True round worms

General Characteristics
Elongated

Bilaterally symmetrical

Cylindrical

Unsegmented
No circulatory system
Separate sexes
Well developed Digestive
system
Reproduction
Oviparous
Larviparous
Parthenogenetic
Digestive system
The adult worm has a complete digestive tract

Mouth
Buccal cavity
Esophagus
Intestine/Midgut.
Rectum
Types of esophagus:

Filariform – Strongyloides
stercoralis

Rhabditiform – Enterobius
vermicularis

Spiruroid - Filarial worms

Strongyliform – Ancylostoma

Stichosoma - Trichuris, Capillaria

and Trichinella
Nervous system
The most important commissure is the CIRCUM-
ESOPHAGEAL RING COMMISSURE

PAPILLAE are minute inflations of the cuticle

Sensory organs: Anterior ( AMPHIDS ) Posterior

( PHASMIDS )
Reproductive system
 The male reproductive organs are
situated in the posterior third of
the body as a single coiled or
convoluted tube

 Accessory copulatory apparatus

consists of one or two unsheathed
copulatory spicules which are
sclerotizations of the cuticle arising
from the dorsal wall of cloaca. This
spicules maybe short or long and
use for attachment of the male to
the female during copulation.

 In some species, a wing-like

appendage or copulatory
bursa/bursa copulatrix maybe
present. Nematodes spermatozoa
are stored in the seminal vesicle.
REPRODUCTIVE SYSTEM
The female reproductive
system may either be a
single or bifurcated tube,
differentiated into ovary,
oviduct, seminal receptacle,
uterus, ovijector, vagina and
a vulva that opens to the
exterior. The ovum passes
from the ovary into the
oviduct (fallopian tube)
where it is fertilized
 PHYLUM NEMATODA
CLASS ADENOPHOREA ( APHASMIDIA )
 Trichuris trichiura
common name : Whip worm
Next most common intestinal
roundworm to Ascaris especially
in urban disadvantage
communities

Habitat: Large intestine – cecum

and rectum

Infective stage: embryonated egg

Diagnostic stage: unembryonated

egg
Occurs quite frequently with
Ascaris probably due to their very
similar epidemiology and method
of transmission to man
Morphology
ADULT
Flesh colored or pinkish slender worms which are
much smaller than Ascaris
The anterior three-fifths of the worm consists of a
fine, hair-like structure which forms the esophagus
while the posterior two-fifths is thick and fleshy and
contains the intestine and reproductive organs.
Adult male
Measures 3 -3.5 cm
With curve posterior end

Adult Female
Measures 3.5 – 5.5 cm
With straight posterior end
Morphology
The esophagus is
characteristically
embedded in glandular
cells called stichocytes.
The tail of the female
worm is straight and
blunt while that of the
male worm is
characteristically curved
Morphology
OVA
Barrel-shaped/Lemon-
shaped/football-shaped
with thick, smooth, double
layer, yellowish-brown egg
shells and two prominent
plugs protruding at both
ends
LIFE CYCLE
Infective stage : Embryonated egg
Mode of Transmission : Ingestion of infective
egg
Portal of Entry : Mouth
*** No larval migration
Habitat : Large Intestine
Portal of Exit : Anus
PATHOGENESIS
Trichiuriasis – light
infection; usually
asymptomatic

Heavy infection : GIT

symptoms, diarrhea,
Rectal Prolapse
DIAGNOSIS
1. DFS (Direct Fecal Smear)
2. Kato Technique or Cellophane Thick smear
3. Kato - Katz Technique
4. Concentration technique
 In heavy infections, stool is frequently mucoid and
contains Chartcot-Leyden Crystals
Control and Prevention

Treatment of cases (Broad Spectrum anti-

helminthes)
Albendazole ; Mebendazole ; Pyrantel pamoate
Mass treatment is advisable
Proper hygiene
Proper waste disposal
Avoid the use of night soil as fertilizer
 Capillaria
philippinensis
common name : Pudoc worm
This was first recognized in the Philippines in 1963
when the first human case dies of the disease in the
PGH

In 1967, an epidemic of Capillariasis took place in

Pudoc West, Tagudin, Ilocos Sur where approximately
1,300 persons became ill and 90 persons died of
infection

Man acquire the disease by ingestion of raw fish

harboring the larval stage
Intermediate hosts:
 Small brackish water fish (Hypseleotris bipartita)
 Bagsit, Birut, Bagsang, Bagsik
Present evidence indicates that it ia a parasite of fish-eating
bird and that in nature, it is a fish-bird cycle. The ability to
infect fish-eating migratory birds suggests that this parasite
may be widely distributed throughout Asia and elsewhere

Common name: Pudoc worm

Habitat: small intestine
Infective stage: filariform larva (L3)
Diagnostic stage: unembryonated egg
MORPHOLOGY
OVA
Peanut-shaped with striated
shells/ Guitar -shaped
Flattened bipolar plugs
Measures 36-45 um by 20 um
The atypical females produce
eggs which are thin-shelled
without polar plugs and are
multi-segmented or
embryonated, these eggs hatch
in utero into first stage larvae
MORPHOLOGY
Adult worm

Male : 1.5 – 3.9mm long ; With spicule

Female : 2.3 – 5.3mm long ; Uterus contains

eggs
There are two types of female worms: the typical
female which has 8 to 10 eggs in utero arranged in a
single row and the atypical female which has 40 to 45
eggs in utero arranged in 2 to 3 rows.
LIFE CYCLE
LIFE CYCLE
Infective stage : Third stage Larva
Mode of Transmission : Ingestion of the infective
larva in the fresh water fish
(BAGSIT : Intermediate Host)
Portal of Entry : Mouth

Definitive Host : Man ; Migrating Birds (Natural

Host)
Habitat : Small Intestine

Portal of Exit : Anus

PATHOLOGY
Causes Borborygmus (Gurgling stomach)
Abdominal pains
Diarrhea
weight loss, malaise, vomiting, anorexia and edema
loss of protein ; malabsorption of fats ; loss of
electrolytes
 death if not treated soon

Responsible for Mystery Disease

DIAGNOSIS
Fecalysis (DFS & Conc. Tech.)
Eggs
Larva
Adult

Duodenal aspirates
Adult worm maybe recovered
Control and Prevention
Treatment of cases - Broadspectrum anti-
helminthes

Management of cases
Electrolyte replacement
High protein diet
 Prevention
Refrain from eating raw fishes
Good sanitary practices
 Capillaria hepatica
common name: Capillary Liver
Worm
MORPHOLOGY
Ova
Lemon-shaped outer shell
Pitted like a golf ball
appearance
Adult
Resembles Trichuris trichiura
LIFE CYCLE
PATHOLOGY
Hepatic capillariasis – acute hepatitis eosinophilia

Dead-end infection
DIAGNOSIS
Liver Biopsy

*** In cases spurious infection larva is found in feces

 Trichinella spiralis
common name : Trichina worm
Trichinella spiralis
Common name: Trichina worm
Common parasite of pig
Causes Trichinellosis, a zoonotic infection in humans
The adults inhabit the small intestine of pig, rat and
man for few weeks.
The encysted larvae are present in the striated muscles
of these hosts
Larviparous
MORPHOLOGY
 One of the smallest
nematode that causes
infection in man
 A single host serves both as
the definitive and
intermediate host
 There are no free-living
stages
MORPHOLOGY
Thread like worm, barely visible by naked eyes

Males
 The spicule an and copulatory sheat are absent
 Identified by the conspicuous conical papillae present in the tail
end
 Short-lived and dies immediately after fertilization of the female
within a week
 1.5mm by 0.4mm
Females
 Larviparous
 They have single uterus, filled with developing eggs in the posterior
region but fully developed and hatched larvae in the anterior region
 3-4mm by 0.6mm
MORPHOLOGY
LARVAE
Spear-like tip
They remain coiled inside muscle cysts, which are only
present in the striated skeletal muscle.
Inside the muscle cysts, the larva continues to develop,
sexually matures and differentiates
Infective stage to man
It remains viable for years before it is dead and
eventually calcified
In the skeletal muscles, a capsule surrounds the larva in
a period of 3 months. The encysted cyst is lemon-shaped
LIFE CYCLE
LIFE CYCLE
*** zoonotic parasite ( animal to human)

HOSTS : wild cats, wild dogs, wild rats, pigs -----à man
(dead end)
Muscles affected by the parasite among human hosts
Muscle of the respiratory system (diaphragm)
Muscle of the heart
Muscle of the limbs
Muscles of the eyes
Muscles of the tongue
PATHOLOGY
Both adult and larvae are pathogenic
Adult female worms present in the intestine cause
gastrointestinal disturbances
Migrating larvae cause various allergic manifestations
such as fever, edema of the face, eosinophilia
Encysted larvae in the skeletal muscle cause muscular
pain
PATHOLOGY
Inflammation

Granulation formation

Calcification
PATHOLOGY
CLINICAL MANIFESTATION
The severity of the clinical manifestations of
trichinellosis depends upon:
Number of larvae ingested
Immune status of the host
Majority of the infections are asymptomatic
 Increased CK, LDH ( muscular enzymes )
PATHOLOGY
In heavy infection, depending upon the sites of the lesion
caused by the parasite three clinical phases of the disease
are described:
1. Intestinal phase
Due to invasion of the intestinal wall by the newborn larvae
Appear 1-2 days after ingestion of undercooked pork and last
nearly 2-3 months
2. Muscle invasion phase
Due to invasion of the muscle by the larvae
This is seen during 7-11 days of ingestion of the infected food
3. Convalescence phase
Marked by the beginning of the encapsulation of the
encysted larvae during the third week of infection
Laboratory diagnosis
Parasitic diagnosis is made most commonly by direct
detection of the first-stage encysted larvae in striated
muscular tissue
Specimen: muscle obtained by biopsy

Serologic = Bachman intradermal test ( in vivo )

=Bentonite Flocculation Intradermal Test ;
ELISA ( in vitro )
Xenodiagnostic = Beck’s
CONTROL AND PREVENTION
Health Education
Cook meat at 77C ( 177 F )
Freezing -15C ( 20 days ) or -30C ( 6 days)

Smoking, Salting, Drying meat is NOT EFFECTIVE in

killing the parasite
 Dioctophyma renale
common name: Giant Kidney worm
Morphology
Adult
Cylindrical, blood red, bell
shaped bursa with spicule

Ova
Barrel-shaped, thick, pitted
golf ball appearance of the
shell
LIFE CYCLE
Intermediate host : Earthworms

Paratenic hosts : fish and frogs

Incidental host : man

Pathology
Destruction of Kidney tissue
Diagnosis
Urine analysis
 PHYLUM NEMATODA
CLASS SECERNENTIA ( PHASMIDS )
 Ascaris lumbricoides
common name: Giant Intestinal
Round worm
Ascaris lumbricoides
Most common and largest intestinal nematode of man
Common name: Giant Intestinal Roundworm
The distribution of the parasite is cosmopolitan
Primarily a parasite specific for man
There are two separate populations and reservations of
the parasite: one consists of adult parasitizing man
and the other of eggs/ova in the environment
Habitat: Small intestine
Infective stage: embryonated egg
Diagnostic stage: fertilized and unfertilized ova
MORPHOLOGY
 Fertilized egg
 Ovoid (broader)
 Measures 35-50 um by 45-75 um
 With thick egg shell
 May have coarse mamillated
albuminous coating
 Corticated or decorticated
 Fine granular germ cell
 Unfertilized egg
 Ovoid (Narrower)
 Measures 88-94 um by 39-44 um
 With thin egg shell
 May have thinner albuminous layer
Corticated or decorticated
 Coarse granular germ cell
 Embryonated egg
 Developing larva is seen within the
shell
MORPHOLOGY
MORPHOLOGY
ADULT
Creamy-white or pinkish-yellow when freshly expelled
Female: bigger, tapered at both ends
Male: smaller, curved posteriorly
The anterior end is provided with 3 lips (trilobite) and a
buccal cavity at the center of the lips
At the junction of the anterior and middle third of the female
worm is a depression around the body where the vagina is
located (genital ring). The male worm aided by its curved tail
should locate this depression during copulation.
The reproductive potential of a mature female worm is about
240,000 eggs per day
Male
Measures 15-25 cm by 2-4 mm
Curved posterior end
With a pair of copulatory spicules

Female
Measures 20-25 cm by 3-5 mm
Straight posterior end
With genital ring (Middle 3rd of the worm)
LIFE CYCLE
Infective stage : Embryonated egg
Mode of Transmission : Ingestion of infective
egg (embryonated egg)
Portal of Entry : Mouth
*** With larval migration
Habitat : Small Intestine
Portal of Exit : Anus
CLINICAL MANIFESTATION AND
PATHOLOGY
Pathology due to larvae migration
- initial pathological lesion in Ascaris is associated
with migrating larvae
- the severity of lesion depends on:
1. Sensitivity of the host
2. Nutritional status of the host
3. Number of the migrating larva
CLINICAL MANIFESTATION AND
PATHOLOGY
B. Pathology due to adult worm
- it produce various pathological lesions in the following
ways:
1. MECHANICAL ACTION – adult worms can cause
obstruction of the intestinal tract in heavy infections
2. SPORIATIVE ACTION – adult worms affect the nutritional
status of the host by robbing off its nutrition
- It leads to malnutrition and retardation of growth and
development
3. ALLERGIC REACTION – metabolites of the living or the
dead adults are toxic and immunogenic
CLINICAL MANIFESTATION AND
PATHOLOGY
Ascariasis
Light infections: Asymptomatic
Migrating larva : pnemonitis, eosinophilia, Loeffler’s
syndrome

Sandbox infection, POT BELLY ( BOLLUS ) ;

appendicitis
DIAGNOSIS
Diagnosis
1. Laboratory Diagnosis
a. DFS (Direct Fecal Smear) - routine
b. Kato Technique or Cellophane Thick smear
c. Kato - Katz Technique
d. Concentration technique
**Stool exam may give NEGATIVE findings in:
1. Worms are still immature in the lumen
2. During larval migration
3. Infection with only male Ascaris worm
4. Extra intestinal infection
DIAGNOSIS
2. Serodiagnosis
- frequently used in the diagnosis of extra intestinal Ascariasis
Commonly used tests include:
1. Indirect Hemagglutination
2. Immunofluorescent Ab
3. Moan Intradermal test
3. Sputum

4. Imaging Method – for extra cellular ascariasis

a. X-ray
b. Ultrasound
c. CT scan
Reservoir, source and Mode of
Transmission
- Man is the only host and reservoir of infection
- Transmission is by FECAL-ORAL
- Infection is common in area with:
a. High density of human population
b. Poor sanitation
c. Habit of people to defecate indiscriminately in and
around settlement
d. Use of infected feces as fertilizer
Control and Prevention

Treatment of cases (Broad Spectrum anti-

helminthes)
Albendazole ; Mebendazole ; Pyrantel pamoate
Mass treatment is advisable
Proper hygiene
Proper waste disposal
Avoid the use of night soil as fertilizer
Toxocara spp

Toxocara canis ( Dog Ascaris/ Dog

Roundworm )

Toxocara cati ( Cat Ascaris/ Cat

Roundworm )
Visceral Larva
COMMON NAME:
 Toxocara canis : Dog ascaris
 Toxocara cati : Cat ascaris
Naturally parasitic in the intestines of dogs and cats that
accidentally infect human (abberant host) producing disease
known as Visceral Larva Migrans (VLM) or Toxocariasis
Life cycle in dogs and cats is the same as the human ascaris
When the embryonated is ingested by man, larvae will hatch
and cannot follow its normal course of development as seen
in their normal host.
The larvae will penetrate the intestinal mucosa and are
carries by the blood stream to the liver, lungs and other
organs
MORPHOLOGY
Adult
Similar to Ascaris lumbricoides
but smaller in size
Body is bent ventrically
 T. canis = Bow Cervical Alae

 T. cati = Arrowhead Cervical Alae

Morphology
OVA
Resemble those of Ascaris but LARGER LESS
ELONGATE WITH THINNER SHELL AND
ALBUMINOID OUTER COVERING
LIFE CYLCE
PATHOLOGY
VISCERAL LARVA MIGRANS
Infection of Visceral organs

OCULAR LARVA MIGRANS

Eye infection
DIAGNOSIS
SEROLOGY
 Enterobius vermiccularis
common name: Pin worm, Seat
worm, Communal worm
Common name: Pinworm or Seatworm
Disease: Enterobiasis or Oxyuriasis
Infective stage and diagnostic stage: embryonated egg
(larva inside the eggs mature within 4 to 6 hours after
oviposition)
Morphology
ADULT
Small, whitish or brown in color.
MALE: measures 2-5 mm in length, the tail is strongly
curved and a single copulatory spicule is present
FEMALE: measures 8-13 mm in length, it has long
pointed tail. The Uteri of gravid female are distended
with eggs
MORPHOLOGY
DIAGNOSTIC FEATURE:
Pair of lateral cuticular wing-like expansion at the
anterior end known as “cephalic alae”
Distinct or prominent esophageal bulb
Morphology

OVA
Elongated, measuring 50-60 by 20-30 microns; wherein
the ventral side is flattened thus the appearance is
similar to letter “D” or characteristically lopsided
There are 2 layers:
Outer thick hyaline albuminous layer
Inner embryonic, lipoidal layer
MORPHOLOGY
The eggs are fully embryonated when laid and will mature
within six hours after oviposition and these are already
infective
Gravid females oviposit 4,600 to 17,000 eggs per day
Eggs are resistant to disinfectant and under cool condition
and may remain viable for 13 days
LIFE CYCLE
LIFE CYCLE
Infective stage : Embryonated egg
Mode of Transmission : Ingestion ; Inhalation ;
Direct contact ; Autoinfection
Portal of Entry : Mouth ; Nose ; Anus
(Depending on the MOT)
Habitat : Large Intestine
Portal of Exit : Anus
PATHOLOGY
Pathology at the site of attachment of the worm
(cecum/ileum)
 Development of minute ulcerations in cecal
mucosa
Pathology due to egg deposition in the perianal
area
Migrating gravid female worm – lays eggs
Produce intense itchiness – PRURITUS ANI
leads to hemorrhages ; pyogenic infection in the
perianal region à restlessness --à insomia
PATHOLOGY
Pathology due to migrating worm in female
patients
 May oviposit in genital organ
 Produce mucoid vaginal discharge
 May enter in the reproductive tract
 Leads to infection
DIAGNOSIS

Scotch Tape Method – should be done in the morning

 Female : oviposit at night

Fecalysis – (DFS) - 5% are demonstrable in stool

*** 10% in rural areas

Washing of hand - Ova maybe be seen

Common modes of transmission:
Hand to mouth transmission
Inhalation of airborne eggs from dust
Autoinfection from the anus
Handling contaminated soiled linens and night
clothes of infected individual
PREVENTION AND CONTROL
Treatment of cases
Broad spectrum anti-helminthes
All members of the family (Communal parasite)

Proper personal hygiene

Sterilization of contaminated linens

***Up to 75% in crowded urban areas

Strongyloides stercoralis
Common name : Threadworm
This nematode is a good example of a facultative
parasite because under certain conditions, it can exist
as a free-living organism, but when conditions in the
soil become unfavorable, it reverts to a parasitic
existence
Of the human nematode infections, only
Strongyloides is capable of perpetuation in man by
producing many generations of infective larvae from
parthenogenetic females
Common name: Threadworm
Habitat: Mucosa of the Small Intestine
Infective stage: filariform larva (L3)
Diagnostic stage: rhabditiform larva (L1)
MORPHOLOGY
Female worm
Free living –shorter than parasitic
 With double bulbed muscular esophageal pharynx

Parasitic female
 Delicate filiform worms (2.2mm)
 Parthenogenetic – requires no male in fertilization
MORPHOLOGY
Male worm
Free living – smaller than female
No parasitic male
Gradually passed in the feces
MORPHOLOGY

Rhabditiform larva
Stage that is passed
in stool
Feeding stage
With short buccal
cavity and elongated
esophagus
With prominent
genital primordium

MORPHOLOGY
Filariform Larva
Longer than RL
With forked or notched tail
S. stercoralis Fila vs Rhabdi
BUCCAL Cavity Esophagus
Filariform None Long
Rhabditiform Short Long
LIFE CYCLE
LIFE CYCLE
Infective stage : Filariform larva
Mode of Transmission : Skin penetration
Portal of Entry : Skin
*** With larval migration
Habitat : Small Intestine
Portal of Exit : Anus

*** with FREE – LIVING CYCLE

*** AUTOINFECTION may also occur
LIFE CYCLE
INDIRECT LIFE CYCLE / HETEROGENIC

Free-living existence in soil => rhabditiform =>

filariform = > copulation => egg => rhabditiform
LIFE CYCLE
AUTOINFECTION

Rhabditiform in intestinal lumen => matures in

filariform => skin penetration ( usually in perianal
area )
PATHOGENESIS
Due to larva
 Dermatitis
 Petechial hemorrhages and itching at the site
of penetration
Ground/ Dew/ Coolie itch
Pulmonary lession
Eosinophilia – characteristics of infection
Loeffler’s syndrome
PATHOGENESIS
Due to adult worm (F)
Destruction of the intestinal mucosa
Abdominal pain and diarrhea
 Malabsorption and hypoalbuminemia
Cochin China diarrhea / Vietnam diarrhea/ Larva
curens
Immunocompromised : Dissimiated
Strongyloidiasis
***PARTHENOGENETIC --à Autoinfection (20-
30yrs)
Due to adult worm (F)
Destruction of the intestinal mucosa
-à Abdominal pain and diarrhea
 --àMalabsorption and hypoalbuminemia

***PARTHENOGENETIC --à Autoinfection (20-
30yrs)
DIAGNOSIS
Direct Microscopy
Harada-Mori
Bearmann Technique
Sputum / Urine
Reservoir, Source, Mode of
Transmission
 1. By penetration of the skin by Filariform
larvae
 2. Transmammary transmission
 3. Ingestion of food and drink contaminated
with larvae
 4. Organ transplant
Control and Prevention

Treatment of cases (Broad Spectrum anti-

helminthes)
Albendazole ; Mebendazole ; Pyrantel pamoate
Mass treatment is advisable
Proper hygiene
Proper waste disposal
Use of footwear
HOOKWORMS and Cutaenous
Migrans
Ancylostoma duodenale
Necator americanus
Ancylostoma caninum
Ancylostoma braziliense
Common names:
Necator americanus – New world hookworm
Ancylostoma duodenale – Old world hookworm
Ancylostoma caninum – Dog hookworm
Ancylostoma braziliense – Cat hookworm
Habitat: Adult – Lumen of the Small Intestine
Infective stage: filariform larva (L3)
Diagnostic stage: ova
Human hookworms are blood-sucking nematodes,
attached to the mucosa of the small intestine among
people living in tropical and subtropical countries
Human Hookworms
A. duodenale vs N. americanus
Necator americanus (Stiles, 1902)
Adults are relatively stout, cylindrical, fusiform, grayish-
white
It has a tendency to go against the general body
curvature at the anterior end, forming a “hook”
The females are longer with a blunt posterior end, the
males are shorter and the posterior end is expanded to
form a fan-like bursa copulatrix used for copulation and
is characteristic for all male hookworm species
Both male and female adult worms have well-developed
buccal capsules characterized by the presence of semi-
lunar cutting plates
Human Hookworms
A. duodenale vs N. americanus
Ancylostoma duodenale (Dubini, 1843)
Adults have in their buccal capsules, two pairs of ventral
teeth similar in size
Body contour tends to follow the general curvature of
the body hence looking like a letter “C”
Necator Ancylostoma
americanus duodenale
New World HW •Old World HW
With 1 pair of •With 2 pairs of
semi-lunar large teeth
cutting plate
MORPHOLOGY
Adult Worm
With cervical
curvature ; F is
longer than M
Male has fan-
shaped posterior
end (copulatory
bursa / bursa
copulatrix) where
RAYS and
SPICULES can be
found
MORPHOLOGY
Anterior with different dental pattern
Basis of species identification
Egg
Ovoidal thin-shelled and colorless.
In the feces, they are already in the 4 to 8 celled stage.
In constipated stool, embryo may already develop inside
the shell
Differentiation of Necator egg from Ancylostoma egg is
difficult and impractical
UNHOLY TRIAD
HOOKWORM VS THREADWORM
HOOKWORM THREADWORM
Buccal Cavity LONG Short
Genital Primodium Short LONG
N. Americanus vs A. duodenale
N. americanus A. duodenale

Dental Pattern Cutting plates 2 pairs of fused teeth

Copulatory bursa Longer than broad Short and board

Dorsal rays Deep cleft and tipds Shallow cleft and tips
bipartite tripartite

Spicules 2 spicules – fused and 2 spicules – UNFUSED

barbed and NOT barbed
LIFE CYLCE
LIFE CYCLE
Infective stage : Filariform larva
Mode of Transmission : Skin penetration
Portal of Entry : Skin
*** With larval migration
Habitat : Small Intestine
Portal of Exit : Anus
PATHOGENESIS
1. Pathology due to the larval stage
a. Ground itch or Coolie itch
b. Pulmonary lesion or Wakana Disease
2. Pathology due to adult worms
a. Hookworm anemia
b. Hypoalbuminemia
DIAGNOSIS
Hookworm infection is diagnosed by the recovery of
eggs on the stool examination using:
a. Direct Fecal Smear (DFS)
b. Kato-Katz technique
c. Concentration techniques
c.1. Brine Floatation Technique
 c.2. Formalin-Ether Concentration
Technique
DIAGNOSIS
When stools have stood for 12 to 24 hours before the
examination was done, some eggs hatched and the
rhabditiform larvae should be differentiated from
those of Strongyloides stercoralis using Harada-Mori
(Culture Method)

Positive OCCULT BLOOD

CUTANEOUS LARVA MIGRANS
A.braziliense vs A. caninum
Ancylostoma braziliense
Cat hookworm
Possesses a pair of large teeth and a pair of
inconspicuous median teeth in the buccal capsule
Ancylostoma caninum
Dog hookworm
Buccal cavity is provided with three pairs of ventral teeth
The cephalic or amphidial gland of the worm secretes an
anticoagulant that delays coagulation of blood
HOOKWORMS
N. A.duodenale A.braziliensi A.caninum
americanus s
Dental feature Cutting plates 2 pairs of 2 ventral pairs 3 ventral pairs
fused teeth of Unfused of fused teeth
teeth

Copulatory Longer than Short and Large, flame- As broad as

bursa broad board shaped long
Rays- Long Rays- stunted
and slender
LIFE CYCLE
PATHOLOGY OF ANIMAL
HOOKWORMS
Forms serpiginous tunnels = CREEPING ERUPTION

“CUTANEOUS LARVA MIGRANS”

ECTOPARASITE = SKIN ONLY

NICE TO KNOW
Ancylostoma ceylanicum
Smallest hookworm species
Common parasite of cats and less frequently of dogs
Factors that contribute to the
transmission of hookworms
1. Suitability of the environment for eggs or larvae
2. Mode and extent of fecal pollution of the soil
3. Mode and extent of contact between infected soil
and skin or mouth
TREATMENT AND PREVENTION
Treatment of cases (Broad Spectrum anti-
helminthes)
Albendazole ; Mebendazole ; Pyrantel pamoate
Mass treatment is advisable
Proper hygiene
Proper waste disposal
Use of footwear

GROUP ACTIVITY
5 members per group
WRITE YOUR NAMES IN A ½ Crosswise Yellow paper
PICK A NAME OF YOUR GROUP
BTS EXO SEVENTEEN WANNAONE
RED VELVET BLACKPINK IOI
I will show pictures of
nematodes then identify, write
the scientific name and
common name of the parasite
In cases of Ascaris ova, write if
Fertilized, Unfertilized or
Decorticated
You’ll have 30 seconds to
identify the parasite
Take note; there can be
multiple parasite in one slide
This is a group effort; identify as many as you can

Winners:
First placer : 100
Second placer: 90
Third placer : 85
NON placer:80
Good LUCK
Slide 1
Slide 2
SLIDE 3
SLIDE $
Slide 6
Slide 7
Slide 8
Slide 9
SLIDE 10
EXTRA INTESTINAL AND BLOOD
NEMATODES
FILARIAL NEMATODES
Arthropod transmitted nematodes
Mostly night - feeding mosquitoes
The sheathed group (retain the embryonic
sheath)
Wuchereria bancrofti, Brugia malayi and Loa loa
The unsheathed group (do not retain the
embryonic sheath)
Onchocerca volvulus, Dipetalonema perstans,
Manzonella pertans
Adult worms are thread-like, they have simple mouth
which is circular or slightly elongated dorsoventrally
and is surrounded by papillae
Adult worms live in the lymphatics, subcutaneous
tissues, connective tissues, muscle and body cavities of
the host
Female adult worms are viviparous. Larvae are called
microfilaria
Humans are the key definitive host
Filarial worms are transmitted through the bite of
arthropod
Periodicity - refers to the rhythmical
appearance of the microfilaria in the
peripheral blood
Nocturnal – appears during the night ( 10 pm – 2
am)
Diurnal – appears during day(10 am – 2 pm )
Superiodic – appears during day and night
 Nocturnal subperiodic – count is peak during night time
 Diurnal subperiodic – count is peak during day time

Non-periodic – no difference in count

 Wuchereria brancrofti
common name: Brancroft’s filarial
worm
MORPHOLOGY
Wuchereria bancrofti
Adult: minute, whitish and thread-like
and are filariform in shape with a smooth
surface. Both anterior and posterior
portion are tapering.
Male – tail is sharply curved ventrally
Female – Viviparous, longer than male
LIFE CYCLE
INTERMEDIATE HOSTS
Aedes poecilus
Anopheles minismus flavirostris
Culex quinquefasciatus
PATHOLOGY
Elephanthiasis of lower
extremeties with
chylocele and Chyluria
Tropical pulmonary
Eosinophilia
DIAGNOSIS
Blood smear
Nocturnal in periodicity
Presence of Sheathed microfilariae free from nuclei at
the tip
Graceful appearance
 Brugia malayi
common
name : Brugian
/ Malayan
filarial worm
B. malayi
Malayan filarial worm
HABITAT : Upper lymph
gland
INTERMEDIATE
HOST :Mansonia, Culex
SAMPLE :Peripheral blood
PERIODICITY: Subperiodic
nocturnal
MORPHOLOGY
Sheathed microfilariae
2 discrete nuclei on the tip
Kinky appearance
W.brancrofti vs B.malayi
Life cycle
PATHOLOGY
“ELEPHANTHIASIS OF UPPER EXTREMITIES”
The clinical manifestation of Malayan Filariasis and
Bancroftian Filariasis nearly the same but with only
few differences
The common sites of elephantiasis include the legs
below the knee and less frequently the arm below the
elbow. Genital involvement and chyluria are absent.
* The diagnosis and treatment are the same as described
in Bancroft's filariasis.
Diagnosis
 Same as W.brancrofti
 Standard method : Peripheral Blood Smear
 wet smear – unstained; motile mf could be seen
 DISADV: cannot be kept for future reference
 Stained smear – differentiation of species ; can be stored for
future reference
 Venous Blood Sample
 Knott’s Concentration Technique : used for low intensity of infection
 *** Microfilariae circulate nocturnally, making blood collection an issue

 Card Test : Antigen detection : parasite specific

 requiring only a small amount of blood has been developed
 Does not require laboratory equipment
 Blood drawn by finger stick
Ultrasonography – demonstrate live worms in the
lymphatics
Foot Biopsy - Normal Skin with areas of chronic
inflammation
 Loa loa
common name : Eye worm
Adult worms move under human skin
Observed beneath skin or passing through
conjunctiva of eyes (‘eye worms’)
Worms = 2 races (attack humans or arboreal
primates)
Sheathed Microfilaria
Nuclei irregularly spaced to tip/
Continuous to the tip
Diurnal in periodicity

Intermediate host
Chrysops
Pathology
Callabar swelling

Disease endemic to rain forest regions of West

& Central Africa
Generally mild & painless (chronic) with 10-15
year incubation period
May cause swellings of skin (Calabar swelling)
Onchocerca volvolus
common name: River Blinding worm
Adults accumulate in subcutaneous
nodules (1cm diameter) which don’t
cause much damage
Mating in nodules produces
microfilariae
Live under skin causing rashes &
wrinkles
Cause blindness when invade eyes
tissues

Early stages of eye damage can be reversed by
drug treatment
Parasiticide ivermectin is most popular
Transfer of worms affected by feeding behaviour
of flies
Waggle mouth parts during biting to increase
wound size & create pool of blood (‘pool feeders’)
MORPHOLOGY
Unsheathed
Free from nuclei

Diagnosis : Skin snips biopsy/ Mazzoti test

Pathology
RIVER BLINDNESS
LET’S REVIEW
Mansonella species
Mansonella perstans
Mansonella steptocerca
Mansonella ozardi
Mansonella species
Unsheathed

Intermediate hosts =
biting midge
Mansonella perstans
Mansonella streptocerca
Mansonella ozzardi
FILARIASIS
Control and Prevention
Most effective method : avoid mosquito bites (for
W.bancrofti and B.malayi)
Sleep under a bed net
Wear long sleeves and trousers
Wear insect repellent on exposed skin, especially
at night

Vector Control :
Killing eggs (oviciding) and killing or disrupting
larva (larviciding) in bodies of stagnant water can
further reduce mosquito populations.


Treatment of filariasis involves two components:
Getting rid of the microfilariae in people's blood
Maintaining careful hygiene in infected persons to reduce the incidence and
severity of secondary (e.g., bacterial) infections.

Anti-filariasis medicines commonly used include:

Diethylcarbamazine (DEC)
reduces microfilariae concentrations
kills adult worms
*** Table salt maybe fortified with DEC.
 Albendazole
kills adult worms
Ivermectin
 kills the microfilariae produced by adult worms
*** The disease is usually treated with single-dose
regimens of a combination of two drugs, one
targeting microfilariae and one targeting adult
worms (i.e.,either diethylcarbamazine and
albendazole, or ivermectin and albendazole
OTHER EXTRAINTESTINAL
NEMATODES
Angiostrongylus cantonensis
Common name : “RAT LUNG WORM”

Barber’s pole appearance

Acquired through ingestion of infective larva in snail

and prawns

Disease: Eye invasion, CNS involvement

( Eosinophillic myeloencephalitis )
Dracunculus medinensis
Common name: “Dragon
worm” : Medina worm” “Serpent
worm” “ Guniea worm” “ Fiery
Serpent of the Israelites “

Longest nematode parasite to

infect man
Adult Male: Catgut Thread

Adult female: larviparous

Intermdiate hosts: Cyclops ( copepods “water fleas” )

Pathogenesis
Formation of blisters, however if the worm fails to reach
the skin, it dies and either disentigrates or become
calcified  presence in mesenteric tissues 
Pseudoperitoneal syndrome  allergic manifestations
Dirofilaria immitis
Common name: Dog Heartworm
Filarial parasite ( unsheathed and partial nocturnal )
Several species of mosquitoes serve as vectors
Very common in dogs
Pathogenesis
Solitary, peripheral nodules in the lung ( coin lesions );
subcutaneous nodules, pulmonary lesions
Gnathostoma spinigerum
Rust colored, cephalic bulb with
four rows of hooks

Acquired through ingestion of

infected fish, birds, snakes

Disease: Gnathostomiasis,
Visceral larva migrans-like
syndrome, CNS involvement
Anisakis
Common name :
Herring’s worm

Definitive host : whales

and Dolphina

3 Intermediate host :
1st = copepod
2nd = small fishes
3rd = larger fishes
Acquire through ingestion of raw fish infected with
larva

Pathogenesis : Granulomatous abscess