Parasitology/Helminths (3 hours)
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1. Defines “Helminth’’
1.1 Lists the helmints classification.
1.2. Defines the structure of helminths
1.3. Defines the life cyles of helminths; lists the egg and larva
structures.
• 2. Lists the clinical tables related with helminths and defines
pathogenetic mechanisms.
• 2.1. Defines the clinical importance of helminths.
• 2.2. Defines the sample taking related with infections of helminths.
• 2.3. Lists the laboratory diagnostic methods.
Nematodes
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Ascaris lumbricoides
Dracunculus medinensis
Enterobius vermicularis
Wuchereria bacrofti
Ancylostoma duodenale
Toxocara spp.
Loa loa
Strongyloides stercoralis
Trichinella spiralis
Trichuris trichiura
Helminths
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Helminth is a general term for a parasitic worm.
The helminths include
 the Platyhelminthes or flatworms (flukes and
tapeworms)
 the Nematoda or roundworms.
Helminths
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all helminths are relatively large (> 1 mm long);
some are very large (> 1 m long).
all have well-developed organ systems and most are active
feeders.
the body is either flattened and covered with plasma
membrane (flatworms)
or cylindrical and covered with cuticle (roundworms).
some helminths are hermaphrodites;
others have separate sexes.
Helminths
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Helminths are worldwide in distribution; infection is most
common and most serious in poor countries.
The distribution of these diseases is determined by climate,
hygiene, diet, and exposure to vectors.
The mode of transmission varies with the type of worm;
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ingestion of eggs or larvae,
penetration by larvae,
bite of vectors,
ingestion of stages in the meat of intermediate hosts.
Worms are often long-lived.
Helminths
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although infections are often asymptomatic, severe pathology
can occur.
worms are large and often migrate through the body, they can
damage the host's tissues directly by their activity or
metabolism.
damage also occurs indirectly as a result of host defense
mechanisms.
almost all organ systems can be affected.
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Helminths are transmitted to humans in many different ways
 by accidental ingestion of infective eggs (Ascaris, Echinococcus,
Enterobius, Trichuris)
 or larvae (some hookworms).
Other worms have larvae that actively penetrate the skin (hookworms,
schistosomes, Strongyloides).
infection requires an intermediate host vector.
the intermediate vector transmits infective stages when it bites the host to
take a blood meal (the arthropod vectors of filarial worms);
the larvae are contained in the tissues of the intermediate host and are
taken in when a human eats that host (Clonorchis in fish, tapeworms in
meat and fish, Trichinella in meat).
The levels of infection in humans therefore depend on
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hygiene (as eggs and larvae are often passed in urine or feces),
climate (which may favor survival of infective stages),
the ways in which food is prepared, a
the degree of exposure to insect vectors.
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Hookworms (Ancylostoma and Necator) actively suck blood from
mucosal capillaries.
The anticoagulants secreted by the worms cause the wounds to
bleed for prolonged periods, resulting in considerable blood loss.
Heavy infections in malnourished hosts are associated with anemia
and protein loss.
Diversion of host nutrients by competition from worms is probably
unimportant, but interference with normal digestion and absorption
may well aggravate undernutrition.
The tapeworm Diphyllobothrium latum can cause vitamin B12
deficiency through direct absorption of this factor.
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Many helminths undertake extensive migrations through body tissues,
which both damage tissues directly and initiate hypersensitivity reactions.
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The skin, lungs, liver, and intestines are the organs most affected.
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Petechial hemorrhages, pneumonitis, eosinophilia, urticaria and pruritus,
organomegaly, and granulomatous lesions
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Feeding by worms upon host tissues is an important cause of pathology,
particularly when it induces hyperplastic and metaplastic changes in
epithelia.
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liver fluke infections lead to hyperplasia of the bile duct epithelium.
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Chronic inflammatory changes around parasites (for example, the
granulomas around schistosome eggs in the bladder wall) have been linked
with neoplasia
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Immune-mediated inflammatory changes occur in the skin, lungs, liver,
intestine, CNS, and eyes as worms migrate through these structures.
Systemic changes such as eosinophilia, edema, and joint pain reflect local
allergic responses to parasites.
The pathologic consequences of immune-mediated inflammation are seen
clearly in intestinal infections (especially Strongyloides and Trichinella
infections).
Structural changes, such as villous atrophy, develop.
The permeability of the mucosa changes, fluid accumulates in the gut
lumen, and intestinal transit time is reduced.
Prolonged changes of this type may lead to a protein-losing enteropathy.
The inflammatory changes that accompany the passage of schistosome
eggs through the intestinal wall also cause severe intestinal pathology.
Heavy infections with the whipworm Trichuris in the large bowel can lead to
inflammatory changes, resulting in blood loss and rectal prolapse.
Nemathodes (roundworms)
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nematodes are cylindrical rather than flattened
the body wall is composed of
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an outer cuticle that has a noncellular, chemically complex
structure,
a thin hypodermis,
musculature.
The cuticle in some species has longitudinal ridges called alae.
The bursa, a flaplike extension of the cuticle on the posterior end of
some species of male nematodes, is used to grasp the female during
copulation.
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Nematodes are usually bisexual.
Males are usually smaller than females,
a curved posterior end, and possess (in some species) copulatory
structures, such as spicules (usually two), a bursa, or both.
The males have one or (in a few cases) two testes, which lie at the
free end of a convoluted or recurved tube leading into a seminal
vesicle and eventually into the cloaca.
Ascariasis
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Ascaris lumbricoides
largest nematode (roundworm) parasitizing the human
intestine
adult females: 20 to 35 cm;
adult male: 15 to 30 cm
Symptoms
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High worm burdens may cause abdominal pain and intestinal
obstruction.
Migrating adult worms may cause symptomatic occlusion of the
biliary tract or oral expulsion.
During the lung phase of larval migration, pulmonary symptoms
can occur
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cough
dyspnea,
hemoptysis,
eosinophilic pneumonitis - Loeffler’s syndrome
Treatment
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albendazole,
mebendazole,
pyrantel pamoate
The most effective method to control ascariasis, as well as other soiltransmitted helminthiasis, is sanitary disposal of feces.
Care must be taken in treating mixed helminthic infections involving
A lumbricoides, because an ineffective ascaricide may stimulate the
parasite to
migrate to another location. Persons in whom asymptomatic ascariasis is
detected incidentally should be treated to prevent the possibility of a
future
abnormal migration of these large worms into extraintestinal sites.
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Drancunculus medinensis
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Dracunculiasis (guinea worm disease)
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isolated areas in a narrow belt of African countries
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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.
After maturation into adults and copulation, the male worms die and the
females (length: 70 to 120 cm) migrate in the subcutaneous tissues
towards the skin surface.
approximately one year after infection, the female worm induces a blister
on the skin, generally on the distal lower extremity, which ruptures.
when this lesion comes into contact with water, a contact that the patient
seeks to relieve the local discomfort, the female worm emerges and
releases larvae.
The larvae are ingested by a copepod and after two weeks (and two
molts) have developed into infective larvae.
Symptoms
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The worm emerges as a whitish filament (duration of
emergence: 1 to 3 weeks) in the center of a painful ulcer,
accompanied by inflammation and frequently by secondary
bacterial infection.
Treatment
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local cleansing of the lesion
local application of antibiotics because of bacterial superinfection.
mechanical, progressive extraction of the worm over a period of
several days.
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no curative antihelminthic treatment available
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winding the protruding worm on a stick
because the worm protrudes only a few centimeters per exposure to
water, this procedure takes, on average, three months to completely
remove the worm.
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Enterobius vermicularis
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Enterobius vermicularis (previously Oxyuris vermicularis)
pinworm infection
adult females: 8 to 13 mm,
adult male: 2 to 5 mm
more frequent in school- or preschool- children and in crowded
conditions
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Eggs are deposited on perianal folds.
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Self-infection occurs by transferring infective eggs to the mouth with hands
that have scratched the perianal area.
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Person-to-person transmission can also occur through handling of
contaminated clothes or bed linens.
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Enterobiasis may also be acquired through surfaces in the environment that
are contaminated with pinworm eggs (e.g., curtains, carpeting).
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Some small number of eggs may become airborne and inhaled. These
would be swallowed and follow the same development as ingested eggs.
Symptoms
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perianal pruritus, especially at night,
invasion of the female genital tract with vulvovaginitis , pelvic
or peritoneal granulomas
anorexia, irritability, and abdominal pain.
The most common symptom is pruritus ani, which disturbs sleep and
which, in children, may be responsible for loss of appetite. abdominal
pain, irritability, and pallor
a cause of appendicitis,
female worms migrate up the vagina and fallopian tubes and into the
peritoneal cavity, where they become encapsulated with
granulomatous tissue.
Recurrent urinary tract infections have been attributed to ectopic
pinworm infections.
Diagnosis
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"Scotch test", cellulose-tape slide test
Eggs can also be found in the stool,
encountered in the urine or vaginal smears.
found in the perianal area, or during ano-rectal or vaginal
examinations.
Treatment
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pyrantel pamoate
advisable to re-treat the patient one month later.
Filariasis
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Wuchereria bacrofti
Brugia malayi
Onchocerca volvulus
Loa loa
Mansonella perstans
M. streptocerca
M. ozzardi
Brugia timori
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Infective larvae are transmitted by infected biting arthropods during a blood
meal.
The larvae migrate to the appropriate site of the host's body, where they
develop into microfilariae-producing adults.
The adults dwell in various human tissues where they can live for several
years.
The agents of lymphatic filariasis reside in lymphatic vessels and lymph
nodes;
 Onchocerca volvulus in nodules in subcutaneous tissues;
 Loa loa in subcutaneous tissues, where it migrates actively;
 Brugia malayi in lymphatics,
 Wuchereria bancrofti; Mansonella streptocerca in the dermis and
subcutaneous tissue;
 Mansonella ozzardi apparently in the subcutaneous tissues;
 M. perstans in body cavities and the surrounding tissues.
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The female worms produce microfilariae which circulate in the blood, except
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Onchocerca volvulus and Mansonella streptocerca, - in the skin,
O. volvulus - the eye.
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The microfilariae infect biting arthropods
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Inside the arthropod, the microfilariae develop in 1 to 2 weeks into infective
filariform (third-stage) larvae.
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During a subsequent blood meal by the insect, the larvae infect the
vertebrate host.
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They migrate to the appropriate site of the host's body, where they develop
into adults, a slow process than can require up to 18 months in the case of
Onchocerca.
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Wuchereria bancrofti - tropical areas worldwide;
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Brugia malayi - Asia;
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Brugia timori -some islands of Indonesia.
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The agent of river blindness, Onchocerca volvulus, - Africa, Latin America,
the Middle East.
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Loa loa and Mansonella streptocerca - Africa;
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Mansonella perstans - Africa and South America;
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Mansonella ozzardi - American continent.
Symptoms
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Lymphatic filariasis most often consists of asymptomatic
microfilaremia.
lymphatic dysfunction causing lymphedema and elephantiasis
(frequently in the lower extremities)
Wuchereria bancrofti- hydrocele and scrotal elephantiasis.
Episodes of febrile lymphangitis and lymphadenitis
Persons who have newly arrived in disease-endemic areas can develop
afebrile episodes of lymphangitis and lymphadenitis.
mostly in Asia, pulmonary tropical eosinophilia syndrome( with
nocturnal cough and wheezing, fever, and eosinophilia)
Symptoms
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Onchocerciasis - pruritus, dermatitis, onchocercomata (subcutaneous
nodules), and lymphadenopathies.
ocular lesions that can progress to blindness.
Loiasis (Loa loa) -often asymptomatic.
Episodic angioedema (Calabar swellings) and subconjunctival
migration of an adult worm can occur.
Infections by Mansonella perstans- angioedema, pruritus, fever,
headaches, arthralgias, and neurologic manifestations.
Mansonella streptocerca -skin manifestations including pruritus,
papular eruptions and pigmentation changes.
Eosinophilia
Mansonella ozzardi - arthralgias, headaches, fever, pulmonary
symptoms, adenopathy, hepatomegaly, and pruritus.
Hookworms
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Ancylostoma duodenale
Necator americanus
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The second most common human helminthic infection (after
ascariasis).
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Worldwide distribution, mostly in areas with moist, warm climate.
Symptoms
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Iron deficiency anemia (caused by blood loss at the site of
intestinal attachment of the adult worms)
cardiac complications.
gastrointestinal and nutritional/metabolic symptoms
local skin manifestations ("ground itch") during penetration by
the filariform larvae,
respiratory symptoms during pulmonary migration of the
larvae.
Diagnosis
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Examination of the eggs cannot distinguish between N.
americanus and A. duodenale. Larvae can be used to
differentiate between N. americanus and A. duodenale, by
rearing filariform larvae in a fecal smear on a moist filter paper
strip for 5 to 7 days (Harada-Mori).
Toxocara spp.
Toxocara canis (dog roundworm)
 T. cati (cat roundworm)
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visceral larva migrans and ocular larva migrans.
the systemic migration of the larval forms of animal helminthic
parasites.
Toxocara species, the common roundworms of dogs and cats,
are the usual cause.
The disease affects mainly children.
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The classic visceral larva migrans syndrome usually occurs in
preschool children with a history of pica (dirt-eating).
Patients who have severe infections often present with eosinophilia,
fever, and marked hepatomegaly which may persist for months;
may be associated respiratory symptoms with wheezing and
coughing.
Pulmonary infiltrates may be seen on chest roentgenograms but
these are usually transient.
Pruritic rashes and chronic urticaria
Neurologic involvement may cause seizures.
Death has been associated with
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myocarditis,
encephalitis,
respiratory syndromes.
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The ocular form of the disease usually occurs in children who are
between school age and young adulthood.
Ocular invasion by the larva may produce retinal granulomas or
endophthalmalitis,
leukokoria (white pupillary reflex),
decreased visual acuity,
strabismus
eye pain.
The syndrome may resemble retinoblastoma; misdiagnosis has
resulted in unnecessary enucleation of the involved eye
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Backyards, children's sandboxes, public parks, and beaches
accessible to dogs are often contaminated with Toxocara ova,
which may remain infective for years.
These areas are potential exposure sites for young children or
others who accidentally ingest the infective eggs.
Children who habitually eat dirt are at particular risk
Diagnosis
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In this parasitic disease the diagnosis does not rest on identification of
the parasite. Since the larvae do not develop into adults in humans, a
stool examination would not detect any Toxocara eggs
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by the clinical findings of visceral involvement in association with
hypergammaglobulinemia, leukocytosis, and eosinophilia.
Liver biopsy may be diagnostic, although the larvae are difficult to find
even in the presence of eosinophilic granulomas
Elevated titers of antibodies against the A and B isohemagglutinins
Toxocara antigens support the diagnosis.
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ELISA using larva-specific antigen has proven a reliable
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Eggs of Toxocara canis. These eggs are passed in dog feces, especially puppies'
feces.
Human infections with Toxocara do not produce or excrete eggs, and therefore
eggs are not a diagnostic finding in human toxocariasis.
The egg to the left is fertilized but not yet embryonated, while the egg to the
right contains a well developed larva. The latter egg would be infective if
ingested by a human (frequently, a child).
Treatment
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Prevention of human infection centers on the appropriate
treatment of Toxocara infections in dogs and cats and on
sanitary disposal of pet feces.
Public education on the necessity of these preventive measures
is needed.Once the soil has become contaminated, infective
eggs persist indefinitely.
There is no treatment of proven efficacy for disease caused by
Toxocara species in humans.
diethylcarbamazine and albendazole
Corticosteroids have been used to decrease the inflammatory
response in ocular infections and in severe respiratory or
cardiac disease.
Strongyloides stercoralis
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The Strongyloides life cycle is more complex than that of most
nematodes with its alternation between free-living and parasitic
cycles, and its potential for autoinfection and multiplication
within the host.
Symptoms
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Most infections with S stercoralis are asymptomatic except for the
ground itch that may occur when infective larvae from the soil
penetrate the skin in large numbers.
Pneumonitis can result from larval invasion in the lung.
Intestinal invasion may lead to epigastric pain and mucous diarrhea.
Eosinophilia is common.
Dissemination of strongyloidiasis into extraintestinal organs sometimes
occurs in persons receiving immunosuppressive drugs.
The infection can be perpetuated by an autoinfection cycle, which can
lead to massive infection, especially in the immunocompromised host.
Linear skin lesions on the lower abdomen and buttocks may also
develop in patients with autoinfection due to penetration of the
perianal skin by infective larvae.
This condition is called larva currens
Diagnosis
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the microscopic identification of larvae (rhabditiform and
occasionally filariform) in the stool or duodenal fluid.
Examination of serial samples may be necessary, and not
always sufficient, because stool examination is relatively
insensitive.
The duodenal fluid can be examined using techniques such as
the Enterotest string or duodenal aspiration.
Larvae may be detected in sputum from patients with
disseminated strongyloidiasis.
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Eosinophilia, epigastric pain, and mucous diarrhea
definitive diagnosis requires finding larvae in the stool or, on rare
occasions, in sputum or urine.
A newly described culture method using agar plates has been
reported to be successful in detecting the parasite.
Larval stages of S stercoralis must be distinguished from hookworm
larvae. The rhabditiform larvae resemble those of hookworms but
can be distinguished by the shorter buccal capsule and larger
genital primordium.
The filariform larvae also resemble those of hookworms, but the tail
is notched and the esophagus is about one-half the length of the
body.
Trichinella spiralis
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Trichinellosis (trichinosis)
In addition to the classical agent T. spiralis
T. pseudospiralis (mammals and birds worldwide),
T. nativa (Arctic bears),
T. nelsoni (African predators and scavengers),
T. britovi (carnivores of Europe and western Asia)
Symptoms
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Muscle involvement may be associated with muscle pain and edema,
elevated serum levels of muscle enzymes (e.g., creatine kinase and
serum glutamic oxaloacetic transaminase).
The diaphragm, intercostal muscles, tongue, and facial muscles are
often involved.
Urticaria and conjunctival or subungual splinter hemorrhages are
common.
serious complications or death may result from invasion of the heart,
lungs, or central nervous system.
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Most cases are acquired from infected pork that is inadequately
cooked.
The most common way that pigs become infected is by
ingestion of garbage containing meat scraps.
Certain ethnic groups whose culinary preferences include raw
pork are at a special risk.
Diagnosis
Any leftover, suspect meat should be examined for Trichinella larvae.
Serum antibodies are not usually detectable before 3 weeks.
 A number of serodiagnostic tests, including
 the bentonite flocculation test,
 ELISA latex agglutination,
 fluorescent antibody,
 complement fixation tests
The bentonite flocculation test, a reliable serodiagnostic method, is
positive in
over 90 percent of cases
 Muscle biopsy
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Trichuris trichura
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Trichuris trichiura, also called the human whipworm.
Symptoms
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Most frequently asymptomatic. Heavy infections, especially in small
children, can cause gastrointestinal problems (abdominal pain,
diarrhea, rectal prolapse) and possibly growth retardation.
lives primarily in the cecum and appendix but can also be found in
large numbers in the colon and rectum.
heavy infections may cause diarrhea, at times containing mucus and
blood.
Anemia may develop, along with weight loss, abdominal pain, nausea,
vomiting, tenesmus, and rectal prolapse.
Nutritional changes can cause stunted growth and clubbing of fingers.
Eosinophilia may also develop in response to worms embedded in the
mucosa.
Diagnosis
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Microscopic identification of whipworm eggs in feces is
evidence of infection
Trematodes
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Clonorchis sinensis
Fasciola hepatica
Paragonimus westermani
Schistosoma haemotobium
Schistosoma japonicum
Schistosoma mansoni
Trematodes
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Trematodes, or flukes, are parasitic flatworms with unique life cycles
involving sexual reproduction in mammalian and other vertebrate
definitive hosts and asexual reproduction in snail intermediate hosts.
These organisms are divided into four groups on the basis of their final
habitats in humans:
the hermaphroditic liver flukes which reside in the bile ducts and infect
humans on ingestion of watercress (Fasciola) or raw fish (Clonorchis
and Opisthorchis);
the hermaphroditic intestinal fluke (Fasciolopsis), which infects
humans on ingestion of water chestnuts;
the hermaphroditic lung fluke (Paragonimus), which infects humans on
ingestion of raw crabs or crayfish;
the bisexual blood flukes (Schistosoma), which live in the intestinal or
vesical (urinary bladder) venules and infect humans by direct
penetration through the skin.
Trematodes
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Signs and symptoms are related largely to the location of the adult
worms.
Schistosoma mansoni and S japonicum (mesenteric venules) eosinophilia, hepatomegaly, splenomegaly, and hematemesis.
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Schistosoma haematobium (vesical venules) - dysuria, hema turia, and
uremia.
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Fasciola hepatica, Clonorchis sinensis- fever, hepatomegaly, abdominal
pain, and jaundice.
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Paragonimus westermani (lungs, brain) - cough, hemoptysis, chest
pain, and epilepsy.
Trematodes
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multicellular eukaryotic helminths.
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Free-swimming larvae (cercariae) are given off by infected snails.
These either penetrate the skin of the human definitive host
(schistosomes) or are ingested after encysting as metacercariae in or
on various edible plants or animals (all other trematodes).
After entering a human the larvae develop into adult males and
females (schistosomes) or hermaphrodites (other flukes), which
produce eggs that pass out of the host in excreta.
These eggs hatch in fresh water into miracidia which infect snails.
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Clonorchis sinensis
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Chinese or oriental liver fluke
Embryonated eggs are discharged in the biliary ducts and in
the stool
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Korea, China, Taiwan, and Vietnam
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found in Asian immigrants, or following ingestion of imported,
undercooked or pickled freshwater fish containing
metacercariae.
Symptoms
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inflammation and intermittent obstruction of the biliary ducts
in the acute phase,
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abdominal pain,
nausea,
diarrhea,
eosinophilia
in long-standing infections,
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cholangitis,
cholelithiasis,
pancreatitis,
cholangiocarcinoma ( may be fatal)
Diagnosis
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Microscopic demonstration of eggs in the stool or in duodenal
aspirate
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The adult fluke can also be recovered at surgery.
Fasciola hepatica
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the sheep liver fluke
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worldwide
Symptoms
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the acute phase (caused by the migration of the immature fluke
through the hepatic parenchyma)
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



the chronic phase (caused by the adult fluke within the bile ducts),


abdominal pain,
hepatomegaly,
fever,
vomiting,
diarrhea,
urticaria
eosinophilia,
can last for months.
intermittent biliary obstruction and inflammation.
ectopic locations of infection (such as intestinal wall, lungs,
subcutaneous tissue, and pharyngeal mucosa) can occur.
Diagnosis





Microscopic identification of eggs is useful in the chronic (adult)
stage.
Eggs can be recovered in the stools or in material obtained by
duodenal or biliary drainage.
False fascioliasis (pseudofascioliasis) refers to the presence of eggs in
the stool resulting not from an actual infection but from recent
ingestion of infected livers containing eggs.
This situation (with its potential for misdiagnosis) can be avoided by
having the patient follow a liver-free diet several days before a repeat
stool examination.
Antibody detection tests are useful especially in the early invasive
stages, when the eggs are not yet apparent in the stools, or in ectopic
fascioliasis.
Paragonimus westermani


the oriental lung fluke
The eggs are excreted unembryonated in the sputum, or
alternately they are swallowed and passed with stool

in the Far East
Symptoms
The acute phase (invasion and migration)

diarrhea,

abdominal pain,

fever,

cough,

urticaria,

hepatosplenomegaly,

pulmonary abnormalities,
 eosinophilia.
During the chronic phase, pulmonary manifestations

cough,

expectoration of discolored sputum,

hemoptysis,

chest radiographic abnormalities.
Extrapulmonary locations of the adult worms ( the brain is involved).
Diagnosis
microscopic demonstration of eggs in stool or sputum,
(not present until 2 to 3 months after infection).
 Eggs are also occasionally encountered in effusion fluid or
biopsy material.

Schistosomiasis





Schistosoma haematobium,
S. japonicum,
S. mansoni
Eggs are eliminated with feces or urine
Schistosoma mansoni is found in parts of South America and
the Caribbean, Africa, and the Middle East; S. haematobium in
Africa and the Middle East; and S. japonicum in the Far East
Symptoms








Many infections are asymptomatic.
acute schistosomiasis (Katayama's fever) may occur weeks
after the initial infection, especially by S. mansoni and S.
japonicum.
fever,
cough,
abdominal pain,
diarrhea,
hepatospenomegaly,
eosinophilia.
Symptoms



Occasionally central nervous system lesions occur:
cerebral granulomatous disease may be caused by ectopic S.
japonicum eggs in the brain,
granulomatous lesions around ectopic eggs in the spinal cord
from S. mansoni and S. haematobium infections may result in a
transverse myelitis with flaccid paraplegia.
Symptoms







continuing infection may cause granulomatous reactions and
fibrosis in the affected organs:
colonic polyposis with bloody diarrhea (Schistosoma mansoni
mostly)
portal hypertension with hematemesis and splenomegaly (S.
mansoni, S. japonicum, S. mansoni)
cystitis and ureteritis (S. haematobium) with hematuria, which
can progress to bladder cancer
pulmonary hypertension (S. mansoni, S. japonicum, more
rarely S. haematobium)
glomerulonephritis
central nervous system lesions
Diagnosis





Microscopic identification of eggs in stool or urine is the most
practical method for diagnosis.
stool examination -S. mansoni or S. japonicum
urine examination - S. haematobium
tissue biopsy (rectal biopsy for all species and biopsy of the
bladder for S. haematobium) may demonstrate eggs when
stool or urine examinations are negative.
antibody detection
Schistosoma
mansoni
Schistosoma
haematobium
Cestodes






Taenia solium
Taenia saginata
Echinococcus granulosus
Echinococcus multilocularis
Diphyllobothrium latum
Hymenolepsis nana
Cestodes

Tapeworms are ribbon-shaped multisegmented flatworms that
dwell as adults entirely in the human small intestine
Taeniasis

Taenia saginata (beef tapeworm)
T. solium (pork tapeworm).

Taenia solium can also cause cysticercosis.


Both species are worldwide in distribution. Taenia solium is
more prevalent in poorer communities where humans live in
close contact with pigs and eat undercooked pork, and in very
rare in Muslim countries.
Symptoms





Taenia saginata taeniasis - mild abdominal symptoms.
The most striking feature consists of the passage (active and
passive) of proglottids-appendicitis or cholangitis
Taenia solium taeniasis is less frequently symptomatic than
Taenia saginata taeniasis.
The main symptom is often the passage (passive) of
proglottids.
The most important feature of Taenia solium taeniasis is the
risk of development of cysticercosis.
Diagnosis

Microscopic identification of eggs and proglottids in feces is
diagnostic for taeniasis, but is not possible during the first 3
months following infection, prior to development of adult
tapeworms.

TAKE EXTREME CARE IN PROCESSING THE SAMPLES!
INGESTION OF EGGS CAN RESULT IN CYSTICERCOSIS!
proglottids of Taenia saginata
Taenia solium
Diagnosis



Injection of India ink in the uterus allows visualization of the
primary lateral branches. Their number allows differentiation
between the two species: T. saginata has 15 to 20 branches on
each side while Taenia solium has 7 to 13
the genital pores in mid-lateral position.
Scolex of T. saginata has 4 suckers and no hooks. T. solium
has 4 suckers in addition to a double row of hooks.
Scoleces of Taenia saginata
Taenia solium
Taenia saginata adult worm
Cysticercosis

The cestode (tapeworm) Taenia solium (pork tapeworm) is the
main cause of human cysticercosis
Symptoms
Cerebral cysticercosis (or neurocysticercosis),
 seizures,
 mental disturbances,
 focal neurologic deficits,
 signs of space-occupying intracerebral lesions.
 death can occur suddenly.
Extracerebral cysticercosis can cause ocular, cardiac, or spinal
lesions with associated symptoms.
Asymptomatic subcutaneous nodules and calcified intramuscular
nodules can be encountered.
Diagnosis





The definitive diagnosis - demonstrating the cysticercus in the
tissue involved.
Demonstration of Taenia solium eggs and proglottids in the
feces diagnoses taeniasis and not cysticercosis.
While suggestive, it does not necessarily prove that
cysticercosis is present.
Persons who are found to have eggs or proglottids in their
feces should be evaluated serologically since autoinfection,
resulting in cysticercosis, can occur.
Antibody detection
Hydatidosis





Human echinococcosis (hydatidosis, or hydatid disease) is caused by
the larval stages of cestodes (tapeworms) of the genus Echinococcus.
Echinococcus granulosus causes cystic echinococcosis, the form most
frequently encountered;
E. multilocularis causes alveolar echinococcosis;
E. vogeli causes polycystic echinococcosis;
E. oligarthrus is an extremely rare cause of human echinococcosis.





Echinococcosis (hydatid disease) results from the presence of one or more
massive cysts, or hydatids, which can develop in any tissue site, including
the liver, lungs, heart, brain, kidneys, and long bones.
The clinical manifestations of this infection therefore vary greatly,
depending on the site and size of the cyst, but resemble those of a slowgrowing tumor that causes gradually increasing pressure.
Infections in the liver, lungs, or subcutaneous tissue sites may be
asymptomatic for many years, but pressure effects eventually develop.
In sensitive or vital areas, hydatids produce a panoply of symptoms, chiefly
owing to mechanical compression or blocking effects but also include
collapse of infected long bones, blindness, and epileptiform seizures.
The rupture of a hydatid cyst may induce sudden anaphylactic shock in a
previously asymptomatic individual.









Echinococcus multilocularis, which normally follows a fox-rodent cycle in northern
Siberia and North America, is occasionally conveyed to human fur trappers via fox
pelts.
In humans it causes a frequently fatal form of echinococcosis. The appearance and
life cycle of this cestode closely resemble those of E granulosus, except for the
restricted range and small number of hosts.
The cyst, however, is extremely dangerous as it lacks the laminated membrane that
confines the cyst of E granulosus, and develops an invasive, uncontrolled series of
connected chambers (hence the designation "multiloculate" and the alternative name
alveolar hydatid).
It therefore resembles a malignant growth, capable of budding off to cause
metastatic spread.
The primary cyst usually forms in the liver.
The disease is usually diagnosed late, when it is inoperable, and ends fatally.
Early radiologic imaging by US, CT, or MR is essential.
Serological tests, particularly with purified E multilocularis antigens, are sensitive and
highly specific.
Treatment with mebendazole, albendazole, or praziquantel, and surgery should
follow.
Symptoms
Echinococcus granulosus infections
 remain silent for years before the enlarging cysts cause symptoms in
the affected organs.

hepatic involvement can result in abdominal pain, a mass in the
hepatic area, and biliary duct obstruction.

pulmonary involvement can produce chest pain, cough, and
hemoptysis.

rupture of the cysts can produce fever, urticaria, eosinophilia, and
anaphylactic shock, as well as cyst dissemination.

in addition to the liver and lungs, other organs (brain, bone, heart)
can also be involved, with resulting symptoms.
Symptoms


Echinococcus multilocularis affects the liver as a slow growing,
destructive tumor, with abdominal pain, biliary obstruction, and
occasionally metastatic lesions into the lungs and brain.
Echinococcus vogeli affects mainly the liver, where it acts as a
slow growing tumor; secondary cystic development is common.
Diagnosis


The diagnosis of echinococcosis relies mainly on findings by
ultrasonography and/or other imaging techniques supported by
positive serologic tests. In seronegative patients with hepatic image
findings compatible with echinococcosis, ultrasound guided fine needle
biopsy may be useful for confirmation of diagnosis; during such
procedures precautions must be taken to control allergic reactions or
prevent secondary recurrence in the event of leakage of hydatid fluid
or protoscolices.
Indirect hemagglutination (IHA), indirect fluorescent antibody (IFA)
tests, and enzyme immunoassays (EIA)
"Hydatid sand". Fluid aspirated from a hydatid cyst will shows
multiple protoscolices (size approximately 100 µm), each of which has
typical hooklets
Treatment


Surgery is the most common form of treatment for
echinococcosis, although removal of the parasite mass is not
usually 100% effective. After surgery, medication may be
necessary to keep the cyst from recurring.
albendazole or mebendazole
Diphyllobothriasis

Diphyllobothrium latum (the fish or broad tapeworm), the
largest human tapeworm


Diphyllobothriasis occurs in areas where lakes and rivers coexist with
human consumption of raw or undercooked freshwater fish.
Such areas are found in the Northern Hemisphere (Europe, newly
independent states of the former Soviet Union (NIS), North America,
Asia), and in Uganda and Chile.
Symptoms
Diphyllobothriasis can be a long-lasting infection (decades).
Most infections are asymptomatic.
 abdominal discomfort,
 diarrhea,
 vomiting,
 weight loss.
 vitamin B12 deficiency with pernicious anemia
 massive infections may result in intestinal obstruction.
 migration of proglottids can cause cholecystitis or cholangitis.
Diagnosis

Microscopic identification of
eggs in the stool is the basis of
specific diagnosis
Hymenolepiasis



Hymenolepis nana (the dwarf tapeworm, adults measuring 15 to 40
mm in length)
Hymenolepis dimnuta (rat tapeworm, adults measuring 20 to 60 cm in
length). Hymenolepis diminuta is a cestode of rodents infrequently
seen in humans and frequently found in rodents.
Eggs of Hymenolepis nana are immediately infective when passed with
the stool and cannot survive more than 10 days in the external
environment

worldwide
Symptoms


asymptomatic
heavy infections with H. nana

weakness,
headaches,
anorexia,
abdominal pain,

diarrhea



Diagnosis

demonstration of eggs in stool
specimens