Unit.

4
Blood and Tissue nematodes
Outline
– General features
– Classification
– Geographical distribution Morphology, differential characteristics, life Cycles,
Laboratory diagnosis, prevention and control of:
• Wuchereria bancrofti
• Brugia malayi/timori
• Loa loa

• Onchocerca volvulus
• Trichinella spiralis
• Dracunculus medinensis
 Learning objective

At the end of this unit the student will be able to:

– Explain the general features of blood and tissue nematodes

– Classify tissue nematodes

– Explain the Geographical distribution, Morphology, differential

characteristics, life Cycles, prevention and control methods of
blood and tissue nematodes
– Collect blood samples in appropriate timing

– Collect skin snip for the diagnosis of O. volvulus

– Detect and identify microfilaria of blood and tissue nematodes

 4.1 Blood and tissue nematodes
General features:
• Adults 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

• The female produce first stage larvae (L1)

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

 Classification:

• Tissue nematodes can be classified based on:

– Habitat in the body

– Clinical manifestation

– Morphology
 Three families/ groups
1. FAMILY FILARIDAE( Filarial worm)
- Common/pathogenic filaria
• Wuchereria bancrofti
• Brugia malayi
• Brugia timori
• Loa loa
• Onchocerca ovolvulus
– Less/non-pathogenic Filaria
• Mansonella perstance
• Mansonella streptocerca
• Mansonella ozardi
2. FAMILY TRICHINELOIDAE

• Trichinella sps

3. FAMILY DRACUNCULIDAE( guinea worm)

• Dracunculus medinensis

Animal tissue nematode rarely infect human

• Dirofilaria sps
• Angiostrongylus cantonensis
• Gnathostoma spinigerem
 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, Loa loa, M. Ozzardi and M. Streptocerca in

subcuraneous tissues

 M. Streptocerca besides reside in the dermis

 M. Perstans resides in body cavities and surrounding tissues

8
 Cont ….

 Three of these are responsible for most of the morbidity:

W. bancrofti and B. malayi cause lymphatic filariasis, and

O. volvulus causes onchocerciasis (river blindness).

9
Diagnosis based on Mf findings:
• Morphologic features:
– Size
– Presence or absence of “ sheath”
– Appearance i.e. curvature, Kinks, coiling etc
– Arrangement of the column of nuclei in the body
– Presence of nuclei at the very tip of the tail

• Other features:
– Periodicity
– Source of specimen
• Factor to be considered when collecting blood

– Collect blood at the correct time

– Concentration technique recommended

– In chronic infection Mf is rarely found in blood

– In LF Mf are higher in capillary blood than

venous blood
– Mf are higher in capillary blood from the ear lob
 Morphology

• Adult
– The adults are long thread like
worms.
– Measure 2 cm – 120 cm (4 – 10 µ
wide)
– Live in body cavities, lymphatic,
and subcutaneous tissues
– Release embryos (microfilaria)
which live in blood or dermis (skin)
– all require an insect or crustaean
vector as intermediate host
• Microfilaria
– The immature first stage larva of filarial worms
– Are motile and live in blood or dermis
– Measure, 150-350 µ long
– Transparent and colorless with rounded or pointed
tail in unstained smear
– Internal structure can be visualized by the use of
fixed stained preparation
– Can be sheathed or unsheathed
Periodicity:-
• Microfilaria of pathogenic filarial
worms that found in the blood (m.f of
filarial worms that causes lymphatic
filariasis and Loasis) show periodicity
Periodicity:-
– Mf are found in the blood in greater number in a
certain hours of a day or a night
– Corresponds to peak biting times of their insect
vector
• Nocturnal periodicity -mf is high in blood during night
hrs
• Diurnal periodicity-mf is high in blood during day hrs
• Nocturnal or diurnal subperiodicity;- mf can found in
blood 24 hrs with slight increase in number during day
or night hrs
Filarial worms Periodicity Main Vector Reservoir
(Synonym) (IH)
O. volvulus Non Periodic Black fly (Simulium) Human
(River blindness)

W. ancrofti (LF) Periodic (N) Culex, Anopheles Human

22 – 04hr
(24hr)
Sub Periodic Aedes Human
20 – 22 (21hr)
14 – 18 (16hr)
B. Malayi (LF) Periodic (N) Anopheles Human
22 – 04hr
(24hr)
Sub Periodic Mansonia Human, Monkey, Cat –
20 – 22 (21hr) Zoonotic
B. Timori (LF) Periodic (N) Anopheles Human
L. Loa (Eye worm) Periodic (D) Deer fly Man, Monkeys
M. streptocerca Non Periodic Midge (Culicoides)
M. perstans Sub Periodic Midge (Culicoides)
M. ozzardi Non periodic Midge16(Culicoides)
• Flarial worm causes 3 main diseases
– lymphatic filariasis (Elephantiasis)
– Loasis
– Onchocerciasis (river blindness)
4.1.1 Lymphatic Filariasis
 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”
 Lymphatic Filariasis
• Large numbers are present in the lymphatics
of the:
Lower extremities (inguinal and obturator groups),

Upper extremities (axillary lymph nodes), and,

Male genitalia (epididymis, spermatic cord, testicle) -

particular for W. bancrofti
 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
– Psychological trauma
– Sexual disability
 Social consequences…..
2. The disease impeds
– Mobility
– Travel
– Educational opportuniity
– Employment opportunity
– Marriage prospect
 Epidemiology of Lymphatic Filariasis

• Endemic in 83 countries
• 1.2 billion at risk
• > 120 million people infected
• > 25 million men suffer from genital disease,
• > 15 million people suffer from lymphoedema
or elephantiasis of the leg
• ~ 2/3 of infected people live in India and
Africa
• Others live in parts of Asia, the Pacific, & in
Central and South America.
Distribution
 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
• island of Indonesia
 Wuchereria bancrofti
Disease: Bancroftian filariasis, Wuchereriasis, elephantiasis
Distribution: tropical and subtropical countries
Morphology:
1. Adult:
– Thready
– Cylinderical oesophagus
– Creamy white in color
– Male:
• About 4cm in lentth
• Curved posterior end
• 2 unequal spicules and has anal papillae

  26
 Wuchereria bancrofti
• Female:
• About 8 cm in length
• 2 sets of genitalia
• Vulva opens close to the posterior end
• Viviparous
2. Micrfilaria:
– 250 x 8 
– Body forms graceful curves
– Body has a column of nuclei separated by free areas
– Rounded anterior and tapered tail ends free of nuclei
– Loose sheath (stretched vitelline membrane) closely fits the body
but projects beyond the head and tail ends.
3. Infective larvae: 1500 – 2000 x 20
– Cylinderical oesophagus

  27
Transmission and life cycle
 Cont ....
• Requires two host
• Human-DH
• Mosquitoes-IH

• Transmission
• Bite female mosquitoes (Genera Culex, Aedes,
Anopheles, Mansonia)
• 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
• 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.
• 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.

 Clinical manifestation.
• Depends on:
– Site occupied by adult
– Number of worms,
– Length of infection and
– Immune response of the host
 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
 Clinical manifestation.
– There may be:
• Recurrent attacks of lymphangitis
– Funiculits
– Epididymitis
– Orchitis, etc...
• Lymphadenitis
• Swelling and redness of affected parts
• Fever, chills, headache, vomiting and malais
b) Obstructive manifestations –
• Fibrosis following the inflammatory process
• Coiled worms inside lymphatics.
• This may result in:
 Dilatation
 Rupture of distended lymphatics
 In the urinary passage – chyluria
 In the pleura – chylothorax
 In the peritoneal cavity – chylous ascitis
 In the testis – chylocoele
 Elephantiasis:
 Hard and thick, rough and fissured skin
 Frequently legs & genitalia (scrotum, penis and vulva)
 Less often arms and breasts.
 Clinical ......
4. Tropical pulmonary eosinophilia
• Pulmonary symptoms: cough, dyspnoea, "asthmatic syndrome".
• Chest X-rays: patchy infiltrates
• Splenomegaly
• High ESR & marked eosinophilia
• No microfilariae in the peripheral blood.
• Serological tests strongly positive

  39
 Diagnosis of W. bancrofti
1. BF (taken at night)

 Thin and thick smears

 Concentration methods

• Lyzed capillary blood technique

• Tube centrifugation lyzed blood technique

• Microhematocrite tube technique

• Membrane filtration technique

• Counting chamber technique

 DEC provocation test

40
 
 Diagnosis of W. bancrofti
 Mf in:
 Aspirates of hydrocele
 Lymph gland fluid
 Chylous urine
2. Intradermal test (antigen from Dirofilaria immitis)

3. Serological tests as IHA, IFA

4. Antigen detection: ICT filariasis test

 
41
43
44
Adult female worm of W. bancrofti Adult male worm of W. bancrofti

45
 Treatment of W. bancrofti
 Diethyl carbamazine (DEC)
 General measures:
 Rest, antibiotics, antihistamines, and bandaging

 Surgical measures for elephantiasis

46
 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

47
4.1.2 Loiasis
 Loiasis
• Caused by filarial worms living in subcutaneous tissue

• Causative agents
• Loa loa (Eye worm)
• Distributed in Rain Forest areas of West Africa
and equatorial Sudan.
 Loa loa (Eye worm)
 Habitat:
 Adults live in:
 Connective tissues under the skin
 Mesentry
 Parietal peritoneum
 Subconjunctival tissue of the eye or thin skinned areas

 Microfilaria in peripheral blood of man during day time

 Infective larvae in the gut, mouth parts and muscles of

chrysops

50
 Loa loa (Eye worm)

 Morphology
 Adult – cylinderical and transparent

 Microfilariae

 Has several curves and kinks

 Sheath which stains best with haematoxylin

 Body nuclei are not distinct and more dense

 Nuclei extend to the end of the tail which is rounded

  51
52
 Transmission
• Horse flies (Tabanidae) in genus Chrysops

• Day-feeding & forest-dwelling

• Also called the “deer fly” or mango fly.

Life cycle
 Life Cycle
• Adult worms continuously migrate through tissue at
a rate of about 1 cm per minute.

• Found in back, chest, axilla, groin, penis, scalp and

eyes.
 Clinical manifastation
• Loiasis is often asymptomatic. 

• Calabar swellings (episodic angioederma)

– Itchy, red, and nonpitting swollen areas in the skin

– 2-10 cm in diameter, Often painful/may be painless

– In any portion of the skin/wrists & ankles most frequent

 Clinical manifastation
• Adult worms also migrate in sub-conjunctival
tissues. 
• They can cause inflammation and irritation but
not blindness
 Laboratory diagnosis
• Mf in stained BF taken during the daytime
• Occasionally the Mf can be found in joint fluid
• Differentiation from mansonella required
(hematoxylin staining)

58
 Loa loa:

Sheathed,

Relatively dense nuclear column

Tail tapers and is frequently coiled, and

Nuclei extend to the end of the tail.

 Mansonella perstans:

Smaller than L. loa

No sheath

Blunt tail with nuclei extending to the end of the tail

60
4.1.3 Onchocerciasis
 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

62
 DISTRUBUTION MAP

Foci are present in Southern

Arabia, Yemen and in S. & C. Tropical Africa between
America the 15° north and the 13°
south
• 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
 Onchocerca volvulus
• Habitat:

– Adult:

• Subcutaneous nodules and in the skin

• Adults can live ~ 8 – 10 years in nodules

– Microfilariae:

• Skin, eye and other organs of the body

– Infective larvae in:

• Gut, mouth parts and65muscles of black fly

 Onchocerca volvulus
Morphology
• Microfilariae:
– 220 to 360 µm by 5 to 9 µm
– No sheath
– Head end is slightly enlarged
– Anterior nuclei are positioned side by side
– No nuclei in the end of the tail
– Tail is long and pointed
66
 Onchocerca volvulus
• Adult:

– Females - 33 to 50 cm in length and 270 to

400 μm
– Males - 19 to 42 mm by 130 to 210 μm. 

67
 Onchocerca volvulus
Transmission:

• By the bite of infected vector (simulium species)

68
 Life cycle
• During a blood meal, infected blackfly introduces L 3
(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 
69
 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

70
• 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

    
71
Life cycle of Onchocerca volvulus

72
 Clinical feature
Onchocerciasis
• Acute onchocerciasis:
– Itchy (pruritic)
– Erythematous
– Papular rash with thickening of the skin

73
 Clinical feature
• Chronic onchocerciasis:
– Elephant or lizard skin Hanging groin

– Leopard skin River blindness

74
 Clinical feature
• Onchocercomata:
– Upper part of the body
(American onchocerchiasis)
– Pelvic region (African form)

• Nodules surrounded by
concentric bands of fibrous
tissue

75
 Laboratory diagnosis
• Mf in skin snips

Skin biopsy Skin fragment

• Mf in urine, blood & most body fluids (in heavy

infection)
– Wet mount preparation Staining

76
77
• Mf must be differentiated from Mf of M.
Streptocerca and M. Ozzardi.
– Mf of O. Volvulus are longer and do not have nuclei
to the end of the tail

78
79
80
 Prevention and control
• Destruction of Simulium

• Avoiding Simulium bites

• Treatment of communities

81
 Treatment
• Ivermectin:
– Paralysis of worms

– Reduces the microfilarial load

• Surgical Care:
– Nodulectomy

– Removes adult worms

82
4.1.4 Trichinellosis
 Trichinella spiralis
 A tissue nematode caused by Trichinella spiralis
 Zoonotic disease
 Disease in humans: Trichinosis, Trichiniasis,
Trichinelliasis, Trichinellosis
 Distribution: Temperate regions where pork is eaten
1. T. Spiralis spiralis – found in temperate regions
2. T. Spiralis nativa – found in the Arctic
3. T. Spiralis nelsoni – found in Africa and S. Europe

 
84
 Trichinella spiralis
 Habitat:
 Adults in the small intestine of man and animals
specially pigs and rats (reservoir hosts)
 Larvae : encysted in muscles

85
 Trichinella spiralis
 Morphology;
1. Adults:
• Attenuated anterior end
• Cellular oesophagus
• Anus or cloaca terminal
Male: 1.5 mm in length
• Posterior end curved ventrally
• 2 caudal papillae
• One set of genitalia

 
86
 Morph ....
 Female: 3.5 mm in length
 Posterior end bluntly rounded
 One set of genitalia
 Vulva opens at the junction of the anterior 5th with the rest
of the body
 Larviparous (viviparous)

87
 Morph ....
2. Encycted larva: in cyst wall formed by tissue reaction
 Larva (1mm) coiled inside the cyst (0.5 x 0.2 mm)
 Larva grows from 0.1 to 1mm (~ 2 weeks to become
infective)
 Lies along the longitudinal axis of muscle fibres
 Cyst usually become calcified

88
 Transmission
• Eating flesh of infected pork (raw/undercooked)

89
Life cycle

90
 Life cycle
 The same host (animal/man) act as DH & IH
 After fertilization, males die and are expelled.
 Females penetrate deeply in the mucosa and lay
 Female lays ~ 1500 larvae in its life span (~ 2 months)

91
• Larvae to the circulation
• Passes through pulmonary filter

• Distributed all over the body (esp. diaphragm, tongue, eye, deltoid,
pectoralis, intercostals, etc)
 Larvae coil and encyst in the long axis of muscles

 Pigs become infected by eating infected flesh from other pigs or ingestion
of infected dead pigs and rats
 Rats are infected by eating flesh of dead pigs or rats and by canibalism

 
92
 Life cycle
 Larvae liberated from the cysts in small intestine
and mature to adults
 Larvae start to be deposited by the female

93
 Pathogenicity
 Intestinal invasion by adult worms
 Abdominal pain, nausea, vomiting, diarrhoea and
colic.

94
 Migration of larvae

95
 Encystment of larvae
 Manifestations depend
up on organs affected.
 > 50 – 100 larvae/gm of
muscle are symptomatic
 < 10 larvae are often
asymptomatic

  96
 Clinical signs & syptoms
 The main findings are:
o Oedema chiefly orbital

o Muscle pain and tenderness

o Headache, fever, rash, dyspnoea, general weakness

o Death occurs in severe cases from exhaustion, heart

failure (myocarditis), pneumonia, etc.

  97
98
 Laboratory diagnosis
1. Immunodiagnosis:
a) Intradermal test (Bachman test)
b) Serological tests:
• Bentonite flocculation (BF)
• Latex agglutination (LA)
• Counter – current electrophoresis (CEP)
• Complement fixation test (CFT)
• IFA and IHA
 

99
 Diagnosis .....
2. Muscle biopsy:
• Direct examination
• After digestion in a pepsin hydrochloric acid medium

3. Eosinophilic leucocytosis in the acute stage

  100
Larvae, freed from Encysted in pressed
their cysts muscle tissue. 

101
102
Adult worm from
intestine wall
 Prevention & control
 Thorough cooking of pork
 770c or freezing at – 150c for 20 days
 – 180c for 24 hours
 Proper breeding of pigs
 Sterilizing garbage
 Antirat campaign
 Inspection of pork in slaughter houses
 Trichinoscope.

103
 Treatment
 Non specific symptomatic treatment:
 Sedatives
 Cortisone and ACTH
 Supportive treatment:
 Rest, fluids, smooth diet and vitamins
 Thiabendazole
 Mebendazole

104
 
4.1.4 Dracunculosis
2.1.3.8. Dracunculus medinenis
“Guinea worm, ”
 Dracunculosis
 Synonyms: Dracontiasis, Dracunculosis, Dracunculiasis

 Causative agent
 Scientific name: Dracunculus medinensis
 Common name: Medina worm or Guinea worm

 
107
 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
 Distribution of
Dracunculus medinensis
Global: Nile valley,
India and areas
where wells are
used for water
supply
Ethiopia:
 Dracunculosis
 Habitat:

 Adults in subcutaneous tissues of man/reservoir

animals

110
 Morphology
I. Adult :thread like, I. Female: About 30 to 100
cylinderical oesophagus cm in length
II. Male: About 3 cm in  Swollen anterior end
length
 Hooked posterior end
 Posterior end coiled
 2 unequal spicules  Inconspicuous
vulva near anterior
end
 

111
 D. medinensis
2. Larva (or embryo):

 600 x 20 
 Rhabditiform oesophagus
 Anterior end rounded
 Tapering and long tail (1/3
body)

112
 Life Cycle of Dracunculus medinensis
• A blister is formed from the female worm's
production of embryos released beneath the skin,
and due to a burning pain that comes with this, the
victims often immerses their legs in water for relief.
• With the sudden drop in temperature that follows,
the blisters usually rupture, releasing the worms.
• These worms may release thousands of infective
juveniles at this time, which enter the water.
Before  The cephalic end of the
fertilized female
pressing on the skin,
produces a papule that
becomes a blister and
then ruptures forming
an ulcer
After
Life Cycle of Dracunculus medinensis

Infective larvae
In water, larvae Must be eaten by Copepod
(Crustacean), the IH,
 Life Cycle of Dracunculus 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.
 Life cycle of D. medinensis
 Man is infected on drinking water containing cyclops
 In the small intestine, the cyclops 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 hygrotropism and geotropism)
 Several months (9 or more) elapse between infection and appearance of the
gravid female at the skin surface

 
117
 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.
 . They penetrate its intestine and settle in the body cavity
to become infective in about 3 weeks

  118
Copepod

119
Life Cycle of D. medinensis

120
 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 turns into a cesicle and

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

 
121
Adult worm of D. medinensis

122
Adult worm of D. medinensis

123
 D. medinensis

Blister containing the worm Ruptured blister with filamentous worm

A B
124
D. medinensis

125
 D. medinensis

Adult Dracunculus in foot

126
B
 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

127
 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

1. 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

 
128
Adult D. medinensis

129
 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.

– 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.