Micropara Lab Parasites Gr123456

GROUP 1.
Kassandra D. Depuyart
Liza Ymanuelle J. Barrientos
Ken Francis G. Ang
Joshua G. Cabrera
Phil Jereg R. Guihama
Name of Parasite: Ascaris Lumbricoides
Common name/ other name: Giant roundworm
I. MORPHOLOGY
*ADULT: MALE AND FEMALE
Male Ascaris does not have any straight tail rather they are
slightly coiled or appear hooked at the posterior end. The cloaca or penial
setae is present in the case of Ascaris male. Males are smaller at 15–31 cm
and tend to have curved tails.
Female Ascaris are larger in size as compared to the males.
The female Ascaris has a straight blunt tail or posterior end. Females
measure 20–35 cm long with straight taisl.
*Egg/ Ova
Fertilized and unfertilized Ascaris lumbricoides eggs are passed in stool of the infected
host. Fertilized eggs are rounded and have a thick shell with an external mammillated
layer that is often stained brown by bile. In some cases, the outer layer is absent
(known as decorticated eggs). Fertile eggs range from 45 to 75 µm in length.
Unfertilized eggs are elongated and larger than fertile eggs (up to 90 µm in length).
Their shell is thinner and their mammillated layer is more variable, either with large
protuberances or practically none. Unfertile eggs contain mainly a mass of refractile
granules. Complete development of the larva requires 18 days under favorable
conditions (moist, warm, shaded soil). However, eggs of Ascaris lumbricoides may
continue to develop and are infectious even when preserved in formalin.
II. LIFE CYCLE
Adult worms live in the lumen of the small intestine. A female may produce
approximately 200,000 eggs per day, which are passed with the feces.
Unfertilized eggs may be ingested but are not infective. Larvae develop to
infectivity within fertile eggs after 18 days to several weeks, depending on
the environmental conditions (optimum: moist, warm, shaded soil). After
infective eggs are swallowed, the larvae hatch, invade the intestinal mucosa,
and are carried via the portal, then systemic circulation to the lungs . The
larvae mature further in the lungs (10 to 14 days), penetrate the alveolar
walls, ascend the bronchial tree to the throat, and are swallowed. Upon
reaching the small intestine, they develop into adult worms. Between 2 and
3 months are required from ingestion of the infective eggs to oviposit ion by
the adult female. Adult worms can live 1 to 2 years.
III. MODE OF TRANSMISSION

Hand to mouth route contaminated with infested soil with the infective eggs.
IV. PATHOLOGY AND SYMPTOMATOLOGY
The pathogenesis of ascariasis is generally related to organ damage and host

reactions to larval migration as well as the number and location of adult
worm in the body. The signs and symptoms of the nematode infection
by Ascaris lumbricoides may include the following: Abdominal discomfort.
Abdominal cramping. Abdominal swelling (especially in children).
V. LABORATORY DIAGNOSIS
The standard method for diagnosing ascariasis is by

identifying Ascaris eggs in a stool sample using a microscope. Because eggs
may be difficult to find in light infections, a concentration procedure is
recommended.
VI. TREATMENT
Anthelmintic medications (drugs that remove parasitic worms from the

body), such as albendazole and mebendazole, are the drugs of choice for
treatment of Ascaris infections, regardless of the species of
worm. Infections are generally treated for 1–3 days.
VII. PREVENTION AND CONTROL
Avoid contact with soil that may be contaminated with human feces,
including with human fecal matter (“night soil”) used to fertilize crops.
Wash your hands with soap and warm water before handling food.
Teach children the importance of washing hands to prevent infection.
Name of Parasite: Wuchereria Bancrofti
Common name/ other name: Filariasis or

Ephantiasis
I. MORPHOLOGY
*Adult: MALE AND FEMALE
The males measure up to 40 mm long.

Females are 80—100 mm long.
Adults of Wuchereria bancrofti are long
and threadlike. Adults are found primarily
in lymphatic vessels, less commonly in
blood vessels.
*Egg/ Ova
The eggs average 40 by 25 μm in size. They lack a true shell, instead being
enclosed in a membrane which stretches to form a sheath over the microfilaria
(embryo). Microfilariae: The embryo itself averages 290 μm by 6-7 μm, though the
sheath surrounding it is slightly larger.
II. LIFE CYCLE
Different species of the following genera of mosquitoes are vectors of W.

bancrofti filariasis depending on geographical distribution. Among them
are: Culex (C. annulirostris, C. bitaeniorhynchus, C. quinquefasciatus, and C.
pipiens); Anopheles (A. arabinensis, A. bancroftii, A. farauti, A. funestus, A.
gambiae, A. koliensis, A. melas, A. merus, A. punctulatus and A.
wellcomei); Aedes (A. aegypti, A. aquasalis, A. bellator, A. cooki, A.
darlingi, A. kochi, A. polynesiensis, A. pseudoscutellaris, A. rotumae, A.
scapularis, and A. vigilax); Mansonia (M. pseudotitillans, M.
uniformis); Coquillettidia (C. juxtamansonia). During a blood meal, an
infected mosquito introduces third-stage filarial larvae onto the skin of the
human host, where they penetrate into the bite wound . They develop in
adults that commonly reside in the lymphatics . The female worms
measure 80 to 100 mm in length and 0.24 to 0.30 mm in diameter, while
the males measure about 40 mm by .1 mm. Adults produce microfilariae
measuring 244 to 296 μm by 7.5 to 10 μm, which are sheathed and have
nocturnal
periodicity,
except the
South Pacific
microfilariae
which have
the absence of
marked
periodicity.
The
microfilariae
migrate into
lymph and
blood
channels
moving
actively through lymph and blood . A mosquito ingests the microfilariae
during a blood meal . After ingestion, the microfilariae lose their sheaths
and some of them work their way through the wall of the proventriculus and
cardiac portion of the mosquito’s midgut and reach the thoracic muscles .
There the microfilariae develop into first-stage larvae and subsequently
into third-stage infective larvae . The third-stage infective larvae migrate
through the hemocoel to the mosquito’s prosbocis and can infect another
human when the mosquito takes a blood meal .
The disease is usually transmitted through the bite of an infectious

mosquito. Overall there are 6 general and 70 species of mosquitoes
responsible for the spread of Wuchereria bancrofti.
Wuchereria bancrofti (Filariasis) infection occurs when a larva carrying

mosquito bites an individual, introducing these larvae into the skin. The larvae
then enters the patient's blood through the skin wound and spread to the
different sites such as lymphatic vessels, subcutaneous tissues or the serous
cavities. Signs and symptoms are fever, inguinal or axillary lymphadenopathy,
testicular and/or inguinal pain, skin exfoliation, and limb or genital swelling -
repeated episodes of inflammation and lymphedema lead to lymphatic damage,
chronic swelling, and elephantiasis of the legs, arms, scrotum, vulva, and
breasts.
The standard method for diagnosing active infection is the identification of

microfilariae in a blood smear by microscopic examination. The microfilariae
that cause lymphatic filariasis circulate in the blood at night (called nocturnal
periodicity).
VI. TREATMENT
The drug of choice is diethylcarbamazine, which can eliminate the

microfilariae from the blood and also kill the adult worms with a dose of 6
mg/kg/day for 12 days, semiannually or annually. A
polytherapy treatment that includes ivermectin with diethylcarbamazine or
albendazole is more effective than either drug alone.
At night. Sleep in an air-conditioned room or. Sleep under a mosquito net.

Between dusk and dawn. Wear long sleeves and trousers and. Use mosquito
repellent on exposed skin. Another approach to prevention includes giving
entire communities medicine that kills the microscopic worms —
and controlling mosquitoes.
Name of Parasite: Loa loa

Common name/ other name: Eye worm or
Loiasis
I. MORPHOLOGY
*ADULT: MALE AND FEMALE
Adult males are smaller at 30-34

mm long and 0.35-0.40 mm wide.
Adult females are 40-70 mm in
length and 0.45-0.60 mm wide.
Adults of Loa loa are often isolated from the sub conjunctiva. The exterior of
the cuticle lacks ridging seen in many Dirofilaria but contains irregularly-
spaced elevations called “bosses”.
Microfilariae of Loa loa
- Are sheathed and measure 230-250 µm long in stained blood smears and
270-300 µm in 2% formalin. The tail is tapered and nuclei extend to the
tip of the tail. Microfilariae circulate in the blood.
II. LIFE CYCLE
The vector for Loa

loa filariasis originates with
flies from
two hematophagous species
of the genus Chrysops (deer
flies), C. silacea and C.
dimidiata. During a blood
meal, an infected fly
(genus Chrysops, day-biting
flies) introduces third-stage
filarial larvae onto the skin
of the human host, where
they penetrate into the bite wound. The larvae develop into adults that
commonly reside in subcutaneous tissue. The female worms measure 40 to
70 mm in length and 0.5 mm in diameter, while the males measure 30 to
34 mm in length and 0.35 to 0.43 mm in diameter. Adults
produce microfilariae measuring 250 to 300 μm by 6 to 8 μm, which are
sheathed and have diurnal periodicity. Microfilariae have been recovered
from spinal fluids, urine and sputum. During the day, they are found in
peripheral blood, but during the noncirculation phase, they are found in
the lungs. The fly ingests microfilariae during a blood meal. After ingestion,
the microfilariae lose their sheaths and migrate from the fly's midgut
through the hemocoel to the thoracic muscles of the arthropod. There the
microfilariae develop into first-stage larvae and subsequently into third-
stage infective larvae. The third-stage infective larvae migrate to the
fly's proboscis and can infect another human when the fly takes a blood
meal.
Loiasis, called African eye worm by most people, is caused by the parasitic
worm Loa loa. It is passed on to humans through the repeated bites of
deerflies (also known as mango flies or mangrove flies) of the genus
Chrysops.
If you have loiasis, you may have itchy, non-painful swellings of the body
that come and go. The swellings can show up anywhere though they are
more common near joints. You may develop an eye worm that crawls across
the surface of your eye. Sometimes you may see a worm that crawls under
your skin.
Diagnosis is by detecting microfilariae in peripheral blood or seeing worms

migrating across the eye.
VI. TREATMENT
Treatment is with diethylcarbamazine and Ivermectin, the drug of choice for
the treatment of onchocerciasis, is a semisynthetic macrolide that is effective
against the microfilariae (but not the adult worms) of Loa loa. A single dose
of 200 mg/kg has been shown to reduce microfilarial levels by 70-90% for
up to 1 year.
Avoid insect bites by wearing long pants and long-sleeved shirts

and avoid the smoke of wood fires to reduce your risk of infection.
NAME OF PARASITE: Echinococcus granulous
COMMON NAMES/OTHER NAMES: Hydatid worm, hyper tape-worm or dog

tapeworm
I.
MORPHOLOGY
*ADULT
*EGG/OVA
The eggs are typical for most taeniid species and are small and round (30-
43µm in diameter), thick-shelled and contain a hexacanth (6-hooked)
embryo (oncosphere). The encysted larval (metacestode) stage is known as a
bladder-worm or hydatid, and it produces multiple infective stages
(protoscoleces, apparent as invaginated scolices already containing suckers
and hooks) either directly from the germinal layer of the cyst wall, or by
forming brood sacs (hydatid sand) by endogenous (internal) or exogenous
(external) budding of the germinal layer. E. granulosus forms fluid-filled
unilocular cysts with endogenous budding of brood capsules, E. vogeli forms
fluid-filled polycystic cysts with exogenous budding, and E.
multilocularis forms fluid-free multilocular or alveolar cysts with exogenous
budding.
II. LIFE CYCLE
The adult Echinococcus granulosus (sensu lato) (2—7 mm long) resides in the small
intestine of the definitive host. Gravid proglottids release eggs that are passed in the
feces, and are immediately infectious. After ingestion by a suitable intermediate host,
eggs hatch in the small intestine and release six-hooked oncospheres that penetrate
the intestinal wall and migrate through the circulatory system into various organs,
especially the liver and lungs. In these organs, the oncosphere develops into a thick-
walled hydatid cyst that enlarges gradually, producing protoscolices and daughter
cysts that fill the cyst interior. The definitive host becomes infected by ingesting the
cyst-containing organs of the infected intermediate host. After ingestion, the
protoscolices evaginate, attach to the intestinal mucosa, and develop into adult
stages in 32 to 80 days.
Humans are aberrant intermediate hosts, and

become infected by ingesting eggs.
Oncospheres are released in the intestine, and
hydatid cysts develop in a variety of organs. If
cysts rupture, the liberated protoscolices may
create secondary cysts in other sites within the
body (secondary echinococcosis).
Human infection occurs by hand-to-mouth transfer of viable tapeworm eggs

from dog feces. The parasite eggs, which can remain viable for weeks, are
distributed via local environmental contamination by feces of tapeworm-
infected canines.
Abdominal pain, nausea and vomiting are commonly seen when hydatids
occur in the liver. If the lung is affected, clinical signs include chronic
cough, chest pain and shortness of breath. Other signs depend on the
location of the hydatid cysts and the pressure exerted on the surrounding
tissues.
Granulosus is endemic suggests a diagnosis of cystic echinococcosis.

Imaging techniques, such as CT scans, ultrasonography,and MRIs, are used
to detect cysts. After a cyst has been detected, serologic tests may be used to
confirm the diagnosis. Alveolar echinococcosis is typically found in older
people.
VI. TREATMENT
Chemotherapy, cyst
puncture, and PAIR
(percutaneous
aspiration, injection of
chemicals and
reaspiration) have
been used to
replace surgery as effective
treatments for cystic echinococcosis.
However, surgery remains the most
effective treatment to remove the
cyst and can lead to a complete
cure.
Wash your hands with soap and

warm water after handling dogs, and
before handling food. Teach children
the importance of washing hands
to prevent infection. Avoid ingestion of
food, water or soil contaminated with stool from dogs.
NAME OF PARASITE: Hymenolepsis diminuta
COMMON NAMES/OTHERS NAMES: Rat tapeworm
I. MORPHOLOGY
*ADULT
Adult Hymenolepis diminuta reach 20 to 60 cm, and up to 90 cm. The

cestode has a long cylindrical body with 4 suckers and an apical organ at its
scolex with no rostellar hooks.
*EGG/OVA
Eggs of Hymenolepis diminuta. These eggs are round or slightly oval, size 70
– 85 µm X 60 – 80 µm, with a striated outer membrane and a thin inner
membrane. The space between the membranes is smooth or faintly
granular. The oncosphere has six hooks.
II.LIFE CYCLE
Eggs of Hymenolepis diminuta are passed out in the feces of the infected
definitive host (rodents, man) . The mature eggs are ingested by an
intermediate host (various arthropod adults or larvae) , and oncospheres
are released from the eggs and penetrate the intestinal wall of the host ,
which develop into cysticercoid larvae. Species from the genus Tribolium are
common intermediate hosts for H. diminuta. The cysticercoid larvae persist
through the arthropod’s morphogenesis to adulthood. H. diminuta infection
is acquired by the mammalian host after ingestion of an intermediate host
carrying the cysticercoid larvae . Humans can be accidentally infected
through the ingestion of insects in precooked cereals, or other food items,
and directly from the environment (e.g., oral exploration of the environment
by children). After ingestion,
the tissue of the infected
arthropod is digested releasing
the cysticercoid larvae in the
stomach and small intestine.
Eversion of the scoleces
occurs shortly after the
cysticercoid larvae are
released. Using the four
suckers on the scolex, the
parasite attaches to the small
intestine wall. Maturation of
the parasites occurs within 20
days and the adult worms can reach an average of 30 cm in length . Eggs
are released in the small intestine from gravid proglottids that
disintegrate after breaking off from the adult worms. The eggs are expelled to
the environment in the mammalian host’s feces .
II. MODE TRANSMISSION
Hymenolepiasis is the most common intestinal tapeworm infection of

humans caused by worm of family cestoda, genus Hymenolepis and
species nana. This infection does not require an intermediate host and
infection can occur directly from one infected person to another by fecal-
oral transmission.
III. PATHOLOGY AND SYMPTOMATOLOGY

Most people who are infected do not have any symptoms. Those who have
symptoms may experience nausea, weakness, loss of appetite, diarrhea, and
abdominal pain. Young children, especially those with a heavy infection,
may develop a headache, itchy bottom, or have difficulty sleeping.
IV. LABORATORY DIAGNOSIS
Diagnosis is based on finding eggs or proglottids in the feces or the adult

worms in the intestine.
V. TREATMENT
Praziquantel is the drug of choice for treatment of H. diminuta infection (2),

but niclosamide is also effective (13, 14). Our patient was initially prescribed
niclosamide, but the treatment regimen was not respected. A single dose of
praziquantel (10 mg/kg) failed to annihilate the tapeworm.
VI. PREVENTION AND CONTROL
Prevention. Good hygiene, public health and sanitation programs, and

elimination of infected rats help to prevent the spread of
hymenolepiasis. Preventing fecal contamination of food and water in
institutions and crowded areas is of primary importance. An effective
prevention and control program should include purchase of parasite-free
animals, insect control, and high standards of animal husbandry and facility
management.
NAME OF PARASITE: Schistosoma mansoni
COMMON NAMES/ OTHER NAMES: Blood fluke
I. MORPHOLOGY
*ADULT
Adults of Schistos
oma mansoni.
Unlike the
flukes, adult
schistosomes have
the sexes
separate, with the
female residing in
a gynecophoral
canal within the
male. Male worms
are robust,
tuberculate and
measure 6-12 mm in length. Females are longer (7-17 mm in length) and
slender.
*EGG/OVA
Schistosoma mansoni eggs are large (114 to
180 µm long by 45-70 µm wide) and have a
characteristic shape, with a prominent
lateral spine near the posterior end. The
anterior end is tapered and slightly curved.
When the eggs are excreted in stool, they
contain a mature miracidium.
II. LIFE CYCLE

Schistosoma eggs are eliminated with feces or urine, depending on species.
Under appropriate conditions the eggs hatch and release miracidia, which
swim and penetrate specific snail intermediate hosts. The stages in the snail
include two generations of sporocysts and the production of cercariae .
Upon release from the snail, the infective cercariae swim, penetrate the skin
of the human host , and shed their forked tails, becoming schistosomulae .
The schistosomulae migrate via venous circulation to lungs, then to the
heart, and then develop in the liver, exiting the liver via the portal vein
system when mature, . Male and female adult worms copulate and reside
in the mesenteric venules, the location of which varies by species (with some
exceptions) . For instance, S. japonicum is more frequently found in the
superior mesenteric veins draining the small intestine , and S.
mansoni occurs more often in the inferior mesenteric veins draining the
large intestine . However, both species can occupy either location and are
capable of moving between sites. S. intercalatum and S. guineensis also
inhabit the inferior mesenteric plexus but lower in the bowel than S.
mansoni. S. haematobium most often inhabitsin the vesicular and pelvic
venous plexus of the bladder , but it can also be found in the rectal
venules. The females (size ranges from 7–28 mm, depending on species)
deposit eggs in the small venules of the portal and perivesical systems. The
eggs are moved progressively toward the lumen of the intestine (S.
mansoni,S. japonicum, S. mekongi, S. intercalatum/guineensis) and of the
bladder and ureters (S. haematobium), and are eliminated with feces or
urine, respectively
S. mansoni is transmitted through water, where freshwater snails of the

genus Biomphalaria act as intermediate hosts. The larvae are able to live in
water and infect the hosts by directly penetrating the skin. Prevention
of infection is done by improved sanitation and killing the snails.
Occasionally some individuals may develop the syndrome after an initial

contact with water contaminated by S. mansoni cercariae . The most
common manifestations are fever, chills, weakness, headache, anorexia,
nausea, vomiting, and general malaise.
Schistosomiasis is diagnosed through the detection of parasite eggs in stool
or urine specimens. Antibodies and/or antigens detected in blood or urine
samples are also indications of infection.
VI. TREATMENT
Most trials report on whether or not the treatment stops eggs excretion;
three reported the person’s recovery from symptoms. The results show that
a single dose of praziquantel (40 mg/kg), as recommended by the World
Health Organization, is an effective treatment for Schistosoma
mansoni infection.
Avoid swimming or wading in freshwater when you are in countries in

which schistosomiasis occurs. Drink safe water. Water used for bathing
should be brought to a rolling boil for 1 minute to kill any cercariae, and
then cooled before bathing to avoid scalding.
NAME OF PARASITE: Gastrodiscoides hominis
COMMON NAMES/ OTHER NAMES: Class: Trematoda
Phylum: Platyhelminths
I. MORPHOLOGY
G. Hominis is a reddish-colored
amphistome with a ventral sucker located
in the posterior end. The anterior region is
narrow and ends with a rounded tip. The
posterior region contains the reproductive
organs including an ovary in the shape of
an oval located under the 2 lobed testes.
*EGG/OVA
Gastrodiscoides Hominis is passed through the feces in egg form where it

can come into direct contact with the water supply or vegetation or it is used
as "night soil"
II. LIFE CYCLE
The eggs of G. Hominis are passed in feces unfertilized usually into some
kind of water source
where they are
ingested by the snail
intermediate host. The
eggs hatch and release
miracidium which
develop from there into
the sporocyst stage
followed by one or
more generations of
redia.
III. MODE OF
TRANMISSION
Gastrodiscoides Hominis is passed through the feces in egg form where it

can come into direct contact with the water supply or vegetation or it is used
as "night soil".
IV. PATHOLOGY AND SYMTOMATOLOGY
While this parasite is typical found in pigs, it can also affect humans.
Usually the infection is asymptomatic but occasionally it can also cause
intestinal problems such as diarrhea, fever, abdominal pain, colic, and an
increase in mucous production.
The diagnosis is made through examination of the feces and detection of
G. Hominis eggs. Only after several digestions of the parasite can the higher
levels be detected because the patient begins to present the symptoms
mentioned before. There have not been any other tests made at this time.
VI. TREATMENT
The treatment for G. Hominis is similar to those of M. yokogawai or H.

heterophyes in that typically a soapsud enema can be effective in removing
the worms.
Prevention of this disease is not difficult when simple sanitary measures are
taken. “Night Soil” should never be used as a fertilizer because it could contain
any number of parasites. Also all food should be washed thoroughly using
filtered water and proper techniques to dispose of waste should observed.
GROUP 4
Deborah Solomom
Tricia Nichole Tabudlong
Christine Talamor
Sherry Ann Tayco
Christel Ann Tianchon
Name of Parasite: Onchocerca volvolus
Common names/ other names: river blindness
I. Morphology
II. LIFE CYCLE

• The male and female worms entwine in nodules in the subcutaneous tissue of the
skin. After mating, the female worm releases around 1000 microfilariae larvae a day
into the surrounding tissue. Microfilariae live for 1–2 years, moving around the body
in the subcutaneous tissue
• The disease spreads by the bite of an infectious blackfly. When a blackfly bites a
person who has onchocerciasis, microscopic worm larvae (called microfilariae) in the
infected person's skin are ingested by the blackfly. The larvae develop over
approximately one week in the fly to a stage that is infectious to humans.
IV. PATHOLOGY & SYMPHATOLOGY
• Onchocerciasis, or river blindness, is a neglected tropical disease (NTD) caused by

the parasitic worm Onchocerca volvulus. It is transmitted through repeated bites by
blackflies of the genus Simulium. The disease is called river blindness because the
blackfly that transmits the infection lives and breeds near fast-flowing streams and
rivers, mostly near remote rural villages. The infection can result in visual impairment
and sometimes blindness. Additionally, onchocerciasis can cause skin disease,
including intense itching, rashes, or nodules under the skin. Worldwide
onchocerciasis is second only to trachoma as an infectious cause of blindness.
• The gold standard test for the diagnosis of onchocerciasis remains the skin snip
biopsy. The biopsy is performed using a sclerocorneal biopsy punch or by elevating a
small cone of skin (3 mm in diameter) with a needle and shaving it off with a scalpel.
In general, the diagnosis of O. volvulus infection should be made with skin snip.
However, when skin snips are negative and clinical suspicion of infection is high, the
general antibody test could be used in an attempt to exclude infection.
VI. TREATMENT
• The recommended treatment is ivermectin, which will need to be given every 6

months for the life span of the adult worms (i.e., 10–15 years) or for as long as the
infected person has evidence of skin or eye infection. Ivermectin kills the larvae and
prevents them from causing damage but it does not kill the adults. There is a
promising treatment using doxycycline that kills the adult worms by killing the
Wolbachia bacteria on which the adult worms depend in order to survive. If you are
infected, it is possible that your doctor will want to treat you both with ivermectin and
with doxycycline.
• There are no vaccines or medications available to prevent becoming infected with O.

volvulus. The best prevention efforts include personal protection measures against
biting insects. This includes wearing insect repellant such as N,N-Diethyl-meta-
toluamide (DEET) on exposed skin, wearing long sleeves and long pants during the
day when blackflies bite, and wearing permethrin- treated clothing. For a description
of the CDC’s information for preventing insect bites. Mass distribution of ivermectin,
donated by Merck & Co., Inc., to all people living in many areas where O. volvulus is
found, is being given to control onchocerciasis.
Name of Parasite: Capillaria philippinensis
Common names/ other names: round worm
I. Morphology
II. LIFE CYCLE

1. Unembryonated, thic-shelled eggs passed in feces.
2. Eggs become embryonated in water.
3. Infective larvae develop in tissue of intermediate host.
4. Ingestion or raw or undercooked infected fish .
5. Adults in small intestinal mocusa.
6. Females may produce two types of eggs: unembryonated eggs (passed in feces) and
embryonated eggs lacking shell ( hatch inside definitive host).
7. Larvae re-invade small intestinal mocusa in autoinfective cycle.
• Once accidentally ingested by a human, the eggs migrate to the liver and mature to
adult worms. Another route of transmission is through the decomposition of infected
animals via eggs in the liver being released into the soil. C. philippinensis is often
found in the tissues of small, freshwater fish.
• Capillaria philippinensis inhabits the small bowel of humans, causing diarrhea and
malabsorption.85,86 Infections have been recognized mostly in the Philippines but
also in Thailand, Taiwan, Japan, Korea, Egypt, China, Indonesia, and Iran. The life
cycle is surmised as follows: water birds harbor the adult worms and excrete ova,
which are ingested by freshwater fish that become infected and produce larvae.
Humans and birds become infected after eating infected fish possessing infective
larvae. These larvae invade the jejunum and ileum, and the resulting adults produce
both eggs and larvae. Unlike almost all helminths that infect humans, with the
exception of Strongyloides stercoralis, the parasite multiplies in the gut. This process
is known as autoinfection and results in an overwhelming infection.
• The specific diagnosis of Capillaria philippinensis is established by finding eggs,

larvae and/or adult worms in the stool or in intestinal biopsies. Unembryonated eggs
are the typical stage found in the feces. In severe infections, embryonated eggs, larvae,
and even adult worms can be found in the feces.
VI. TREATMENT
• Mebendazole 400 mg/day given in divided doses for 20 days for new cases and for 30
days for relapses of cases. Eggs and parasites disappear from feces within 4 days and
symptoms within a week. Albendazole has also been found effective in treating
intestinal capillariasis using the same dosage as Mebendazole.
• Cook fish thoroughly before eating. Avoid eating raw fish. Use sanitary toilet for
disposal of human waste.Capillariasis is an intestinal parasitism caused by smallest
nematodes that infect humans called Capillaria Philippinesis.
Name of Parasite: Toxocara cati
Common names/ other names: feline roundworm
I. Morphology
II. LIFE CYCLE

• The adult worms live in the small intestine and the female produces eggs that are
passed in the feces of the cat. The egg is typically passed containing a single cell, and
after a period of time in the environment, two molts occur within the eggshell to
produce the infective third-stage larva
• Dogs and cats that are infected with Toxocara can shed Toxocara eggs in their feces.
Adults and children can become infected by accidentally swallowing dirt that has been
contaminated with dog or cat feces that contain infectious Toxocara eggs.
• Infection of cats with the eggs of Toxocara cati occurs when ingested larvae penetrate
the stomach wall and migrate through the liver, lungs and trachea until they reach the
small intestine where they develop into adults. You can experience the Breathing
difficulties, Abdominal pain,Weakness, Rash,and Generalised itching.
• A blood test is available that looks for evidence of infection with Toxocara larvae. In
addition to the blood test, diagnosis of toxocariasis includes identifying the presence of
typical clinical signs of VT or OT and a compatible exposure history.
VI. TREATMENT
• Treatment for Toxocara cati infections in cats is rather simple. There are a number of
anthelmintics that will kill the adult worms, including emodepside, fenbendazole,
milbemycin, and moxidectin. However, most drugs are ineffective against the
immature parasites.

• Controlling Toxocara infection in dogs and cats will reduce the number of infectious
eggs in the environment and reduce the risk of infection for people. Have your
veterinarian treat your dogs and cats, especially young animals, regularly for
worms.Clean your pet’s living area at least once a week; every day is better. Feces
should be either buried or bagged and disposed of in the trash. Wash your hands after
handling pet waste.Do not allow children to play in areas that are soiled with pet or
other animal feces and cover sandboxes when not in use to make sure that animals do
not get inside and contaminate them. Wash your hands with soap and warm water
after playing with your pets or other animals, after outdoor activities, and before
handling food or eating.Teach children the importance of washing hands to prevent
infection.
Name of Parasites: Diphyllobothrium Mansonoides
Common name/other name: Spirometra mansonoides or Diphyllobothrium

Lantum
I. Morphology( egglova, larval stage, adult)
II. Life cycle

Eggs are passed unembryonated in feces
Under appropriate conditions, the eggs mature (approximately 18 to 20 days) and

yield oncospheres which develop into a coracidia
After ingestion by a suitable crustacean (first intermediate host) the coracidia develop
into procercoid larvae
Procercoid larvae are released from the crustacean upon predation by the second
intermediate host (usually a small fish) and migrate into the deeper tissues where they
develop into a plerocercoid larvae (spargana), which is the infectious stage for the
definitive host
Because humans do not generally eat these small fish species raw, the second
intermediate host probably does not represent an important source of human
infection. However, these small second intermediate hosts can be eaten by larger
predator species that then serve as paratenic hosts
In this case, the plerocercoid migrates to the musculature of the larger predator fish;
humans (and other definitive host species) acquire the parasite via consumption of
undercooked paratenic host fish
In the definitive host, the plerocercoid develops into adult tapeworms in the small
intestine. Adult diphyllobothriids attach to the intestinal mucosa by means of two
bilateral groves (bothria) of their scolex
The adults can reach more than 10 m in length, with more than 3,000 proglottids.
Immature eggs are discharged from the proglottids (up to 1,000,000 eggs per day per
worm) and are passed in the feces. Eggs appear in the feces 5 to 6 weeks after
infection.
III. Mode of Transmission
Diphyllobothrium latum (D. latum), which is the most common cause of

diphyllobothriasis, also called the “fish tapeworm” or the “broad tapeworm,” is
transmitted to humans by the ingestion of fish which harbor infectious larvae of the
genus Diphyllobothrium causing a wide-ranging spectrum of disease and severity.
IV. Pathology and Sympathology
Most infections are asymptomatic. However symptoms can include abdominal

discomfort, diarrhea, vomiting, and weight loss. Vitamin B12 deficiency leading to
pernicious anemia may occur. Complications include intestinal obstruction and gall
bladder disease caused by migration of proglottids.
V. Laboratory Diagnosis
Microscopic identification of eggs in the stool is the basis of family level diagnosis;
genus level identification based on eggs is difficult due to overlap in morphological
features. Eggs are usually numerous and can be demonstrated without concentration
techniques. Identification of proglottids passed in the stool is also of diagnostic value.
VI. Treatment
Treatment for this parasitic infection, as well as most tapeworm infections, is

praziquantel in those without contraindications. A 25 mg/kg dose is noted to be highly
effective against D. latum infections.Lower doses at 10 mg/kg have been noted to be
effective against other species of Diphyllobothrium but have shown poor efficacy
against D. latum in experimental animal models.A single dose was found to have high
cure rates. Side effects of praziquantel include weakness, headache, dizziness,
abdominal pain, fever, and possibly urticaria.
An alternative anthelminthic drug used for D. latum infections is a single dose of
niclosamide, which is given either in a single 2-gram dose for adults or a 1-gram dose
for children older than six years of age.
Praziquantel can be given in pregnancy.
VII. Prevention and Control
This infections can be easily prevented. Use the following guidelines:
* Cook fish at a temperature of 130°F (54.4°C) for five minutes.
* Freeze fish below 14°F (-10.0°C).
* Follow proper food safety handling, such as washing hands and avoid cross-
contamination with raw fish and fruits and vegetables.
* Avoid contact with any animal known to be infected with a tapeworm.
* Exercise caution when eating and traveling in developing countries
Name of Parasite: Taenia Multiceps
Common Name/ Other names: Coenurus tapeworm or Coenurosis
I.Morphology
II.Life Cycle
Eggs and gravid proglottids are shed in feces of the infected definitive host (canids)
into the environment image , where they are immediately infectious and may be
ingested by an intermediate host image . Eggs hatch in the intestine of the
intermediate host and oncospheres are released image that circulate in blood until
they lodge in suitable organs (including skeletal muscle, eyes, brain and subcutaneous
tissue). After about three months, oncospheres develop into coenuri, which contain
numerous protoscolices. The definitive host becomes infected by ingesting the tissue of
an infected intermediate host containing a coenurus image . The protoscolices evert,
attach to the small intestinal wall image , and develop into adult cestodes in the
definitive canid host image .
Humans become infected after the accidental ingestion of eggs on fomites or in food
and water contaminated by feces of the infected definitive host image . Eggs hatch in
the intestine, and oncospheres are released image that circulate in blood until they
lodge in suitable organs and after about three months develop into coenuri image .
Coenuri of T. multiceps are usually found in the eyes and brain; those of T. serialis are
usually found in subcutaneous tissue.
III. Mode of transmission
Taenia (Multiceps) multiceps is the causative agent of the rare condition called Gid.
The disease occurs in ruminants as well as many other mammalian species. The larval
parasite, ingested from fecal-contaminated food and water, invades the brain and
spinal cord and develops as a bladderworm that causes pressure necrosis of the
nervous tissues. The resultant signs of hyperesthesia, meningitis, paresis, paralysis,
ataxia, and convulsions are observed. Diagnosis is usually made at necropsy.
Eliminating transfer from the canid hosts prevents the disease
IV. Pathology and Sympathology
Symptoms of Taenia Multiceps (coenurosis) require several years to develop and

depend on the organ infected. Involvement of the brain can cause increased
intracranial pressure, seizures, loss of consciousness, and focal neurologic deficits. A
coenurus in subcutaneous tissue or muscle may manifest as a fluctuant, tender
nodule. If the eyes are involved, vision may be impaired.Diagnosis of coenurosis is
typically made after surgical removal, which is also the primary treatment. Surgery is
typically done for symptomatic, space-occupying lesions.
In the definitive host, taeniasis can be diagnosed by finding proglottids in the feces, on
the animal, or in the environment, and taeniid eggs in the feces by fecal flotation,
sedimentation or other techniques. While the proglottids are still moist, their
morphology can help identify the organism to the genus level. Injecting the proglottid
with India ink can reveal structural details and aids in distinguishing some species.
PCR and other genetic techniques can more reliably identify the specific organism, but
are rarely used for taeniasis in animals except in research. Repeated sampling may be
needed to detect the eggs, as they are shed intermittently, and are not concentrated
efficiently by the usual flotation methods. Taeniid eggs are dense and brown, with a
striated embryophore coat. Coproantigen assays can detect taeniid antigens in feces,
but do not usually distinguish different species. Diagnosis of cysticercosis or
coenurosis can be difficult in live animals. In sheep, T. multiceps coenurosis is
sometimes suspected if there is refraction upon palpation of the skull behind the horn
buds and consistent clinical signs. Imaging studies such as MRI or ultrasound are
used occasionally, especially in smaller animals, and biopsies may be helpful if the
cyst is accessible
VI. Treatment
Currently the only treatment that can be recommended is the surgical removal of the
coenurus cyst from the brain of the affected animal . This treatment can be very
successful, and most cases will show a dramatic recovery, with return to full
neurological function, however not all affected animals can undergo surgery as it
largely depends on the location of the cyst. The vet will have to decide whether there is
a chance the animal will recover or whether it is better to destroy the affected animal
humanely to prevent further suffering.
The best control and prevention of coenurosis is to prevent dogs from having access to
sheep and cattle carcasses and not to feed them uncooked meat. If this is not possible,
the control and prevention of coenurosis should be based on routine anthelmintic
dosing of dogs, preferably every three months. Public footpaths running through the
sheep fields used by people walking their dogs can be a particular problem. Farmers
could display a sign explaining the disease risks and encouraging local people walking
their dogs on these fields to have their dogs wormed.
Name of Parasites:Paragonimus Westermani
Common Name/ Other Name:Japanese Lung Fluke
I. Morphology (egglova, larval stage, adult).
II. Life Cycle

Paragonimus has a quite complex life-cycle that involves two intermediate hosts as
well as humans.
Eggs first develop in water after being expelled by coughing (unembryonated) or

being passed in human feces. In the external environment, the eggs become
embryonated. In the next stage, the parasite miracidia hatches and invades the first
intermediate host such as a species of freshwater snail.
Miracida penetrate its soft tissues and go through several developmental stages
inside the snail but mature into cercariae in 3 to 5 months.
Cercariae next invade the second intermediate host such as crabs or crayfish and
encyst to develop into metacercariae within 2 months. Infection of humans or other
mammals (definitive hosts) occurs via consumption of raw or undercooked
crustaceans. Human infection with P. westermani occurs by eating inadequately
cooked or pickled crab or crayfish that harbor metacercariae of the parasite.
The metacercariae encysted in the duodenum, penetrate through the intestinal wall
into the peritoneal cavity, then through the abdominal wall and diaphragm into the
lungs, where they become encapsulated and develop into adults. The worms can also
reach other organs and tissues, such as the brain and striated muscles, respectively.
However, when this takes place completion of the life cycles is not achieved, because
the eggs laid cannot exit these sites (CDC).
Transmission of the parasite P. westermani to humans and mammals primarily

occurs through the consumption of raw or undercooked seafood. In Asia, an estimated
80% of freshwater crabs carry P. westermani. In preparation, live crabs are crushed
and metacercariae may contaminate the fingers/utensils of the person preparing the
meal. Accidental transfer of infective cysts can occur via food preparers who handle
raw seafood and subsequently contaminate cooking utensils and other foods.
Consumption of animals which feed on crustaceans can also transmit the parasite, for
cases have been cited in Japan where raw boar meat was the source of human
infection. Food preparation techniques such as pickling and salting do not exterminate
the causative agent. For example, in a Chinese study eating "drunken crabs" was
shown to be particularly risky because the infection rate was 100% when crabs are
immersed in wine for 3–5 minutes and fed to cats/dog.
IV. Pathology
Once in the lung or ectopic site, the worm stimulates an inflammatory response
that allows it to cover itself in granulation tissue forming a capsule. These capsules
can ulcerate and heal over time. The eggs in the surrounding tissue become pseudo
tubercles. If the worm becomes disseminated and gets into the spinal cord, it can
cause paralysis; capsules in the heart can cause death. The symptoms are localized in
the pulmonary system, which include a bad cough, bronchitis, and blood in sputum
(hemoptysis).
Diagnosis is based on microscopic demonstration of eggs in stool or sputum, but

these are not present until 2 to 3 months after infection. However, eggs are also
occasionally encountered in effusion fluid or biopsy material. Furthermore, you can
use morphological comparisons with other intestinal parasites to diagnose potential
causative agents. Finally, antibody detection is useful in light infections and in the
diagnosis of extrapulmonary paragonimiasis. In the United States, detection of
antibodies to Paragonimus westermani has helped physicians differentiate
paragonimiasis from tuberculosis in Indochinese immigrants (CDC).
VI. Treatment
According to the CDC, praziquantel is the drug of choice to treat paragonimiasis.

The recommended dosage of 75 mg/kg per day, divided into 3 doses over 3 days has
proven to eliminate P. westermani. Bithionol is an alternative drug for treatment of
this disease but is associated with skin rashes and urticaria. For additional
information, see the recommendations in The Medical Letter (Drugs for Parasitic
Infections).
Prevention programs should promote more hygienic food preparation by

encouraging safer cooking techniques and more sanitary handling of potentially
contaminated seafood. The elimination of the first intermediate host, the snail, is not
tenable due to the nature of the organisms' habits. A key component to prevention is
research, more specifically the research of everyday behaviors. This recent study was
conducted as a part of a broader effort to determine the status of Paragonimus species
infection in Laos. An epidemiological survey was conducted on villagers and
schoolchildren in Namback District between 2003 and 2005. Among 308 villagers and
633 primary and secondary schoolchildren, 156 villagers and 92 children had a
positive reaction on a Paragonimus skin test. Consequently, several types of crabs
were collected from markets and streams in a paragonimiasis endemic area for the
inspection of metacercariae and were identified as the second intermediate host of the
Paragonimus species. In this case study, we see how high prevalence of
paragonimiasis is explained by dietary habits of the population. Amongst
schoolchildren, many students reported numerous experiences of eating roast crabs in
the field. Adult villagers reported frequent consumption of seasoned crabs (Tan Cheoy
Koung) and papaya salad (Tammack Koung) with crushed raw crab. In addition to this
characteristic feature of the villagers' food culture, the denizens of this area drink
fresh crab juice as a traditional cure for measles, and this was also thought to
constitute a route for infection.
Name of Parasites:
Echinostoma Ilocanum
Common Name/ Other Name: Trematodes
I. Morphology (egglova, larval stage, adult)

II. Life Cycle
Echinostoma have three hosts in their life cycle: a first intermediate host a second
intermediate host and a definitive host Snail species such as Lymnaea pp. are
common intermediate hosts for Echinostoma, although fish and other bivalve molluscs
can also be intermediate hosts for these parasites.
Echinostoma species have low specificity for their definitive hosts and can infect a
variety of different species of animal including amphibians, aquatic birds, mammals
and humans. A definitive host which is infected with Echinostoma will shed
unembryonated Echinostoma eggs in their faeces.
When the eggs are in contact with fresh water they may become embryonated,
and will then hatch and release miracidia. The miracidia stage of Echinostoma is free-
swimming, and actively penetrates the first intermediate snail host, which then
becomes infected.
The main source of human infection is large freshwater snails, Pila luzonica (in the
Philippines) and Viviparus javanicus (in Indonesia), and rats and dogs are animal
reservoir hosts. The principal mode of human infection is consumption of raw or
undercooked snails.
IV. Pathology
Pathogenicity likely varies depending on the infecting species. Catarrhal

inflammation often occurs due to the penetration of the sharp-spined collar into the
intestinal mucosa, which creates ulcerative lesions. In heavy infections,
gastrointestinal signs/symptoms may occur. Peripheral eosinophilia is usually
present. A small number of fatal cases of Artyfechinostomum (= Echinostoma)
malayanum, in which heavy worm burdens caused anemia, malnutrition, or intestinal
perforation, have been reported.
During endoscopy, an adult flat worm was seen with mild portal hypertensive
gastropathy (McCormack’s classification) and erosive duodenopathy. The worm was
removed and its morphological characteristics were studied which revealed flat leaf
like structure, reddish-gray in color measuring approximately 10 mm in length by 2
mm in width. Oral sucker, ventral sucker, uterus and testes were clearly observed in
the adult worm but its head collar with collar spines around the oral sucker were not
visible. The adult worm resembled the Echinostoma species, Clonorchis sinensis and
Opisthorchis felineus. Since, neither the facilities for genetic confirmation nor for
fixing, staining and mounting of the adult worm was present at our institute, the
worm was preserved in 10% formalin and waited until the next morning for the
analysis of the stool sample of the patient to reach the possible diagnosis by studying
the morphology and characteristics of the ova laid by the worm.
VI. Treatment
Patient was treated with praziquantel 40 mg/kg (single dose) which is the drug of
choice for Echinostoma species infection by which he got improved and on follow up
stool examination after 2 weeks revealed no ova of Echinostoma species with
confirmed resolution of the abdominal pain.

Prevention can be implemented by health education to discourage the
consumption of raw or incompletely cooked molluscs and fish, as for other food-borne
trematode infections. However, programmes to control echinostomiasis have had
limited success compared to other helminthiasis owing to several factors. Among these
are the broad specificity for the second intermediate host and the existence of reservoir
hosts (Gutierrez, 2000). Moreover, the first intermediate hosts are able to serve as the
second intermediate hosts. The presence of low host specificity causes the difficulties
to the successful control of the medically important echinostome parasites. This
should be kept in mind when designing health promotion strategies.
Group 6
Name of parasite: Enterobius Vermicularis
Common names/other names: human pinworm/ common names “seatworm” and

“threadworm”
I. MORPHOLOGY
ADULT: MALE OR FEMALE
Adult males of Enterobius vermicularis: Adult males of Enterobius vermicularis

measure up to 2.5 mm long by 0.1-0.2 mm wide
Adult females of Enterobius vermicularis: adult females measure 8-13 mm long by

0.3-0.5 mm wide.
EGGS/OVA: The eggs of Enterobius vermicularis measure 50—60 µm by 20—30 µm.

They are transparent, elongate to oval in shape, and slightly flattened on one side.
They are usually partially embryonated when shed.
I. LIFE CYCLE
Gravid adult female Enterobius vermicularis deposit eggs on perianal folds .

Infection occurs via self-inoculation (transferring eggs to the mouth with hands that
have scratched the perianal area) or through exposure to eggs in the environment (e.g.
contaminated surfaces, clothes, bed linens, etc.) . Following ingestion of infective
eggs, the larvae hatch in the small intestine and the adults establish themselves in
the colon, usually in the cecum . The time interval from ingestion of infective eggs
to oviposition by the adult females is about one month. At full maturity adult females
measure 8 to 13 mm, and adult males 2 to 5 mm; the adult life span is about two
months. Gravid females migrate nocturnally outside the anus and oviposit while
crawling on the skin of the perianal area . The larvae contained inside the eggs
develop (the eggs become infective) in 4 to 6 hours under optimal conditions .
III. MODE OF TRANSMISSION - Pinworm infection is spread by the fecal-oral route,

that is by the transfer of infective pinworm eggs from the anus to someone's mouth,
either directly by hand or indirectly through contaminated clothing, bedding, food, or
other articles.
IV. PATHOLOGY AND SYMPTOMATOLOGy - itching of the anal or vaginal area.
Insomnia, irritability, teeth grinding and restlessness.
Occasional stomach pain and nausea.
V. LABORATORY DIAGNOSIS -The most common means of diagnosing pinworm

infection is via the “Scotch tape” test, where a clear adhesive cellulose tape is applied
to the anal area early in the morning before bathing or defecation. This is then
observed under a microscope for the presence of pinworm eggs.
VI. TREATMENT - The medication used for the treatment of pinworm are either
mebendazole, pyrantel pamoate, or albendazole. Any of these drugs are given in one
dose initially, and then another single dose of the same drug two weeks later. Pyrantel
pamoate is available without prescription.
VII. PREVENTION AND CONTROL - This includes washing hands with soap and
warm water after using the toilet, changing diapers, and before handling food. Keep
fingernails clean and short, avoid fingernail-biting, and avoid scratching the skin in
the perianal area. Teach children the importance of washing hands to prevent
infection
Name of parasite: Taenia asiatica
Common names/ other names: Asian taenia or Asian tapeworm
I. MORPHOLOGY
The morphology, clinical manifestations, diagnosis, and management of intestinal

infection with the adult T. asiatica tapeworm are similar to those for infections with T.
saginata (beef tapeworm), but infection is acquired by eating pork, not beef. Adult T.
asiatica range in size from 4 to 8 meters. Pigs are the intermediate hosts for T.
asiatica. Humans are infected by eating cysticerci (larvae) in raw or undercooked pork.
After ingestion, the cysticerci mature into adult worms in the small intestine of
humans.
II. LIFE CYCLE
The life cycle of T asiatica is indirect and digenetic, and is completed in humans as the
definitive host, and the intermediate host is mostly pigs (including wild boar in
Taiwan), and possibly cattle on rare occasion.
Eggs of T. saginata passed in the faeces of an infected person are only infectious to
cattle. Humans are infected by ingestion of raw or undercooked beef infected with
Cysticercus bovis, the larval stage of T. saginata. In humans, the adult tapeworm
develops in the intestine over 2–3 months. The cycle of infection repeats when
infectious eggs are passed in the faeces and later ingested by cattle, slowly migrating
into the flesh and transforming into the larval stage.
Infections by T. solium may follow a similar cycle, with consumption of infected pork
leading to the subsequent development of adult tapeworms. However, human infection
may also occur through the consumption of T. solium eggs. This occurs by direct
transfer from the faeces of an infected person, or through ingestion of contaminated
food or water. When the eggs of T. solium are ingested by either humans or pigs, the
embryos escape the shells and penetrate the intestinal wall, with subsequent spread of
larvae to various tissues to produce cysticercosis.
IV. PATHOLOGY & SYMPTOMATOLOGY
T. asiatica causes intestinal infection. Humans infected with adult T. asiatica worms
are asymptomatic or have mild gastrointestinal symptoms. They may see proglottids
(tapeworm segments) in their stool.
The laboratory diagnosis of human intestinal taeniasis for decades had been based on
the detection of bile-stained eggs and the gravid proglottids of the adult worm passed
in the feces. Recent studies reveal that microscopic examination of eggs or the gravid
proglottids alone is not a reliable method of differentiating T. saginata from T. asiatica
because of their similarities. Hence it is hypothesized that the exact epidemiologic
prevalence of T. asiatica might be underestimated. Newer methods of reliable detection
and differentiation of these parasites include serological and molecular methods.
VI. TREATMENT
Treatment of T. asiatica infection is with a single oral dose of praziquantel 5 or 10

mg/kg. Alternatively, a single 2-g dose of niclosamide (not available in the US) is given
as 4 tablets (500 mg each) that are chewed one at a time and swallowed with a small
amount of water. For children, the dose of niclosamide is 50 mg/kg (maximum dose 2
g) once. Stools should be reexamined for Taenia ova 1 and 3 months after treatment to
verify cure. Infection can be prevented by cooking whole cuts of meat to ≥ 63° C (≥
145° F) as measured with a food thermometer placed in the thickest part of the meat,
then allowing the meat to rest for 3 minutes before carving or consuming. Ground
meat should be cooked to ≥ 71° C (≥ 160° F). Ground meats do not require a rest
period.
The most effective way to prevent taeniasis is to cook food thoroughly. This means
cooking meat to a temperature above 140°F (60°F) for five minutes or more. Measure
the meat temperature with a cooking thermometer.
After cooking meat, allow it to stand for three minutes before cutting it. This can help
destroy any parasites that may be in the meat. Learn more about meat safety.
In the United States, laws requiring the inspection of animals and meat help reduce
the chance that tapeworms will be spread.
Proper hand hygiene is also important for preventing the spread of this disease.
Always wash your hands after using the bathroom and teach your children to do the
same. Also, drink bottled water if you live in or travel to an area where water must be
treated.
Name of Parasite: HYMENOLEPIS NANA
Common names/other names: Dwarf tapeworm (Hymenolepis nana, also known as

Rodentolepis nana, Vampirolepis nana, Hymenolepis fraterna, and Taenia nana)
I. MORPHOLOGY (egg/ova,larval stage, adult)
EGG/OVA: These eggs are oval and smaller than those of H. diminuta, with a size
range of 30 to 50 µm.
LARVAL STAGE: Larvae subsequently emerge and reattach to the intestinal wall to
complete their development into adult tapeworms in 2 - 3 weeks
ADULT: Hymenolepis nana (the dwarf tapeworm, adults measuring 15 to 40 mm in
length).
II. LIFE CYCLE
Life Cycle:
Eggs of Hymenolepis nana are immediately infective when passed with the stool and
cannot survive more than 10 days in the external environment . When eggs are
ingested by an arthropod intermediate host (various species of beetles and fleas
may serve as intermediate hosts), they develop into cysticercoids, which can infect
humans or rodents upon ingestion and develop into adults in the small intestine. A
morphologically identical variant, H. nana var. fraterna, infects rodents and uses
arthropods as intermediate hosts. When eggs are ingested (in contaminated food or
water or from hands contaminated with feces), the oncospheres contained in the eggs
are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and
develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return
to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa
and develop into adults that reside in the ileal portion of the small intestine producing
gravid proglottids . Eggs are passed in the stool when released from proglottids
through its genital atrium or when proglottids disintegrate in the small intestine . An
alternate mode of infection consists of internal autoinfection, where the eggs release
their hexacanth embryo, which penetrates the villus continuing the infective cycle
without passage through the external environment . The life span of adult worms is
4 to 6 weeks, but internal autoinfection allows the infection to persist for years.
Intermediate hosts of hymenolepis spp.
nana, and humans can become infected with the latter by direct ingestion of eggs.
Within the arthropod host, the eggs develop into cysticercoids, which can infect the
mammalian host upon ingestion and develop into adults in the small intestine.
● Symptoms develop if large number of worms
● May include abdominal pain, diarrhea, anorexia, irritability
V. LABORATORY
Nana eggs in stool specimens, primarily from the wet preparation examination of the
concentration sediment. The eggs are most easily seen on a direct wet smear or a wet
preparation of the concentration sediment. Adult worms The scolex has four suckers
and a short rostellum with hooks.
VI. TREATMENT
● Praziquantel, adults and children, 25mg/kg in a single-dose therapy.
● Niclosamide*: adults, 2 gm in a single dose for 7 days; children 11-34 kg, 1 gm

in a single dose on day 1 then 500 mg per day orally for 6 days; children > 34
kg, 1.5 gm in a single dose on day 1 then 1 gm per day orally for 6 days.
Prevention. Good hygiene, public health and sanitation programs, and elimination of
infected rats help to prevent the spread of hymenolepiasis. Preventing fecal
contamination of food and water in institutions and crowded areas is of primary
importance.
Name of Parasite: Parastrongylus cantonensis
Common names/ other names: Rat lungworm, Angiostrongylus cantonensis
I. MORPHOLOGY
A. cantonensis is a nematode roundworm with 3 outer protective collagen layers, and

a simple stomal opening with no lips or buccal cavity leading to a fully developed
gastrointestinal tract. Males have a small copulatory bursa at the posterior. Females
have a “barber pole” shape down the middle of the body, which is created by the
twisting together of the intestine and uterine tubules. The worms are long and slender
- males are 15.9-19 mm in length, and females are 21-25 mm in length
Adult male (top) and female (bottom) A. cantonensis worms. Note copulatory bursa at
posterior of male, and characteristic “barber pole” spiral in female.
II. LIFE CYCLE
The adult form of A. cantonensis resides in the pulmonary arteries of rodents, where it
reproduces. After the eggs hatch in the arteries, larvae migrate up the pharynx and
are then swallowed again by the rodent and passed in the stool. These first stage
larvae then penetrate or are swallowed by snail intermediate hosts, where they
transform into second stage larvae and then into third stage infective larvae. Humans
and rats acquire the infection when they ingest contaminated snails or paratenic
(transport) hosts including prawns, crabs, and frogs, or raw vegetables containing
material from these intermediate and paratenic hosts. After passing through the
gastrointestinal tract, the worms enter circulation. In rats, the larvae then migrate to
the meninges and develop for about a month before migrating to the pulmonary
arteries, where they fully develop into adults.
Humans are incidental hosts; the larvae cannot reproduce in humans and therefore
humans do not contribute to the A. cantonensis life cycle. In humans, the circulating
larvae migrate to the meninges, but do not move on to the lungs. Sometimes the larvae
will develop into the adult form in the brain and CSF, but they quickly die, inciting
the inflammatory reaction that causes symptoms of infection.
Transmission is based on food-borne routes, ingestion of raw or insufficiently

cooked contaminated mollusks, crustacean, or other hosts; or ingestion of vegetables
contaminated with infectious larvae.
Symptomatic treatment is indicated for symptoms such as nausea, vomiting,

headache, and in some cases, chronic pain due to nerve damage or muscle atrophy.
Repeat lumbar puncture may be required to lower intracranial pressure and relieve
headaches.
Diagnosis of the human infection caused by A. costaricensis can be
made by examining biopsied or surgical specimens and confirming the presence of
the parasites or their eggs. Graeff-Teixeira et al. (1991) established histopathological

patterns for diagnosis. Also, an enzyme-linked immunosorbent assay (ELISA)
was developed that demonstrated a sensitivity of 86% and a specificity of 83% when
used with sera adsorbed with Ascaris suum antigens (Graeff-Teixeira et al., 1997).
ANGIOSTRONGYLIASIS 229
In endemic areas, meningitis or meningoencephalitis caused by A. cantonensis is
suspected in the presence of the characteristic signs of eosinophilia in the blood and
eosinophilic pleocytosis of the cerebrospinal fluid. In places such as Thailand,
where infection of the central nervous system caused by Gnathostoma spinigerum
has a high prevalence, the two diseases must be differentiated. Punyagupta et al.
(1990) indicate that gnathostomiasis causes sharp pain in the nerve roots, signs of
cerebral and spinal disease, and yellowish or bloody cerebrospinal fluid. Although
most reports indicate that only in a few cases can the parasite be found in patients’
cerebrospinal fluid or eyes, Hwang and Chen (1991) reported having recovered it by
lumbar puncture in 41.5% of 84 pediatric cases. Serologic tests are useful for
confirming the presumptive diagnosis (Legrand and Angibaud, 1998). Two varieties of
ELISA have shown a specificity of 100%, but sensitivity of just 50% to 60%
(Eamsobhana et al., 1997).
VI. TREATMENT
Treatment of angiostrongylus is not well defined, but most strategies include a

combination of anti - parasitics to kill the worms, steroids to limit inflammation as the
worms die, and pain meds to manage the symptoms of meningoencephalitis.
Anti-Helminthics
Anti-helminthics are often used to kill off the worms, however in some cases this
may cause patients to worsen due to toxins released by the dying worms.
Albendazole, ivermectin, mebendazol, and pyrantel are all commonly used, though
albendazole is usually the drug of choice. Studies have shown that anti-helminthic
drugs may shorten the course of the disease and relieve symptoms. Therefore anti-
helminthics are generally recommended, but should be administered gradually so as
to limit the inflammatory reaction.
Anti-Inflammatories
Anti-helminthics should generally be paired with corticosteroids in severe
infections to limit the inflammatory reaction to the dying parasites. Studies suggest
that a two week regimen of a combination of mebedizole and prednisolone significantly
shortened the course of the disease and length of associated headaches without
observed harmful side effects [8]. Other studies suggest that albendazole may be more
favorable, because it may be less like to incite an inflammatory reaction. The Chinese
herbal medicine long-dan-xie-gan-tan (LDGXT) has also been shown to have a similar
anti-inflammatory effect, and in mild cases may be used alone to relieve symptoms
while infection resolves itself.
While human angiostrongyliasis is not very prevalent, except in a few
areas of high endemicity, prophylaxis is important because there is no known

therapeutic treatment for the infection. Theoretically, angiostrongyliasis could be
controlled by reducing rodent and mollusk populations, though practical application
seems doubtful. Preventive measures for individuals consist of thoroughly washing
vegetables, and hands after garden or field work; not eating raw or undercooked
mollusks and crustaceans; and not drinking water that may be unhygienic.
Experiments have shown that incubation of infective A. costaricensis larvae for 12
hours at 5°C in 1.5% sodium hypochlorite kills all the larvae. Incubation in saturated
sodium chloride or in commercial vinegar reduced the number of larvae but failed
to prevent the infection in mice (Zanini and Graeff-Teixeira, 1995).
Name of Parasite: Dracunculus Medinensis
Common Name: Guinea worm disease nematode ›dracunculiasis worm

II. Humans become infected by drinking unfiltered water containing copepods (small
crustaceans) which are infected with larvae of D. medinensis . Following ingestion,
the copepods die and release the larvae, which penetrate the host stomach and
intestinal wall and enter the abdominal cavity and retroperitoneal space.
III. Dracunculiasis is transmitted by drinking unsafe stagnant water contaminated by
copepods (water fleas) that contain Dracunculus medinensis larvae. The copepods
are digested in the human gastrointestinal tract and release the larvae, which
penetrate the gut wall.
IV. Pathology - The roundworm, Dracunculus medinensis, causes dracunculiasis or
Guinea worm disease. Humans become infected by drinking unfiltered water
containing small crustaceans that are infected with larvae of Dracunculus
medinensis. The worm emerges from the skin in the middle of an ulcer as a
white-looking filament.
Symptomatology - Guinea Worm Disease; Fiery Serpent) Dracunculiasis is infection

with
Dracunculus medinensis. Symptoms are a painful, inflamed skin lesion, which

contains an adult worm, and debilitating arthritis. Diagnosis is by inspection.
Treatment is slow removal
of the adult worm.

V. Dracunculiasis is an infection with Dracunculus medinensis. Symptoms are a
painful,
inflamed skin lesion, which contains an adult worm, and debilitating arthritis.
Diagnosis is by inspection. Treatment is slow removal of the adult worm.
Dracunculiasis is close to being eradicated. Humans become infected by drinking
unfiltered water containing copepods (small crustaceans) which are infected with
larvae of D. medinensis . Following ingestion, the copepods die and release the
larvae, which penetrate the host stomach and intestinal wall and enter the abdominal
cavity and retroperitoneal space.
VI. There is no specific drug treatment for guinea worm disease. Rather, the infection
typically is managed through the careful removal of the worm in its entirety. Soaking
the site of the blister in a container of water encourages the worm to emerge. Once it
has broken through the skin, gentle traction is applied to the worm, speeding its
emergence, which may take several days or weeks. The worm usually is wrapped
around a piece of gauze or a stick to maintain tension and prevent the worm from
retracting into the body. Topical antibiotics often are applied to the site of the wound
to prevent infection with another organism during the extraction period. Aspirin or
ibuprofen may be administered to relieve pain and reduce inflammation.
VII. Guinea worm disease can be prevented by avoiding drinking unsafe water.
Teaching
people to follow these simple control tactics can completely prevent the spread of the
disease: Drink only water from protected sources (such as from boreholes or hand dug
wells) that are free from contamination
Name of Parasite: Clonorchis Sinensis
Common names/other names: chinese liver fluke
I. Morphology (adult, eggs, miracidium, sporocyst, redia, cercaria and

metacercaria)
eggs are small, ranging in size from 27 to 35 µm by 11 to 20 µm. The eggs are oval
shaped with a convex operculum that rests on visible “shoulders” at the smaller end of
the egg. At the opposite (abopercular) end, a small knob or hook-like protrusion is
often visible.
Clonorchis sinensis adults are flattened, lance shaped, and measure approximately
10 to 25 mm long by 3 to 5 mm wide. The oral and ventral suckers (acetabulum) are
relatively small. Like other flukes, they are hermaphroditic.
II. Life cycle
Clonorchis sinensis eggs are discharged in the biliary ducts and in the stool in an
embryonated state . Eggs are ingested by a suitable snail intermediate host .
Eggs release miracidia , which go through several developmental stages
(sporocysts , rediae , and cercariae ). The cercariae are released from the
snail and, after a short period of free-swimming time in water, they come in contact
and penetrate the flesh of freshwater fish, where they encyst as metacercariae .
Infection of humans occurs by ingestion of undercooked, salted, pickled, or smoked
freshwater fish . After ingestion, the metacercariae encysted in the duodenum
and ascend the biliary tract through the ampulla of Vater . Maturation takes
approximately one month. The adult flukes (measuring 10 to 25 mm by 3 to 5 mm)
reside in small and medium sized biliary ducts.
III. Mode of transmission
The eggs of Clonorchis are ingested by freshwater snails. After the eggs hatch,
infected snails release microscopic larvae that then enter freshwater fish. People
become infected by eating infected raw or undercooked fish containing the larvae.
IV. Pathology & symptomatology
Clonorchis sinensis clinical manifestation
Clonorchiasis is an infection with the liver fluke Clonorchis sinensis. Infection is

usually acquired by eating undercooked freshwater fish. Symptoms include fever,
chills, epigastric pain, tender hepatomegaly, diarrhea, and mild jaundice. Diagnosis is
by identifying eggs in the feces or duodenal contents.
V. Laboratory diagnosis
Ova and parasite (O&P) stool examinations for liver fluke eggs is the only available way
to diagnose Clonorchis infection. More than one stool sample may be needed to
identify the eggs.
VI. Treatment
Praziquantel or albendazole are the drugs of choice to treat Clonorchis infection.
VII. Prevention and control
Clonorchis infection can be prevented by avoiding raw or undercooked freshwater fish.

Lightly salted, smoked, or pickled fish can contain infectious parasites. Clonorchis
infection does not result from drinking river water or other non-potable water.
Parasite name: Metagonimus Yokogawai
Common name: Fluke worm
I. Morphology:
The flukes of the Genus Metagonimus are characterized by their small body, 1.0-2.0
mm long by 0.4-0.6 mm wide, laterally located ventral sucker, absence of genital
sucker or ventrogenital apparatus, and egg size. Metagonimus takahashii differs from
M. yokogawai in the position of two testes (anterior testis separated from the posterior
testis), the distribution of vitelline follicles (more abundant and crossing over the
posterior-most end), and by larger size of eggs (M. yokogawai, 28-30 mm; M.
takahashii, 32-36 mm). Metagonimus miyatai morphologically differs from M.
yokogawai and M. takahashii in the position of the posterior testis (separated greatly
from the anterior one), the distribution of vitelline follicles (never crossing over the
posterior testis), and the intermediate size of eggs (28-32 mm).
II. Life Cycle
Metagonimiasis is transmitted through eating undercooked fish caught in water

polluted with infected fecal matter. By nature of its mode of transmission, M.
yokogawai tends to be more a disease of rural and underprivileged populations.
The Heterophyid worms cause mild symptoms which include abdominal pain,
diarrhea, easy fatigability, weakness and anorexia. For this reason, these infections
are overlooked by the patients and physicians. Attention should be paid to the
infection caused by these minute sized intestinal flukes as their eggs are small and
can penetrate through the walls of the intestinal capillaries and lymphatics. The eggs
can be carried to the myocardium, brain and spinal cord causing emboli and
granulomatous reactions.
The diagnosis is based on the microscopic identification of eggs in the stool. However,
the eggs are indistinguishable from those of Heterophyes heterophyes and resemble
those of Clonorchis and Opisthorchis. Specific diagnosis is based on identification of
the adult fluke evacuated after antihelminthic therapy, or found at autopsy.
VI. TREATMENT
Praziquantel is recommended in both adult and pediatric cases with dosages of 75

mg/kg/d in 3 doses for 1 day. Praziquantel is a Praziniozoquinoline derivative that
alters the calcium flux through the parasite tectum and causes muscular paralysis
and detachment of the fluke. Prizaquantel should be taken with liquids during a meal
and as provided commercially as Biltricide. Praziquantel is not approved by the U.S.
Food and Drug Administration (FDA) for treatment of metagonimiasis, but is approved
for use on other parasitic infections.
Praziquantel has some side effects but they are generally relatively mild and transient
and a review of evidence shows it overall a well-tolerated drug. Possible side effects
include abdominal pain, allergy, diarrhea, headache, liver problems, nausea or
vomiting, exacerbation of porphyries, pruritus, rash, somnolence, vertigo, or dizziness.
In fact, in 2002, the World Health Organization recommended the use of Praziquantel
in pregnant and lactating women, though controlled trials are still needed to verify
this.
Another possible drug option is Tetrachloroethylene, a chlorinated hydrocarbon, but

its use has been superseded by new antihelminthic drugs (like Praziquantel). A 1978
study also looked at the efficacy of several drugs on metagonimiasis infection,
including bithionol, niclosamide, nicoflan, and Praziquantel. All drugs showed lower
prevalence of eggs in feces, however only Praziquantel showed complete radical cure.
Therefore, the authors concluded Praziquantel was the most highly effective, was very
well tolerated, and was the most promising drug against metagonimiasis.
Several public health prevention strategies could help lower the rates of
metagonimiasis. One is to control the intermediate host (snails). This can be done
through use of molluscidals. Another is to use education to ensure all people,
especially in areas were the disease regularly occurs, fully cook all fish. This could
potentially be problematic and not as effective as hoped as many of the people affected
by metagonimiasis eat raw or pickled fish as part of a traditional, long-seated dietary
practice. Additionally, implementing more sanitary water conditions would reduce the
continual reintroduction of eggs to water sources, thus restarting the lifecycle.
Complete control of metagonimiasis presents several potential problems because it
does have several reservoir hosts, thus eradication is unlikely.
Group 2
Name of parasite: Trichuris trichiura
Common names/other names: Human whipworm
I. MORPHOLOGY
 ADULT: MALE OR FEMALE
- Adult males of Trichuris trichiura are 30-45 millimeters long,

with a coiled posterior end.
- Adult females are 35-50 millimeters with a straight posterior

end. Both sexes have a long, whip-like anterior end.
 EGGS/
OVA:
Trichuris trichiura eggs are 50-55 micrometers by 20-25

micrometers. They are barrel-shaped, thick-shelled and
possess a pair of polar “plugs” at each end. The eggs are
unembryonated when passed in stool.
II. LIFE CYCLE:
 The unembryonated eggs are passed with the stool . In the soil,
the eggs develop into a 2-cell stage , an advanced cleavage
stage , and then they embryonate ; eggs become infective in 15
to 30 days. After ingestion (soil-contaminated hands or food), the
eggs hatch in the small intestine, and release larvae that
mature and establish themselves as adults in the colon . The
adult worms (approximately 4 cm in length) live in the cecum and
ascending colon. The adult worms are fixed in that location, with
the anterior portions threaded into the mucosa. The females begin
to oviposit 60 to 70 days after infection. Female worms in the
cecum shed between 3,000 and 20,000 eggs per day. The life span
of the adults is about 1 year.
III. MODE OF TRANSMISSION -Trichuris is spread via fecal-oral
transmission. Eggs are deposited in soil through human feces. After 10-
14 days in soil, eggs become infective.
IV. PATHOLOGY & SYMPTOMATOLOGY -Signs and Symptoms. Trichuris

trichiura (Trichuriasis), also known as whipworm, colonizes the cecum
and ascending colon and may cause anemia, abdominal discomfort,
bloody diarrhea, stunted growth, and, in overt cases, may lead to rectal
prolapse.
V. LABORATORY DIAGNOSIS - The standard method for diagnosing the

presence of whipworm is by microscopically identifying whipworm eggs in
a stool sample. Because eggs may be difficult to find in light infections, a
concentration procedure is recommended.
VI. TREATMENT - Anthelminthic medications (drugs that rid the body of

parasitic worms), such as albendazole and mebendazole, are the drugs of
choice for treatment. Infections are generally treated for 3 days. The
recommended medications are effective.
VII. PREVENTION AND CONTROL -The best way to prevent infection is to

always: Avoid ingesting soil that may be contaminated with human feces,
including where human fecal matter or wastewater is used to fertilize
crops. Wash your hands with soap and warm water before handling food.
Name of Parasite: SPIROMETRA ERINACEIEUROPAEI
Common Names/ other Name: TAPEWORM
I. Morphology
: EGG- Spirometra Erinaceieuropaei eggs are ovoid in shape with tapered ends.
LARVA ADULT- Adult Spirometra are typically large worms with long bodies
consisting of three distinguishable body sections: the scolex, the neck, and the
strobilia. Overall body length can reach up to several meters; however, this can
vary depending on host species as well as other factors.The scolex is the spoon
shaped anterior portion of the worm and consists of the head with
attachments. Instead of hooks and distinct suckers (like most tape worms), S.
erinaceieuropaei have two bothria (grooves on the scolex that contain weak
muscles that perform a sucking action). The neck is unsegmented and located
between the scolex and the rest of the body.
II. Life Cycle:
The S. erinaceieuropaei life cycle is complex and consists of three hosts. The
life cycle starts when eggs of such parasites are discharged via feces from the
so-called definitive host. During this period, the eggs are immature not until
they reach a freshwater source. Once in freshwater, the eggs hatch to become
first stage larvae (coracidia). From here, coracidia are ingested by crustaceans
(copepods), which become the first intermediate host. Inside the first
intermediate host, the coracidia develop into procercoid larvae; however, this is
still considered the first larval stage. Next, copepods are eaten by fish, reptiles,
or other amphibians that become the second intermediate host. Inside the
second intermediate host, the larvae will burrow into the intestinal tract where
they develop into plerocercoid larvae (the final larval stage). In the final larvae
stage, S. erinaceieuropaei migrate to subcutaneous tissue and/or muscles. To
the final stage, the second intermediate host is eaten by a definitive host. A
couple of weeks later, the parasite will mature into adult tapeworms and its life
cycle continues. Adult tapeworms can survive up to 30 years in their definitive
host (typically dogs and cats
III. Mode of Transmission:
There are three ways in which humans can be infected with this parasite. 1.
Eating raw or undercooked meats from snakes, frogs, and other four-footed
animals 2. Drinking of contaminated water infected by copepods. 3. Using raw
snake or frog flesh in poultices that encounter intact human skin (Spirometra
larvae have been shown to penetrate skin and cause infection in this manner.)
IV. . PATHOLOGY AND SYMPTOMATOLOGY Infection by the migratory
plerocercoid larvae of the cestodes Spirometra mansonoides and other Spirometra
spp. (including Spirometra erinaceieuropaei) is termed sparganosis. Clinical
symptoms vary with the location of the larvae. Only a few hundred cases of
sparganosis have been reported. The primary hosts vary and include dogs and
birds. Clinical symptoms depend upon the location of the lesions and often
include headache, seizures, and weakness.
Migrating spargana cause various symptoms depending on the final location in

the host. Spargana may locate anywhere, including subcutaneous tissue, breast,
orbit, urinary tract, pleural cavity, lungs, abdominal viscera and the central
nervous system. The migration in subcutaneous tissues is usually painless, but
when spargana settle in the brain or spine a variety of neurological symptoms
may occur, including weakness, headache, seizure, and abnormal skin
sensations, such as numbness or tingling. If the inner ear is involved, the patient
may experience vertigo or deafness.
VI. TREATMENT
Oral, subcutaneous, or intramuscular administration of praziquantel at 30

mg/kg body weight to cats experimentally infected with
Spirometraerinaceieuropaei cleared all animals of their infections (Fukase et al.,
1992). Treatment of 22 cats with naturally acquired infections by the
intramuscular or subcutaneous administration of 34 mg/kg body weight
eliminated the cestodes from the treated animals. Note: this treatment is with
doses of praziquantel that are greater than those required to treat intestinal
dipylidiasis and taeniasis in cats.

Prevention would require that cats be dissuaded from hunting which is liable to
be an impossibility. Thus, it will be necessary to perform fecal examinations on
cats living in areas where this parasite is present. Because of the nature of this
parasite to undergo periods when eggs are not present in the feces, it may be
necessary to perform more than one fecal examination each year to insure that a
cat is free of this parasite.
Name of Parasite: fasciola hepatica
Common names/ other names: LIVER FLUKE
I. Morphology: The Adult Worm - Averaging 30mm in length and 13 mm in

width, Fasciola hepatica is one of the largest flukes in the world. The adult
worm has a very characteristic leaf shape with the anterior end being
broader than the posterior end and an anterior cone-shaped projection.
II. LIFE CYCLE:
III. MODE OF TRANSMISSION: There is no vector in Fasciola hepatica

transmission. Transmission occurs through the ingestion of raw, fresh-water
vegetation on which the flukes in their metacercariae form are encysted.
IV. PATHOLOGY & SYMPHATOLOGY: The young worms move through the
intestinal wall, the abdominal cavity, and the liver tissue, into the bile ducts,
where they develop into mature adult flukes that produce eggs. The pathology
typically is most pronounced in the bile ducts and liver. Fasciola infection is both
treatable and preventable.
V. LABORATORY DIAGNOSIS: The standard way to be sure a person is infected
with Fasciola is by seeing the parasite. This is usually done by finding Fasciola
eggs in stool (fecal) specimens examined under a microscope. More than one
specimen may need to be examined to find the parasite.
VI. TREATMENT: Triclabendazole. Triclabendazole, a benzimidazole compound
active against immature and adult Fasciola parasites, is the drug of choice for
treatment of fascioliasis.
VII. PREVENTION AND CONTROL: Individual people can protect themselves by
not eating raw watercress and other water plants, especially from Fasciola-
endemic grazing areas. As always, travelers to areas with poor sanitation should
avoid food and water that might be contaminated (tainted).
Name of Parasite: SCHISTOSOMA JAPONICUM
Common names/ Other names: ORIENTAL BLOOD FLUKE
I. MORPHOLOGY:
The S. japonicum worms are yellow or yellow brown. By electron microscopy
there are no bosses or spines on the dorsal surface of the male, which is ridged
and presents a spongy appearance. Many spines cover the inner surface of the
oral sucker and extend to the pharyngeal opening. The oral sucker shows a rim
with spines of variable size and sharpness inward and outward from the rim. The
ventral sucker possesses many spines which are smaller than in the oral sucker.
The lining of the gynecophoric canal is roughened by minute spines. The
integument of the female is ridged and pitted and possesses fewer spines than in
the oral sucker, the ventral sucker, and the gynecophoric canal of the male.
Anterior to the acetabulum, the integumental surfaces are devoid of spines.
However, in the other areas, spines are equally distributed except for the vicinity
of the excretory pore.
EGGS
The eggs of Schistosoma japonicum are large and more
rounded than other species, measuring 70-100 µm long by
55-64 µm wide. The spine on S. japonicum eggs is smaller
and less conspicuous than other species. Eggs are shed
in stool.
LARVAL DEVELOMENT
Miracidium- not much bigger than the egg. It is free-
swimming, ovoid, covered with cilia, and could easily be mistaken for protozoan.
Sporocyst- This stage has no mouth or gut; it takes its food directly from the
snail it lives in. Each sporocyst reproduces asexually -- creating daughter
sporocysts.
Cercaria- sporocyst lives and grows inside a snail host, completing another round
of asexual reproduction, giving the offspring have a different structure.
ADULT
MALE
Males are shorter and stouter than females and
have a long groove on their underside in which
the female (should one arrive) attaches herself.
FEMALE
The females measure 2 cm by 0.4 mm.
II. LIFE CYCLE
The life cycles of Schistosoma japonicum and Schistosoma mansoni are very
similar. In brief, eggs of the parasite are released in the feces and if they come in
contact with water they hatch into free-swimming larva, called miracidia. The
larva then has to infect a snail of the genus Oncomelania such as species of
Oncomelania hupensis within one or two days. Inside the snail, the larva undergo
asexual reproduction through a series of stages called sporocysts. After the
asexual reproduction stage cercaria (another free-swimming larva) are generated
in large quantities, which then leave (shed into the environment) the snail and
must infect a suitable vertebrate host. Once the cercaria penetrates the skin of
the host it loses its tail and becomes a schistosomule. The worms then migrate
through the circulation ending at the mesenteric veins where they mate and start
laying eggs. Each pair deposits around 1500–3500 eggs per day in the vessels of
the intestinal wall. The eggs infiltrate through the tissues and are passed in the
feces.

 Mainly by contact with contaminated water. Infective free-swimming larval
forms (cercariae) penetrate directly through the skin.
 Symptoms of schistosomiasis are not caused by the worms themselves
but by the body’s reaction to the eggs. Many infections are
asymptomatic. A local cutaneous hypersensitivity reaction following skin
penetration by cercariae may occur and appears as small, itchy
maculopapular lesions. Acute schistosomiasis (Katayama fever) is a
systemic hypersensitivity reaction that may occur weeks after the initial
infection, especially by S. japonicum. Manifestations include systemic
symptoms/signs including fever, cough, abdominal pain, diarrhea,
hepatosplenomegaly, and eosinophilia.
 Occasionally, Schistosoma infections may lead to central nervous system
lesions. Cerebral granulomatous disease may be caused by ectopic S.
japonicum eggs in the brain, and granulomatous lesions around ectopic
eggs in the spinal cord may occur in S. mansoni and S. haematobium
infections. Continuing infection may cause granulomatous reactions and
fibrosis in the affected organs (e.g., liver and spleen) with associated
signs/symptoms.
 Pathology associated with S. mansoni and S. japonicum schistosomiasis
includes various hepatic complications from inflammation and
granulomatous reactions, and occasional embolic egg granulomas in
brain or spinal cord.
V. LABORATORY AND DIAGNOSIS

 Diagnosis is established by demonstrating eggs in feces or urine by direct
wet mount or formalin ethyl acetate concentration methods.
 Zinc sulfate concentration is not satisfactory for recovery of heavy
schistosome eggs.
 Eggs may be detected in biopsies of rectum, bladder or occasionally liver.
 Egg hatching methods may occasionally be requested to determine
viability or less commonly, to detect a limited infection.
 Feces mixed in distilled water is placed in a flask, covered with foil (to
keep out light), with neck or a sidearm exposed to bright light.
 Miracidia, if present, actively swim to the light and can be detected using
a hand lens.
VI. TREATMENT
Infections with all major Schistosoma species can be treated with praziquantel.
The timing of treatment is important since praziquantel is most effective against
the adult worm and requires the presence of a mature antibody response to the
parasite. For travelers, treatment should be at least 6-8 weeks after last exposure
to potentially contaminated freshwater.

The best way to prevent schistosomiasis is to take the following steps if you are
visiting or live in an area where schistosomiasis is transmitted:
1. Avoid swimming or wading in freshwater when you are in countries in which
schistosomiasis occurs. Swimming in the ocean and in chlorinated swimming
pools is safe.
2.Drink safe water. Although schistosomiasis is not transmitted by swallowing
contaminated water, if your mouth or lips come in contact with water containing
the parasites, you could become infected. Because water coming directly from
canals, lakes, rivers, streams, or springs may be contaminated with a variety of
infectious organisms, you should either bring your water to a rolling boil for 1
minute or filter water before drinking it. Bring your water to a rolling boil for at
least 1 minute will kill any harmful parasites, bacteria, or viruses present. Iodine
treatment alone WILL NOT GUARANTEE that water is safe and free of all
parasites.
3.Water used for bathing should be brought to a rolling boil for 1 minute to kill
any cercariae, and then cooled before bathing to avoid scalding. Water held in a
storage tank for at least 1 – 2 days should be safe for bathing.
4.Vigorous towel drying after an accidental, very brief water exposure may help to
prevent parasites from penetrating the skin. However, do not rely on vigorous
towel drying alone to prevent schistosomiasis.
Group 5
NAME OF PARASITE: STRONGYLOIDES STERCORALIS

COMON NAMES/ OTHER NAMES: PARASITIC ROUNDWORM/ THREADWORM,
PINWORMS, NEMATODES
I. MORPHOLOGY
Strongyloides stercoralis is one of the smallest parasites known to infect humans.
Female filariform larvae (males are thought to be non-parasitic) are slender and
fast-moving, being approximately 50 µm in diameter and between 350-600 µm in
length.
STRONGYLOIDES STERCORALIS OVA

II. LIFE CYCLE
Strongyloides stercoralis is classified as a soil-transmitted helminth. This means

that the primary mode of infection is through contact with soil that is
contaminated with free-living larvae. When the larvae make skin contact, they
can penetrate it and migrate through the body, eventually finding their way to the
small intestine where they burrow and lay their eggs. Unlike other soil-
transmitted helminths such as hookworm and whipworm, whose eggs do not
hatch until they are in the environment, the eggs of S. stercoralis hatch into
larvae in the intestine. Most of these larvae will be excreted in the stool, but some
of the larvae may mature and immediately re-infect the host either by burrowing
into the intestinal wall, or by penetrating the skin around the anus. This
characteristic of S. stercoralis is termed auto-infection. The significance of
autoinfection is that unless treated for S. stercoralis, persons may remain
infected throughout their lifetime.
In addition to contact with soil and auto-infection, there have been rare cases of
person-to-person transmission in the following:
 Organ transplantation
 Institutions for people with cognitive disability requiring assistance with daily
living
 Long-term care
facilities
 Daycare centers
IV. PATHOLOGY & SYMPTOMALOGY
The gold standard for the diagnosis of Strongyloides infection is serial stool
examination. However, traditional stool examinations are insensitive and require
up to seven stool exams to reach a sensitivity of 100%. Specialized stool exams
include Baermann concentration, Horadi-Mori filter paper culture, quantitative
acetate concentration technique, and nutrient agar plate cultures. Duodenal
aspirate is more sensitive than stool examination, and duodenal biopsy may
reveal parasites in the gastric crypts, in the duodenal glands, or eosinophilic
infiltration in the lamina propria. Frequently, larvae can be seen by a simple wet
mount in fluid from a bronchoalveolar lavage (BAL).
VI. TREATMENT
Treatment for strongyloidiasis is recommended for all persons found to be
infected, whether symptomatic or not, due to the risk of developing hyper
infection syndrome and/or disseminated strongyloidiasis. Furthermore, it is
recommended that patients be considered for testing prior to being initiated on
any immunosuppressive therapy, particularly corticosteroids.
*Treatment for Acute and chronic strongyloidiasis
1. Ivermectin, in a single dose, 200 µg/kg orally for 1—2 days
Relative contraindications include the following:
 Confirmed or suspected concomitant Loa loa infection
 Persons weighing less than 15kg
 Pregnant or lactating women
Alternative
2. Albendazole, 400 mg orally two times a day for 7 days.
Relative contraindications:
 Hypersensitivity to benzimidazole compounds or any component of product
 Use should be avoided in the 1st trimester of pregnancy
In patients with positive stool examination for Strongyloides and persistent
symptoms, follow-up stool exams should be performed 2—4 weeks after
treatment to confirm clearance of infection. If recrudescence of larvae is observed,
retreatment is indicated.
*Hyperinfection syndrome/Disseminated strongyloidiasis
If possible, immunosuppressive therapy should be stopped or reduced, and:
Ivermectin, 200 µg/kg per day orally until stool and/or sputum exams are
negative for 2 weeks. For patients unable to tolerate oral therapy, such as those
with ileus, obstruction, or known or suspected malabsorption, published case
reports have demonstrated efficacy with rectal administration. If oral and/or
rectal administrations are not possible, there have been instances where
Investigational New Drug (IND) exemptions for the veterinary subcutaneous
formulation of ivermectin have been granted by the FDA.

The best way to prevent Strongyloides infection is to wear shoes when you are
walking on soil, and to avoid contact with fecal matter or sewage. Proper sewage
disposal and fecal management are keys to prevention. Furthermore, if you
believe that you may be infected, the best way to prevent severe disease is to be
tested and, if found to be positive for disease, treated.
You should discuss testing with your doctor if you are
 Taking steroids or other immunosuppressive therapies
 About to start taking steroids or other immunosuppressive therapies
 A veteran who served in the South Pacific or Southeast Asia
 Infected with Human T-cell Lymphotropic Virus-1 (HTLV-1)
 Diagnosed with cancer
 Going to donate or receive organ transplants
Standard precautions should be observed for patients hospitalized with
strongyloidiasis. Wearing gloves and gowns, good hygiene, and diligent
handwashing is important when encountering the patient’s feces.
Name of parasite: BRUGIA TIMORI

Common names/other names:
I. MORPHOLOGY
 The microfilariae of Brugia timori are longer and morphologically distinct
from those of Brugia malayi and Wuchereria bancrofti, with a cephalic
space length-to-width ratio of about 3:1. B. timori more closely resembles
the symptoms caused by B. malayi and morphologically resembles B.
malayi.
II. LIFE CYCLE

 The life cycle of Brugia timori is very similar to that of Wuchereria
bancrofti and Brugia malayi, leading to nocturnal periodicity of the
disease symptoms. Eosinophilia is common during acute stages of
infection. So far Brugia timori has only been found in the Lesser Sunda
Islands of Indonesia.

 By the bite of an infected mosquito; B. malayi transmitted by various
species of Mansonia, Anopheles and Aedes; B. timori transmitted by
Anopheles barbirostris INCUBATION PERIOD: Variable; allergic
manifestations may appear as early as a month after infection;
microfilariae may not appear in blood until 3-6 months after infection.
 The typical vector for Brugia malayi filariasis are mosquito species from
the genera Mansonia and Aedes. During a blood meal, an infected
mosquito introduces third-stage filarial larvae onto the skin of the
human host, where they penetrate into the bite wound. The affected
lymphatic vessels become distended and tender, and the overlying skin
becomes erythematous and hot. Abscess formation and ulceration of the
affected lymph node occasionally occurs during B. malayi infection,
more often than in Bancroftian filariasis.
 The first step towards developing a diagnosis of lymphatic filariasis is to
establish a history of exposure in endemic areas. Laboratory tests can
follow this basic clinical procedure. These tests may include:
 Basic serology testing of peripheral blood for microfilariae
detection, keeping theperiodicity of the microfilariae in mind.
 A skin biopsy can also be performed, but this test is generally
reserved for the infection by tissue-dwelling nematodes
(Onchocerca volvulus).
VI. TREATMENT
 As to the treatment of B. Malayi infection, diethylcarbamazine has been
found to reduce the microfilaria count and to kill the adult worms; the
severe febrile reactions of microfilaria carriers to the initial doses of this
drug may be reduced by administration of the steroid prednisolone.
 Prevention includes giving entire communities medicine that kills the
microscopic worms — and controlling mosquitoes. Annual mass
treatment reduces the level of microfilariae in the blood and thus,
diminishes transmission of infection.
TOXACARA CANI
MORPHOLOGY:
LIFE CYCLE:
MODE OF TRANSMISSION:
Dogs and cats that are infected with Toxocara can shed Toxocara eggs in their
feces. Adults and children can become infected by accidentally swallowing dirt
that has been contaminated with dog or cat feces that contain
infectious Toxocara eggs.
PATHOLOGY & SYMPTOMATOLOGY:
Toxocara canis, the parasitic roundworm of the dog may infect aberrant hosts
including mice and humans. The present study examined the behavioral and
pathological changes at each of three postintubation periods (Period 1: 8-10 days,
2: 49-51 days, and 3: 84-86 days postintubation, respectively) in independent
groups of mice intubated with 1000 eggs of T. canis. Eight-ten days after
intubation Toxocara infected animals typically showed depressed levels of activity
relative to saline-intubated controls. The scope and severity of behavioral changes
were attenuated when different mice were tested 49-51 days after infection, and
then became more severe when
the third set of animals was
tested 84-86 days after
intubation. While brain
pathology increased over the
three periods, visceral organs
showed marked pathology 8-10
days after intubation followed by
a decrease in severity. These data
suggest that Toxocara associated
pathological changes in visceral organs and in the brain have behavioral
consequences in mice. Given the similarity in migratory pathways of this parasite
in rodents and humans, and the findings of T. canis larvae in human brain
tissue, the results of this animal study may have implications concerning the
possible etiology of behavioral disorders for children who have a known history of
pica for dirt.
Toxocariasis is an infection caused by the ingestion of larvae of the dog
roundworm Toxocara canis or the cat roundworm Toxocara cati. The soil of parks
and playgrounds is commonly contaminated with the eggs of T canis, and
infection may cause human disease that involves the liver, heart, lung, muscle,
eye, and brain.
LAB DIAGNOSIS
A blood test is available that looks for evidence of infection with Toxocara larvae.
In addition to the blood test, diagnosis of toxocariasis includes identifying the
presence of typical clinical sign.
TREATMENT
For OLM, surgery, steroids, and anthelminthic (anti-parasitic) chemotherapy are
the preferred methods of treatment.Visceral toxocariasis can be treated with
antiparasitic drugs such as albendazole or mebendazole. Treatment of ocular
toxocariasis is more difficult and usually consists of measures to prevent
progressive damage to the eye.
PREVENTION & CONTROL
Wash your hands with soap and warm water after playing with your pets or
other animals, after outdoor activities, and before handling food or eating. Teach
children the importance of washing hands to prevent infection. Teach children
that it is dangerous to eat dirt or soil.
DIPHYLOBOTHRIUM LATUM
MORPHOLOGY
The adult worm is ivory or yellowish grey in color, measuring 3-10 meters in
length. The head (scolex) is small, spatulated or spoon shaped, has a pair of slit
grooves (bothria) ventrally and dorsally and has no rostellum (a beaklike
projection on the head) and no hookless.
LIFE CYCLE
When the egg of D. latum passed out along with the faeces of the infected host
(man) meets water, the ciliated embryo (coracidium, Fig. 107.4) escapes from the
egg and swims in the water. It is ingested by a Cyclops (Fig. 107.5, 6) and
transforms into procercoid larva. When the infected Cyclops is ingested by a fish,
procercoid develops into plerocercoid or sparganum (Fig. 107.8) larva in the fish
which is infective to man. On consuming insufficiently cooked fish, man becomes
infected. The plerocercoid larva develops into an adult worm, ultimately the eggs
are excreted in the feces.
MODE OF TRANSMISSION
Is one of the
pseudophyllidean cestodes
transmitted via aquatic
species. 5 Human infection
with D. latum is acquired by
eating uncooked freshwater
fish containing the parasite's
plerocercoid cysts.
PATHOLOGY AND
SYMPATHOLOGY
Diphyllobothrium latum infects the person by tapeworms of the genus
Diphyllobothrium (commonly D. latum and D. nihonkaiense). Diphyllobothriasis
mostly occurs in regions where raw fish is regularly consumed; those who
consume raw fish are at risk of infection. Most infections are asymptomatic.
However, symptoms can include abdominal discomfort, diarrhea, vomiting, and
weight loss. Vitamin B12 deficiency leading to pernicious anemia may occur.
Diseases caused by diphyllobothrium latum: the largest tapeworms that can
infect people, can grow up to 30 feet long. While most infections are
asymptomatic, complications include intestinal obstruction and gallbladder
disease caused by migration of proglottids.
LABORATORY DIAGNOSIS
Diagnosis made by finding the typical brown, oval, operculate eggs in feces using
standard recovery techniques
Eggs: measure 58 - 76 μm by 40 - 51 μm and in addition to the operculum, have
a small round knob-like projection on the a opercular end
Scolex: elongated; displays a pair of longitudinal grooves known as bothria, which
replace the usual suckers
Gravid proglottids: wider than long, have genital pores located midventral,
adjacent to centrally located, rosette shaped uterus
TREATMENT
Praziquantel: adults and children, one dose, 5 - 10 mg/kg orally
Niclosamide: adults 2 gm orally once; children 50 mg/kg (maximum 2 gm) orally
once
PREVENTION AND CONTROL
How can I prevent Diphyllobothrium infection?
 Do not eat raw or undercooked fish.
 Cook meat and fish properly before you eat it
 Drinking water is clean
 Follow proper food safety handling, such as washing hands and avoid cross
contamination with raw fish and fruits and vegetables.
The FDA recommends the following for fish preparation or storage to kill
parasites.
 Cooking
o Cook fish adequately (to an internal temperature of at least 145° F [~63°
C]).
 Freezing
o At -4°F (-20°C) or below for 7 days (total time), or
o At -31°F (-35°C) or below until solid, and storing at -31°F (-35°C) or
below for 15 hours, or
o At -31°F (-35°C) or below until solid and storing at -4°F (-20°C) or below
for 24 hours.
Taenia Solium
MORPHOLOGY
- The adult Taenia solium has a head (scolex) that consists of four suckers and a
rostellum with a double crown of hooks, and unsegmented narrow neck, and a
large body formed by several hundred proglottids. The entire body is called a
strobila and may range in size from two to eight meters long.
LIFE CYCLE
- Solium. The adults produce proglottids which
mature, become gravid, detach from
the tapeworm, and migrate to the anus or are
passed in the stool (approximately 6 per
day). T. saginata adults usually have 1,000 to
2,000 proglottids, while T. Solium adults have an
average of 1,000 proglottids. The eggs contained
in the gravid proglottids are passed with feces. T.
saginata may produce up to 100,000 and T.
Solium may produce 50,000 eggs per proglottid
respectively.
-
- T. solium taeniasis is acquired by humans through the ingestion of the
parasite's larval cysts (cysticerci) in undercooked and infected pork.
Human tapeworm carriers excrete tapeworm eggs in their faeces and
contaminate the environment when they defecate in open areas.
-
Opisthorchis felineus
MORPHOLOGY The adults of Opisthorchis felineus differ from those of
Opisthorchis viverrini mainly in larval development and morphology; however,
the eggs of O. felineus are 30 by 11 µm while those of O. viverrini are 27 by 15
µm. Specimens of the genus Metorchis have much wider bodies and spherical
testes.
The life cycle is very similar to that of Clonorchis sinensis. The eggs hatch only
after they are ingested by the appropriate snail (Bithynia leachi). Ultimately a
cercaria develops that has eyespots and a large tail fin. The cercaria penetrates a
fresh-water fish, typically of the carp family, between the scales and encysts as a
metacercaria within the muscles. Cats become infected by eating infected fish.
Once eaten, the fluke migrates through the ampule of Vater into the bile ducts
where it matures (Vogel, 1934)
MODE OF TRANSMISSION How does one become infected with Opisthorchis?

The eggs of Opisthorchis are ingested by freshwater snails. After the eggs hatch,
infected snails release microscopic larvae that then enter freshwater fish. People
become infected when eating infected raw or undercooked fish containing the
larvae.
PATHOLOGY AND SYMPTOMATOLOGY- Most pathologic manifestations result
from inflammation and intermittent obstruction of the biliary ducts. In mild
cases, manifestations include dyspepsia, abdominal pain, diarrhea, or
constipation. With infections of longer duration, the symptoms can be more
severe, and hepatomegaly and malnutrition may be present. LABORATORY
DIAGNOSIS- Diagnosis is based on microscopic identification of eggs in stool
specimens. However, the eggs of Opisthorchis are practically indistinguishable
from those of Clonorchis. The adult fluke can also be recovered at surgery.
Serologic testing is currently not available for Opisthorchis infection
TREATMENT- For treating Opisthorchis felineus, a dose of 60 mg/kg of the drug
was given for 5 days after which 75% cure rates were obtained. A dose of 100
mg/kg given on alternate days for 5 or 10 days may be needed to get 80% cure
rates against O. viverrini. PREVENTION AND CONTROL Do not eat raw or
undercooked freshwater fish. Lightly salted, smoked, or pickled fish can contain
infectious parasites. Drinking river water or other nonpotable water will not lead
to infection with Opisthorchis.
HETEROPHYES HETEROPHYES
MORPHOLOGY
All Heterophyes species are small trematodes, under 2 mm long. Their outer
surface is covered by tiny spikes. The pharynx is long and well developed. The
caecae of the intestine extend to the tail end of the worm. The genital pore is
surrounded by a sucker with spiky structures. The identification of Heterophyes
is commonly based on the number of these spikes. The sucker of the genital pore
is close and posterio-lateral to the well-developed ventral sucker (acetabulum).
The testes are side by side, close to the distal parts of the intestinal caecae. The
ovary is located medially. The vitellar glands are located at the anterior side of the
testes and grouped symmetrically. The general morphology and internal organs of
H. heterophyes are presented in Fig. 3.11.
LIFE CYCLE
Adults release embryonated eggs each with a fully-developed miracidium, and
eggs are passed in the host’s feces . After ingestion by a suitable snail (first
intermediate host), the eggs hatch and release miracidia which penetrate the
snail’s intestine. Genera Cerithidia and Pironella are important snail hosts in
Asia and the Middle East respectively. The miracidia undergo several
developmental stages in the snail, i.e. sporocysts, rediae, and cercariae. Many
cercariae are produced from each redia. The cercariae are released from the snail
and encyst as metacercariae in the tissues of a suitable fresh/brackish water fish
(second intermediate host). The definitive host becomes infected by ingesting
undercooked or salted fish containing metacercariae. After ingestion, the
metacercariae excyst, attach to the mucosa of the small intestine and mature into
adults (measuring 1.0 to 1.7 mm by 0.3 to 0.4 mm). In addition to humans,
various fish-eating mammals (e.g., cats and dogs) and birds can be infected by
Heterophyes heterophyes .
Flukes are parasitic flatworms that infect various parts of the body (eg, blood
vessels, gastrointestinal tract, lungs, liver) depending on the species.
Heterophyiasis is acquired by eating infected raw or undercooked fish from
freshwater or brackish water containing metacercariae (encysted stage). After
ingestion, metacercariae are encysted and attach to the mucosa of the small
intestine. There, they develop into adults, growing to about 1.0 to 1.7 mm by 0.3
to 0.4 mm. Infection with Metagonimus yokogawai, a related trematode, has been
reported after eating raw or undercooked freshwater or brackish fish in the Far
East, Siberia, Manchuria, the Balkan states, Israel, and Spain. Intestinal
infection with Nanophyetus salmincola has been reported after ingestion of raw
or undercooked salmon. Adult flukes can cause abdominal pain and diarrhea
Pathology and Symtomatology - Each worm causes a mild inflammatory reaction
at its site of contact with the intestine. In heavy infections which are common
cause damage to the mucosa and produce intestinal pain and mucosa diarrhea. -
Heterophyes heterophyes is endemic in the Far East, Middle East, and Egypt.
Heterophyiasis is acquired by eating infected raw or undercooked fish from
freshwater or brackish water containing metacercariae (encysted stage). After
ingestion, metacercariae excyst and attach to the mucosa of the small intestine.
Laboratory Diagnosis
Laboratory diagnosis of Heterophyes heterophyes is by stool microscopy. The ova
of H.heterophyes are difficult to distinguish from other heterophyid species and
some other flukes but collection of the adult worm allows accurate identification
of the species. Treatment - Treatment of heterophyiasis is with praziquantel 25
mg/kg orally 3 times a day for 1 day for H. heterophyes and M. yokogawai and 20
mg/kg orally 3 times a day for 1 day for N.
PREVENTION AND CONTROL

Prevention involves not eating raw or undercooked fish that may contain these
intestinal flukes.
ANCYLOSTOMA DUODENALE
COMMON NAME: OLD WORLD HOOKWORM

❖MORPHOLOGY
● ADULT MALE AND FEMALE
● FEMALE IS 10-13 MM IN LENGTH BY 0.6 IN DIAMETER
● MALES ARE 8-11 MM BY 0.4 MM
● POSTERIOR ENDS HAS AN UMRELLA-SHAPE BURSA WITH RIBLIKE RAYS
● TWO PAIRS OF CURVED TEETH ON THE VENTRAL WALL OF ITS BUCCAL
CAPSULE
● EGG/OVA
● EGGS APPEAR AS OVAL THIN-SHELLED BODIES
● MEASURING 55-77 UM IN LENGTH BY 35-42 UM IN WIDTH
● FRESHLY EXCRETED EGGS CONTAIN A DEVELOPING EMBRYO IN THE
EARLY STAGES OF CLEAVAGE (2-8 CELLS)
● RHABDITIFORM LARVA - THIN SIZE: 200-400U - LONG BUCCAL CAVITY -
RHABIDITIFORMOESOPHAGUS, VERY SMALL GENITAL - POINTED TAIL END
● FILARIFORM LARVA - SIZE: 600-700U - CYLINDRICAL OESOPHAGUS (1/3 OF
THE BODY LENGTH) - SHARPLY POINTED TAIL
❖LIFE CYCLE ● Most adult worms are eliminated in 1 to 2 years, but the
longevity may reach several years. Some A. duodenale larvae, following
penetration of the host skin, can become dormant (hypobiosis in the intestine or
muscle). These larvae are capable of re-activating and establishing patent,
intestinal infections.
❖MODE OF TRANSMISSION
● Anyclostoma Duodenale is a kind of Hookworm. It is transmitted primarily by
walking barefoot on contaminated soil and through the ingestion of larvae. This
larvae can mature into a form that can penetrate the skin of humans.
❖PATHOLOGY AND SYMPTOMATOLOGY
● Duodenale infect a person through the oral route (known as Wakana
syndrome), they may experience nausea, vomiting, pharyngeal irritation, cough,
dyspnea, and hoarseness. The most serious symptoms of Ancylostoma infection
develop during the last phase when the adult worms establish themselves in the
human intestine.
● DISEASE CAUSED BY ANCYLOSTOMA DUODENALE: Two common
hookworm infections in humans are ancylostomiasis and necatoriasis, caused by
the species Ancylostoma duodenale and Necator americanus respectively. The
disease can be prevented on an individual level by not walking barefoot in areas
where the disease is common.
❖LAB DIAGNOSIS
● The standard method for diagnosing the presence of hookworm is by
identifying hookworm eggs in a stool sample using a microscope. Because eggs
may be difficult to find in light infections, a concentration procedure is
recommended.
❖TREATMENT
● Anthelminthic drugs: Benzimidazoles(albendazole 400mg once on empty
stomach, mebendazole 100mg 2 times for 3 days)
● In some cases, levamisole and pyrantel pamoate (11 mg/kg/day for 3 days)
may be used
● Efficacy of single dose treatment for hookworm infection is 72% for albendazole,
15% for mebendazole, 31% for pyrantel pamoate
● World Health Organization does recommended anthelmintic treatment in
pregnant women after the first trimester.
● It is also recommended that if the patient also suffers from anemia that ferrous
sulfate (200 mg) be administered three times daily at the same time as
anthelmintic treatment; this should be continued until hemoglobin values return
to normal which could take up to 3 months.
● Hookworm infection can be treated with local cryotherapy when the hookworm
is still in the skin.
❖PREVENTION AND CONTROL ● Preventing unhygienic defecation and
avoiding direct skin contact with the soil such as wearing shoes, using barriers
when seated on the ground) are effective in preventing infection but difficult to
implement in many endemic areas. Periodic mass treatment of susceptible
populations at 3- to 4-month intervals has been used in high-risk areas. Risk of
developing cutaneous larva migrans can be reduced by the following: -Avoiding
direct skin contact with potentially infested beach sand or other soil where dogs
or cats have defecated. -Treating cats and dogs for hookworm
NECATOR AMERICANUS
COMMON NAME: HUMAN HOOKWORM
OTHER NAME: Necator americanus Stiles, 1902
❖MORPHOLOGY
● MALE AND FEMALE ADULT
● FUMALES ARE 9-11 MM IN LENGTH BY 0.4 MM IN DIAMETER
● MALES ARE 7-9 MM BY 0.3 MM
● SMALLER THAN A. DUODENALE
● A PAIR OF SEMILUNAR CUTTING PLATES ON THE VENTRAL WALL OF
BUCCAL CAPSULE
● EGGS
● RESEMBLES THOSE A. DUODENALE
● LONGER AND MORE ELONGATED THAN A.DUODENALE
● DAILY EGG OUTPUT IS 9,000 EGGS
● RHABDITIFORM LARVA - THIN SIZE: 200-400U - LONG BUCCAL CAVITY -
RHABIDITIFORMOESOPHAGUS, VERY SMALL GENITAL - POINTED TAIL END
● FILARIFORM LARVA - SIZE: 600-700U - CYLINDRICAL OESOPHAGUS (1/3
OF THE BODY LENGTH) - SHARPLY POINTED TAIL
❖LIFE CYCLE
● Adult N. americanus specimens range from 5 to 11 millimetres (0.2 to 0.4 inch).
The worms then live in the intestine for many months, and some may persist for
as long as 10 years. Continual reinfection and acquired partial resistance result
in a more or less constant number of worms harboured. Infective larvae when
swallowed can develop in the intestine without preliminary lung passage, but this
mode of transmission is not common in nature.
● Transmission of N. americanus larvae occurs through exposed skin, by

environmental acquisition from soil, feces, and other contaminated surface.
Vertical transmission among neonates is also possible
. ❖PATHOLOGY AND SYMPTOMATOLOGY

● The pathology of N. americanus is divided into two stages – larvae and
adults. The larvae penetrate the uninfected skin and travel through various
organs, including the respiratory tract and lymph nodes. Once in the lymph
nodes, the larvae start entering the blood, lungs, and intestines.
● DISEASE CAUSED BY NECATOR AMERICANUS:

Necatoriasis is the condition of infection by Necator hookworms, such as
Necator americanus. This hookworm infection is a type of helminthiasis
(infection) which is a type of neglected tropical disease.
❖LAB DIAGNOSIS
● The most common method for diagnosing N. americanus is through
identification of eggs in a fecal sample using a microscope. N. americanus
eggs have a thin shell and are oval shaped, measuring roughly 56–74 by 36–
40 μm.
❖TREATMENT
● The most common treatment for N. americanus infection are
benzimidazoles, specifically albendazole and mebendazole.
● Benzimidazoles kill adult worms by binding to the nematode’s β-tubulin
and subsequently inhibiting microtubule polymerization within the parasite.
● The efficacy of single-dose treatments for hookworm infections were: 72%
for albendazole, 15% for mebendazole, and 31% for pyrantel pamoate.
● A current concern with this parasite is the increase in drug resistance,
such as benzimidazoles and mebendazoles.
❖PREVENTION AND CONTROL

● The best way to avoid hookworm infection is not to walk barefoot in areas
where hookworm is common and where there may be human fecal
contamination of the soil. Also, avoid other skin contact with such soil and
avoid ingesting it. Infection can also be prevented by not defecating outdoors
and by effective sewage disposal systems.
PARASITE NAME: ANISAKIS
COMMON NAME: HERRING WORM

OTHER NAME: Anisakis simplex (Rudolphi, 1809) ›Anisakis simplex B
❖MORPHOLOGY ● The larvae of the family Anisakidae are characterized by

the presence of three bilobed lips, a boring tooth near the dorsal lip, large
excretory gland cells in their anterior region, and a ventriculus between the
esophagus and the intestine.
❖LIFE CYCLE ● Adult stages of anisakid nematodes reside in the stomach

of marine mammals, where they are embedded in the mucosa in clusters.
Unembryonated eggs produced by adult females are passed in the feces of
marine mammals . The eggs become embryonated in water, undergoing two
developmental molts , and hatch from the eggs as free-swimming
ensheathed third-stage (L3) larvae. These free-swimming larvae are then
ingested by crustaceans. The ingested larvae grow within the crustacean
hemocoel, and become infective to fish and cephalopod paratenic hosts.
After preying upon infected crustaceans, the digested L3 larvae migrate from
the paratenic host intestine into the abdominal cavity, and eventually to the
tissues of the mesenteries and skeletal muscle. Through predation, tissue-
stage L3 larvae can be transmitted among paratenic hosts . Fish and squid
maintain L3 larvae that are infective to humans and marine mammals .
❖MODE OF TRANSMISSION ● The transmission of this disease occurs

when infective larvae are ingested from fish or squid that humans eat raw or
undercooked.
❖PATHOLOGY AND SYMPTOMATOLOGY ● Anisakis pathology is due
mainly to two mechanisms: allergic reactions (from isolated urticaria and
angioedema to life-threatening anaphylactic shock associated with
gastrointestinal symptoms or ‘gastroallergic anisakiasis’), and direct tissue
damage, due to invasion of the gut wall, development of eosinophilic
granuloma, or perforation (gastric or intestinal anisakiasis).
● DISEASE CAUSED BY ANISAKIS: Anisakiasis is a parasitic disease

caused by anisakid nematodes (worms) that can invade the stomach wall or
intestine of humans. The transmission of this disease occurs when infective
larvae are ingested from fish or squid that humans eat raw or undercooked.
❖LAB DIAGNOSIS ● The only method for diagnosing anisakiasis, other than
endoscopy, is immunological examination (e.g., by examining Anisakis-
specific IgA, IgG, and IgE). The sensitivity is as high as 70%-80%[12,13], but
the results take time (a week) and, therefore are not at all helpful in the
clinical field.
❖TREATMENT ● Endoscopic removal of the larvae ● Possibly albendazole ●
Endoscopic removal of the larvae is curative. ● Treatment of presumptive
anisakiasis with albendazole 400 mg orally twice a day for 6 to 21 days may
be effective, but data are limited.
❖PREVENTION AND CONTROL ● Do not eat raw or undercooked fish or
squid. The FDA recommends the following for seafood preparation or storage
to kill parasites. • Cooking (Seafood in General) o Cook seafood adequately
(to an internal temperature of at least 145° F [~63° C]). • Freezing (Fish) o At
-4°F (-20°C) or below for 7 days (total time), or o At -31°F (-35°C) or below
until solid, and storing at -31°F (-35°C) or below for 15 hours, or o At -31°F
(-35°C) or below until solid and storing at -4°F (-20°C) or below for 24 hours.
TAENIA SAGINATA
Common name: THE BEEF TAPEWORM
I. MORPHOLOGY (egg/ova, larval stage, adult):
EGG/OVA
Larval Stage
Larval encystment usually occurs in striated muscle and the central
nervous
system, and within 8 to 11 weeks the larvae, termed Cysticercus solium
(cellulosae) in dogs and Cysticercus bovis in cattle, become infectious.
Cysticerci
are ellipsoid, translucent bladder-like cysts in which an inverted scolex has
developed.
Adult
T. saginata is a long flattened ribbon-like tapeworm that is white in color. It
is
about 6 to 7 millimeters in width. The adult T. saginata usually grows to be
about
4 to 8 meters in length, with about 1000 segments called proglottids.
T. saginata has 15 to 20 branches and no hooks in the scolex.
II. LIFE CYCLE

● Taeniasis is the infection of humans with the adult tapeworm of Taenia
saginata or Taenia solium. Humans are the only definitive hosts for T.
saginata and T. solium. Eggs or gravid proglottids are passed with feces.
1. The eggs can survive for days to months in the environment. Cattle (T.
saginata) and pigs (T. solium) become infected by ingesting vegetation
contaminated with eggs or gravid proglottids
2. In the animal’s intestine, the oncospheres hatch
3. Invade the intestinal wall, and migrate to the striated muscles, where they
develop into cysticerci. A cysticercus can survive for several years in the
animal.
Humans become infected by ingesting raw or undercooked infected meat
4. In the human intestine, the cysticercus develops over 2 months into an
adult
tapeworm, which can survive for years. The adult tapeworms attach to the
small
intestine by their scolex
5. Reside in the small intestine
6. Length of adult worms is usually 5 m or less for T. saginata (however it
may
reach up to 25 m) and 2 to 7 m for T. solium. The adults produce proglottids
which mature, become gravid, detach from the tapeworm, and migrate to
the
anus or are passed in the stool (approximately 6 per day). T. saginata adults
usually have 1,000 to 2,000 proglottids, while T. solium adults have an
average of
1,000 proglottids. The eggs contained in the gravid proglottids are released
after
the proglottids are passed with the feces. T. saginata may produce up to
100,000
and T. solium may produce 50,000 eggs per proglottid respectively.

● Taenia saginata passed in the faeces of an infected person are only
infectious to cattle. Humans are infected by ingestion of raw or
undercooked beef infected with Cysticercus bovis, the larval stage of T.
saginata. In humans, the adult tapeworm develops in the intestine over
2–3 months.

● Humans are the sole definitive host. When humans ingest infected raw or
incompletely cooked beef, the cysticercus develops into a reproductive
adult in the small intestine in - 3 months. Symptoms are rare but may
include abdominal discomfort and diarrhea. Unlike T. solium, the eggs of T.
saginata are not infectious to humans and their ingestion does not result in
cysticercosis. Taeniasis due to T. solium is usually characterized by mild
and non-specific signs and symptoms; 6-8 weeks after ingestion of the
cysticerci, abdominal pain, nausea, diarrhea or constipation might arise
and last until the tapeworm dies following treatment (otherwise it may live
many years).
● The laboratory diagnosis of human intestinal taeniasis for decades had
been based on the detection of bile stained eggs and the gravid proglottids
of the adult worm passed in the feces. Recent studies reveal that
microscopic examination of eggs or the gravid proglottids alone is not a
reliable method of differentiating T. saginata from T. asiatica because of
their similarities.
VI. TREATMENT
-Praziquantel
-Alternatively, niclosamide (outside the US)
● Treatment of T. saginata infection is with a single oral dose
of praziquantel 5 or 10 mg/kg.
● Alternatively, a single 2-g dose of niclosamide (not available in the US) is
given as 4 tablets (500 mg each) that are chewed one at a time and
swallowed with a small amount of water. For children, the dose of
niclosamide is 50 mg/kg (maximum dose 2 g) once.
● Treatment can be considered successful when no Taenia ova are identified
in stool 1 and 3 months after treatment.
● T. saginata infection can be prevented by cooking whole cuts of beef to ≥
63° C (≥ 145° F) as measured with a food thermometer placed in the
thickest part of the meat, then allowing the meat to rest for 3 minutes
before carving or consuming. Ground beef should be cooked to ≥ 71° C (≥
160° F). Ground beef does not require a rest period.

▪ One way to prevent taeniasis is to cook meat to safe temperatures. A food
thermometer should be used to measure the internal temperature of
cooked meat. Do not sample meat until it is cooked. USDA recommends
the following for meat preparation.
▪ For Whole Cuts of Meat (excluding poultry) Cook to at least 145° F (63° C)
as measured with a food thermometer placed in the thickest part of the
meat, then allow the meat to rest for three minutes before carving or
consuming.
▪ For Ground Meat (excluding poultry) Cook to at least 160° F (71° C);
ground meats do not require a rest time.
● According to USDA, “A ‘rest time’ is the amount of time the product
remains at the final temperature, after it has been removed from a grill,
oven, or other heat source. During the three minutes after meat is
removed from the heat source, its temperature remains constant or
continues to rise, which destroys pathogens.”
DIPYLIDIUM CANINUM
Common name: FLEA TAPEWORM
I. MORPHOLOGY (egg/ova, larval stage, adult):
EGG/OVA
Dipylidium caninum is a common tapeworm of dogs and cats, but is
occasionally
found in humans. It has many common names including the “flea
tapeworm”,
“cucumber tapeworm”, and “double-pored tapeworm”
Larval Stage
Canids and felids are the normal hosts for Dipylidium caninum. The
intermediate
host is usually the larval stages of the dog or cat flea (Ctenocephalides spp.)
and
occasionally Trichodectes canis (the dog louse).
Adult
The adult tapeworms (measuring up to
60 cm in length and 3 mm in width)
reside in the small intestine of the host,
where they each attach by their scolex
II. LIFE CYCLE

● Gravid proglottids are passed intact in the feces or emerge from the
perianal region of the host image. In the environment, the proglottids
disintegrate and release egg packets, which are also occasionally found
free in the feces image. The intermediate host (most often larval stages
of the dog or cat flea Ctenocephalides spp.) ingests egg packets, and
the oncosphere within is released into the larval flea’s intestine. The
oncosphere penetrates the intestinal wall, invades the insect’s
hemocoel (body cavity), and develops into a cysticercoid image. The
cysticercoid remains in the flea as it matures from a larva into an adult
image. The vertebrate host becomes infected by ingesting the adult flea
containing the cysticercoid image. In the small intestine of the
vertebrate host, the cysticercoid develops into the adult tapeworm after
about one month. The adult tapeworms (measuring up to 60 cm in
length and 3 mm in width) reside in the small intestine of the host,
where they each attach by their scolex image. Gravid, double-pored
proglottids detach from the strobila (body) and are shed in the feces.
Humans also acquire infection by ingesting the cysticercoid
contaminated flea. Children are most frequently infected, possibly due
to close contact with flea-infested pets’ image.
● Dipylidium caninum is a tapeworm that commonly infects dogs and
cats. Transmitted by ingestion of an infected flea, D. caninum
occasionally affects humans, especially children.

● Dipylidium caninum is the common tapeworm of dogs and cats and
occasionally humans. Cat fleas, Ctenocephalides felis are the
intermediate hosts. Adults embed into the mucosa of the small intestine,
small numbers may cause no symptoms but larger numbers can cause
hemorrhagic enteritis and occasionally death in young animals. Most
infections are asymptomatic, but sometimes these symptoms may be
identified in an infected individual: mild diarrhea, abdominal colic,
anorexia, restlessness, constipation, rectal itching, and pain due to
emerging proglottids through the anal cavity.
● Dipylidium caninum eggs in stool specimens, primarily from the wet
preparation examination of the concentration sediment. The eggs are
most easily seen on a direct wet smear or a wet preparation of the
concentration sediment.
VI. TREATMENT
● Treatment for both animals and humans is simple and very effective. A
prescription drug called praziquantel is given, either orally or by
injection (pets only). The medication causes the tapeworm to dissolve
within the intestine. Since the worm is usually digested before it passes,
it may not be visible in your dog’s stool. The drugs are generally
well-tolerated.

To reduce the likelihood of infection you should:
1. Control fleas on your pet, and in their indoor and outdoor
environments.
2. Have your veterinarian treat your dogs and cats promptly if they
have tapeworms.
3. Clean up after your pet, especially in playgrounds and public parks.
Bury the feces, or place it in a plastic bag and dispose of it in the
trash.
4. Do not allow children to play in areas that are soiled with pet or other
animal feces.
5. Teach children to always wash their hands after playing with dogs
and cats, and after playing outdoors.
FASCIOLA GIGANTICA
COMMON NAME: Giant liver fluke
I. MORPHOLOGY
Egg
Fasciola gigantica very rarely infects humans. Reported cases are mainly
from Africa. The life cycle,
transmission, morphology, clinical presentation, and treatment of the F.
gigantica trematode and its
infections are very similar to those of F. hepatica.
II. LIFE CYCLE:

Immature eggs are discharged in the biliary ducts and passed in the stool.
1. Eggs become embryonated in freshwater over ~2 weeks
2. Embryonated eggs release miracidia
3. Which invade a suitable snail intermediate host
4. In the snail, the parasites undergo several developmental stages
(sporocysts , rediae, and
cercariae). The cercariae are released from the snail
5. And encyst as metacercariae on aquatic vegetation or other substrates.
Humans and other
mammals become infected by ingesting metacercariae-contaminated
vegetation (e.g., watercress)
6. After ingestion, the metacercariae encysted in the duodenum
7. And penetrate through the intestinal wall into the peritoneal cavity. The
immature flukes then
migrate through the liver parenchyma into biliary ducts, where they mature
into adult flukes and
produce eggs
8. In humans, maturation from metacercariae into adult flukes usually
takes about 3–4 months;
development of F. gigantica may take somewhat longer than F. hepatica.
III. MODE OF TRANSMISSION:

Transmission occurs through the ingestion of raw, fresh-water vegetation on
which the flukes in their
metacercariae form are encysted. The plants become exposed to the
metacercariae when the body of water
that the vegetation is growing in becomes contaminated by eggs in the fecal
matter of an infected host.

The young worms move through the intestinal wall, the abdominal cavity,
and the liver tissue, into the
bile ducts, where they develop into mature adult flukes that produce eggs.
The pathology typically is most
pronounced in the bile ducts and liver.
Fasciola infection is both treatable and preventable. More usually the
invasive phase lasts many weeks,
with the most common symptoms being intermittent fever, hepatomegaly,
and abdominal pain, although
up to 50% of infections may be subclinical. Abdominal pain is usually in the
epigastrium or right
hypochondrium. Other symptoms include malaise and wasting.
Even during the chronic phase of infection, it can be difficult to find eggs in
stool specimens from people
who have light infections. Certain types of blood tests can be helpful for
diagnosing Fasciola infection,
including routine blood work and tests that detect antibodies (an immune
response) to the parasite.
VI. TREATMENT
➔ Triclabendazole, a benzimidazole compound active against immature and
adult Fasciola
parasites, is the drug of choice for treatment of fascioliasis.
➔ As with all medications, use of triclabendazole should be individualized.
➔ Triclabendazole is given orally, with food, to improve absorption.
According to the FDA
approved product, the recommended dosage regimen (for patients at least 6
years of age) is two
doses of 10 mg/kg given 12 hours apart.
➔ Triclabendazole resistance has been documented, particularly in infected
animals but also in some
infected humans.
Additional Perspective About Therapy
➔ On the basis of limited data, nitazoxanide might be effective therapy in
some patients. The drug is
given orally, with food. The dosage regimen for adults is 500 mg po bid
(twice a day) for 7 days.
➔ Praziquantel, which is active against most trematodes (flukes), typically is
not active against
Fasciola parasites. Therefore, praziquantel therapy is not recommended for
fascioliasis.
➔ In some patients who have biliary tract obstruction, manual extraction of
adult flukes (e.g., via
endoscopic retrograde cholangiopancreatography [ERCP]) may be indicated.
VII. PREVENTION & CONTROL

No vaccine is available to protect people against Fasciola infection.
In some areas of the world where fascioliasis is found (endemic), special
control programs are in place or
are planned. The types of control measures depend on the setting (such as
epidemiologic, ecologic, and
cultural factors). Strict control of the growth and sale of watercress and
other edible water plants is
important.
Individual people can protect themselves by not eating raw watercress and
other water plants, especially
from Fasciola-endemic grazing areas. As always, travelers to areas with poor
sanitation should avoid food
and water that might be contaminated (tainted). Vegetables grown in fields
that might have been irrigated
with polluted water should be thoroughly cooked, as should viscera from
potentially infected animals.
FASCIOLOPSIS BUSKI
COMMON NAME: Giant Intestinal Fluke
I. MORPHOLOGY
Fasciolopsis buski is usually elongated, oval in shape, without a cephalic
cone. Its size varies depending
on the host species, and is between 2 and 10 cm in length and 0.8 and 3 cm
in width.
Egg
➔ Size: About 140 um x 80 um
➔ Shape: Ellipsoidal, thin shell. Small, indistinct operculum.
➔ Color: Yellowish-brown. Shell is transparent.
➔ Stage when passed in feces: Embryonated. Filled with yolk cells in which
an indistinct germinal
cell is embedded.
Adults
➔ Size: 2 to 7.5 cm long, 0.8 to 2 cm wide.
➔ Shape: Elongated ellipsoid.
➔ F. buski is hermaphroditic. Female organs are found in the anterior half,
while the testes are found
in the posterior half.
II. LIFE CYCLE
Causal Agent: The trematode Fasciolopsis buski, the largest intestinal fluke
of humans.
Immature eggs are discharged into the intestine and stool .
1. Eggs become embryonated in water
2. Eggs release miracidia
3. which invade a suitable snail intermediate host .
4. In the snail the parasites undergo several developmental stages
(sporocysts , rediae , and
cercariae). The cercariae are released from the snail
5. encyst as metacercariae on aquatic plants .
6. The mammalian hosts become infected by ingesting metacercariae on the
aquatic plants. After
ingestion, the metacercariae excyst in the duodenum
7. attach to the intestinal wall. There they develop into adult flukes (20 to 75
mm by 8 to 20 mm) in
approximately 3 months, attached to the intestinal wall of the mammalian
hosts (humans and
pigs) .
8. The adults have a lifespan of about one year.

Humans (and pigs) pass eggs in their feces, which develop in water and
infect snails as intermediate hosts.
After further development, the parasites leave the snail intermediate host
and encyst on water plants.
Humans become infected as a result of eating these contaminated water
plants raw (or undercooked).

Fasciolopsiasis, infection of humans and swine by the trematode
Fasciolopsis buski, a parasitic worm.
The adult worms, 2–7.5 cm (0.8–3 inches) long, attach themselves to the
tissues of the small intestine of
the host by means of ventral suckers; the sites of attachment may later
ulcerate and form abscesses.
What are the signs and symptoms of fasciolopsiasis?
Many people do not have symptoms from Fasciolopsis infection. However,
abdominal pain and diarrhea
can occur 1 or 2 months after infection. With heavy infections Fasciolopsis
flukes can cause intestinal
obstruction, abdominal pain, nausea, vomiting, and fever.
Microscopic identification of eggs, or more rarely of the adult flukes, in the
stool or vomitus is the basis
of specific diagnosis. The eggs are indistinguishable from those of F.
hepatica.
VI. TREATMENT
Four relatively new broad spectrum anthelmintics (thiabendazole,
mebendazole, levamisole and pyrantel
pamoate) were compared with two older anthelmintics, (tetrachloroethylene
and hexylresorcinol) to treat
heavy Fasciolopsis buski infections in 17 children aged 4-13 years in
hospital. Tetrachloroethylene was
the most effective drug in these 17 children and another 49. Large numbers
of worms were expelled and
faecal egg counts were markedly reduced (99%).The mean number of worms
per child was 122 with a
range of 7 to 818. All the other anthelmintics tested were ineffective; no
worms or only a few were
expelled after treatment. However, the oral administration of
tetrachloroethylene and hexylresorcinol
were associated with severe anaphylactic reactions which were prevented by
prior treatment with
antihistamines.
VII. PREVENTION & CONTROL

● Involves not eating freshwater plants in areas where Fasciolopsis buski is
endemic.
● Cook all aquatic plants well before eating them (in boiling water).
● In endemic areas, prevent fecal contamination (from humans or pigs) of
water where aquatic
plants are grown. Do not feed raw aquatic plants to pigs.

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GROUP 1.

Liza Ymanuelle J. Barrientos

Ken Francis G. Ang

Phil Jereg R. Guihama

Name of Parasite: Ascaris Lumbricoides

Common name/ other name: Giant roundworm

II. LIFE CYCLE

III. MODE OF TRANSMISSION

IV. PATHOLOGY AND SYMPTOMATOLOGY

The pathogenesis of ascariasis is generally related to organ damage and host

The standard method for diagnosing ascariasis is by

Anthelmintic medications (drugs that remove parasitic worms from the

VII. PREVENTION AND CONTROL

Name of Parasite: Wuchereria Bancrofti

Common name/ other name: Filariasis or

*Adult: MALE AND FEMALE

The males measure up to 40 mm long.

II. LIFE CYCLE

Different species of the following genera of mosquitoes are vectors of W.

III. MODE OF TRANSMISSION

The disease is usually transmitted through the bite of an infectious

IV. PATHOLOGY AND SYMPTOMATOLOGY

Wuchereria bancrofti (Filariasis) infection occurs when a larva carrying

The standard method for diagnosing active infection is the identification of

The drug of choice is diethylcarbamazine, which can eliminate the

VII. PREVENTION AND CONTROL

At night. Sleep in an air-conditioned room or. Sleep under a mosquito net.

Name of Parasite: Loa loa

Adult males are smaller at 30-34

II. LIFE CYCLE

The vector for Loa

III. MODE OF TRANSMISSION

Diagnosis is by detecting microfilariae in peripheral blood or seeing worms

VII. PREVENTION AND CONTROL

Avoid insect bites by wearing long pants and long-sleeved shirts

NAME OF PARASITE: Echinococcus granulous

COMMON NAMES/OTHER NAMES: Hydatid worm, hyper tape-worm or dog

II. LIFE CYCLE

Humans are aberrant intermediate hosts, and

Human infection occurs by hand-to-mouth transfer of viable tapeworm eggs

IV. PATHOLOGY AND SYMPTOMATOLOGY

Granulosus is endemic suggests a diagnosis of cystic echinococcosis.

VII. PREVENTION AND CONTROL

Wash your hands with soap and

NAME OF PARASITE: Hymenolepsis diminuta

COMMON NAMES/OTHERS NAMES: Rat tapeworm

Adult Hymenolepis diminuta reach 20 to 60 cm, and up to 90 cm. The

II. MODE TRANSMISSION

Hymenolepiasis is the most common intestinal tapeworm infection of

III. PATHOLOGY AND SYMPTOMATOLOGY

Diagnosis is based on finding eggs or proglottids in the feces or the adult

Praziquantel is the drug of choice for treatment of H. diminuta infection (2),

VI. PREVENTION AND CONTROL

Prevention. Good hygiene, public health and sanitation programs, and

NAME OF PARASITE: Schistosoma mansoni

COMMON NAMES/ OTHER NAMES: Blood fluke

II. LIFE CYCLE

III. MODE OF TRANSMISSION