Introduction to Helminths

GENERAL CHARATRISTICS:-
1. Helminths are elongated flat or round worm like parasites measuring few
millimeters to meters.
2. Belonging to kingdom Animalia.
3. They are eukaryotic multicellular (Metazoa) and bilaterally symmetrical.

4. In general, helminths exist in three morphological forms—(1) adult form (or

the worm), (2) larval form and (3) eggs.
5. Based on their reproduction, helminths can be classified into the following:
a. Oviparous: Most of the helminths (Cestoda, trematodes and many

nematodes) are oviparous, i.e. after fertilization, the adult worm laid
eggs which develop then hatch.
b. Viviparous: Only few nematodes directly discharge the larval forms

after fertilization (e.g. filarial worm and Trichinella)

c. Ovoviviparous: They lay egg containing larva that immediately hatches

out (e.g. Strongyloides).

Various helminths have distinct morphology of eggs which can be used to
differentiate the helminths
6. They belong to two phyla of medical importance:-

1. Phylum Platyhelminthes (flat worms)— it includes two classes:

a. Class: Cestoda (tapeworms)

b. Class: Trematoda (flukes or diageneses)

2. Phylum: Nemathelminths: (Nematodes) (Round worms)

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 The classification of all the medically important helminths according to
their habitat in man is depicted in Table.

Properties Cestodes Trematodes Nematodes

Leaf-like and Elongated, cylindrical and
Shape Tape-like and segmented
unsegmented unsegmented
No sucker, no hooklets.
Suckers present, some Suckers present Some have
Head end
have attached hooklets No hooklets Well developed buccal
capsule
Complete from mouth to
Alimentary canal Absent Present but incomplete
anus
Body cavity Absent Absent Present
Monoecious
Sexes Monoecious Diecious
(except schistosomes)
Requires two hosts Requires one host
Requires three hosts
Life cycle (except Hymenolepis and (except filarial worms and
(except Schistosoma)
Diphyllobothrium) Dracunculus)
Cysticercus, Cercaria,
hydatid cyst metacercaria, Rhabditiform larva ,
Larva forms coenurus, cysticercoid, Redia, filariform larva and
coracidium, plerocercoid miracidium and microfilaria
and procercoid sporocyst
Intestinal nematodes:
- Ascaris lumbricoides
- Enterobius vermicularis
Hymenolepis nana
- Trichuris trichiura
- Hymenolepis diminuta
- Strongyloides stercoralis
- Echinococcus species Fasciola hepatica
Hookworms:
- Taenia saginata - Schistosoma spp.
- Ancylostoma duodenale
- Taenia solium
Blood & tissue nematodes
- Taenia Multiceps
(Filarial worms):
- Loa loa
- Wuchereria bancrofti

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 Phylum: Nemathelminths:
(Nematodes) (Round worms)

GENERAL CHARATRISTICS:-
1. Nematodes have cylindrical/filariform un-segmented bodies, with a body
cavity (pseudocele), in which all the viscera are suspended.
2. Their bodies consist of 3 layers, an outer tough layer which usually resist
digestion (cuticle/integument), a middle layer (hypodermis), & lastly an
inner somatic muscular layer which helps the worm to move by sinuous
flexion.
3. Their digestive system is complete, consisting of an anteriorly placed
mouth, leading to an esophagus, which varies in size & shape in different
types of nematodes, there is also an intestine which leads into the rectum &
eventually opens through the anus.
4. The nematodes are diecious (separate males & females).
5. Males are generally smaller than females, & their posterior end is curved or
coiled ventrally, while females have pointed posterior end.
6. In the male, the rectum & the ejaculatory duct both open into a common
cavity (cloaca).
7. In addition to the normal male structures, males also have copulatory
structures such as spicules, bursa, or both.

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8. Female nematodes may produce undeveloped eggs (oviparous), or larvae
(viviparous), & some lay eggs containing developed larvae which
immediately hatch out (ovoviviparous).

9. The life cycle of nematodes consists typically of 4 larval stages (L1

L4), & the adult form, the cuticle is shed while passing from
one stage to the other, this is called (molting).

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 Ascaris lumbricoides
(The largest intestinal nematode)

 Its name (lumbricoides) is derived from its resemblance to the

common earthworm (lumbricus).
 Largest worm nematodes.
Morphology:
A. Adult worm:
1. Female are larger & thicker than male.
2. Female ~20 – 35 cm in length, as thick as a lead pencil.
3. Male ~10 – 20 cm in length, more slender.

4. Creamy
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 white in color with pinkish cast & finely striated cuticle.
5. Mouth with three oval lips supplied with sensory papillae.
6. Club-shaped esophagus.
7. Male posterior end is curved & has 2 copulatory spicules.

B. Eggs:
Two types of eggs are passed by the female worms:
a. Fertilized eggs: (inseminated by a male): Oval, fertilized
ovum covered by an outer albuminous mamillated layer,
yellowish-brown (bile stained), inner thick hyaline layer.

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 b. Infertile eggs (unfertilized):
 Found in about two fifths of all infections & in absence of
male.
 Longer, narrower, contain a mass of protoplasm with refractile
granules.
 Thinner inner shell with irregular coating of albumin.
Sometimes, the outer albuminous coat is lost & the eggs
appear colorless & are known as (Decorticated eggs).
 Ascaris eggs are the most resistant eggs in soil; they can
survive for months in sewage/feces, & up to 4 years in the
environment/soil.
 Exposure to temperature down to -12C° has no effect on the
eggs.
 Eggs are resistant to chemicals (10% formalin stool
preservative, disinfectants) & desiccation (drying).
 Eggs are destroyed by temperature above 40C°, & exposure
to direct sunlight for ~15hrs.

(A) (B) (C)

Eggs of Ascaris lumbricoides (saline mount) (A) unfertilized egg; (B) fertilized egg;
(C) decorticated fertilized egg

Epidemiology:
Cosmopolitan, more common in:
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  Warm countries & where sanitation is poor.
 Where night soil (human excreta) is used for fertilization.
 Where pig manure is used as a fertilizer swine Ascaris
(Ascaris suum) intestinal obstruction.
-Same incidence in both sexes, more in children (bad hygiene).
Life cycle:
Habitat: Small intestine.
Infective stage: fully embryonated eggs.
Definitive host: humans.
 Adult worms inhabit small intestine of humans (85% jejunum,
15% ileum).
 They do not attach to the intestinal wall, rather they maintain their
position by constant movement upwards (thus they are frequently
found in stools).
 They obtain their nourishment from semi-digested food of the
host, which could cause malnutrition, especially in children.
 Female worm has an average daily output of 200,000 eggs, both
fertilized & unfertilized.
 Fertilized eggs are passed in feces immature/un-segmented, thus
freshly passed eggs are not infective, & cannot cause
autoinfection.
 These eggs can survive in the environment/soil for up to 4 years
waiting for favorable conditions (moist, O2, warm temperature
°
~20C – 30C°).
 Upon reaching soil, with the favorable conditions & within 3
st
weeks eggs become larvae (L1 = 1 stage Rhabditiform larva);
then larvae within eggs molt to become (L2 = 2nd stage
Rhabditiform larva).
 Man gets infected orally by ingestion of fully embryonated eggs
containing (L2 = 2nd stage Rhabditiform larva) through

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 contaminated hands, foods, water, or house flies transmitting
eggs to food.
 After ingestion, eggs hatch in the duodenum, & the Rhabditiform
larvae (actively motile) are liberated, they penetrate the intestinal
mucosa, & are carried out by blood or lymphatics to the right
side of the heart, then to the pulmonary circulation.
 Once they reach the lung, they are filtered out by the pulmonary
capillaries into the alveoli where they grow & molt twice to give
(L4 = 2nd stage filariform larvae) within ~2 weeks.
 Filariform larvae migrate through the respiratory passages to
reach the esophagus then the small intestine, where they molt
for the last time to reach maturity (adult worm).
 Females begin to lay eggs after ~2 months from the beginning of
the infection.
 -Life span of the worm is ~1 year.
Ascariasis:
 Usual infection, consisting of ~5 – 10 worms, often goes
unnoticed (asymptomatic), & it’s only discovered by routine stool
examination, or by discovery of an adult worm passed in the stool.

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 Life cycle of Ascaris lumbricoides
Clinical features due to migrating larva:
1. Larval migration may produce host sensitization resulting in allergic
manifestations, such as: pulmonary infiltration, asthmatic attack,
cough, moderate fever, with peripheral eosinophilia, this is
called eosinophilic pneumonia (Loeffler’s syndrome).
2. Large number of larvae migrating through lungs rupture of
pulmonary capillaries hemorrhagic pneumonia
3. Some larvae may reach the left side of the heart by the pulmonary
veins systemic circulation embolus to various organs.
Clinical features due to adult worms:
 Patients may complain of vague abdominal pain or dyspepsia.
 Malnutrition & growth retardation (especially in children).
Complications:

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  Serious & sometimes fatal effects of ascariasis are due to
(migration of adult worms), fortunately such migrations are not
common, & are induced by drugs (anesthesia), fever, & spicy
food.
 The worm maybe regurgitated, vomited, escapes through the
external nares, or rarely inhaled into the bronchus.
 Perforation of the intestinal wall, migration to peritoneal cavity
causing peritonitis.
 May come out through abdominal wall usually at umbilicus in
children & inguinal region in adults.
 Intestinal volvulus, intussusception, obstruction.
 Invasion of bile duct, gall bladder obstructive jaundice.
 Invasion of liver & appendix has also been reported.
 May occlude ampulla of Vater acute hemorrhagic pancreatitis.
 Worms may carry bacteria to these sites producing abscesses.
 The metabolites (by products) of living or dead worms produce
toxic manifestations in sensitized persons, such as: edema of
face, giant urticaria (hives), asthma, insomnia, loss of appetite
& loss of weight.
 Increased levels of immunoglobulins (IgG & especially IgE).
Diagnosis:
During migratory stage (Ascaris pneumonia):-
1. In sputum of bronchial washing we may find:
st
 3rd stage larvae (L3 = 1 stage filariform larvae).
 Charcot Leyden crystals.
 Eosinophils
2. Blood picture shows: eosinophilia.
3. X-ray (radiology): Transient patchy lung infiltrates.
During intestinal stage:-
1. Eggs in stool (or even adult worms).

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 2. X-ray (radiology): Barium meal shows worms as filling defects,
sometimes even the worms intestinal tracts are outlined as well
by the barium they have ingested.
3. Cholangiogram: may show the worms in the gall bladder or bile
duct.
Treatment:
1. Drug of choice: Albendazole (Zentel).
2. Mebendazole (Vermox) poorly absorbed from intestine.

3. Pyrantel pamoate (Combantrin) poorly absorbed from

intestine.
4. Piperazine citrate (Antepar) readily absorbed from intestine,

not used in renal or hepatic impaired function, or convulsion

disorder.
Note: Most of these drugs act by paralyzing the helminth, so the worm
loses its ability to move upstream in order to maintain its position and
then the peristaltic movement carries the worm out.
 Endoscopic removal of worms from biliary tract.
 In case of intestinal obstruction nasogastric suction until vomiting
is controlled, then after 1-2hrs initial dose of Piperazine is given
through nasogastric tube, & although Albendazole would seem the
logical choice for treatment of this complication, stimulation of
migratory activity might be a reason not to use it.
 If vomiting recurs, suction must be resumed, & additional doses may be
given.
 If there is no vomiting, second dose is given orally 24hrs after the first,
& repeated every 12 hrs.
 Surgical intervention is indicated if the obstruction is complete or in
cases of failed medical treatment.
Prevention:
 Avoid using night soil as fertilizer.

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 Enterobius vermicularis
(Oxyuris, pinworm, seat worm)

Morphology:
A.Adult worm:
1. Yellowish-white in color.
2. Cuticle expands at the anterior end forming a pair of cervical
alae.
3. Double bulbed esophagus (bulb shaped esophagus).
4. Female have a long sharply pointed tail (pinworm).

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 5. Male have a curved tail with a single spicule.

B. Eggs:
1. Oval, asymmetrical shaped.

2. Flattened at one side & convex at the other (D shaped).

3. Colorless (not bile stained).

4. Translucent shell with moderate thickness.

5. Eggs are very resistant to disinfectants.

6. Eggs contain developed larvae.

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Epidemiology:
 Worldwide, common in crowded areas.
 Whites more susceptible than blacks.
 Occurs in all socioeconomic levels.
 In all ages, but more common in children.
Life cycle:
 Definitive host: Humans are the only known host for this worm.
 Habitat:- Mature worms inhabit the Cecum (ileocecal junction)
& adjacent portions of both large & small intestines.
 Infective stage:- Fully embryonated egg containing first stage
larva (L1 = 1st stage Rhabditiform larva).
Gravid females, containing from 10,000 to 15,000 eggs migrate (usually
at night or rest time) to the perianal & perineal regions, where they
deposit their sticky eggs (eggs remain viable for 2 weeks).
Note: The male is seldom seen, as it does not migrate, & it usually dies
after mating.
Eggs mature (become infectious) within ~6hrs, they contain fully
developed larvae.
Fully embryonated egg containing first stage larva (L1 = 1st stage
Rhabditiform larva) is the infective stage.
Upon ingestion of eggs larvae hatch in the duodenum, then molt a
couple of times to reach maturity, & then descend to the cecum.
It takes ~4 - 6 weeks from ingestion of eggs to perianal migration
(oviposition).
Life span of the worm is ~2months (in absence of autoinfection).
Mode of infection:-
Man gets infected by:
 Foods & drinks exposed to contaminated dust.
 Airborne (inhalation).
 Auto-infection: patient scratch perianal area contamination of
hands & nails hand to mouth transmission.

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  Retro-infection: eggs hatch on perianal skin release of larvae
which crawl back into the anus then to the cecum & mature into
adults.

Life cycle of Enterobius vermicularis

Enterobiasis / oxyuriasis:
 About 1/3 of the infections are asymptomatic.
 Symptoms occur mainly in children & are more common in
females than in males.
 Perianal itching (pruritus ani) is the main & sometimes only
symptom, especially at bedtime.
 Scratching may lead to dermatitis.

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  Worm may wander into the female vulva, vagina, uterus,
fallopian tubes, sometimes even reaching the peritoneum,
where it may become embedded & die, leading to granuloma
formation around eggs or worms.
 May also cause ectopic vulvovaginitis or urethritis in
females.
 Invasion of appendix may occur  appendicitis.
 Other sites rarely involved are lung & liver.
 Other symptoms include: irritability, enuresis, insomnia,
grinding of teeth, poor appetite, abdominal pain, nausea &
vomiting.
 Eosinophilia is uncommon, but has been reported.
Diagnosis:
 Clinically suspected in children with nocturnal perianal itching,
or discovery of adult worms on the feces or on perianal region.
 Eggs in feces found only in 5% of infected persons.
 Eggs best obtained by swabbing perianal region in the
morning (before bathing or defecation) by using scotch/
adhesive/ cellophane tape technique (Graham technique).
 Graham technique: An adhesive tape is applied to the perianal
region, then spread on a microscope slide & examined; this
technique has to be repeated on 3 consecutive days because
of the irregular migration of gravid female.
 A number of commercial detection kits are available.
Treatment:
1. Treatment of entire family is needed.
2. Warm tap water enemas.
3. Drug of choice: Albendazole (Zentel), it should be repeated
in 2 weeks in order to kill any worms that might have
hatched from eggs.

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 4. Mebendazole (Vermox).
5. Pyrantel pamoate (Combantrin).
6. Piperazine citrate (Antepar).
7. Pyrvinium (Viprynium).
Prevention:
1. Washing hands & cut nails
2. Cleaning bed sheets & underwear of infected children.
3. Protect food from dust.

Trichuris trichiura
(Whipworm)

The name (Trichuris) means (hair-like tail), this name is not quite
correct, because it is the anterior end that is hair-like not the tail, the
name (Trichocephalus) which is correct, was later given, but the first
name has the priority.

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Morphology:
A. Adult worm:
1. An attenuated, anterior 3/5, which is colorless & traversed by a
narrow cellular esophagus (stichosome) resembling a string of
beads.
2. Thicker, pinkish-gray, posterior 2/5, containing intestine, & a
single set of reproductive organs.
3. Blunt posterior end of female & a coiled posterior end of male
which contain a single copulatory spicule & a retractile sheath.

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 B. Eggs:
1. Eggs are barrel or lemon shaped with plug-like, translucent, polar,
mucus, prominences.
2. They have yellowish outer shell (bile-stained), & transparent inner
shell.
3. Eggs are less resistant to desiccation, heat & cold, than Ascaris
eggs, yet they can remain viable in soil for several years.

Epidemiology:
 Worldwide distribution, but more common in tropical areas &
where sanitation is poor.
 Children are more affected.
 Environmentally coextensive with Ascaris.
Life cycle:
 Definitive host: It’s mainly human parasite, but some strains infect
monkeys & pigs.
 Habitat: Adult worms inhabit large intestine mainly cecum & to a
lesser extent appendix & colon down to rectum, embedding its
anterior end in the intestinal mucosa.
 Infective stage: fully embryonated eggs containing (L1 = 1st stage
Rhabditiform larva).
 Females produce 3000 to 10,000 eggs/day.
 These eggs pass in feces immature/un-segmented, thus freshly
passed eggs are not infective, & cannot cause autoinfection.
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 Upon reaching soil, with the favorable conditions (moist, warm,
shade) & within 3 weeks eggs become embryonated (L1 = 1st stage
Rhabditiform larva).
 Mode of infection: Man gets infected orally by ingestion of fully
embryonated eggs containing (L1 = 1st stage Rhabditiform larva)
through contaminated hands, foods, water, or house flies
transmitting eggs to food.
 In the small intestine, egg-shells gets digested, & activated larva
escapes from the egg.
 Larvae penetrate the intestinal villus & they remain in the intestinal
crypts for several days, where they grow & molt.
 Larvae then pass to the cecal area where they reach maturity.
 The developmental period from ingestion of eggs to oviposition by
females, takes ~1 - 3 months.
 Life span of the worm is ~4 - 8 years.

Life cycle of Trichuris trichiura

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Trichuriasis:
Asymptomatic in mild cases
In heavy chronic infections, anterior ends of the worms embedded in the
intestinal mucosa of the host, produce damage, leading to the following
signs & symptoms:
1. Blood loss (0.005ml/worm/day): the worms suck some blood, but the
hemorrhage that occurs at their site of attachment is the greater
source of blood loss, infection by 200 worms or more may cause:
 Iron deficiency anemia
 Dysentery & Tenesmus
 Growth retardation
2. Abdominal pain & tenderness.
3. Nausea & vomiting.
4. Anorexia & Weight loss.
5. Rectal prolapse: due to edema of rectum produced by worms
embedded in that area.
6. Appendicitis.
7. Moderate eosinophilia.
Diagnosis:
Finding characteristic lemon shaped eggs in the feces.
Treatment:
1. Drug of choice: Albendazole (Zentel).
2. Mebendazole (Vermox).
3. Anti-diarrheal: Loperamide (Imodium), help by increasing contact
time between the anthelmintic drug & the parasite.

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 Strongyloides stercoralis
(The smallest intestinal nematode)
(Dwarf threadworm)

Morphology:
A. Adult worm:
1. Colorless with finely striated cuticle.
2. Short buccal cavity leading to a cylindrical esophagus.
3. Gravid females have paired uteri containing 5-10 eggs each.
4. Males are not seen in human infections because they don’t have
penetrative power, therefore they don’t invade the intestinal wall.
5. It seems likely that the larvae produced by females while in the host,
develop (Parthenogenetically).

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B. Eggs:
1. Oval, thin-shelled, transparent.
2. Eggs of Strongyloides are ovoviviparous (segmented) eggs, i.e they
immediately hatch out to larvae.

Epidemiology:
 Prevalent in tropical & subtropical areas, where warmth, moisture, &
lack of sanitation favors its free living cycle.
 Cats & dogs may both be infected, human infections from a canine
source has been reported.
 Strongyloides fuelleborni Parasite of African monkeys.

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  Strongyloides fuelleborni kellyi infect mainly infants
swollen belly sickness treated by Thiabendazole
(Mintezol).
Life cycle:
Free living form inhabits the soil.
Habitat: Parasitic form inhabits the duodenum & upper jejunum of
humans, but in heavy infections the pylorus, small & large intestines,
the proximal biliary & pancreatic passages, all may be involved.
Definitive host: Humans.
Infective stage: filariform larva (L3).
Mature females (containing eggs) invade & embed themselves in the
intestinal mucosa.
This parasite has 3 types of life cycle:
1. Direct life cycle:
 Eggs are deposited in the intestinal mucosa by mature females.
 Eggs hatch into Rhabditiform larva (L1), then pass into the
lumen of the intestine & out with feces.
 In the soil & after 2 – 3 days of feeding, Rhabditiform larva molt
twice long, slender, non-feeding infective filariform larva
(L3).
Mode of infection:
Human gets infected by walking barefoot or coming in direct
contact with the soil containing the filariform larva.
 The infective filariform larva penetrates the human skin
venous circulation right side of the heart lungs
penetrate alveoli pass through respiratory passages
esophagus swallowed, reaching the small intestine.
 In the small intestine filariform larvae molt twice to become
mature, penetrate & embed themselves in the intestinal mucosa.
 Oviposition in ~1 month from the initial infection.
 Occasionally, some larvae may pass into the arterial circulation &
reach various organs of the body.

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2. Indirect (free-living) cycle:
 Rhabditiform larvae in the soil may develop into sexually mature
free-living males & females.
 Fertilization occur in the soil, after which females lay eggs that
hatch into Rhabditiform larvae which then molt twice
filariform larvae.
 These filariform larvae can either enter a new host, or repeat the
free-living cycle.
 The indirect cycle appears to be associated with optimal
environmental conditions as in tropical countries, whereas the
direct method is more frequently seen in less favorable colder
conditions.
3. Autoinfection:
 Rhabditiform larvae may feed & molt within the intestinal tract,
develop into filariform larvae then penetrate the intestinal
mucosa (Internal autoinfection), or perianal skin (external
autoinfection), where they enter the venous circulation &
complete rest of the cycle.
 Autoinfection is responsible for maintaining the infection as long
as 30 – 40 years.

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Strongyloidiasis (Cochin-China diarrhea):
 Many infections are light & go unnoticed (asymptomatic).
 Skin rashes & itching resembling (ground itch of hookworms) are
sometimes seen following penetration of skin by larvae (larva currens),
skin lesions due to penetration are generally minor, (hives) urticaria are
rare.
 Pulmonary lesions are generally not sever but in heavy infections,
patchy pneumonitis with larvae in the sputum may be seen, this
condition is associated with asthmatic type wheezing & cough,
resembling (tropical pulmonary eosinophilia seen in filariasis).
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 Moderate infections may cause burning mid epigastric pain &
tenderness (resembling peptic ulcer), nausea & vomiting, diarrhea &
constipation, protein malnutrition, malabsorption, steatorrhea.
 In heavy infections & if involving the large intestine, infection may give
rise to symptoms mimic that of ulcerative colitis (melena,
gastrointestinal bleeding, blood per rectum).
- Eosinophilia is common. - Total serum IgE is usually elevated.

Hyper infection Syndrome & Disseminated Strongyloidiasis:

 At times, normal life cycle of the parasite is altered, with an
increase in the proportion of Rhabditiform larvae that transform
into filariform larvae while still within the gut, this result in a large
increase in the worm burden.
 If only the gastrointestinal tract & lungs are involved, this
condition is known as hyper infection syndrome.
 When the number of migrating larvae is so great as to injure other
organs, beyond the gut & lungs, this is called disseminated
Strongyloidiasis.
 In these two cases, ulcerations of mucosa can be produced, along
with fibrosis & inflammatory infiltration of the submucosal layer,
gram-negative bacteria could also be observed in some cases.
 Patients with hyper infection syndrome usually present with fever,
gastrointestinal symptoms, dyspnea, wheezing, hemoptysis,
cough, & weakness.
 In disseminated strongyloidiasis, micro-hemorrhages may occur
around larvae disseminated to the CNS, granuloma surrounding
the larvae is also common in many affected organs.
Diagnosis: (Eggs are not the best method)
 Clinically (Suggestive): Atypical bronchitis/pneumonitis, followed in
few weeks by mucus/watery diarrhea, epigastric pain & eosinophilia.
 Larvae in sputum.
 Larvae in stools.

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  In severe diarrhea or with use of strong purgative eggs in stools.
 Stool concentration may be necessary.
 Barium meal x-ray in severe infection loss of mucosal pattern &
tubular narrowing (Pipe stem deformity).
 Eosinophilia in 10% - 40% of the cases, absent in hyper infection
syndrome.
 Other methods that help revealing larvae in stools:

Entero/string test Baermann technique

Agar plate culture Filter paper strip

Treatment:
1. Drugs of choice: Albendazole (Zentel) or Ivermectin.
2. Mebendazole (Vermox).
3. Thiabendazole (Mintezol) was the drug of choice, but it has a high
incidence of side effects.
Prevention:
 Avoid walking barefooted in soil.
 Wearing shoes & gloves while handling soil.

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 Hookworms
Ancylostoma duodenal

Morphology:
A. Adult worm:
- Cylindrical, whitish worm, its anterior end is bent dorsally, hence the
name (hookworm).
- Anterior end (buccal capsule) has 2 pairs of sharp teeth (4 teeth), & 2
plates.
- Worm uses these teeth & plates to cut & attach to the intestinal
mucosa.
- Male about 1cm in length, its posterior end has cuticular umbrella-like
expansion known as (Copulatory bursa) with 2 long spicules.
- Female about 1.3cm in length, it has 2 sets of genitalia, & its posterior
end is pointed.

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B. Eggs:
- Oval, transparent (not bile stained) surrounded by thin hyaline shell.
- When passed in feces, the eggs contain a segmented (but immature)
ovum, usually with 4 Blastomeres.
- There is a clear space between the segmented ovum & egg shell.

Epidemiology:
- Ancylostoma duodenal Present in Libya
- Necator americanus Not present in Libya (Central/South America)
- Widespread in areas where people defecate on the ground, don’t wear
shoes & handle mud.

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Life cycle:
- Habitat: Adult worms inhabit the small intestine (duodenum &
jejunum) of humans, & they maintain their position by attaching (via
their buccal capsule = teeth & plates) to the intestinal mucosa.
- Females produce ~20,000 eggs per day.
- These eggs pass in feces immature, thus, freshly passed eggs are not
infective, & cannot cause autoinfection.
- Upon reaching soil, with the favorable conditions (moist, warm, shade,
O2) & within few days, the immature embryo in the egg develops into
(L1 = 1st stage Rhabditiform larva).
- Rhabditiform larva hatch, then molt twice to form (L3 = 1st stage
filariform larva) which is the infective stage. (Infective stage)
Mode of infection:
- Humans get infected by:
 Walking barefoot or coming in direct contact with the soil
containing the filariform larva.
 Via GIT mucous membranes if larva is ingested in contaminated
foods or water.
 Trans-mammary or Trans-placental (rare).
- Filariform larvae penetrate the skin/mucous membranes venous
circulation right side of the heart lungs penetrate alveoli
pass through respiratory passages esophagus swallowed,
reaching the small intestine.
- Larvae molt in the small intestine to reach maturity & attach to
intestinal mucosa.
- Usually it takes ~5weeks from the time of infection until oviposition.

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 Ancylostomiasis:
1. Cutaneous phase (ground itch/dew itch):
 Begins when larva penetrate skin.
 Causing edema, erythema, macules, papules, urticaria, & pruritus.
 Its severity is proportionate to the number of infecting larvae.
 At times, pyogenic bacteria are introduced to the skin with the invading
larvae.
2. Pulmonary phase (Loeffler’s syndrome = eosinophilic pneumonia = larval pneumonitis):
- Pulmonary phase is usually asymptomatic, but in some cases, it gives rise to
Loeffler’s syndrome.
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 - Causing fever, dry cough, expectoration, wheezes, hemoptysis, petechial
hemorrhage, leukocytosis, & sore throat.
3. Intestinal phase (the most important phase):
- Begins with Painful eosinophilic enteritis, as a result of worms attachment
& their release of hyaluronidase, which degrades mucosa & erodes blood
vessels.
- Intermittent abdominal pain, loss of normal appetite, & desire to eat soil
(geophagy).
- Pica: ingestion of non-food substances as seen in anemic & hysterical
patients.
- Blood loss (intestinal hemorrhage) which is exacerbated by bleeding at the
sites of former attachment, & by anticoagulants produced by the worms.
- Blood loss per worm is ~0.2ml/day, patients with heavy infections may lose
up to 200ml of blood per day.
- With chronic infection:
 Chronic blood loss, depletion of iron stores, toxic products produced by
worms depresses bone marrow Microcytic hypochromic anemia
(iron deficiency anemia).
 Anemia Bone marrow hyperplasia.
 Anemia hypertrophy of the heart congestive heart failure.
 Hypoproteinemia generalized edema.
 Children may show physical, mental, & growth retardations, along with
cognitive impairments due to blood loss & malnutrition.
 Increase susceptibility to infections + Rapid progression of HIV.
Diagnosis:
- Stool examination for detection of eggs.
- Culture of stool to differentiate larva from that of Strongyloides.
- Fecal Occult Blood Test (FOBT).
Treatment:
- Iron supplements for anemia.
- Albendazole (Zentel). -Mebendazole (Vermox).
- Levamisole (Ergamisol) for mixed Ascaris & Ancylostoma infection.
Prevention:
- Avoid walking barefooted in soil.
- Wearing shoes & gloves while handling soil.
- Common sense.
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