LECTURE NOTES ON

MEDICAL HELMINTHOLOGY
Dr.rer.nat. Afiat Berbudi, dr., M.Kes
Dept.of Biomedical Sciences
Parasitology Division Click “Esc”button
Faculty of Medicine When finished
Universitas Padjadjaran
Introduction to
Medical Helminthology

 Medical helminthology : the study of parasitic

worms (helminthes/ vermes/cacing) affecting
human, which :
 Spend part or the entire life cycle in a
human host or
 Animal parasite causing disease in human
Introduction to Medical Helminthology
CLASS
1. Nematoda
CLASSIFICATION 2. Trematoda
3. Cestoidea

HELMINTHES

NEMATHELMINTHES PLATYHELMINTHES

NEMATODES TREMATODES CESTODES

 NEMATODES

Classification based on Habitat

HABITAT

INTESTINAL BLOOD AND TISSUE

NEMATODES NEMATODES

SOIL TRANSMITTED FILARIA and

OTHER (NON-STH)
HELMINTHS (STH) DRACUNCULUS
 INTESTINAL NEMATODES

SOIL TRANSMITTED NON-SOIL TRANSMITTED

HELMINTHS HELMINTHS

• Ascaris lumbricoides Enterobius vermicularis

(adult worm and eggs ) (Oxyuris vermicularis, )
• Trichuris trichiura
• Hookworm
Trichinella spiralis
 Necator americanus
 Ancylostoma duodenale
• Strongyloides stercoralis -

Tissue Nematodes
 Introduction to Medical Helminthology
CLASS
1. Nematoda

NEMATODES
2. Trematoda
3. Cestoidea

General characteristics

 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)
 Introduction to Medical Helminthology

NEMATODES CLASS
1. Nematoda
General characteristics 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
 Introduction to Medical Helminthology
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
 Introduction to Medical Helminthology
NEMATODES CLASS
1. Nematoda
General characteristics 2. Trematoda
3. Cestoidea

 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 their anterior 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
 Introduction to Medical Helminthology
NEMATODES CLASS
1. Nematoda
2. Trematoda
Life cycle 3. Cestoidea

 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
 Introduction to Medical Helminthology

NEMATODES CLASS
1. Nematoda
Life cycle 2. Trematoda
3. Cestoidea

 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
 Introduction To Medical Helminthology
NEMATODES CLASS
1. Nematoda
Pathogenicity 2. Trematoda
3. Cestoidea

 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
 Introduction To Medical Helminthology
CLASS

NEMATODES
1. Nematoda
2. Trematoda
3. Cestoidea
Pathogenicity

 The local reaction from intestinal parasites result from

irritation, invasion of the intestinal wall and occasionally
penetration to extraneous site

 The degree of local or general reaction – depend upon the

sensitivity of the host to the protein product of the parasite

 Intestinal mucosa is damaging by biting and bloodsucking, by

lytic ferment secreted by the parasite and by mechanical
irritation
 Introduction To Medical Helminthology

NEMATODES CLASS
1. Nematoda
Pathogenicity 2. Trematoda
3. Cestoidea
 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 are appeared late in the immune reaction
Th2
 NEMATODES

Classification based on Habitat

HABITAT

INTESTINAL BLOOD AND TISSUE

NEMATODES NEMATODES

SOIL TRANSMITTED FILARIA and

OTHER (NON-STH)
HELMINTHS (STH) DRACUNCULUS
Introduction to Medical Helminthology

NEMATODES
CLASS
1. Nematoda
2. Trematoda
Classification based on Habitat 3. Cestoidea

 Soil Transmitted Helminthes

 Ascaris lumbricoides
 Trichuris trichiura Importance
 Hookworm (Necator americanus, Ancylostoma
duodenale)
 Strongyloides stercoralis

 Non-Soil Transmitted Helminthes

 Enterobius vermicularis
 Trichinella spiralis

Importance
 Filaria and Dracunculus
 Wuchereria bancrofti
 Brugia malayi
 Brugia timori
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
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
Ascaris lumbricoides
LIFE CYCLE
INSIDE THE HUMAN BODY
 Ingestion of mature eggs
Mature eggs
Ingested

 Hatched in the gaster, larva Migration of larva

penetrates the wall of the
inside the
intestine and enter into blood
circulation circulatory system

 To the right heart chamber,

Larva Adults
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
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
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
Ascariasis in one area :
 Pyrantel pamoate
 prevalence > 30 %, treatment 3x/year
 Mebendazol
 prevalence (20-30) %, treatment 2x
/year  Oxantel pamoate
 prevalence
 Piperazine
(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
( 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)
Trichuris trichiura (Life Cycle)
LIFE CYCLE
 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)

http://www.med-chem.com/para-site.php?url=org/trictric
Infection 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 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
Infection by Trichuris trichiura
PREVENTION
Treatment

Drugs available:
Elimination of source of infection
 Oxantel pamoate
 Improved personal hygiene (hand
 Mebendazol
washing,(drug
toiletoftraining)
choice)
 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
LIFE CYCLE
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
 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 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
Patient with atrophic glossitis
anemi hipokrom also show fingernail deformity
mikrositer yang (koilonichia)
disebabkan infection
berat HOOKWORM
 Fingernail becomes thin and
 Tampak lidah halusconcave with elevated ridge
dan kurang papila

source : Atlas Parasitologi Kedokteran, Zaman P. Alih Bahasa : Anwar C.; Mursal Y.
Infection by HOOKWORM

Diagnosis
 Identify eggs from feces sample
 Identify larva from :
Fecal culture
Old feces sample
 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
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
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)
Infection by
Strongyloides stercoralis
Diagnosis
Find and identify
 Rhabditiform larva :
 From fresh feces
 Gastric (duodenal) juice
*Eggs :
 In heavy diarrhea
 After administration of laxative
Infection by
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
Enterobius vermicularis

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 scratching 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

o The worm causes disease, called trichinosis.
o There are 3 clinical stadium:
o Intestinal invasion that is done by worm (1-2 days
after eating infectious muscle).
o Larva migration (7-28 days after eating infectious
muscle). It results cerebral disturbing, cardiac
distrubing, fever, even die.
o 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 (LESS
IMPORTANT !)
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
 FILARIA

TOPICS
(As problem of Public Health in Indonesia)

 Wuchereria bancrofti
 Brugia malayi
 Brugia timori

All species above – nocturnal periodicity

 Distribution of lymphatic filariasis

Hoerauf et al. 2011

Institute for Medical Microbiology, Immunology and Parasitology (IMMIP)
5
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

 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
MAIN MOSQUITO VECTORS

 W. bancrofti  rural: vektor Aedes, Anopheles dan Mansoni

urban: Culex fatigan, Anopheles

 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
 Wuchereria bancrofti
Periodicity

PERIODICITY (WHO, 1967)

 Commonly nocturna, also in Indonesia
 In Polynesia, subperiodic diurna, vector
Aedes polynisiensis
Life Cycle
 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
 Brugia malayi
LIFE CYCLE AND PERIODICITY

Nocturna, vector Anopheles barbirostris

(farm)
Subperiodic nocturna, vector Mansonia
uniformis, M. indiana (swamp)
Life Cycle of B. malayi
LYMPHATIC FILARIASIS LIFE CYCLE
Adult worm

Microfilariae
HUMAN
BODY

MOSQUITO
Infective larva (L3) BODY
Larva L1

Mansonia, Anopheles,
Larva L2 Culex, Aedes
 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.
Example of filariasis from Malaysia
 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
 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
 Asymptomatic Microfilaraemic

 Microfilaraemic carrier
 No sign and symptom of infection
 Source of infection to others