The document discusses several nematode parasites including Enterobius vermicularis (pinworm), Dracunculus medinensis (guinea worm), and filarial worms such as Wuchereria bancrofti and Brugia malayi. It provides details on the morphology, life cycles, transmission, symptoms, diagnosis and treatment of these parasites. Key information includes that pinworms infect the intestines and guinea worms emerge from blisters in the skin after a year of maturation, while filarial worms reside in the lymphatic system and bloodstream, being transmitted by mosquitoes.

2. Nematode general
morphology

3. Enterobius vermicularis
Dracunculus medinensis
Wuchereria bancrofti
Brugia malayi
Onchocerca vulvolos
Loa loa

4. Enterobius vermicularis
 The pinworms are one of the most
common intestinal nematodes. The
adult worms inhabit the cecum and
colon. Right after mating, the male
dies. Therefore, the male worms are
rarely seen. The female worms
migrate out the anus depositing
eggs on the perianal skin. Humans
get this infection by mouth and by
autoinfection.

5. I. Morphology
 1. Adults: The adults look like a pin and are
white in color. The female worm measures about 8
to 13 mm in size and is fusiform in shape. The
male adult is only 2-5mm. The tail of a male is
curved. They die right after mating, thus males are
rarely seen. The anterior end tapers and is flanked
on each side by cuticular extensions called
“ cephalic alae”. The esophagus is slender,
terminating in a prominent posterior bulb , which
is called esophageal bulb. The cephalic alae and
esophageal bulb are important in identification of
the species.
 2. Egg: 50 to 60m by 25 µm, persimmon seed-
like, colorless and transparent, thick and
asymmetric shell, content is a larva.

6. Adult worm of E. vermiculais

8. Morphology -- Egg
• Oval in shape, 50~60×25μm in average, a
larva inside
• Clear, colorless and doubly refractive egg
shell, flattened on one side

9. molt molt 3 times
Adults Newly laid Infective Larvae Adults
eggs 6h eggs
Life cycle

10. II. Life Cycle
1. site of inhabitation: cecum and
colon
2. infective stage: embryonated egg
3. infective route: by mouth
4. without intermediate host and
reservoir host
5. life span of female adults: 1-2
months

11.  Humans are the only host in nature
 No intermediate host (direct life cycle)
 No larval migration between organs
Characteristics of life cycle

12. III. Symptomatology
About one-third of pinworm-infected persons
are asymptomatic, The adult worms may
cause slight irritation of the intestinal mucosa.
Major symptom is anal pruritus, which
associates with the nocturnal migration of the
gravid females from the anus and deposition
of eggs in the perianal folds of the skin.
Restlessness, nervousness, and irritability,
probably resulting from poor sleep associated
with anal pruritus,. In young girls, migration
of the worms may produce vaginitis and
salpingitis or granuloma of the peritoneal
cavity.

13. Adult Pinworms on the perianal
skin

14. IV. Diagnosis
Diagnosis depends on recovery of
the characteristic eggs. The eggs and
the female adults can be removed from
the folds of the skin in the perianal
regions by the use of the cellophane
tape method. The examination should
be made in the morning, before the
patient has washed or defecated

15. V. Treatment and prevention
Since the life span of the pinworm is less
than two months, the major problem is
reinfection. Albendazole is the drug of
choice. Repeated retreatment may be
necessary for a radical cure.
Prevention: 1. treat the patients and
carriers 2. individual health 3. public
health 4. health education and hygienic
habits

16.  VI. Epidemiology
Geographical distribution—
cosmopolitan in temperate zones
with about 30 to 50% of the
population infected. It is more
common in white than colored
people and more prevalent in
children than adults. Enterobiasis is
most common where people live
under crowded conditions such as
orphanages, kindergartens, and
large families

19. Dracunculus
medinensis

20. Taxonomy
 Class: Secernentea
 Subclass: Spiruria
 Order: Spirurida
 Superfamily: Drancunculoidea
 Family: Dracunculidae
 Common names- Guinea Worm, Medina Worm,
Serpent Worm,Dragon Worm

21. History
Known as a parasite of humans
since about 1530 B.C.
Guinea worm is thought to be the
"fiery serpent" referred to in the
Bible.
The symbol of a Physician is the
"Caduceus". The serpents are
believed to represent the Guinea
worm.
Persian physicians removing the
D. medinensis parasite from
patient during the 9th century-

22. Hosts
Definitive: Humans
Intermediate: Copepod

23. Distribution
Except for a few remote
villages in the Rajastan desert of
India and in Yemen, Guinea
worm disease now occurs only in
Africa.
Infected areas in Africa lie in a
band between the Sahara and the
equator.
Presently, only 9 countries are
endemic: Sudan, Ghana, Nigeria,
Mali, Togo, Burkina Faso,
Ethiopia, Niger, and Ivory Coast.
>50% of all cases of Guinea
worm disease are reported from
southern Sudan.

24. Distribution
Smaller numbers of cases
are reported from
Ethiopia, Chad, Senegal,
and Cameroon.
Most cases occur in poor
rural villages that are not
visited by tourists.

25. Morphology
•One of the largest nematodes known.
•Adult females have been recorded up
to 800 mm long
•Few males known do not exceed 40
mm.
•The mouth is small and triangular and
is surrounded by a quadrangular,
sclerotized plate.
•Lips are absent.
•The esophagus has a large glandular
portion
•Spicules of the male are unequal and
490 to 730 um long. The gubernaculum
ranges from 115 to 130 um long.

26. Morphology
A: Adult D. medinensis
worms. (A) The adult female
guinea worm is a long,
slender worm ranging from
30 to 120 cm in length and
from 0.09 to 0.17 cm in
width.
B: Three mature guinea
worms.
 Note the tiny size of the
mature male (mm)
compared with the
mature female (mf) and
especially the markedly
elongated and
serpiginous, gravid
female worm (gf). The
gravid female shows an
extruded uterus (eu)

27. Characteristics
 Only helminthic parasite transmitted solely through
water.
 But usually occurs during drought
 Everyone is forced to drink from the same stagnant
water supplies or pay for well.
 Three conditions to be met before D. medinensis can
complete it’s life cycle.
 The skin of an infected individual must come in
contact with water
 The water must contain the appropriate species of
microcrustacean
 The water must be used for drinking
 Believed the parasites feed on blood due to the gut often
being filled with dark brown gut material

28. Life Cycle

29. Life Cycle
 Humans become infected by drinking unfiltered water containing
copepods (small crustaceans) which are infected with larvae of D.
medinensis
 Following ingestion, the copepods die and release the larvae, which
penetrate the host stomach and intestinal wall and enter the abdominal
cavity and retroperitoneal space.
 The worm molts again 20 days and 43 days post infection
 Females are fertilized by the third month.
 After maturation into adults and copulation, the male worms die and
the females (length: 70 to 120 cm) migrate in the subcutaneous tissues
towards the skin surface
 Approximately one year after infection, the female worm induces a
blister on the skin, generally on the distal lower extremity, which
ruptures.
 When this lesion comes into contact with water, which the patient seeks
to relieve the local discomfort, the female worm emerges and releases
larvae
 The larvae are ingested by a copepod and after two weeks (and two
molts) have developed into infective larvae

30. Diagnosis
 Diagnosis is made from the local blister,
worm or larvae.
 The outline of the worm under the skin.
 Some people claim to be able to feel the
worm moving towards the surface of the
skin.
 Finding Calcified worms.

31. Epidemiology
 Dracunculiasis may result in three
major disease conditions
 Emergent adult worms
 Secondary bacterial infection
 Nonemergent worms
 When worms do not emerge they degenerate and
release antigens causing fluid filled abscesses or
allergenic reactions.
 If the worms become calcified they can cause
inflammation or if they remain in a joint, arthritis.
 Can cause paraplegia if it worm gets into the central
nervous system.

32. Pathology
 None until the female worms cause an allergic reaction by releasing
metabolic wastes into host. This occurs at the onset of migration to the
skin.
 a rash accompanied by severe itching
 nausea
 vomiting
 diarrhea
 dizziness
 edema
 Reddish papule-blister (local itching and intense burning).
 Blister ruptures, becomes abscessed-very painful.
 Secondary bacterial infections of opening possible.
 Retreating worm can draw bacteria under skin as well.
 There may be later symptoms
 fibrosis of the skin, muscles, tendons and joints (may interfere with
locomotion or use of limbs)
Blister

33. Pathology
Adult in joint 
Calcified lesion in soft
tissues 

34. Treatment
 Drug Therapy—Metronidazole
 To help prevent bacterial infections
 Anti-inflammatory to help reduce swelling
 Treatment includes the extraction of the adult guinea
worm by rolling it a few centimeters per day
 Usually takes weeks or months depending on how long the
worm is.
 Exposing area to cold water helps remove worm faster.
 Preferably by multiple surgical incisions under local
anesthesia.
 Infection does not make a person immune

35. Control
 Construction of copings around well heads
or the installation of boreholes with hand
pumps.
 Borehole is a deep and narrow well.
 Coping is a cap/cover over a well
 Key is to prevent copepod growth by controlling
sunlight. Light increases the food source of the
copepod.

36. Order Filariata
 Filarial worm
1. Wuchereria bancrofti
2. Brugia malayi
3. Onchocerca
4. Loa

37. Common Characteristics
 Biohelminth
 Need intermediate host
 Location (residing site)
 Tissue and blood
 Ovoviviparous (larviparous)
 adult female deposit larvae

38. Filaria
 2 types of filaria
 Lymphatic filaria
 Tissue filaria
 Subcutaneous tissue (O.volvulus, L.loa)
 Peritoneal cavity (M.perstans)
 All species are transmitted by insect
vectors
 8 species could infect human being

39. Most Important Species
 Tissue filaria
 Onchocerca volvulus: river blindness
 Loa loa: subcutaneous swelling
 Lymphatic filaria
 W. Bancrofti
 B. Malayi

40. Morphology
 Adult
 Grossly a
white silk,
thread-
like
 W.b >
B.m

41.  Microfilaria (Mf)
 Appear in host peripheral circulation
during night
 Structure
 Cephalic space
 Somatic nuclei
 Caudal nuclei
 Sheath, etc.

42. Differentiation of Mfs Between W.b
and B.m
W.b B.m
Size Large Small
Curvature Smooth Kinky
Cephalic space Short Long
Somatic nuclei Clear & separated Fused
Caudal nuclei None 2

43. Microfilariae measure 270 by 8 m, have a sheath and
a tail with terminal constriction, elongated nuclei and
absence of nuclei in the cephalic space. They have
nocturnal periodicity.
(Wet mount preparation).

44. Microfilaria of Brugia malayi

45. Microfilaria of Wuchereria bancrofti

46. Brugia malayi: the cephalic space is longer than broad
(in W.bancrofti is as long as broad).

50. Main Points of Life Cycle
 Location (adult): lymphatic system
 W.b: superficial and deeper
e.g. lower limbs, groin, scrotum, etc.
 B.m: superficial
e.g. mainly in lower limbs
 Infective stage: filariform larva
 Infection route: mosquito inoculation
 Discharge stage: microfilaria

51.  Intermediate host & vector:
mosquito
 W.b: Culex (Anopheles)
 B.m: Anopheles (Aedes)
 Infection threshold
 15-100Mf/20mm
 Mf show nocturnal periodicity

52.  Nocturnal periodicity
 Mfs appear in the peripheral blood in high
density during the night, but hide in the
pulmonary capillaries during the daytime
while the host is awaken.
 W.b: 10 Pm ~ 2 Am
 B.m: 8 Pm ~ 4 Am

53. Pathogenesis
 Main pathogenic factor
 Adult
 Acute stage
 Lymphangitis, Lymphadenitis
 B.m: lower limbs
 W.b: limbs & uro-gential
(epididymitis, orchitis)

54.  Chronic stage
 Elephantiasis could be seen in both
filarial infection
 W.b: chyluria, hydrocele

55. Lymphatic filariasis: elephantiasis is the last
consequence of the swelling of limbs and scrotum.

56. Early hydrocoel in a Tanzanian man with W.bancrofti infection

57. Lymphatic filariasis: elephantiasis of scrotum.
Genital manifestations are frequent in
W.bancrofti infections while they are rare during
B.malayi infections.

58. Bancroftian filariasis:Elephantiasis of scrotum

59. Epidemiology
 Distribution:
 Tropic region, coexist with mosquito
 W.b: global
 B.m: Asia
 China
 15 provinces, mixed
 Shandong,Tai wan,Hainan only W.b

60. Lymphatic filariasis have a wide geographic distribution.
W.bancrofti and B.malayi infect some 128 million people,
and about 43 million have symptoms.
B.malayi infection is endemic in Asia
(China, Corea, India, Indonesia, Malaysia, Philippines, Sri
Lanka). W.bancrofti has a larger distribution : Asia
(China, India, Indonesia, Japan, Malaysia, Philippines, South-
East Asia, Sri Lanka, Tropical Africa, Central and South
America, Pacific Islands.

61. Endemic links
 Source of infection
 Patient
 Mosquito
 W.b: Culex (Anopheles)
 B.m: Anopheles (Aedes)
 Susceptible population: human
 Natural & social factors

62. Laboratory Diagnosis
 Etiological examination
 Stained thick blood smear: first choice of
methods
 Blood drop microscopy: used in the field
 Hetrazan induced method
 Lymph node biopsy

63. Principle of Control
 Mass treatment: Hetrazan
 Hetrazan-salt: 0.3%, 6 months
 Elephantiasis-baking bandage
 Mosquito biting control

64. Biological characteristics
 Zoonosis
 Ovoviviparous
 Adult & larva live in the same host
individual
 Adult: small intestine
 Larva: striated muscle

65. ONCHOCERCA
VOLVULUS

66. TAXONOMY
Kingdom: Animalia
Phylum: Nematoda
Class: Secernentea
Order: Spirurida
Family: Filariidae
Genus: Onchocerca
Species: O. volvulus

67. ONCHOCERCA VOLVOLUS
 A helminthes worm
 The male is usually 2-3 cm long;
the female is usually 50 cm long
 Adults occur in the subcutaneous
tissue and in nodules
 Microfilaria are usually 300 X 8
micrometers long
 An adult female worm can produce
over 1000 microfilariae in a day,
resulting in millions over a lifetime
 Adult worms have a life span of 10-
15 years
 Lips and a buccal capsule are
absent
Adult O. volvolus
Microfilaria

68. ONCHOCERCIASIS
 Commonly known as river blindness
 The world’s second leading infectious cause of blindness
 The World Health Organization's (WHO) estimates the
global prevalence is 17.7 million, of whom about 270,000
are blind

69. DISTRIBUTION
 Tropical Africa between the 15° north
and the 13° south (high endemicity in
Burkina Faso and Ghana)
 Foci are present in Southern Arabia,
Yemen and in America (Mexico,
Guatemala, Colombia, Ecuador, Brazil,
Venezuela)
 Predominantly located in rural
agricultural villages located near rapidly
flowing streams

70. DISTRUBUTION MAP

71. LIFE CYCLE
Onchocerciasis is linked with
fast flowing rivers where
Simulium blackflies breed.
An infected female blackfly
takes a blood meal from a host.
The hosts skin is stretched by
the fly’s apical teeth and cut by
its mandible.

72. LIFE CYCLE
The third stage larvae enter
subcutaneous tissue, migrate,
form and lodge in nodules, and
slowly mature into adult worms.
New worms form new nodules
or find existing nodules and
cluster together.
The smaller male worms may
travel through nodules and
mate.

73. LIFE CYCLE
After mating, eggs form inside
the female worm, develop into
microfilariae and leave the worm
one by one.
Thousands of microfilariae
migrate in the subcutaneous
tissue.

74. LIFE CYCLE
Some microfilariae die causing
skin rashes, lesions, intense
itching, or skin depigmentation.
Microfilariae also can travel to
the eye, causing blindness.

75. LIFE CYCLE
The infected host is bitten by
another female fly. Microfilariae
are transferred from the host to
the blackfly, where they develop
into infective larvae.
Inside the fly, the larvae travel to
the fly’s thoracic muscles and
develop into a third stage
larvae. The cycle begins
again…

76. OVERVIEW OF LIFE CYCLE

77. ONCHOCERCIASIS
 The intensity of human infection (number of worms in an individual) is related to the number of
infectious bites endured by an individual.
 Blindness is almost always in persons with intense infection.
 An individual may be asymptomatic. Those with symptoms usually experience nodules, skin
rashes, eye lesions, bumps under the skin. The eye lesions can manifest into blindness.
 Incubation periods last from nine to 24 months after the initial bite.
 The hosts white blood cells usually release cytokines that effect the infected tissue and thus killing
the microfilariae, which causes “lizard skin” (swelling and thickening of skin) and “leopard skin”
(loss of pigment).

78. DIAGNOSIS
 The most common is fresh examination of blood-free skin
snips; however, this does not always show the presence of
the parasite.
 Serologic testing for antibodies is available; however, a
positive result doesn’t guarantee onchoceriasis.

79. TREATMENT
 Ivermectin (mectizan) is administered as an oral
dose of 150 micrograms per kilogram (maximum
12 mg) every 6-12 months.
 The drug paralyses the microfilariae and prevents
them from causing itching.
 Ivermectin does not kill the adult worm; it does
prevent them from producing additional offspring.
 Surgical removal of the nodules is also available.
 There is no vaccine.

80. FURTHER PREVENTION
 Avoiding the day when the Simulium
blackflies tend to bite
 Using insecticides such as DEET
 Wearing long sleeves and pants

81. Loa loa
The eye worm
Chrysops (deer fly

82. Loa loa
The most troublesome infection sites -
- conjunctiva
●Pathogenic stage:
Adult worm
● Intermediate host：
Chrysops
● Mildly pathogenic
● Adult worms wander
through out the body
(1.5cm/min) and cause
pathology

83. Loa loa
Cabalar swelling

84. Loa loa
Loa loa adult in Calabar swelling x section

85. Epidemiology
Loa loa
 Loaiasis is now
limited to the African
equatorial rain forest
and southern Sudan
Infection rates are
highest in regions with
muddy ponds and
swamps

87. Prevention
 Treatment of the patients
Surgical removal of wandering adult worms from the
conjunctiva is advisable
Chemotherapy: Diethylcarbamazine/Ivermectin (effective
to kill microfilariae), but may both have severe side-effects
 Control of insect vector population
 Protective netting and screening to shield individuals