Transcript Trematodes (Flukes)

Trematodes (Flukes)
and Cestodes
Jose A. Serpa, M.D.
Assistant Professor
Baylor College of Medicine
References
The Travel and Tropical Medicine Manual by Elaine Jong and
Christopher Sandford. Fourth Edition, 2008
Principles and Practices of Infectious Diseases. Mandel, Bennett
and Dolin. Sixth Edition, 2005
DPDx. Laboratory Identification of Parasites of Public Health
Concern (CDC). Second Edition, 2006.
Special thanks to Dr. A.C. White Jr. for allowing me to use some of
his slides
Agenda
1. Trematodes (flukes): definition and
classification
2. Schistosomes, liver flukes and lung flukes
3. Cestodes: Intestinal tapeworms
4. Cestodes: Tissue (cyst) stage (cysticercosis
and ecchinococcosis)
Cayetano Heredia National Hospital and Institute
of Tropical Medicine Alexander von Humboldt,
Lima , Peru
1. Trematodes
Trematodes
The flukes, or trematodes, are
leaf-shaped parasites with a blind
bifurcate intestinal tract
Size varies from 1 mm to more
than 10cm
Most are hermaphroditic, except
schistosomes
Classification
1. Blood flukes (Schistosomes)
2. Hepatobiliary (Clonorchis sinensis, Opistorchis
spp. and Fasciola hepatica)
3. Lung flukes (Paragonimus)
4. Intestinal flukes (Metagonymus, Heterophyes,
Fasciolopsis)
Eggs of trematodes
From DPDx, website for laboratory diagnosis of parasitic diseases of the Division of Parasitic Diseases, National Centers for
Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA, [http://www.dpd.cdc.gov/DPDx/].
2. A. Schistosomiasis
Schistosomiasis
Trematode infection caused by “blood flukes”
which live in venules of the gastrointestinal and
genitourinary tract
There are approximately 200 million persons
infected in the world (120 million are
symptomatic and 100 000 die each year)
It affects 74 countries (80% of cases occur in
Sub-Saharan Africa)
Human Schistosomes and their
geographic distribution
S. mansoni: Africa,
Brazil, Middle East,
Caribean
S. haematobium: Africa,
Middle East
S. japonicum: China,
Phillipines, SE Asia
S. mekongi: Laos,
Cambodia
S. intercalatum: Central
Africa (less common)
Life cycle
Cercariae penetrate human skin during
contact or immersion in fresh water
inhabited by infected snails
Cercariae transform into schistosomulae
, go into bloodstream and then migrate to
liver and lung where they mature (4-6
weeks)
Adult male and female pair and migrate to
the Sup Mes vein (S. japonicum and S.
mekongi), Inf Mesenteric vein (S.
mansoni) or venous plexus sorrounding
the bladder (S. hematobium)
Eggs are excreted in feces or urine and
deposited in fresh water. They hatch,
miracidia emerge and infect snails of
certain species. Cercariae emerge from
infected snails
Clinical syndromes
Asymptomatic
Schistosome (cercarial) dermatitis
Acute Schistosomiasis
Chronic Schistomiasis
Schistosome dermatitis
It is due to skin
penetration of cercaria
Pruritic maculopapular
rash
It can last from hours
(first time exposed) to
days (previously
sensitized)
Acute Schistosomiasis (Katayama
fever)
Occurs at the time of initial parasite egg-laying
(hypersensitivity to egg- associated Ags) about 2-8
weeks after infection
Consists of fever, rash/urticaria, cough, abdominal pain,
diarrhea, hepatosplenomegaly and eosinophilia
Usually in persons from non-endemic areas
More common with S. mansoni and S. haematobium
Chronic Schistosomiasis
Intermittent dysentery and bowel
obstruction
Hepatosplenic disease
Urinary tract disease
Less common: Lung or CNS disease
Hepatosplenic
schistosomiasis
Occurs in S. mansoni , S. japonicum
and S. mekongi
Pathogenesis: granulomas around
embolized eggs that become trapped
in small portal veins (liver)
Initial stage: hepatomegaly
Later stages: Periportal fibrosis 
blocks portal blood flow which leads to
portal hypertension (splenic
congestion, ascites and esophageal
bleed)
HBV or HCV coinfection worsens
prognosis
Urinary tract disease
Occurs in S. haematobium
infections
Passage of eggs through the
bladder wall cause hematuria
and dysuria (inflammation and
ulcerations)
Granulomatous lesions with
subsequent fibrosis of the
bladder wall cause urinary
reflux and obstruction
(hydroureter, hydronephrosis,
chronic bacteriuria, renal failure
and squamous carcinoma of
bladder)
Lung and CNS schistosomiasis
Eosinophilic pneumonitis results when eggs reaching the
general circulation are trapped in the alveolar capillaries
Aberrant migration of adult worms or embolization of
eggs to the spinal cord or brain can cause transverse
myelitis (S. mansoni or S. haematobium) or seizures (S.
japonicum) respectively
Keep in mind…
Acute infection of humans with avian species of Schistosomes can
result in an allergic skin reaction called swimmer’s itch (can not
mature in the human host and die in the skin). NO need of
antiparasitic therapy
Pathogenic adult Schistosoma can persist in the human host for
decades so infections can present in non endemic areas among
immigrants from endemic regions
An interesting association
Prolonged and recurrent Salmonella bacteremia and/or
bacteriuria has been reported in patients chronically
infected with schistosomiasis
Diagnosis
Persons with a history of freshwater exposure in
endemic areas (even if eosinophilia is absent)
Identification of eggs in stool or urine samples
Identification of eggs in tissues (e.g. rectal or
bladder mucosa)
Serologic tests (CDC): FAST-ELISA (99%
sensitive) and immunoblot (species-specific)
Imaging studies (US, CT, MRI) as clinically
indicated
Schistosoma eggs
Schistosoma eggs in tissues
Treatment
Praziquantel is the drug of choice
Dosing: 40mg/kg in 2 divided doses on a single
day (S. mansoni and S. haematobium) or
60mg/kg in 3 divided doses 4-6h apart on a
single day (S. Japonicum)
Artemisinins (e.g. artemether) has
antischistosomal as well as antimalarial activity
Steroids can be used along with praziquantel for
Katayama fever or CNS disease
Prevention and control of
Schistosomiasis
Avoid contact with fresh water in endemic areas
Annual mass drug administration of praziquantel
Environmental measures to control the snails
and promote sanitary disposal of human
excrement (cost beyond the reach of poor
countries)
2. B. Liver flukes
Liver flukes
 They include:
1. Clonorchis sinensis
2. Opisthorchis sp.
3. Fasciola hepatica
Clonorchis and Opisthorchis
Largely found in the Far East,
Southeast Asia and Russia
The hermaphroditic adult
worms measure 5 to 25mm x
2 to 5mm and inhabit the
intrahepatic biliary ducts
Humans become infected by
eating raw or inadequately
cooked fish
Life cycle
Clinical syndromes
Asymptomatic eosinophilia
RUQ abdominal pain with jaundice
Acute biliary obstruction
Acute pancreatitis
Recurrent pyogenic cholangitis
Cholangiocarcinoma
Diagnosis and Treatment
Based on identification
of eggs in the stool or
adult worms during
surgery or ERCP
Imaging studies (US, CT
or MRI) can demonstrate
biliary dilation
Praziquantel is the drug
of choice (75mg/kg in 3
divided doses 4-6h
apart).
Surgery or ERCP for
acute biliary obstruction
Fasciola hepatica
Large liver fluke (adult worm
measures 3.0 x 1.5 cm) that
lives in the bile ducts of its
mammalian hosts (humans,
sheep and cattle)
Reported in 61 countries from
Europe, North Africa, Asia and
South America (Bolivia and
Peru)
More than 3 million cases in
the world
Transmission
Parasite eggs passed in stools
hatch into miracidia which
infects fresh water snails.
Cercaria emerge from snails and
attach to aquatic plants (encyst
as metacercaria)
Humans ingest contaminated
aquatic plants (e.g. water cress)
Metacercaria excyst, penetrate
the intestinal wall, enter the
peritoneum, and then pass
through the liver capsule to the
biliary tract
Clinical syndromes
1. Acute phase
 Associated with parasite migration (duodenum –
peritoneal cavity – liver) and burrowing through the liver
 Causes fever, abdominal pain, hepatomegaly and
eosinophilia
2. Chronic phase
 Due to biliary involvement
 Intermittent “biliary colic”, cholangitis
Diagnosis and management
Serology for acute phase
Demonstration of eggs in stools, bile or
duodenal aspirates
Imaging studies (US, CT) show linear
hepatic tracts
Treatment is with triclabendazole
(10mg/kg once or twice). Also bithionol,
nitazoxanide.
2. C. Lung flukes
Lung flukes
Most important species:
Paragonimus westermani, P.
heterotremus, P. skrjabini, P.
miyazakii (Asia), P. africanus, P
uterobilateralis (Africa), P.
mexicana, P ecuadoriensis (South
and Central America)
Cases reported from Asia, Africa
and Central and South America
Life cycle
Adult worms lay eggs that are
coughed up in the sputum or
swallow and passed in the
stools
Eggs hatch in freshwater and
develop into miracidia that
infects snails (cercaria)
Cercaria infects freshwater
crustaceans (metacercaria)
Humans are infected when
eating raw or inadequately
cooked crabs or crayfish
Metacercaria excyst in the
duodenum  peritoneum 
diaphragm  pleura  lung
Clinical manifestations
Pulmonary paragonimiasis
Extrapulmonary paragonimiasis
Pulmonary paragonimiasis
Resembles pulmonary tuberculosis
Initial stages: cough productive of brownish
sputum with intermittent hemoptysis
Chronic stages: profuse expectoration, dyspnea,
hemoptysis, pleural effusions and pneumothorax
CRX: infiltrates, cavities, cysts, nodules, pleural
effusions
Extrapulmonary paragonimiasis
Ectopic migration of eggs from the bowel
Most common: CNS, skin, liver, peritoneum
CNS: brain lesions (seizures, headaches, visual
disturbances), meningitis
Skin: Migratory lesions (resemble cutaneous
larva migrans)
Diagnosis and treatment
Identification of eggs in stools or sputum
Gram or AFB stain in sputum may destroy eggs
Serology: Immunoblot from CDC (Sen: 96%, Sp:
100%)
Drug of choice is praziquantel (75mg/kg/day
divided in 3 doses for 2 days)
Adult flukes
3. A. Cestodes
Intestinal tapeworms
Tapeworms (adult stage)
 Tapeworms are segmented flat worms that have a head or scolex
(which attaches to the intestine) and rhomboid-shaped segments
termed proglottids
 The tapeworms elongates from each scolex by forming proglottids
(which contain male and female reproductive organs). Adult
tapeworms may reach lengths of 4.5 – 10m
Clinically important tapeworms
Tapeworm
Common name
Transmission
Taenia solium
Pork tapeworm
Ingesting meat (pork)
containing larvae
Taenia saginata
Beef tapeworm
Ingesting meat (beef)
containing larvae
Dyphilobotrium sp.
Fish tapeworm
Ingesting fish containing
larvae
Hymenolepis sp.
Dwarf tapeworm
Accidental ingestion of fecal
material (containing eggs)
Dipyllidium caninum
Dog tapeworm
Accidental ingestion of dog
fleas
Life cycle: generalities
 The proglottids (containing eggs) shed periodically in the feces
 Eggs are ingested by an intermediate host - cow, pig, fish. Then the
eggs hatch and larvae emerge, penetrate the gut and migrate to the
tissues (especially the muscle)
 The lifecycle is completed when humans ingest encysted larvae-
containing meat
Epidemiology
– T. solium is prevalent worldwide (60 million) but rare in US except in
immigrants from endemic areas of Latin America and Asia
– T. saginata is found worldwide (60 million), especially in Africa and Latin
America. In the US, it is seen among people who eat raw or
undercooked beef (e.g. steak tartare)
– D. latum is prevalent worldwide (10 million) particularly among people
who ingest raw, pickled, or marinated fish. D. latum in the US has been
associated with sushi and sashimi made of raw pacific salmon and
some Scandinavian pickled fish dishes (carp, herring, smelt)
– H. nana and H. diminuta(dwarf, 2cm long) is prevalent worldwide (30
million) especially in children. Because of person to person spread,
nurseries and day-care facilities are sites of transmission
Life cycle of Dyphillobotrium
Life cycle of Hymenolepis
Life cycle of Dipylidium
Clinical manifestations
Most infections are asymptomatic or with
minor abdominal symptoms.
Patients may complain of passing worms
D. latum can compete for absorption of
vitamin B12 causing B12 deficiency.
Diagnosis and treatment
Eggs can be identified in the stools, but
this may require repeated examinations
The eggs of T. saginata and T. solium
indistinguishable
Gravid proglottids or the scolex can be
examined to tell the species apart
Treatment is praziquantel
Tapeworm eggs
Tapeworms
3. B.
Cestodes
Tissue cysts (larval stage)
Cysticercosis
It is a tissue infection (e.g. subcutaneous tissues, brain, eye, muscle, heart,
etc) caused by the larval stage of Taenia solium.
Neurocysticercosis = cysticercosis of the nervous system
Cysticercosis is prevalent in Latin America, Sub-Saharan Africa, India,
China and Southeast Asia
– Serosurveys in endemic areas: up to 10% infection rates. Studies from
India, Mexico, Peru, and Ecuador documented that up to half of patients with
adult onset seizures had evidence of neurocysticercosis by imaging studies
– In the US, NCC is primarily a disease of immigrants (Hispanics from Central
America). Local transmission has been documented in the setting of
household tapeworm carriers
Life cycle of Taenia solium
Pathophysiology
There is typically an incubation period of several years before onset of
clinical symptoms
This quiescent phase results from the parasite’s ability to evade the host
immune system. However as the cysticerci age, they lose this ability which
leads to an intense inflammatory reaction (causing seizures)
Over a few months, the inflamed lesion either resolves radiographically or
is replaced by a small calcification
Cysticerci in the cerebral ventricles often cause obstructive hydrocephalus
as a result of mechanical obstruction
Types of neurocysticercosis
Neurocysticercosis can cause a wide spectrum of clinical forms
depending on the number of parasites, their location, and the degree
of host inflammation
It can be broadly divided into:
1. Parenchymal: solitary lesion, multiple lesions
2. Extra-parenchymal disease:
a.
b.
c.
Intraventricular cysts
Subarachnoid cysts
Spinal cord cysts
Parenchymal NCC
A solitary degenerating
parenchymal lesion is perhaps
the most common presentation
of neurocysticercosis
worldwide
Seizures are the main clinical
manifestation of this type of
NCC
Other symptoms: headaches,
neurologic focal deficits
Extra-parenchymal NCC
Intraventricular
Intraventricular cysts typically
present with increased
intracranial pressure from
obstructive hydrocephalus
Headache, nausea,
papilledema and altered
mental status can also be
present
Extra-parenchymal NCC
Subarachnoid
Subarachnoid NCC causes a wide
range of symptoms. Cysts in the
fissures (especially the Sylvian fissure)
can enlarge to several cm and cause
mass effect
Basal subarachnoid cysticercosis
carries the worst prognosis since
numerous cysticerci may fill the basilar
cisterns leading to arachnoiditis. This
can present as meningitis, stroke or
communicating hydrocephalus
Most of these patients frequently have
concomitant ventricular and/or
parenchymal disease
Calcifications: inactive lesions?
Diagnosis
Imaging studies: MRI and CT
Serology: Enzyme-linked immunoelectrodifusion transfer blot (EITB)
More accurate in serum than in CSF. The assay has a nearly 100%
specificity and 98% sensitivity for those with multiple cysticerci.
(sensitivity is only 70% in patients with a single parenchymal cyst)
Screening for taeniasis in patients or household contacts(?)
Diagnostic criteria
Absolute criteria: Histopathology, Parasites seen in eye, MRI with cyst and
scolex
Major criteria: CT/MRI consistent with NCC, +EITB, resolution (spontaneous
or with ABZ/PZQ), single enhancing lesion <20 mm w/o Symptoms or signs
of other disease
Minor criteria: CT compatible, clinical manifestations c/w NCC, cysticercosis
outside CNS (e.g. muscle calcifications)
Epidemiologic criteria: Household contact of tapeworm carrier, residence or
prolonged travel to endemic area
Definitive diagnosis: one absolute criterion or two major plus one minor and one
epidemiologic criterion
2. Probable diagnosis: one major plus two minor criteria, one major plus one minor plus
one epidemiologic criteria, or three minor plus one epidemiologic criteria
1.
Treatment
Symptomatic therapy must be the initial goal of management in
neurocysticercosis. (anti-epileptic medications, surgical CSF
diversion procedures, and corticosteroids respectively)
Antiparasitic medications also play an important although still
controversial role in the treatment of NCC
Surgery (VP shunts, open craniotomy and especially endoscopic
removal of cysts) also play a role in selected cases
Treatment consensus
Viable or degenerating parenchymal cysts: AED, steroids,
antiparasitics
Intraventricular cysts: endoscopic removal of cysts or VPS followed
by antiparasitics and steroids
Subarachnoid: Steroids, antiparasitics (repeated courses?) +/- VPS
Calcifications: AED (current rec’s against use of antiparasitics)
Hydatid cyst
It is an infection of liver and lung due to the encysted larva of the
cestode Echinococcus spp.
Two main species:
1. E. granulosus: Cystic hydatid disease. Endemic in sheep raising
areas of the world (e.g South America, Middle East). There are
small foci in the US (California, Utah and Alaska)
2. E. multilocularis: Alveolar hydatid disease. Endemic in Alaska,
Central Europe and Northern Japan
Dogs and wild canines are the definitive hosts (adult worms in
intestines). Sheep and catle (E. granulosis) or rodents (E.
multilocularis) are the intermediate hosts (hydatic disease)
Life cycle
Clinical manifestations and
diagnosis
Hydatid cyst disease (E. granulosus) presents with a slowly
expanding mass lesion usually in the liver (60%) or lungs (25%).
The most serious complications result from cyst rupture, which can
cause anaphylaxis or numerous daughter lesions.
Alveolar hydatid disease (E. multilocularis) presents with an
expanding infiltrative process (90% in the liver).
Diagnosis: Imaging studies (US, CT), serology (ELISA at CDC) is
83% sensitive
Treatment
In experienced centers, E. granulosus cysts are now mainly treated
by PAIR procedure (percutaneous aspiration, injection of scolidical
agents, and reaspirations).
PAIR should be undertaken while on albendazole therapy (spilled
cyst fluid can spread infection to other areas such as the peritoneal
cavity)
Chemotherapy alone may be attempted with albendazole for small
or inoperable lesions
Surgical removal is the treatment of choice for complicated cysts
(e.g. communication with the biliary tract) and for E. multilocularis.
Consider pre- and post-operative albendazole