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Phylum: Nemathelminthes
(Round worms)
Class: Nematoda
General characters:
1)Separate sexes
 Males smaller than females, and commonly has a
curved posterior end.
2)Un-segmented, elongated cylindrical, round worms.
3)Body cavity containing body fluid, in which the
digestive and genital systems float.
4)Size: varies from less than one mm to nearly one meter
in length.
5)The body wall is made up of 3 layers:
a. Outer laminated non cellular cuticle;
which may inflate anteriorly forming cervical alae
(Enterobius vermicularis) or posteriorly forming
copulatory bursa (Ancytostoma).
On the cuticle there may be papillae, expansions or
spines.
b. Thin syncytial layer or hypodermis that secretes
the cuticle.
c. Single muscular layer, divided into 4 quadrants by
the hypodermal lines, its arrangement varies in
different nematodes and helps in classification.
6) Digestive system:
A straight tube starting at the anterior head end,
by the mouth which is provided with facilities
for attachment e.g lips, teeth, and plates which
ends by the anus posteriorly.

Mouth leads to oesophagus, with tri-radiate
lumen (one dorsal and two subventral) ,varies in
shapes according to the species of the nematode
parasite, and helps in identification.
Types of oesophagus:
i-Cellular esophagus: a narrow row of cells
attached to the esophagus (Trichocephalus
trichiuris , Trichinella spiralis & Capallaria).
ii – Muscular: simple tube surrounded with a
straited muscular wall:
a) One segment:
i- Club- shaped oesophagus (Ascaris).
ii- Cylindrical esophagus (Filariae)
Club- shaped
Cylindrical
b.
Two segments:
1- Double – bulbed oesophagus, with anterior club
shaped portion and posterior spherical part
(Oxyuris = Enterobius vermicularis)
2- Rhabditiform oesophagus, with an anterior
cylindrical portion and pyriform posterior
portion and a narrow constriction in between
(Strongyloides stercoralis).
Double – bulbed
Rhabditiform
- After the esophagus is the intestine which proceeds
until it opens in the anus on the ventral surface in
female or it joins the genital duct which open in
cloaca in male (subterminal except in Trichiuris
and Trichinella).
7)
Reproductive organs:
Male: curved posterior end.
- In the form of single coiled convoluted tubule,
Testes followed by vas deferens, seminal vesicle
and finally opens by ejaculatory duct with the
anus in the cloaca posteriorly.
- The cuticle may show expansion (Copulatory
bursa) with or without spicules that help in
differentiation.
Female: - straight posterior end
One or 2 genital systems joining to open by a
single vagina in the vulva.
- Each has a glandular ovary→ oviduct→
receptaculum seminis →uterus and vagina.
 Egg of parasitic nematode may hatch in the
external environment and controlled by suitable
factors as temperature, moisture and oxygen. Or
it may hatch after ingested by the host and
stimulated by carbon dioxide tension, salts, PH
and temperature. In both types larva undergoes
4 molts until it becomes adult.
8 -Excretory system : consists of two longitudinal
lateral canals running in the lateral lines .
-the lateral canals join in terminal duct→
excretory pore in the region of the oesophagus.
9 - No circulatory system : the fluid in the body
cavity contain heamoglobin, glucose, proteins,
salts and vitamins that fulfill the function of
blood .
10- Nervous system: consists of nerve ring around
the esophagus and 6 nerve trunks pass to the
head and others to the posterior end.
-Sensory organs are in the labial, cervical, anal &
genital regions.
1) By ingestion of eggs:
o Directly infective when passed in stool
(Enterobius).
o Infective after a period of maturation outside
(Ascaris and Trichocephalus), by the larvated
eggs.
2) Ingestion of larvae:
o Larva itself: in Trichostrongylus colubriformes
and Hookworms through food and drink.
o Larva in muscles: Trichina capsule in muscles of
pigs.
o Larva in insect: Medina worm in cyclops.
3) Penetration of skin:
o Larval penetration: Hook worm and Strongyloides.
o Insect bite: Filarial worms.
•
Human nematodes are divided according to the
habitat of adult worms into:
Intestinal nematodes
Small intestine:
1.
Ascaris lumbricoides.
2.
Hookworms (Ancylostoma duodenal and Necator
americanus).
3.
Strongyloides stercoralis (Dwarf thread worm).
4.
Trichostrongylus colubriformis.
5. Capillaria philippinensis.
6.
Trichinella spiralis. (considered as both intestinal
and tissue nematode).
Large intestine:
1. Enterobius vermicularis.
2. Trichiuris trichiura.
Tissue nematodes
1.
2.
3.
4.
Filariae.
Dracunculus medinensis (Medina worm).
Larva migrans (visceral and cutaneous).
Trichinella spiralis (considered as both intestinal
and tissue nematode).
Intestinal nematodes
1) Ascaris lumbricoides
(The giant intestinal round worm)
Distribution:
 Cosmopolitan (more prevalent) in warm
regions with poor sanitation.
 Affect all ages but children are more
commonly and heavily infected by their
frequent exposure to contaminated soil.
Adult morphology:
1)
Long cylindrical with tapering ends.
2)
Pink or yellowish creamy in color.
3)
Finely striated cuticle.
4)
Mouth: at the anterior and, with 3 lips; one dorsal and two
subventral with a small triangular buccal cavity. Each lip is
provided with 2 sensory papillae and fine teeth.
5)
Esophagus: muscular club- shaped followed by the intestine
to open in anus in female and cloaca in male.
Female:
o
20-40 cm × 6 mm
o
with straight posterior end
o
two sets of genitalia
o
vulva at the junction of anterior and
middle thirds of the body ventrally.
Male:
o 15-20 cm × 3 mm
o posterior end curved ventrally
o one set of genital organs and 2 small equal
spicules
Ascaris male posterior end
Life Cycle:
Habitat: the adult worms live free in the small intestine
(jejunum). Each female lays 200.000 eggs per day
regularly. Its life span is about one year .
Definitive host: man .
Infective stage: egg
rhabditiform larva .
containing
a
second
stage
Stages in the life cycle: egg in the soil  larvated egg
(with 2nd stage rhabditiform larva) , ingested by
man larva adult in the small intestine .
Size
Shape
Fertilized
Unfertilized
60 × 45 µ
90 × 45 µ
Oval with 2 coverings:
1.Outer thick regular
albuminous
mammillations.
2.Inner thick egg shell.
Long and narrow Similar to
1. Less developed fertilized egg
thin irregular except that the
mammillated
albuminous
mammillations. layer is lost.
2. thin egg shell
Color Brownish
Content Immature ovum (one
cell stage)
Decorticated
brownish
Refractile
granules
N.B. The unfertilized eggs are found not only in the
absence of males but in about two fifths of all
infections,
since
repeated
copulations
are
necessary for the continuous production of fertile
eggs.
Ascaris lumbricoides -- the
human round worm
Ascaris
• Fully embryonated eggs are
swallowed and L2 hatches in
the stomach and penetrate
stomach or duodenal mucosa
• Larvae enter blood stream and
leave through alveoli into lung
• Larvae molt several times in
the lungs L3/L4 move up and
get swallowed
• 2-3 months after infection the
adult worms start laying eggs
(200,000 daily)
• Eggs are shed with the feces
and embryonate within 2-3
weeks
Eggs are voided with stool, mature in the soil after 2
weeks under suitable conditions (25ºc, humidity,
shade
and
oxygen),
develops
1st
stage
Rhabditiform larva within the shell. After one
more week, the larva molts into 2nd stage
rhabditiform larva within the egg (infective stage).
Methods of infection:
Ingestion of mature eggs containing 2nd stage
rhabditiform larva, contaminating food (green raw
vegetables), water or hands. Cockroaches and house
flies may carry the larvated eggs to human food
(mechanical transmission).
Inhalation of mature eggs to the nasopharynx.
- Egg hatches in the small intestine, liberating the
larva (freshly laid eggs with no larva inside are
not capable of causing infection).
- Rhabditiform larva comes out of the egg to the
lumen of the small intestine, penetrate the
mucosa to reach the circulation, carried to the
right side of the heart  pulmonary arteries 
lung. The larva breaks out of capillaries into lung
alveoli and moults twice (2nd and 3rd moults).
- The larva creeps along the bronchioles  bronchi 
trachea  larynx  pharynx, then swallowed to
reach the small intestine where it moults once (4th
moult and becomes adult).
- Eggs appear in feaces 2-3 months after infection.
- The life span of a female Ascaris in human body is
about one year, then dies. So if a person shows
infection with Ascaris for several years, it only
means that this person is continuously re-infected.
N.B. In massive infection, some larvae may reach the general
circulation to be filtered in various organs as abnormal foci
in: lymph glands, spleen, kidneys, brain or spinal cord.
When reaching the kidney they may find their way to urine
and attract attention. In such ectopic sites, larvae are
unable to grow to maturity and most of them are destroyed.
Pathogenesis and Clinical Manifestations
Disease: Ascariais:
The usual infection consisting of 5 – 10 worms, often goes
unnoticed by the host and is discovered on a routine stool
examination or by the discovery of an adult worm passed
spontaneously in stool.
The pathogenic effects of ascariasis are due to the following
mechanisms:
1.Allergic reactions to the parasitic stages.
2.Effect of the adult on host nutrition.
3.Mechanical effect of the adult worm.
4.Wandering larvae and adults.
5.Microorganisms carried with larvae during migration.
Migrating larvae:
1.Lung: In light infection, there is slight damage with unnoticed
pathological lesions.
In heavy infection, the migrating larvae in the lungs result in
lobular pneumonitis, there is cellular infiltration, serous exudates
and some haemorrhage causing cough and bronchial irritation,
(asthmatic attack), expectoration with blood stained sputum and
aedema of lips, microscopically the larvae may be detected in the
sputum, with many oesinophils .
2.General circulation: Occasionally some larvae reach the
general circulation and distributed to various organs as lymph
nodes, brain, spleen & kidneys (ectopic sites) leading to abnormal
clinical manifestations as a result of visceral larva migrans
Adult worm: in the intestine may cause abdominal discomfort
with distension, colic, diarrhea or constipation, vomiting and
dyspepsia due to production of anti-enzymes (anti-peptic and antitryptic substances that interfere with protein digestion).
1.Traumatic
a.In
effects:
heavy infection  intestinal obstruction.
b.Obstruction
c.Appendix
of the bile ducts by the worms  obstructive jaundice.
 appendicitis.
d.Obstruction
of ampulla of Vater  acute hemorrhagic pancreatitis.
e.Perforation of
intestinal wall  peritonitis.
f.Some
worms may ascend via the stomach and oesophagus to
the nasopharynx, enter the larynx causing suffocation especially
in children.
g.It may come out of mouth or nose or even go to Eustachian
tube from the pharynx resulting in damage of the middle ear.
2.Toxic
effects: metabolic by -products of living or dead worms
may give rise to fever, allergic manifestations (urticaria and
asthma)
and
nervous
irritability
(insomnia
and
even
convulsions)
3.Nutritional
impact: loss of appetite  malnutrition and
impairment of growth, with vitamin A and C deficiency.
Ascaris
• Infection depends on fecal
contamination of food, water or
soil
• Eggs are sensitive to sun light
but otherwise extraordinarily
resistant (ascarosides - special
glycolipids secreted by the
embryo)
• Fertilized eggs are shorter and
rounder than unfertilized
Ascaris
• Occasional pulmonary symptoms
• Intestinal phase mostly asymptomatic,
but worms can lead to malnourishment
in children
• Dangerous complications are mostly
observed in children under 10
• Volvulus, a mass of knotted worms
obstructing the intestine
• Penetration of the bile duct and liver by
adult worms
• Penetration of the intestinal wall,
followed by peritonitis
• Wandering and obstruction can be
linked to certain medications
Diagnosis
Clinical: symptom of intestinal ascariasis are indistinguishable
from those of other intestinal helminthic infections.
Laboratory
1. Detection of eggs in stool. (direct smear, after concentration,
Stoll’s technique).
2. Detection of migrating larvae in sputum or better in gastric
lavage contents.
3. Detection of adults passing out with or without stool or in
vomitus.
4. Eosinophilia (7 – 12%).
5. Radiology: Barium meal shows cylindrical filling defect
(string sign).
6. Biopsy.
Treatment
Drugs
Levamizol hydrochloride (Ketrax): 2 mg/kg as a single
oral dose
Mebendazole (Antiver, vermox) or Flubendazole
(Fluvermal).
Piperazine citrate, hydrate or adipate (parazine,
vermizine or uvilon).
Surgical
For treatment of complications e.g intestinal
obstruction, obstruction of appendix or bile ducts .
Control
1.
2.
3.
4.
5.
6.
7.
8.
Mass treatment of infected persons.
Sanitary disposal of excreta.
Health education.
Cleanliness (washing hands before meal).
Proper washing of green raw vegetables.
Pure water supply.
Control of flies and other insects.
Stool should not be used as a fertilizer unless being
treated by chemicals or temperature of 50°C or
higher to kill eggs.
Toxocara canis & Toxocara cati
These two species are ascarid parasites of dogs and cats. They
are cosmopolitan. Both are similar in biology and morphology
Adult Toxocara has three
lips and a pair of cervical
alae.
Mature male:
4-6 cm.
Mature female: 6-10 cm.
Toxocara eggs:
Dark brown with pitted shells
Size: 85 × 75 
Passes immature in dogs’ stool.
Life cycle:
– Puppies are infected through mother’s milk soon
after birth or prenatally.
– They remain susceptible to reinfection until sexually
mature, then acquire some resistance to reinfection.
Mode of infection in man:
• Accidental swallowing of larvated eggs of Toxocaca
by man with contaminated food ,drink or hands 
Visceral larva migrans.
• The 2nd stage rhabditiform larvae hatch in the small
intestine, pierce the mucous membrane and are
carried with blood to the liver, lungs, brain, eyes,
heart and other tissues where they produce
eosinophilic granulomatous lesions. Larvae remain
for several weeks or months without any growth or
development till they die.
Enterobius vermicularis
(Oxyuris, pinworm, seatworm)
Geographical distribution:
o Cosmopolitan, more common in children than
adults.
o More common in temperate and cold climate
than hot climate because of less frequent
bathing and changing of under wears.
Morphology:
oTranslucent cuticle, finely transversely striated.
oThere are 2 wings like expansions (cervical alae) at the
anterior end. The mouth with 3 small retractile lips,
followed by small buccal cavity.
oThe oesophagus: double- bulbed . Intestine opens by the
anus ventrally, some distance from the posterior end.
Female: 1cm with a long thin sharply pointed tail
occupying about 1/3 total length (hence the common
name pin worm), 2 sets of genital organs and vulva at
the junction of the anterior fourth with the rest of the
body.
Male: shorter than female 0.5 cm, its posterior end curved
ventrally, one set of genital organs that open with the
anus in the cloaca and one spoon- shaped spicule.
Eggs:
• Size:50x25µ
• Shape: plano-convex
• Shell: 2 layers and covered by a
3rd outer thin albuminous sticky
layer.
• Colour : colourless.
• Contents: fully developed larva.
female
male
Life cycle:
o Habitat: Adult worm live in the caecum,
appendix and adjacent parts of small and large
intestine .
o Definitive host: Only man.
o Infective stage: fully embryonated eggs
containing fully developed larvae when laid, so
eggs are immediately capable of starting
infection when swallowed.
o The adults are short lived (40-50 days)
o the male dies after fertilization and expelled with
feces
o the gravid fertilized female migrate down the
bowel (especially at night) when eggs are fully
developed and come out of the anus to lay eggs
around the anus and peri-anal region.
o Each female deposits about 10.000 eggs then dies
after laying all its eggs. So continuous infection
means repeated swallowing of eggs causing
infection to go on.
o It takes 2-4 weeks to complete the life cycle (from
time of swallowing eggs till eggs laid by the
female).
Mode of infection:
o Ingestion of eggs through contaminated food and drink .
o Autoinfection: movements of female to peri-anal region at
time of egg deposition causes intense irritation and itching 
eggs are carried under finger nails to the mouth after
scratching of peri-anal skin (anus to mouth infection), this can
be discovered in about one- third of infected children .
o Retro-infection: eggs hatch on the peri-anal region and larvae
migrate back through the anus to the rectum and caecum .
o Air- borne infection: eggs can fall in the underwear and in the
sheets and blankets.
o Contact with patients (Direct hand to hand or indirect contact
by handling contaminated articles as clothes, bed linens, toilet
seats, door knobs )
Pathogenisis and clinical picture of Enterobiasis,
Oxyuriasis:
oPerianal irritation, with nocturnal itching and
enuresis, insomnia, irritability, restlessness, neurosis
and inability to concentrate
oPruritus ani due to:
1- Nocturnal migration of the female worm on the
perianal skin
2- Skin sensitization due to worms ruptured during
scratching
3- Straitions on the cuticle.
4- Sticky material on the eggs.
Pathogenisis and clinical picture
– Vaginitis and salpingitis, with irritation,
vaginal discharge, and even granuloma
around eggs or worms.
– Irritation of intestinal mucosa with minute
ulcers, haemorrhage and 2ry bacterial
infection at site of attachment.
– Obstructive appendicitis.
Diagnosis:
o Clinical.
o Laboratory:
• Detection of adult worms in feces or on the peri-anal
region.
• Detection of eggs:
a. In stool: seldom found, unless uterus of gravid female
ruptures during migration to the peri-anal region.
b.In urine of female patient.
c. On peri-anal region by swab, which must be done early
in the morning before defecation or bathing and should
be repeated for several days before the patient is
considered free.
Types of swabs:
–Scotch adhesive tape swab.
–Vaseline swab.
–N.I.H. (National Institute of Health) swab.
Treatment:
o Mebendazole
(vermox),
Pyrantel
pamoate
(Combantrin) or Flubendazole (Fluvermol): as
single oral dose
* a 2nd dose must be given after 2 weeks to prevent
re-infection.
o Local: mercurial ointment is applied to the perianal skin especially at night relieve itching and
kills females that come out to deposit eggs and
prevent dispersal of eggs.
Control:
– Mass treatment of the whole companions
of the infected person.
– Personal cleanliness.
– Protection of food and drink from
contamination by dust and hands of
patients.
Adult Pinworm:
Life Cycle:
Females in perianal region:
Trichuris trichiura
(Trichocephalus trichiurus)
Whipworm
Geographical distribution:
• Cosmopolitan, more common in worm moist
regions.
• More sensitive to the effect of desiccation and
direct sun light than Ascaris.
Morphology :
Adult body is demarcated into
• an anterior thin part or whip-like (3/5) contains a cellular
oesophagus, and
• a posterior thick part bluntly rounded (2/5) contains the rest
of organs.
Male : 3-4 cm. in length
• coiled posterior end
• single copulatory spicule inside a retractile sheath
• terminal cloaca.
Female : 4-5 cm. in length
• straight blunt posterior end
• has one set of genitalia
• the vulva opens at the junction of thin and thick parts.
• Anal orifice is terminal
FEMALE
MALE
T. trichiurus egg
• Barrel-shaped.
• Yellowish-brown.
• 50 X 25 µ.
• Thick-shell.
• Bipolar mucoid plugs.
• Contains an immature embryo.
• The egg requires 3-5 weeks for
the larva to develop inside and
become infective.
Life Cycle
• Habitat: large intestine mainly the caecum but is also
found in the appendix and lower ileum.
• Definitive host : man.
• Reservoir host: some mammals.
• Stages in the life cycle: Egg→larva → adult .
• Infective stage: egg containing first stage larva.
• Method of infection: Ingestion of larvated egg with
contaminated food and drinks.
• The female is oviparous.
• Number of eggs deposited/female/day is about 2000 eggs.
Ova pass with stool 2 months after infection.
• Life span: 4-6 years.
The adult parasite T.trichiurus deeply embedding its
thin anterior portion into the sub-mucosa.
Pathogenicity and clinical manifestations of
Trichuriasis:
o Light infection is asymptomatic.
o Heavy chronic infection manifests with:
• Frequent, small, blood-streaked diarrheal stools.
• Abdominal pain and tenderness.
• Dysentery.
• Rectal prolapse.
• Hypo- or hyperchromic anemia.??
• Appendicitis.
•Protein loosing enteropathy.
• Intestinal wall perforation and peritonitis.
•Eosinophilia (30-60 %) in acute heavy infection.
Diagnosis:
o Clinical: difficult.
o Laboratory.
•Stool examination for the characteristic egg
(diagnostic stage). Ova should be quantified
since light infections may not require treatment.
•Proctoscopy: The worms can be seen attached
to the inflamed and ulcerated rectal mucosa.
Treatment:
– Mebendazole (Vermox or Antivir) or
Flubendazole (Fluvermal).
Control:
– Treatment of infected patients.
– Sanitary disposal of human stool.
– Strict hygienic measures for hands, food
and drink.
– Control of house fly.