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Phylum Nematoda

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
APAPILLAE 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
AADULT
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.
.
AAdult male
AMeasures 3 -3.5 cm
AWith curve posterior end

AAdult Female
AMeasures 3.5 – 5.5 cm
AWith straight posterior end
Morphology

stichocytes


Morphology
OVA
Barrel-

shaped/Lemonshaped/football-shaped with thick,


smooth, double layer, yellowishbrown egg shells and
two prominent plugs protruding at both ends
LIFE CYCLE
AInfective stage : Embryonated egg
AMode of Transmission : Ingestion of infective
egg
APortal of Entry : Mouth
A*** No larval migration
AHabitat : Large Intestine
APortal 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

A Treatment of cases (Broad Spectrum


antihelminthes)
AAlbendazole ; Mebendazole ; Pyrantel pamoate
AMass treatment is advisable
A Proper hygiene
A Proper waste disposal
A 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 fisheating 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
AOVA
APeanut-shaped with striated
shells/ Guitar -shaped
AFlattened bipolar plugs
AMeasures 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
A Adult worm
A Male : 1.5 – 3.9mm long ; With spicule
A 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
A Infective stage : Third stage Larva
A Mode of Transmission : Ingestion of the infective
larva in the fresh water fish
(BAGSIT : Intermediate Host)
A Portal of Entry : Mouth
A Definitive Host : Man ; Migrating Birds (Natural
Host)
A Habitat : Small Intestine
A Portal of Exit : Anus
PATHOLOGY
ACauses Borborygmus (Gurgling stomach)
AAbdominal pains
ADiarrhea
Aweight loss, malaise, vomiting, anorexia and
edema
Aloss of protein ; malabsorption of fats ; loss of
electrolytes
A death if not treated soon

AResponsible for Mystery Disease


DIAGNOSIS
AFecalysis (DFS & Conc. Tech.)
AEggs
ALarva
AAdult

ADuodenal aspirates
Adult worm maybe recovered

Control and Prevention


ATreatment of cases - Broadspectrum
antihelminthes AManagement of cases
AElectrolyte replacement
AHigh protein diet
A Prevention
ARefrain from eating raw fishes
AGood 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
A Thread like worm, barely visible by naked eyes

A 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
A 1.5mm by 0.4mm
A Females
Larviparous
They have single uterus, filled with developing eggs in the posterior
region but fully developed and hatched larvae in the anterior region
A 3-4mm by 0.6mm
MORPHOLOGY
ALARVAE
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
A *** zoonotic parasite ( animal to human)

A HOSTS : wild cats, wild dogs, wild rats, pigs -----


à man (dead end)
A Muscles affected by the parasite among human
hosts
A Muscle of the respiratory system (diaphragm)
A Muscle of the heart
A Muscle of the limbs
A Muscles of the eyes
A Muscles of the tongue
PATHOLOGY
ABoth 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
AInflammation
AGranulation formation
ACalcification
PATHOLOGY
ACLINICAL 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
A Unfertilized egg
A Fertilized egg A Ovoid (Narrower)
A Ovoid (broader) A Measures 88-94 um by 39-44 um
A Measures 35-50 um by 45-75 um
A With thick egg shell A With thin egg shell
A May have coarse mamillated A May have thinner albuminous layer
albuminous coating A Corticated or decorticated
A Corticated or decorticated A Coarse granular germ cell
A Fine granular germ cell A Embryonated egg
A 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
A Male
A Measures 15-25 cm by 2-4 mm
A Curved posterior end
A With a pair of copulatory spicules

A Female
A Measures 20-25 cm by 3-5 mm
A Straight posterior end
A With genital ring (Middle 3rd of the worm)
LIFE CYCLE
AInfective stage : Embryonated egg
AMode of Transmission : Ingestion of
infective egg (embryonated egg) APortal of
Entry : Mouth
A*** With larval migration
AHabitat : Small Intestine
APortal 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
A 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

A Treatment of cases (Broad Spectrum


antihelminthes)
AAlbendazole ; Mebendazole ; Pyrantel pamoate
AMass treatment is advisable
A Proper hygiene
A Proper waste disposal
A 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
A T. canis = Bow Cervical Alae

A T. cati = Arrowhead Cervical Alae


Morphology
OVA
Resemble those of Ascaris but LARGER LESS
ELONGATE WITH THINNER SHELL AND
ALBUMINOID OUTER COVERING
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
A 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

A 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
AInfective stage : Embryonated egg
AMode of Transmission : Ingestion ; Inhalation
; Direct contact ; Autoinfection
APortal of Entry : Mouth ; Nose ; Anus
( Depending on the MOT)
AHabitat : Large Intestine
APortal of Exit : Anus
PATHOLOGY
APathology at the site of attachment of the
worm (
cecum/ileum)
A Development of minute ulcerations in cecal
mucosa

APathology due to egg deposition in the


perianal
area
AMigrating gravid female worm – lays eggs
AProduce intense itchiness – PRURITUS ANI
Aleads to hemorrhages ; pyogenic infection in
the perianal region à restlessness --à insomia
PATHOLOGY
APathology due to migrating worm in female
patients
A May oviposit in genital organ
A Produce mucoid vaginal discharge
A May enter in the reproductive tract
A Leads to infection
DIAGNOSIS
A Scotch Tape Method – should be done in the
morning
A Female : oviposit at night

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


A *** 10% in rural areas
A 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


ATreatment of cases
ABroad spectrum anti-helminthes
AAll members of the family (Communal parasite)
AProper personal hygiene
ASterilization of contaminated linens
A***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
A Female worm
AFree living –shorter than parasitic
A With double bulbed muscular esophageal pharynx

AParasitic female
A Delicate filiform worms (2.2mm)
A Parthenogenetic – requires no male in fertilization
MORPHOLOGY
A Male worm
AFree living – smaller than female
ANo parasitic male
AGradually passed in the feces
MORPHOLOGY
ARhabditiform larva
AStage that is passed in stool
AFeeding stage
AWith short buccal cavity and elongated
esophagus
AWith prominent genital primordium
A

MORPHOLOGY
AFilariform Larva
ALonger than RL
AWith forked or notched tail
S. stercoralis Fila vs Rhabdi
BUCCAL Cavity Esophagus

Filariform None Long


Rhabditiform Short Long
LIFE CYCLE
LIFE CYCLE
AInfective stage : Filariform larva
AMode of Transmission : Skin penetration
APortal of Entry : Skin
*** With larval migration
AHabitat : Small Intestine
APortal of Exit : Anus A***
with FREE – LIVING CYCLE
A*** 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
A Dermatitis
A Petechial hemorrhages and itching at the
site of penetration
A Ground/ Dew/ Coolie itch
APulmonary lession
AEosinophilia – characteristics of infection
ALoeffler’s syndrome
PATHOGENESIS
Due to adult worm (F)
ADestruction of the intestinal mucosa
AAbdominal pain and diarrhea
AMalabsorption and hypoalbuminemia
ACochin China diarrhea / Vietnam diarrhea/ Larva
curens
AImmunocompromised : Dissimiated
Strongyloidiasis
A ***PARTHENOGENETIC --à Autoinfection (
20-30yrs)
A Due to adult worm (F)
A Destruction of the intestinal mucosa
A -à Abdominal pain and diarrhea
A--àMalabsorption and hypoalbuminemia
A
A ***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

A Treatment of cases (Broad Spectrum


antihelminthes)
AAlbendazole ; Mebendazole ; Pyrantel pamoate
AMass treatment is advisable
A Proper hygiene
A Proper waste disposal
A 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
ANecator 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 welldeveloped
buccal capsules characterized by the presence of semi-
lunar cutting plates

Human Hookworms
A. duodenale vs N. americanus
AAncylostoma 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”
ANecator
americanus
ANew World HW
AWith 1 pair of
semi-lunar
cut ting plate
Ancylostoma
duo denale
• Old World
HW
• With 2 pairs
of large teeth
MORPHOLOGY
A Adult Worm
AWith cervical
curvature ; F is
longer than M
AMale has
fanshaped
posterior end
(copulatory bursa
/ bursa copulatrix)
where
RAYS and SPICULES can be found
MORPHOLOGY
A Anterior with different dental pattern
ABasis of species identification
A 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 bipartite Shallow cleft and tips tripartite

Spicules 2 spicules – fused and barbed 2 spicules – UNFUSED and NOT barbed
LIFE CYCLE
AInfective stage : Filariform larva
AMode of Transmission : Skin penetration
APortal of Entry : Skin
A*** With larval migration
AHabitat : Small Intestine
APortal 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
AAncylostoma braziliense
Cat hookworm
Possesses a pair of large teeth and a pair of inconspicuous
median teeth in the buccal capsule
AAncylostoma 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. americanus A.duodenale A.braziliensis A.caninum

Dental feature Cutting plates 2 pairs of fused teeth 2 ventral pairs of 3 ventral pairs of fused
Unfused teeth teeth

Copulatory bursa Longer than broad Short and board Large, flame-shaped As broad as long Rays-
Rays- Long and slender stunted
LIFE CYCLE
PATHOLOGY OF ANIMAL
HOOKWORMS
Forms serpiginous tunnels = CREEPING ERUPTION
“CUTANEOUS LARVA MIGRANS”

ECTOPARASITE = SKIN ONLY


NICE TO KNOW
AAncylostoma 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


A Treatment of cases (Broad Spectrum
antihelminthes)
AAlbendazole ; Mebendazole ; Pyrantel pamoate
AMass treatment is advisable
A Proper hygiene
A Proper waste disposal
A 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

READY?????? START
WAIT >.< !!!!!!!!!!!!!!!
After the 10th slide, your group has 5 more minutes to
finalize your answers
Slide 1
SLIDE 3
SLIDE $
Slide 6
Slide 7
Slide 8
Slide 9
SLIDE
10
YOU NOW HAVE 5 minutes to
Finalize your answer
NOW WE’RE DONE !!! ARE YOU
READY TO FACE THE JUDGMENT???
DONE WITH NEMATODES????
NAH!!!! We’re just halfway....
enough with the intestines Let’s
have some Blood

EXTRA INTESTINAL AND


BLOOD NEMATODES
FILARIAL NEMATODES
AArthropod transmitted nematodes
AMostly night - feeding mosquitoes
AThe sheathed group (retain the embryonic
sheath
)
AWuchereria bancrofti, Brugia malayi and Loa loa
AThe unsheathed group (do not retain the
embryonic sheath)
AOnchocerca 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
A Periodicity - refers to the rhythmical
appearance of the microfilaria in the
peripheral blood
ANocturnal – appears during the night ( 10 pm – 2
am)
ADiurnal – appears during day(10 am – 2 pm )
ASuperiodic – appears during day and night
A Nocturnal subperiodic – count is peak during night time
A Diurnal subperiodic – count is peak during day time
ANon-periodic – no difference in count

Wuchereria brancrofti
common name: Brancroft’s filarial
worm
MORPHOLOGY
AWuchereria 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
AINTERMEDIATE 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
AB. 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
A Standard method : Peripheral Blood Smear A
wet smear – unstained; motile mf could be seen
A DISADV: cannot be kept for future reference
A Stained smear – differentiation of species ; can be stored
for future reference
A Venous Blood Sample
A Knott’s Concentration Technique : used for low intensity of
infection A *** Microfilariae circulate nocturnally, making blood
collection an issue

A Card Test : Antigen detection : parasite specific


A requiring only a small amount of blood has been
developed
A Does not require laboratory equipment
Blood drawn by finger stick
AUltrasonography – demonstrate live worms in
the lymphatics
AFoot Biopsy - Normal Skin with areas of
chronic
inflammation
Loa loa
common name : Eye worm
AAdult worms move under human skin
AObserved beneath skin or passing through
conjunctiva of eyes (‘eye worms’)
AWorms = 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

A Disease endemic to rain forest regions of


West & Central Africa
A Generally mild & painless (chronic) with
10-15 year incubation period
A May cause swellings of skin (Calabar
swelling)
Onchocerca volvolus common name:
River Blinding worm
AAdults accumulate in
subcutaneous nodules (1cm
diameter) which don’t cause
much damage
AMating in nodules produces
microfilariae
ALive under skin causing
rashes & wrinkles
ACause blindness when invade eyes
tissues
A
AEarly stages of eye damage can be reversed by
drug treatment
AParasiticide ivermectin is most popular
ATransfer of worms affected by feeding
behaviour of flies
AWaggle 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
A Mansonella perstans
A Mansonella steptocerca
A Mansonella ozardi
Mansonella species
Unsheathed

Intermediate hosts = biting midge

Mansonella perstans
Mansonella streptocerca
Mansonella ozzardi
FILARIASIS
AControl and Prevention
AMost effective method : avoid mosquito bites (
for W.bancrofti and B.malayi)
ASleep under a bed net
AWear long sleeves and trousers
AWear insect repellent on exposed skin,
especially at night
A
AVector Control :
AKilling eggs (oviciding) and killing or
disrupting larva (larviciding) in bodies of
stagnant water can further reduce mosquito
populations.
AA
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

A*** The disease is usually treated with


singledose 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
NOW we’re done with nematodes

kaya pa????

Kaya !!!!!!
Hwaiting ( Figthing )
THANK YOU FOR LISTENING

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