2.2.

Tissue nematodes
General feature:
• Adults which live in the tissues of human (lymphatic
system, subcutaneous tissues or muscle)
• Long thread - like worms
• Requires two host to complete their life cycle.
• Females are viviparous, larvae hatch in the uterus
• The female produce first stage larvae (L1)

By: MA 2
The immature L1 stage larva is called Microfilariae

Small , slender, motile forms

L1 require blood sucking insects (IH) to develop

to infective form (L3)

No reproduction in the vector, rather

development

By: MA 3
 Classification:
1. FAMILY FILARIDAE( Filarial worm)
- Common/pathogenic filaria
• Wuchereria bancrofti
• Brugia malayi
• Brugia timori
• Loa loa
• Onchocerca volvulus
2. FAMILY TRICHINELOIDAE
• Trichinella sps
3. FAMILY DRACUNCULIDAE( guinea worm)
• Dracunculus medinensis

By: MA 4
 FAMILY FILARIDAE ( Filarial worm)
• Flarial worm causes 3 main diseases
• lymphatic filariasis (Elephantiasis):caused
by W.bancrofti and B.malayi
• Loasis caused by Loa loa
• Onchocerciasis (river blindness): caused by
O.volvulus

By: MA 5
 FAMILY FILARIDAE ( Filarial worm)
General features:

Filariae live as adults in various human tissues

Agents of LF reside in lymphatic vessels and lymph nodes

O.Volvulus in subcutaneous tissues

Loa loa in subcutaneous tissues

By:6MA
 Lymphatic Filariasis
• Disease caused by filarial worms living in
the human lymphatic system
• Causative agents
• Wuchereria bancrofti
• Brugia malayi
• Burigia timori
• These worms lodge in the lymphatic
system
• They live for four to six years, producing
millions of minute larvae that circulate in
the blood”
By: MA 7
 Lymphatic Filariasis
• Large numbers are present in the lymphatic of the:
Lower extremities

Upper extremities (axillary lymph nodes), and,

Male genitalia (epididymis, spermatic cord, testicle)
- particular for W. bancrofti

By: MA 8
 Social consequences
It is one of the most debilitating and disfiguring
diseases of the world
1. Disfigurement of the limbs and genitals leads
to:
– Stigma
– Anxiety
– Ostracization (Expel from
a community or group)
– Psychological trauma
– Sexual disability

By: MA 9
 Social consequences…..
2. The disease impedes
– Mobility
– Travel
– Educational opportunity
– Employment opportunity
– Marriage prospect

By: MA 10
 Distributin
• Wuchereria bancrofti
• affects an estimated 119 million individuals and
disfigures 40 million.
• Wide distribution (Africa, SE Asia, Indonesia, South
Pacific Islands)

• Brugia malayi
• Limited distribution (China, India, SE Asia, Indonesia,
Philippines)

• Brugia timori
• Limited distribution (island
By: MA
of Indonesia) 11
 Wuchereria bancrofti
Transmission and life cycle

By: MA 12
 Cont ....
• Requires two host
• Human-DH
• Mosquitoes-IH
• Transmission
• Bite female mosquitoes (Genera Culex,
Aedes, Anopheles, Mansonia)

By: MA 13
• Infective larvae deposited onto
human skin during the mosquito's
blood meal
• Enter through the mosquito bite
puncture wound or local
abrasions.
• In humans:
– Parasites passes to the
lymphatic system
– Undergo further molts
– Become adult male and female
worms
By: MA 14
• Adult female worms produce thousands of
sheathed microfilariae per day
• Mf can be found in blood 9 months after infection
(W.bancrofti) and 3 months (Burigia species)
• Normally found in peripheral circulation in evening.

By: MA 15
• Microfilariae ingested during blood meal
from infected person
• Penetrate the mosquito stomach wall
• Enter the body cavity (hemocoel)
• Migrate to the insect's flight muscles for
growth.
• After 2 molts, the L3 migrate through the
head,
• Reach the proboscis of the mosquito.

By: MA 16
 Clinical manifestation.
• Depends on:
– Site occupied by adult
– Number of worms,
– Length of infection and
– Immune response of the host

By: MA 17
 Clinical manifestation.

1. Many infections are asymptomatic

2. Circulating Mf probably do not cause pathology
3. The main pathological lesions are:
a) Inflammatory manifestations – due to toxic
products of living or dead adult worms

By: MA 18
 Clinical manifestation.
– There may be:
Recurrent attacks of:-
• Lymphangitis- inflammation of lyphatic vessels
• Funiculitis-especially an inflammation of the
spermatic cord
• Epididymitis
• Orchitis-Inflammation of one or both testes;
characterized by pain and swelling
• Lymphadenitis
• Swelling and redness of affected parts
• Fever, chills, headache, vomiting and malais
By: MA 19
 Elephantiasis:
 Hard and thick, rough and fissured (fine cracks) skin
 Frequently legs & genitalia (scrotum, penis and
vulva)
 Less often arms and breasts.

By: MA 20
By: MA 21
 Diagnosis of W. bancrofti
1. BF (taken at night)
 Thin and thick smears
 Concentration methods
 Mf in:
 Aspirates of hydrocele (serous fluid accumulates in
a body sac)
 Lymph gland fluid
 Chylous urine
2. Intradermal test (antigen from Dirofilaria immitis)
3. Serological tests
By:22MA
4. Antigen detection:
 Differential diagnosis

• Podoconiosis (syn. lymphatic siderosilicosis or

lymphoconiosis):
– Very slow onset of oedema
– Lymphoedema
– Elephantiasis (mostly limited to below the knee)
• Caused by immune response to certain minerals.
• No hydrocoele, no eosinophilia, no nocturnal
microfilaraemia
•
By:23MA
Podoconiosis
• is the result of a genetically determined abnormal
inflammatory reaction to mineral particles in irritant red clay
soils derived from volcanic deposits
• Is barefoot populations living on irritant soil
• also known as nonfilarial elephantiasis

By: MA 24
Podoconiosis
• is a disease of the lymph vessels of the
lower extremities that is caused by
chronic exposure to irritant soils. It is the
second most common cause of
tropical lymphedema after filariasis
• and is characterized by prominent
swelling of the lower extremities, which
leads to disfigurement and disability

By: MA 25
 Treatment of W. bancrofti

 Diethyl carbamazine (DEC)

 General measures:
 Rest, antibiotics, antihistamines, and bandaging

 Surgical measures for elephantiasis

By:26MA
 Prevention and control of W. bancrofti

 Control of mosquitoes
 Avoid mosquito bite
 Treat patients
 Health education
 Global LF elimination program strategy:
 Mass drug administration
 Care for chronic cases

  By:27MA
ONCHOCERCIASIS
• Is a filarial disease caused by O. Volvulus
• Commonly known as river blindness
• The world’s second leading infectious cause of blindness
• WHO estimates the global prevalence is 17.7 million, of
whom about 270,000 are blind

By: MA 28
• Occurs most widely along the
courses of fast running rivers
in the forests and Savannah
areas of west and central
Africa
• Also occurs in the Yemen, Arab
Republic, Central and South
America

By: MA 29
Onchocerca volvulus
• Habitat:
• Adult:
• Subcutaneous nodules and in the skin
• Adults can live ~ 15 years in nodules
• Microfilariae:
• Skin, eye and other organs of the body
• Infective larvae in:
• Gut, mouth parts and muscles of black fly

By:30
MA
Onchocerca volvulus

Transmission:

• By the bite of infected vector (simulium species)

By:31
MA
Life cycle
• During a blood meal, infected blackfly introduces L3
(infective stage) larvae onto the skin of the human
• L3 penetrate into the bite wound   
• In subcutaneous tissues the larvae develop into adult filariae
• Adult commonly reside in nodules in subcutaneous
connective tissues 

By:32
MA
Life cycle
• The female worms produce Mf for ~ 9 years
• Mf have a life span ~ 2 years 
• Mf found:
• Typically in the skin and in the lymphatics of
connective tissues
• Occasionally in peripheral blood, urine and
sputum

By:33
MA
• A black fly ingests the Mf during a blood meal
• Mf migrate from the blackfly's midgut through the
hemocoel to the thoracic muscles 
• Mf develop into L1 larvae and then to L3 
• L3  migrate to the blackfly's proboscis
• Infection occurs when the fly takes a blood meal

    

By:34
MA
Life cycle of Onchocerca volvulus

By:35
MA
Clinical feature
Onchocerciasis
• Acute onchocerciasis:
• Itchy (pruritic)
• Erythematous
• rash with thickening of the skin

By:36
MA
Clinical feature
• Chronic onchocerciasis:
• Elephant or lizard skin Hanging groin

• Leopard skin River blindness

By:37
MA
Clinical feature

• Onchocercomata:
• Upper part of the body (American
onchocerchiasis)
• Pelvic region (African form)

• Nodules surrounded by concentric

bands of fibrous tissue

By:38
MA
Laboratory diagnosis
• Mf in skin snips

Skin biopsy Skin fragment

• Mf in urine, blood & most body fluids (in heavy infection)
• Wet mount preparation Staining

By:39
MA
Prevention and control

• Destruction of Simulium

• Avoiding Simulium bites

• Treatment of communities (~APOC)

By:40
MA
Treatment
• Ivermectin:
• Paralysis of worms
• Reduces the microfilarial load
• Surgical Care:
• Nodulectomy
• Removes adult worms

By:41
MA
Dracunculus medinenis
“Guinea worm, ”

By: MA 42
 Dracunculosis
 Synonyms: Dracontiasis, Dracunculosis,
Dracunculiasis
 Causative agent
 Scientific name: Dracunculus medinensis
 Common name: Medina worm or Guinea worm

 
By:43MA
 Epidemiology
 Most common in areas of limited water
supply where individuals acquire water
by physically entering water sources.
– “Walk-in well”
– Water holes in parts of Africa
 Habitat:
 Adults in subcutaneous tissues of man/reservoir
animals

By: MA 44
 Transmission & Life cycle of D. medinensis
 Man is infected on drinking water containing cyclops
 In the small intestine, the cyclop is digested , larvae liberated
and penetrate through the duodenal wall and migrate to the
subcutaneous tissues probably via lymphatics.
• At this point the females are fertilized by the males, and the
males die.  The females then migrate to the skin, reach sexual
maturity, and produce juveniles. 
 They tend to go to parts most likely to come in contact with
water as the lower extremities (positive geotropism)
 Several months (9 or more) elapse between infection and
appearance of the gravid female at the skin surface

By:45MA
 Life cycle of D. medinensis
 Male dies after copulation
 The cephalic end of the fertilized female pressing on the
skin, produces a papule that becomes a blister and then
ruptures forming an ulcer
 When the ulcer contacts water, a loop of the uterus
prolapses through a rupture in the anterior end of the
worm and larvae are discharged.
 Water cyclops ingest the larvae

 
By:46MA
 Life cycle of D.medinensis
• Once within the
copepod, the infective
juvenile larvae moves
into the hemocoel
where they develop
into 3rd stage juveniles.
• These get consumed
when humans drink
water with infected
copepods.
By: MA 47
Copepod

By:48MA
Life Cycle of D.medinensis

By:49MA
 Pathogencity of D.medinensis
 Early manifestatiosn are produced when the female
worm approaches the skin. It liberates a toxic substance
that results in local erythema, tenderness and pain.
 This is followed by formation of a blister that ultimately
ulcerates
 There may be local or systemic symptoms as urticaria,
pruritus, pain, dyspnoea, nausea and vomiting, which
subside with rupture of the blister
 The ulcer may be secondarily infected producing
cellulitis and induration
 Eosinophilia
 cellulitis - An inflammation of body tissue (especially
that below the skin) characterized
By:50MA
by fever and swelling
Adult worm of D.medinensis

By:51MA
Adult worm of D.medinensis

By:52MA
 D.medinensis

Blister containing the worm Ruptured blister with filamentous worm

A B
By:53MA
D. medinensis

By:54MA
 D. medinensis

Adult Dracunculus in foot

B By:55MA
 Diagnosis of D. medinensis
 Laboratory tests to investigate dracunculiasis are
limited because the larvae are normally washed
into water

 A diagnosis is usually made when the blister has

ruptured and the anterior end of the female
worm can be seen

By:56MA
 Diagnosis of D. medinensis
 If required, laboratory confirmation of the
diagnosis can be made as follows:
1. Place a few drops of water on the ulcer to encourage
discharge of the larvae

2. After a few minutes collect the water in a plastic bulb

pipette or pasteur pipette

3. Transfer the water to a slide and examine

microscopically using 10x objective – motile larvae will
be observed
By:57MA
 Prevention & Treatment
• People with an open Guinea worm wound
should not enter ponds or wells used for
drinking water.
• Water can be boiled, filtered through tightly
woven nylon cloth, or treated with a larvae-
killing chemical.
• No medication is available to end or prevent
infection.
– The only treatment is to remove the worm
over many weeks by winding it around a small
stick and pulling it out a tiny bit at a time.
By: MA 58
 Prevention & Treatment
– Sometimes the worm can be pulled out completely within
a few days, but the process usually takes weeks or months.
– The worm can be surgically removed before the wound
begins to swell.
– Antihistamines and antibiotics can reduce swelling and
ease removal of the worm.

By: MA 59
Adult D. medinensis

By: MA 60