell and irregular  FEMALE
mamillated coating filled o Mouth with 3 lips
with refractile granules o Cuticle
(Lecithin) o Genital girdle- female reproductive organ
o Sensory papillae- their sense of organ
 *The copulation of A. lumbricoides form like letter T
 Lay 200,000 eggs per day. Eggs can develop and
embryonated or pass through feces
 Eggs are diagnostic stage
 A distinct grove is often seen surrounding the worm at the
level of the vulvar opening called the vulvar waste or
genital girdle and it is believe to facilitate mating
 Seen in sputum
 Larva: morphology is similar to adults
 Adult: polymyarian type (cells are numerous and project
well into body)
 Smooth striated cuticles
 Terminal mouth with 3 lips (2 ventral, 1 dorsal) and
sensory papillae (sense of touch)
 Males –ventrally curved posterior with two spicules
 Females - paired reproductive organs in posterior 2/3
(Vulvar waste)
 Life cycle: In soil, it takes 2-3 weeks for eggs to develop
into infective stage under favorable conditions
(temperature, moisture and humidity). The larvae reach
their 3rd stage, molts and
 embryonates, only this when swallowed can humans be
infected. (Ingestion)
 infective stage is your embryonated egg
 Pathogenesis:
o Reactions of tissues to invading larvae
o Irritation of intestines (intestinal spasm) by adult
 MALE: and extraintestinal migration

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o Usual infections of 10-20 worms
may go unnoticed.
o Obstructs pancreas (acute pancreatitis) and cause
appendicitis
o Heart and Lung migration-produces symptoms
similar to pneumonia (Loeffler’s syndrome)
when a re infection occurs subsequently there
may be intense cellular reaction in the migrating
larvae in the lungs with the infiltration of
eosinophils, macrophages, and epithelioid cells.
This Ascaris pneumonia characterize by low
grade fever, dry cough, asthmatic quizzing,
urticaria eosinophilia. The sputum is often blood
tinged and may contain char coat laded crystals
o The larvae may occasionally found in sputum but
may often seen in gastric washers
o Natural habitat: small intestines
 LIFE CYCLE IN YOUTUBE
(https://www.youtube.com/watch?v=Y61wwcXnpF8)
o Ascariasis an infection of the small intestine caused by
Ascaris lumbricoides.
o Infections with these parasites are more common
where sanitation is poor and raw human feces are used
as a fertilizer.
o Ascaris lumbricoides is the large round worm of the
phylum nematoda.
o It is the most common parasitic worm in humans.
o Fertilized OVA or the eggs of the worms contaminate
the food and are ingested with it.
o After ingestion they reach the small intestine and eggs
hatch out into larval forms.
o The larva crosses the duodenum region of the small
intestine and gets released into the bloodstream from
there it is carried into the liver and heart and then
enters the lungs.
o In the lungs the larvae grow and shed their skin which
is known as moulting.
o After three weeks the larvae passes from the
respiratory system to be coughed up swallowed and
finally returns to the small intestine.
o Due to the increase in the number of worms in our
body sometimes they may emerge from anus nose and
mouth also.
o In the small intestine the larva matures into an adult
male or female worm and fertilization occurs at this
stage of life cycle.
o The male worm is smaller in size than the female is
ascaris sperm male verbs are 15 to 20 centimeters in
length while females are 20 to 35 centimeters in
length.
o The female worm produces 200,00 eggs per day for 12
to 18 months. These eggs excreted out in stool and
become infectious after two to three weeks in soil
fertilized eggs can persist in soil for 10 years or more.
o These eggs contaminate food and the cycle restarts.
o Let's solve some questions based on this topic:
o Question 1: Ascaris lumbricoides infection occurs
through?
1. Sole of uncovered feet
2. Contaminated water and food
3. Improperly cooked measly pork
4. from air through inhalation.
SY 2021 - 2022
1st
BSMLS
*This question was asked in Rajasthan PMT 2008.
Solution the fertilized eggs are present in soil which
contaminate the food and water hence option 2 is
correct.
o Question number 2: Ascaris is complete its life cycle
in?
1. Only in man
2. Man and sheep
3. Man and mosquito
4. Man and cow.
*Solution: Ascaris is monogenetic so it competes as
life cycle in a single host that is man hence option 1 is
correct.
o Question 3: Which is not true in Ascaris infection.
More common in children
Does not produce tonsillitis
The number can be 500 to 5000
Infection can be cured even without medication
*Solution: Ascariasis disease need proper
medication it cannot be cured without medication
hence option 4 is correct.
 LIFE CYCLE OF ASCARIS
o It start with the ingestion of the infective stage.
Man acquires infection by ingestion of food and
water contaminated with the embryonated egg.
o The embryonated egg will form into the first
stage of the worm which is the Rhabditiform
larva, it is liberated in that duodenum
o Larvae borrows through the mucous membrane
of the intestine, after it destroy the intestinal
linings, the parasites will go to the circulation, if
they reach the lungs, trachea and pharynx, from
there they are re-swallowed and reach small
intestines.
o The Rhabditiform in small intestine will develop
into adult worm
 Fertilized egg- pass through feces
 Country who have poor sanitation use feces as fertilizer
 Unfertilized- can develop in soil (embryonated)
 Infective Stage: embryonated egg
 Diagnostic stage: unfertilized egg, fertilized egg, and adult
 Procedures: Direct fecal smear, kato thick, kato katz
 Note: If negative in stool exam:
o No infection,
o Early infection
o All MALE WORM infection, Ascariasis only
 Treatment: Albendazole, Mebendazole, Pyrantel pamoate

HOOKWORMS
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MR. JOHN MARIO CALIGUIRAN,
RMT
 a. Necator americanus (American o Then they can now migrate via blood
hookworm, American murderer, New world stream
hookworm) cause infection in humans o It will reach the pharynx and ultimately
 b. Ancylostoma duodenale (old world hookworm) it will shallow by the host, then they
cause infection in humans will settle in small intestine and
 c. Ancylostoma braziliense (cat hookworm) develop into adult worms
 d. Ancylostoma caninum (dog hookworm) o Adult worms in small intestine they can
now copulate, description is letter “Y”
o Female will lay eggs and pass through
feces
o Feces in the eggs will mature,
o Then, embryonation or development in
the soil
o After that, it will turn into rhabditiform
larvae, and it will hatch and they can
now mold twice
o Then, filarifom larvae
 Pathogenesis: skin at point of entry (ground
itch/dew itch)
 Mazza Mora/Water sore
Blastomeres
 Larval migration into lungs – Visceral Larva
 4-8 circles
Migrans
 Morphology
 Cutaneous larva migrans (Creeping eruption - it
 Eggs
is form due to subcutaneous migration of
 It is difficult to distinguish
filariform larva, there is a reddish, itchy papule,
between Necator americanus
more commonly infection in animal hookworms
& Ancylostoma duodenale
than in human hookworms) :
 Bluntly round ends with thin
o A. braziliense and A. caninum
hyaline shell
 2 to 8 cell stages of division  Small intestine infections
 “Morula ball”  Microcytic/hypochromic anemia such as Iron
 Adult: Necator americanus- small, cylindrical, deficiency anemia and hypoalbumemia
fusiform grayish white
 Posterior end of male has broad caudal bursa with
rib like rays
 Caudal bursa is use to hold the female when they
are mating
 Buccal capsule (mouth) has ventral pairs of
semilunar cutting plates
 Head is curved opposite to curvature of body,
hence “hookworm”
 Ancylostoma duodenale- larger than Necator
 Buccal capsule has 2 pairs of curved ventral teeth
 Rhabtidiform: long buccal cavity, short genital
primordium, first stage of larva of worms
 Filariform: shorter esophagus, sheathed tail, it
can develop to adult
 Male copulatory bursa:
 Bipartite (2 digits): Barbed & bristle like N.
americanus
 Tripartite (3 digits): Simple & not barbed A.
duodenale
 Life cycle: Adult worm attaches to mucosa of
intestines, females oviposit eggs and passes into  This hookworms release anticoagulants for it to
feces, in soil embryo develops into rhabtidiform not stop the bleeding, if you have chronic or
larva after 2 days, and develops into filariform prolonged bleeding you’ll have anemia,
larva after 7 to 10 days. decreased iron
 Life cycle of Ancylostoma duodenale  Agent of laziness (poor white population) tropical
o Mode of transmission: Penetration of anemia (Puerto Rico)
skin of man which is the definitive host  Infective Stage: filariform larva
o The Filariform larvae will be the one to  Diagnostic stage: eggs
penetrate the skin that can be found in  Procedures: Direct fecal smear, kato katz, kato
soil thick and Harada Mori

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MR. JOHN MARIO CALIGUIRAN,
RMT
 Infective Stage: embryonated eggs
 Treatment: Mebendazole (not for children below  Diagnostic stage: embryonated eggs
2 yrs), Albendazole (not for pregnant)  Procedures: DFS, Kato thick, Kato Katz, FECT
 Treatment: mebendazole

STRONGYLOIDES STERCORALIS
 Other name: Threadworm
 Morphology:
o Eggs: Transparent, Segmented
 Adult:
o Female has double-bulbed muscular
esophagus and straight cylindrical intestines
o Male has ventrally curved tail and a
gubernaculum with no caudal alae
 Rhabtidiform: elongated esophagus and pyriform
N. americanus (adult mae) posterior, short buccal cavity, larger genital
 2 ventral primordium
 2 dorsal chitinous cutting plates  Filariform: smaller than hookworm, with cleft at tip
A. duodenale (adult male) of tail
 4 ventral teeth  Adult filariform larvae has notch tail
 2 dorsal knot-like teeth  Long esophagus almost 40% of total body length
(female)
TRICHURIS TRICHIURA

 Other name: whipworm because of the appearance of

adult worm
 Morphology
o Eggs:
 Barrel/football/Japanese lantern
with bipolar plugs
 When in soil, much prone to
dessication
 Adult: holomyarian (cells are
small, numerous and closely
packed in narrow zone)
 Anterior 3/5 portion is traversed
by narrow esophagus resembling
“string of beads”
 Generally, has thick and fleshy
posterior and threadlike anterior
 Female has rounded posterior and
lays 3000 to 10,000 eggs
 Testis or male reproductive are in
the middle of the body

 Life cycle: Inhabits large intestine, after copulation

female deposits eggs that is passed into feces, under
good conditions, eggs embryonate in 2-3 weeks. No
lung migration.
o Ingestion of embryonated egg with infective
of Rhabdtifrom larvae
o Larvae liberated through one of the poles
o Liberated in small intestines but passed
down to your cecum and will develop in
adult worms
 Asymptomatic
 Pathogenesis:
o Petechial hemmorhage
o Provide good site for entamoeba histolytica
o Appendicitis
o Rectal prolapse
o Trichocephaliasis other name for trichuriasis
a chronic GIT disorder

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MR. JOHN MARIO CALIGUIRAN,
RMT
 Treatment: Albendazole

OTHER INTESTINAL NEMATODES (NON SOIL

TRANSMITTED)
 1. Enterobius vermicularis
 2. Capillaria philippinensis

ENTEROBIUS VERMICULARIS
 Formerly known as oxyuris vermicularis
 Other names: oxyuris, pinworm, seatworm, society worm
 Common names: Pinworm, seatworm.
 Common associated disease and condition names:
o Enterobiasis, pinworm infection.
 Morphology:
o Eggs:
 “D-shaped”, elongated, flattened on
one side
 Outer, triple albuminous covering
 Inner lipoidal membrane
 Eggs become infective outside host for
 Enters host through skin penetration, larva enter 4-6 hours
circulation via heart, lung’s respiratory tree, esophagus,  “Tadpole like embryo” – eggs is
then will reach small intestine decribe as
 In the small intestine, larvae mature into adult worm  Adult: males has curved tail and single spicule, usually
 Adult female embedded in the mucosa of small intestine
dies after copulation, with lateral wings or cephalic alae
lays egg containing larva
 Larva when develop, will form Rhabditiform larva.
 Rhabditiform larva can develop into filariform in bowel.
o Filariform larva can cause autoinfection or
autoreinfection by penetrating perianal skin
 Other forms of Rhabditiform larvae can develop into adult
worms. Free living adult worn in soil can copulate
resulting to embryonated egg
 Embryonated egg develop into Rhabditiform larva then
develop into filariform larva.
 Life cycle: filariform larva infects through skin
penetration, passes through lungs and larynx. Females
reproduce by parthenogenesis. Autoreinfection
happens when rhabtidiform larva passes into large
intestine and further develop into filariform larva.
 Pathogenesis: skin penetration
 Autoreinfection & migration into body
 Disseminated infection in immunosuppressed
patients/cochin china diarrhea
 Strongyloidiasis, infection cause by S. stercoralis is
generally benign and asymptomatic
 Blood eosinophilia and larva in stool being the only
indication of infection

 Infective Stage: filariform larva

 Diagnostic stage: rhabtidifrom larva
o Hookworm – thin shell and morula balls
appearance
o S. stercoralis – worm in microscope with
morula balls

 Procedures:
o 1. Baermann funnel
o 2. Harada mori
o 3. Beale’s string test

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MR. JOHN MARIO CALIGUIRAN,
RMT
o Adult worm migration- appendicitis, vaginitis,
endometritis, salpingitis
 Appendicitis
 Vaginitis – inflammation of vagina
 Endometritis – inflammation of uterus
 Salpingitis – inflammation of fallopian
tube
o Familial disease
o Mother’s complex: Pruritus ani, Lack of sleep,
Extraintestinal enterobiasis
 Infective Stage: embryonated eggs
 Diagnostic stage: embryonated eggs
 Procedure: Scotch tape swab technique/ graham’s scotch
adhesive tape swab
 Treatment: pyrantel pamoate
CAPILLARIA PHILIPPINENSIS

 Mode of transmission – ingestion of contaminated hand,

food, drink, clothing and dust
 Enterobius vermicularis infection can be transmitted via
inhalation
 Egg (with infective larva) swallowed by man (definitive
host)
 The egg shell is dissolved by the digestive juices and larva
liberated in small instestine
 Liberated larva migrates towards cecum
 Develops into adult worm
o Tip of the adult worm is called cephalic alae
 Eggs laid at the perianal skin by the gravid female
 Scratching of the perianal skin and when ingested can
cause autoinfection
 In soil, eggs develop to embryonated egg (with infective
larva inside)
 Autoinfection occurs because of the ingestion of eggs due
to scratching of perianal area with fingers leading to
deposition of eggs under the nails. This type of infection is
mostly common in children. Anus to mouth
 Retroinfection, in this process the eggs lay on the perianal
skin immediately hatch into the infective stage larva and
migrate through the anus to develop into worm in the
colon. Anus to colon
 Life cycle: Found in lower intestines, female worms
migrate down and exit to anus and deposit eggs, each
female can lay up to 11,000 eggs, after deposition of eggs,
female dies. Eggs on perianal region embryonates, it is
prone to dessication, however in moist condition can
survive for 13 days.
 Pathogenesis:
o Mild catarrhal infection of intestines
o Pruritus ani
o Insomnia of children
UNCOMMON INTESTINAL NEMATODES
 Other names: mystery worm, pudoc worm (discovered in
Philippines in 1963)
Morphology:
 Eggs: peanut shaped, Guitar-shaped, striated shells and
flattened bipolar plugs
 Adult: members of superfamily Trichuroidea
(characteristically has thin filamentous anterior end and
slightly thicker posterior end)
 Esophagus (stichosome) has rows of secretory cells called
stichocytes
 Male: with chitinized spicule (spicule sheath)
 Female: have eggs in utero
 Life cycle: female worms deposits eggs which
embryonates in soil or water and ingested by freshwater
fish, it then hatches in the intestines of fish into larvae, fish
being eaten by humans (usually uncooked) and develops
into human intestines. Birds act as reservoir host when they
eat the fish that is infected.
 Pathogenesis: borborygmi, protein losing enteropathy,
malabsorption, low levels of electrolytes and high
immunoglobulin E
o Borborygmi – refers to the characteristic
growling and grumbling sound that stomach
and intestine make as food or fluid or gas pass
through
 Infective Stage: filariform larva
 Diagnostic stage: eggs in direct fecal smear or stool
concentration methods, ELISA
 Treatment: electrolyte replacement and high protein diet

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1. Toxocara canis (dog ascarid) and Toxocara cati (cat  Infective Stage: 3rd stage larva
ascarid)- eggs resemble Ascaris but is larger. Causes visceral  Diagnostic stage: adult worm
larva migrans and nematode endolphthalmitis  Treatment: albendazole, thiabendazole, mebendazole
2. Anisakis spp. – causes herring disease, infects humans after
eating fish containing larva.
TRICHINELLA SPIRALIS
3. Trichostrongylus- similar to hookworm eggs, but has pointed
eggs, an intestinal nematode of herbivores  Other names: garbage worm, muscle worm, pork worm
4. Oesophagostomum spp.: worms resemble Hookworms. Causes  Discovered by Richard Owen in 1835.
unilocular disease/”dapaong tumor” or “turtle in the belly”  3 subspecies:
5. Baylisascaris procyonis- causes fatal visceral larva migrans in o Trichinella spiralis spiralis (temperate regions)
infants o Trichinella spiralis nativa (arctic regions)
6. Eustrongyloides spp.- parasite of wading birds, human infection o Trichinella spiralis nelsoni (Africa)
reported through ingestion of “sushi” and bait minnows
7. Gongylonema spp- intermediate hosts are cockroaches and other
insects, human infection is through ingestion of these insects or
contaminated water.
8. Acanthocephala spp- thorny headed worms (Moniliformis
moniliformis, Macracanthorhychus hirudinaceus,
Macracanthorhychus ingens, Bulbusoma) requires arthropod
intermediate hosts such as beetles and cockroaches, also
accidentally through sashimi
TISSUE NEMATODES

 Parastrongylus cantonensis  Morphology

 Trichinella spiralis o Larva: Spear-like burrowing anterior tip
 Dracunculus medinensis o Adult:
 male - single testis, has posterior
cloaca with a pair of appendages and
PARASTRONGYLUS CANTONENSIS
conical papillae
 Female (3.5mm)- has an oviduct,
seminal receptacle, coiled uterus,
vagina and vulva, club shaped uterus
((viviparous/larviparous)
 Life cycle: the host (humans, cats, dogs, cats, pigs, bears,
foxes, walruses, other carnivores and omnivores) serve as
final and intermediate hosts. Larvae are usually found in
 Other name: rat lungworm (discovered by Chen in 1935 muscles.
from rats in Canton, China)  Requires 2 host to complete its life cycle. Propagated by
 Morphology rats
o Eggs: Delicate hyaline shells , unembryonated  Pathogenesis:
o Adult: pale and filiform o (1) enteric phase
o Male - well developed kidney shaped and single o (2) convalescent phase
 lobed caudal bursa o (3) encapsulation
o Female- barber’s pole pattern of uterus  Cardinal signs/symptopms: Severe myalgia, periorbital
 Life cycle: 1st stage larva first infect intermediate hosts edema, eosinophilia
(snails), mode of infection is done by penetration or  Note: Trichinellosis is a self-limiting disease, prognosis is
ingestion. It develops into 3rd stage larva in snails. Rats good
ingest snails harbouring the 3rd stage, they are the  Infective Stage: encysted larva
definitive hosts.  Diagnostic stage: encysted larva
 1st Intermediate hosts (snails): Achatina fulica (giant  Procedures:
African snail), Pomacea canaliculata Hemiplecta o Muscle biopsy (gold standard)
sagittifera, Helicostylamacrostoma, Vaginilus plebeius, o Chemistry tests (Elevated creatinine
Veronicella altae phosphokinase, lactate dehydrogenase,
 Pathogenesis: acute occipital or bitemporal headache. o and myoglobin)
Large numbers of charcot leyden crystals in meninges.
Human Eosinophillic meningitis. Note that prognosis is
good (disease is mild)

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o Beck’s xenodiagnosis (Albino
rats were fed by infected meat and observe for
presence of parasite after 2 weeks)
 Immuno-tests: Bentonite flocculation, Intradermal test
(Bachmann)
 Confirmatory: Western blot, Latex agglutination
Algorithm for diagnosis of Acute Trichinellosis in humans
Group Symptom
A Fever, eyelid, Facial edema, myalgia
B Diarrhea, neurological signs, cardiac signs, conjunctivitis,
sublingual hemorrhages, cutaneous rash
C Eosinophilia, high total IgE, high muscular enzymes
D Positive serology, seroconversion, positive muscular biopsy
 Treatment: Thiabendazole
 Prevention: meat should be cooked at 77°C, or
freezed, storing at -15°C for 20 days or -30°C for six
days. Smoking or salted or even drying is not effective
DRACUNCULUS MEDINENSIS
 Other names: fiery serpent of the east, guinea worm
 Morphology
o Adult: Inhabits cutaneous and subcutaneous
tissues
 1st intermediate host- copepod/water flea
LESSON 7: INTESTINAL NEMATODES
 Enterobius vermicularis
 Ascaris lumbricoides
 Capillaria philippinens
 Trichiuris trichiuria
 Hookworms
 Strongyloides stercoralis
INTRODUCTION:
The term nematode means “roundworm” because members of the
phylum Nematoda can be viewed as a cross-section and may range
from a few millimeters to more than 1 meter in length. A common
characteristic found in nematodes is that both male and female
representatives exist, unlike other parasites. As a general conclusion,
the male roundworm is generally smaller than the female. Body
development is rather complex with an exterior covering called a
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cuticle which covers several layers of underlying musculature, a
complex nerve cord and a well-developed digestive system.
Functional sexual organs are present in the male and in addition the
body of the male ends in either a curved or coiled tail. Humans are
considered the definitive host for the species of roundworms that are
considered medically important for the parasitic nematode infections.
Where fertilized eggs or larvae are the means for reproducing adult
roundworms, three routes are generally involved by which the host
becomes infected. Depending on the species of nematode, the adult
female nematode is able to produce an infection in the following
ways:
 Ingestion of eggs by a susceptible host can result in
immediate infection
 After a required period of external development, usually in
the soil, either eggs or larvae reach an infective stage
before developing the capability to infect a host, often by
skin penetration
 Eggs or larvae are transmitted to a new host by insect
vectors
ENTEROBIUS VERMICULARIS
 Pinworms are prevalent around the world, and although
they are not a serious threat to the overall health of the
individual, they do cause some discomfort through anal
irritation and nervousness mostly in small children.
 The most prevalent type of human worm infection in the
United States and perhaps around the world is by that of the
pinworm.
 The term worms in children are a common lay term for
pinworms. This frequently used reference to pinworms is
almost universal as a descriptive name for this parasite,
which is an organism of the genus and species Enterobius
vermicularis. Because many children put their dirty fingers
into their mouths, they are more susceptible to this type of
infection.
 The condition is most often confirmed by microscopic
examination of the characteristic eggs where one side of
the egg is flattened.
 All parasites require a host and some may require up to
three different hosts for development and infection, but for
pinworms, only the human serves as a host, where the
organism develops into an adult and serves as a vessel for
transmission to others.
 Treatment with medication is available to kill the parasites,
and to be completely effective, all members of the family
should be treated when a single family member is
diagnosed with a pinworm infection.
 Personal hygiene and sanitary living conditions are
necessary to avoid becoming infected and then reinfected.
 Although pinworm infections are relatively harmless, they
are a nuisance but are easily treated, and ridding the entire
family of the annoying symptoms of the disease is required
to effectively control the infection.
GENRAL CHARACTERISTIC OF E. VERMICULARIS
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 Enterobius vermicularis is called a pinworm due to its long
pointed tail that resembles a straight pin in the adult worm.
 These pinworms may be visible in the stools of those
infected, and are readily visible in the feces of children
with heavy infections, but the diagnosis is generally made
by the presence of eggs.
 Rarely, eggs may become airborne and be inhaled and
swallowed.
 Retroinfection, or the migration of newly hatched larvae
from the anal skin back into the rectum, may occur but the
frequency with which this happens is unknown.
LIFE CYCLE
1. Gravid adult female Enterobius vermicularis deposit eggs
on perianal folds.
2. Infection occurs via self-inoculation (transferring eggs to
the mouth with hands that have scratched the perianal area) or
through exposure to eggs in the environment (e.g. contaminated
surfaces, clothes, bed linens, etc.)
3. Following ingestion of infective eggs, the larvae hatch in
the small intestine and the adults establish themselves in the colon,
usually in the cecum.
4. The time interval from ingestion of infective eggs to
oviposition by the adult females is about one month. At full maturity
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adult females measure 8 to 13 mm, and adult males 2 to 5 mm; the
adult life span is about two months. Gravid females migrate
nocturnally outside the anus and oviposit while crawling on the skin
of the perianal area.
5. The larvae contained inside the eggs develop (the eggs
become infective) in 4 to 6 hours under optimal conditions.
SYMPTOMS
Symptoms often range from being asymptomatic to any or several of
the following signs and symptoms. An itchy anus due to an
inflammatory response to the adult worm, especially at night, will be
the most frequent symptom exhibited. In addition to this
manifestation, any or all of the following may be present:
 Irritability may occur in children along with nervousness
and disruptive behavior
 With severe scratching of the anus, the skin may break
down and progress to a secondary bacterial infection
 Rare cases appear to cause anorexia, or loss of appetite
 Somewhat vague or ill-defined feelings of not being well
may be present
 Female children may also have an itchy and inflamed
vagina
 Adult worms may be seen in the stools
 Eggs may be seen with the naked eye, clinging to the skin
around the anus
 Pinworms do not contribute to abdominal pain but have,
perhaps erroneously, been attributed to cases of
appendicitis as they have been observed in tissue specimens
such as the appendix.
DISEASE TRANSMISSION
The infection is spread via the fecal-oral route by ingestion or
inhalation of embryonated ova. The disease may also be transmitted
by fomites (inanimate objects that are contaminated by organisms)
and from soiled fingers, dirty bed linens, toilet seats, and clothing.
The disease is found throughout the world and spreads quickly
through families and groups in close contact with each other, such as
in day care centers for young children.
HOSTS
Oxyurid nematodes (pinworms) generally exhibit high host
specificity. Humans are considered the only host for E. vermicularis,
although occasional infections have been reported in captive
chimpanzees. Geographic Distribution E. vermicularis occurs
worldwide, with infections occurring most frequently in school- or
preschool-children and in crowded conditions.
TREATMENT AND PREVENTION
 The physician will most likely request a procedure to test a
sample of the patient’s feces to make a positive
identification of pinworms as the cause for symptoms of
infection.
 Medication is available to kill the worms and this is usually
prescribed for the infected person and all members of the
household. Usually one dose is followed up with a second
dose 2 weeks later to take care of any surviving worms.
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 Although safe for humans, a prescription  Geographic distribution is associated with climate and poor
from the physician is required before starting the sanitation.
medication.  The eggs of A. lumbricoides require a in order for the
 A repeat preparation should be examined following embryonated ovum to mature and become infective.
completion of treatment to ensure complete eradication.  Infection rates are elevated in poverty-stricken areas that
 All family members should take the medication, regardless have poor sanitation.
of whether they are experiencing symptoms, because the  Transmission is through the fecal-oral route, usually
condition is quite contagious and some are asymptomatic, through the ingestion of eggs on contaminated material.
showing no evidence of the common symptoms and signs  Ascaris eggs are capable of survival within harsh
of infection. environmental conditions, including dry or freezing
 Treatment for relieving the itching of the anus can be temperatures.
effective with the use of various types of soothing anti-itch
creams or similar preparations. PATHOGENESIS
 Recurrence of the infection is likely if bed linens and bed  Many A. lumbricoides infections are asymptomatic.
clothes are not thoroughly washed to kill both eggs and  The presentation of symptoms correlates with the length of
worms, and if personal hygiene is not practiced, including infection, the number of worms present, and the overall
thorough hand washing following trips to the bathroom and health of the host.
when playing with other children.  Intestinal symptoms range from mild to severe intestinal
obstruction.
ASCARIS LUMBRICOIDES  Some patients will develop pulmonary symptoms and
 Ascaris lumbricoides, sometimes considered the “large
present with immune-mediated hypersensitivity
roundworm,” is one of six worms classified by Linnaeus,
who performed most of his observations and studies pneumonia.
between the 1730s and 1750s.  The worms may cause an immune condition known as
 His work took him to countries throughout several areas of Löffler’s syndrome characterized by peripheral
the world, which confirmed the widespread range of the eosinophilia.
parasite.
 Linnaeus is credited with giving the scientific name to
Ascaris lumbricoides, along with other plants and animals.
 The chief source of most of the infections by this parasite is
the practice of using human feces to fertilize soil where
food is grown.
 The adult worm lives in the intestine and the female
produces eggs that pass with fecal materials, where the
larvae within the eggs develop and reach an infective stage
in soil.
 Foods grown and gathered from agricultural areas where
the soil is contaminated by feces containing eggs from this
species may directly transmit the eggs to humans when
food contaminated with infective eggs is eaten and the
larvae emerge from the ingested eggs in the intestine.
 The history of ascariasis is long and has been determined
to have been an infection plaguing humans since before
recorded history.
 Ascaris lumbricoides is the most common and the largest
roundworm.
 The parasite has a worldwide distribution with higher
prevalence in the tropical regions.
 Eggs are ingested and hatch in the duodenum, penetrate the
intestinal wall, and migrate to the hepatic portal circulation.
 The adult worms live and reproduce in the lumen of the
small intestine. The ovum is a thick, oval mammillated
(outer protrusions) and embryonated egg. LIFE CYCLE
 The eggs are passed in the feces and become infective 2 to
6 weeks following deposition, depending on the
environment.
 A. lumbricoides life cycle is classified as an indirect life
cycle; transmission is not via a direct route from one host to
the next.

EPIDEMIOLOGY

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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.
Larvae develop to infectivity within fertile eggs after 18 days to
several weeks, depending on the environmental conditions (optimum:
moist, warm, shaded soil).
3. After infective eggs are swallowed, the larvae hatch, invade
the intestinal mucosa, and are carried via the portal, then systemic
circulation to the lungs.
4. 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.
5. Upon reaching the small intestine, they develop into adult
worms. 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.
LABORATORY DIAGNOSIS
 Female worms have an extremely high daily output of eggs,
making diagnosis relatively easy through the identification
of eggs in feces.
 The large, broadly oval mammillated ova are typically
stained brown from bile.
 Some eggs will be decorticated, or lacking the
mammillated outer cover.
 Infertile eggs may be oval or irregular shaped with a thin
shell and containing internal granules.
 Adult worms may also be identified in feces.
 The male is smaller (15 to 31 cm) with a curved posterior
end and contains three well-characterized lips.
 Larvae may be found in sputum or gastric aspirates as a
EPIDEMIOLOGY
result of larval migration during development within the
human host.
TREATMENT AND PREVENTION
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 Anti-helminthic treatment is recommended for all
infections.
 Preferred therapy includes oral albendazole, mebendazole,
or pyrantel pamoate.
 Prevention is managed through proper sanitation and good
hygiene.
TRICHURIS TRICHIURA
 Trichuris trichiura, whipworm, has a worldwide
distribution.
 Unlike other intestinal nematodes discussed in this module,
there is no tissue migration phase within the life cycle of T.
trichiura.
 The human whipworm (Trichuris trichiura or
Trichocephalus trichiuris) and previously known as
Trichuris trichiura, is one of the most prevalent parasitic
roundworms found worldwide.
 The existence of the organism has been documented for
many years and in the older literature it was described as
causing a condition called trichuriasis when it infects the
large intestine of the human.
 Whip with a long and slender thread-like anterior portion
and with thicker, wider “handles” at the posterior end that
is long and slender, described as a threadlike caudal
portion.
 The male is characterized by a slightly coiled tail, whereas
the female has a rounded and somewhat blunt posterior that
is not coiled.
 The adult worm ranges from 30 to 50 mm with a range of
35 to 50 mm for the female.
 The male is slightly smaller than the female, ranging from
30 to 45 mm in length.
 The eggs have a mucogelatinous plug at each terminal end
of the elongated egg that is bile-stained and barrel-shaped.
 A smooth but thick shell covers the egg, which is from 45
to 55 μm in length and 20 to 23 μm in width.
 Trichuris trichiura is typically found in moist, warm
climates around the world.
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 Infections are relatively common in Asia,
Africa, and South America, with some cases identified in
the southeastern United States.
 Often the nematode is identified in co-infections along with
A. lumbricoides.
 Poor hygiene is associated with increased transmission,
especially in children.
 Humans are infected by ingestion of the eggs.
 Larvae are released in the intestine where they mature into
adult worms.
 Eggs are then passed in the feces and deposited in the soil.
 The eggs require a warm, moist environment for
embryonation in order to become infective to another host.
LIFE CYCLE
1. The unembryonated eggs are passed with the stool.
2. In the soil, the eggs develop into a 2-cell stage, an
advanced cleavage stage , and then they embryonate ; eggs become
infective in 15 to 30 days.
3. After ingestion (soil-contaminated hands or food), the eggs
hatch in the small intestine, and release larvae that mature and
establish themselves as adults in the colon.
4. The adult worms (approximately 4 cm in length) live in the
cecum and ascending colon. The adult worms are fixed in that
location, with the anterior portions threaded into the mucosa.
5. The females begin to oviposit 60 to 70 days after infection.
Female worms in the cecum shed between 3,000 and 20,000 eggs per
day. The life span of the adults is about 1 year.
LABORATORY DIAGNOSIS
 Diagnosis is typically from the identification of eggs and
rarely the adult worm within the feces.
 An adult female may produce up to 20,000 eggs per day.
However, during the lengthy development of mature worms
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within the intestine, there may be no shedding of eggs for
up to 3 months.
 Eggs appear as brown barrel-shaped structures. They are
unembryonated and contain a thick wall with hyaline polar
plugs at each end.
 The adult female worm ranges in size from 35 to 50 mm
and demonstrates a gradually increasing width from
anterior to posterior, with a straight end.
 The adult male ranges in size from 30 to 45 mm and
demonstrates the same broadening morphology with a
coiled posterior end.
TREATMENT AND PREVENTION
 Therapy may or may not be indicated, dependent on the
nutritional status of the host, the length of infection, and the
level of worm burden.
 Anthelmintics such as albendazole are recommended when
necessary.
 Prevention includes practicing proper hygiene and
sanitation as well as the disposal of dirt or soil
contaminated with feces.
CAPILARIA PHILIPINENSIS
 Capillaria philippinensis was first recognized as a human
parasite in the late 1960s and now has a well-known wide
distribution.
 This parasite is prevalent in the northern Philippines, hence
the name C. philippinensis, and has also been found in
Thailand, Japan, Taiwan, Iran, and Egypt.
 The parasite reproduces in the gut, resulting in
autoinfection and hyperinfection very similar to that
observed in S. stercoralis.
EPIDEMIOLOGY
 Human infection is thought to occur from the ingestion of
uncooked fish harboring infective larvae.
 In the Philippines, where the organism is prevalent, the
people ingest a large spectrum of raw seafood, including
fish, shrimp, crabs, and snails.
 In addition, defecation in the fields or water sources where
snails, shrimp, and crabs are collected is common.
 The life cycle of the parasite is currently not fully
understood.
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LIFE CYCLE
LABORATORY DIAGNOSIS
TREATMENT AND PREVENTION
1. Typically, unembryonated, thick-shelled eggs are passed in
the human stool and become embryonated in the external
environment in 5—10 days.
2. After ingestion by freshwater fish, larvae hatch, penetrate
the intestine, and migrate to the tissues.
3. Ingestion of raw or undercooked fish results in infection of
the human host.
4. The adults of Capillaria philippinensis are very small
(males: 2.3 to 3.2mm; females: 2.5 to 4.3 mm) and reside in the
human small intestine, where they burrow in the mucosa.
5. In addition to the unembryonated, shelled eggs which pass
into the environment, the females can also produce eggs lacking
shells (possessing only a vitelline membrane, which becomes
embryonated within the female’s uterus or in the intestine.
6. The released larvae can re-invade the intestinal mucosa and
cause internal autoinfection.
7. This process may lead to hyperinfection (a massive number
of adult worms).
PATHOGENESIS
 Symptoms vary with the level of worm burden.
 The larvae are ingested and reside in the small intestine
where they burrow into the mucosa.
 Because of the mechanical insertion into the intestinal wall,
patients lose weight rapidly as a result of malabsorption
and fluid loss.
 Longterm infections lasting weeks to months may result in
death attributable to a severe loss of electrolytes,
particularly potassium (hypokalemia), and associated organ
failure.
 Intestinal capillariasis initially manifests as
abdominal/gastrointestinal disease, which can become
serious if not treated because of autoinfection.
 A protein-losing enteropathy can develop which may result
in complications such as cardiomyopathy, severe
emaciation, cachexia, and death.
 In the first recognized outbreak of intestinal capillariasis,
the case fatality rate was over 10%.
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 Diagnosis is typically from the identification of eggs, adult
worms, or larvae in stool specimens.
 The eggs resemble those produced by T. trichiura.
 They are somewhat smaller with a thick, striated shell and
less prominent polar plugs.
 Female worms produce the characteristic thick-shelled eggs
as well as thin-shelled and free larvae.
 Anthelmintic agents including albendazole and
mebendazole are recommended.
 Adequate preparation and cooking of seafood, including
fish, snails, crabs, and shrimp in endemic areas, are
encouraged.
HOOKWORMS
 Hookworms are known to have a worldwide distribution
with two species known to infect humans, Ancylostoma
duodenale and Necator americanus.
 They are the second most common helmintic infection
reported in humans.
 The eggs and rhabditiform larvae of the two species are
indistinguishable.
 Differentiation of the species is based on the morphology
of the buccal capsule and the adult male copulatory bursa.
 Another category of a widespread nematode is the
hookworm (refers to a number of species), which is also a
roundworm and lives in the small intestine of its host. Its
eggs and worms are frequently found in the fecal
specimens of those infected with hookworms.
 The two major species, Ancylostoma duodenale and
Necator americanus, range over broad areas of both the
Old and the New World.
 These two species are much smaller than the large
roundworm called Ascaris lumbricoides and include
additional physical complications in the infected victim
through migration into the body’s tissues.
 Obstruction of the gastrointestinal tract that may be
experienced with an A. lumbricoides roundworm
infestation is less frequent in hookworm infestations.
 The most significant risk from hookworm infection is the
development of anemia, which is caused by depletion of
dietary iron, proteins, and iron supplements that are
absorbed in the digestive tract.
 The worms extract blood large amounts of blood and in
addition may damage the mucosa of the intestinal tract and
cause blood to appear in the feces.
 The blood loss through the tools may require testing for
occult blood, which is a condition caused by broken down
red blood cells that are not visible to the naked eye.
 It is possible to become infected with hookworms by direct
contact with contaminated soil, generally through walking
barefoot, or accidentally swallowing contaminated soil.
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 The adult stages of A. duodenale and N. 2. These released rhabditiform larvae grow in the feces and/or
americanus are seldom seen for identification, but they are the soil, and after 5 to 10 days (and two molts) they become
similar in appearance. filariform (third-stage) larvae that are infective.
 The eggs are indistinguishable as there is only a slight 3. These infective larvae can survive 3 to 4 weeks in favorable
difference in size between the two species. environmental conditions. On contact with the human host,
 The eggs of N. americanus are slightly larger than those of typically bare feet, the larvae penetrate the skin and are
A. duodenale and measure from 55 to 75 μm in length, with carried through the blood vessels to the heart and then to
a width of between 35 and 40 μm. the lungs.
 A.duodenale and N. americanus also differ in their 4. They penetrate into the pulmonary alveoli, ascend the
mouthparts or buccal cavities. The buccal capsule of A. bronchial tree to the pharynx, and are swallowed.
duodenale has visible teeth, whereas N. americanus has 5. The larvae reach the jejunum of the small intestine, where
specialized structures called cutting plates. they reside and mature into adults.
6. Adult worms live in the lumen of the small intestine,
typically the distal jejunum, where they attach to the
intestinal wall with resultant blood loss by the host.
7. Most adult worms are eliminated in 1 to 2 years, but the
longevity may reach several years.
NOTE: Some A. duodenale larvae, following penetration of the host
skin, can become dormant (hypobiosis in the intestine or muscle).
These larvae are capable of re-activating and establishing patent,
intestinal infections. In addition, infection by A. duodenale may
probably also occur by the oral and the transmammary route. A.
ceylanicum and A. caninum infections may also be acquired by oral
ingestion. A. caninum-associated eosinophilic enteritis is believed to
result following oral ingestion of larvae, not percutaneous infection.
N. americanus does not appear to be infective via the oral or
transmammary route.

LIFE CYCLE

1. Eggs are passed in the stool, and under favorable conditions

TABLE 6-1 DIFFERENTIATION OF N. AMERICANUS
(moisture, warmth, shade), larvae hatch in 1 to 2 days and
AND A. DUODENALE
become free-living in contaminated soil.
Genus and species Necator Ancylostoma
americanus duodenale

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New World Old Worm Stage Adult
Common name hookworm, hookworm Size Females 10-12 mm in length;
American Murderer male slightly shorter
Etiologic agent Necatoriasis, Ancytostomiasis, Shae Round and elongated with a
Uncinariasis Wakana disease long pointed tall
Infective stage Filariform larva Filariform larva Motility Not reported
Definitive host Humans Humans Other features Well-developed mouthparts for
Portal of entry Usually via skin Usually via attaching to intestinal mucosa
penetration rather ingestion rather
than ingestion than skin LABORATORY DIAGNOSIS
penetration  Hookworms are typically diagnosed by the presence of
Mode of Skin > Mouth Mouth > skin eggs or rhabditiform larvae found in stool specimens.
transmission  The eggs and larvae of the two species are
Habitat Small intestine Small intestine indistinguishable.
(jejunum, ileum) (duodenum,  The eggs are oval and thin-shelled and contain a clearly
jejunum) visible four- to eight-cell stage embryo.
Maturation in 49-56 53  There is a characteristic clear space between the shell and
Host (days) the developing embryo.
Mode of Oral attachment to Oral attachment to  Recovery and identification of eggs on direct smear or from
attachment mucosa by sucking mucosa by sucking concentration methods is recommended.
Mode of nutrition Sucking and Sucking and  Eggs may appear distorted on permanently stained smears.
ingesting blood ingesting blood
 The rhabditiform larvae are typically 250 to 300 µm with
Pathogenesis Larva-ground/dew Larva-ground/dew
a long buccal capsule and an inconspicuous genital
itch, creeping itch, creeping
primoridum.
eruption; adult-IDA eruption; adult-IDA
 The larger filariform larvae are approximately 500 µm,
Microcytic, Microcytic,
with a pointed tail and a esophageal to intestinal ratio of
Hypochromic Hypochromic
1:4.
Anemia Anemia
 Both the rhabditiform and filariform larvae must be
Laboratory Concentration Concentration
differentiated from S. stercoralis.
diagnosis methods and Direct methods and Direct
 Fresh stool stored at room temperature may result in
Fecal Smear Fecal Smear
continued maturation and hatching of larvae.
Treatment Albendazole, Albendazole,
 Larvae may be cultured according to the Harada-Mori
mebendazole, or mebendazole, or
method.
pyrantel pamoate pyrantel pamoate
Length of adult 5-9 for males; 9-11 8-11 for males; 10-
TREATMENT AND PREVENTION
shape for females 13 for females
Shape Head curved Head continuous in  Anthelmintic agents including albendazole, mebendazole,
opposite to same direction as and pyrantel pamoate are indicated. However, as a result of
curvature of body, the body variation in species and geographic distribution, some
giving a hooked agents may not be effective in a specific population of
appearance to parasites, and regional recommendations should be
anterior end followed because of potential drug tolerance or resistance.
Temp at which 20-35 15-35  Avoid contaminated soil and beaches.
90% of eggs hatch  Wear appropriate footwear such as enclosed shoes in
(C) potentially contaminated areas.
Diagnostic Semilunar cutting Male- Tripartite  As a result of the immunosuppressive activity associated
feature- adult plate; bipartite dorsal ray with the production of hookworm proteins, vaccination
dorsal ray may only be partially effective.
Diagnostic morula Same  Currently no preventive vaccine exists. However, a protein,
feature-egg ASP-2, secreted by infective larvae of N.
 americanus is being investigated as a potential recombinant
MICROSCOPIC DIAGNOSTIC FEATURE vaccine.
GENERAL CLASSIFICATION- HOOKWORM ADULT
Organism A. duodenale and N. STRONGYLOIDES STERCORALIS
americanus  Infection with Strongyloides stercoralis is less common
Specimen required Feces than other intestinal nematodes.

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 The organism is endemic in the tropics and causes a severe life-threatening condition called “swollen
subtropical regions of Asia, Latin America, and Africa. belly syndrome.”
 A limited geographic distribution exists in the United States
and Europe. LIFE CYCLE
 S. stercoralis, commonly referred to as the threadworm,
may inhabit the intestine or exist as a freeliving organism in
the soil.
 The life cycle can be classified as direct, indirect (free-
living phase), or autoinfective.
 The filariform (infective larvae) penetrate the skin and
migrate via the circulatory system to the heart and lungs.
 The organism enters the bronchial tree and then is
swallowed, where it lives in the digestive tract and matures
into an adult worm.
 In the intestine the filariform larvae may also penetrate the
mucosa, resulting in autoinfection.
 The female worm produces eggs by parthenogenesis (a
form of asexual reproduction where growth and
development occur without fertilization), because parasitic
adult male worms are nonexistent.
 Within the indirect life cycle, the rhabditiform
(noninfective) larvae develop into mature males and
eggproducing females.
The Strongyloides stercoralis life cycle is complex, alternating
 The free-living life cycle may revert to the production of
between free-living and parasitic cycles and involving autoinfection.
infective larvae at any time.
In the free-living cycle:
 S. stercoralis is transmitted via direct penetration in
1. Rhabditiform larvae are passed in the stool of an infected
endemic areas.
definitive host.
 Person-to-person transmission occurs within 2. Develop into either infective filariform larvae (direct
institutionalized groups, in day care centers, and among development) or free-living adult males and females that mate
homosexual men. and produce eggs.
3. From which rhabditiform larvae hatch and eventually become
infective filariform (L3) larvae
4. The filariform larvae penetrate the human host skin to initiate
the parasitic cycle.
5. This second generation of filariform larvae cannot mature into
free-living adults and must find a new host to continue the life
cycle.
Parasitic cycle:
1. Filariform larvae in contaminated soil penetrate human skin
PATHOGENESIS when skin contacts soil, and migrate to the small intestine.
 Infections may be asymptomatic or consist of a variety of 2. It has been thought that the L3 larvae migrate via the
disseminated strongyloidiasis syndromes. bloodstream and lymphatics to the lungs, where they are
 Reinfection is more commonly associated with eventually coughed up and swallowed. However, L3 larvae
immunocompromised patients. appear capable of migrating to the intestine via alternate routes
 Acute infections may develop a localized pruritic, (e.g. through abdominal viscera or connective tissue).
erythematous papular rash. 3. In the small intestine, the larvae molt twice and become adult
 Some patients develop a macropapular or urticarial (red and female worms.
raised) rash on the buttocks, perineum, and thighs. 4. The females live embedded in the submucosa of the small
 The migration of larvae may cause epigastric pain, nausea, intestine and produce eggs via parthenogenesis (parasitic males
diarrhea, and blood loss. do not exist), which yield rhabditiform larvae.
 Hyperinfection, an increased worm burden within the lungs 5. The rhabditiform larvae can either be passed in the stool, or can
and intestines, may occur. cause autoinfection.
 Disseminated infections may also result in larvae within the
central nervous system, kidneys, and liver. LABORATORY DIAGNOSIS
 A second species, Strongyloides fuelleborni, a primate
parasite, has been isolated from humans in Africa and

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 9 CLINICAL
SY 2021 - 2022

m
1st
BSMLS
MR. JOHN MARIO CALIGUIRAN,
RMT
 The rhabditiform larva is the primary the flariform larvae are more
diagnostic stage for strongyloidiasis in humans through slender than the rhabditiform
microscopic examination of stool. stage
 The larvae are 250 to 300 µm long with a short buccal Motility Rhabditiform larvae are motile in
capsule, a large bulb on the esophagus, and a prominent the soil and penetrate skin of
genital primordium. those coming in contact
 The filariform larvae are larger (up to 500 µm) and have a Other Features Free-living cycle in the soil may
notched tail with an esophageal to intestinal ratio of 1:1. revert to production of infective
 The eggs, which are rarely identified, are segmented with a flariform larvae
thin shell.
 S. stercoralis larvae are the most common found in human
stool specimens.
 Depending on the fecal transit time though the intestine and
the patient’s condition, both rhabditiform and rare
filariform may be present.
 If stool examination is delayed, embryonated ova may be
present.
 Parasite recovery from stool may be enhanced by the
Baermann funnel technique. TREATMENT AND PREVENTION
 The basic method is to wrap the sample in a paper tissue or  Ivermectin is the recommended treatment for
cloth and submerge it in a funnel filled with water. The uncomplicated infections.
nematodes will clump and sink to the bottom of the funnel  Albendazole is an alternative, but has not proven to be as
where they can be recovered. effective.
TABLE 6-2: DIFFERENTIATION OF S. STERCORALIS  Hyperinfection and disseminated conditions require
AND HOOKWORM LARVAE anthelmintic therapy in combination with broadspectrum
BUCCA BUL TAIL GENITAL antibiotics to prevent secondary bacterial enteric infections.
L B PRIMORDIU  In addition, patients taking immunosuppressive
CAVITY M medications should discontinue use during infection and
Hookworm- Long yes small treatment.
rhabditiform  Follow-up examinations are indicated and treatment should
Hookworm- Long no pointed be reinstituted if larvae are identified within 2 weeks
filariform following cessation of therapy.
Strongyloides- Short yes large  Immunocompromised individuals and patients taking
rhabditiform immunosuppressive medications should avoid
Strongyloides- Short no notched contaminated beaches and other areas.
filariform 

MICROSCOPIC DIAGNOSTIC FEATURE

GENERAL CLASSIFICATION- NEMATODAL
THREADWORM
Organism Strongyloides stercoralis
Specimen required Feces
Stage Most often the adult larval form
is the primary infective form as
the rhabditiform larva
Size Two form of larva; rhabditiform
larva are 200-250 um, which
show short buccal capsule
(mouth), prominent genital
primordium; flariform larvae are
approximately 500 um in length
and possess notched tall with
equal lengths of esophagus and
intestinal tract
Shape Larva are elongated and slender,
hence the term threadworms as

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