LECTURE NOTES ON

MEDICAL
HELMINTHOLOGY
 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
 CLASS
1. Nematoda
CLASSIFICATION 2. Trematoda
3. Cestoidea

HELMINTHES

NEMATHELMINTHES PLATYHELMINTHES

NEMATODES TREMATODES CESTODES

 NEMATODES CLASS
1. Nematoda
General characteristics 2. Trematoda
3. Cestoidea

The spesies 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
Inner body cavity (pseudocoelom)
 NEMATODES
General characteristics CLASS
1. Nematoda
2. Trematoda
3. Cestoidea

Have intestinal, reproductive, nervous and excretory

system
No circulatory system
Three stages : egg, larva and adult

Separate sex organs (male and femile) :

Male smaller than femile
Male commonly has a curved posterior end
 NEMATODES
CLASS
1. Nematoda
General characteristics 2. Trematoda
3. Cestoidea

Nematodes live as
1. The free-living, are widely distributed in water and
soil
2. The parasitic spesies, live in plants, mollusks,
annelids, arthropods and vertebrates
Over 80.000 spesies are parasite of vertebrate

Classification Based on
The existence of phasmid (a caudal chemo
receptor)
The habitat of the adult worm
 NEMATODES
General characteristics

Adult worm react to touch, heat, cold and probably to

chemical stimulus
Intestinal nematode maintain their positions :
By oral attachment to the mucosa Ancylostoma, Necator
By anchorage with there attenuated ends Trichuris
By penetration of the tissues Strongyloides
By retention in the folds of the mucosa and pressure against it -
Ascaris

The methods of obtaining food may be classed as

Sucking with ingestion of blood Ancylostoma
Absorpsion of lysed tissue by immbedded worms
Trichuris
Feeding on the intestinal contents Ascaris
Absorption of nourishment from the body fluids filarial
worms
 NEMATODES
Life cycle

Simple or complex live cycles within and without the

definitive host
Multiplication during the larval stages rarely occurs
In some genera (Strongyloides) beside as parasit it can
be the free-living phase for one or more generations
Most nematodes have only one host the larvae passing
from host to host directly or after free-living existence
 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 damaging by biting and bloodsucking,
by lytic ferment secreted by the parasite and by
mechanical irritation
 NEMATODES
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
Pathogenicity

The antigen-antibody combination :

Localize the irritating excretions and secretions of the parasite
Immobilize the parasite
Inhibit its physiologic activities
Retard its development
Some time destroy the parasite
The immobilized worms are surrounded by inflammatory
reaction
Eosinophils, which appear late in the immune reaction, are
probably associated with the detoxication of foreign protein
and form a barrier to absorption
The presence of the antibodies and tissue sensitization is of
practical importance in diagnostic serological and skin test
 NEMATODES
Classification based on Habitat

HABITAT

INTESTINAL BLOOD AND TISSUE

NEMATODES NEMATODES

SOIL TRANSMITTED FILARIA and

OTHER (NON-STH)
HELMINTHS (STH) DRACUNCULUS
 NEMATODES
Classification based on Habitat
Soil Transmitted Helminthes
Ascaris lumbricoides
Trichuris trichiura
Hookworm (Necator americanus, Ancylostoma
duodenale) Importanc
Strongyloides stercoralis e

Non-Soil Transmitted Helminthes

Enterobius vermicularis Importanc
Trichinella spiralis e

Filaria and Dracunculus

Wuchereria bancrofti
Brugia malayi
Brugia timori
Disease caused by Soil transmitted helminthes
DEFINITION Soil transmitted helminths :

NEMATODE WORMS WHICH REQUIRE

PERIOD OF DEVELOPMENT AND
MATURATION DURING ITS LIFE
CYCLE ON SOIL

IMMATURE INTO
INFECTIVE
 SOIL TRANSMITTED HELMINTHS
IN INDONESIA

Wet and humid tropical

Remain a public climate
health problem Lack of hygiene and
High prevalence sanitation
Very common and Because Low level of education
important disease and socio-economic
status
High population density
Poor life habit
 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
Infection by Ascaris lumbricoides
( ASCARIASIS )
DISTRIBUTION
Cosmopolitan
Prevalence 70-90 %
Primarily affects underfives and school
children

HABITAT
Lumen of the intestine :
Jejunum
Media ileum
 Infection by Trichuris trichiura
( TRICHURIASIS )
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)
 Infection by Hookworm
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

HABITAT
Small intestine (jejunum)
In heavy infection : duodenum, colon
 Infection by
Strongyloides stercoralis

HOST, HABITAT AND DISTRIBUTION

Man is the definitive Host

Habitat of female worm, mucosal
lining of :
Duodenum

Jejunum (proximal )

Found very cosmopolitan, especially

in the tropical and subtropical
region
 Ascaris lumbricoides
LIFE CYCLE
INSIDE THE HUMAN BODY
Ingestion of mature eggs Mature eggs
Ingested

Hatched in the gaster, Migration of larva

larva penetrates the wall inside the
of the intestine and enter circulatory system
into blood circulation
To the right heart Adults
Larva
chamber, into the lungs
Alveoli bronchioles - bronchus -
trachea - swallowed
Arrived in the intestine and
becomes mature adult
Source : Medical Parasitology in Plates
Piekarski G. Infertile eggs
 Trichuris trichiura
LIFE CYCLE

In human body
C

Eggs hatch
(Proximal intestine)

Maturation in soil (3-5 weeks)

Adult in colon, In Soil
especially in Caecum

Eggs in
Feces
 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 Immature
egg

In Soil
Infective larvae

Mature
Filariform larvae egg
Immature
egg
Rhabditiform larvae Hatch in soil
Strongyloides stercoralis
LIFE CYCLE
Life cycle in human body
A

Larvae exit from

Capillary, entered
Alveoli

Larvae enter
Lung

Adult in
duodenum, especially
Larvae entered Proximal duodenum
Blood stream

Filariform l arvae Rhabditiform l arvae

penetrate skin in Feces

Filariform larvae
Rhabditiform larvae
Infective stage
B in soil

Egg
Development

FREE LIVING Free living

CYCLE adult in soil

Rhabditiform
larvae

Life cycle in soil

 Ascaris lumbricoides
PATHOGENESIS AND CLINICAL SYMPTOMS
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
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
 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)
Infecion by 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
 Infection by 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
 Infection by 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
 Infection by 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, mental retardation
 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)

Patient
Glositis atrofik pada with atrophic glossitis
anemi hipokrom
also show fingernail
mikrositer yang
deformity (koilonichia)
disebabkan infection
Fingernail becomes thin and
berat HOOKWORM
Tampak lidah concave
halus with elevated ridge
dan kurang papila

source : Atlas Parasitologi Kedokteran, Zaman P. Alih Bahasa : Anwar C.; Mursal Y.
 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)
Ascaris lumbricoides
Diagnosis
Identify the eggs found in feces using
following methods :
Direct smear method
Concentration method
Sedimentation method
Identify larva found in sputum
Identify adult worm found expelled from
anus, mouth, nostril
Quantitative lab method to measure
level of infection
- Stoll method
- Kato Katz method
Additional : chest X-ray
Infection Trichuris trichiura
Diagnosis
Identify egg worm found in fecal
sample
Identify adult worm from prolapsed
rectum (by proctoscopy)
Measure level of infection by counting
Number of eggs per gram feces with Stoll
method and Kato katz method.
Number of female worm expelled through
deworming
Infection by HOOKWORM

Diagnosis
Identify eggs from feces sample
Identify larva from :
Fecal culture
Old feces sample
 Infection by
Strongyloides stercoralis
Diagnosis
Find and identify
Rhabditiform larva :
From fresh feces
Gastric (duodenal) juice
Eggs :
In heavy diarrhea
After administration of
laxative
 Ascaris lumbricoides
Mass treatment
BasedTreatment
on prevalence of
Drug available
Ascariasis 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
ASCARIASIS
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
PREVENTION
Treatment

Drugsavailable:
Elimination of source of infection
Improved
Oxantel pamoate personal hygiene (hand
Mebendazol (drugtoilet
washing, of choice)
training)
Through washing of sold
vegetables
Health education
Provision of sanitary public toilet
 HOOKWORM
ANTIHELMINTHICS
Tetrachlorethylen
Mebendazole
Albendazole
Pyrantel pamoate
Bitoskanate
Bephenium hidroxynaphtoate
PREVENTION
Same as with Ascariasis but
with the addition of :
wearing shoes during work
in plantation or mine area
 Infection by
Strongyloides stercoralis
TREATMENT AND PREVENTION

Drugs given
Thiabendazole
Mebendazole
Pyrvinium pamoate
PREVENTION for Strongyloidiasis
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 dont 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) food (person eats food with

infectious hand after scartching anal
area)

Eggs crack in duodenum & larvas appear

Larvas become mature (be worm) in ileum

 Infection by
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.
 Infection by
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).
 Infection by Trichinella spiralis
E. DIAGNOSIS
> Muscle biopsy
> Immunological diagnosis.

F. TREATMENT
> Thiabendazole.

G. PREVENTION
> Cooking meat (esp. pig muscle) perfectly
> Destroying mouse, etc.
 BLOOD AND TISSUE
NEMATODE
THERE ARE THREE GROUPS :
Filaria dan Dracunculus
Larva Migrans (TROPICAL MEDICINE)
Rarely found nematode :
- Angiostrongylus cantonensis
- Capillaria hepatica
- Gnatostoma spinigerum
FILARIA AND DRACUNCULUS

Wuchereria bancrofti
Brugia malayi
Brugia timori
Loa loa
Onchocerca volvulus
Acanthocheilonema
perstans
Mansonella ozzardi
Dracunculus medinensis
 FILARIA
LIFE CYCLE

Insect as a vector : Anopheles, Aedes,

Mansoni, Culex juga Simulium, Chrysops
atau Culicoides
Habitat : blood, lymph, muscle, conective
tissue, serous cavity
 GENERAL LIFE CYCLE OF FILARIAE

MALE & FEMALE

ADULT WORM IN TISSUE

LARVAE MIGRATE TO
FINAL LOCATION AND FEMALE
DEVELOP TO ADULT PRODUCE
MICROFILARIAE

MICROFILARIAE
HUMAN INFECTED
TO BLOOD
WHENVECTOR BITES
OR SKIN

HUMAN

INFECTED LARVAE VECTOR MICROFILARIAE

IN VECTOR INGESTED BY VECTOR

DEVELOPMENT
IN VECTOR
 FILARIA

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
Lymphatic filariasis

Wuchereria bancrofti
Brugia malayi
Brugia timori
Life Cycle of B malayi
 THE DEVELOPMENT IN THE MOSQUITO : 10 12 DAYS
MICROFILARIAE APPEAR IN THE BLOOD :
Wuchereria bancrofti : minimum after 8 months
Brugia malayi : minimum after 3 months
THE ADULT MAY LIFE AND PRODUCE MICROFILARIAE FOR
MORE THAN 18 YEARS
LIFE SPAN OF MICROFILARIAE APPROXIMATELY 1 YEAR
LYMPHATIC FILARIASIS LIFE CYCLE
Adult worm

Microfilariae
HUMAN
BODY

MOSQUITO
Infective larva (L3) BODY
Larva L1

Mansonia, Anopheles,
Larva L2 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 10-20 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
 TROPICAL PULMONARY EOSINOPHILIA

IS A SYNDROME OF IMMUNOLOGICAL HYPERRESPONSIVENESS TO

MICROFILARIAE IN THE LUNGS
IS A CLASSICAL EXAMPLE OF OCCULT FILARIASIS; Filarial Infection
where Microfilariae are not found in the Blood
Male more common than in Female
Microfilariae are absent from the blood but have been
Recognized in Lung biopsies and adult worms have been seen
on Ultrasonography
 TROPICAL PULMONARY EOSINOPHILIA

Clinical

PAROXYSMAL COUGHING AND WHEEZING THAT IS WORSE

AT NIGHT
EOSINOPHIL COUNTS ABOVE 3000 CELLS/MM3 OF BLOOD
EXTRAPULMONARY MANIFESTATIONS OCCUR
SPLENOMEGALY
LYMPHADENOPHATY
HEPATOMEGALY
 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

 SPECTRUM OF CLINICAL MANIFESTATIONS OF
LYMPHATIC FILARIASIS IN ENDEMIC AREAS

CHRONIC TROPICAL
ASYMTOMATIC FILARIAL
NONE LYMPHATIC PULMONARY
MICROFILAREMA FEVER
PATHOLOGY EOSINOPHILLIA
 Grading of lymphoedema

Grade 1
Reversible pitting
oedema
 Acute manifestations
Characterised by recurrent attacks of fever
associated with inflammation of lymph nodes
(adenitis) and /or lymph vessels
(adenolymphangitis, ADL)
Involvement of genitalia lymphatic in male
funiculitis, epididymitis or orchitis
Lasting for 4-5 days
Repeated episode important in the progression
of disease
 Acute manifestation: ADL
Acute Filarial Lymphangitis
Cord-like structure with retrograde lymphangitis:
painful, red and tenderness
Systemic reaction mild, distal oedema rare
Recurrent at same site common
ADL with secondary bacterial infection
Most common form of ADL
Associated with fever, chills, myalgia and headache
Cellulitis and oedematous, subside after each attack
Acute adenolymphangitis
(ADL)
Subcutaneous abscess may form and
rupture releasing chylous fluid
 Chronic manifestation
Major signs
Hydrocoele
Chyluria
Rupture of lymphatic lining the bladder leading to passage of
lymph in the urine
May resolve spontaneously
Lymphocytes in urine
Lymphoedema
elephantiasis
 Chronic manifestation
Major signs
Hydrocoele
Chyluria
Lymphoedema
Swelling due to collection of lymph fluid in soft
tissue
Pitting oedema, may or may not be reversible
Thickened skin
elephantiasis
 Chronic manifestation
Major signs
Hydrocoele
Chyluria
Lymphoedema
Elephantiasis
Irreversible, non-pitting oedema with fibrotic and
verrucous skin changes (thickening, folding,
hyperkeratosis, pigmentation, ulceration)
Skin & soft tissue infection common
 Grading of lymphoedema

Grade 2
Irreversible oedema
No skin changes
 Grading of lymphoedema

Grade 3
Irreversible oedema
Skin thickened
 Grading of lymphoedema

Grade 4 (5,6 & 7)

Irreversible oedema
Skin thickened,
fibrotic & verrucous
changes
(elephanthiasis)
 Chronic manifestation

Only a small proportion of filarial-infected

population affected
Immigrants tend to develop chronic manifestation
more often and sooner than indigenous people
Occurrence of major signs differ between places
 Chronic manifestations: Pathology
Adult worm
Host response Reticular cells hyperplasia
Worm factors?
Thrombosis & inflammatory reaction
Dilatation of lymph vessel
Granulomatous reaction with giant cells,
Dysfunctional valve histocytes, epitheloid cells
Retrograde lymph flow
Healing with re-canalization

Transient oedema Dying worms

Intense inflammatory reaction with
granuloma formation
Healing with fibrosis
Secondary
Loss of architecture & complete obliteration bacterial
infection
Elephantiasis & other chronic
manifestations
 Lymphatic vessel dilatation, valve
incompetency, lymphatic back flow,
pooling & oedema
 Asymptomatic Microfilaraemic

Microfilaraemic carrier
No sign and symptom of infection
Source of infection to others
Evidence of sub-clinical infections:-
40% with sub-clinical hematuria/proteinuria: low grade
renal damage. Complete reversal after clearing Mf
Lymphoscintigraphy: markedly dilated, tortuous lymphatics
and abnormal lymph flow
 Secondary bacterial infection of chronic
lymphoedema

Commonest cause of morbidity in

lymphatic filariasis
Recurrent attack of lymphadenitis,
lymphangitis and cellulitis
May last for more than 1 weeks,
5-6 times a year
Unable to work, going to school
 Cause
Chronic swelling, lost of skin
architecture
Crack and fissures, point of entry
of bacterial
Poor hygiene aggravate the
situation
 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
 Brugia malayi
ELEPHANTIASIS BY B. malayi

Not involving external genitalia

Sumber : Atlas of Medical Parasitology. Radomyos P., dkk.
 Brugia timori

With giemsa, sheath not clear

Size longer than B. malayi
Vector : Anopheles barbirostris (sawah)
Lesi mild/moderate at lower extremity
bellow the knee
Reservoir host is not found
 Loa loa
Etiologic agent of loiasis
Adult worms actively migrate throughout the
subcutaneous and deep connective tissue
Vector is the day-bitting mano fly, amember species of
Chrysops.
Life cycle:
- adult male 20-35 mm long, 0.5 mm wide
- adult female longer, 50-70 mm length
 Human eye

Adult worms migrate in Female produces

subcutaneous tissue, causing microfilaria which circulate
transient Calabar swelling in the blood stream

Infective larva penetrates skin Microfilaria ingested by

after being deposited during mango fly during blood
bite and develops to maturity in meal; develops into
subcutaneous tissue. infective larvae

Chrysops
 Onchocerca valvulus
Causes onchocersiasis or river blindness
Intermediate host and vector blackfly or buffalo gnat (genus Simulium)
Since microfilariae are found in the skin, the specimen of choice for the
diagnosis of onchocersiasis is a skin biopsy or skin snip.

Infective larva actively Microfilaria ingested by

penetrates skin after being black fly during blood meal
deposited there when fly bites develops into infective
larva

Female produces worm-like

Develops to maturity in unsheathed eggs (microfilariae)
subcutaneous tissue which are found in skin

Adult female worms live in

subcutaneous nodule
Male worms migrate in
subcutaneous tissues
 DIAGNOSIS

1. CLINICAL DIAGNOSIS
2. PARASITOLOGICAL DIAGNOSIS
Blood Specimen should be obtained at the time or the day
when the peak concentration of microfilariae is expected
3. IMMUNOLOGICAL AND POLYMERASE CHAIN REACTION
(PCR)
4. ULTRASONOGRAPHY
 TREATMENT
DEC :
Microfilaricidal Host are Eliminated
Adult Some are Eliminated
INVERMECTIN (MECTIZAN)
Microfilaricidal Host are Eliminated
Adult No Effect

DEC per oral

6 mgr/Kg BW/day. In there devided doses after food for 12 days
Treatment must be repeated every 6 months for as long as the
person remains Microfilaraemic or has Symptoms
 TREATMENT

ANTIFILARIAL DRUGS
Diethylcarbamazine citrate
(DEC, HETRAZAN, BANOCIDE, NOTEZINE)
DEC :
Is a Microfilaricidal agent also capable of Killing a
Proportion of the Adult Wuchereria bancrofti,
Brugia malayi, and Brugia timori
INVERMECTIN (MECTIZAN)
Is a Potent Microfiraricide but has no Microfilaricidal
effect
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.
(Oncomelania hupensis linduensis )
 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 EGGS 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 free-

swimming 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
Swallowed by vector1
EGGS within MIRACIDIUM
(water snail)
faeces (cilliated larvae)

SPOROCYST
Mating EGGS

REDIA
Grow mature in
biliary tract
CERCARIA
Crossing fish (vector2)
Swallowed by skin
METACERCARIA
definitive host forming METACERCARIA
(cyst) in fish skin/muscle
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 completely-grown
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
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 in size and has
operculum. Immature eggs are lied in billiary
duct and exit with feces.
 Life cycle
Hepatic tissues are infiltrated
Eggs are expelled within feces with eggs, immature eggs
are lied in billiary duct

Eggs mature in water

Penetrate Glissons capsule,
and hatch after 9-15 days
hepatic tissue, then into billiary duct
at optimum temperature 22-250C
in 12 weeks in adult

Miracidia enter
intermediate host I and develop Penetrate intestinal wall,
to become sporocysts, rediae I, Enter peritoneal cavity
rediae II in 3 weeks , and cercariae

Cercariae move toward Metacercariae exit

Intermediate host II the cyst in duodenum

At night, in 8 hours,
become metacercariae Metacercariae penetrate
definitive hosts
 Clinical Symptom
Until metacercaria penetrate Glissons 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 Sometimes, into ectopic place

go out to bronchioles like mesentery, pleura or brain,
and reach adulthood here

Then, they are coughed

with sputum or swallowed
In 3-6 hours, enter abdominal cavity
and expelled with feces
and penetrate abdominal wall, stay
for several days before penetrating
Hatch in water become
diaphragm, to pleural cavity and enter
MIRACIDIUM after
bronchioles
maturation (2-3 weeks)

In intermediate hosts I,
MIRASIDIA become REDIAE I, In duodenum, encystations happens,
REDIAE II, and finally CERCARIAE penetrate intestinal wall (in 30-60 minutes)

In intermediate hosts II,

cercariae become METACERCARIAE Metacercariae penetrate
in 5 months 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