Blood and tissue nematodes Introduction to blood and tissue nematodes Classification Clinical features

1. 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

2. 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

3. 2.1.3 Blood and tissue nematodes
2.1.3.1. General features:
• 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)

4. 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

5. 2.1.3.2. Classification:
• Tissue nematodes can be classified based on:
– Habitat in the body
– Clinical manifestation
– Morphology

6. 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

7. 2. FAMILY TRICHINELOIDAE
• Trichinella sps
3. FAMILY DRACUNCULIDAE( guinea worm)
• Dracunculus medinensis
Animal tissue nematode rarely infect human
• Dirofilaria sps
• Angiostrongylus cantonensis
• Gnathostoma spinigerem

8. 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
2.1.3.3. FAMILY FILARIDAE ( Filarial worm)

9. 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).
Animal reservoirs play no role of significance in most
places, except in sub-periodic B. malayi.
9
Cont ….

10. 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

11. • 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

12. FAMILY FILARIDAE( Filarial worm)
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

13. • 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

14. Periodicity:-
• Microfilaria of pathogenic filarial
worms that found in the blood (m.f of
filarial worms that causes lymphatic
filariasis and Loasis) show periodicity

15. 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

16. 16
Filarial worms
(Synonym)
Periodicity Main Vector
(IH)
Reservoir
O. volvulus
(River blindness)
Non Periodic Black fly (Simulium) Human
W. ancrofti (LF) Periodic (N)
22 – 04hr
(24hr)
Culex, Anopheles Human
Sub Periodic
20 – 22 (21hr)
14 – 18 (16hr)
Aedes Human
B. Malayi (LF) Periodic (N)
22 – 04hr
(24hr)
Anopheles Human
Sub Periodic
20 – 22 (21hr)
Mansonia Human, Monkey, Cat –
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 Midge (Culicoides)

17. • Flarial worm causes 3 main diseases
–lymphatic filariasis (Elephantiasis)
–Loasis
–Onchocerciasis (river blindness)

18. 2.1.3.4. Lymphatic Filariasis

19. 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”

20. 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

21. 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

22. Social consequences…..
2. The disease impeds
– Mobility
– Travel
– Educational opportiity
– Employment opportunity
– Marriage prospect

23. 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.

24. Distribution

25. 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
• Leser sunda, island of Indonesia

26. 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

27. 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.
27

28. Wuchereria bancrofti
3. Infective larvae: 1500 – 2000 x 20
– Cylinderical oesophagus
28

29. W. Bancrofti & B. Malayi
29

30. Transmission and life cycle

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

32. • 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

33. • 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.

34. • 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.

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

36. 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

37. 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

38. 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

39.  Elephantiasis:
 Hard and thick, rough and fissured skin
 Frequently legs & genitalia (scrotum, penis and vulva)
 Less often arms and breasts.

41. 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
• Responds very well to therapy with DEC
41

42. 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
42

43. 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
43

45. 45

46. 46

47. Adult female worm of W. bancrofti
47
Adult male worm of W. bancrofti

48. 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, eosinophilia, nocturnal microfilaraemia
48

49. Treatment of W. bancrofti
 Diethyl carbamazine (DEC)
 General measures:
 Rest, antibiotics, antihistamines, and bandaging
 Surgical measures for elephantiasis
49

50. 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
50

51. 2.1.3.5. Loiasis

52. 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.

53. 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
53

54. 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
54

55. 55

56. Transmission
• Horse flies (Tabanidae) in genus Chrysops
• Day-feeding & forest-dwelling
• Also called the “deer fly” or mango fly.

57. Life cycle

58. 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.

59. Clinical manifastation
• Loiasis is often asymptomatic.
• Calabar swellings (episodic angioedema)
– 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

60. Clinical manifastation
• Adult worms also migrate in sub-conjunctival
tissues.
• They can cause inflammation and irritation but
not blindness

61. 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)
61

63. 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
63

64. 64
Mf of Loa loa
Mf of M. pestans

65. 2.1.3.6. Onchocerciasis

66. Onchocerciasis
• Is a filarial disease caused by O. Volvulus
66

67. ONCHOCERCIASIS
• 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

68. DISTRUBUTION MAP
Tropical Africa between
the 15° north and the 13°
south
Foci are present in Southern
Arabia, Yemen and in S. & C.
America

69. • 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

70. 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 and muscles of black fly
70

71. 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
71

72. 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.
72

73. Onchocerca volvulus
Transmission:
• By the bite of infected vector (simulium species)
73

74. 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
74

75. 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
75

76. • 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
76

77. Life cycle of Onchocerca volvulus
77

78. Clinical feature
Onchocerciasis
• Acute onchocerciasis:
– Itchy (pruritic)
– Erythematous
– Papular rash with thickening of the skin
78

79. Clinical feature
• Chronic onchocerciasis:
– Elephant or lizard skin Hanging groin
– Leopard skin River blindness
79

80. Clinical feature
• Onchocercomata:
– Upper part of the body
(American onchocerchiasis)
– Pelvic region (African form)
• Nodules surrounded by concentric
bands of fibrous tissue
80

81. Laboratory diagnosis
• Mf in skin snips
• Mf in urine, blood & most body fluids (in heavy
infection)
– Wet mount preparation Staining
81
Skin biopsy Skin fragment

82. 82

83. • 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
83

84. 84

85. 85

86. Prevention and control
• Destruction of Simulium
• Avoiding Simulium bites
• Treatment of communities (~APOC)
86

87. Treatment
• Ivermectin:
– Paralysis of worms
– Reduces the microfilarial load
• Surgical Care:
– Nodulectomy
– Removes adult worms
87

88. 2.1.3.7. Trichinellosis

89. 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
89

90. Trichinella spiralis
 Habitat:
 Adults in the small intestine of man and animals
specially pigs and rats (reservoir hosts)
 Larvae : encysted in muscles
90

91. 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
91

92. 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)
92

93. 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
93

94. Transmission
• Eating flesh of infected pork (raw/undercooked)
94

95. Life cycle
95

96. 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)
96

97. • 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 97

98. Life cycle
 Larvae liberated from the cysts in small intestine
and mature to adults
 Larvae start to be deposited by the female
98

99. Pathogenicity
 Intestinal invasion by adult worms
 Abdominal pain, nausea, vomiting, diarrhoea and
colic.
99

100.  Migration of larvae
100

101.  Encystment of larvae
 Manifestations
depend up on organs
affected.
 > 50 – 100 larvae/gm
of muscle are
symptomatic
 < 10 larvae are often
asymptomatic
101

102. 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.
102

103. 103

104. 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
104

105. Diagnosis .....
2. Muscle biopsy:
• Direct examination
• After digestion in a pepsin hydrochloric acid medium
3. Eosinophilic leucocytosis in the acute stage
105

106. 106
Larvae, freed from
their cysts
Encysted in pressed
muscle tissue.

107. 107
Adult worm from
intestine wall

108. 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.
108

109. Treatment
 Non specific symptomatic treatment:
 Sedatives
 Cortisone and ACTH
 Supportive treatment:
 Rest, fluids, smooth diet and vitamins
 Thiabendazole
 Mebendazole
109

110. Dracontiasis

111. 2.1.3.8. Dracunculus medinenis
“Guinea worm, ”

112. Dracunculosis
 Synonyms: Dracontiasis, Dracunculosis, Dracunculiasis
 Causative agent
 Scientific name: Dracunculus medinensis
 Common name: Medina worm or Guinea worm
112

113. 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

114. Distribution of
Dracunculus medinensis
Global: Nile valley,
India and areas
where wells are
used for water
supply
Ethiopia:

115. Dracunculosis
 Habitat:
 Adults in subcutaneous tissues of man/reservoir
animals
115

116. Morphology
I. Adult :thread like,
cylinderical oesophagus
II. Male: About 3 cm in
length
 Posterior end coiled
 2 unequal spicules
I. Female: About 30 to 100
cm in length
 Swollen anterior end
 Hooked posterior end
 Inconspicuous
vulva near anterior
end
116

117. D. medinensis
2. Larva (or embryo):
 600 x 20 
 Rhabditiform oesophagus
 Anterior end rounded
 Tapering and long tail (1/3
body)
117

118. 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.

119. Before
After
 The cephalic end of the
fertilized female
pressing on the skin,
produces a papule that
becomes a blister and
then ruptures forming
an ulcer

120. Life Cycle of Dracunculus medinensis
Infective larvae
In water, larvae Must be eaten by Copepod
(Crustacean), the IH,

121. 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.

122. 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
122

123. 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
123

124. Copepod
124

125. Life Cycle of D. medinensis
125

126. 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 126

127. Adult worm of D. medinensis
127

128. Adult worm of D. medinensis
128

129. D. medinensis
129
Blister containing the worm Ruptured blister with filamentous worm
A B

130. D. medinensis
130

131. D. medinensis
131
Adult Dracunculus in foot
B

132. 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
132

133. 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
133

134. Adult D. medinensis
134

135. 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.