CLINICAL PARASITOLOGY
LECTURE /SECOND SEMESTER
APHASMID NEMATODES
reproductive system
TRICHURIS TRICHIURA ● Male – watch-spring coil appearance
● Female – blunted rounder posterior end;
Common Name: Whipworm vulva opens at anterior extremity of fleshy
portion
Infective Stage: Embryonated Egg
Habitat: Large Intestine
Mode of Transmission: Ingestion of egg via
contaminated food/water
Diagnostic Specimen: Feces ●
● The whipworm derives its name from its
characteristic whiplike shape; the adult
(male, 30-45 mm; female, 35-50 mm) buries
its thin, threadlike anterior half into the
intestinal mucosa and feeds on tissue
secretions, not blood. This relative tissue
invasion causes occasional peripheral
eosinophilia.
● The cecum and colon are the most
commonly infected sites, although in
heavily infected individuals, infection can
be present in more distal segments of the GI
tract, such as the descending
I. MORPHOLOGY
● Adult: the worm looks like a buggy whip,
the anterior ⅗ is slender and the posterior ⅖
is thick. It is pinkish gray in color. The II. LIFE CYCLE
female worm is 3-5 cm in length and has a
long slender esophageal region. The male is 1. Site of inhabitation: cecum
smaller than the female and has a curved 2. Infective stage: embryonic egg
tail. The reproductive organs of male and 3. Infective mode and route: passively
female are all double tubules. swallowed by the mouth
● Egg: it is barrel or spindle in shape and 50 x 4. Without intermediate host and reservoir host
20μm in size. It is brownish and has a 5. The life span of the adult is about 3-5 years
translucent polar plug at either end. The
content of the egg is an
undeveloped cell
ADULT WORM
● 2.5 – 5 cm long
● Whipworm /
Trichocephalus trichiura
● Geog distrib /
Epidem
● Anterior end (2/3)
with slender esophagus
● Posterior end (fleshy 1/3) with digestive &
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3. Heavy infection: Bloody diarrhea,
emaciation, prolapse of the anus may occur.
- Loss of height of microvilli
- Infiltration of plasma cells,
lymphocytes, sometimes
eosinophils between the crypts
- Mechanical - appendicitis
- Allergic – eosinophils and Charcot
Leyden in the colonic exudate
- 2-6 years old : diffuse colitis →
chronic diarrhea, dysentery (more
chronic than amoebic), tenesmus,
rectal prolapse, clubbed fingers,
malnutrition, hypochromia
Whipworm in the gut
III. LABORATORY DIAGNOSIS Prolapsed Rectum
● Microscopic identification of whipworm
eggs in feces is evidence of infection.
Discover the eggs in feces by saturated
brine flotation method or direct fecal smear.
● DFS – ova; size depends on treatment status
- “light” = < 10 ova / smear
- “heavy” = > 50 ova / smear
- “massive” = TNTC; unequally
distributed
● Centrifugal flotation or sedimentation – for
light infections V. TREATMENT
● Proctoscopy – rectal mucosa
● Mebendazole – 100 mg bid x 3 days
● Difetarsone and oxantel pamoate
IV. PATHOLOGY
1. Light infection: Asymptomatic
2. Middle infection: Clinical manifestations
are usually abdominal
pain,anorexia,diarrhea, constipation.
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Capillaria spp. I. LIFE CYCLE
● Causal Agents:
- The nematode (roundworm)
Capillaria philippinensis causes
human intestinal capillariasis.
● Two other Capillaria species parasitize
animals, with rare reported instances of
human infections.
● They are C. hepatica ,which causes in
humans hepatic capillariasis, and C.
aerophila ,which causes in humans
pulmonary capillariasis .
CAPILLARIA PHILIPPINENSIS
Common Name: NA
Infective Stage: Encysted Larvae
Habitat: smallI Intestine ● Ova embryonate in fresh water Raw fish
eaten (freshwater fish – ipon – Hypseleotris
Mode of Transmission: Ingestion of bipartita) – hatch inside fish intestine
raw/undercooked contaminated fish ● Borborygmi; intractable diarrhea,
abdominal pain, weight loss, loss of
Diagnostic Specimen: Feces appetite, malabsorption without villi
changes
● Pudoc worm, Mystery ● Death after onset of pneumonia, heart
Disease failure, hypokalemia or cerebral edema.
● Pudoc, Tagudin, Ilocos Sur -
1967 Capillaria philippinensis egg under light
● IH – birot, bagsang, bagtu microscopy. Roll over the image for a view of
● Habitat: jejunum unembryonated
● Females w/ eggs in utero – 8 C. philippinensis eggs inside an adult female .
to 10 eggs arranged in a single row
or 40-45 eggs
arranged in 2 to 3 rows
The adults of Capillaria philippinensis
(males: 2.3 to 3.2 mm; females: 2.5 to 4.3
mm)
II. GEOGRAPHIC DISTRIBUTION
● Capillaria philippinensis is endemic in the
Philippines and also occurs in Thailand.
● Rare cases have been reported from other
Asian countries, the Middle East, and
Colombia.
● Rare cases of human infections with C.
hepatica and C. aerophila have been
reported worldwide.
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OVA Capillaria hepatica eggs
Capillaria
philippinensis Trichuris trichiura
● Smaller ● Larger
● Less prominent ● More prominent
mucous plugs mucous plugs
● Striated egg ● Not striated
shell ● Football shaped
● Peanut shaped
● Laid in early Capillaria hepatica eggs in liver tissue
segmentation
CAPILLARIA AEROPHILA III. CLINICAL FEATURES
● adult worms reside in the epithelium of the ● Intestinal capillariasis (caused by C.
tracheo- bronchial tract of various animals. philippinensis) manifests as abdominal pain
Eggs are produced, coughed up, swallowed and diarrhea, which, if untreated, may
by the animal, and excreted in its feces. The become severe because of autoinfection.
eggs become embryonated in the soil. ● A protein-losing enteropathy can develop
Ingestion of infective eggs completes the which may result in cachexia and death.
cycle. Transport or paratenic hosts may ● Hepatic capillariasis (C. hepatica) manifests
also intervene in the cycle. as an acute or subacute hepatitis with
eosinophilia, with possible dissemination to
CAPILLARIA HEPATICA other organs. It may be fatal.
● Pulmonary capillariasis(C. aerophila) may
● Adult worms reside in the liver of various present with fever, cough, asthma, and
animals, especially rats. pneumonia, and also may be fatal.
● The females produce eggs that are retained
in the liver parenchyma. IV. LABORATORY DIAGNOSIS
● When the infected animal is eaten by
another animal, the eggs are released by ● The specific diagnosis of C. philippinensis
digestion, excreted in the feces of the is established by finding eggs, larvae and/or
second animal, and become embryonated in adult worms in the stool, or in intestinal
the soil. biopsies.
● Alternately, the eggs can be released ● Unembryonated eggs are the typical stage
following the death and decomposition of found in the feces. In severe
the first animal, and mature in the soil. infections, embryonated eggs, larvae, and
● Following ingestion by a subsequent host, even adult worms can be found in the feces.
these infective eggs release larvae in the ● The specific diagnosis of C. hepatica
intestine that migrate through the portal infection is based on demonstrating the
circulation to the liver, where they develop ● adult worms and/or eggs in liver tissue at
into adults. biopsy or necropsy. (Note: identification of
C. hepatica eggs in the stool is a spurious
finding, which does not result from
infection of the human host, but from
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ingestion by that host of livers from infected I. HABITAT
animals.)
● The specific diagnosis of C. aerophila is ● Mucosa of small intestine of pig, rat, bear,
based on demonstrating eggs in stool or in and man
lung biopsy ● Striated muscles - encysted larvae
● No free-living forms
II. MORPHOLOGY
DIOCTOPHYMA RENALE
● Commonly called the giant kidney worm ,
Dioctophyma renale has been found most
frequently in mustelids and in wild and
domestic carnivores in practically all parts
of the world. Infrequent occurrences of the
parasite have been recorded in pigs, horses,
cattle and man
I. LAB DIAGNOSIS & TREATMENT
● Eggs, larvae or adult worms in the stool
● Mebendazole – 200 mg bid x 20 days
● Albendazole – 400 mg OD x 10 days
TRICHINELLA SPIRALIS
Common Name: Trichina worm
Infective Stage: Encysted larvae
Habitat: Striated muscle tissue
Mode of Transmission: Ingestion of
raw/undercooked contaminated meat
Diagnostic Specimen: Skeletal muscle
biopsy/blood (LDH, Aldolase, CPK,eo ct)
● Responsible for the potentially fatal disease
called trichinosis.
● Females produce live young. ● Thin & pointed anterior half of body
● Juveniles penetrate skeletal muscles where ● Pair of claspers at posterior end
they burrow and develop into cysts in the ● Viviparous nematode
muscle tissue called nurse cells. ● Life span: about six weeks, and in that time
● Transmission occurs when meat from an can produce up to 1,500 larvae
animal
● containing nurse cells is ingested, the
juvenile worms
● are liberated into the intestine where they
mature.
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IV. PATHOGENESIS
III. LIFE CYCLE
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V. CLINICAL FEATURES VI. DIAGNOSIS
INDIRECT METHODS
● History
- Eating pork 2 weeks earlier
- Recent - gastroenteritis
● Blood Examination
- Eosinophilia (20 -95%)
● Serology
- Hypergammaglobinemia - IgE
- ELISA - Confirmatory test: TSL-1
secreting antigens
- Bentonite flocculation test
- Latex fixation test
● Bachman intradermal test
- 1:5000 or 1:10000 dilution of larval
antigen
- Wheel 15 to 20 minutes
● Radiological examination
- calcified cysts
● Molecular methods
- PCR
VII. TREATMENT
● Mild cases
- Supportive treatment
● Moderate cases
- Albendazole (BID; 8 days)
- Or momendazole
● Severe cases
- Add Glucocorticoids-Prednisolone
KEY POINTS
● Smallest nematode
● Host-optimum & alternative
● Viviparous
● Infective form
● Muscles commonly involved
● Pathogenesis & clinical features
● Diagnosis & treatment
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