The document provides background information on helminths (parasitic worms). It discusses their lifecycles, transmission methods, locations within the host body, and impacts on human health. Specifically, it covers the major groups of intestinal nematodes (roundworms) that commonly infect humans, including their classification, lifecycles involving egg/larval stages and environmental transmission, clinical symptoms, and methods of diagnosis through fecal sample examination.

1. HELMINTHOLOG
Y
1
Mr Ng’andu. S

2. BACKGROUND TO HELMINTHS
 The term “helminth” (Greek helmins-’worm’) originally referred to intestinal worms, but now
comprises many other worms, including tissue parasites as well as many free-living species
 Helminthic parasites have an outer protective covering, the cuticle or integument which may
be tough and armed with spines or hooks.
 The cuticle of live helminths is resistant to intestinal digestion
 The eggs or larvae are produced in enormous numbers—as many as 200,000 or more per
female per day.
 Helminths differ from protozoa in their inability to multiply in the body of the host.
 Protozoa multiply in the infected person so that disease could result from a single infection.
But helminths apart from very rare exceptions do not multiply in the human body so that a
single infection does not generally lead to disease. Heavy worm load follows multiple
infections.
2

3. BACKGROUND TO HELMINTHS
 Parasitic worms, commonly referred to as helminths, are the most common parasites
infecting humans.
 They are macroparasites and adults can generally be seen with the naked eye.
 They are transmitted to humans through food, water and soil, arthropod and molluscan
vectors.
 Majority of the parasitic worms are intestinal worms that are soil-transmitted and infect the
gastrointestinal tract.
 Other parasitic worms such as schistosomes reside in blood vessels.
3

4. BACKGROUND TO HELMINTHS
 Parasitic worms live in and feed in living hosts. They receive nourishment and protection
while disrupting their hosts' nutrient absorption.
 This can cause weakness and disease of the host. In their adult form, parasitic worms cannot
multiply in humans.
 Helminths are able to survive in their mammalian hosts for many years due to their ability to
manipulate the immune response by secreting immunomodulatory products.
 All parasitic worms produce eggs that have a strong shell to protects them against a range of
environmental conditions.
 The eggs can therefore survive outside their hosts, in the environment for many months or
years. 4

5. BACKGROUND TO HELMINTHS
 Based on their shape and other characteristics, helminths are classified into two
broad groups:
1) The cylindrical (round) worms belonging to the Phylum Nemathelminthes
(Class Nematoda) commonly called Nematodes and
2) The flat worms belonging to the Phylum Platyhelminthes.
 The flat worms in turn are classified into two categories—the leaf-like Trematodes
(Class Trematoda) or flukes and the tape-like Cestodes (Class Cestoda) or
tapeworms.
5

6. THE ROUNDWORMS
 Nematodes comprise the group of organisms containing the largest number of
helminth parasites of humans.
 Humans are definitive hosts for many roundworms of medical importance.
 The adult female produces fertilized eggs, or larvae which may be infective to new
host in three ways:
i. Eggs are immediately infective after ingestion by humans
ii. Eggs or larvae require a period of development in the environment to become
infective
iii. Eggs or larvae are transmitted to a new host by an insect.
6

7. THE ROUNDWORMS
 Developing larvae go through a series of 4 molts with the third stage, the
filariform larva*, being most often the infective stage.
 Infection with roundworms can be by ingestion of infective eggs or larvae or by
larval penetration of skin or by transmission of larvae through insect bite.
 About one-half of the nematodes parasitic for man are intestinal, the others are
found in various tissues.
 Pathogenicity of intestinal nematodes may be due to larval migration through
body tissues, piercing of intestinal wall, bloodsucking activities of worms or
allergic reactions to secretions, worms or larvae. 7

8. INTESTINAL NEMATODES
 General Life Cycle of Intestinal nematodes
 Humans ingest infective eggs. Hookworm and Strongyloides stercoralis are
exceptions, in these filariform larvae penetrate the skin to gain entry.
 Male and female adults develop in the intestine. With Ascaris lumbricoides, and
Strongyloides stercoralis larvae penetrate the intestinal mucosa and initiate a heart
– lung cycle enroute to the intestinal tract to mature to adults.
 Fertilized eggs are produced
 Diagnostic stage - eggs or larvae in feces.
 Larvae develop within the egg in warm, moist soil (except for Strongyloides
stercoralis, whose eggs hatch in the intestine, with larvae passing in the feces)
8

9. INTESTINAL NEMATODES
 Enterobius vermicularis - The Pinworm
 It is a group infection especially common among children, often associated with low
sanitation and hygiene.
 Humans are the only known host
 Eggs are ingested, hatch in intestine, larvae mature, adults live in the colon.
 Gravid females migrate to the perianal area at night to lay eggs.
 Eggs develop to the infective stage within 4-6 hours.
 Eggs are resistant to drying, and can survive for extended periods in cool, moist
environment. Viable eggs can be found on bed linens, towels, furniture, windowsills,
door jams and in dust.
 Cleaning eggs from the environment and treating all persons in the household is
important in order to break life cycle.
 Eggs are found only rarely in fecal samples because release is most often external to
the intestines. 9

10. INTESTINAL NEMATODES
 Diagnosis of the Pinworm
(1) Recovery and identification of eggs or adults from the perianal region utilizing
the cellophane tape preparation.
(2) Specimens must be collected the first thing in the morning upon waking,
especially before bathing or bowel movements.
(3) Eggs are rarely found in fecal samples because release is usually external to
the intestines.
 Pathology and symptoms
Most cases are asymptomatic
Other symptoms may be due to the migration of the female out of the anus to lay her
eggs and include: severe perianal itching due to hypersensitivity reaction, loss of sleep,
irritability, slight irritation of the intestinal mucosa, and vulval irritation in girls from
migrating worms (after egg laying, worm may migrate into the vagina instead of the
anus).
10

11. INTESTINAL NEMATODES
 Trichuris trichiura - The Whipworm
 Life cycle
(1) Infective, fully embryonated eggs are ingested, larvae hatch in small
intestine, penetrate and develop in the intestinal villi, return to lumen and
migrate to the area of the cecum.
(2) Larvae mature and live in the colon. Worms embed their anterior
portion (as much as two-thirds of the worm) into the mucosa.
(3) Eggs are released into the stool.
(4) Eggs must undergo development in the soil for a period of time
(approximately 10 days to 3 weeks) before they become infective.
(5) The worm’s life span is estimated to be 4 - 8 years.
11

12. INTESTINAL NEMATODES
 Diagnosis of the Whipworm
 Through recovery and identification of eggs in the feces.
 Pathology and symptoms
 Slight infections - are usually asymptomatic, no treatment is necessary.
 Heavy infections - surface of colon is entangled with worms which causes bloody
or mucoid diarrhea, weight loss and weakness;
 Infections with 200 or more worms in children may cause a chronic dysentery,
profound anemia and growth retardation, abdominal pain and tenderness.
 Distribution:
 It is the third most common intestinal helminth infection.
 Higher prevalence in warm countries and areas of poor sanitation, especially in
countries which utilize "night soil" for fertilizer.
 Common among children and in the institutionalized mentally retarded*. 12

13. INTESTINAL NEMATODES
 Ascaris lumbricoides- The large intestinal Roundworms
 Life cycle - complex, involves a heart-lung cycle:
(1) Humans ingest embryonated eggs containing infective larvae.
(2) Larvae hatch from the eggs in the small intestine, penetrate the intestine wall, enter the bloodstream, migrate
to the liver, travel to the lung via the blood stream.
(3) Larvae break out of lung capillaries into alveoli, travel to the bronchioles, and are coughed up to the pharynx.
They are swallowed and return to the intestine. Two molts to 4th stage larvae take place in alveoli.
(4) Larvae mature to adults in the small intestine.
(5) The large, muscular worms do not attach to the intestinal wall, but maintain their position by constant
movement.
(6) Undeveloped eggs are passed in the feces. These eggs embryonate in the soil and are infective after
approximately two weeks to one month. The egg shell is very thick, making it quite resistant to environmental
changes.
(7) Eggs remain infective for up to 5 years if protected from direct sunlight and desiccation.
13

14. INTESTINAL NEMATODES
 Diagnosis of Ascaris lumbricoides
 Through recovery and identification of eggs and/or adults in the feces.
 Pathology and symptoms
(1) Pneumonia - associated with migration of larvae in the lungs.
(2) Obstruction of the intestines, appendix, or common bile duct.
(3) Vomiting and abdominal pain.
(4) May cause malnutrition in children with heavy infections or poor diet.
(5) Some infections are asymptomatic .
 Eggs of Ascaris lumbricoides thrive best in clay soil with dense shade, heavy rain
and warm climate.
14

15. INTESTINAL NEMATODES
 Ascaris is the largest intestinal nematode.
 Mixed infections with T. trichiura are common.
 If both are present it is best to treat the Ascaris infection first, since it is the more
likely of the two to migrate.
 Any non-specific therapy, or (especially) administration of anesthesia can cause
worms to migrate, including penetrating the intestinal wall; forcing through the
pyloric and cardiac valves of the stomach, thus entering the esophagus, or
crawling into the common bile duct. All are potentially dangerous.
 Adult worms may rarely be recovered from the anus, mouth, throat or nose.
15

16. INTESTINAL NEMATODES
 Hookworms- two species
i. Necator americanus
ii. Ancylostoma duodenale
 Life cycle
(1) Under optimal conditions, eggs in fecally contaminated soil develop and hatch within 24
to 48 hours, becoming rhabditiform larvae. Growth and development continue to take
place in the soil as the larvae feed on bacteria and organic material and undergo a first
molt.
(2) After about 7 days the worms stop feeding and molt a second time, transforming from
the rhabditiform larvae to infective filariform larvae.
(3) Infective larvae do not feed and can survive for approximately 2 weeks without a host.
They usually live in the upper layers of the soil, and when the soil is cool and moist,
they climb to the highest point covered by a film of moisture. They extend their bodies
into the air and remain waving about in this position until driven down by drying of their
surroundings or by heat, or until they come in contact with the skin of a suitable host.
16

17. INTESTINAL NEMATODES
 Life cycle of hookworms ctd…
4. Infections are acquired when the third stage filariform larvae penetrates the skin
of a human.
5. Larvae enter the lymphatic system or bloodstream, and travel to the lungs. After
maturating in the lungs, the larvae migrate up the trachea to be swallowed and
reach the small intestine, where they mature.
6. Immature adults attach to the intestinal mucosa by means of their stout mouth
parts and suck blood and tissue juices of the host.
7. About five weeks after infection, the worms have undergone a final molt to
become sexually mature adults. Fertilization occurs, and the females begin to
release eggs. Worm life span is about 1 year. 17

18. INTESTINAL NEMATODES
 Diagnosis of hookworms:
 Recovery and identification of eggs (rarely larvae) in the feces.
 Cannot differentiate Hookworm species by egg appearance.
 To determine if a significant infection is present make a saline direct smear, count the number of eggs on the
entire smear, if there are less than 5 eggs per smear it is indicative of a light infection (usually no anemia), 20 or
more eggs per smear is clinically significant, and 100 or more per smear is indicative of a very heavy infection.
 Pathology and symptoms of hookworms:
 After repeated infections severe allergic itching at site of penetration may occur (cutaneous larva migrants).
 During migration through the lungs, patients may experience a sore throat and / or bloody sputum.
 Heavy intestinal infections may result in enteritis, anemia, weakness, and loss of strength due to the anemia.
 Chronic intestinal infections may experience slight anemia, weakness, weight loss and non-specific gastro-
intestinal symptoms.
 A combination of nutritional and disease factors are commonly seen in endemic areas. Children may exhibit
stunted growth and intellectual development.
18

19. INTESTINAL NEMATODES
 Moist, warm regions of the world where the skin frequently contacts the soil is
optimal for heavy hookworm infections, especially in areas of poor sanitation.
 Delayed fecal examination can result in eggs hatching. The technologist must
then differentiate the larvae from those of Strongyloides stercoralis.
 In heavy infections, blood loss can be up to 100 milliliters/day. In these instances,
one must provide dietary and iron support with drug treatment.
19

20. INTESTINAL NEMATODES
 Hookworm, Ascaris, and whipworm are known as soil-transmitted helminths (STH).
Together, they account for a major burden of disease worldwide and classified as a
neglected tropical disease
 The main species of the STH that infect people are the roundworm (Ascaris
lumbricoides), the whipworm (Trichuris trichiura) and hookworms (Necator
americanus and Ancylostoma duodenale).
 There is no direct person-to-person transmission, or infection from fresh faeces,
because eggs passed in faeces need about 3 weeks to mature in the soil before
they become infective.
 Since these worms do not multiply in the human host, re-infection occurs only as a
result of contact with infective stages in the environment 20

21. INTESTINAL NEMATODES
 Strongyloides stercoralis - The Threadworm
 Life cycle
(1) Infective third stage filariform larvae penetrate skin, and enter the lymphatic
system or bloodstream.
(2) Larvae migrate to the lungs, break out of lung capillaries into alveoli.
(3) After maturation, larvae travel up to the pharynx, are swallowed, and return to the
intestine.
(4) Larvae mature to adults and attach to the mucosa of the small intestine.
(5) Parthogenetic Females only - no parasitic males.
(a) Females are believed to be capable of unisexual reproduction, no fertilization
required.
(b) Produce viable eggs.
21

22. INTESTINAL NEMATODES
 Life cycle of Strongyloides stercoralis ctd
(6) Eggs hatch in mucosa – larvae have 3 pathways of existence:
(a) First stage rhabditiform larvae (non-infectious) are passed in feces, live in the soil,
mature into a free-living adult males and females, which produce eggs. Within 2-3
days rhabditiform larvae hatch from these eggs.
Within 24 hours these develop into other free-living adults or molt to become
infective filariform larvae. They can live up to two weeks in soil. Filariform larvae
must penetrate skin.
(b) Rhabditiform larvae live in soil and develop into infective filariform larvae which
penetrate the skin.
(c) First stage larvae develop into infective stage larvae in the intestine (autoinfection)
and causes hyperinfection.
Note: Eggs hatch in the intestine and are not usually passed in stool specimens. 22

23. INTESTINAL NEMATODES
 Diagnosis Strongyloides stercoralis
Through recovery and identification of larvae in the feces or recovery and
identification of eggs in duodenal drainage.
 Pathology and symptoms of Strongyloides stercoralis
Skin – allergic reactions; raised, itchy, red blotches at the site of larval penetration.
Lungs - pneumonia.
 Intestinal - abdominal pain, diarrhea/constipation, vomiting, weight loss, variable
anemia, increased eosinophil count.
Light infections are usually asymptomatic.
Heavy infection - bowel becomes edematous and congested.
Death may occur in immunosuppressed patients due to heavy autoinfection and larval
migration throughout the body with bacterial infections secondary to larval spread and
intestinal leakage. 23

24. INTESTINAL NEMATODES
 Parasitic female is parthogenetic; no parasitic males exist.
 While hookworm infection dies out over a period of some years after the patient has
moved from an endemic area, strongyloidiasis may persist for years, regardless of
change in location, due to autoinfection (internal infection).
 Strongyloidiasis is difficult to treat.
 (a) Thiabendazole – the drug of choice, but it has side effects.
 (b) Mebendazole - is better tolerated, but less effective.
 (c) Albendazole - is tolerated fairly well
 (d)Ivermectin has been found effective.
 In cases with severe diarrhea, embryonated eggs* may be present in stool
specimens. 24

25. BLOOD & TISSUE NEMATODES
Trichinella spiralis - trichinosis
 Trichinella spiralis is a parasite of carnivorous mammals. It is especially common in
rats and swine fed uncooked garbage and slaughterhouse scraps.
 Human infections occur most often as a result of consumption of raw or undercooked
pork
Life cycle of Trichinella spiralis
i. Infective stage larvae are ingested in meat products (encysted larvae are in the
muscle of infected and undercooked pork, deer, walrus, bear).
ii. Tissue is digested, larvae are freed in the intestine. They mature into adult males
and females.
iii. Female in the deep mucosa releases larvae. These disseminate throughout the
body via the bloodstream. (No eggs)
iv.Larvae encyst in striated muscle.
25

26. BLOOD & TISSUE NEMATODES
 Diagnosis of Trichinella spiralis through:
Identification of encysted larvae in muscle biopsy. Muscles richest in blood supply are
preferred for biopsy - larvae spread via bloodstream.
Serology becomes positive 3 to 4 weeks after infection.
A history of eating undercooked pork, deer, walrus or bear is indicative whenever
appropriate symptoms appear.
26

27. BLOOD & TISSUE NEMATODES
 Diagnosis of Trichinella spiralis
 Pathology and symptoms of Trichinella spiralis
Fever, muscle pain, bilateral periorbital edema, and increased eosinophil count
warrant a presumptive diagnosis.
Intestinal phase – patients experience small intestinal edema and inflammation,
nausea, vomiting, abdominal pain, diarrhea, headache and fever.
Migrational phase - high fever, blurred vision, edema, cough and pleural pains lasting
one month with heavy infection.
Muscle phase – acute, local inflammation with edema and pain of the musculature.
 Trichinella spiralis has cosmopolitan in distribution; worldwide among meat-eating
populations
27

28. BLOOD & TISSUE NEMATODES
 The Filariae
Filariae are long thread-like nematodes that inhabit portions of the human
subcutaneous tissues and lymphatic system.
Female worms produce eggs. The eggs modify, becoming elongated and worm-like in
appearance and adapting to life within the vascular system.
These modified eggs, referred to as microfilariae, are capable of living a long time in
the vertebrate host, but cannot develop further until ingested by an intermediate host
and vector, an insect.
The microfilariae transform into infective larvae in the insect and are deposited in the
skin of the next suitable host when the insect next takes a blood meal.
28

29. BLOOD & TISSUE NEMATODES
 General life cycle Filariae
(1) Human infection is acquired when infective larvae enter the skin at the
arthropod’s feeding site.
(2) Larval migration and development takes place in the tissue.
(3) Adults are in various tissues (species determined) and mature and produce
microfilariae.
29

30. BLOOD & TISSUE NEMATODES
 Wuchereria bancrofti – a blood & lymphatic dweller.
 The infection often results in elephantiasis. Commonly called “Bancroft's Filariasis.”
 Onchocerca volvulus – the “blinding filarial.” Infections involve the dermis and
subcutaneous tissues, where adults gather within nodules.
 Vectors:
Wuchereria bancrofti – Culex, Aedes, & Anopheles mosquitoes.
Onchocerca volvulus – Simulium flies (blackfly)
30

31. BLOOD & TISSUE NEMATODES
 Diagnosis
W. bancrofti, is diagnosed by detection and identification of microfilaria in stained
blood smears.
O. volvulus - microfilariae are found in skin scrapings around nodules. Microfilariae
are found only in skin, not in the blood stream.
31

32. BLOOD & TISSUE NEMATODES
 Pathology and symptoms
 W. bancrofti
Swelling due to allergic reaction occurring around the worms produces obstruction.
Each individual reacts differently. Very few develop elephantiasis, but in some this is
extensive.
 O. volvulus
Characterized by fibrotic nodules encapsulating adults.
Blindness occurs due to the presence of microfilariae in all ocular structures. This
parasite is a major cause of blindness in Africa.
Control is difficult because Simulium flies breed in running water.
32

33. TREMATODE PARASITES
 The life cycle of the medically important trematodes involves a sexual cycle in
humans (definitive host) and asexual reproduction in freshwater snails
(intermediate hosts)
 Transmission to humans takes place either via penetration of the skin by the free-
swimming cercariae of the schistosomes or via ingestion of cysts
 The important trematodes are:
i. Schistosoma species (blood flukes)
ii. Fasciola hepatica
33

34. TREMATODE PARASITES
 SCHISTOSOMA
 Disease: Schistosomiasis
1. Schistosoma mansoni and Schistosoma japonicum affect the gastrointestinal tract
2. Schistosoma haematobium affects the urinary tract
Important properties of Schistosomes
 Adult schistosomes exist as separate sexes but live attached to each other
 S. mansoni and S. japonicum adults live in the mesenteric veins, whereas S.
haematobium lives in the veins draining the urinary bladder.
 Schistosomes are therefore known as blood flukes
34

35. TREMATODE PARASITES
 General Life Cycle of Schistosomes
• Humans are infected when the free-swimming, fork-tailed cercariae penetrate the
skin
• They differentiate to larvae (schistosomula), enter the blood, and are carried via the
veins into the arterial circulation
• Those that enter the superior mesenteric artery pass into the portal circulation and
reach the liver, where they mature into adult flukes
• S. mansoni and S. japonicum adults migrate against the portal flow to reside in the
mesenteric venules
• S. haematobium adults reach the bladder veins through the venous plexus between
the rectum and the bladder
35

36. TREMATODE PARASITES
 General Life Cycle of Schistosomes contd
• In their definitive venous site, the female lays fertilized eggs, which penetrate the
vascular endothelium and enter the gut or bladder lumen, respectively
• The eggs are excreted in the stools or urine and must enter fresh water to hatch
• Once hatched, the ciliated larvae (miracidia) penetrate snails and undergo further
development and multiplication to produce many cercariae
• Cercariae leave the snails, enter fresh water, and complete the cycle by
penetrating human skin
• The three schistosomes use different species of snails as intermediate hosts
36

37. Feature S. japonicum S. mansoni S. haematobium
Testes (male) 6-7 in a single file 8 -9 in a zigzag row 4 -5 in groups
Ovary (female) In the middle of the
body; contains 50 or more
eggs
Anterior to the middle of
the body; contains 1-3 eggs
Behind the middle of the body;
contains 20 – 30 eggs
Intestine Short Longest Long
Egg Lateral knob Lateral spine Terminal spine
Intermediate host Oncomelania Biomphalaria and Australorbis Bulimus (Physopsis
Definitive Host Man and domestic
animals
Man Man
37

38. 38

39. TREMATODE PARASITES
• Pathogenesis of Schistosomes
• Most of the pathologic findings are caused by the presence of eggs in the liver, spleen, or
wall of the gut or bladder
• Eggs in the liver induce granulomas, which lead to fibrosis, hepatomegaly, and portal
hypertension
• The granulomas are formed in response to antigens secreted by the eggs
• Hepatocytes are usually undamaged, and liver function tests remain normal
• S. mansoni eggs damage the wall of the distal colon (inferior mesenteric venules), whereas
S. japonicum eggs damage the walls of both the small and large intestines (superior and
inferior mesenteric venules)
• The damage is due both to digestion of tissue by proteolytic enzymes produced by the egg
and to the host inflammatory response that forms granulomas in the venules
• The eggs of S. haematobium in the wall of the bladder induce granulomas and fibrosis,
which can lead to carcinoma of the bladder 39

40. TREMATODE PARASITES
• Clinical Findings
• Most patients are asymptomatic, but chronic infections may become symptomatic
• The acute stage, which begins shortly after cercarial penetration, consists of itching and
dermatitis followed 2 to 3 weeks later by fever, chills, diarrhea, lymphadenopathy, and
hepatosplenomegaly
• Eosinophilia is seen in response to the migrating larvae
• This stage usually resolves spontaneously
• The chronic stage can cause significant morbidity and mortality
• In patients with S. mansoni or S. japonicum infection, gastrointestinal hemorrhage,
hepatomegaly, and massive splenomegaly can develop
• Patients infected with S. haematobium have hematuria as their chief early complaint
• Superimposed bacterial urinary tract infections occur frequently
• Diagnosis depends on finding the characteristic ova in the feces or urine 40

41. TREMATODE PARASITES
• Fasciola hepatica
• Sheep liver fluke, causes disease primarily in sheep and other domestic animals
• Humans are infected by eating watercress (or other aquatic plants) contaminated by
larvae (metacercariae) that excyst in the duodenum, penetrate the gut wall, and
reach the liver, where they mature into adults
• Hermaphroditic adults in the bile ducts produce eggs, which are excreted in the
feces
• The eggs hatch in fresh water, and miracidia enter the snails
• Miracidia develop into cercariae, which then encyst on aquatic vegetation
• Sheep and humans eat the plants, thus completing the life cycle
• Diagnosis is made by identification of eggs in the feces 41

42. CESTODE PARASITES
• Clinically important cestodes pathogenic to man are:
• Taenia solium (pork tapeworm),
• Taenia saginata (beef tapeworm),
•
• Echinococcus granulosus and E. multilocularis (hydatid).
• Epidemiology
• These cestodes have a worldwide distribution but incidence is higher in
developing countries.
• Infection rate is as high as 10% in the third world.
42

43. CESTODE PARASITES
• T. saginata
• Can be up to 4 to 6 meters long and 12 mm broad
• It has a pear-shaped head (scolex) with four suckers but no hooks or neck.
• It has a long flat body with several hundred segments (proglottids).
• Each segment is about 18 x 6 mm with a branched uterus (15-30
branches).
• T. solium is slightly smaller than T. saginata.
• It has a globular scolex with four suckers and a circular row of hooks
(rostellum) that gives it a solar appearance.
• There is a neck and it has a long flat body (0.1 meter in length).
• The proglottids are 5 x 10 mm with a 7-12 branch uterus.
 The proglottids of Taenia species can be identified by the number of uterine
branches; 7-13 for T. solium and 15-20 for T. saginata
• The eggs of T. solium and T. saginata are indistinguishable
43

44. 44

45. CESTODE PARASITES
• Life cycle
• A tapeworm larval cyst (cysticercus) is ingested with poorly cooked infected
meat; the larva escapes the cyst and passes to the small intestine where it
attaches to the mucosa by the scolex suckers.
• The proglottids develop as the worm matures in 3 to 4 months. The adult
may live in the small intestine as long as 25 years and pass gravid
proglottids with the feces.
• Eggs extruded from the proglottid contaminate and persist on vegetation for
several days and are consumed by cattle or pigs in which they hatch and
form cysticerci
• T. solium eggs can also infect humans and cause cysticercosis (larval
cysts in lung, liver, eye and brain) resulting in blindness and neurological
disorders. 45

46. CESTODE PARASITES
• Pathology
• Gastrointestinal symptoms are due to the presence of the tape worm.
• Cysticercosis symptoms are a result of inflammatory/immune responses.
• Antibodies are produced in cysticercosis and are useful epidemiological
tools.
• Diagnosis
• Through the recovery of eggs or proglottids in stool or from the perianal area.
Cysticercosis is confirmed by the presence of antibodies.
• Treatment and control
• Praziquantel is the drug of choice.
• A thorough inspection of beef and pork, adequate cooking or freezing of
meat are effective precautions, since cysticerci do not survive temperatures
below -10o C and above 50o C.
46

47. CESTODE PARASITES
• Echinococcosis (hydatid)
• Echinococcus granulosus is the main causative agent of hydatid cysts
• This is the smallest of all tapeworms (3 to 9 mm long) with only 3
proglottids.
• Epidemiology
• The organism is common in Eastern Africa, Asia, Australia, southern Spain,
southern parts of South America and northern parts of North America; the
incidence being higher in rural areas of affected regions.
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48. CESTODE PARASITES
• Life cycle of Echinococcus granulosus
 The adult worm lives in domestic and wild carnivorous animals.
 Eggs, passed by infected animals, are ingested by the grazing farm animals or man,
localize in different organs and develop into hydatid cysts containing many larvae
(proto-scolices or hydatid sand).
 When other animals consume infected organs of these animals, proto-scolices
escape the cyst, enter the small intestine and develop into adult worms.
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49. CESTODE PARASITES
• Life cycle of Echinococcus granulosus
 Echinococcus eggs, when swallowed by man, produce embryos that penetrate the
small intestine, enter the circulation and form cysts in liver, lung, bones, and
sometimes, brain.
 The cyst is round and measures 1 to 7 cm in diameter, although it may grow to be
30 cm.
 The cyst consists of an outer anuclear hyaline cuticula and an inner nucleated
germinal layer containing clear yellow fluid.
 Daughter cysts attach to the germinal ayer, although some cysts, known as brood
cysts, may have only larvae (hydatid sand).
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50. CESTODE PARASITES
 Diagnosis of Echinococcosis (hydatid)
 Clinical symptoms of a slow-growing tumor accompanied by eosinophilia are
suggestive.
 Intradermal (Casoni) test with hydatid fluid is useful. Pulmonary cysts and calcified
cysts can be visualized using x-rays.
 Antibodies against hydatid fluid antigens have been detected in a sizable
population of infected individuals by ELISA or indirect hemagglutination test.
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51. CESTODE PARASITES
 Treatment and control of Echinococcosis (hydatid)
 Treatment involves surgical removal of cyst or inactivation of hydatid sand by
injecting the cyst with 10% formalin and its removal within five minutes.
 It has been claimed that a high dose of Mebendazole results in some success.
 Preventive measures involve avoiding contact with infected dogs and cats and
elimination of their infection.
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52. 52

53. SUMMARY
Organism Transmission Symptoms Diagnosis Treatment
Taenia saginata Cyst in beef Epigastric pain,
vomiting, diarrhea
Proglottids or eggs in
stool or perianal area
Praziquantel
Taenia solium Cyst in pork Epigastric pain,
vomiting, diarrhea
Proglottids or eggs in
stool or perianal area
Praziquantel
T. solium Cysticercosis Oro-fecal Muscle pain and
weakness, ocular and
neurologic problems
Roentgenography,
anti-cysticercal
antibody (EIA)
Praziquantel
E. granulosus Oro-fecal Large cysts produce
various symptoms
depending on the
location of the
organism.
Roentgenography,
anti-hydatid fluid
antibody (EIA), Casoni
skin test
Surgery, formalin
injection and drainage,
Praziquantel
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54. ASSIGNMENTS
1. Describe epidemiology of the Soil-transmitted helminth infections (geohelminths) in Tanzania
2. Describe regulation or modulation of the host immune system by helminth parasites
3. Describe the epidemiology of schistosomiasis in Tanzania
4. Describe the epidemiology of Onchocerciasis in Tanzania
54