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Parasitology - Nematodes
Medical Technology (Southwestern University PHINMA)
Studocu is not sponsored or endorsed by any college or university
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lOMoARcPSD|18320988
P2  CLINICAL PARASITOLOGY | NEMATODE INFECTIONS
Compiled by VJC and GA
1. Based on life stages (laying eggs or larva):
1.A. Oviparous
PHYLUM NEMATODA
– “roundworms”
 Eggs w/ segmented ovum
– bilaterally symmetrical helminthes
 hookworm
– elongated cylindrical bodies; complete digestive tract
 Trichostrongylus spp.
– with sensory chemoreceptor
– sexes – typically separate
 Eggs w/ unsegmented ovum
* Male – smaller than female; curved posterior end
 Ascaris spp.
 Heteroxenous – more than one host
 Homoxenous – only one host
 Eggs w/ unsegmented ovum
– usual cycle:
w/ mucus plug at both ends
Egg stage  Larval stage  Adult stage
 Trichuris spp.
Side notes:
 Eggs containing larva
 Smallest worm: Trichinella spiralis
 Enterobius spp.
 Longest worm: Dracunculus medinensis (up to 1m)
 Largest worm: Dioctophyma renale
 Largest common worm: Ascaris lumbricoides
1.B. Viviparous/Larviparous
ACQUISITION:
 Ingestion of fully embryonated ova
 directly gives birth to larvae
 Trichuris trichiura
 no egg stage; filarial worm
 Ascaris lumbricoides
 Trichinella spp.
 Enterobius vermicularis
 Dracuncular spp.
 Ingestion of fully embryonated encysted larva
1.C. Ovoviviparous
 lays eggs that immediately
 Trichinella spiralis
 Capillaria philippinensis
hatch out
 Strongyloides spp.
 Larval skin penetration (thigmotropism
 Hookworm Ancyclostoma
 Hookworm Necator
2. According to habitat:
 Bites of arthropod / skin inoculation
2.A. Small Intestine
 Wuchereria bancrofti
 Capillaria philippinensis
 Brugia malayi
 Ascaris lumbricoides
 Strongyloides stercoralis
 hookworms:
Necator
Ancyclostoma
CLASSIFICATIONS: according to…
2.B. Large Intestine
1. life stages
2. habitat
 Trichuris trichiura
3. presence/absence of caudal chemoreceptor
 Enterobius vermicualris
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lOMoARcPSD|18320988
P2  CLINICAL PARASITOLOGY | NEMATODE INFECTIONS
Compiled by VJC and GA
3. According to presence/absence
of caudal chemoreceptor:
3.A. Phasmids
 with caudal chemoreceptor
 Ascaris lumbricoides
 Strongyloides stercoralis
 hookworms
3.B. Aphasmids
 without caudal chemoreceptor
 Trichuris trichiura
 Enterobius vermicualris
 Aka. Giant roundworm
 Capillaria philippinensis
 Most common intestinal nematode
 Trichinella spiralis
 Frequent in tropics (moist and warm climate)
 Estimated infected individuals: >1 Billion (70% from Asia)
Varying degrees of pathology:
(a) Tissue reaction to the invading larvae
(b) Irritation of the intestine by mechanical and
SOIL-TRANSMITTED HELMINTHS (STH)
 Ascaris lumbricoides
toxic action of the adult
(c) Other complications due to heavy infection and
 Trichuris trichiura,
extra intestinal migration
 Hookworms
Produces:
 Pepsin inhibitor 3 (PI-3)
STH INFECTIONS
– Diseases of poverty
 protects worms from digestion
– Contribute to malnutrition & impairment of cognitive
performances; reduce work capacity & productivity
 Phosphorylcholine
 suppresses lymphocyte proliferation
Soil – Major role in development and transmission
PARASITE BIOLOGY
 So called “polymyarian type” of somatic
muscle arrangement
 Cells: numerous; project well into body cavity
 WORMS:
 whitish/pinkish: large w/ thick cuticles
 have terminal mouth w/ 3 lips & sensory papillae
 mature: cylindrical w/ tapering ends
 ADULTS:
 Reside in but do not attach to the mucosa of the
small intestines.
 Morphology is similar to larval
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P2  CLINICAL PARASITOLOGY | NEMATODE INFECTIONS
Compiled by VJC and GA
MALES
FEMALES
Length: 12 to 31 cm long
Length: 22 to 35 cm long
Width: 2 to 4 cm wide
Width: 3 to 6 cm wide
Posterior end:
Posterior end:
ventrally curved w/ 2 spicules
Reproductive organ
Reproductive organ:
Reproductive organ:
single, long, tortuous tubule
paired in the posterior 2/3
Spicules: 2; broad
Vulva: opens at middle
lays 200,000 eggs per day
(more worm load = less eggs laid)
DIFFERENT EGG STAGES
1. Unfertilized
corticated
2. Unfertilized
decorticated
 EGGS
– deposited in the soil through defecation of
infected person
3. Fertilized
corticated
 Embryonation – Eggs to develop into infective stage
– 2 to 3 weeks; in the soil
– in suitable temp, moisture, & humidity
4. Fertilized
 EMBRYONATED EGGS
– Survive in moist shaded soil for a few months to 2
decorticated
years in tropical and sub-tropical areas
 but longer in temperate regions
Infertile Eggs vs Fertile Eggs
INFERTILE EGGS
88 to 94 μm x 40 to 44 μm
5. Embryonated
FERTILE EGGS
60 to 70 μm x 30 to 50 μm
( longer and narrower )
Shell: thin
*appearance:
Shell: thick, transparent, hyaline
 outer layer: thick
 as supporting structure
 inner membrane:
Unfertilized: oblong
Fertilized: round
Corticated: granulated/coarse outer membrane
Decorticated: agranulated/smooth outer membrane
delicate vitelline, lipoidal
 highly impermeable
Outer membrane:
Outer membrane:
 irregular mammilated
 coarsely mammilated
coating filled w/ refractile
granules
 Difficult to identify;
(found not only in the
albuminous covering
 Infective Stage: fully embryonated egg
– (When ingested) hatch in the lumen of small intestine
 releasing the larvae
– Larvae migrate to the cecum or proximal colon
 may be absent or lost in
 where they penetrate the intestinal wall
“decorticated” eggs
– Larvae enter the venules to go to the liver
 (At oviposition) have an
ovoid mass of protoplasm
absence of males)
 will develop into larvae
 Found in 2 of 5 infections
in about 14 days
 through the portal vein
– On to the heart & pulmonary vessels
 where they break out of capillaries to enter the air sacs
– In the lungs
 larvae undergo molting before migrating to the larynx
and oropharynx
– To be swallowed into the digestive tract
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P2  CLINICAL PARASITOLOGY | NEMATODE INFECTIONS
Compiled by VJC and GA
 Heavy infections cause:
 Hepato-tracheal migration phase: 14 days
 Dvlpmt of Egg-laying adult: 9–11 weeks (after egg ingestion)
 bowel obstruction (due to bolus formation)
 Life span of adult worm: 1 year
 intussusception, or volvulus
 that may result in bowel infarction
 LARVAE
 intestinal perforation
– up to 2 mm long and 75 um in diameter
– Undergo two molts to reach their 3rd stage within
 Serious/fatal effects:
– Due to erratic migration of adult worms
the egg and become embryonated
 Humans are infected only when this infective egg is
 may be regurgitated and vomited
 may escape through the nostrils
swallowed
 (rarely) inhaled into the trachea
PATHOGENESIS AND CLINICAL
MANIFESTATIONS
 Invading bile ducts
– through the ampulla of Vater and enter the
 Majority: Asymptomatic
gallbladder or liver
 Estimated 120 – 220 million cases exhibit morbidity
– Biliary ascariasis
 severe colicky abdominal pain
 fever,
 due to: movement of worms in biliary tract
urticaria, malaise, intestinal colic, nausea,
vomiting, diarrhea, and CNS disorders
 Bolus
formation
– Acute appendicitis = worms lodging in appendix
 Larval
migrations
– Pancreatitis = worms occluding the pancreatic duct
 may cause pneumonitis and bronchospasm
 Ectopic
– Abscess = due to intestinal bacteria carried to the
migration
migration sites
– Acute peritonitis or chronic granulomatous
 appendix, bile duct, pancreatic duct
peritonitis = penetration through intestinal wall
into peritoneal cavity
ASCARIASIS
– Contributed to a total of 1.85 million disabilityadjusted life years (DALYs) in 2004.
– Usual infection: 10 to 20 worms
– Continuous biting or pricking of the
intestinal mucosa for food may:
- Irritate: nerve endings in the mucosa
 Unnoticed unless discovered by stool exam or the
- Result to: intestinal spasm
 leads to: intestinal obstruction
spontaneous passing of worms in the stool
 During lung migration
– Larvae may cause host sensitization
EPIDEMIOLOGY
 Results in allergic manifestations like:
 lung infiltration
 Endemic in S.E. Asia, Africa, Central & South America
 asthmatic attacks
 East Asia & Pacific islands – highest # of cases
 edema of the lips
 5–15 years old – highest intensities of infection
– Penetration through the lung capillaries
 Results in difficulty of breathing and fever
 Prevalence in the Philippines:
– Public elem school (high risk group): 80% – 90%
similar to pneumonia
– Preschool children – 30.9%
 Vague abdominal pain – most frequent complaint
– School-age children – 27.7%
 Eosinophilia – present during larval migration
 Moderate infections may produce:
 Lactose intolerance
 Vitamin A malabsorption
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P2  CLINICAL PARASITOLOGY | NEMATODE INFECTIONS
Compiled by VJC and GA
 Adverse reactions to these anthelminthics
DIAGNOSIS
- Rare, mild, and transient
 Clinical diagnosis: inaccurate
- Epigastric pain, headache, diarrhea, nausea,
 Bec. symptoms are vague and indistinguishable
vomiting, and dizziness
- minimized by deworming tablet (after a meal)
 Stool exam techniques: (eggs and adults)
– Direct fecal smear (DFS)
 Preventive chemotherapy
 less sensitive than Kato thick Smear & Kato-Katz
- through (MDA) with anthelminthics, either alone or
in combination, even without stool exam
– Kato thick Smear (qualitative diagnosis)
 WHO suggests coverage of at least 75% of target population
 individual and mass screening
 IHCP targets MDA coverage of at least 85% of target population
– Kato-Katz techniques (quantitative diagnosis)
 WHO recommends targeting other high-risk groups:
 individual and mass screening
 Women of child- bearing age
 intensity of helminth infection in epg
 Pregnant women
– Concentration techniques, such as (FECT)
 by confirming presence of eggs in feces
 MDA in the Philippines
- part of Integrated Helminth Control Program (IHCP) of DOH
- conducted in elem schools every January and July
* Adult worm visualized in the intestines by: barium meal examination
for school-age children through (DepEd)
 MDA for preschool-age children
TREATMENT
– conducted under the Garantisadong Pamabata
 Any of the broad-spectrum anthelminthics
program through DOH and LGU
(single dose; oral):
 MDA in filariasis-endemic areas
 Mebendazole (cure rate: 96.5%)
– Albendazole and diethylcarbamazine
 Albendazole (cure rate: 93.9%)
 Pyrantel pamoate (cure rate: 87.9%)
*reinfection may take place immediately after deworming
 May receive albendazole or mebendazole:
 Pregnant women in 2nd or 3rd trimester
 Lactating women
Albendazole
– 400 mg single dose
– 200 mg (12-23 months old)
 Ineligible for MDA with albendazole/mebendazole:
 Children less than 1 year old
 Pregnant women in 1st trimester
Mebendazole
– 100mg – 2x a day for 3 days
Pyrantel pamoate
– 10 mg/kg (max. 1 g) single dose
 Benefits of regular deworming
– Iron stores, growth and physical fitness,
cognitive performance, and school attendance
Others:
– Nutritional indicators such as reduced wasting,
Ivermectin
– As effective as albendazole
stunting, and improved appetite.
– Single dose if given at a dose of 200 μg/kg
 Use of anthelminthics in livestock
Nitazoxanide
– 500 mg twice a day for 3 days
– Results in anthelminthic resistance to all drug classes
– 1-3 years old (100 mg twice a day for 3 days)
– 4-11 years old (200 mg twice a day for 3 days)
 “WASHED” – water, sanitation, hygiene, edu, deworming
Benzimidazoles (e.g. Such as Albendazole & Mebendazole)
– Bind to the parasites’ b-tubulin
 disrupting the parasite microtubule polymerization
– Result: death of adult worms (several days)
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P2  CLINICAL PARASITOLOGY | NEMATODE INFECTIONS
Compiled by VJC and GA
LIFE CYCLE:
1. adult worm in small intestine (diagnostic stage)
2. feces in soil through defection (diagnostic stage)
a. fertilized egg
b. unfertilized egg (no biological development)
3. embryonation; fully embryonated egg (infective stage)
*larva molts twice inside the egg
4. ingestion or skin penetration
5. small intestine (hatch)
6. lung migration
7. tracheal migration
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P2  CLINICAL PARASITOLOGY | NEMATODE INFECTIONS
Compiled by VJC and GA
MALES
FEMALES
Length: 30 - 45 mm
Length: 35 - 50 mm
Posterior end: coiled w/ 1
Posterior end: blunt
spicule & retractile sheath
Reproductive organ:
Reproductive organ:
single, long, tortuous tubule
paired in the posterior 2/3
PATHOGENESIS AND
CLINICAL MANIFESTATIONS
 Aka Whipworm
 STH; classified as “holomyarian type” of somatic
muscle arrangement in cross-section
 Cells: numerous; closely packed in narrow zone
 Anterior portion (embedded in mucosa) causes
petechial hemorrhages
 Predispose to amebic dysentery; bec. ulcers provide suitable
site for tissue invasion of E. histolytica
 Mucosa – hyperemic and edematous
PARASITE BIOLOGY
 Enterorrhagia (or intestinal bleeding) – common
 Lumen of appendix – (filled with worms) leading to
 WORMS
 Anterior (three-fifths):
appendicitis/granuloma formation
– attenuated; traversed by narrow esophagus
 due to consequent irritation & inflammation
(resembling string of beads)
 Heavy chronic trichuriasis – blood-streaked diarrheal
 Posterior (two-fifths):
– contains the intestine
stools, abdominal pain, tenderness, nausea, vomiting,
– 1 set of reproductive organs
anemia, weight loss.
 Females:
– lay 3,000–10,000 eggs per day
 Over 5,000 epg = symptomatic
– produce 60 million eggs over its average
 Over 20,000 epg = severe diarrhea; dysenteric syndrome
lifespan (2 years)
 Inhibit Cecum and Colon
 Secrete TT47
DIAGNOSIS
 Pore-forming protein
 Allows worms to imbed their whip-like portion into the
 DFS
 Kato cellophane thick smear
intestinal wall
 Kato-katz technique (quantitative)
 LARVAE
 FECT
– Not usually described
 Bec. larvae escape and penetrate intestinal villi
soon after embryonated eggs are ingested
TREATMENT
 Remain in intestinal villi for 3–10 days
 Mebendazole – 100mg – 2x a day for 3 days
EGGS
 Albendazole – (alternative)
– Size: 50 – 54 um long x 23 um wide
– Shape: lemon or football with plug-like
translucent polar prominences
– Outer shell: yellowish
– Inner shell: transparent
– Fertilized egg – unsegmented at oviposition
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P2  CLINICAL PARASITOLOGY | NEMATODE INFECTIONS
Compiled by VJC and GA
– Embryonic developmt – in soil; outside the host
 2–3 weeks to become embryonated
LIFE CYCLE:
1. unembryonated eggs passed in feces (diagnostic stage)
2. 2-cell stage
– (if swallowed) embryonated eggs go to small
intestine; undergo 4 larval stages
 12–3 weeks to become adult worms
3. advanced cleavage
4. ingestion embryonated eggs (infective stage)
5. in small intestine: larvae hatch
6. in cecum: adult
– compared to Ascaris:
 Eggs

in soil are more susceptible to desiccation
No heart-lung migration
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P2  CLINICAL PARASITOLOGY | NEMATODE INFECTIONS
Compiled by VJC and GA
TREATMENT
 Electrolyte replacement and high CHON diet
 Mebendazole 200 mg a day for 20 days
 Albendazole 400 mg once a day for 10 days
PREVENTION AND CONTROL
 Avoid eating raw fish
 Good sanitary practice
 Proper waste disposal
 Educational programs
PARASITE BIOLOGY
 aka Pudoc’s worm
LIFE CYCLE:
 tiny; residing in the small intestine
1. unembryonated eggs (diagnostic stage)
 Infective Stage: third stage larvae
2. in soil or water: embryonated eggs
 natural hosts: fish-eating birds
3. in the intestine of the fish:
 incidental hosts: humans
eggs hatch and infective larvae develop (infective stage)
4. ingestion of raw undercooked infected fish
 from superfamily Trichinelloidea
5. in intestines: infective larvae (infective stage)
 first recorded in Northern Luzon
in intestines: female worms produce larvae
 reinvade intestinal mucosa
 result: internal autoreinfection
EGGS
– Size: 5 – 45 um long x 20 – 25 um wide
– Shape: peanut shape with flattened bipolar plugs
MALES
FEMALES
Size: 1.5 – 3.9 mm
Size: 2.3 – 5.3 mm
Spicule: (reproductive organ) Reproductive organ and
230–300 um; unspined sheath
digestive tract: posterior end
Anterior end: thin filamentous
Anterior end: narrow
Posterior end: shorter
Posterior end: wider
PATHOGENESIS AND
CLINICAL MANIFESTATIONS
 Borborygmus (gurgling stomach)
 Abdominal pains, Diarrhea, Weight loss, Malaise
 Anorexia, Vomiting, Edema
DIAGNOSIS
 DFS (eggs in feces)
 Duodenal aspiration
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P2  CLINICAL PARASITOLOGY | NEMATODE INFECTIONS
Compiled by VJC and GA
2. INVASION
• Larval migration
• Fever, facial ellema, urticaria, pain, swelling, weakness
3. CONVALESCENT
• Encystment
• Fever, weakness, pain and other symptoms
In Severe Cases:
• Gastric and intestinal hemorrhages
 Aka garbage round worm
• Myocardial and neurological complications
 Whitish in color
• Pericardial effusion, congestive heart failure, meningitis,
 1.5 – 3.5mm x 0.04 –0.06mm
meningoencephalitis, and cerebral lesions
 larviparous
LARVA
– Size: 80–120um x 5.6um at birth; but reaches
900–1,300um x 35–40um after entering muscle fiber
– has a spear-like burrowing anterior tip
DIAGNOSIS
• Biochemical test : chemical evidence of muscle damage
• Peripheral blood eosinophilia: High counts strengthens
the diagnosis
MALES
Size: 1.5mm x 0.04mm
Reproductive organ:
single testes
FEMALES
• Serology
• Muscle biopsy (definitive diagnosis)
Size: 3.5mm x 0.06mm
Reproductive organs:
Single ovary, Oviduct, Coiled uterus,
TREATMENT
Seminal receptacle, Vagina & valve
Produce 1,500 larvae or more
• Thiabendazole 2x a day for 7 days
in her lifetime
• Mebendazole
PATHOGENESIS AND
CLINICAL MANIFESTATIONS
PREVENTION AND CONTROL
 Severity depend on the intensity of infection
• Meat should be cooked at 77°C
• 10 larvae = asymptomatic
• Freezing –15°C for 20 days or –30°C for 6 days
• 100 or more = more symptoms
• Meat inspection and keeping pigs rat-free
• 1000/ more = severe; fatal
• Health education
* “Measly Pork” – Infected meat
 3 PHASES:
1. Enteric
2. Invasion
3. Convalescent
1. ENTERIC
• Incubation and intestinal invasion
• Parasite gets inside the body of the host until such
time signs and symptoms may show
• Diarrheal constipation, vomiting, abdominal cramps,
malaise and nausea
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lOMoARcPSD|18320988
P2  CLINICAL PARASITOLOGY | NEMATODE INFECTIONS
Compiled by VJC and GA
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lOMoARcPSD|18320988
P2  CLINICAL PARASITOLOGY | NEMATODE INFECTIONS
Compiled by VJC and GA
PATHOGENESIS AND
CLINICAL MANIFESTATIONS
 Mild catarrhal inflammation of the intestinal mucosa
 Irritation of the perianal region
 Intense itching
 Insomnia due to the pruritus
 Poor appetite, weight loss, irritability, grinding of teeth,
and abdominal pain
 Aka human pinworm
 Classification based on somatic muscle arrangement:
DIAGNOSIS
meromyarian
 Airborne (because very light eggs)
 Causes enterobiasis/oxyuriasis,
 gold standard: scothtape method
 characterized by perianal itching/pruritus ani
 adult worms in perianal region
PARASITE BIOLOGY
TREATMENT
 Adult worms
 drugs of choice:
– Anterior end:
• Albendazole 400mg
cuticular alar expansions & prominent esophageal bulb
• Mebendazole 100mg
– in the cecum
 secondary drug of choice:
• Pyrantel Pamoate 11mg/kg single dose
 Rhabditiform larva
– 140-150um by 10um
– Has esophageal bulb
PREVENTION AND CONTROL
– No cuticular expansion
 Personal hygiene
 Proper hand washing
 Infected person should sleep alone
EGGS
– Size: 50-60 um x 20-30 um
– Asymmetrical; inverted D-shape
(one side flattened; other side convex)
– very light but has very thick shell
– shell covering: triple albuminous
– become fully-embryonated
(within 6 hours; in the perianal region)
MALES
Size: 2–5mm x 0.1–0.2mm
Single spicule;
Curved tail
FEMALES
Size: 8–13mm x 0.4 mm
Anterior end:
prominent esophageal bulb;
long pointed tail
Rarely seen bec. they usually Lay 4,672–16,888 eggs a day
die after copulation
(average 11,105 eggs)
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lOMoARcPSD|18320988
P2  CLINICAL PARASITOLOGY | NEMATODE INFECTIONS
Compiled by VJC and GA
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