UNIT – THREE

HELMINTHS
Learning objective

At the end of this unit the students will be able to:

 Define helminths
 Describe the general features of helminths
 Describe the taxonomic classification of
helminths
Outline

 Introduction to helminths
 General features of helminths
 classification of helminths
3.1. Introduction to Helminths

Medical helminthology: study of these parasitic

worms and their medical consequence

Helminths derived from the Greek word

“helminths” or “helminthose” meaning worm
 Helminths……………..

 Either free living or parasitic organisms belonging to

phylum:
 Nemathelminthes(round worm)

 Platyhelminthes(flat worm ),

 Aacanthocephala (spinyheaded worms )or

 Aannelida (segmented worm )

 3.2.General features of helminths

Multicellular forms with specialized organs

 Adult worms vary in size (6mm->10m)

 Their life cycles may be simple or complex

 Pathology, clinical sign and symptoms:

 Depend on the location of the organisms

 May be caused by adults, larva, or egg

HELMINTHS………….

 Laboratory diagnosis mainly depends on

 Detection and identification egg , larva or

embryo and rarely adults

Classification of helminths
 Summary

 Define helminths

 Define medical helminthology

 Describe the general features of helminths

 Classify helminths
Helminths……………….

The next topic will be on Nemathelminths

HELMINTHS……………

4. Nemathelminths
 Learning objective

At the end of this unit the students will be able to:

 Describe the general epidemiological aspects of
nematodes
 Discuss the characteristics of each nematode
 Explain the life cycle of each nematode
 Apply the necessary laboratory procedures for
the detection and identification of nematodes
 Outline
 General features of Nemathelminths
 Burden and impact on human life
 Classification of nemathelminths
 Intestinal nematodes
 General features
 For each species:
 Epidemiology , morphology, transmission life
cycle , clinical features, laboratory diagnosis
treatment, prevention& control
 N
4.1. General features of Nemathelminths

 Round in cross-section

 Unsegmented

 Digestive system complete

 Possess mouth, oesophagus and anus

 Have separate sexes

Nemathlminths……………..

 Can be oviparous/ovoviviporous/viviparous
 Egg (ova) -Larva(L1-L4)-Adult

 Possess a shiny cuticle (smooth/spined/ridged)

 Mouth is surrounded by lips or papillae

Nemathlminths……………
 Have Four larval stages
4.2. Burden and impact on human life
 ≈ 500,000 spp.
globally
• Most are free
living
 Abundant pathogens
in life-stock and pets
 Important pests of
many crops
 Cause numerous
human diseases
•The warm regions of the world = worm regions.
•High burden
•In the rural villages
•unsanitary overcrowded cities
•'big three' (Ascaris, Trichuris & Hookworm) is common
•Temperate and cold climates are not spared.
 4.3. Classification of Nemathelminths
 INTESTINE NEMATODE  BLOOD & TISSUE
 Small intestine NEMATODE
 Ascaris  Adults or larval stage in
lumbricoides tissue
 Hook worm
 Filaria –
 Wuchereria bancrofti
 Strongyloides
 Brugia malayi
stercoralis
 Large intestine  Onchocerca volvulus
 Trichuristrichuria  Loa loa
 Enterobius  Trichinella spiralis,
vermicularis  Draconculus medinensis
Cont…
 Animal nematode of less medically important or
low occurrence
INTESTINAL NEMATODE BLOOD & TISSUE
 Toxocara catti & NEMATODE
Toxocara cani  M. ozardi,
 A. canninum & A.  M. peristance,
braziliens  M. stereptocerca
 Cappilaria species
 S. fulliborni
 Trichostrongylus
species
 4.4. INTESTINAL NEMATODES
General features

 Live in gastro-intestinal tract

 In humans, often spread by poor hygiene related to

feces

 Most species are geo-helminths (soil transmited)

 Female worms are oviparous

 Humans are the only or major host of intestinal nematode

 eNe
 Transmission:

 Ingestion of infective egg

 Larva penetrating skin
 Laboratory diagnosis:
 Egg in faeces ( most often)
 Larva in faeces
 Recovering egg in the skin around the anus
 Occasional adult worms: A. lumricoudes, E.
vermicularies
 Cont…
 It includes
 Ascarislumbricoides
 Trichuris trichiura

 Enterobius vermicularis

 Strongyloides stercoralis

 Ancylostoma duodenale

 Nectator amircanus

 Before becoming adults in their human host, the larvae of A.

lumbricoides, S. stercoralis , and hookworms have heart lung
migration
 4.4.1. Ascaris lumbricoides
 Also known as large intestinal round worm

 the first human helminth recorded in chinse

medical literature(about 300-200 B.C.)

Epidemiology
 world wide
1.45 billion people are infected annually

WHO estimated it resulted in 60,000 persons death

in 1995
Ascaris……..
Ascaris………….
 Transmission and Life Cycle

 Transmission
 A. lumbricoides is spread by faecal pollution of
soil
 Infective stage:- egg containing 2nd stage larva

 A person acquire infection by

1- Ingestion of food or water contaminated with
infective eggs

2-eating soil(geophge) frequently seen in children

Ascaris…………

3-putting contaminated finger or toys with infective

egg in to mouth

4- rarely by inhalation of eggs carried in air

 Ascaris……………
 The infection is common in areas with
 high density of human population

Poor sanitation

Habit of people to defecate

indiscriminately in and around settlements

Use of infected faeces as fertilizer

 Life cycle
 Fully embryonated eggs are swallowed & L2
hatches in the stomach & penetrate stomach or
duodenal mucosa

 L2 enter blood stream & leave through alveoli into

lung

 Then molt several times in the lungs to L3/L4

 Then move up and get swallowed

Ascaris……………..

 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
Ascaris…………….
 Ascaris……………
Pathogenesis:
1. “Verminous” pneumonia, lung tissue damage
due to migratory larvae.

2. Bowel obstruction - too many adult worms.

3. Parasite secretes trypsin inhibitor, prevents host

from digesting proteins.

4. Aberrant migration of “irritated” adult worms to:

a. Common duct
b. Liver
c. Pharynx
d. Peritoneum
 Ascaris.................

 With heavier worm

loads a tangled mass
of worms can obstruct
the bowel, or an
individual worm can
block a duct
Laboratory Diagnosis
A. Finding and identification of eggs in the stool.
 Direct wet mount
 adequate for detecting moderate to heavy

infections
 concentration technique may be used In light
infection, Sodium chloride floatation technique &
Formolo-ether concentration technique

B. Adult worms occasionally passed in the stool or

through the mouth or nose
Ascaris…………

C. Larvae can be identified in sputum or gastric

aspirate during the pulmonary
 migration phase (examine formalin-fixed
organisms for morphology
 The diagnostic form is the egg in feces. Unmated females
lay non fertilized eggs.
Ascaris……………..
5 types of Ascaris eggs in stool
A. Fertilized Egg With Double Shell
 Size: about 70m
 Shape: oval, or some times round
 Shell: The two layer are distinct,
rough , brown, covered with little
lumps
 external shell and smooth,
thick, colorless internal shell.
 Colour: brown external shell, and the
contents are colorless or pale yellow.
 Content: a Single rounded granular
central mass.
Ascaris…………….

B. Unfertilized Egg With

Double Shell
 size: 80-90m
 shape; more elongated
(elliptical)
 shell: brown, puffy external
shell and thin internal shell.
 content: full of large round
very refractile granules
Ascaris………….
C. Semi-decorticated Fertilized Egg
Similar to Type A but With out the
external Shell
 Shell: single , smooth, thick and
colourless or very pale yellow.
 Content: a single rounded
colourless granular central mass.
Ascaris……………

D. Semi-Decorticated  Ascaris…….
Unfertilized Egg
 Shell: a single smooth thin
colourless shell (double line)
 Content: large rounded
colourless refractile
granules.
Ascaris…………
E. Embryonated Egg
 Ascaris…………..
Treatment
Mebendazole

Prevention and Control

1.Prevention of infection by
 washing hands before eating & trimming finger

 Avoid eating uncooked foods such as vegetables

Ascaris……….

2. Preventing soil become faecally polluted by

 sanitary disposal of faeces in
latrines
 avoiding the use of night soil as a
fertilizer

3.Treatment and health education

• Mass de-worming programmes repeated at 3-6
month intervals, have been advocated in areas of
high prevalence
 4.4.2.Trichuris trichiura
 Common name : whipworm, due to the whip-
like form of the body.

Epidimology
 The third most common round worm of
humans worldwide

 Infections
more frequent in areas with tropical
weather and poor sanitation practices, and
among children
Trichuris…………
~ 112 billion cases world-wide

 ~ 1.05 billion people are infected annually

 In Ethiopia
 One national survey showed 36.1%

 On
study in central and northern plateaus:
mean prevalence of 49%
 Trichuris…………
Habitat
 Adult:
large intestine (caecum) and
appendix

 Eggs: In the faeces, not infective when

passed
 Trichuris………….
Morphology
 Adults: whip-like shape, anterior 3/5th of the worm
resembles a whip & the posterior 2/5 th are thick
Male : Size 30-45 mm , coiled tail
Female: 35-50mm, straight thick tail
Trichuris……………..
Egg:
Size: 50-54m
Shape: "tea tray eggs” or
barrel- shaped with a
colorless protruding mucoid
plug at each end
Shell: fairly thick and smooth,
with two layers & bile stained
Color: yellow brown
Content: a central granular
mass which is Unsegmented
ovum
 Trichuris…………

 Transmission and life Cycle

Transmission
 Ingestion of embryonated egg in

contaminated water , food or from

contaminated hand

life Cycle
 The unembryonated eggs are passed with the
stool of infected individuals
Trichuris..............

 Mature within three weeks of being deposited in

soil.
require a warm, moist environment with
plenty of oxygen to ensure embryonation
The embryonated eggs are extremely
resistant to environmental conditions

 When embryonated eggs are swallowed larvae are

released into the upper duodenum

 then attach themselves to the villi of small intestine

or invade the intestinal walls
Trichuris…………….

 After 3-10 days they move down to the caecum &

ascending colon where they mature into adult
worms
 The adult worms are fixed with the anterior

portions threaded into the mucosa

 The females begin oviposit 60 to 70 days

after infection& shed 3,000 - 20,000 eggs per
day

 The life span of the adults is about 1 year

Clinical features
 Are largely determined by the worm burden:

 < 10 worms are asymptomatic (99% asymptomatic)

 Heavy worm burden

 Mechanical damage to the intestinal mucosa

 Chronicprofuse mucus and bloody diarrhea with

abdominal pains and edematous prolapsed
rectum
Trichuris……………..
 Anaemia from blood loss and iron deficiency,
malnutrition, weight loss and sometimes
death
Each adult worm sucks about 0.005
ml of blood per day

 Rarely a child will develop congestive cardiac

failure because of anaemia and fluid retension
hypoproteinemia and oedema
Trichuris vulpes (dog whip worm in
the intestine of an infected dog
The diagnostic stage is the egg in fecal samples.
Trichuris…………….
Laboratory diagnosis
1.Finding of characteristics egg in faeces

2. Sigmoidoscopy may enable visualisation of worms

Treatment
 Mebendazole

 Treat the iron deficiency anaemia

Prevention and Control : the same as described for

A. lumbricodes
 4.4.3. Enterobius vermicularls
. Common name: “Pin Worm” or “threadworm” or “
seat worm”

Epidimology
 occurs world-wide

 Children (5-14 years ) are more commonly

infected than adults

 Occur in group living together

Entrobious…………..

 Pinworms eggs can

be spread throughout
a house and difficult
to eliminate.
 Small children are
most apt to pick them
up during the
“teething stage.”
 Entrobious………………

 In Ethiopia : 5 % school children in rural

communities in Gonder region had
E. Vermicularis eggs under their finger nails
and that only 0.5% of them were found to shed
eggs in the stool

 Recent studies done using routine stool

examination method, a prevalence rate up to 1%
were reported
 Entrobious……………
Habitat
 Adult: Caecum & appendix
 Gravid female: Caecum & rectum
 Eggs: deposited on perianal skin & occasionally
in faeces

Morphology
 Adults: Color: yellow white
Male: Size 2-5mm Coiled tailed
Female: 8-13mm, thin pointed tail
Morphology of Enterobius vermicularis adult
female

They are small white worms with pointed tail

swollen cuticle at anterior end prominent
esophageal end bulb
 Entrobious……………..
 Egg
Size: 50-60m
Shape: oval but flattened
on one side, rounded
on the other side
Shell : Smooth and thin
but with double shell
Content: either a small
granular mass or a
small curved up larvae
Entrobious................
Transmission and Life cycle

Transmission

 Person –to- person transmission(ingestion and

air borne)
 Eggs remains viable 20 days

 Autoinfection

 Retro infection
Life cycle
 Ingestion embryonated eggs, usually carried on
fingernails, clothing, bedding or house-dust.

 Eggs hatch in stomach, larvae migrate to caecal

region where they mature into adults

 Copulation takes place in the caecum

 Gravid females migrate nocturnally outside the anus

and oviposit on the perianal area
 1 pin worm lay over 10,000 -15,000 eggs eggs /day
Entrobous……………..
 With in 4-6 hours being laid the egg contain
infective larvae

 Perianal itching from the eggs Induces scratching,

and hence the eggs are transmitted to the mouth on
the fingers

 Retroinfection, or the migration of newly hatched

larvae from the anal skin back into the rectum

 interval from ingestion of infective eggs to

oviposition by the adult females is about one month

 The life span of the adults is about two months

Clinical features
 Nocturnal anal pruritis.
 The cause of this is unknown, but may be related to
the intensity of the infestation, and/or an allergic
reaction to parasite

 Sleeplessness, because of the irritation

 Vulvovaginitis, and even urethritis may occur

in girls when migrating worms lay their eggs
in these sites
 Abdominal pain or appendicitis resulting from
the worms are considered to be very rare
Adult Pinworms on the perianal skin
Egg of E. vermicularis and scotch tape preparation
Laboratory Diagnosis
1.Finding eggs from perianal skin using adhesive
tape or swab method

 Done by pressing transparent adhesive tape

("Scotch test", cellulose-tape slide test) on the
perianal skin and then examining the tape
placed on a slide.
 Alternatively, anal swabs or "Swube tubes" (a
paddle coated with adhesive material) can also
be used.
 Collect sample in the morning, before
defecation and washing,
 The “Scotch Tape
Test”
 place a piece of
Scotch Tape on the
anal area.
 The tape is placed on
a slide and examined
under a microscope
for the flat sided eggs.
Entrobious…………………

2. Finding eggs in the faeces

 Eggs can also be found stool, but less
frequently

 Lessthen 10% found in stools, i.e. not a useful

examination;

 occasionallyeggs can be found in the urine or

vaginal smears
Entrobious……………….

3. Finding of female worms from perianal skin

or faeces
 Adult worms are also diagnostic, when found
in the perianal area, or during ano-rectal or
vaginal examinations
 Entrobious……………..

Treatment
 Pyrental Pamoate or Mebendazole

Prevention and Control

1.Treating all members of a family in which

infection has occurred

2. Wearing tight-fitting cotton pants to infected

children
 Entrobious……………..

3. Washing of the anal skin each morning

4.Washing of clothing worn at night

5. washing hands after using toilet and before

eating , avoidance of putting fingers in the mouth
& trimming finger
 4.2.4.Strongyloides stercoralis
 Common names: name: Dwarf thread
worm

Epidemiology
 Found worldwide

 An estimated 50 to 100 million cases

 Favors warmer tropical and subtropical

climate
Strongyloides……………
 Strong. Ster. Cont.
 In Ethiopia
 not highly prevalent in most areas and is

found in the same geographical areas with

hookworm
 rates up to 44% reported from 41 of the

50 communities in central and northern

Ethiopia
 The infection is rare or absent in many

arid lowland areas, including the Ogaden

and pastoral areas in the Awash Valley
Strong. Ster. Cont.

 Worms can be free-living

in the soil or live in a host.
 The definitive host is
humans, but may also affect
other primates and dogs
Strong. Ster. Cont.

 S. stercoralis show the following characteristics

1. Parasitic males are absent
2. Parasitic females are present in the submocusa
of small intestine which produce egg
parthenogenically
3. Can develop in to free living generation in the
soil out side the human host
4. Has internal out infection
Habitat
 Has both free living and parasitic generations
 Parasitic Adult females: buried in the
mucosal epithelium of the small intestine of
man

 Rhabditiform larvae: Passed in the faeces

and external environments

 Filariform larvae: soil and water the infective

stage
Strong. Ster. Cont.

 Free living male and female : on external

environment

 Egg : laid in the sub mucosa of small

intestine
Morphology
The size and shape of the worm are dependent
on whether it’s parasitic or free-living.

• Free-living females – 1 mm by 60 µm
• Parasitic females – 2.2 mm by 45 µm
• Eggs – 55 µm by 30 µm:as soon as they
are laid in sub mucosa, the rhabditiform larvae
Larvae
Rhabditiform larvae Filariform larvae
(non-infective form) (pathogenic form)
Morphology-Larva
 Rhabditiform Larvae  Filariforml Larave
 Size: 200-300m  About 600-700m
long ; 15m thick  Cylinderical
 Motility: very actively esophagus
motile in the stool  Bifid tail end
 Tail: Moderately
tapered
 Short buccal cavity
and rhabiditiform
esophagus
 Transmission and Life cycle
 Transmission
1. Commonly by penetration of skin by filariform larva

2. Ingestion of food or water contaminated with

filariform larva( oral rout)

3. Rarely: Transmamary & Organ transplantation

4. Autoinfection with rhabidit form larva

 Strong. Ster. Cont.

Life Cycle
 Complex , Two types of cycles exist:
1.Free-living (indirect) cycle
Rhabditiform larvae(stool) molt 4x free-
living adult males and females produce eggs

rhabditiform larvae develop to free living

adult males or females

Filariform larvae(this initiate parasitic life cycle)

 Strong. Ster. Cont.

2.Parasitic (direct) cycle

Rhabditiform larvae(stool) molt 2x develop
to filarifrom penetrate skin lung Alveolar
space bronchial tree pharynx
swallowed &develop to adult female in small
intestine(molt 2x) produce egg by
parthenogenesis which yield rhabditiform larvae
Strong. Ster. Cont.

 Autoinfection, the rhabditiform larvae become

infective filariform larvae in the host
tissue ,penetrate

intestinal mucosa (internal
autoinfection) or perianal area (external
autoinfection)
Life cycle

Parasitic life cycle

Free-living cycle
Clinical feature
 It is usually asymptomatic, in symptomatic cases
 People with weaker immune systems

such as elderly people and children

are more susceptible
1.Cutaneous phase
 large number of larva produce itching and
erythema at the site of infection within 24 hours of
invasion

2.Pulmonary phase: The migratory larva in the

lung producing bronchopneumonia and full blown
pneumonitis
3. Intestinal phase : Invasion by adult worms may
produce abdominal pain and mucus diarrhea ,
nausea vomiting and anemia

Auto- and hyper-infection syndromes

 characterized by massive larval invasion of the lung
or any other organ including CNS, which is fatal

 occurs when the immune status of the host

suppressed by either drugs, malnutrition or the
concurrent diseases
Laboratory Diagnosis
1.Finding the larvae in faeces or in duodenal
aspirates using direct or concentration method
by microscopy
 In hyper-infection syndrome the larva may

be found in sputum, urine and in other

specimens
 Examination of serial samples may be

necessary because direct stool

examination is relatively insensitive
 Strong. Ster. Cont.
 The stool can be examined in wet mounts:
 Directly

 After concentration (formalin-ethyl acetate)

 After recovery of the larvae by the baermann funnel
and water emergence semi-concentration
technique

 After
culture by the harada-mori filter paper
technique

 After culture in agar plates

 Strong. Ster. Cont.

2. Serological tests
 Antibody Detection

 Indicated when the infection is suspected and the

organism cannot be demonstrated by:
 duodenal aspiration, string tests, or
 by repeated examinations of stool
 Use antigens derived from filariform larvae for the
highest sensitivity and specificity
 EIA) s currently recommended because of its
greater sensitivity (90%).
 IFA and IHA tests can be used
Treatment
Ivermectin or thiabendozole

Prevention and Control

1.Sanitary disposal of faeces in latrine
2. avoid use of night soil as a fertilizer

3. Wearing protective footwear

4.Treatment of infected individuals and Health

education
 Properly dispose of
human wastes.

Wear Shoes.

…Don’t eat dirt.

 Strongyloides fuelleborni

Geographical Distribution

 Widely distributed in Zimbabwe, Zambia, Papua

New Guinea, co-exists with S.stercoralis in
Ethiopia

 It is a common parasite of old world monkeys ,

apes &dog
 Strong. Ster. Cont.

Transmission and life cycle

Transmission
 Skin penetration by filariform larvae
 Transmammary

Habitat:-Has both free living and parasitic life

Life cycle
 similar to S.stercoralis except it shed eggs in the
feaces
 Strong. Ster. Cont.
Pathology and treatment: similar to S.stercoralis

Laboratory diagnosis
 Finding eggs in fresh stool specimens

Egg:-Resembles eggs of hookworms but are

shorter and smaller
-Colorless, Oval and 50 by 35μm in size
-Contain partially developed larvae
 N.B. If there is a delay in examining the feaces , the larva
will hatch
 Strong. Ster. Cont.

Prevention and Control

 The same as described for S. stercoralis
 4.2.5. Hook Worms
 Are hematophagous nematodes

 Two major species

Ancylomstoma duodenale
Necator americanus

 Less important : A. ceylanicum, A.

braziliense ,A. caninum , A.tubaeforme, A.
buckleyi
Epidimology
 widely distributed throughout the tropics and
subtropics

 more than 1 billion people are infected world-

wide

 cause daily blood loss of 7 million liters

 Most commonly infected are children,

agricultural workers and miners
 Ancylostoma is found in Europe around the
Mediterranean, on the West coast of South
America and in parts of China and India

 Necator is found over much of the western

hemisphere, Africa and South East Asia
 In Ethiopia : Necator americanus are more
common than Ancylostoma duodenale

highest infection rates: Ilubabor,

Kefa ,Welega

A.duodonale is associated with areas of

poor soil coverage and high rate of
drainage

N.americanus is found in red soil areas

on flat plain
 Altitudeand moisture is the major factor
affecting their distribution

 Hook worm infection is absent in low ,hot

dry areas of Ethiopia and above 2500m alt
Habitat
 Adult:
Jejunum and less often in the duodenum
of man

 Eggs: In the faeces; not infective to man

 Rhabditiform and filariform larvae: free in soil

and water
Morphology : Adult
A.duodenale N.americanus
pathogen city more pathogenic less pathogenic

Size longer and thicker short and thinner

male 8mm 7-9mm
female 10-13mm 9-11mm

Buccal capsule large and oval small and round

Jaw like teeth cutting plates

Buccal cavity short,10-15 m long ,15-16 m in

in length length
lumen is large lumen is short
 A.duodenale N.americanus
Shape of head slightly conical rounded

Esophagus-
Intestinal junction no gap gap
 Head is slightly bend
(hook) and
 the mouth carries
characteristic teeth
(Ancylostoma) or
plates (Necator)
 The posterior end of
the male worm is
elaborated into a
copulatory bursa
 Teeth in their buccal cavity enable their
attachment to intestinal mucosa - from where
they suck their host's blood

 The worm's mean life span Is 1 - 3 years, and

Egg:
 2x egg are produced by A. duodenale
(20,000egg/day) than N. americanus

Size : 65-40m
Shape: oval
Shell: very thin and appears as black line
Colour: the cells inside are pale gray
Content: contains an ovum which appears
segmented usually 4-8 blastomeres
 Rhabiditiform Larvae Filariform Larvae
1.Size 250-500m 600- 700 m

2.Bucal cavity long short

3.Oesophages 1/3 body length 1/4 body length

4.Tail Pointed end Sharply pointed

end
Hookworm rhabditiform larva Hookworm filariform larva
Life cycle
 Eggs are passed in the stool , and under favorable
conditions (moisture, warmth, shade),

 rhabditiform larva larvae hatch in 1 to 2 days in the

feces and/or the soil

 After 5 to 10 days (and two molts) they become

become filariform (third-stage) larvae that are
infective
 larvae can survive 3 to 4 weeks in favorable
environmental conditions.
 On contact with the human host, the larvae
penetrate the skin and are carried through the
veins to the heart and then to the lungs

 They penetrate into the pulmonary alveoli, ascend

the bronchial tree to the pharynx, and swallowed

 The larvae reach the small intestine, where they

reside and mature into adults
 they attach to the intestinal wall with resultant
blood loss by the host
Clincal features
 arise from a combination of intestinal
inflammation and progressive iron/protein-
deficiency anemia

 Most individuals with hookworm infection are

asymptomatic (90%)

 high loads of the parasite(20 - 100 worms)

coupled with poor nutrition (inadequate intake of
protein and iron) eventually lead to anemia
 Skin penetration and associated secondary
bacterial infection can result in “ground itch”

 Pulmonary phase is usually asymptomatic

 Intestinal phase: adult worms attach to the

mucosa and feed on blood. Worms continuously
move to new places exacerbating bleeding
continued

 Hookworms on
the bowel
mucosa
Hookworms
 The main concern with hook
worm disease is blood loss
 0.03 ml (N.a.) to 0.26 ml (A.d)
per worm,
 up to 200 ml per day in heavy
infections
 Chronic heavy infection results
in anemia and iron deficiency
 Together with malnutrition
infection can severely stunt
growth and development in
children
 Anemia leads to weakness and
fatigue in adults
 Symptoms of hookworm infection depending on the site at which the
worm is present and the burden of worms

Table 2. Clinical features of hookworm disease

Site Symptoms Pathogenesis

Cutaneous invasion
Local erythema, macules,
Dermal and subcutaneous
papules (ground itch)
migration of larva
Bronchitis, pneumonitis Migration of larvae
Pulmon
and, sometimes, through lung,
ary
eosinophilia bronchi, and trachea
Attachment of adult
Gastro- Anorexia, epigastric pain
worms and injury to
intestina and gastro-intestinal
upper intestinal
l hemorrhage
mucosa
Iron deficiency, anemia,
Hematol
hypoproteinemia, edema, Intestinal blood loss
ogic
cardiac failure
Laboratory Diagnosis
1.Finding eggs in faeces
 A.duodenale and N.americanus eggs
morphologically indistinguishable
 Microscopic identification of eggs in the stool is the
most common method
 The recommended procedure:

1. Collect a stool specimen.

2. Fix the specimen in 10% formalin.
3. Concentrate using the formalin–ethyl acetate
sedimentation technique
4. Examine a wet mount of the sediment.
The diagnostic stage is the egg in the feces.
Eggs of both species look the same
 freshly passed faeces should be examined

 If more than 12 hours old ,a larva may be seen

inside the egg

 If more than 24 hours old ,the larva hatch

 hookworm : deep buccal cavity
 S. stercoralis : shorter buccal cavity
Eggs that can be mistaken with hookworm
egg

 Trichostrongylus species
 Ternidens deminutus

 S. fuelleborni

 oesophagostum species
 Trichostrongylus species : pseudo-hook
worms

- mainly parasites of ruminants, equines

and rodents

-a person becomes infected by ingesting

third stage larvae in contaminated food
or drink
- The adult worm live in small intestine with head
penetrating the mucosal wall and suck blood

- Egg: passed in faeces

 longer and thinner than hook worm egg,
measuring 85-115 μm in length
 More pointed at on or both ends

 Usually appears more segmented

Trichostrongylus eggs
 Ternidens deminutus

parasite of monkey and baboons
 Transmission is by ingesting third stage larva
 Adult worm : in the large intestine
 Suck blood and anemia( in heavy infection )
 egg in faeces has similar structure with hookworm , but
much larger , measuring about 85 μm in length and
contains more cells
 oesophagostum species
 Infection by ingesting infective larva

 Larvaedevelop in large intestine where they form

nodules and abscesses

 Adult : leave the nodule and attached to intestinal

wall

 Eggs is about the same size of that of hookworm,

but is passed in advanced stage of development
2.PCR
 For diagnosis of A.duodenale infection
 Epidemiological studies and monitoring of

success of control programs

3. Serological tests (IgG and IgE)

Treatment
 Pyrantel pamoate, Mebendazole or
Thiabendazole
 if anemic : high protein diet supplemented with
ferrous sulphate, folic acid and vitamin B12

Prevention and control

 As described for Strongyloides stercoralis
 Larva migrans
1. CUTANEOUS LARVA MIGRANS
2. VISCERAL LARVA MIGRANS
3. OCULAR LARVA MIGRANS

1. CUTANEOUS LARVA MIGRANS

 Caused by larvae of cat hook worm (Ancylostoma
braziliense) & dog hook worm (Ancylostoma
caninum) in man

 Commonly seen in children in the tropics and sub

tropics
 The filariform form larva are able to infect by skin
as well as by mouth

 When the larvae invade the skin , the produce

itching papule which become creeping or extending
red linear skin lesions in the skin within 2 or 3 days

 Movement of larva may extend the lesion several

millimeters/day
 Image 037_02. Cutaneous Larva Migrans. Cutaneous larva migrans lesions of the foot of a 10-
year-old girl. In the United States this dog and cat hookworm infection is most commonly seen
in the southeastern states. These raised, serpiginous, pruritic, migrating eruptions may extend
rapidly.

Red Book Online Visual Library, 2006. Image 037_02. Available at:
http://aapredbook.aappublications.org/visual. Accessed December 7, 2007

Copyright ©2006 American Academy of Pediatrics

 Image 037_01. Cutaneous Larva Migrans. Cutaneous larva migrans lesions on lower leg
(caused by hookworm larvae of Ancylostoma braziliense and Ancylostoma caninum).

Red Book Online Visual Library, 2006. Image 037_01. Available at:
http://aapredbook.aappublications.org/visual. Accessed December 7, 2007

Copyright ©2006 American Academy of Pediatrics

 Image 037_05. Cutaneous Larva Migrans. Cutaneous larva migrans infection of the foot in an
adolescent male

Red Book Online Visual Library, 2006. Image 037_05. Available at:
http://aapredbook.aappublications.org/visual. Accessed December 7, 2007

Copyright ©2006 American Academy of Pediatrics

 Image 037_04. Cutaneous Larva Migrans. Adult who noted a migrating skin lesion on left thigh
for 2 weeks.

Red Book Online Visual Library, 2006. Image 037_04. Available at:
http://aapredbook.aappublications.org/visual. Accessed December 7, 2007

Copyright ©2006 American Academy of Pediatrics

Laboratory diagnosis
 Can be made by inspection of lesions along with the
characteristics history of exposure

Treatment
 Oral or topical application of thiabendazole or DEC

Prevention and control

 Deworming of cats and dogs
 Removed of vagrant cats and dogs from areas of
human habitation
2. VISCERAL LARVA MIGRANS
 Migration of larval nematodes of the
 dog ascarid (Toxocara canis ) ,

 the cat ascarid (Toxocara catis )

 larave don't complete their normal cycle of

development as their movement is arrested at
some level of the human body
 Toxocara canis

 the dog ascarid

 Larvacauses visceral larva migrans(VLM)

(toxocariasis or toxocaral disease) & ocular
larva Migrans(OLM) (granulomatous
opthalmitis) in man

 Causes a common infection in dogs through out

the world

 Infection rates in dogs varies from 2-90%

 Adult are in small intestine of canid: dogs , fox
 high egg production, larvae in egg
capsules for long periods of time

 Human ,especially children, & rodents can be

paratenic hosts; they harbor migrating larvae

 Human become ingested by ingesting infective

egg
 children playing with puppies or in parks or in
other areas contaminated with dog faeces , are
particularly at risk
Life cycle
 In dog is similar to that of Ascaris lumbicoides in
man

 Unembroynated egg passed in faeces

 it requires further maturation outside the host

 The infective egg ingested by dog, rodents and

human and the larvae hatch in small intestine
 In puppies younger than 5 weeks , the larvae
complete migratory and developmental cycle
similar to that of Ascaris lumbicoides in human
host and grow to adult in the intestine

 In adult puppies , adult dogs or human host ,the

larvae unable to complete their development

 In these hosts , the larvae may wander in the tissue

for some time and encyst as second stage larvae
 In pregnant bitches , dormant L2 larvae excyst/
reactivated by hormonal change and cross the
placenta to grow to adult worm in the fetuses

 In human the L2 which hatch in the gut , migrate

through tissues causing VLM or if trapped in the
eye ,OLM
VISCERAL LARVA MIGRANS(VLM)

 In the course of migration ,they cause

eosinophilic inflammation followed granuloma
formation around dead larvae

 Characterized by persistent eosinophilia in the

peripheral blood ,fever & often occurring along
with the involvement of the lung or liver or both
Ocular Larva Migrans (OLM)
 is potentially more serious as the retina may
damaged and in extreme cases may result in
loss of visions or sever ocular inflammation
 Toxocara catis
 The cat ascarid

 Cosmopolitan distribution

 It’s life cycle similar to Toxocara canis except there is

no transplacental transmission

 It’s egg develop to L2 in earthworm, cockroaches , mice

& dogs

 Cats become infected by ingesting mice harboring

larvae in their tissues

 Larval T. cati infection in human rarely cause VLM

Laboratory diagnosis of VLM
 Findingof larvae in biopsies, especially liver, but
larvae are only rarely found

 Serological tests using L2 of Toxocara as an

antigen

Treatment
 Thiabendazole & DEC

 Corticosteroids:
sever pulmonary , myocardial&
eye inflammation
Prevention and control
 Antihelminthic treatment of dogs

 Excluding dogs from children playing areas

 Improve sanitation ,education , Safe water

supply & Chemotherapy to interrupt transmission
infective egg to water, food or human hands
 summary
1. write the common name, infective and diagnostic
stage of all intestinal nematodes

2. List the possible sources of specimen for the

diagnosis of intestinal nematodes

3. Discuss the main differences between

rhabiditiform and filariform larvae of hook worm
and S.stercoralis.
5.List intestinal nematodes do not have heart lung migration
in their life cycle?

6. What are the difference between adult N. americanus and

A. duodenale ?

7. mWrite the prevention and control of intestinal nematodes

8. Define larvae migrans

9.List the causative agents of larva migrans