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LECTURE NOTES ON
MEDICAL
HELMINTHOLOGY
Dept. of Parasitology FK Unpad
Introduction to
Medical Helminthology
 Medical helminthology : the study of
parasitic worms (helminthes/
vermes/cacing) affecting man, which :
– Spend part or the entire life cycle in a
human host or
– Animal parasite causing disease in
human
CLASSIFICATION
HELMINTHES
NEMATHELMINTHES
NEMATODES
PLATYHELMINTHES
TREMATODES
CESTODES
General characteristics of Nematodes
 The species parasitic in man range in length from
2 mm (Strongyloides stercoralis) to over a meter
(Dracunculus medinensis)
 The adult is an elongate cylindrical worm,
bilaterally symmetrical like a thread; also known as
roundworm
 Unsegmented
 Body covered by fine and smooth cuticle,
sometimes striated
 Has inner body cavity (pseudocoelom)
Nematodes Life cycle




Transmission to a new host :
 Ingestion the mature infectious egg or larva
 Penetration of the skin or mucous membranes by the
larva
Some species have an intermediate host – usually an
arthropod
The same animal both the definitive and intermediate host
of Trichinella spiralis
Nematodes, do not multiply in man
Nematodes Pathogenicity




The effect of parasitic nematodes upon the host depends
upon : species, the intensity of the infection and the
location of the parasite
Simultaneous infection with several species of intestinal
nematodes is common in tropical and subtropical
countries
Injury may be produced by adult and larval parasites
Intestinal parasites produce less local and systemic
effect than tissue parasites
Nematodes Pathogenicity

The local reaction from intestinal parasites result from
irritation, invasion of the intestinal wall and occasionally
penertation to extraneous site

The local reaction in the liver, lungs (and other) – may
destroy or encapsulate the larvae

The degree of local reaction – depend upon the
sensitivity of the host to the proteic product of the
parasite

Intestinal mucosa is damaged by biting and
bloodsucking, by lytic ferment secreted by the parasite
and by mechanical irritation
Pathogenicity
The general reaction are produced by loss of blood,
absorption of toxin, nervous reflexes and proteic
sensitization
 The larvae of certain species, produce local and general
reaction
 In unatural host the larvae may be pass through their
invasive stages, never become established as adult
parasite – paratenic host
 Immunity is acquired through the invasion of the tissues
by the parasite and its larvae or through the absorption of
its products
 Immunity is both humoral and cellular

NEMATODES
Classification based on Habitat
HABITAT
INTESTINAL
NEMATODES
SOIL TRANSMITTED
HELMINTHS (STH)
BLOOD AND TISSUE
NEMATODES
OTHER (NON-STH)
FILARIA and
DRACUNCULUS
NEMATODES

Soil Transmitted Helminthes
 Ascaris lumbricoides
 Trichuris trichiura
 Hookworm (Necator americanus,
Ancylostoma duodenale)
 Strongyloides stercoralis

Non-Soil Transmitted Helminthes
 Enterobius vermicularis
 Trichinella spiralis

Filaria and Dracunculus
 Wuchereria bancrofti
 Brugia malayi
 Brugia timori
Important
Important
Disease caused by Soil transmitted helminthes
DEFINITION Soil transmittedhelminth :
NEMATODE WORMS WHICH REQUIRE
PERIOD OF DEVELOPMENT AND
MATURATION DURING ITS LIFE
CYCLE ON SOIL
IMMATURE
INTO
INFECTIVE
SOIL TRANSMITTED HELMINTHS
GENERAL CHARACTERISTICS OF STH
INFECTION
 Non-acute and not fatal
 Occurs primarily in slum areas
 Children are commonly infected with :
 Ascaris lumbricoides
 Trichuris trichiura
 Young adults mostly infected with
hookworms (in the plantations and
mining area) :
 Necator americanus
 Ancylostoma duodenale
Ascaris lumbricoides
DISTRIBUTION
Cosmopolitan
Prevalence 70-90 %
Primarily affects underfives
and school children
HABITAT
Lumen of the intestine :
 Jejunum
 Media ileum
Ascaris lumbricoides
LIFE CYCLE
 Ingestion of mature eggs
Mature eggs
Ingested
 Hatched in the gaster,
Migration of larva
inside the
larva penetrates the wall
of the intestine and enter circulatory system
into blood circulation
 To the right heart
Larva
chamber, into the lungs
 Alveoli – bronchioles - bronchus trachea - swallowed
Adults
 Arrived in the intestine and
becomes mature adult
Source : Medical Parasitology in Plates
Piekarski G.
Infertile eggs
Ascaris lumbricoides
PATHOGENESIS AND CLINICAL SYMPTOMS
Disease ; Ascariasis
Complaints due to direct effect by
(1). Larva
 Allergic manifestation : urticaria,
swollen lips, asthma attack
 Loffler Syndromes :
 Ascaris pneumonia (coughing)
 Hyper-eosinophilia
 Thorax X-ray : temporary white spots
 Larva migration
Ascaris lumbricoides
DISTRIBUTION
 Cosmopolitan
 Prevalence 70-90 %
 Primarily affects underfives
and school children
HABITAT
Source : Dept. of Parasitologi FKUP, 1999
 Lumen of the intestine :
Adult worms expelled after
deworming
 Jejunum
 Media ileum
Source : Color Atlas of Medicine and Parasitology. 1977
Peters W. & Gillers H.M.
Ascaris lumbricoides
PATHOGENESIS AND CLINICAL SYMPTOMS
Complaints due to direct effect by
(2). Adult worm
 Irritations of the mucosal folds
 Blocking of the intestine - ileus
 Erratic migration
 Competes in the absorption of
food and vitamins
 Release of toxic metabolic
products
Ascaris lumbricoides
Diagnosis
Laboratory diagnosis
 Identify the eggs found in feces
using following methods :


Direct smear method
Concentration method
 Identify larva found in sputum
 Identify adult worm found expelled
from anus, mouth, nostril
 Do quantitative lab method to
measure level of infection
 Additional : chest X-ray
Ascaris lumbricoides
Mass treatment
Treatment
Based
on prevalence of
Drug available
A. lumbricoides
in one area :
 Pyrantel pamoate
 prevalence
> 30 %, treatment 3x/year
 Mebendazol
 prevalence (20-30) %, treatment 2x
 Oxantel pamoate
/year
 Piperazine
 prevalence
(10-20) %, treatment 1x
/year  Albendazole
 prevalence < 10 %, individual
treatment in positive cases only
Ascaris lumbricoides
PREVENTION
 treatment of individual case
 Provision of sanitary public bath, wash
and toilet facilities
 Media information and health education
 Routine health check up of children
Infection by
Trichuris trichiura
Distribution
 Trichuriasis - cosmopolitan
 Primarily in hot and humid areas
 prevalence 80-90 %, especially among
underfives and school children
Habitat
 Caecum, appendix, colon (proximal end)
Mode of infection  oral
 Infective eggs embedded under
fingernail (hand to mouth infection)
 Ingested with contaminated food/drinks
(carried by insect vector: cockroach,
flies)
Trichuris trichiura
LIFE CYCLE
In human body
C


Eggs hatch
(Proximal intestine)
Maturation in soil (3-5 weeks)
Adult in colon,
especially in Caecum
Eggs in
Feces
In Soil
Trichuris trichiura
PATHOLOGY AND CLINICAL SYMPTOMS
Disease : Trichuriasis
Heavy infection worm migrate to
colon, rectum
 Prolapsus recti, worm found in
mucosal lining (due to frequent
defecation)
Trichuris trichiura
PATHOLOGY AND CLINICAL SYMPTOMS
Chronic and heavy infection
 Heavy anemia (Hb = 3 gr%) (1
worm absorb 0,005 cc
blood/day)
 Abdominal pain, nausea,
weight loss, vomiting
 Prolapsus recti
 Headache, fever
Mixed infection may
occur with Ascaris
lumbricoides,
hookworm and
Entamoeba histolytica
Trichuris trichiura
Diagnosis
 Identify egg worm found in fecal
sample
 Identify adult worm from
prolapsed anus and rectum (by
proctoscopy)
 Measure level of infection by
counting :
 Number of eggs per gram feces
 Number of female worm expelled
through deworming
Trichuris trichiura
PREVENTION
Treatment
 available:
Elimination of source of infection
Drugs
 Improved
personal hygiene (hand
 Oxantel
pamoate
 Mebendazol
(drug
of training)
choice)
washing,
toilet
 Through washing of sold
vegetables
 Health education
 Provision of sanitary public toilet
Infection by Hookworm
PREFERENTIAL HABITAT
 Small intestine (jejunum)
 In heavy infection : duodenum, colon
GEOGRAPHIC DISTRIBUTION
Cosmopolitan, especially :
– Tropical equator
– Coal/tin mines, coffee/rubber
plantations
 Ideal soil for egg development :
– Sandy soil
– Clay soil
– Muddy soil hindered from excessive
dryness or wetness
HOOKWORM
LIFE CYCLE
In human body
Larvae exit from
Capillary and
entered Alveoli
Larvae entered
Pulmonary
Adult in intestine
( jejunum )
Larvae entered
Blood stream
Eggs in
feces
Filariform l arvae
penetrate skin
In Soil
Immature
egg
Infective larvae
Filariform larvae
Mature
egg
Immature
egg
Rhabditiform larvae
Hatch in soil
HOOKWORM
PATHOLOGY AND CLINICAL SYMPTOMS
 Disease: Ancylostomiasis
 Synonym: Uncinariasis, necatoriasis
 infection by A. duodenale are more
serious than N. americanus
 Chronic infection rarely produce
acute manifestation
 Tissue damage and symptoms are
caused by :
– Larva stage
– Adult worm
HOOKWORM
PATHOLOGY CAUSED BY LARVA STAGE
 Larva penetrates the skin maculopapules - erythema - heavy
itching : ground itch/dew itch
 In sensitive patient, larva carried in
the circulation, may cause:
– Bronchitis / Pneumonitis
HOOKWORM
PATHOLOGY CAUSED BY ADULT WORM
 Hooked to the intestinal mucosal wall :
abdominal pain, nausea, diarrhea
 Absorbing 0,2-0,3 ml of blood/day/worm :
progressive anemia, hypo chrome,
microcytic type of Fe deficiency anemia
 Heavy anemia (Hb may reach 2 gr %) :
– Dyspnea, physical weakness, headache
– Rapid pulse beat, cardiac weakness
– Children : physical growth retardation,
mental
HOOKWORM
PATHOLOGY CAUSED BY ADULT WORM
(Anemia by HOOKWORM)
Blood smear of patient with heavy infection caused by hookworm
indicating Fe deficiency anemia with low MCHC and low serum Fe
concentration
Source : Color Atlas of Medicine and Parasitology. 1977 Peters W. & Gillers H.M.
HOOKWORM
PATHOLOGY CAUSED BY ADULT WORM
(Anemia by hookworm)
 Atrophic glossitis found with hypo
chromic microcytic anemia,
caused by heavy infection of
hookworm
 Tongue surface become smooth
and lacking of papillae
HOOKWORM
PATHOLOGY CAUSED BY ADULT WORM
(Anemia by hookworm)
 Glositis atrofik
pada with atrophic glossitis
 Patient
anemi hipokrom
also show fingernail
mikrositer yang
deformity (koilonichia)
disebabkan infection
 Fingernail becomes thin and
berat HOOKWORM
concave
with elevated ridge
 Tampak lidah
halus
dan kurang papila
source : Atlas Parasitologi Kedokteran, Zaman P. Alih Bahasa : Anwar C.; Mursal Y.
HOOKWORM
Diagnosis
 Identify eggs from feces sample
 Identify larva from :
– Fecal culture
– Old feces sample
HOOKWORM
TIHELMINTHICS
trachlorethylen
ebendazole
bendazole
rantel pamoate
oskanate
phenium hidroxynaphtoate
PREVENTION
 Same as with Ascariasis but
with the addition of :
wearing shoes during work
in plantation or mine area
Infection by
Strongyloides stercoralis
HOST, HABITAT AND DISTRIBUTION
 Man is the definitive Host
 Habitat of female worm,
mucosal lining of :
 Duodenum
 Jejunum (proximal end)
 Found very cosmopolitan,
especially in the tropical and
subtropical region
Strongyloides stercoralis
LIFE CYCLE
Life cycle in human body
A
Larvae exit from
Capillary, entered
Alveoli
Larvae enter
Lung
Adult in
duodenum, especially
Proximal duodenum
Larvae entered
Blood stream
Filariform l arvae
penetrate skin
Filariform larvae
Infective stage
Rhabditiform l arvae
in Feces
Rhabditiform larvae
in soil
B
Egg
Development
FREE LIVING
CYCLE
Free living
adult in soil
Rhabditiform
larvae
Life cycle in soil
Strongyloides stercoralis
CLINICAL FEATURES
 Disease : Strongyloidiasis,
Strongyloidosis, Cochin China
diarrhea
 Level of infection :
 Mild - asymptomatic
 Moderate
 Heavy and chronic
In moderate infection
 Female worm embedded in the
mucosal wall of duodenum
 Burning sensation and stinging
pain in the epigastrium
 Nausea, vomiting, diarrhea and
constipation
In heavy and chronic infection
 Loss of body weight; Anemia
 Dysentery (chronic); Slight fever
 May be accompanied by secondary
bacterial infection where worm inhabits
the entire intestinal epithelium up to the
distal colon)
Strongyloides stercoralis
Diagnosis
Find and identify
 Rhabditiform larva :
– From fresh feces
– Gastric (duodenal) juice
*Eggs :
– In heavy diarrhea
– After administration of
laxative
Strongyloides stercoralis
TREATMENT AND PREVENTION
Drugs given
 Thiabendazole
 Mebendazole
 Pyrvinium pamoate
PREVENTION
 Similar to the prevention of hookworm
 Autoinfection is prevented by means of :
– Avoid constipation
– Anal hygiene
NON-SOIL TRANSMITTED HELMINTHS
= Members of intestinal nematode that have
transmissions are not via soil.
= It happens because egg or larva of non-soil
transmitted helminths don’t do maturation
process (to become infectious) in the soil.
NON-SOIL TRANSMITTED
HELMINTHS
1. Enterobius vermicularis
2. Trichinella spiralis
Enterobius vermicularis
A.
MORPHOLOGY
> Enterobius vermicularis = Oxyuris vermicularis =
pinworm.
> In its life, this worm (ovipar) develops from:
egg
larva
worm.
> Its egg is oval, assymetry, that contains embrio.
> This worm has lateral ala cephalic in anterior tip.
> One female worm can produce 11.000 eggs in one
day.
> The female worm will die after producing eggs.
> The male worm will die after copulation.
B.
LIFE CYCLE of Enterobius vermicularis
Female & male worms do copulation in cecum & around
(appendix, ascending colon & ileum)
Pregnant female worms migrate at night & produce eggs in anus
& around (anal area)
After several hours, eggs become mature & infectious, then come to
host, via:
air (person inhalates)
with
scartching anal area)
food (person eats food
infectious hand after
Eggs crack in duodenum & larvas appear
Larvas become mature (be worm) in ileum
Enterobius vermicularis
C.
SPREADING
> Cosmopolite (spread around the world), especially in
children.
D.
PATHOLOGY & CLINIC
> The worm causes disease, called enterobiasis.
> This disease has clinical symptoms:
- Ithcing in anal area (pruritus ani) at night.
- In girl, this disease can make inflammation in
fallopian
tube (salpingitis).
- Intestine is seldom disturbed, etc.
Enterobius vermicularis
E.
DIAGNOSIS
> Scotch adhesive tape swab method, is done before
taking a bath or defecating.
F.
TREATMENT
> Mebendazole, thiabendazole, etc.
G. PREVENTION
> Washing hand before eating
> Cutting long fingernail, etc.
Trichinella spiralis
A.
MORPHOLOGY
> Trichinella spiralis = porkworm.
> In its life, this worn (vivipar) develops from larva
worm.
> Its larva can become cyst (circular larva which is
covered by
hyaline capsule).
> This worm has stylet mouth to invade intestine or
muscle tissue.
> One female worm can produce about 1.350-2.000
larvas.
> The male worm will die after copulation.
B. LIFE CYCLE of Trichinella spiralis
Female & male worms do copulation in mouse/pig/person duodenum to
cecum
Pregnant female worms enter to intestinal villi and then lymphatic sinus
Pregnant female worms bear larvas in lymphatic sinus
Larva is brought by lymphatic flow, to thorachic duct, right heart, lung,
left heart, and then to around body
Host (person/pig/etc) can die
Larva enter to mouse/pig/person muscle tissue & make cysts (larva can
live until 30 years in muscle)
Health person eats meat (pig muscle) before cooked perfectly
Cyst wall rupture & larva release & larva become mature (be worm) in
health person duodenum
The worm can also pass placenta & mammary
Trichinella spiralis
C.
SPREADING
> Cosmopolite (spread around the world).
D.
PATHOLOGY & CLINIC
> The worm causes disease, called trichinosis.
> There are 3 clinical stadium:
- Intestinal invasion that is done by worm (1-2 days
after
eating infectious muscle).
- Larva migration (7-28 days after eating infectious
muscle).
It results cerebral disturbing, cardiac
distrubing, fever, even
die.
-Forming cyst & healing process (90 days after eating
infectious muscle).
BLOOD AND TISSUE
NEMATODE
THERE ARE THREE GROUPS :
— Filaria dan Dracunculus
— Larva Migrans (TROPICAL MEDICINE)
— Rarely found nematode (LESS
IMPORTANT !)
FILARIA
LIFE CYCLE
 Insect as a vector : Anopheles, Aedes,
Mansoni, Culex juga Simulium, Chrysops
atau Culicoides
 Habitat : blood, lymph, muscle, conective
tissue, serous cavity
BLOOD AND TISSUES NEMATODE
Filaria – caused Filariasis
TOPICS
(As problem of Public Health in Indonesia)
 Wuchereria bancrofti
 Brugia malayi
 Brugia timori
All species above – nocturnal periodicity
LIFE CYCLE OF FILARIA
 In the human body, found stages :
– Adult filaria – lymph node and vessel, difficult to find – not important
– Microfilariae – pralarvae stage – in the peripheral blood – important for diagnostic
 Microfilariae, must be attention about :
– Morphology for identified species of filaria
– Periodicity for chose right time for take blood
 Periodicity – when microfilariae found in most number :
– Nocturnal Periodicity – only in the night
– Subperiodic nocturnal – in the night more number than in the daytime
– Diurnal Periodicity – only in the daytime
– Subperiodic diurnal – in the daytime more number than in the night
– Nonperiodic – same number in the daytime and in the night
MORPHOLOGY OF MICROFILARIAE

Appearance graceful or stiff

Sheathed, its clear in part of the head or the tail (the three of
them are sheathed)

“Nuclei” in the body : spread in average or in groups, show in
the part of :

Head – without nuclei, named cephalic space, compare its length
with its wide

Tail, contain the nuclei or not
PRIMARY CAUSE
 Wuchereria bancrofti
 Brugia malayi
 Brugia timori
Life Cycle of B. malayi
LYMPHATIC FILARIASIS LIFE CYCLE
Adult worm
Microfilariae
HUMAN
BODY
Infective larva (L3)
MOSQUITO
BODY
Larva L1
Larva L2
Mansonia, Anopheles,
Culex, Aedes
MAIN MOSQUITO VECTORS
 W. bancrofti  Anopheles sp
 B. malayi  Mansonia sp
 B. timori  An. barbirostris
Wuchereria bancrofti
Habitat and Distribution
HABITAT
Vessel and lymph node
(bellow the diaphragm)
Can live 10-18 years
Microfilaria in blood,
penetrate placenta
3 times metamorfosa
DISTRIBUTION :
 Urban bancroftian filariasis, vektor
Culex fatigans
 Rural bancroftian filariasis, vektor
Aedes, Anopheles dan Mansoni
Wuchereria bancrofti
Periodicity
PERIODICITY (WHO, 1967)
 Commonly nocturna, also in Indonesia
 In Polynesia, subperiodic diurna, vector
Aedes polynisiensis
Wuchereria bancrofti
Clinical
DIVIDED IN :
 Biologic incubation
periode
 Asymptomatic periode
 Acute stage
 Chronic stage
 Biologic incubation periode asymptomatic, amicrofilaremi
larva - microfilaremi (± 1 year)
 Asymptomatic Periode asymptomatic, microfilaremi

symptom (-), microfilaria (+),
especially in endemic area
Wuchereria bancrofti
Clinical
 Acute stage - symptomatic, microfilaremi
 Acute alergic filarial lymphangitis
– Lymphangitis, limphadenitis (±)
– Filaria fever, alergic symptom (±)
 Chronic stage - symptomatic, microfilaremi
— Elephantoid tissue formation at lower extremity
and scrotum
— Adult worm die : microfilaria reduce
PERIODICITY





Nocturnal Periodicity
Sub periodic nocturnal
Diurnal Periodicity
Sub periodic diurnal
Non periodic
All 3 species have nocturnal periodicity
Clinical manifestation




Acute filariasis
Chronic filariasis
Atypical presentation
Asymptomatic carrier
Chronic manifestations:
Pathology
Adult worm
Host response
Reticular cells hyperplasia
Worm factors?
Dilatation of lymph vessel
Granulomatous reaction with giant cells,
histocytes, epitheloid cells
Dysfunctional valve
Retrograde lymph flow
Transient oedema
Thrombosis & inflammatory reaction
Healing with re-canalization
Dying worms
Intense inflammatory reaction with
granuloma formation
Healing with fibrosis
Loss of architecture & complete obliteration
Elephantiasis & other chronic
manifestations
Secondary
bacterial
infection
Lymphatic vessel dilatation, valve
incompetency, lymphatic back flow,
pooling & oedema
Brugia malayi
LIFE CYCLE AND PERIODICITY
• Definitive host : human, monkey, dog,
cat
• In vector 6-8,5 days, 2 times metamorf
Nocturna, vector Anopheles barbirostris
(farm)
Subperiodic nocturna, vector Mansonia
uniformis, M. indiana (swamp)
Brugia malayi
CLINICAL, THERAPY AND PREVENTION
CLINICAL:
 Main symptom : fever, limphangytis,
limphadenitis
 Elephantiasis : lower extremity bellow knee,
elbow,inguinal, rarely scrotum
THERAPY :
 Hetrazan, po 0,1 gr, 3-4 x/day, as long as 10 days
PREVENTION :
 Pentachlorophenol (dowicide G), kill water plant
Pistia stratioides, Eichornia, Salvinia
Example from Thailand
ELEPHANTIASIS by B. malayi
Not involving external genitalia
Courtesy Prof. Radomyos P. Mahidol U.
Example of filariasis from Malaysia
Filariasis Case at Pusat Pencegah
Penyakit Untut – Kepala Batas
Filariasis research - IMR
Blood Trematoda
(Schistosoma sp.)
There are four species of schistosome
which are infective to humans:
 Schistosoma mansoni, found in Africa,
Brazil, Venezuela, Suriname , Puerto
Rico, and the Dominican Republic.
 Freshwater snails of the Biomphalaria
genus are an important host for this
trematode.
 S. japonicum whose common name is
simply blood fluke is found widely
spread in Eastern Asia and the
southwestern Pacific region. In Taiwan
this species only affects animals, not
humans. Freshwater snails of the
Oncomelania genus are an important
host for S. japonicum.
 S. mekongi is related to S. japonicum and
affects both superior and inferior mesenteric
veins. S. mekongi differs in that it has
smaller eggs, a different intermediate host,
and longer prepatent period in the
mammalian host.
 S. haematobium, commonly referred to
as the bladder fluke, originally found in
Africa, the Near East, and the
Mediterranean basin, was introduced into
India during World War II. Freshwater
snails of the Bulinus genus are an
important host for this parasite
 Schistosoma mansoni causes intestinal
schistosomiasis
 Schistosoma haematobium causes
urinary schistosomiasis
 Schistosoma japonicum and
Schistosoma mekongi cause Asian
intestinal schistosomiasis
HABITAT
 S. Haematobium  Venous vessel (Vv)
of urinary bladder, colon; Hepar
 S. Japonicum  Vv. of intestine; Hepar
 S. Mekongi  Vv. of intestine; Hepar
 S. Mansoni  Vv. of Colon, Rectum;
Hepar
EPIDEMIOLOGY
Disease of schistomiasis or bilharzasis in
Indonesia only schistomiasis japonica found
in middle sulawesi, relate to agriculture
getting water from irrigation.
Group of age hit by between 5-50 year.
Mass treatment every 6 month.
S. japonicum
 The S. japonicum worms are yellow or
yellow-brown. The males of this species
are slightly larger than the other
Schistosomes and they measure ~ 1.2cm
by 0.5 mm. The females measure 2cm by
0.4 mm. The adult worms are longer and
narrower than the related S. mansoni
worms.
S. japonicum
 This Parasite at human being cause
oriental of schistosomiasis,
schistosomiasis japonica, katayama
fever or Snail Fever disease
Katayama Fever
 Acute schistosomiasis (Katayama's fever) may
occur weeks after the initial infection,
especially by S. mansoni and S. japonicum.
Manifestations include:
 Abdominal pain
 Cough
 Diarrhea
 Eosinophilia
 Fever
 Fatigue
 Hepatosplenomegaly

Faeces with egg of s. JAponicum have contact with water

Those egg will hatch and release free-swimming larva called Miracidia

Miracidia will infect Oncomelaria hupensis by penetrating their skin

Inside the snail they will undergo asexual reproduction, and will become
sporocysts

Further reproduction will produce large number of Cercaria, which is freeswimming larva

Cercaria can infect us by penetrating our skin

After penetration, they will loose their tail and become Schistosomule

Enter circulation, and end at the mesenteric veins

There, they will undergo sexual reproduction and produce egg

Egg will penetrate the tissue and are passed with the faeces
S. mansoni
 The male S. mansoni is
approximately 1 cm long (0.6
to 1.4 cm) and is 0.11 cm
wide. It is white and it has a
funnel-shaped oral sucker at
its anterior end
 The female has a cilindric
body, longer and thinner than
the male (1.2 to 1.6 cm long
by 0.016 cm wide). The female
parasite is darker and it looks
gray. The darker color is due
to the presence of a pigment
(hemozoin) in its digestive
tube
CLINICAL SYMPTOM AND PATHOLOGY
Similar with S. japonicum, but it
is lighter
MORPHOLOGY AND LIFE CYCLE
Adult Worm of fairish male about 1,3
cm and female about 2,0 cm. its life in
small vena flank. Egg found in urine,
and rectum genitals
Pathology
 It can break the wall of the urinary bladder
 The most characteristic symptom is
haematuria.
 Dysuria also can occur.
 Inflammatory reaction to eggs in the bladder
wall and later fibrosis and calcification often
leads to mucosal hyperplasia and papilloma
formation
 In Egypt vesical schistosomiasis has been
considered a common cause of malignancy
of the bladder in male agricultural workers
Lab Diagnosis
 Microscopic identification of eggs in stool or urine is
the most practical method for diagnosis
 Stool examination should be performed when infection
with S. mansoni or S. japonicum is suspected, and
urine examination should be performed if S.
haematobium is suspected. Dark urine is a significant
clinical sign of urinary schistosomiasis
 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.
 The eggs of S. haematobium are ellipsoidal with a
terminal spine, S. mansoni eggs are also ellipsoidal
but with a lateral spine, S. japonicum eggs are
spheroidal with a small knob.
Treatment
 Schistosomiasis is readily treated using
a single oral dose of the drug
Praziquantel
Prevention
 The main focus of prevention is eliminating the
water-borne snails which are natural reservoirs for
the disease. This is usually done by identifying
bodies of water, such as lakes, ponds, etc., which
are infested, forbidding or warning against
swimming and adding niclosamide, acrolein,
copper sulfate, etc., to the water in order to kill the
snails.
 Individuals can guard against schistosomiasis
infection by avoiding bodies of water known or
likely to harbor the carrier snails
Liver Trematodes
 Clonorchis sinensis
 Dicrocoelium dendriticum
 Opistorchis felineus
 Opistorchis viverini
 Fasciola hepatica
Clonorchis sinensis
Epidemiologiy
- China, Japan, Korea, Taiwan, Vietnam
Habitat
- Biliary tract, pancreatic tract
Host
- definitive : human, cat, dog
- vector 1 :
Water snail genus of Bulimus, Thiara, or species
Melanoides tuberculatus
- Vector 2 :
Fish family of
Cyprinidae, Salmonidae,
Gobiidae, Anabantidae
Morphology
- Elongated, flat,
transparent, bulging
on posterior
- Oval egg, thickened
on posterior, found
within faeces
LIFE CYCLE
Eggs within
Mirasidium
faeces
(cilliated larvae)
Swallowed by vector1
(water snail)
Sporocyst
Mating  Eggs
Redia
Grow mature in
biliary tract
Cercaria
Swallowed by
Crossing fish (vector2)
skin 
definitive host
forming metascercaria
(cyst) in fish skin/muscle
Metacercaria
Diagnosis
- Eggs within faeces
- Immunology diagnosis
Prevention
- Avoid eating raw fish  must be completely
cooked
Dicrocoelium dendriticum
Epidemiology
- Cosmopolite for lamb & other herbivores in Asia,
Africa, Europe & America
Morphology
- Mature form: flat, slender
- Eggs: dark brown, thick wall, contain completelygrown mirasidium
Host
- Definitive: lamb
- Vector 1: snail genus of Abida, Zebrina
- Vector 2: ant, species Formica fusca
Life Cycle : comparable to C. sinensis
Fasciola hepatica
Epidemiology



Is the first
trematode found
Causes fasciolatic
hepatic
Is cosmopolite
mainly in country
with large farm
(mostly sheep),
infection in human
often happens in
Cuba, France,
England, and
Aljazair.
Habitat and host




Habitat is mainly in billiary duct, may
penetrate hepatic tissue causing abses.
Definitive hosts are human, sheep and
other cattle.
Intermediate host I is family Lymnaeidae,
especially genus Lymnaea.
Intermediate host II is water plants
especially Nasturtium officinale.
Morphology





Big size, 30 x 13 mm
Integuments is scaly
Posterior end without thorn
Unique shape, like shoulder because it
has kerucut kepala
Batil isap kepala (1 mm) and stomach
are almost same in size and adjacent
 Caecum is hyper branching until posterior
end
 Hyper branching testis is lied between 2/4
– ¾ posterior body, one is behind the
other
 Ovary branches, anterior to testis and
smaller
 Uterus is short, curved, located between
ootype and porus genital.
 Egg is 130-150 x 63-90 µ in size and has
operculum. Immature eggs are lied in
billiary duct and exit with feces.
Life cycle
Eggs are expelled within feces
Eggs mature in water
and hatch after 9-15 days
at optimum temperature 22-250C
Hepatic tissues are infiltrated
with eggs, immature eggs
are lied in billiary duct
Penetrate Glisson’s capsule,
hepatic tissue, then into billiary duct
in 12 weeks in adult
Miracidia enter
intermediate host I and develop
to become sporocysts, rediae I,
rediae II in 3 weeks , and cercariae
Penetrate intestinal wall,
Enter peritoneal cavity
Cercariae move toward
Intermediate host II
Metacercariae exit
the cyst in duodenum
At night, in 8 hours,
become metacercariae
Metacercariae penetrate
definitive hosts
Clinical Symptom
 Until metacercaria penetrate Glisson’s capsule,
these is no complain. But trauma and necrotic
lesion rise during migration through hepatic
tissues.
 In heavy infection, epithelia is scraped and
young worm will return to hepatic parenchyma,
form abscess pouch, and hepatic tissues are
infiltrated with eggs.
 When larvae migrates to peritoneal cavity, focus
ectopic may happen in blood vessel, lungs,
subcutaneous tissue, brain ventricles, and eyes
where abscess will be formed.
 Symptoms : colic, ikterus obstructiva, cough and
vomiting, abdomen rigidity, acute epigastria pain,
leukocytosist and eosinophily until above 60%
Diagnosis
 Eggs are found in feces, duodenal fluid, or
bile. Patient, who will be examined, do not
eat liver.
 Need early diagnosis to prevent fatal liver
damage.
 Serodiagnostic test is very helpful, although
it is not an routine diagnostic tool.
Prevention
 Treating patient and cattle that act as
reservoir.
 Incinerating water snails.
 Cooking vegetables that will be eaten.
Lung Trematode
 Paragonimus westermani
 Disease : Paragonimiasis ,
Pulmonary distomiasis
Paragonimus westermani

Epidemiology
– It is cosmopolite in
human, mainly east
in Japan, Philippine,
Korea, China,
Muangthai, Taiwan,
Africa, etc.
– In Indonesia, it is
autochthon infection
in animal. In human,
as import case.
Host
 Definitive hosts are human and mammalians
such as dog and cat
 Intermediate hosts I are Semisulcaspira
libertina (Japan), Brotia asperata (Philipina),
B. costula episcpalis (Malaysia), Syncera sp.,
and Melania.
 Intermediate hosts II are freshwater crabs
genus Potamon, Eriocheir, Sesarma sp., and
crayfish.
Life cycle
From the pouch, eggs
go out to bronchioles
Then, they are coughed
with sputum or swallowed
and expelled with feces
Hatch in water after
maturation (2-3 weeks)
In intermediate hosts I,
miracidia become Rediae I,
Rediae II, and finally cercariae
In intermediate hosts II,
cercariae become metacercariae
in 5 months
Sometimes, into ectopic place
like mesentery, pleura or brain,
and reach adulthood here
In 3-6 hours, enter abdominal cavity
and penetrate abdominal wall, stay
for several days before penetrating diaphragm,
to pleural cavity and enter bronchioles
In duodenum, encystations happens,
penetrate intestinal wall (in 30-60 minutes)
Metacercariae penetrate
definitive hosts
Clinical signs and pathology
 Around parasite, leukocyte infiltration happens
and is followed by forming fibrosis capsule and
form cyst containing 2 worms, purulent blood,
and eggs.
 Lungs : (1) nonsuppurative, (2) tubercle-like, (3)
suppurative, (4) ulcerative.
 First fever, shaking chills, dry cough, then
hemaptoe with sticky and rush-colored sputum
mainly when wake up in the morning.
 Physical examination reveals a
bronchopneumonia or bronchiectasi with
pleural effusion.
Diagnosis
 Finding eggs in sputum, aspiration
pleural fluid, and feces
 Serology test with intradermal test,
complement fixation test.
Treatment and Prevention
TREATMENT
- Praziquantel
PREVENTION
 Treating patients
 Cooking crab before being eaten
 Cestodes are members of phylum
Platyhelminthes, also known as
tapeworms.
General morphology
 Scolex : organ of attachment,usually
bearing suckers or hooks
 Neck : part which it grows
 Strobilla : the boby, consist of
proglotids (segments)
 Proglotids
Immature :segment that is
attached to
the neck
Mature : has a reproductive
structure
Gravid (pregnant): filled with eggs.
Tegument: covers adult cestode, allows
materials to enter and
be excreted from
waste to
the body
 Hermaphrodite, each proglotid has a male
and female reproductive structure.
• Is not yet found in Indonesia
• Resides in ileum of human, dogs, and
cats
Morphology
• Adult worm 3 – 10m, can be as long as
60m, with 3000-4000 proglotids.
• In the place of sucker or hooks, are two
shallow sucking grooves called bothria.
• Operculated eggs
LIFE CYCLE
• Adult tapeworms resides in
ileum. Self fertilization will
occur and eggs are produced
• Unembryonated eggs is
release with feces.
• eggs will develop into
onchosphere which contains
a ciliated embryo.
• egg disintegrate releasing
the ciliated embryo ,
• Coracidium
is eaten
coracidium,
larva stage
I. by copepod, and inside it will develop to larva stage
II called procercoid.
• If copepode is eaten by fish, procercoid will penetrate into fish’s muscle,
and develop to larva stade III called plerocercoid/sparagnum.
• human will be infected by this larva. It will attach to mucous membrane
of intestine and developes into adult tapeworms.
Pathogenesis
Disease: diphyllobothriasis
Usually asymptomatic, can cause abdominal
pain, weight loss, diarrhea, vomiting,deficiency of
vit B12.
Diagnosis
Eggs or proglotids found in feces.
Treatment
Niclosamide, praziquantel, bithionol, atabrin
Prevention
Avoid ingestion of undercooked fish
• Also called porkworm and resides in
jejenum of human.
• Larva is known as cycticercus celullosae
10 x 5 mm. usually inhabit the muscle.
Morphology
• Adult worm is 2 – 4m
• Has a rostellum with two rows of hooks
plus four suckers.
• Genital pores located lateral to proglotids.
• Eggs doesn’t have opperculum, but
contains onchosphere.
L i f e cycle
 Eggs are digested out in the stomach of the pig.
 Using its hook and lysis substrate, the
oncosphere will then penetrate intestinal wall
into blood stream and reside in muscle forming
cysticercus celullose.
 Human will be infected by digestion of
undercooked pork.
 The larva will attach inside the small intestine,
and develop into adult tapeworms that can
produce eggs.
 These eggs will then pass through feces
Pathogenesis
• Disease: cysticercosis
• Most cases are asymptomatic.
Diarrhea, abdominal pain may occur.
• If cysticercus migrate to brain, can cause
neurocysticercosis. Headaches, seizures, even
death can occur.
Diagnosis
Gravid proglotids or egg in feces, CT scan, MRI.
Treatment
Praziquantel and niclosamide, also surgical
removal.
• Also known as beef
worm.
• Larva is called
cysticercus bovis,
Morphology
• Adult beefworm is
5m,but can grow as
far as 25m
.
• Has four suckers,
but no hooks.
Hymenolepsis diminuta
 Habitat
small intestine
 Definitive hosts
rats, also common in humans
 Intermediate hosts
grain beetle or flea
 Epidemiology
cosmopolite, found in Indonesia
Hymenolepsis diminuta
 Morphology
Adult worms 10-60 mm long, 3-5 mm
wide, have 800-1000 proglotids.
Rounded scolex bears a small rostellum
with four suckers, proglotid 0,8 mm long
and 2,5 mm wide.
Eggs without the polar filaments, sized 6080μm.
Tapeworm
matures in
small intestine
Ingestion of
arthropod host
containing
cysticeroid larvae
Adult worms in
small intestine
Life cycle
Development of
cysticeroid
larvae
Infective embryonated
egg in feces
(diagnostic stage)
Ingestion by
Arthropod host
Hymenolepsis diminuta
 Transmission
Transmission or infection occurs by
ingestion of infected beetles or other
arthropods, usually in grains and cereals
 Pathogenesis
Symptoms, if any, are mild, and usually
include diarrhea, nausea, and slight
abdominal pain
 Diagnosis
Recovery of characteristic eggs in feces
Hymenolepsis diminuta
 Treatment
Niclosamide, Praziquantel
 Prevention
Limit exposure of grains and cereals to
rats and insects.
Dyphilidium caninum
 Synonym
Double-pore dog tapeworm
 Definitive hosts
Cats and dogs,,, also found in humans’
small intestine.
 Intermediate hosts
Dog/cat flea; Ctenocephalides canis and
C.felis.
Dyphilidium caninum
 Morphology
Adult tapeworm is 10 to 50 cm in length. Several rows
of tiny hooklike spines are present on the coneshaped rostellum.
The uterus in the gravid proglottid contains numerous
packets of eggs, each packet containing 5 to 20 eggs.
Colorless eggs ~ 30-60μm in diameter, with a six
hooked oncosphere present in each egg.
The eggs are enclosed in membrane-bound packets.
Dyphilidium caninum
 Transmission
Infection after ingestion of cysticeroid larvae.
 Pathogenesis
Most of infected individuals are asymptomatic,
although some with a heavy worm burden may
experience mild gastrointestinal symptoms,
such as nausea, diarrhea, indigestion, and
slight abdominal pain.
Scolex
attaches to
intestinal wall
Tapeworm
matures in
small intestine
Human
host
Ingestion of
flea containing
cysticeroid larvae
Life cycle
External
environment
Development
of
cysticercoid
larvae
in flea
Ingestion by
dog/cat flea
Gravid
proglottids or
packets of eggs
Dyphilidium caninum
 Diagnosis
Recovery of characteristic gravid proglottids and
egg packets (following rupture of proglottids) in
human feces.
 Treatment
Niclosamide, Praziquantel.
 Prevention
Good veterinary care of cats and dogs, keeping
animal freely from parasites.
Good personal hygiene.
Hymenolopsis nana
 Morphology:
 smallest tapeworm, 25-40mm, found in mice and other
rodents, doesn’t need intermediate host
 the scolex bears a short rostellum with one row of hooks,
along with four suckers
 proglottids 2 mm wide and 1mm long
 Sac-like gravid uterus is usually full of eggs
 Egg: round to oval thin-shelled, 30-45 micrometer, contains
an inner envelope with two polar thickenings, each having
four to eight filaments, which extend into the space within
the shell
Hymenolopsis nana
 Transmission: Infection is usually
transmitted by ingestion of infective eggs.
Although most cases are asymptomatic,
mild gastrointestinal symptoms, such as
diarrhea, abdominal pain, and weight may
occur
Hymenolopsis nana
 Laboratory Diagnosis:
recovery of
characteristic eggs in
human feces. Adult
worms and proglottids
are rarely seen in the
stool
Hymenolopsis nana
 Treatment and Prevention: Praziquantel is
the treatment of choice for infection with H.
nana. Niclosamide is also effective. Good
sanitary practices are essential in the
prevention of infection
Echinococcus granulosus
 Morphology: hydatid tapeworm, 4 mm in
length, scolex bearing four suckers,
numerous hooks, and three proglottids
 Eggs: although not found, but it is identical
to those of Taenia species
Echinococcus granulosus
 Transmission and Pathogenesis
Ingestion of eggs, usually by hand-to-mouth contact with
infected dog feces. Symptoms vary, depending on the
location of the cyst in tissue. Although cysts may form in
many areas of the body, the lung and the liver are most
commonly affected. Pulmonary symptoms, such as
cough and chest pain, may develop with lung infection.
One serious complication of hydatid cyst disease is the
risk of anaphylactic shock, following rupture of the cyst.
Echinococcus granulosus
 Laboratory Diagnosis:
The eggs are not found in human feces. The
diagnosis of hydatid cyst disease may be made by
radiographic and serologic studies. A combination
of assays, including enzyme immunoassay and
immunoblot techniques, has been suggested ti
diagnose hydatid cyst disease. The demonstration
of hydatid sand is also diagnostic.
Echinococcus granulosus
 Treatment and prevention
Although surgical removal of hydatid cyst
has long been considered the treatment
of choice, several antihelminthic agents
are now available. These include
praziquantel and mebendazole. Infection
is also prevented by good personal
hygiene to prevent hand-to-mouth
transmission of eggs from dogs to
humans, avoidance of ingestion of sheep
viscera by dogs, and antihelminthic
treatment of dogs, as necessary