Helminthes

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

Int…
 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
Higher, 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

Laboratory Diagnosis
 Laboratory diagnosis mainly depends on detection and
identification egg , larva or embryo and rarely adults

HELMINTHES
NEMATHELMINTHES
(NEMATODES)
PLATYHELMINTHES
TREMATODES CESTODES
Classification of helminths

General features of Nemathelminths
 Round in cross-section
 Unsegmented
 Digestive system complete
 Possess mouth, oesophagus and anus
 Have separate sexes

Features…
 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

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.
•The burden of disease is not evenly spread within
developing countries
•The majority of worms are found in the poorest sections of
the community, compounding poverty, and social
deprivation.
•High burden
•In the rural villages
•unsanitary overcrowded cities
•'big three' (Ascaris, Trichuris & Hookworm) is common
•Temperate and cold climates are not spared.

Classification of Nemathelminths
 Intestine nematodes
 Adults or larval stage in the
intestine
 Small intestine
 Ascaris lumbricoides
 Hook worm
 Strongyloides
stercoralis
 Large intestine
 Trichuris trichuria
 Enterobius
vermicularis
 Blood & tissue nematodes
 Adults or larval stage in
tissue
 Filaria –
 Wuchereria bancrofti
 Brugia malayi
 Onchocerca volvulus
 Loa loa
 Trichinella spiralis,
 Draconculus medinensis

Animal nematode of less medically important
or low occurrence
INTESTINAL NEMATODEs
 Toxocara catti &
Toxocara cani
 A. canninum & A.
braziliens
 Cappilaria species
 S. fulliborni
 Trichostrongylus
species
BLOOD & TISSUE
NEMATODEs
 Mansonella ozardi,
 M. peristance,
 M. stereptocerca

INTESTINAL NEMATODES
General features
 Humans are the only or major host of intestinal
nematodes
 Live in gastro-intestinal tract
 Often spread by poor hygiene related to feces
 Most species are geo-helminthes (soil transmitted)
 Female worms are oviparous

Pathogenesis
 Major source of chronic ill health
 Compromising the growth potential, and
intellectual achievements of children all over the
world

Life cycle
 Intestinal nematodes share similar life cycles
that have evolved in response to new ecological
niches
 The core nematode life cycle involves
development from an egg through 5-stages of
growth.
 The 1st 4-stages(L1, L2, L3, L4) are larval
 The 5th & final stage of development is a
sexually mature adult worm.
 At each stage the cuticle of the parasite moults.

Transmission
 Usually only two sites of entry for intestinal
nematodes infecting humans:
 Ingestion of infective egg
 Larva penetrating skin
Laboratory diagnosis:
 Eggs ( most often) and Larvae in faeces
 Recovering egg in the skin around the anus
(perianal area)
Occasional adult worms: A. lumricoudes, E.
vermicularies

Cont…
 Intestinal nematodes infecting humans includes
 Ascaris lumbricoides
 Trichuris trichiura
 Enterobius vermicularis
 Strongyloides stercoralis
 Ancylostoma duodenale
 Nectator amircanus

Ascaris lumbricoides
 Also known as large intestinal round worm
 Is a member of the family Ascoridoidea
 Possess a mouth that has three conspicuous
lips
 Are pathogenic in their adult stage
Epidemiology
 world wide

1.45 billion people are infected annually
WHO estimated it resulted in 60,000 persons death
in 1995

 In Ethiopia
ranges from 17% to 77.7%
Highest rate in school children (2/3rd)
Distributions affected by altitude and
climate
was 29% in highlands, 35% in the
temperate areas and 38% in the
lowlands

A.lumbricoides…
 Habitat
Adult: In the small intestine
Egg: In the faeces
 extremely resistant to adverse
environmental condition and
chemicals
 remains viable in soil and dust
for up to 10 years

Morphology….
 Adult worm is a long whitish pink cylindrical worm
tapering at both ends, curving ventrally in the
male
 Females reach 49cm with a diameter of 3-6mm
 Males are much smaller, slightly more than half of
the size of females.

Morphology….
Males:
 have one or two copulatory spicules, but no
bursa copulatrix, Usually no caudal alae
 Female worms produce up to 240, 000eggs/day,
which corresponds to just under 3000eggs/gram
of faeces.

Egg
 Ascaris eggs vary widely in size and appear in
two forms:
I. Fertilized:
golden brown, ovoid and mammilated
about 30-40µm wide & 50-60µm long with a
dense outer irregular shell & a more
translucent regular inner shell.
The thick external mammilated layer is often
lost, giving a decorticate appearance -

Eggs….
 Evidence of segmentation or embryonation is
often seen.
II. Unfertilized: is larger & more elongated with a
length of about 89-95µm and 40-50µm width
 The internal structure of the egg is poorly
differentiated

Transmission and Life Cycle
 Transmission
A. lumbricoides is spread by faecal pollution of
soil
Is favored by conditions that improve the survival
of eggs in the soil, in particular warm moist shady,
conditions
Infective stage: embryonated egg (egg containing
2nd stage larva)

Transmission…
A person acquires infection by
1- Ingestion of food or water contaminated with
embryonated eggs
2-eating soil(geophge) frequently seen in children
3-putting contaminated finger or toys with infective
egg in to mouth
4- rarely by inhalation of eggs carried in air

Transmission….
 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 larvae
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

Life cycle….
 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

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;
common duct, liver, Pharynx, peritoneum

Pathogenesis…
 With heavier worm
loads a tangled mass
of worms can obstruct
the bowel, or an
individual worm can
block a duct

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
& Formol-ether concentration technique
B. Adult worms occasionally passed in the stool or
through the mouth or nose

Lab diagnosis….
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 unfertilized eggs.

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.
 Color: brown external shell, & the
contents are colorless or pale yellow.
 Content: a Single rounded granular
central mass.

Ascaris eggs….
B. Unfertilized Egg With Double
Shell
 size: 80-90m
 shape; more elongated
(elliptical)
 shell: brown, puffy external
shell & thin internal shell.
 content: full of large round very
refractile granules

C. Semi-decorticated fertilized egg
Similar to Type A but With out the
external Shell
 Shell: single , smooth, thick
and colorless or very pale
yellow.
 Content: a single rounded
colorless granular central
mass.
Ascaris eggs….

Ascaris eggs….
D. Semi-Decorticated
Unfertilized Egg
Shell: a single smooth
thin colorless shell
(double line)
Content: large rounded
colorless refractile
granules.

Ascaris eggs….
E. Embryonated Egg

Treatment
 Mebendazole, 200 mg, for adults and
 100 mg for children, for 3 days is effective.

Prevention and control
1.Prevention of infection by
 washing hands before eating & trimming
finger nails
 Avoid eating uncooked foods such as
vegetables

Prevention…
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

Trichuris trichiura
 Common name : whipworm, due to the whip-like
form of the body.
Epidemiology
The third most common round worm of humans
worldwide
Infections more frequent in areas with tropical
weather & poor sanitation practices, and among
children

~ 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%

Habitat
 Adult: large intestine (caecum) & appendix
 Eggs: In the faeces, not infective
when passed
Morphology
Adults: whip-like shape, anterior 3/5th of the worm
resembles a whip & the posterior 2/5th
are thick
Male : Size 30-45 mm , coiled tail
Female: 35-50mm, straight thick tail

Eggs
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

Transmission and life Cycle
Transmission
 Ingestion of embryonated egg in
contaminated food, water, or from
contaminated hand
life Cycle
 The unembryonated eggs are passed with the
stool of infected individuals

Life cycle….
 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

Life cycle…..
 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/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
 Chronic profuse mucoid & bloody diarrhea
with abdominal pains &
 edematous prolapsed rectum

Clinical features….
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, fluid retention
hypoproteinemia & oedema

The diagnostic stage is the egg in fecal samples.

Laboratory diagnosis
1.Finding of characteristic eggs in faeces
2. Sigmoidoscopy may enable visualisation of
worms
Treatment
 Mebendazole, 200 mg for adults &
 100 mg for children, for 3 days is effective.

 Sanitary disposal of faeces in latrine
 Avoidance of the use of night soil as a fertilizer
 Treatment of infected individuals and health
education.

Enterobius vermicularls
. Common name: “Pin Worm” or “threadworm” or “
seat worm”
Epidemiology
 occurs world-wide
 Children (5-14 years ) are more commonly
infected than adults
 Occur in group living together

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

Epidemiology….
In Ethiopia :
 5 % school children in rural communities in Gondar
region had E. Vermicularis eggs under their finger
nails and that only 0.5% of them were found to
shed eggs in the stool
 in routine stool examination method, a prevalence
rate up to 1% were reported

Habitat
 Adult: Caecum, appendix and adjacent
portions of the ascending colon
 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

They are small white worms with
pointed tail
swollen cuticle at anterior end
prominent esophageal end bulb

Morphology…
 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

Transmission and Life cycle
Transmission
 Person –to- person transmission: occur through
handling & sharing of contaminated clothes or
bed linens
 through surfaces in the environment that are
contaminated with pinworm eggs
 Self (Autoinfection) - occurs by transferring
infective eggs to the mouth with hands that have
scratched the perianal area

Transmission …
 Children who suck their fingers are more likely to be
infected
 Exposure to viable eggs on soil (Ingestion)
 Air borne: Some small number of eggs may become
airborne and inhaled
Eggs remain viable 20 days
 Autoinfection
 Retro infection may occur after hatching on the anal
mucosa

Life cycle
 Ingestion of 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

Life cycle…..
 With in 4-6 hours being laid the egg contain
infective larvae
 Perianal itching from the eggs Induces scratching,
& hence the eggs are transferred to the mouth via
fingers
 Retro-infection: 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 1month

Pathogenesis
 Mild perianal itching and excoriation
 Appearance of eggs or worms in an ectopic
location
 Atopic worms may result in a granulomatus
response
 In the perianal area causing vaginitis and
postmenopousal bleeding
 Granulomas in the peritoneum

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 the parasite
 Sleeplessness, because of the irritation
 Vulvovaginitis, & 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

1.Finding eggs from perianal skin using adhesive tape
or swab method
Done by pressing transparent adhesive tape
("Scotch test", cellulose-tape) 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,

Lab diagnosis…
 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.

Lab diagnosis…
2. Finding eggs in the faeces
Less then 10% found in stools, i.e. not a useful
examination;
occasionally eggs can be found in the urine or
vaginal smears

Diagnosis…
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

Treatment
 Two doses (10 mg/kg; maximum of 1g) each of
Pyrental Pamoate two weeks apart give a very
high cure rate.
 Mebendazole is an alternative.
*The whole family should be treated, to avoid
reinfection

1. Treating all members of a family in which
infection has occurred
2. Wearing tight-fitting cotton pants to infected
children
3. Washing of the anal skin each morning
4. Washing of clothing worn at night
5. washing hands after using toilet and before
eating
6. avoidance of putting fingers in the mouth &
trimming finger

Strongyloides stercoralis
 Common names: Dwarf thread worm
Epidemiology
 Found worldwide
 An estimated 50 to 100 million cases
 Favors warmer tropical and subtropical
climate

Epidemiology….
 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
 infection is rare or absent in many arid lowland
areas, including the Ogaden and pastoral areas
in the Awash Valley

Characterstics
1. Parasitic males are absent
2. Parasitic females are present in the submocusa
of small intestine which produce eggs
parthenogenically
3. Can develop in to free living generation in the
soil out side the human host
4. Has internal autoinfection

Habitat
 Has both free living and parasitic generations
 Parasitic Adult females: buried in the mucosal
epithelium of the small intestine of man
 Free living male and female: on external env`t
 Rhabditiform larvae: Passed in the faeces &
external environments
 Filariform larvae infective stage: soil & water.
 Egg : laid in the sub mucosa of small intestine

Morphology
• 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 submucosa, the rhabditiform larvae will hatched

Larvae
Rhabditiform larvae
(non-infective form)
Filariform larvae
(infective form)

Morphology…
 Rhabditiform Larvae
Size: 200-300m long
; 15m thick
Motility: very actively
motile in the stool
Tail: Moderately
tapered
Short buccal cavity
and rhabiditiform
esophagus
 Filariforml Larave
About 600-700m
Cylinderical
esophagus
Bifid tail end

 Transmission
1. Commonly by penetration of skin by filariform
larva
2. Ingestion of food or water contaminated with
filariform larva( oral route)
3. Rarely: Transmamary & Organ transplantation
4. Autoinfection with rhabidit form larva

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)

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

Life cycle….
 Autoinfection, the rhabditiform larvae become
infective filariform larvae in the host tissue
penetrate intestinal mucosa (internal
autoinfection) or
 perianal area (external autoinfection)

Parasitic life cycle
Free-living cycle

Clinical feature
 It is usually asymptomatic, in symptomatic cases
 People with weaker immune systems such as
elderly people & children are more susceptible.
1.Cutaneous phase
 large number of larva produce itching & erythema
at the site of infection within 24 hours of invasion

Clinical…
2.Pulmonary phase: The migratory larva in the
lung producing bronchopneumonia & full blown
pneumonitis
3. Intestinal phase : Invasion by adult worms may
produce abdominal pain & mucoid diarrhea ,
nausea, vomiting and anemia.

Clinical….
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

1. Finding the larvae in faeces or duodenal
aspirates using direct or concentration method
by microscopy
 In hyper-infection syndrome the larva may be
found in sputum, urine and other specimens
 Examination of serial samples may be
necessary because direct stool examination is
relatively insensitive

Diagnosis…
 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

Diagnosis….
2. Serological tests
 Antibody Detection
 Indicated when the infection is suspected
and the organism cannot be demonstrated
by:
 duodenal aspiration, string tests, or
 repeated examinations of stool
 Use antigens derived from filariform larvae
for the highest sensitivity and specificity

Diagnosis….
 EIA currently recommended because of its
greater sensitivity (90%).
 IFA and IHA tests can be used

Treatment
Ivermectin or thiabendozole

1. Sanitary disposal of faeces in latrine
2. Avoidance of use of night soil as a fertilizer
3. Wearing protective footwear
4. Treatment of infected individuals and Health
education

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

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
faeces

Pathology and treatment
 Similar to S.stercoralis
 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 faces ,
the larva will hatch.

The same as described for S. stercoralis

 Are hematophagous nematodes
 Two major species
Ancylomstoma duodenale
Necator americanus
 Less important : A. ceylanicum, A. braziliense
,A. caninum , A.tubaeforme, A. buckleyi
Hook Worms

Epidemiology
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

 In Ethiopia : Necator americanus is 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
Epidemiology….

Epidemiolgy…
 Altitude and moisture are the major factors
affecting their distribution
 Hook worm infection is absent in low ,hot
dry areas of Ethiopia and above 2500m
alttitude

 Adult: Jejunum and less often in the
duodenum of man
 Eggs: In the faeces; not infective to man
 Rhabditiform & filariform larvae: free in soil
and water
Habitat

Adult Adult
A.duodenale N.americanus
Size longer and thicker short and thinner
male 8mm 7-9mm
female 10-13mm 9-11mm
Buccal capsule large &oval small & round
Jaw like teeth cutting plates
Buccal cavity short,10-15m long ,15-16
m length m length
lumen is large lumen is short
Morphology of Adult hookworm

A.duodenale N.americanus
Shape of head slightly conical rounded
Esophagus-
Intestinal junction no gap gap
pathogenecity more pathogenic less
pathogenic
Morphology….

 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 & appears as black line
Color: the cells inside are pale gray
Content: contains an ovum which
appears segmented usually 4-8 blastomeres
Morphology….

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
Morphology of larvae

Hookworm filariform larva
Hookworm rhabditiform larva

Transmission and life cycle
Transmission
 Penetration of the skin by filariform larvae
 Ingestion of the filariform larvae present in the soil
or transmammary
 For A.duodnale, but N.americanus requires
transmammary migration
 Transplacental: rare

Life cycle
 Eggs are passed in the stool, under favorable
conditions (moisture, warmth, shade),
 Rhabditiform larvae hatch in 1 to 2 days in the feces
and/or soil
 After 5 to 10 days (and two molts) they become
filariform (third-stage) larvae that are infective
 larvae can survive 3 to 4 weeks in favorable
environmental conditions.

Life cycle….
 On contact with the human host, the larvae
penetrate the skin & are carried through the veins
to the heart, 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 & mature into adults
they attach to the intestinal wall with resultant
blood loss by the host

Clinical features
 Arise from a combination of intestinal inflammation &
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 &
iron) eventually lead to anemia

Clinical ….
 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

Clinical….
 Blood loss, 0.03 ml (N.americanus.) to 0.26 ml
(A.duodnale) per worm,
 up to 200 ml per day in heavy infections
 Chronic heavy infections result in anemia & iron
deficiency
 Malnutrition, stunt growth & poor mental dev`t in
children
 Anemia leads to weakness & 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
Dermal
Local erythema, macules,
papules (ground itch)
Cutaneous invasion
and subcutaneous
migration of larva
Pulmona
ry
Bronchitis, pneumonitis and,
sometimes, eosinophilia
Migration of larvae
through lung, bronchi,
and trachea
Gastro-
intestinal
Anorexia, epigastric pain
and gastro-intestinal
hemorrhage
Attachment of adult
worms and injury to
upper intestinal
mucosa
Hematol
ogic
Iron deficiency, anemia,
hypoproteinemia, edema,
cardiac failure
Intestinal blood loss

1. Finding eggs in faeces
 Microscopic identification of eggs in the stool is the
most common method
• A.duodenale & N.americanus eggs
morphologically indistinguishable

Lab diagnosis…
 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 for
characteristic eggs.

• 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 will hatched
and misslead with strongyloides larva
 hookworm : deep buccal cavity
 S. stercoralis : shorter buccal cavity
Diagnosis….

Diagnosis…
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
 As described for Strongyloides stercoralis

summary
1. write the characteristics of nemathelminthes
2. Write the infective and diagnostic stage of medically
important intestinal nematodes
3. List the possible sources of specimen for the
diagnosis of intestinal nematodes
4. Discuss the main differences between rhabiditiform
and filariform larvae of hook worm and S.stercoralis.

Summary…
5. Which intestinal nematodes do not undergo heart
lung migration in their life cycle?
6. What are the differences between adult N.
americanus and A. duodenale ?
7. Write the prevention and control means of
intestinal nematodes.

References
1. Guerrant RL, Walker, DH, Weller PF (2006).
Tropical Infectious Diseases. Principles, pathogens
& practices. 2nd Edition.
2. Gillespie SH & Pearson RD (2001). Principles &
practices of clinical Parasitology.
3. Cheesbrough M (2005). District laboratory practice
in Tropical Countries. 2nd edition updated. Part one.
Cambridge.
4. CDC.
5. Awole M & Cheneke W(2006). Medical Parasitology
for medical laboratory technology students.
Upgraded lecture notes series.

Nematodes
 Blood and Tissue nematodes

Outline
General features
 Classification
 Geographical distribution, morphology, differential
characteristics, life Cycles, laboratory diagnosis, prevention
and control of:
 Wuchereria bancrofti
 Brugia malayi/timori
 Loa loa
 Onchocerca volvulus
 Trichinella spiralis
 Dracunculus medinensis

Learning objective
At the end of this unit the student will be able to:
 Explain the general features of blood and tissue nematodes
 Classify tissue nematodes
 Explain the Geographical distribution, Morphology, differential
characteristics, life Cycles, prevention and control methods of
blood and tissue nematodes
 Collect blood samples in appropriate timing
 Collect skin snip for the diagnosis of O. volvulus
 Detect and identify microfilaria of blood and tissue nematodes

2.1.3.1 General features
Adults:
 are long thread - like worms
 live in the tissues of human lymphatic system,
subcutaneous tissues or muscle
 Requires two host to complete their life cycle.
 Females are viviparous, larvae hatch in the uterus
 The female produce first stage larvae (L1)

 The immature L1 stage larva is called
Microfilariae.
 Microfilariae:
 Small, slender, motile forms
 L1 require blood sucking insects (IH) to
develop to infective form (L3)
 No reproduction in the vector, rather
development

2.1.3.2. Classification:
 Tissue nematodes can be classified based on:
Habitat in the body
Clinical manifestation
Morphology

Three families/ groups
1. FAMILY FILARIDAE( Filarial worm)
Common/pathogenic filaria
 Brugia malayi
 Brugia timori
 Loa loa
 Onchocerca volvulus
Less/non-pathogenic Filaria
 Mansonella perstance
 Mansonella streptocerca
 Mansonella ozardi

2. Family Trichineloidae
 Trichinella species
3. Family Dracunculidae( guinea worm)
• Dracunculus medinensis
Animal tissue nematodes rarely infect human
 Dirofilaria spps
 Angiostrongylus cantonensis
 Gnathostoma spinigerem

General features:
 Filariae live as adults in various human tissues
 Agents of LF reside in lymphatic vessels &
lymph nodes
• O. Volvulus, Loa loa, M. Ozzardi and M.
Streptocerca in subcutaneous tissues
• M. Streptocerca besides reside in the dermis
• M. Perstans resides in body cavities and
surrounding tissues
160
2.1.3.3. FAMILY FILARIDAE
( Filarial worm)

 Three of these are responsible for most of the
morbidity:
 W. bancrofti & B. malayi cause lymphatic
filariasis,
 O. volvulus causes onchocerciasis (river
blindness).
 Animal reservoirs play no significance role in
most places, except in sub-periodic B. malayi.
161
Cont ….

Diagnosis based on Mf findings:
 Morphologic features:
 Size
 Presence or absence of “ sheath”
 Appearance i.e. curvature, Kinks, coiling etc
 Arrangement of the column of nuclei in the body
 Presence of nuclei at the very tip of the tail
 Other features:
 Periodicity
 Source of specimen

 Factors to be considered when collecting blood
Collect blood at the correct time
Concentration technique recommended
In chronic infection Mf is rarely found in blood
In lymphatic filariasis Mf are higher in capillary
blood than venous blood??
Mf are higher in capillary blood from the ear lob

FAMILY FILARIDAE( Filarial worm)
Morphology
 Adult
The adults are long thread
like worms.
Measure 2 cm – 120 cm
(4 – 10 µm wide)

Morphology…..
Live in body cavities, lymphatic, and
subcutaneous tissues
Release embryos (microfilaria) which live in
blood or dermis (skin)
all require an insect or crusteacian vector as
intermediate host

 Microfilaria
The immature first stage larva of filarial worms
Are motile and live in blood or dermis
Measure, 150-350 µ long
Transparent and colorless with rounded or pointed
tail in unstained smear
Internal structure can be visualized by the use of
fixed stained preparation
Can be sheathed or unsheathed

Periodicity:
 Microfilaria of pathogenic filarial worms that
found in the blood which causes lymphatic
filariasis and Loiasis show periodicity.
Mf are found in the blood in greater number in
a certain hours of a day or night.
Corresponds to peak biting times of their
insect vector

Periodicity…
 Nocturnal periodicity: mf is high in blood
during night hrs
 Diurnal periodicity: mf is high in blood during
day hrs
 Nocturnal or diurnal sub-periodicity: mf can
found in blood 24 hrs with slight increase in
number during day or night hrs

170
Filarial worms
(Synonym)
Periodicity Main Vector
(IH)
Reservoir
O. volvulus
(River blindness)
Non Periodic Black fly (Simulium) Human
W. ancrofti (LF) Periodic (N)
22 – 04hr (24hr)
Culex, Anopheles Human
Sub Periodic
20 – 22 (21hr)
14 – 18 (16hr)
Aedes Human
B. Malayi (LF) Periodic (N)
22 – 04hr (24hr)
Anopheles Human
Sub Periodic
20 – 22 (21hr)
Mansonia Human, Monkey, Cat –
Zoonotic
B. Timori (LF) Periodic (N) Anopheles Human
L. Loa (Eye worm) Periodic (D) Deer fly Man, Monkeys
M. streptocerca Non Periodic Midge (Culicoides)
M. perstans Sub Periodic Midge (Culicoides)
M. ozzardi Non periodic Midge (Culicoides)
Black fly

 Filarial worms cause 3 main diseases
lymphatic filariasis (Elephantiasis)
Loiasis
Onchocerciasis (river blindness)

Lymphatic Filariasis
• Disease caused by filarial worms living in the
human lymphatic system
• Causative agents
• Wuchereria bancrofti
• Brugia malayi and Burigia timori
• These worms lodge in the lymphatic system
• They live for four to six years, producing millions
of minute larvae that circulate in the blood”

Lymphatic…
 Large numbers are present in the lymphatics of
the:
 Lower extremities (inguinal & obturator
groups),
 Upper extremities (axillary lymph nodes), &
 Male genitalia (epididymis, spermatic cord,
testicle) - particular for W. bancrofti

Social consequences
It is one of the most debilitating and disfiguring
diseases of the world
1. Disfigurement of the limbs and genitals leads
to:
 Stigma
 Anxiety
 Ostracization
 Psychological trauma
 Sexual disability

Social consequences…..
2. The disease impeds
 Mobility
 Travel
 Educational opportunity
 Employment opportunity
 Marriage prospect

Epidemiology of L. Filariasis
 Endemic in 83 countries
 1.2 billion at risk
 > 120 million people infected
 > 25 million men suffer from genital disease,
 > 15 million people suffer from lymphoedema or
elephantiasis of the leg
 ~ 2/3 of infected people live in India and Africa
 Others live in parts of Asia, the Pacific, & in Central
and South America.

Distribution
 affects an estimated 119 million individuals
and disfigures 40 million.
 Wide distribution (Africa, SE Asia, Indonesia,
South Pacific Islands)
 Brugia malayi
 Limited distribution (China, India, SE Asia,
Indonesia, Philippines)
 Brugia timori: Leser sudan, island of Indonesia

Wuchereria bancrofti
Disease: Bancroftian filariasis, Wuchereriasis,
elephantiasis
Distribution: tropical and subtropical countries
Morphology:
1. Adult:
 Thready
 Cylinderical oesophagus
 Creamy white in color
180

W.bancrofti…
Male:
 About 4cm in lentth
 Curved posterior end
 2 unequal spicules and has anal papillae
• Female:
 About 8 cm in length
 2 sets of genitalia
 Vulva opens close to the posterior end
 Viviparous

W. bancrofti...
2. Microfilaria:
250 x 8 
Body forms graceful curves
Body has a column of nuclei separated by free
areas
Rounded anterior & tapered tail ends free of nuclei
182

W. bancrofti
 Loose sheath (stretched vitelline membrane)
closely fits the body but projects beyond the head
& tail ends.
3. Infective larvae: 1500 – 2000 x 20
 Cylinderical oesophagus
183

Cont ....
• Requires two host
• Human-DH
• Mosquitoes-IH
Transmission
• Bite of female mosquitoes
(Genera Culex, Aedes, Anopheles, Mansonia)

• Infective larvae deposited onto
human skin during the mosquito's
blood meal
• Enter through the mosquito bite
puncture wound or local
abrasions.
 In humans:
 Parasites passes to the lymphatic
system
 Undergo further molts
 Become adult male & female
worms

 Adult female worms produce thousands of
sheathed microfilariae per day
 Mf can be found in blood 9 months after infection
(W.bancrofti) & 3 months (Burgia species)
 Normally found in peripheral circulation in evening.

 Microfilariae ingested during blood meal from
infected person
 Penetrate the mosquito stomach wall
 Enter the body cavity (hemocoel)
 Migrate to the insect's flight muscles for growth.
 After 2 molts, the L3 migrate through the head,
 Reach the proboscis of the mosquito.

Clinical manifestation
 Depends on:
Site occupied by adult
Number of worms,
Length of infection and
Immune response of the host

Clinical manifestation.
1. Many infections are asymptomatic
2. Circulating Mf probably do not cause pathology
3. The main pathological lesions are:
a) Inflammatory manifestations: due to toxic
products of living or dead adult worms

Clinical…
 There may be:
 Recurrent attacks of lymphangitis
 Funiculits
 Epididymitis
 Orchitis, etc...
 Lymphadenitis
 Swelling and redness of affected parts
 Fever, chills, headache, vomiting & malais

b) Obstructive manifestations
• Fibrosis following the inflammatory process
• Coiled worms inside lymphatics.
• This may result in:
 Dilatation
 Rupture of distended lymphatics in the
 urinary passage – chyluria
 pleura – chylothorax
 peritoneal cavity – chylous ascitis
 testis – chylocoele

 Elephantiasis:
 Hard and thick, rough and fissured skin
 Frequently legs & genitalia (scrotum, penis &
vulva)
 Less often arms and breasts.

Clinical ......
4. Tropical pulmonary eosinophilia
 Pulmonary symptoms: cough, dyspnoea,
"asthmatic syndrome".
 Chest X-rays: patchy infiltrates
 Splenomegaly
 High ESR & marked eosinophilia
 No microfilariae in the peripheral blood.
 Serological tests strongly positive
 Responds very well to therapy with DEC
196

Diagnosis of W. bancrofti
1. BF (taken at night)
 Thin and thick smears
 Concentration methods
 Lyzed capillary blood technique
 Tube centrifugation lyzed blood technique
 Microhematocrit tube technique
 Membrane filtration technique
 Counting chamber technique
 DEC provocation test
197

Diagnosis...
 Mf in:
 Aspirates of hydrocele
 Lymph gland fluid
 Chylous urine
2. Intradermal test (antigen from Dirofilaria immitis)
3. Serological tests as IHA, IFA
4. Antigen detection: ICT filariasis test
198

Adult female worm of W. bancrofti
202
Adult male worm of W. bancrofti

Differential diagnosis
 Podoconosis (syn. lymphatic siderosilicosis or
lymphoconosis):
Very slow onset of edema
Lymphoedema
Elephantiasis (mostly limited to below the knee)
 Caused by immune response to certain minerals.
• No hydrocoele, eosinophilia, nocturnal
microfilaraemia 203

Treatment of W. bancrofti
 Diethyl carbamazine (DEC)
 General measures:
 Rest, antibiotics, antihistamines, and bandaging
 Surgical measures for elephantiasis
204

• Control of mosquitoes
 Avoid mosquito bite
 Treat patients
 Health education
 Global LF elimination program strategy:
 Mass drug administration
 Care for chronic cases
205

Loiasis
• Caused by filarial worms living in subcutaneous
tissue
• Causative agents
• Loa loa (Eye worm)
 Distributed in Rain Forest
areas of West Africa &
equatorial Sudan.

Loa loa (Eye worm)
 Habitat:
 Adults live in:
 Connective tissues under the skin
 Mesentry
 Parietal peritoneum
 Subconjunctival tissue of the eye or thin
skinned areas

208

Loa loa Habitat..
 Microfilaria in peripheral blood of man during day
time
 Infective larvae in the gut, mouth parts and
muscles of chrysops
209

Morphology….
 Adult – cylinderical and transparent
 Microfilariae
 Has several curves and kinks
 Sheath which stains best with haematoxylin
 Body nuclei are not distinct and more
dense
 Nuclei extend to the end of the tail which is
rounded

Transmission
 Horse flies (Tabanidae) in genus Chrysops
 Day-feeding & forest-dwelling
 Also called the “deer fly” or mango fly.

Life Cycle
 Adult worms continuously migrate through tissue at
a rate of about 1 cm per minute.
 Found in back, chest, axilla, groin, penis, scalp and
eyes.

Clinical manifastation
 Loiasis is often asymptomatic.
 Calabar swellings (episodic angioedema)
Itchy, red, and nonpitting swollen areas in the skin
2-10 cm in diameter, Often painful/may be painless
In any portion of the skin/wrists & ankles most
frequent

Clinical manifestations
 Adult worms also migrate in sub-conjuctival tissues.
 They can cause inflammation & irritation but not
blindness

 Mf in stained BF taken during the daytime
 Occasionally the Mf can be found in joint fluid
 Differentiation from mansonella required
(hematoxylin staining)
217

 Loa loa:
 Sheathed,
 Relatively dense nuclear column
 Tail tapers & is frequently coiled, and
 Nuclei extend to the end of the tail.
 Mansonella perstans:
 Smaller than L. loa
 No sheath
 Blunt tail with nuclei extending to the end of
the tail
219

220
Mf of Loa loa
Mf of M. pestans

Onchocerciasis
 Is a filarial disease caused by O. Volvulus
 Commonly known as river blindness
 The world’s second leading infectious cause of
blindness
 WHO estimates the global prevalence is 17.7 million,
of whom about 270,000 are blind
222

DISTRUBUTION MAP
Tropical Africa between
the 15° north and the 13°
south
Foci are present in Southern
Arabia, Yemen and in S. & C.
America

 Occurs most widely along
the courses of fast running
rivers in the forests &
Savannah areas of west and
central Africa
 Also occurs in the Yemen,
Arab Republic, Central and
South America

Onchocerca volvulus
 Habitat:
Adult:
 Subcutaneous nodules and in the skin
 Adults can live ~ 8 – 10 years in nodules
Microfilariae:
 Skin, eye and other organs of the body
Infective larvae in:
 Gut, mouth parts and muscles of black fly
226

Onchocerca volvulus
Morphology
 Microfilariae:
220 to 360 µm by 5 to 9 µm
No sheath
Head end is slightly enlarged
Anterior nuclei are positioned side by side
No nuclei in the end of the tail
Tail is long and pointed
227

Onchocerca volvulus
 Adult:
Females - 33 to 50 cm in length and 270 to 400
μm
Males - 19 to 42 mm by 130 to 210 μm.
228

Onchocerca volvulus
Transmission:
 By the bite of infected vector (simulium species)
229

Life cycle
 During a blood meal, infected black fly introduces L3
(infective stage) larvae onto the skin of the human
 L3 penetrate into the bite wound
 In subcutaneous tissues the larvae develop into adult
filariae
 Adult commonly reside in nodules in subcutaneous
connective tissues
230

Life cycle
 The female worms produce Mf for ~ 9 years
 Mf have a life span ~ 2 years
 Mf found:
Typically in the skin and in the lymphatics of
connective tissues
Occasionally in peripheral blood, urine and sputum
231

Life cycle…..
 A black fly ingests the Mf during a blood meal
 Mf migrate from the black fly's midgut through the
hemocoel to the thoracic muscles
 Mf develop into L1 larvae and then to L3
 L3 migrate to the black fly's proboscis
 Infection occurs when the fly takes a blood meal
232

Life cycle of Onchocerca volvulus
233

Clinical feature
Onchocerciasis
 Acute onchocerciasis:
Itchy (pruritic)
Erythematous
Papular rash with thickening of the skin
234

Clinical feature
 Chronic onchocerciasis:
 Elephant or lizard skin Hanging groin
 Leopard skin River blindness
235

Clinical feature
 Onchocercomata:
Upper part of the body
(American onchocerciasis)
Pelvic region (African form)
• Nodules surrounded by
concentric bands of fibrous
tissue
236

 Mf in skin snips
 Mf in urine, blood & most body fluids (in heavy
infection)
 Wet mount preparation Staining
237
Skin biopsy Skin fragment

 Mf must be differentiated from Mf of M.
Streptocerca and M. Ozzardi.
Mf of O. Volvulus are longer and do not have
nuclei to the end of the tail
239

 Destruction of vector (Simulium)
 Avoiding Simulium bites
 Treatment of communities (~APOC)
242

Treatment
 Ivermectin:
Paralysis of worms
Reduces the microfilarial load
 Surgical Care:
Nodulectomy
Removes adult worms
243

Trichinella spiralis
 A tissue nematode caused by Trichinella spiralis
 Zoonotic disease
 Disease in humans: Trichinosis, Trichiniasis,
Trichinelliasis, Trichinellosis
 Distribution: Temperate regions where pork is eaten
1. T. Spiralis spiralis – found in temperate regions
2. T. Spiralis nativa – found in the Arctic
3. T. Spiralis nelsoni – found in Africa and S.
Europe 245

 Habitat:
 Adults in the small intestine of man and animals
especially pigs and rats (reservoir hosts)
 Larvae : encysted in muscles
246

 Morphology;
1. Adults:
 Attenuated anterior end
 Cellular oesophagus
 Anus or cloaca terminal
Male: 1.5 mm in length
 Posterior end curved ventrally
 2 caudal papillae
 One set of genitalia
247

Morph ....
 Female: 3.5 mm in length
 Posterior end bluntly rounded
 One set of genitalia
 Vulva opens at the junction of the anterior 5th
with the rest of the body
 Larviparous (viviparous)
248

Morph ....
2. Encycted larva: in cyst wall formed by tissue
reaction
 Larva (1mm) coiled inside the cyst (0.5 x 0.2 mm)
 Larva grows from 0.1 to 1mm (~ 2 weeks to
become infective)
 Lies along the longitudinal axis of muscle fibres
 Cyst usually become calcified
249

Transmission
 Eating flesh of infected pork (raw/undercooked)
250

Life cycle...
 The same host (animal/man) act as DH & IH
 After fertilization, males die and are expelled.
 Females penetrate deeply in the mucosa and lay
 Female lays ~ 1500 larvae in its life span (~ 2
months)
 Larvae to the circulation
 Passes through pulmonary filter
252

 Life cycle......
 Larvae coil & encyst in the long axis of muscles
 Pigs become infected by eating infected flesh
from other pigs or ingestion of infected dead
pigs and rats
 Rats are infected by eating flesh of dead pigs or
rats and by canibalism
253

Life cycle
 Larvae liberated from the cysts in small intestine
and mature to adults
 Larvae start to be deposited by the female
254

Pathogenicity
 Intestinal invasion by adult worms
 Abdominal pain, nausea, vomiting, diarrhoea and
colic.
255

 Encystment of larvae
 Manifestations
depend up on
organs affected.
 > 50 – 100
larvae/gm of
muscle are
symptomatic
 < 10 larvae are
often asymptomatic
257

Clinical signs & syptoms
 The main findings are:
 Oedema chiefly orbital
 Muscle pain and tenderness
 Headache, fever, rash, dyspnoea, general
weakness
 Death occurs in severe cases from exhaustion,
heart failure (myocarditis), pneumonia, etc.
258

1. Immunodiagnosis:
a) Intradermal test (Bachman test)
b) Serological tests:
 Bentonite flocculation (BF)
 Latex agglutination (LA)
 Counter – current electrophoresis (CEP)
 Complement fixation test (CFT)
 IFA and IHA
260

Diagnosis .....
2. Muscle biopsy:
 Direct examination
 After digestion in a pepsin hydrochloric acid
medium
3. Eosinophilic leucocytosis in the acute stage
261

263 Adult worm from intestine wall

Prevention & control
 Thorough cooking of pork
 770c or freezing at – 150c for 20 days
 – 180c for 24 hours
 Proper breeding of pigs
 Sterilizing garbage
 Antirat campaign
 Inspection of pork in slaughter houses
 Trichinoscope.
264

Treatment
 Non specific symptomatic treatment:
 Sedatives
 Cortisone and ACTH
 Supportive treatment:
 Rest, fluids, smooth diet and vitamins
 Thiabendazole
 Mebendazole
265

2.1.3.8. Dracunculus medinenis
“Guinea worm, ”

Dracunculosis
 Synonyms: Dracontiasis, Dracunculosis,
Dracunculiasis
 Causative agent
 Scientific name: Dracunculus medinensis
 Common name: Medina worm or Guinea worm
268

Epidemiology
 Most common in areas of limited water
supply where individuals acquire water by
physically entering water sources.
“Walk-in well”
Water holes in parts of Africa

Distribution of
Dracunculus medinensis
Global: Nile valley,
India and areas
where wells are
used for water
supply
Ethiopia:

Dracunculosis
 Habitat:
 Adults in subcutaneous tissues of man/reservoir
animals
271

Morphology
I. Adult :thread like,
cylinderical oesophagus
II. Male: About 3 cm in
length
 Posterior end coiled
 2 unequal spicules
I. Female: About
30 to 100 cm in
length
 Swollen
anterior end
 Hooked
posterior end
 Inconspicuous
vulva near
anterior end
272

D. medinensis
2. Larva (or embryo):
 600 x 20 
 Rhabditiform
oesophagus
 Anterior end rounded
 Tapering and long tail
(1/3 body)
273

Life Cycle of Dracunculus
medinensis
 A blister is formed from the female worm's
production of embryos released beneath the skin,
due to a burning pain that comes with this, the
victims often immerses their legs in water for relief.
 With the sudden drop in temperature that follows, the
blisters usually rupture, releasing the worms.
 These worms may release thousands of infective
juveniles at this time, which enter the water.

Before
After
 The cephalic end of the
fertilized female
pressing on the skin,
produces a papule that
becomes a blister and
then ruptures forming
an ulcer

Life Cycle of Dracunculus medinensis
Infective larvae
In water, larvae Must be eaten by Copepod
(Crustacean), the IH,

Life Cycle of Dracunculus medinensis
 Once within the
copepod, the infective
juvenile larvae moves
into the hemocoel where
they develop into 3rd
stage juveniles.
 These get consumed
when humans drink
water with infected
copepods.

Life cycle of D. medinensis
 Man is infected on drinking water containing cyclops
 In the small intestine, the cyclops is digested , larvae
liberated and penetrate through the duodenal wall
and migrate to the subcutaneous tissues probably
via lymphatics.
 At this point the females are fertilized by the males,
and the males die. The females then migrate to the
skin, reach sexual maturity, and produce juveniles.
278

Life cycle
 They tend to go to parts most likely to come in
contact with water as the lower extremities
(positive hygrotropism and geotropism)
 Several months (9 or more) elapse between
infection and appearance of the gravid female at
the skin surface
 Male dies after copulation

Life cycle of D. medinensis
 The cephalic end of the fertilized female pressing on
the skin, produces a papule that becomes a blister
and then ruptures forming an ulcer
 When the ulcer contacts with water, a loop of the
uterus prolapses through a rupture in the anterior
end of the worm and larvae are discharged.
 larvae penetrate the intestine and settle in the body
cavity to become infective in about 3 weeks
280

Life Cycle of D. medinensis
282

Pathogencity of D. medinensis
 Early manifestatiosn when the female worm
approaches the skin. It liberates a toxic substance
that results in local erythema, tenderness and pain.
 Formation of a blister that turns into a cesicle &
ultimately ulcerates
 Local or systemic symptoms as urticaria, pruritus,
pain, dyspnoea, nausea and vomiting, which
subside with rupture of the blister
 The ulcer may be secondarily infected producing
cellulitis and induration
 Eosinophilia
283

Adult worm of D. medinensis
284

Adult worm of D. medinensis
285

D. medinensis
286
Blister containing the worm Ruptured blister with filamentous worm
A B

D. medinensis
288
Adult Dracunculus in foot
B

Diagnosis of D. medinensis
 Laboratory tests to investigate dracunculiasis are
limited because the larvae are normally washed
into water
 A diagnosis is usually made when the blister has
ruptured and the anterior end of the female worm
can be seen
289

Diagnosis of D. medinensis
 If required, laboratory confirmation of the diagnosis
can be made as follows:
1. Place a few drops of water on the ulcer to
encourage discharge of the larvae
2. After a few minutes collect the water in a plastic
bulb pipette or pasteur pipette
3. Transfer the water to a slide and examine
microscopically using 10x objective – motile
larvae will be observed
290

Prevention & Treatment
 People with an open Guinea worm wound should
not enter ponds or wells used for drinking water.
 Water can be boiled, filtered through tightly woven
nylon cloth, or treated with a larvae-killing chemical.
 No medication is available to end or prevent
infection.

 The only treatment is to remove the worm over
many weeks by winding it around a small stick
and pulling it out a tiny bit at a time.
 Sometimes the worm can be pulled out
completely within a few days, but the process
usually takes weeks or months.
 The worm can be surgically removed before the
wound begins to swell.
 Antihistamines and antibiotics can reduce
swelling and ease removal of the worm.

Summary
 Write the general characteristics of blood and
tissue nematodes
 What are the basis for classification of tissue
nematodes
 Write the diagnostic and differential
characteristics of microfilariae of tissue
nematodes
 What are the factors to be considered in
collection of samples for diagnosis
 Write the vectors responsible for transmission of
blood and tissue nematodes

References
1. Guerrant RL, Walker, DH, Weller PF (2006). Tropical
Infectious Diseases. Principles, pathogens & practices.
2nd Edition. Elsevier Inc
2. Gillespie SH & Pearson RD (2001). Principles &
practices of clinical Parasitology. John Wiley & sons
LTD
3. Cheesbrough M (2005). District laboratory practice in
Tropical Countries. 2nd edition updated. Part one.
Cambridge.
4. www.CDC.gov.
5. Awole M & Cheneke W(2006). Medical Parasitology for
medical laboratory technology students. Upgraded
lecture notes series.
6. Jaffeey & Leach. Atlas of Medical Helminthology &
protozology. 2nd edition.

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