Taenia Species
1. Taenia saginata asiatica (Asian
Tapeworm)

Taxonomy Debate: Some
consider this a distinct species,
while others classify it as a
subspecies of Taenia saginata
based on DNA similarities.
2. Taenia multiceps (Multiceps
multiceps)
Rare Human Infection:
 It is a rare parasitic infection in
humans, primarily affecting
herbivorous animals.
Morphology:
Larvae (Coenurus):
Morphological Features:

Similar to T. saginata, but with key
differences:
 Characterized by a unilocular
cyst containing multiple scolices
(hooks), which is why it is
called Multiceps.
 Intermediate Host: Pig (as
opposed to cow in T. saginata).
 Cysticerci Location: Primarily in
the liver (instead of muscles).
 Scolex Features: Contains
hooklets, which may be absent in
mature worms.
 Size: Smaller, with 300-1,000
proglottids (segments).
Geographic Distribution:
 Found mainly in Taiwan, Korea,
China, Malaysia, Thailand.
 Not reported in India.
Clinical Features:
 Clinical presentation, diagnosis,
and treatment are similar to T.
saginata.
Diagnosis and Treatment:
 Similar to T. saginata, including
stool examination for
proglottids/eggs and possible
imaging for cysticerci.

Adult Worm:
 Length: 40-60 cm.
 Scolex: Pear-shaped with 4
suckers and an armed rostellum
with 2 rows of hooklets.
 Eggs: 30 µm in size, similar to
other Taenia species.

Life Cycle:
 Definitive Host (where adult
tapeworm lives): Dog, fox, and
wolf.
 Intermediate Host (where
larvae develop): Herbivores like
sheep.
 Humans can serve as accidental
intermediate hosts if they
ingest contaminated food/water
containing eggs.
 Oncospheres (eggs) hatch in
the intestine, penetrate the walls,
and migrate to various organs,
especially the CNS (Central
Nervous System), where they
transform into the larval form
(coenurus).

Clinical Manifestations:
 The disease mainly affects
herbivores’ CNS and is called gid,
characterized by unstable gait
and giddiness.
 In humans, space-occupying
lesions in the CNS lead to:




Headache
Vomiting
Paralysis
Seizures
Epidemiology:
 Occurs mainly in developing
countries where dog
populations are not controlled.
 Affected regions include:


Africa: Uganda, Kenya, Ghana,
South Africa
The Americas: Brazil, Mexico,
Canada, the United States
 India: A few cases reported, with
a notable recent case of cerebral
coenurosis from NIMHANS,
Bangalore in 2011.

Diagnosis:
 Based on gross and histological
examination of the coenurus
following surgical removal.
 Neuroimaging (CT or MRI) may
also be used to visualize
space-occupying lesions.

Treatment:
 Surgical removal of the coenurus
(larval cysts).
 Anti-parasitic medications may
be used in certain cases, though
surgery is typically the main
approach.
Key Points to Remember:
 T. saginata asiatica is primarily
distinguished by its pig-based
lifecycle and the location of
cysticerci (liver vs. muscle in T.
saginata).
 T. multiceps involves a complex
lifecycle with dogs as definitive
hosts and herbivores like sheep
as intermediate hosts. Humans
become infected accidentally,
usually through ingestion of
eggs from contaminated food or
water.
 Both tapeworm species share
similarities in diagnosis and
treatment but have distinct
epidemiological patterns and
clinical manifestations.
Echinococcus Species
Echinococcus Overview:


Echinococcus is a genus that
causes hydatid disease in
humans.
Four species infect humans:
 E. granulosus – Causes cystic
hydatid disease.
 E. multilocularis – Causes
alveolar hydatid disease.
 E. vogeli and E. oligarthrus –
Cause polycystic hydatid
disease.
Echinococcus granulosus
(Cystic Hydatid Disease)
History:
 Also known as dog tapeworm.
 Hydatid cysts were recognized
as early as Hippocrates and
Galen.
 Hartmann (1695) demonstrated
the adult form in dogs.
 Goeze (1782) described the
larval form (hydatid cyst).
Structure:
Head (Scolex):
 Shape: Pyriform (pear-shaped),
about 300 µm in diameter.
 Features: 4 suckers and a
rostellum (armed with two rows
of hooklets).
Neck:
 Short and thick.
Strobila (Body):

Composed of 3 proglottids
(segments):
Larval Form (Hydatid Cyst):
1. Immature segment
2. Mature segment
3. Gravid segment (broader than
the others, filled with 100–1,500
eggs).
 Found in the liver and other
viscera of humans and
herbivores (e.g., sheep, cattle).
 The proglottids are similar to
those of other cyclophyllidean
cestodes.
Habitat:


Adult Worms:
 Reside in the intestine of dogs
(the definitive host).
Morphology of Echinococcus
granulosus:
Adult Worm:

Size:
 3–6 mm in length (much smaller
than other cestodes).
Eggs:
Morphology:
 Similar to Taenia eggs.
 Oncosphere contains 6 hooklets,
surrounded by an embryophore
(protective outer layer).
Larval Form (Hydatid Cyst):
 The hydatid cyst is the larval
form of Echinococcus granulosus.
 Found primarily in the liver, lungs,
or other viscera of intermediate
hosts (humans, herbivores).
Echinococcus granulosus:
Life Cycle and Development
Life Cycle of Echinococcus
granulosus

The life cycle of Echinococcus
granulosus involves two hosts:
Definitive Hosts (where adult
worms live):
 Dogs and other canine animals
(foxes, wolves).
Intermediate Hosts (where larval
forms develop):
 Eggs are ingested from
contaminated food, water, or
surfaces.
2. Transformation to Larva
(Hydatid Cyst):
 After ingestion, the eggs release
oncospheres (larvae) in the
duodenum due to the rupture of
the embryophore (outer shell).
 The oncospheres penetrate the
intestinal wall and enter the
portal circulation
(bloodstream).
3. Migration to Organs:
 Herbivores such as sheep,
cattle, and occasionally humans
(humans are an accidental
intermediate host).
 Oncospheres are carried by the
bloodstream to the liver
(60–70% of cases), lungs, or
rarely other organs.
Mode of Transmission:
4. Host Immune Response:
 Humans and other intermediate
hosts acquire the infection by
ingesting E. granulosus eggs
found in dog feces
(contaminated food, water, soil).
 Rarely, flies can serve as
mechanical vectors, transferring
eggs from feces to food or
surfaces.
 The immune system attempts to
destroy the larvae, causing an
inflammatory response around
the site of infection.
 While many oncospheres are
destroyed, some escape
destruction and develop into
hydatid cysts.
Development in Humans
(Accidental Intermediate Host)
 The oncospheres are encysted by
fibrous tissue (produced by
fibroblasts), forming a
fluid-filled cyst called a hydatid
cyst.
 Cysts grow at a rate of 1 cm per
month.
1. Ingestion of Eggs:
5. Formation of Hydatid Cyst:
 Full cyst development takes
10–18 months in sheep
(intermediate host).
6. Maturation of Hydatid Cyst:
 Once mature, the hydatid cyst
becomes infective to dogs and
other definitive hosts.
 Humans are a dead-end host
because dogs do not consume
human organs.
Development in Dogs (Definitive
Host)
1. Infection by Consumption of
Contaminated Viscera:
 Dogs or other canines acquire
the infection by consuming the
viscera (organs) of infected
intermediate hosts (e.g., sheep)
that contain mature hydatid
cysts.
2. Transformation of Hydatid Cyst
to Adult Worm:
 The hydatid cyst (larva)
develops into an adult
tapeworm in the dog's intestine.
 The adult worm matures and
produces eggs, which are
excreted in the dog’s feces.
 Key Points to Remember:
 Humans act as accidental
intermediate hosts in the life
cycle of Echinococcus granulosus.
 Transmission to humans occurs
through ingestion of eggs from
dog feces.
 The larval stage (hydatid cyst)
forms in the liver, lungs, or other
organs, leading to hydatid
disease.
 Hydatid cysts grow slowly,
maturing over 10–18 months.
 Dogs acquire infection by
consuming the infected viscera
of intermediate hosts and pass
the eggs in their feces.
 Humans are dead-end hosts,
meaning the cycle does not
complete in humans.
Echinococcus granulosus:
Pathogenicity and Clinical
Features
Pathogenicity:
The pathogenicity of Echinococcus
granulosus is primarily due to the
deposition and growth of hydatid
cysts in various organs.
Hydatid Cyst: Structure and
Characteristics
3. Transmission to Other Hosts:
Shape & Size:
 The eggs in the feces are
infective to intermediate hosts
(including humans), continuing
the cycle.
 Fully developed hydatid cysts are
unilocular (one chamber) and
subspherical.
 Size: Varies from a few
millimeters to more than 30 cm
(common size 5-8 cm).
Cyst Wall:

Pericyst (Outer Layer):
 Host-derived fibrous tissue and
blood vessels due to the host’s
immune response.

Ectocyst (Middle Layer):
 Parasite-derived tough, elastic,
glycan-rich, acellular hyaline
layer (approx. 1 mm thickness).
 Resembles the white of a
hard-boiled egg.

Endocyst (Inner Layer):
 Parasite-derived germinal layer
(22-25 µm thickness).
 Forms the brood capsules and
hydatid fluid.
 Produces protoscolices (future
heads of tapeworms).
Hydatid Fluid:
 Clear, colorless to pale yellow.
 pH: 6.7, Specific Gravity:
1.005–1.010.
 Contains sodium chloride,
sodium sulfate, sodium
phosphate, succinates.
 Antigenic, toxic, and
anaphylactic.
Brood Capsules and Protoscolices:
 Brood capsules are formed in the
endocyst, containing
protoscolices.
 Hydatid sand: Granular deposit
formed by detached brood
capsules and protoscolices.
Types of Hydatid Cysts:
 Primary Cyst: Directly formed
from the oncosphere after
ingestion.
 Secondary Cysts: Result from
the breakage of primary cysts
due to trauma, leading to
dissemination to other organs.
 Acephalocyst: Cysts lacking
brood capsules and
protoscolices.
 Endogenous Daughter Cysts:
Formed when the brood capsule
breaks within the cyst, producing
smaller cysts inside.
Fate of the Hydatid Cyst:
 Spontaneous Resolution: Some
cysts may resolve on their own.
 Rupture: Can lead to:


Formation of secondary cysts.
Anaphylactic reaction due to
leakage of hydatid fluid.
Clinical Features of Hydatid
Disease
Age of Onset:
 Infection typically occurs in
childhood but often manifests in
adult life.
Most Common Locations:
 Liver (60-70%, mainly the right
lobe).
 Lung (20-30%).
 Rarely: Spleen, kidneys, brain,
heart, bones.
Asymptomatic Cases:

 Many cases are asymptomatic
and only detected incidentally
through imaging studies.
Outcome and Disease Progression
Symptoms:
 Symptoms primarily result from
the pressure effects or
complications caused by the
cysts.
Fever.



Pressure Effects:




Palpable abdominal mass.
Hepatomegaly (enlarged liver).
Abdominal tenderness.
Portal hypertension and ascites
(fluid accumulation in the
abdomen).
Obstruction:
 Daughter cysts may erode into
organs like the biliary tree or
bronchi, causing:
 Cholestasis (bile flow
obstruction).
 Dyspnea (difficulty breathing).
Secondary Bacterial Infection:
 May cause pyogenic abscess
formation in hydatid cysts.
Reactions:
 Cyst rupture can release hydatid
fluid, leading to severe allergic
reactions, including:


Hypotension (low blood
pressure).
Syncope (fainting).
Outcome depends on cyst
size and location.
Extrahepatic Cysts: More
common in younger children,
found in organs like lungs,
brain, and orbit.
Multiple Cysts: Found in
20-40% of cases, with
involvement of multiple
organs.
Key Points to Remember:
 Echinococcus granulosus forms
hydatid cysts, which grow slowly
and are typically asymptomatic
until large enough to cause
organ compression.
 Liver and lung are the most
common sites for cyst formation.
 Anaphylactic reactions can
occur if cysts rupture.
 Multiple cysts or involvement of
multiple organs is seen in a
significant proportion of cases.
Laboratory Diagnosis of
Echinococcus granulosus
Infection
1. Microscopic Examination of
Hydatid Fluid:

Procedure:
o Aspirate hydatid fluid
from cyst and examine
under the microscope
o
o
for brood capsules
and protoscolices.
Hydatid sand can be
detected by placing a
drop of centrifuged
fluid between two
slides and rubbing
them together. The
grating sensation
indicates sand grains.
Purulent material can
be treated with
hydrochloric acid for
better visibility.

Confirmatory Tests:


2. Histological Examination:


Surgically removed cysts are
examined for cyst wall layers
and brood capsules using
histopathological stains:
o Giemsa stain
o Hematoxylin and
Eosin (H & E)
o Periodic Acid-Schiff
(PAS) stain
These stains help demonstrate
the three cyst wall layers
(pericyst, ectocyst, endocyst)
and attached brood
capsules.
3. Antibody Detection:
Screening Tests (60-90%
Sensitivity):



Indirect Hemagglutination
(IHA)
Latex Agglutination Test
(LAT)
Indirect Fluorescent
Antibody (IFA) Test
Enzyme-Linked
Immunosorbent Assay
(ELISA)
Immunodiffusion and
Electroimmunodiffusion:
Detect antigen-5 (arc-5).
Western Blot: Detects
antibody against antigen B
fragment (8-12 kDa band).
92% sensitivity, 100%
specificity. Specific for IgG4
antibodies.
o
Antigen B is preferred
for
seroepidemiological
studies.
Additional Notes:


Antibody tests can’t
differentiate between recent
and past infections.
Liver cysts show better
serological results than
extrahepatic cysts. Alveolar
echinococcosis shows better
results than cystic
echinococcosis.
4. Antigen Detection:

Tests for detecting specific
antigens in serum or urine:
o
ELISA, CIEP
(Counter-current
Immunoelectrophoresi
s), LAT.

These methods can
differentiate between recent
and past infections and serve
as prognostic markers for
treatment monitoring.
5. Imaging Methods:
X-rays:
 Simple, inexpensive method to
detect hepatomegaly and
calcified cysts (can also detect
cysts in lungs).
Ultrasound (USG):
 Imaging method of choice due
to low cost and high diagnostic
accuracy (90%).
 Detects both single and
multiple cystic lesions.
 Water lily sign: Fluid leakage
causes germinal layer collapse,
which floats in the cyst cavity.
 Daughter cysts: Appear as cysts
within cysts, cartwheel or
honeycomb appearance.
 Detects complications like
biliary obstruction.
 Monitors treatment response
and is used in epidemiological
studies.
Computed Tomography (CT):
 90-100% sensitivity for cyst
detection.
 More accurate for detecting
number, location, and
complications of cysts.
 Better than USG for detecting
calcified cysts (calcification
takes 5-10 years to develop).
 Superior for detecting
extra-hepatic cysts and
distinguishing from other cystic
lesions.
 Prognostic marker: Can be used
to monitor disease progression.
Magnetic Resonance Imaging
(MRI):
 Higher contrast resolution
provides clearer images of cysts.
 Can be used as an alternative to
CT scans but poor at detecting
calcified cysts.
6. Molecular Methods:


PCR targeting mitochondrial
DNA has been developed for
Echinococcus genotyping.
PCR-RFLP (Restriction
Fragment Length
Polymorphism) can identify
10 genotypes (G1-G10).
o
o
G1 genotype is the
most common in India.
Each genotype has a
host specificity and
geographical
distribution.
7. Skin Test (Casoni Test):


Immediate hypersensitivity
reaction to hydatid fluid
antigens.
Developed by Casoni in 1911:
o
Procedure: Inject 0.2
mL of antigen into one
arm and sterile saline
o
in the other arm as a
control.
Interpretation: A large
wheal (≥5 cm) with
pseudopodia forms at
the test site within 30
minutes in sensitive
patients.


Limitations:



Low sensitivity (60-80%).
False positives due to
cross-reaction with other
cestodes.
Obsolete: Largely replaced by
serological tests.
8. Other Tests:


Eosinophilia: Present in
20-25% of cases.
Hypergammaglobulinemia:
Common in patients with
hydatid disease.
Monitoring Treatment Response:


Imaging methods (USG, CT,
MRI): Monitor cyst size
reduction or disappearance.
Antigen detection: Antigen
levels decrease as the patient
improves.
Key Points to Remember:


Imaging (especially USG and
CT) is essential for detecting
cysts and monitoring
progression.
Antibody and antigen
detection tests are valuable
for diagnosis, but cannot
differentiate between past
and recent infections.
Molecular methods (PCR)
offer high specificity for
identifying genotypes and
understanding regional
epidemiology.
Casoni test is now obsolete
due to low sensitivity and false
positives.
Treatment of Echinococcus
granulosus Infection
1. Treatment Considerations:

Decision-Making: Based on
size, location,
manifestations of cysts, and
the overall health of the
patient.
2. PAIR (Puncture, Aspiration,
Injection, and Re-aspiration):
Alternative to surgery.
Steps involved:
1. Percutaneous puncture of the
cyst.
2. Aspiration: Remove 10–15 mL of
cyst fluid.
3. Injection of scolicidal agents (e.g.,
hypertonic saline, cetrimide, or
ethanol).
4. Re-aspiration: Remove fluid after
5 minutes.
Benefits of PAIR:
 Higher cure rate.
 Lower recurrence rate.
 Less complications and shorter
hospitalization compared to
surgery.
Indications for PAIR:
 Larger hepatic cysts.
 Cysts within cysts.
 Multiple cysts.
 Cysts with detached
membranes.
Contraindications for PAIR:
 Superficially located cysts (risk
of rupture).
 Inaccessible cysts or
extrahepatic cysts.
 Cysts communicating with the
biliary tree.
3. Surgery:
Definitive treatment but should be
reserved for:
 PAIR contraindicated or
refractory cases.
 Secondary bacterial infections.
 Advanced disease.
Disadvantages of Surgery:
 High recurrence rate (2–25%).
 Postoperative complications
(10–25%).
Preoperative Use of Albendazole:
 Reduces cyst size and prevents
recurrence.
 Dosage: 15 mg/kg/day, divided
into two doses.
 Given 4 days before to 4 weeks
after surgery or PAIR.
4. Antiparasitic Agents:
Albendazole:
 Drug of choice.
 Used to reduce cyst size before
PAIR or surgery and to prevent
recurrence.
 Administered for 4 days before
and up to 4 weeks after the
procedure.
Alternative: Praziquantel (used
when albendazole is not available or
suitable).
5. Percutaneous Thermal Ablation:



Non-invasive method.
Involves radiofrequency
ablation of the cyst's
germinal layer.
Offers an alternative to PAIR
in certain cases.
Key Points to Remember:
 PAIR offers a minimally
invasive option with fewer
complications and a higher cure
rate than surgery.
 Surgery is the gold standard
when PAIR is not suitable but
carries higher risks of recurrence
and complications.
 Albendazole is crucial for
preoperative preparation and
preventing recurrence, while
praziquantel is an alternative.
 Percutaneous thermal ablation
is a non-invasive option to
consider for cyst management.
Echinococcus multilocularis,
Echinococcus oligarthrus, and
Echinococcus vogeli:
Laboratory Diagnosis:Imaging
Methods:

USG, CT Scan, and MRI:

Detect cyst number, size, extent
of the lesion, and calcification.
Antibody Detection Tests:
Echinococcus multilocularis
(Alveolar Hydatid Disease)
Morphology:

Size: Smaller than E.
granulosus (1.2 – 3.7 mm in
length).
Life Cycle:
Hosts:
 Definitive Host: Foxes, wolves
(also dogs and cats).
 Intermediate Host: Small wild
rodents (e.g., squirrels, voles,
mice).
 Human: Accidental intermediate
host.
ELISA:
 Sensitive (86-97%).
 Cross-reacts with E. granulosus
(false positives).
Western Blot (using Em-18
antigen):
 Highly sensitive (97%) and
specific (100%).
 Does not cross-react with E.
granulosus.
Histopathology:
 PAS staining (Periodic Acid
Schiff) after FNAC (Fine Needle
Aspiration Cytology) or biopsy:
Similar to E. granulosus life cycle,
with differences in hosts.

Clinical Features:
Treatment and Prevention:

Causative Agent of Alveolar
(Multilocular) Hydatid
Disease:
o
o
Cysts have multiple
locules (cavities).
Cysts lack fluid or free
brood capsules or
scolices.
Detects multiloculated cysts
and necrosis.

Similar to E. granulosus
treatment:
o
o
Surgery or PAIR
(Puncture, Aspiration,
Injection, and
Re-aspiration).
Albendazole for
preoperative treatment
and to prevent
recurrence.
Echinococcus oligarthrus &
Echinococcus vogeli
Hosts:


Definitive Hosts:
o
o

E. oligarthrus: Wild
felids (wild cats, jaguars,
pumas).
E. vogeli: Wild brush
dogs.
Intermediate Hosts: Rodents
(e.g., paca, spiny rats,
opossums).
Life Cycle:

 Only 80 cases of polycystic
hydatid disease reported so far.
 Most cases are seen in humid
tropical forest areas of Central
and Northern South America:
Similar to E. granulosus.
Clinical Features:
E. oligarthrus:
 Rare human infections.
 4 cases reported: 3 involving the
orbit and 1 involving the heart.
E. vogeli:
 Most common in the liver (80%)
followed by lungs and other
organs.
 Symptoms are similar to cystic
echinococcosis.
Epidemiology:
 E. oligarthrus and E. vogeli are
very rare in humans:
Brazil, Colombia, Panama,
Venezuela.
Laboratory Diagnosis:

Dependent on imaging,
histopathology, serology, or
molecular methods (e.g.,
PCR).
Treatment and Prevention:

Similar to E. granulosus
treatment.
Key Points to Remember:
 E. multilocularis causes alveolar
hydatid disease with multiple
locules and no brood capsules.
It's diagnosed with Western blot
using Em-18 antigen.
 E. oligarthrus and E. vogeli
rarely infect humans and cause
polycystic hydatid disease.
Cases are mostly seen in tropical
regions of South America.
 Diagnosis relies on imaging,
serology, and histopathology.
 Treatment is similar to that of E.
granulosus, including
albendazole, PAIR, and surgery
for more severe cases.
Hymenolepis nana
General Overview


Common Name: Dwarf
tapeworm.
Smallest cestode infecting
humans.
Etymology of Hymenolepis



Hymen: Thin membrane
covering the eggs.
Lepis: Covering.
Nana: Small size.
Discovery

First detected by Bilharz in
1857 in the small intestine.
Epidemiology


Most common tapeworm
infection globally, affecting
50-75 million people.
Prevalence: 0-4%, with higher
prevalence in children (up to
16%).
 Rostellum: Single row of 20-30
hooklets.
Neck:
 Long and gives rise to
proglottids.
Strobila:
 Composed of 200 segments
(proglottids).
 Mature proglottids: Contain
both male and female
reproductive organs.
 Genital pore: Opens laterally on
the same side.
 Uterus: Lobulated wall.
 Testes: Three testicular follicles.
Egg



Size: 30-47 µm.
Shape: Round to slightly oval.
Structure:
o


Morphology
Adult Worm



Size: Small (1-4 cm).
Resides in the upper
two-thirds of the ileum.
Structure: Consists of head,
neck, and strobila.
o
o
Head/Scolex:
 Globular shape.
 4 suckers.
Two membranes:

Outer egg shell.
Inner
embryophore
containing yolk
granules.
Oncosphere: Contains
6 hooklets.
Polar filaments: 4-8
filaments emerging
from thickened poles
of the embryophore.
Appearance: Non-bile stained
(colorless in saline mount).
Infective Form: Eggs.
Larva


Form: Cysticercoid.
Structure: Solid, except for
the proximal part, which is
vesicular and contains the
scolex.
Key Points to Remember
Mode of Transmission:
1. Ingestion of contaminated food
and water with eggs.
2. Autoinfection: Ingestion of eggs
released in the small intestine,
leading to reinfection.
 H. nana is the smallest cestode
and can be identified by its
distinct egg morphology
(non-bile stained, two
membranes, polar filaments).
 The adult worm has a scolex
with hooklets and a strobila with
many proglottids.
 The egg is the infective and
diagnostic form.
 Prevalence is high in children,
with 50-75 million affected
worldwide.
Lifecycle Process:
Hymenolepis nana: Life Cycle,
Diagnosis, and Treatment High-Yield Notes

Life Cycle of Hymenolepis nana
Indirect Life Cycle
Direct Life Cycle
Hosts:
Hosts:
 Definitive host: Humans.
 Intermediate hosts: Insects (e.g.,
rat fleas like Pulex irritans and
Xenopsylla cheopis).
 Definitive host: Humans (only
host).
 Other hosts: Rodents (rats and
mice).
 Eggs hatch in the small intestine.
 Larvae penetrate the intestinal
wall and develop into
cysticercoid larvae in 4–5 days.
 The intestinal villi rupture,
releasing the larvae into the gut
lumen.
 Larvae mature into adult worms
in 10–12 weeks.
 The adult worm undergoes
fertilization and produces eggs.
 Eggs are passed in the feces,
which are infective to humans.
Autoinfection ensures
persistence of infection, despite
the worm's lifespan of only 4–10
weeks.
Mode of Transmission:
 Rare: Humans acquire infection
by ingesting fleas containing
cysticercoid larvae.
Lifecycle Process:
 Eggs are ingested by insects
(fleas).
 Embryo hatches and penetrates
the insect's intestine, developing
into cysticercoid larvae.
 Infected fleas are consumed by
humans, and the larvae develop
into adult worms in the human
intestine.
 The adult worm produces eggs,
which are passed in the feces.
Clinical Features and Pathogenicity


Usually asymptomatic.
Severe infections with
1000–2000 worms may
cause:
o
o
o
o
o
Anorexia
Abdominal pain
Headache
Dizziness
Diarrhea
Laboratory Diagnosis of H. nana

Stool Examination:
o
Detect non-bile
stained eggs with
polar filaments
between the shell
membranes.

Eosinophilia: May be present
in some cases (≥5%
eosinophils).
Treatment

Praziquantel:
o
o

Dose: 25 mg/kg once.
Effective against both
adult worms and
cysticercoid larvae in
the intestine.
Nitazoxanide:
o
o
Dose: 500 mg twice a
day for 3 days.
Alternative treatment.
Key Points to Remember
 Direct Cycle: No intermediate
host; autoinfection is common,
leading to persistent infection.
 Indirect Cycle: Fleas are the
intermediate hosts, and human
infection is rare.
 Diagnostic Clue: Non-bile
stained eggs with polar
filaments are characteristic.
 Treatment: Praziquantel is the
drug of choice, with
Nitazoxanide as an alternative.
Hymenolepis diminuta and
Dipylidium caninum:
Hymenolepis diminuta (Rat
Tapeworm)


rostellum with 1–7
rows of hooklets.
Life Cycle

1. Definitive host: Dogs
and cats (humans are
rarely infected).
2. Intermediate host:
Insects (primarily fleas).
Common Name: Rat tapeworm.
Similarity to H. nana: Similar to
H. nana, but with some
differences (see table 10.6).
Life Cycle:
 Indirect cycle only (unlike H.
nana, which has both direct and
indirect cycles).
 Intermediate host: Essential for
the life cycle. Insects such as
lepidopterans, myriapods, and
beetles act as the intermediate
hosts.
 Definitive host: Rodents,
typically rats.
 Human Infection: Rare, with
fewer than 500 reported cases
(mainly in India, Japan, and Italy).



Common Name:
Double-pored tapeworm.
Common Hosts: Dogs and
cats (humans are rarely
infected).
Morphology

o
Resembles the indirect
cycle of H. nana.
Clinical Features


Mostly Asymptomatic.
Rare symptoms may include:
o
o
o
o
o

Indigestion
Loss of appetite
Diarrhea
Pruritus ani (itching
around the anus)
Abdominal pain
Children are more commonly
affected.
Laboratory Diagnosis
Adult Worm:
o
Mode of Transmission:
o Humans acquire the
infection by ingesting
fleas containing
cysticercoid larvae.
Life Cycle Similarity:
o
Dipylidium caninum
(Double-Pored Tapeworm)

Hosts:
Length: 10–70 cm.
Scolex: Contains four
oval suckers and a

Stool Examination:
 Eggs: 25–40 µm in size, typically
in groups of 15 (called egg
packets).
 Proglottids: Barrel-shaped (3.2
mm wide), resembling cucumber
seeds when fresh and rice grains
when dry.

Proglottids contain two sets of
reproductive organs with two
genital pores, hence the name
double-pored tapeworm.
Treatment

Praziquantel: Drug of choice
for treatment.
Key Points
 H. diminuta: Rat tapeworm, has
an indirect cycle with insects as
the intermediate host. Rare
human infection.
 D. caninum: Double-pored
tapeworm, commonly infects
dogs and cats. Human infection
occurs through ingestion of
fleas containing cysticercoid
larvae.
 Laboratory Diagnosis: Eggs in
egg packets and barrel-shaped
proglottids.
 Treatment: Praziquantel is the
treatment of choice for both
infections.