4a71c4c1709e4ee3adc9118ffc6e5d83

2021-2022
Introduction
:‫رؤيه كلية التمريض‬

‫ان تكون الكلية رائدة ومتميزة فى مجال التعليم والممارسات التمريضية والبحث العلمى وخدمة‬
‫المجتمع لالرتقاء بالمنظومة الصحية وتحقيق اهداف التنميه المستدامة على المستوى المحلى والقومى‬
.‫واالقليمى والدولى‬
.
:‫رسالة كلية التمريض‬
‫اعداد خريج مؤهل وكفء فى مجال التعليم والممارسات التمريضية والبحث العلمى وخدمة المجتمع‬
.‫قادرا على االبتكار ومنافسا محليا وقوميا واقليميا وفقا للقيم المهنيه واالخالقية‬
Course specification:
University: Menoufia
Faculty of nursing .
Department offering the course: Medical Parasitology.
1-Data of the course:
Title of the course :Medical parasitology
Year: 1st year of nursing B.CH program
Code: MED 109
Specialty: Medical Parasitology
Teaching and learning methods: Credit hour system
Lectures: 2 hours (every week for 15 weeks)
2-Objectives of the course:
-To provide students with introduction of parasites , biological,

epidemiological and mode of transmission of some parasites causing diseases
to humans .
-To enable students to understand the pathogenesis, clinical presentation and
complication of parasitic diseases .
-To enable students to reach diagnosis and know the general outline of
treatment, prevention and control of parasitic infection
3-Intended learning outcomes :
By the end of the course ,students should be able to perform:
a-knowlage and understanding:

a1.Describe the common diseases caused by helminthes ,protozoa and
arthropods as regard life cycle ,pathogenesis ,clinical features ,differential
diagnosis ,complication and medical important.
A2 .point out the methods of recovery of parasites and their culture methods
as well as immunological and molecular methods used for diagnosis of
parasitic infections.
a 3.Define the principles of management for common parasitic disease.
A4. Record the dual effect between professional work and environment.
A5. Describe characteristic gross and microscopic pictures of different
pathologic lesions within those organ systems and the associated functional
disturbances.
b- Intellectual skills :
b1 . Assess the different ion of behavior and ecology of different parasite
species and stages in the environment.
b2 . Diagnosis different helminthes and some protozoa .
b3. Carry out a protection to their society and environment from
dissemination of parasites.
b4. Differentiate between parasites: inhabiting the same geographical
location, also those affecting the same organ and parasites present in the
same sample.
b5. Make the proper decision to solve problems in the field of Parasitology
b6. Select from the different diagnostic tools the ones that help reaching a
final diagnosis in the field of medical Parasitology
d) General and Transferable Skills
At the end of the program the graduate should be able to:

d1. Perform active and good connection at all fields. Techniques.
d2. Do self-assessment.
d3. Use available sources to get knowledge.
d4. Put bases and indicators for evaluation of other's work
4- Attendance criteria:
Students should be according to the faculty by attending laws.
References:
1- Department course books.

2- Diagnostic medical parasitology: Garcia L.S and Bruckner.2008
3- Journal of parasitology .Journal of Helminthology and WWW.
Pubmed . com
4- CDC web site
5- Clinical parasitology :Satoskar AR.Simon GL, Hotez PJ and Tsuji M
2009 , Landes Bioscience
MEDICAL PARASITOLOGY
For
Nursing Students
Index
Subject Page
I. 1
II. CHAPTER 2: TREMATODA ............................................... 3
III. CHAPTER 3: NEMATODA ................................................ 18
IV. CHAPTER 4 45
CHAPTER 5 63
V.
VI. CHAPTER 6 65
VII. CHAPTER 7 98
i
List of Figures
Figure Title Page
Fig. (1) Life cycle of Fasciola gigantica 5
Fig. (2) Life cycle of Fasciola hepatica 10
Fig. (3) Life cycle of Schistosomes 14
Fig. (4) Life cycle of Ascaris 25
Fig. (5) Life cycle of Ancylostoma 29
Fig. (6) Life cycle of Strongyloides stercoralis 32
Fig. (7) Life cycle of Trichuris trichiura 36
Fig. (8) Life cycle of Enterobius 39
Fig. (9) Life cycle of Wuchereria bancrofti 43
Fig. (10) Life cycle of Trichinella spiralis 48
Fig. (11) Life cycle of Taenia saginata 54
Fig. (12) Life cycle of Taenia solium 57
Fig. (13) Life cycle of Hymenolepis nana 61
Fig. (14) Life cycle of Hymenolepis diminuta 64
Fig. (15) Life cycle of Echinococcus granulosus 68
Fig. (16) Life cycle of Entamoeba histolytica 78
Fig. (17) Life cycle of Giardia lamblia 84
Fig. (18) Life cycle of Trichomonas vaginalis 88
Fig. (19) Life cycle of Leishmaniasis 92
Fig. (20) Life cycle of Malaria 99
Fig. (21) Life cycle of Toxoplasma gondii 107
ii
Introduction
Introduction
 Parasite: Is an organism, which lives on or within another organism called
host.
 Host : Is a living organism that harbours the parasite.
 Types of hosts:-
1) Definitive host (D.H) : It is the host which harbours the mature adult
stage of the parasite or in which sexual reproduction of the parasite
take place.
2) Intermediate host (I.H) : It is the host which harbours larval stage
(immature or non sexually reproducing forms of the parasites).
3) Reservoir host (R.H) : It is an animal that harbours the mature stage of
the parasite as in human. It acts also as a source of infection to man
and maintains the parasite in nature.
4) Vector : An arthropod which carries the parasite from one host to
another.
- The relationship between the organism and its host occurs in the
following forms:-
1) Commensalism : It is a relationship between two living organisms
where one benefits (commensal), while the other (host) is not harmed.
2) Parasitism : It is a relationship between two living organisms where one
benefits (parasite), while the other (host) is harmed.
3) Mutualism : It is a beneficial relationship between two living organisms
where both drive a benefit and can successfully live apart.
 Types of parasitism:-
1) Ectoparasite: One that lives on or in the skin but not within the body of
its host (infestation).
2) Endoparasite : One that lives in the internal organs or tissues of its host
(infection).
1
Introduction
3) Temporary or Intermittent parasite : One that visits its host only for a
short period of time for its meal.
4) Permanent parasite: One that spends its life cycle on or in the body of
its host.
5) Opportunistic parasite: One that causes disease only in
immunodeficient patients (AIDS), while in immunocompetent
individuals, the parasite may exist in a latent form producing no
symptoms.
 Medical parasitology is classified into:-

1) Medical helminthology (deals with parasitic worms or helminths):-
 Phylum : Platyhelminthes (flat worms) Class:Trematoda
Class: Cestoidea
 Phylum : Nemathelminthes (round worms) Class: Nematoda

2) Medical entomology
3) Medical protozoology
2
Phylum: Platyhelminthes
Phylum : Platyhelminthes (Flat worms)
I. Class : Trematoda (Flukes)

Trematodes includes the following parasites:-
 Hepatic flukes :-
- Fasciola gigantica.
- Fasciola hepatica.
 Intestinal fluke :-
- Heterophyes heterophyes.
 Blood flukes :-
- Schistosoma mansoni.
- Schistosoma haematobium.
 Hepatic flukes
1) Fasciola gigantica (Giant liver fluke)
 Geographical distribution :-
 Common parasite of herbivorous animals especially in cattle raising
countries .
 Human infections are found in many parts of the world e.g. West
Africa, America, Europe and Egypt.
 Habitat : Bile ducts in liver.
 D.H : Cattle, sheep and occasionally man.
 I.H : Snail (Lymnaea cailliaudi).
 Morphological characters :-
1. Adult:-
 The worm is large fleshy, measuring 6 1.5cm.
 The body is flat leaf like. Formed of anterior small conical portion,
shoulder and parallel sides.
2
2. Egg (D.S):-
 Size : 140 70 µm.
 Shape : Oval.
 Shell : Thin operculated.
 Color : Yellowish brown.
 Content : Immature (ovum & yolk cells).
3. Miracidium:-
4. Sporocyst:-
5. Redia:-
6. Cercaria:-
 Formed of body and tail.
 Body with oral and ventral suckers, simple intestinal caeca.
 Cystogenous glands under the cuticle that secreate the cyst.
 Tail : Simple (leptocercous cercaria).
7. Encysted metacercaria (I.S):-
 Spherical about 250µm in diameter.
 The cercaria losses its tail and secreate a thick cyst wall.
 The infected stage to herbivorous animals and human.
 Present in green aquatic vegetations and water.
 Life cycle:-
 Adult worms live in the bile ducts of herbivorous animals (primarily
sheep and cattle) and occasionally man.
 Immature eggs (D.S) pass out of the liver with the bile into the intestine
to feaces. If they fall into water, the eggs will complete their
development into miracidia in 2 weeks.
 The miracidium has about 24hr to find a suitable snail host (Lymnaea
cailliaudi) where it develops into sporocyst, 1st and 2nd generation
rediae and finally cercariae come out from the snail to water in about
3
30 days.
 Cercaria leaves the snail, loses its tail and produces a thick, transparent
cyst wall around itself and encysts on aquatic plants or freely in water
(I.S).
 Infection occurs by ingestion of encysted metacercaria with aquatic
vegetations or in water.
 Juvenile flukes excyst in the small intestine and penetrate the intestinal
wall, migrate in the peritoneal cavity to the liver, penetrate the capsule
and burrow into the hepatic parenchyma to the bile duct where it
matures in about 2 months. Adult worm can live as long as 10 years.
Figure (1): Life cycle of Fasciola gigantica
4
 Pathogenesis :-
- Disease : Fascioliasis, liver rot.
1) Migratory phase: During the migration of juveniles, tissues are
mechanically destroyed and inflammation appears around
migratory tracks.
2) Biliary phase:-
 In the bile ducts, adult flukes cause inflammation and
hyperplasia of the epithelium 🠆 oedema which stimulate
fibrous tissue and thickening of the ducts. Cholangitis and
cholecystitis combined with the large body of the flukes 🠆
mechanical obstruction.
 Obstruction produced back pressure and atrophy of liver
parenchyma, cirrhosis and possibly jaundice.
 Gall bladder: Usually enlarged and oedematous with
thickening of the wall 🠆 fibrous adhesion to adjacent organs.
3) Ectopic locations: Migrating juveniles may lose way and reach
ectopic sites such as eye, brain, skin, lungs, kidneys, diaphragm
& subcutaneous tissue.
 Clinical pictures :-
1) Invasive or acute phase: Due to migration of juvenile fluke up to
the bile ducts. The major symptoms of this phase are:-
- Fever (40 - 42 oc).
- Abdominal pain.
- Intestinal disturbances: Loss of appetite, flatulence, nausea and
diarrhea.
- Hepatomegaly, splenomegaly and ascites.
- Anaemia (is not caused by hematophagia but by chemically
released proline from adult worms).
5
2) Chronic or obstructive phase: Due to adult fluke in the bile duct.

- Biliary colic and epigastric pain.
- Fatty food intolerance.
- Nausea, jaundice and pruritus.
- Right upper quadrant tenderness.
 Diagnosis :-
1) Clinical : Patient history of prolonged fever, hepatomegaly and high
eosinophilia.
2) Laboratory :-
a. Direct :-
1. Finding the eggs in the patient stool (direct and concentration
methods).
2. Ultrasonography.
3. Computerized tomography (CT).
b. Indirect :-
1. Intradermal tests using Fasciola prepared antigen.
2. Serological diagnosis: Detection of antibodies or antigens in the
patient's serum by I.H.A, C.F.T, ELISA.
3. Molecular techniques : PCR
4. Eosinphilia.
 Treatment :-
 Triclabendazole (Fasinex) : 10 mg/kg in a single oral dose.
 Prevention and Control :-
 Mass treatment of infected human and reservoir animals.
 Snail control.
 Protection :-
- Elimination of aquatic vegetations.
- Pure water supply.
- Proper washing or cooking of aquatic vegetations.
- Health education.
6
2) Fasciola hepatica
- It differs from F.gigantica in the following:-
Items F. gigantica F. hepatica

Distribution Africa ,Asia and Egypt Common in Europe
Reservoir host Cattle and buffaloes Sheep
Size 6 1.5 cm 3 1 cm
Longer and slender Wide anteriorly and
with small anterior cone pointed posteriorly
Shape
and parallel sides (converging) with large
anterior cone
Intermediate Lymnaea cailliaudi Lymnaea trancatula
host
Intestinal fluke
Heterophyes heterophyes
 Egypt: Mainly found in the north part of Delta especially in Borollos and
Manzala lakes.
 Far East : China, Japan, Korea, Taiwan.
 Turkey.
 Habitat :-
 Small intestine (deeply embedded between villi).
 D.H : Man and fish eating animals (dogs &cats).
 I.H : 1st 🠆 Pirenella conica snail.
2nd 🠆 Fish e.g. Mugil cephalus (Boury) and Tilapia nilotica (Bolty).
7

1. Adult:-
 Pear shaped with broad round posterior end, 1.5 - 3 0.5 mm.
2. Eggs (D.S):-
 Size : 30 15 µm
 Shape : Oval.
 Shell : Thick with anterior operculum and a small knob at posterior
end.
 Color : Yellowish brown.
 Content : Mature (miracidium).
3. Miracidium, sporocyst and redia are similar to those of Fasciola.
4. Cercaria:-
 Formed of body and membranous tail (lophocercous cercaria).
 Body contains oral and ventral suckers, primitive gut, 2dark eye
spots and 7 pairs of penetrating glands.
 V- shaped bladder.
 Life cycle:-
 Adult worms live in small intestine of the definitive host (man and fish
eating animals).
 Mature eggs pass with faeces (D.S). In brackish water, they are
ingested by P. conica snail (1st I.H) that lives in lakes of Borollos and
Manzala in Egypt.
 Egg hatches inside the snail and miracidium is liberated.
 Miracidium develops to sporocyst 🠆 1stand 2nd generation rediae 🠆
cercariae that leave snail to water in about one month.
 Lophocercus cercaria pierces skin and encysts in muscle tissue of the
2nd intermediate host (2nd I.H) which is Mugil cephalus (Boury) and
Tilapia nilotica (Bolty) fish 🠆 encysted metacercaria
8
 Infection is acquired by eating fish containing encysted metacercaria

(I.S) either raw or improperly cooked (grilled) or salted less than 10
days(Feseekh).
 In the small intestine, the cyst wall is dissolved and the encysted
metacecaria is embedded between the villi to develop into adult worm.
 Eggs appear in feaces within 2 - 3 weeks after infection.
Figure (2): Life cycle of Fasciola hepatica

 Pathogenesis and symptomatology :-
- Diseases : Heterophyiasis.
1) Intestinal phase:-
Each worm causes a mild inflammatory reaction at its site of contact
with the intestine. In heavy infections, damage of the mucosa occur 🠆
colicky abdominal pain and mucus diarrhea.
2) Ectopic sites:-
Sometimes eggs can inter the blood stream (due to its minute size) and
be carried as emboli to other organs especially heart (myocarditis &
heart failure) and brain (neurological disorders).
01
 Diagnosis :-
1) Clinical.
2) Laboratory: Identification of eggs in the stool (direct and concentration
methods).
 Treatment :-
 Praziquantel (Biltricide, drug of choice): 25mg/kg twice daily for one
day.
 Control :-
1) Mass treatment of patients, fishermen and infected animals.
2) Proper cooking of fish and salting not less than 10 days.
3) Snail control.
4) Periodic examination and health education of fishermen to avoid
defecation in water.
Blood flukes
Schistosomes
 Species :-
 Schistosoma haematobium.
 Schistosoma mansoni.
 Blood flukes differ from other trematodes in the following :-

1. Separate sexes.
2. Female : Long cylindrical.
3. Intestinal caeca reunite into a single caecum.
4. Testes: More than two.
5. Egg without operculum but spine.
6. No radia stage.
7. Forked tail cercaria is the infective stage (no encysted metacercaria).
00
Schistosoma haematobium
 Geographical distribution:-
1. Along the Nile Valley (Egypt, Sudan and Ethiopia).
2. South America, East and West Asia.
3. Middle East.
 Habitat : Vesical and pelvic venous plexuses.
 D.H : Man.
 I.H : Bulinus trancatus snail.
 R.H : Non (species specific).
1) Male :-
 Size : 10 1 mm.
2) Female :-
 Size : 20 0.25 mm.
3) Egg:-
 Shape : Oval.
 Size : 140 60 µm.
 Shell : Thin with terminal spine.
 Color : Translucent.
 Contents : Mature (fully developed miracidium).
4) Miracidium : Similar to Fasciola but without eye spots.
5) No redia stage.
6) Cercaria : Formed of body and tail:-
 Body : Oral and ventral suckers, primitive gut and 5 pairs of
penetration glands.
 Tail : Forked (Furcocercus cercaria).
01
 Life cycle:-
 Adult worms live in the vesical and pelvic venous plexuses in man
(D.H), the parasite migrates to terminal capillaries in the wall of the
urinary bladder.
 Female leaves the male (being more slender), it migrates alone into a
more narrow venule to lay eggs one by one while it retracting
backwards until the venule becomes full.
 Eggs pass to the perivascular tissues of the urinary bladder and other
tissues of urogenital system to reach the lumen and pass in urine
mainly in the last drops (terminal haematuria).
 When egg reaches the fresh water, the miracidium hatches within 20
minutes and survives for 24 hours, it perishes if it doesn’t find its snail
host.
 The miracidium penetrates the soft structure of the snail intermediate
host (Bulinus trancatus) where it develops into 🠆1st&2nd generation
sporocysts 🠆 cercariae (no redia stage) in about 1 - 2 months.
 Cercaria pierces skin when water begins to evaporate, penetration
is helped by penetration gland secretions and activity of the
muscular tail.
 Drinking water may lead to infection as cercaria can pierce buccal
mucosa but if ingested, it is easily killed by gastric juice.
 The cercaria enters the body leaving its tail outside (schistosomulum) to
reach the blood stream 🠆 Rt. side of the heart 🠆 lung 🠆 Lt. Side of
heart 🠆 systemic circulation 🠆 intestinal capillary bed 🠆 intrahepatic
branches of portal vein where it matures in 3 weeks.
 The mature male carries the female and migrates out the liver to pelvic
and vesical plexuses to deposit the eggs. Eggs appear in urine about 8
- 10 weeks after infection.
02
Figure (3): Life cycle of Schistosomes

- Disease :Schistosomiasis haemtobium, urinary bilharziasis.
- The clinical aspects of this infection are divided into 4 stages :-
1) Stage of invasion :-
a. Skin lesion due to cercarial penetration.
b. Local dermatitis, irritation, itching and papular rash.
2) Stage of migration :-
a. Lung : Irritation due to passage of cercaria causing minute
haemorrhage , cough, sputum, dyspnea and eosinophilia
(verminous pneumonia).
b. Liver : Enlarged tender liver and spleen.
c. Toxic symptoms : Due to metabolic products of maturing
parasites causing anorexia, headache, malaise, fever and muscle
pain.
03
3) Stage of egg deposition (acute stage) :-

- Active escape of eggs in urine produce tissue damage and manifested
by :-
1. Frequency of micturation.
2. Burning sensation during micturation.
3. Terminal haematuria 🠆 iron deficiency anaemia.
4. Dull pain in the loin and supra pelvic (urinary bladder).
4) Stage of tissue reaction, repair and fibrosis (chronic or late stage)
:-
 Granuloma formation is the main pathogenic lesion that develops
around the eggs in tissues. Soluble egg antigen from miracidium
stimulates the cellular immune response of the host.
 The granuloma consisting of eosinophils, plasma cells and
macrophages. The formation of granuloma and fibrosis leading to
bilharzial nodules, papillomata, sandy patches and reduced egg
output.
1. Bladder : Fibrosis, 2ry bacterial infection, stones, sandy patches
and malignancy.
2. Ureter : Stenosis, hydroureter, hydronephrosis 🠆 2ry bacterial
infection  renal failure.
3. Urethra: Stenosis and fistula.
4. Genital organs: Affection of prostate and testes and spermatic
cord in male and vagina and vulva in female.
 Diagnosis :-
1) Clinical.
2) Laboratory :-
a. Direct methods :-
1. Demonstration of eggs in the urine. The urine sample is examined
microscopically by either direct smear or by concentration after
04
sedimentation or centrifugation. The last drop must be included in the

sample.
2. Cases with free or no eggs (chronic): Bladder biopsy by using
Cystoscope.
b. Indirect methods :-
1. Eosinophilia.
2. Anaemia :-
a. Iron deficiency anaemia (due to chronic loss of blood).
b. Haemolytic anaemia (due to hyper-splenism).
3. Intradermal test.
4. Serological tests :-
-IHAT, CFT, IFAT and ELISA.
-Circum oval precipitin test (viable eggs + tested serum) 🠆
precipitation around the eggs in positive cases due to presence
of antibodies in serum reacting with miracidum antigen.
-Recently: Detection of circulating Schistosoma antigens by
using of monoclonal antibodies can limit the cross reactions
with other tests.
 Treatment :-
 Parziquantel (Biltricide): 40mg /kg as a single oral dose.
 Metrifonate (Bilarcil): 10mg/kg single dose every other week for 3
doses.
 Surgical: In complicated cases.
05
Intestinal Schistosomiasis
- Caused mainly by S.mansoni and S.japonicum. Their defferences are

detected in the following table:-
Item S.haematobium S.mansoni S.japonicum

Distribution Nile Valley, Africa, Nile Delta, Africa, Far East
Middle East, South Middle East, South
Europe America
Size 10 1mm Smaller, 8 1mm 15 0.5 mm
Tubercle Fine Coarse No tubercles
(smooth)
Male
Testes 3 - 5, big in a line 6 - 9, small and in cluster 6 - 8, in a line

Caeca Reunite in the Reunite in the anterior Reunite at the
posterior half half posterior 1/4 of
the body
Size 20 0.25 mm Smaller, 14 0.15 mm 26 0.25 mm
Ovary Posterior 1/3 of the Anterior 1/3 of the body In the middle
and body
Femal
caeca
e
Uterus Long with 20 - 30 Short 1 - 4 ova. Short with 50

ova eggs
Vitelline Small, in the post. In post. 1/2 of the body
glands 1/3 of the body Big, extended to 2/3 of the body
D.H Man
R.H  In nature: Non Monkeys & rodents Domestic animals
 Experimentally: (dog, cat, pig &
monkeys &rodents cattle)
Habitat Vesical and pelvic Small branches of Superior & inf.
venous plexuses inferior mesenteric vein mesenteric
of rectum &pelvic colon venous plexuses
Size 140 60 µm 150 65 µm 85 65 µm
Shape Oval with terminal Oval with lateral spine Ovoid with
Eggs
spine minute knob

Shell Thin, non operculated
Colour Translucent
Content Mature (fully developed miracidium)
Snail (I.H) Bulinus truncatus Biomphalaria Onchomelania
alexandrina
Diagnosis Egg in urine Egg in stool
06

- Diseases : Schistosomiasis mansoni or intestinal bilharziasis.
1) Stage of invasion and migration : Like schistosomiasis
haematobium.
2) Stage of egg deposition (acute schistosomiasis) :-
 The adult worms in the intrahepatic branches of portal vein are
settled down, pair and migrate to mesenteric veins. The couple
worms migrate from the portal vein to the mesenteric veins.
 Eggs deposited in the pelvic colon and rectum. Expulsion of eggs
in stool  tissue damage and haemorrhage.
 Symptoms:-
-Abdominal pain.
-Frequent motion, dysentery with blood and mucus in stools.
3) Stage of tissue reaction, repair and fibrosis (chronic or late stage) :-
 Trapped eggs in the intestinal wall 🠆 formation of polyps,
papillomata and sandy patches.
-Later on, the intestinal wall becomes fibrosed and thickened 🠆
stricture of the wall, sinuses, fistula and rectal prolapse.
 Embolic lesions :-
Some eggs are swept back into the blood stream to different organs:-
- Liver: Periportal fibrosis 🠆 portal hypertension 🠆 hepatosplenomegaly,
ascitis and oesophageal varices.
- Lung: Biharzial cor pulmonal.
- Brain: Cerebral schistosomiasis (more common with S. japonicum than
S.mansoni and hematobium).
- Skin and kidney.
07
 Diagnosis :-
1) Clinical.
2) Laboratory :-
a. Direct method :-
1. Detection of eggs in the stool by direct smear or concentration
by sedimentation techniques.
2. Kato thick faecal smear (will be discussed later).
3. Rectal swab examined microscopically for eggs.
4. Rectal biopsy and liver biopsy in chronic stage.
b. Indirect methods: Like S. haematobium.
 Treatment :-
 Parziquantel (Biltricide): 40mg /kg as a single oral dose.
 Oxamniquine (Vancil) 15mg /kg twice a day for 2days after meal.
 Surgical: In complicated cases.
 Prevention and control of schistosomiasis :-
1) Personal prophylaxis
2) Health education
3) Mass treatment and follow up of patients
4) Snail control
08
Phylum: Nemathelminthes
Phylum : Nemathelminthes
Class : Nematoda
(Round worms)
 General characters:
1) They are elongated, unsegmented, cylindrical worms with tapering

ends. Their length range from 1mm to more than one meter.
2) Bilaterally symmetrical.
3) Separate sexes. The male is smaller and its posterior end is curved
ventrally to help in holding female during copulation while the female
posterior end is straight.
4) The body is covered by a cuticle made of scleroprotein (resist the

digestive Juices and enzymes of the host).
5) The body wall consists of three layers:-
a. Cuticle: Outer laminated non- cellular protective layer. It may be

smooth or have striations, spines or papillae.
b. Hypodermis: It is a syncytial layer that secretes the cuticle, it shows

4 longitudinal lines of thickening. Two lateral ones enclose excretory
canals while the dorsal and the ventral are containing the dorsal and
the ventral nerve cords.
c. Muscle layer: Single layer of non striated fibers divided into 4

sectors by the four thickenings of the hypodermis.
6) The body cavity contains body fluid in which lie different systems e.g.
digestive, reproductive, excretory & nervous systems.
7) The digestive system: A simple starting with mouth and ends by anus.
a. Mouth: Anterior provided with the lips, teeth, plates and sensory
papillae.
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b. Oesophagus varies in shape and structure:-
 Cellular.
 Muscular:-
 Club shaped.
 Double bulbed (anterior club shaped part and posterior

spherical part).
 Rhabditiform (anterior club part and posterior pyriform part

with a constriction in-between).
 Cylindrical or filariform (muscular anterior part and glandular

posterior part).
 The oesophagus 🠆 intestine (lined with columnar cells) 🠆

rectum terminates at anus that opens ventrally in female near the
posterior end and joins to the genital opening and opens in cloaca
in male.
8) Reproductive system:-
a. The female has two sets of genitalia. The genital system consists of
double tubes. Each consists of one ovary 🠆 oviduct 🠆 seminal
receptacle 🠆 uterus. The two uteri join to form one vagina that
opens ventrally by vulva. Female worms may lay eggs (oviparous),
mature eggs containing larvae (ovoviviparous) or may give larvae
(larviparous or viviparous).
b. The male has one set of genitalia formed of one coiled tube
differentiated into a testis 🠆 vas deferens 🠆 seminal vesicle &
ejaculatory duct that terminates with the rectum in the cloaca. Male
has accessory copulatory organs as spicules, papillae, bursa,
cement glands or gubernaculums.
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9) Excretory system: Consists of two lateral longitudinal excretory canals

connected by a transverse tube 🠆 open by excretory pore in the
cervical region at the level of oesophagus (no flame cells).
10) Nervous system: Consists of a nerve ring surrounding the oesophagus

🠆 nerve trunks extend ventrally and dorsally.
11) Life cycle: Usually nematodes pass through the sequence of egg
development (by moulting).
 Fertilized female 🠆 passes eggs 🠆 hatche 🠆 larvae 🠆 moult
three times🠆 4 larval stages then moult again 🠆 adult.
 The 1st and 2nd stage larvae (L1, L2) are called rhabditiform
larvae. The 3rd and 4th stage larvae (L3, L4) are called filariform
larvae.
Classification of nematodes
I. According to habitat
A. Intestinal nematodes (adults in the intestine):-
1. Small intestine of man:-
 Ascaris lumbricoides
 Ancylostoma duodenale
 Necator americanus
 Strongyloides stercoralis
 Trichinella spiralis
 Trichostrongylus colubriformis
 Capillaria phillippinensis
Large intestine of man:-

 Enterobius vermicularis
 Trichuris trichiura
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2. Small intestine of dogs & cats:-

 Ancylostoma caninum
 Ancylostoma braziliense
 Toxocara canis & cati
B. Tissue nematodes:-
1. Adults in tissues:-
 Filariae
2. Larvae in tissues:-
 Larvae of Ancylostoma caninum & Ancylostoma braziliense 🠆
cutaneous larva migrans.
 Larvae of Toxocara canis & cati 🠆 visceral larva migrans.
 Larvae of some filariae.
I. Nematodes of small intestine

1) Ascaris lumbricoides
(Giant intestinal worm)
 Geographical distribution: Cosmopolitan, occurs in all ages but mainly

in children who exposed to contaminated soil.
 D.H: Man.
 Habitat: Small intestine (jejunum).
 Morphological characters:-
1) Adults:-
 Male: 15 - 25 cm long × 3mm width. The posterior end is curved
ventrally and the tail is bluntly pointed.
 Female: 20 - 35 cm long × 0.5 cm width, straight posterior end, 2
sets of genitalia.
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 Eggs:-
a) Fertilized egg:
 Size: 60 × 45 µm
 Shape: Oval to round.
 Shell: Inner thick shell and outer mamillated coat.
 Color: Golden brown (bile stained).
 Content: Immature (one - cell stage).
b) Unfertilized egg:
 Size: 90 × 45 µm
 Shape: Elongated.
 Shell: Thinner with ill developed mamillated coat.
 Color: Yellowish brown.
 Content: Multiple refractile granules (no embryo, completely fill
the egg shell).
c) Decorticated egg: Fertilized or unfertilized egg that loses the
mammillated layer.
 N.B: The host who harbouring the female worm only passes unfertilized
eggs.
 Life cycle:
 The adult worms live free in the small intestine of man (D.H).
 The immature eggs in stool 🠆 the soil 🠆 mature egg (2nd rhabditiform
larva (I.S).
 Man infects by ingestion of mature egg containing 2nd stage rhabditiform
larva with contaminated food (green vegetables), water or hands.
 Egg hatche in the duodenum 🠆 pierce the mucous membrane of small
intestine to enter the mesenteric venules 🠆 pulmonary arteries to the
lung.
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 Larvae reach the pharynx & swallowed to reach the small intestine
where they moult to adult worms.
 Eggs appear in stool after 2 - 3 months.
 With hyperinfection, filariform larvae can reach the left side of the heart
to the general circulation and distributed to different organs (visceral
larva migrans).
Figure (4): Life cycle of Ascaris
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 Pathogenesis and symptomatology:-

- Disease: Ascariasis.
1) Larval migratory phase:-
1. verminous pneumonia (Loeffler's syndrome) that presented by
fever, cough with blood tinged sputum, dyspnea, and eosinophilia
(20%).
2. Visceral larva migrans.
2) Intestinal phase:
 Light infection 🠆 no symptoms.
 Colic, abdominal distension, vomiting, diarrhea or constipation,
dyspepsia, epigastric pain or even peptic ulcer.
 Malnutrition and underdevelopment of children with heavy infection.
 Vit. A deficiency.
3) Complications:
 Nervous irritability (insomnia and convulsion).
 Intestinal obstruction.
 Peritonitis.
 Pancreatitis.
 Appendicitis.
 Cholecystitis and obstructive jaundice.
 Liver abscess.
 Vomiting.
 Diagnosis:-
1) Clinical.
2) Laboratory:-
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a) Direct:
 Detection of eggs in stool by direct or concentration methods.

 Detection of the adult worms in stools.
 Detection of migrating larvae in sputum or gastric juice.
b) Indirect:
 Eosinophilia 20%
 Treatment:-
1) Mebendazole (vermox): 100 mg (one table) twice daily for 3 days.
 Prevention and control (5 F):-
1) Health education.
2) Mass treatment of patients.
3) Sanitary sewage disposal.
4) Sanitary water supply.
5) Proper washing of green vegetables (food).
6) Avoid defecation in soil & using human excreta as manure (feaces).
7) Washing hands before meals (fingers).
8) Fly control.
2) Hookworms
Ancylostoma duodenale
 Geographical distribution: Cosmopolitan, widely distributed in tropical
and subtropical countries.
 Habitat: Small intestine and particularly jejunum.
 D.H: Man.
1) Adults:-
 Male:-
-Size: 10 mm in length.
 Female:-
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-Size: 12 mm in length.
2) Egg:-
 Size: 60×40µm.
 Shape: Oval with blunt poles.
 Shell: Thin.
 Color: Translucent.
 Contents: Immature (4-cell stage) with empty space between the
shell and contents.
3) Filariform larva (infective stage):-
 600 - 700 µm in length.
 Filariform (cylindrical) oesophagus: one fourth of the body length.
 Pointed tail end
 Sheathed.
 Life cycle:
 Adult worms live in the jejunum.
 The immature egg matures in soil 🠆 hatches 🠆 3rd stage rhabditiform
(I.S).
 Man is infected by penetration of the skin or mucous membrane of the
mouth by the infective filariform larva.
 The larva passes through blood 🠆 reaches pharynx 🠆 swallowed to
reach the small intestine.
 In the small intestine it moults and matures to adult.
 Eggs appear in faeces after 6 - 8 weeks.
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Figure (5): Life cycle of Ancylostoma

- Disease: Ancylostomiasis.
1. Skin invasion: (ground itch, creeping eruption or dew itch):-
 Causes local dermatitis at the site of entry with irritation and

itching followed by erythema, oedema and papular rash 🠆
2ry bacterial infection.
2. Larval migratory phase:-
a) To the lung (Loeffler's syndrome or verminous pneumonia):-
 Causes fever, cough, dyspnoea, expectoration of blood
tinged sputum and eosinophilia.
b) Visceral larva migrans.
3. Intestinal phase:-
 Nausea, vomiting, pain, flatulence, constipation, diarrhea or
blood loss.
 Hypochromic microcytic aneamia.
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 Hypoproteinaemia.
 Physical and mental retardation.
 Diagnosis:-
1) Clinical.
2) Laboratory:-
Direct:
 Stool examination for egg detection.
Indirect:
 Blood examination for anaemia.
 Treatment:-
1) Mebendazole (Vermox): one tablet (100 mg) twice daily for 3 days.
 Prevention and control:-
1) Personal hygiene
2) Mass treatment of patients.
3) Avoid using of human excreta as manure (should be treated with

chemical disinfectants or stored before used).
4) Sanitary sewage disposal of human excreta.
5) Health education to avoid defecation on the ground.
6) Wearing shoes and gloves and avoid walking bare footed.
3) Strongyloides stercoralis
(Dwarf thread worm)
 Geographical distribution: Cosmopolitan, more in tropical and
subtropical regions including Egypt.
 Habitat: In the parasitic form 🠆 the adult lives in the duodenum and
jejunum of the small intestine of man where the female embedded
completely into the submucosa, while the male found free in the lumen.
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 D.H: Man.
 R.H: May be dogs, cats and monkeys
1) Male (either parasitic or free – living):-
 Size: 0.7 mm × 50 µm.
2) Parasitic female:-
 Size : 2.2 mm × 30 - 50 µm
3) Free – living female:-
 Size: 1mm × 60 µm.
4) Egg (rarely found in stool):-
 Size: 50 × 30 µm.
 Shape: Oval.
 Shell: Very thin.
 Color: Translucent
 Content: Mature (contain rhabditiform larva).
5) Rrhabditiform larva (D.S):-
 200µm × 20 µm.
 Short buccal cavity.
 Rhabditiform oesophagus (1/3 body length).
 Posterior end is blunt.
6) Filariform larva (I.S):-
 Size: 600-700 µm in length.
 Cylindrical (filariform) oesophagus (1/2 body length).
 Notched tail tip.
 Non sheathed.
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 Life cycle:-
 Adult worm lives in the small intestine of man (duodenum and jejunum)
and occasionally dogs, cats and monkeys.
 After fertilization 🠆 rhabditiform larvae passes stool.
 In soil, rhabditiform larva develops by one of the two following life
cycles according to the environmental conditions:-
1. Direct cycle: When the environmental conditions in soil are
unfavorable, the rhabditiform larvae 🠆 infective filariform larvae (I.S)
in 2 - 3 days.
2. Indirect cycle: When the environmental conditions in soil are
favourable for free living, rhabditiform larvae 🠆 free living male and
female within 2 day.
Figure (6): Life cycle of Strongyloides stercoralis
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 Mode of infection:-
1) Human infection occurs by penetration of the skin or mucous
membrane of mouth by infective filariform larvae 🠆 venous circulation
🠆 pharynx 🠆 swallowed 🠆 reach the small intestine.
- The larvae moult twice during migration to become adult worms.
- Rhabditiform larvae appear in stool after 4 weeks of infection.
2) Autoinfection
- Internal autoinfection: by penetrating the intestinal mucosa.
- External autoinfection: by penetrating the perianal skin.

- Disease: Strongyloidiasis, Cochin – China diarrhea.
1) Skin invasion:-
- Cutaneous larva migrans.
- Creeping eruption.
2) Larval migratory phase:-

a) To the lung (Loeffler's syndrome or verminous pneumonia):-
- Fever, cough, dyspnea, haemoptysis and high eosinophilia

resembling tropical pulmonary eosinophilia.
b) Visceral larva migrans.

3) Intestinal phase:-
- Light infection: Usually asymptomatic.
- Heavy infection: Epigastric pain and tenderness (duodinitis),

nausea, vomiting and watery mucus diarrhea alternates with
constipation.
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 Diagnosis:-
1) Clinical.
2) Laboratory:-
Direct:
a. Stool examination for rhabditiform larvae.
b. Stool culture.
Indirect:
c. Eosinophilia.
d. Serological tests (CFT, IHA, ELISA).
 Treatment:-
1) Thiabendazole.
 As hookworms.
II. Nematodes of large intestine
1) Trichuris trichiura
Trichocephalus trichiurus
(Whipworm)
 Geographical distribution: Cosmopolitan especially in warm countries,

common in children.
 Habitat: Large intestine (caecum and appendix), the anterior thin part of
the worm embedded deeply in the intestinal wall.
 D.H: Man.
1) Adults:-
 Male:-
-3 - 4cm.
 Female:-
-4 - 5 cm.
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2) Egg (D.I):-
 Size: 50 ×25 µm.
 Shape: Barrel shaped.
 Shell: Thick with two polar prominences.
 Color: Brownish.
 Content: Immature (one cell stage).
 Life cycle:-
 The adult worms live in the large intestine, usually in caecum and
appendix (sometimes sigmoid and rectum).
 Immature eggs pass in stool and when the environmental conditions
are suitable in about 3weeks.
 Man infected by ingestion of eggs containing the 1st stage rhabditiform
larvae (I.S) with contaminated food or water.
 Larva in the large intestine, moults 4 times and matures to adult stage
(without migratory cycle).
 Eggs appear in stool after 2 - 3 months.
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Figure (7): Life cycle of Trichuris trichiura

- Disease: Trichuriasis, Trichocephaliasis.
 Light infection: Asymptomatic.
 Heavy infection leads to:-
1) Haemorrhage and mucosal ulceration.
2) Distension, nausea, vomiting, low abdominal pain which may
simulate chronic appendicitis and bloody diarrhea.
3) Dysentery
4) Appendicitis & abscess.
5) Peritonitis
6) Anaemia:-
 Microcytic hypochromic anaemia.
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 Hyperchromic pernicious anaemia.

7) Eosinophilia.
 Diagnosis:-
1) Clinical.
2) Laboratory:-
 Stool examination: For egg detection and sometimes the adult
worm.
 Proctoscopy: Shows hanging worms attached to the mucosa.
 Eosinophilia.
 Treatment:-
 Mebendazole (Vermox)
 Prevention and control: As Ascaris.
1) Enterobius vermicularis
Oxyuris vermicularis
(Pinworm, Seatworm)
 Cosmopolitan.
 More common in cold climate than hot climate and in children.
 More prevalent among groups of people e.g. families, army camps,
schools and prisoners.
 Habitat: Large intestine, especially caecum, adjacent parts of ileum and
appendix.
 D.H: Man, especially children.
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1) Adults:-
 Male:-
-5 mm.
 Female:-
-10 mm.
2) Egg (D.S & I.S):-
 Size: 50 × 25 µm.
 Shape: D-shaped or planoconvex (one side is flat and the other is
convex).
 Shell: Thick double layers covered by outer albuminous sticky layer.
 Content: Mature (fully developed larvae).
 Life cycle:-
 Adult worms live in the caecum, appendix & lower ileum of man (D.H).
After fertilization, male dies and passes outside with faeces, while the
gravid female migrates at night to the perianal region where mature
eggs are laid and sticked to the skin of the perianal region. Sometimes
the female worm enters the urethra or vagina of female patients.
 Man is infected by ingestion of mature eggs with contaminated food,

drinks or hands.
 Eggs hatch in the small intestine and larvae moult to develop into adults
in the large intestine (caecum).
 Eggs appear in the stool after 2 - 4 weeks from infection.
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Figure (8): Life cycle of Enterobius
1) Autoinfected: Children are commonly infected.

2) Retroinfection: Eggs hatch in caecum or in the perianal area 🠆 larvae
come out 🠆 return to rectum to develop into adult worms.
3) Air-borne infection due to inhalation of dust contaminated with eggs
(swallowed).
4) Direct contact with patients (hand to hand) or indirect contact with
contaminated articles (clothes, toilet seats & bed linens).
5) Contaminated food or drinks with eggs.
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- Disease: Enterobiasis.
1) Itching of the perianal region (pruritus ani) especially at night.
2) Sometimes the migrating female may enter the female urethra or
vagina especially in children leading to:
- Urethritis & nocturnal enuresis.
- Vulvo -vaginits.
3) Appendicitis.
 Diagnosis:-
1) Clinical.
2) Laboratory:-
1. Detection of adult worms in the stool or perianal region.

2. Detection of eggs in stool or around perianal ergion by:
 Direct methods.
 Perianal region by swabs:-
1. N.I.H swab (National Institute of Health.
2. Scotch adhesive tape swab.
 N.B: Swabs should be taken in the morning before defecation or

bathing.
3. Urine examination for eggs.
 Treatment:-
- Treatment should be accompanied with good hygiene.
1. Mebendazole (Vermox):.
2. Local ointment to the perianal area e.g. white precipitate ointment.
3. Other members of the family or school should also treated.
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1) Washing hands before meals and after defecation.

2) Cutting fingers nails.
3) Boiling of internal clothes & bed linens.
4) Children should wear tight clothes to prevent scratching at night.
5) Washing of toilet seats with disinfectant to avoid contamination.
6) Protection of food from contamination by infected hands, dust and
flies.
7) Treatment of whole family in the same time.
8) Fly control.
III. Tissue Nematodes

 General characters:-
1) Adults or larvae live in the extraintestinal tissues.
2) Adult worms are slender and thread like.
3) Cylindrical (filariform) oesophagus.
4) Females are larviparous (T. spiralis, D. medinensis & filariae).
5) Require an arthropod as intermediate host for their life cycle (D.
medinensis & filariae).
Wuchereria bancrofti
(Bancroft's filarial worm)
1) Tropical and subtropical regions.

2) Far East.
3) Egypt especially in Rasheed, Abu Rawash, Kerdasa, Damietta, Sharkia
& some sporadic localities in Menoufiya Governorate.
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 Habitat: Lymph nodes and lymph vessels of lower limbs, external

genitalia and trunk.
 D.H: Man.
 I.H (vector): Mainly Culex pipiens..
1) Male:
- 3 - 4 cm × 0.1 mm
2) Female:-
- 7 - 10 cm ×0.2 mm.
3) Microfilaria (D.S) Fig.(9):-
- 250 µm × 8 µm.
4) Infective filariform larvae (I.S):-
- In the mouth part of mosquito.
- 1500 - 2000 µm × 20 µm.
 Life cycle:-
 Adult worms live in lymph nodes and lymph vessels of the lower
limbs and external genitalia. Female deposits microfilariae that
carried to the peripheral blood at night (nocturnal periodicity).
 Microfilariae are taken by Culex piniens mosquito (I.H) with its blood
meal.
 The rhabditiform larvae moult into infective stage (I.S) filariform

larva.
 The filariform larva migrates to the labium.
 During mosquito blood meal 🠆 the infected filariform larva pierces

the skin or enters through the puncture wound by its active
penetration.
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Figure (9): Life cycle of Wuchereria bancrofti

- Disease : Bancroftian filariasis or elephantiasis.
1) Asymptomatic phase: Occurs in endemic areas where patients remain
asymptomatic but with patent microfilaria in their blood.
2) Acute inflammatory phase:-

 Symptoms:-
1. Fever, chills & headache & toxemia.
2. Local lymphangitis.
3. Lymphadenitis.
4. Affection of the lymphatics of the epididymis and testes
(epididimo-orchitis), Scrotaum (varicocoele & hydrocoele) and
spermatic cord (funiculitis) in males and vulva in females.
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3) Tropical pulmonary eosinophilia (Occult filariasis):-

 It is characterized by:-
1. Occurs in endemic areas of filariasis.
2. The microfilariae are seen in the lung tissues.
3. Marked eosinophilia
4) Obstructive (chronic) phase:-
- The obstruction of lymph flow.
 Effects of obstruction:-
a. The lymph vessels become dilated, distended and varicosed.
b. Oedema.
c. Rupture of distended vessels:-
- In pleural sac 🠆 chylothorax.
- Peritoneal sac 🠆 chylous ascitis.
- Tonica vaginalis of testis 🠆 chylocele.
- Intestine 🠆 chylous diarrhea.
d. Elephantiasis: It is a result of complex immune responses in a
long duration (5 - 10 years).
Symptoms:
- Thickening of the affected part.
- The skin become hard, dense, cracked and non pitting with
loss of elasticity.
- The skin appears rough, folded, stretched and fissured.
- Elephantiasis is usually affected most dependent parts e.g.:
Legs, scrotum.
- Blood sample is negative for microfilaria.
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 Diagnosis:-
1) Clinical.
2) Laboratory:
 Direct:
A. Blood examination for microfilariae: Blood should be obtained at
night (10 p.m. - 2 a.m.).
 Several techniques are available as follows:-
1. Wet mount preparation.
2. Stained thin and thick blood film.
3. Concentration techniques.
4. Diethylcarbamazine (Hetrazan) provocative test: 100 mg of
hetrazan (1 - 2 tablets) given orally to suspected person in
day time 🠆 microfilariae appear in the peripheral blood after
one hour in positive cases.
B. Examination of urine (chyluria) for microfilaria:-
C. Aspiration of lymph nodes or hydrocele.
D. X-ray for calcified adult.
E. Indirect methods:
Immunodiagnosis:-
-Serological tests (ELISA, IFAT, CFT & IHAT).
- Detection of circulating filarial antigen
F. PCR.
G. Eosinophilia.
 Treatment:-
1) Di - ethyl - carbamazine citrate (DEC, Hetrazan): The drug of choice.

2) Surgical treatment is required in sever elephantiasis in limbs, breast and
genetalia e.g. hydrocoele and varicocoele.
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1) Mass treatment of infected patients in endemic areas.

2) Chemoprophylaxis by DEC.
3) Mosquito control: Insecticides, wire screen & skin repellants.
4) Environmental sanitation.
Trichinella spiralis
(Trichina worm)
 Geographical distribution: Cosmopolitan, mainly in pork eating

countries e.g. America and Europe.
 Habitat: Adult worm lives in the small intestine mainly duodenum and
jejunum and larvae in muscles of man and animals, so man and animals
act as D.H & I.H.
 D.H, I.H: Rat, pig & Man.
1) Adults:-
 Thread like nematode, the anterior end is thinner than posterior end.
 Lipless mouth.
 Cellular oesophagus (1/3 body length).
 Terminal anus in female and terminal cloaca in male.
 Female:-
- 3mm × 100 µm.
 Male:-
- 1.5 mm × 50 µm.
2) Larva:-
 0.1 mm in length.
 Rhabditiform oesophagus.
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 Deposited directly in the intestinal wall.

 Carried by the blood to the active striated muscles.
3) Encysted Larva:-
 1mm in length.
 Coild and encysted by fibrous capsule 🠆 cyst (0.5x0.2mm).
 The cyst lies along the longitudinal axis of the muscle fibers.
 The cyst usually calcified within 6 - 12 months.
 Life cycle:-
 The adults live in the small intestine of man (D.H), pigs and rats (R.H).
 After fertilization the male dies and expelled, while the female
penetrates the intestinal wall to lays larvae (0.1 mm) in the submucosa.
 Larvae are carried by the blood to liver 🠆 Rh side of the heart 🠆 lung 🠆
Lt side of the heart 🠆 general circulation 🠆 to all parts of the body
especially the active striated muscles (eye lid, tongue, muscles of
mastication, deltoid, intercostals muscles and diaphragm) where they
are coiled and encysted as a result of host reaction in the long axis of
muscles forming an oval cyst (0.5 0.2 mm).
 Man is infected by ingestion of undercooked pork containing the
encysted larvae. In the small intestine, larvae are released and mature
to adults in 48 hours.
 Pigs are infected by eating flesh from infected pig or dead pigs or
infected rats.
 Rats are infected by eating infected rat (cannibalism) or infected pig’s
muscles.
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Figure (10): Life cycle of Trichinella spiralis

- Disease: Trichinosis, trichiniasis or trichinelliasis.
- There are two main phases for infection:-
1) Enteral phase (affecting the intestine):-
 This phase occurs from 2 to 7 days after infection.
 Eosinophilia detected early and increased.
2) Parenteral phase: (outside the intestine):-
Larvae migrate in the blood 🠆 invade different tissue 🠆 initiate

inflammatory reaction and presented by:-
a. Fever and urticarial rash due to toxaemia.

b. Muscles: Pain and tenderness of the affected muscle:-
c. Splinter haemorrhage under the nails (a common symptom)
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d. Larynx: Hoarseness of voice.

e. Heart: Myocarditis 🠆 may lead to heart failure.
f. Lung: Pneumonia.
g. Brain: encephalitis and meningitis.
h. In severe cases, death can occur 4-6 weeks after the infection
and is usually caused by myocarditis, encephalitis or
pneumonia.
i. Eosinophilia: 20 - 50%.
 Diagnosis:-
1) History: Eating improperly cooked meat.

2) Clinical:
3) Laboratory:-
1) Direct:-
a. Stool examination: For larvae or adult (possible during enteral
phase).
b. Blood examination for detection of larvae.
c. Muscle biopsy.
d. Trichinoscopy: To see larvae in muscle
e. X ray for calcified cyst.
f. CT for brain lesions.
2) Indirect:-
a. Eosinophilia (20 - 50%).
b. Intradermal test (Bachman test).
c. Serological tests: CFT, IHA, IFAT, ELISA, (BFT) & (LAT).
22
 Treatment:-
1) General treatment:-
 Bed rest and fluid therapy
 Sedatives.
 Corticosteroids.
2) Specific therapy:-
 Thiabendazole (Mintezol): 25 mg / kg twice daily for 10 - 14 days.
 Mebendazole (Vermox): 200 mg 3 times daily for 2 weeks.

1) Treatment of the patient.
2) Avoid eating pork or proper cooking or freezing of pork.
3) Proper inspection of pig’s meat in slaughter houses by trichinoscope.
4) Treatment of pigs.
5) Proper breading places for pigs and heat treatment of garbage used in
feeding pigs.
6) Rodent control.
22
Class: Cestoidea
II. Class : Cestoidea (Tapeworms)

Subclass : Cestoda
 General Characters :-
1) Adults: Flat, ribbon like and segmented.

2) Their length varies from few millimeters to several meters.
3) The body is formed of :-
1. Scolex (head) with organs of fixation :-
a) Suckers either :-
-4 true cup shaped muscular sucker , or
-2 false suckers as grooves (bothria).
b) Rostellum with one or more circles of hooks. Fig.(7 - 2)
2. Neck is the region of growth.
3. Strobila: Formed of segments (proglottids).
 Immature segments: They lie anterior and contain immature
genital organs.
 Mature segments: Follow the immature ones and contain fully
developed genital organs.
 Gravid segments: They lie posterior and contain uteri filled with
eggs.
4) The genital system :-
 Cestodes are hermaphrodites having both male and female genital
systems in each mature segment.
 Reproduction : Is by self fertilization in the same segment or by
cross ferilization between different segments.
 Male organs : Testes (at least 3, small scattered) 🠆 vasa efferentia
🠆 vas deferens 🠆 seminal vesicle 🠆 ejaculatory duct 🠆 cirrus and
cirrus sac 🠆 common genital pore.
15
Class: Cestoidea
 Female organs : Bilobed ovary in the posterior part of the segment

🠆 oviduct 🠆 ootype 🠆 uterus 🠆 vagina open in common genital
pore.
-Uterus : Either vertical or transverse, blind or with a separate
pore.
-Vitelline glands : Either compact mass or small scattered follicles
open in ootype.
Cestodes are classified according to habitat into
I. Intestinal cestodes II. Tissue cestodes

(Adult in the small intestine of man) (Larvae in the tissues of man)
(Man is the D.H) (Man is the I.H)
1. Taenia saginata 1. Hydatid cyst (larva of E.granulosus

or E.multilocularis) 🠆 Hydatidosis.
2. Taenia solium
3. Hymenolepis nana
4. Hymenolepis diminuta
1) Taenia saginata
(Beef tapeworm, Bald tapeworm)
 Geographical distribution: - Cosmopolitan, especially in cattle-

raising countries.
 D.H : Man
 I.H : Herbivorous animals (cattle, sheep and camels).
 Habitat: Small intestine.
15
Class: Cestoidea

1) Adult :-
 Size : 4 - 10 meters.
2) Egg (D.S):-
 Size : 30 - 40 µm in diameter.
 Shape :Spherical.
 Shell : Thick, radially striated emberyophore.
 Color : Brownish.
 Content : Mature hexacanth embryo (onchosphere larva).
3) Cysticercus bovis (I.S):-
 Size: 1 × 0.5 cm.
 Shape: Oval cyst lined with germinal epithelium containing fluid and
surrounded by fibrous tissue reaction formed by the intermediate
host (cattle).
 Scolex: Invaginated with 4 suckers (without hooks).
 Life cycle:-
 The adult worm lives in the upper small intestine of man (D.H). Mature
eggs and gravid segments pass in faeces (D.S). Eggs may be released
in the perianal region if the gravid segment ruptured during passing.
 Cattle (I.H) and other herbivorous animals (camels & sheep) are
infected by ingestion of eggs or gravid segments with grass.
 The egg hatches in the duodenum 🠆 released hexacanth embryo 🠆
penetrates the mucosa of the small intestine 🠆 enters the intestinal
venule 🠆 Rt side of the heart 🠆 lung 🠆 Lt side of the heart 🠆 systemic
circulation 🠆 distributed all over the body especially the active skeletal
muscles (tongue, jaw, neck, shoulder, thigh and forearm), heart and
brain where it develops into cysticercus bovis (I.S) within 2 months. It
15
Class: Cestoidea
remains viable for one year, then dies and becomes calcified.
 Human infection occurs by eating beef either raw or improperly cooked
e.g. steaks, hamburgers or grilled (kabab) containing viable cysticercus
bovis. In the small intestine, the invaginated scolex of the cysticercus
evaginates in response to bile salt and attaches to mucous membrane
🠆 adult worm in 3 months.
Figure (11): Life cycle of Taenia saginata
- Disease :Taeniasis saginata.

1) Intestinal irritation e.g. nausea, vomiting, hunger pains, colic, diarrhea
or constipation.
2) Toxic manifestations: Due to worm products e.g. dizziness, headache,
insomnia & delirium.
15
Class: Cestoidea
3) Intestinal obstruction.
4) Loss of weight.
5) Anxiety and nervousness due to continued migration of proglottids out
of the anus 🠆 irritation & itching.
 Diagnosis :-
1) Detection of eggs by stool examination (direct and concentration
methods).
2) Perianal swabs by scotch tape for eggs (will be discussed later).
3) Detection of gravid segments in the stool to differentiate between
Taenia species.
 Treatment : Similar to D. latum.
 Prevention and control :-
1) Treatment of patients.
2) Avoid defecation in soil & sanitary sewage disposal.
3) Proper cooking of meat or deep freezing ( 10oc for 5 - 10 days).
4) Proper inspection of meat in slaughter houses and infected meat should
be destroyed.
5) Prevention of cattle to graze in contaminated areas.
1) Taenia solium
(Pork tapeworm)
 Pork-eating countries e.g. America, Europe.

 Not common in Islamic countries.
 D.H : Man.
 I.H : Pigs and occasionally man.
11
Class: Cestoidea
 Habitat : Small intestine
 Morphology:-
1) Adult :-
 Size: 4 - 6 meters in length.
2) Egg (D.S & I.S): Similar to T. saginata.
3) Cysticercus cellulosa: Similar to cysticercus bovis, but detected in pork
and the invaginated scolex carries 4 suckers and hooks.
 Life cycle :Similar to T. saginata except :-
1) Intermediate host : Pig.
2) Infected larva called cysticercus cellulosa.
3) Man acts as D.H (harbours the adult in the small intestine) by eating
infected pork and also acts as I.H (harbours the cysticercus cellulosa in
his tissues) by eating T. sodium eggs and develops a condition known
as cysticercosis.
15
Class: Cestoidea
Figure (12): Life cycle of Taenia solium

1) Taeniasis solium: Due to ingestion of undercooked pork containing
cysticercus cellulosa (the same clinical pictures as taeniasis saginata).
2) Cysticercosis : It develops when man ingested the T. solium eggs with
food or drink  development of larvae (cyticercus cellulosa) in his
tissues. (will be discussed later).
 Diagnosis : Similar to T. saginata.
 Treatment : Similar to T. saginata but :-
1) Niclosamide is contraindicated because it disintegrates the worms,
15
Class: Cestoidea
releasing large number of eggs in the intestine which increase the

possibility of cysticercosis (internal autoinfection).
2) Atebrine causes nausea and vomiting. Anti-emetic must be given one
hour before administration of Atebrine to avoid antiperistalsis and
internal autoinfection.
 Control : Similar to T. saginata.
 Differences between T. saginata and T. solium :-
Item T. saginata T. solium
Distribution Cattle raising countries Pig raising countries
Disease Taeniasis saginata Taeniasis solium
Size 4 - 10 meters 4 - 6 meters

Adult
Rostellum with 2 rows of

Scolex No rostellum or hooks.
taenoid hooks.
D.H Man in both

Life cycle
Morphologically similar
Egg
Infect cattle only Infect pigs & man
Cattle, sheep & camel

I.H Pigs & occasionally man
only
Larva Cysticercus bovis Cysticercus cellulosa
 Cysticercus bovis in  Cyeticercus cetllulosa in

I.S to man undercooked beef undercooked pork
 Eggs 🠆 cysticercosis.
15
Class: Cestoidea
4) Hymenolepis nana
(Vampirolepis nana or Dwarf tapeworm)
 Geographical distribution: Cosmopolitan and more common among

children.
 It is prevalent in Egypt.
 Habitat: Small intestine (both adult & larval stage).
 D.H: Man.
 R.H: Rodents (rats & mice).
 I.H: Man, sometime flea larva & beetles.
1) Adult:-
 Size: The smallest tapeworm in man, about 1 - 4 cm 1 mm.
2) Egg (D.S & I.S):-
 Size: 35 - 50 µm in diameter.
 Shape: Spherical.
 Shell: 2 layers.
- Outer thin layer.
- Inner embryophore with 2 polar thickenings, each with 4 - 8
filaments.
 Content: Mature hexacanth embryo (onchosphere).
3) Cysticercoid nana:-
 Size: 0.5- 1mm in length.
 Shape: Oval cyst containing fluid.
 Scolex: Upright in position, carrying suckers & hooks.
 Tail: Posterior (Cercocystic cysticercoid).
15
Class: Cestoidea
 Life cycle:-
1) Direct cycle:-
 The adult worm lives in the intestinal wall of man, rats & mice (D.H).
 Mature eggs and gravid segments pass in stool.
 Infection occurs by ingestion of eggs with food (green raw vegetables)
and water or by autoinfection (contaminated hands).
 The egg hatches 🠆 onchosphere is librated in the small intestine 🠆
penetrates the intestinal villi & develops into cysticercoid larva in
submucosa 🠆 after one week, it returns to the lumen, attaches to
mucosa and matures to adult worm within 2 weeks.
 This direct cycle is easily spread between groups of people lived

together e.g. families, school children….etc, as it doesn't need external
development (man acts as D.H & I.H).
2) Indirect cycle:-
 Sometimes, eggs in soil ingested by flea larva or other insects (beetles,
flour insects and cockroaches) (I.H) 🠆 hatch in the intestine 🠆
onchosphere penetrates the intestine 🠆 body cavity where
cercocystic cysticercoid develops.
 Ingestion of flea or other insects with food 🠆 libration of cysticercoid in
intestinal lumen 🠆 attaches to the mucosa 🠆 develops into adult.
 N.B: The cysticercoid remains in flea larva until it develops into adult
flea.
56
Class: Cestoidea
Figure (13): Life cycle of Hymenolepis nana
1) Ingestion of eggs with food or drink directly or indirectly by the
house fly.
2) Autoinfection either external (faeco-oral route) or internal

(disintegration of gravid segments inside the intestine 🠆 libration of
eggs containing mature hexacanth embryo 🠆 penetrates the
submucosa 🠆 changes to cysticercoid larva 🠆 it returns back to the
lumen 🠆 matures to adult).
3) Ingestion of flea, flea larva or other insects containing cysticercoid.
 Clinical Picture:
- Disease: Hymenolepiasis nana.
 Abdominal pain, anorexia, vomiting and diarrhea.
 In heavy infection: Nervous manifestations occur due to absorption
of metabolic products of the adults  dizziness, insomnia &
55
Class: Cestoidea
convulsions.
 Diagnosis: Stool examination to detect the eggs (direct and
concentration).
 Treatment:-
1) Anti-cestodal drugs.
2) Praziquentel: 15-20 mg/kg as a single oral dose.
 N.B:-
- All family members must be treated at the same time.
- Repeat the treatment after 2-3 weeks to destroy the embedded
cysticercoids in submucosa.
1) Mass treatment of the patients.
2) Personal cleanliness (washing hands after defecation and before
eating) to avoid autoinfection.
3) Proper sewage disposal.
4) Avoid using human excreta as fertilizer.
5) Proper washing of vegetables.
6) Protect food from flies.
7) Insect control.
8) Rodent control.
4) Hymenolepis diminuta
(Rat tapeworm)
 Geographical distribution: Cosmopolitan.

 D.H: Rats, mice and rarely man (children).
 I.H: Rat flea larvae and other insects as beetles and cockroaches.
 Habitat: Small intestine.
55
Class: Cestoidea
1) Adult:-
 Size: 20 - 60 cm × 4 mm.
2) Egg (D.S):-
 Size: 60 - 70µm in diameter.
 Shape: Broad oval.
 Shell: Two layers, outer thin layer and inner embryophore with polar
thickening without filaments.
 Color: Yellowish.
 Content: Mature hexacanth embryo (onchosphere).
3) Cysticercoid diminuta: Similar to H. nana, while scolex without hooks.

 Life cycle:-
 The adult worm lives in small intestine of rodents (mice, rats) and rarely
man (D.H).
 Eggs pass in stool and ingest by an insect (I.H) e.g. larva of fleas, grain
beetles or cockroaches.
 The egg hatches in the intestine of the insects 🠆 Onchosphere
penetrates the intestine 🠆 body cavity where develops into cysticercoid
(cercocystic cysticercoid).
 The D.H infected by ingestion of insect vectors containing cysticercoid
larva (I.S) with food.
 The cysticercoid liberates in the small intestine 🠆 attaches to the
mucosa 🠆 matures to adult worm within 3 weeks.
55
Class: Cestoidea
Figure (14): Life cycle of Hymenolepis diminuta
55
Class: Cestoidea
 Diagnosis, treatment and control similar to H. nana.

- Differences between H. nana & H. diminuta:-
Items H. nana H. diminuta
Size 1 - 4 cm × 1 mm 20 - 60 cm × 4 mm
Retractile rostellum with Invaginated rostellum
Scolex
Adult
one row of hooks without hooks

Mature Smaller, 3 testes close to Bigger, 3 testes apart
segments each other in the middle from each other
Gravid Smaller, about 0.5 × 0.1 Larger, about 5 ×
segments mm 1mm
Size 35 - 50 µm in diameter 60 - 70 µm in diameter
Shape Spherical Broad oval
Eg
g
Inner embryophere with Without polar filaments

Shell
polar filaments
Color Translucent Yellowish
Scolex with suckers & Scolex with suckers
Cysticercoid
hooks only
Man and occasionally rats Rats, mice &
D.H
& mice occasionally man
Man & sometimes insects
Larva of fleas, grain
I.H (like larva of fleas or grain
beetles & cockroaches
beetles)
Eggs or cysticercoid larvae cysticercoid larvae in
I.S
in insect insect only
- Ingestion of eggs with - Ingestion of insects
food or drink containing cysticercoid
- Internal or external auto- larva
Mode of infection infection
- Ingestion of insects
containing cysticercoid
larva
51
Class: Cestoidea
 Tissue cestodes
They are cestodes that infect different tissues of man by their larval stage
causing serious diseases e.g. D. mansoni, T. solium, M. multiceps, E.
granulosus, E. multilocularis, and H. nana.
2) Echinococcus granulosus
(Hydatid worm)
 Geographical distribution : Cosmopolitan.

 Habitat : Small intestine.
 D.H: Dogs, foxes and other canines.
 I.H: Sheep, cattle, pigs and occasionally man.
1) Adult:-
 Size : 3 - 6mm.
2) Egg (I.S to man and herbivorous): Similar to Taenia egg.
3) Hydatid cyst (D.S in man and herbivorous):-
 Simple unilocular hydatid cyst:-
 The most common type.
 Size : Variable from pin's head to head of the foetus (1 mm - 20
cm).
 Shape : More or less spherical.
 Structure:-
1. Pericyst : Fibrous capsule.
2. Cyst wall: 2 layers:-
a) Outer laminated non-cellular, 1mm thick.
b) Inner cellular germinal layer which secretes the laminated
layer and produces scolices, brood capsules and
55
Class: Cestoidea
daughter cysts.
3. Contents:-
a) Multiple scolices arise from the germinal layer.
b) Brood capsule: Sac of germinal layer only containing
group of scolices.
c) Endogenous daughter cyst: Similar to mother cyst.
d) Exogenous daughter cyst: Due to increase of the
intracystic pressure  herniation of both laminated and
germinal layer outside the mother cyst and may separate
from it.
e) Hydatid fluid
f) Hydatid sand: Scolices, hooks, brood capsules and
daughter cysts separated from germinal layer and floating
in hydatid fluid. Fig.(13 - 5)
 Other types of hydatid cyst :-
1) Sterile cyst.
2) Osseous cyst:.
3) Calcified cyst:.
4) Multilocular (Alveolar) hydatid cyst : Caused by E. multilocularis.
 D.H: Red foxes and other wild canines.
 I.H: Rodents and occasionally man.
5) Polycystic hydatid cyst.
 Life cycle of Echinococcus granulosus :-
 Adult worm lives in the small intestine of dogs and other canines (D.H)
🠆 eggs pass in faeces 🠆 swallowed by man, sheep, cattle & camels
(I.H).
 Man ingested the eggs along contaminated food, drink with dogs faeces
or by handling dogs whose hair are usually contaminated with eggs.
55
Class: Cestoidea
 The onchoshere hatches in intestine 🠆 blood stream 🠆 various organs

and develops into hydatid cysts.
 The commonest sites:-
 Liver (70%).
 Lung (20%).
 Other organs such as brain, bone, spleen, kidney, muscles,

heart, thyroid & eyes (10%).
 Dogs and others canines (D.H) were infected by eating hydatid cysts
present in herbivorous organs around slaughter houses 🠆 adult in the
small intestine.
 The cycle in man is considered as a blind cycle.
Figure (15): Life cycle of Echinococcus granulosus
55
Class: Cestoidea
Hydatid disease
(Echinococcosis or Hydatidosis)
 Definition: It is a parasitic infection of both humans and other mammals

such as sheep, cattle and rodents with hydatid cyst, the larval stage of
different Echinococcus species.
 Types of human echinococcosis:-
1) Cystic echinococcosis.
2) Alveolar echinococcosis.
3) Polycystic echinococcosis.
 Local inflammatory reaction around the hydatid cyst.
 The symptoms depend on the size & site of the cyst.
 Large sized cysts 🠆 pressure atrophy of affected organs:-
 Liver 🠆 enlargement and dysfunction.
 Lung 🠆 pain, cough and dyspnea.
 Brain 🠆 epilepsy.
 Eye 🠆 protrusion of the eye ball.
 Bones 🠆 Pain & spontaneous fracture.
 Spontaneous rupture of cyst into peritoneal cavity or pleura may lead
to severe allergic reaction (anaphylactic shock) or secondary cysts.
 Abscess formation.
55
Class: Cestoidea
 Diagnosis:-
1) Clinical:-
 History of contact with dogs.
 Hydatid thrill.
2) Laboratory:-
a) Direct:-
1. X-ray for calcified cyst.
2. Ultrasonography, CT scan and MRI.
3. Scolices in sputum or urine.
b) Indirect:-
1. Eosinophilia.
2. Intradermal test
3. Serological tests: IHAT, CFT, IFAT, ELISA and precipitin or
flocculation test.
4. PCR: Nucleic acid detection.
 Treatment:-
1) Surgical removal of the cyst.
2) Percutaneous treatment (PAIR)
- This procedure is indicated in inoperable cases and who have
drug resistance (no response to medical treatment).
3) Medical treatment:-
 Indications: In inoperable cases and before and after surgery.
-Albendazole.
-Mebendazole (Vermox).
 Disadvantages:-
1. It may lead to drug resistance.
2. It is used for long time in high dose.
56
Class: Cestoidea

1) Dogs (D.H):-
- Periodic examination and treatment of pet dogs.
- Elimination of stray dogs.
- Infected organs in slaughter houses should be destroyed and not
fed to dogs.
2) Man (I.H):-
- Health education to avoid kissing, handling or playing with dogs.
- Personal hygienic measures.
- Avoid contamination of food or drink with dog faeces.
- Fly control.
55
Medical Arthropodology
Myiasis
 Definition: Infection of human or animals tissues with larvae of dipterous
flies.
 Classification:
I. According to the biology (habit) of the fly:-
1) Specific myiasis (obligatory tissue parasites): Caused by larvae of
certain flies which normally develop in living tissues of man or
animals e.g.:
 Dermatobia (human botfly): Female deposits eggs on other
blood sucking insects like mosquitoes or flies (Stomoxys). When
such insects bite man or animals for blood meal, the eggs hatch
and larvae penetrate intact skin 🠆 nodular cutaneous myiasis.
 Oestrus (sheep botfly): Female deposits eggs accidentally in the
eye (conjunctiva) or nose of man 🠆 hatch 🠆 larvae 🠆 ocular and
nasopharyngeal myiasis.
2) Semispecific myiasis (obligatory necrobiots): larvae of some flies
which mainly live on decaying matters and animals,may
occasionally live on living tissues of man or animals if open wounds
or ulcers are present e.g. Calliphora, and Sarcophaga.
3) Accidental myiasis: larvae of some flies may get in human tissues
accidentally through ingestion of contaminated food or drink, or
deposition on urethral opening or anal orifice e.g. Musca and
Fannia.
II. According to affected tissues:
1) Gastric myiasis: Due to ingestion of larvae of some flies with food or
drink e.g. Eristalis larva in man.
2) Intestinal myiasis: Due to either ingestion of eggs or larvae of some
flies with food or drink (e.g. Musca ) or deposition of eggs or larvae
27
Medical Arthropodology
of other flies (e.g. Fannia) near the anal orifice during sleep or
defecation in open latrines.
3) Urogenital myiasis: Due to deposition of eggs of Fannia (latrine fly):-
 On the urethral opening during sleep or defecation 🠆 urethra 🠆
urinary bladder 🠆 cystitis.
 On vaginal opening in female 🠆 Larvae enter the vagina 🠆
vaginitis.
4) Ocular and nasopharyngeal myiasis: invasion of larvae of some flies
to the conjunctiva and the nose 🠆 severe irritation and oedema, e.g.
Oestrus.
5) Aural myiasis: flies eggs are deposited on purulent discharge in ear
🠆 hatch 🠆 larvae enter the external ears 🠆 middle and internal ears
🠆 severe lesion e.g. Sarcophaga.
6) Cutaneous myiasis:-
 Intact skin:- e.g. Dermatobia.
A. Broken skin (wounds or ulcers): e.g. Calliphora.
Diagnosis:-
1- Clinical: Appearance of the lesions and symptoms.
2- Laboratory:-
- Identification of larva in the lesion by its posterior spiracles.
 Treatment:-
Manual or surgical removal of larvae by forceps under local
anaesthesia from skin wounds, eye, ear and nose.
27
Class: Sporozoa
Medical Protozoology
It is the study of protozoa of medical importance. Protozoa are microscopic
unicellular organisms capable of performing all physiologic functions of life.
 Morphological characters:-
1) Protozoa are made of protoplasm that differentiated into nucleoplasm
and cytoplasm which consists of outer thin hyaline ectoplasm and inner
voluminous granular endoplasm.
2) The ectoplasm functions including: Ingestion of food, excretion of waste
products, respiration, protection and locomotion.
3) The endoplasm is concerned with metabolism and reproduction.
4) Nucleus is concerned with reproduction. It consists of nuclear
membrane, nucleoplasm (nuclear sap) and chromatin. It may be one or
more, vesicular or compact.
 Biology of protozoa:-
1) Nutrition: By absorption through the body surface, phagocytosis,
diffusion through the body surface or pinocytosis.
2) Respiration: Either aerobic for protozoa living in tissues or blood or
anaerobic for protozoa living in the intestinal lumen.
3) Locomotion:-
- By pseudopodia (amoeboid movement) 🠆 as amoebae.
- By cilia that covered the body 🠆 as ciliates.
- By flagella which are whip-like filaments (single or multiple).
- By undulant movement (gliding) 🠆 as sporozoa.
4) Excretion: By diffusion through the body surface or cytopyge.
5) Secretions: Protozoa secrete:-
- Digestive ferments and pigments.
- Material for the cyst wall formation
- Proteolytic enzymes
- Hemolysins and cytolysins
47
Class: Sporozoa
- Toxic and antigenic substances.

6) Reproduction:-
a. Asexual reproduction:-
- Simple fission: e.g. amoebae, flagellates (longitudinal) & ciliates
(transverse).
- Multiple fission: e.g shizogony in sporozoa.
b. Sexual reproduction:-
- Conjugation.
- Gametogony.
7) Encystation: Formation of cysts that resist unfavourable conditions
outside the body and for protection against digestive juice of the
gastrointestinal tract.
Classification of Phylum Protozoa
According to the organ of locomotion According to the habitat
1- Class Rhizopoda (Amoebae) 1- Intestinal protozoa:

 move by pseudopodia. Amoebae, flagellates, ciliates
2- Class Ciliata (Ciliates) and intestinal coccidia
 move by cilia. 2- Blood protozoa:
3- Class Zoomastigophora (Flagellates) Blood flagellates, Plasmodium
 move by flagella. species and Babesia
4- Class Sporozoa (Plasmodia & Coccidia) 3- Tissue protozoa:
 move by gliding. Toxolasma ,Sarcocystis
and tissue flagellates
4- Buccal protozoa:
Entamoeba gingivalis
Trichomonas tenax
5- Urogenital protozoa:
Trichomonas vaginalis
47
Class: Sporozoa
1) Class: Rhizopoda
(Amoebae)
 General characters:-
1) Move by pseudopodia.
2) Multiply asexually by simple binary fission.
3) Contain vesicular nucleus.
4) Form cyst.
This class includes:-
1- Amoebae of large intestine:-
- Entamoeba histolytica.
- Entamoeba coli.
2- Amoeba of buccal cavity:-
- Entamoeba gingivalis.
3- Free living amoebae:-
- Pathogenic free living amoebae: Naeglaria fowleri and Acanthamoeba
species.
- Non pathogenic free living amoebae: Coprozoic amoebae.
Entamoeba histolytica
 Geographical distribution: Worldwide especially in the temperate
zone.
 Habitat: Large intestine (caecum, colonic flexures and sigmoidorectal
region).
 D.H: Man
 R.H: Dogs, pigs, rats and monkeys
1) Trophozoite stage (Vegetative form or tissue form):-
- Size: 20µm (15 - 30 µm).
47
Class: Sporozoa
- Shape: Irregular.
- Cytoplasm: Differentiated into ectoplasm and endoplasm.
- Ectoplasm (Outer): Clear with a single finger like pseudopodia.
- Endoplasm (Inner): Granular with:
a. Nucleus:-
- Size: 5 - 6 µm.
- Shape: Spherical with small and central Karyasome.
- Peripheral chromatin: Fine granules of uniform size and
regularly arranged on the inner surface of the nuclear
membrane.
b. Food vacuoles: May contain RBCs (no bacteria).
2) Cyst Stages: include
a. Precyst stage.
b. Immature cyst (Uninucleate cyst and Binucleate cyst):-
 Uninucleate cyst: contain 1 nucleus
 Binucleate cyst: contain 2 nuclei-
c. Mature cyst (Quadrinucleate cyst):-
- Size: 15 µm (10 - 20 µm).
- Shape: Rounded with thick cyst wall.
- Contents:-
 4 nuclei similar to the nucleus of trophozoite but smaller in
size.
 Glycogen vacuoles and chromatoid bodies (stored food) tend
to disappear in mature cyst as the cyst gets older.
- The infective stage.
44
Class: Sporozoa
 Life cycles:-
 Entamoeba (E) histolytica trophozoite lives in the large intestine.
 Infection occurs by ingestion of mature cysts (I.S) (Quadrinucleate
cyst).
 Cysts are excyst in the small intestine (ileo-coecal junction) liberating
trophozoites with 4 nuclei (metacysts) 🠆 divides 3 times by binary
fission 🠆 produce 8 trophozoites which migrate to the large intestine.
 In asymptomatic carriers and cysts passers trophozoites 🠆
produce immature cysts 🠆 multiply 🠆 mature cysts, which are passed
in the faeces (usually found in firm stool).
 In symptomatic patients, the trophozoites invade the intestinal
mucosa (intestinal disease) forming flask-shaped ulcers or reach the
bloodstream to extraintestinal sites such as the liver, brain, and lungs
(extra-intestinal disease).
Figure (16): Life cycle of Entamoeba histolytica
47
Class: Sporozoa
Mode of transmission:-
1) Contaminated foods (ex. green vegetables) or drinks or hands with
human excreta containing mature cyst.
2) Handling food by infected food handlers as cookers and waiters.
3) Flies and cockroaches that carry the cysts from faeces to exposed food.
4) Autoinfection (faeco-oral or hand to mouth infection).
 Disease: Amoebiasis or amoebic dysentery.
 Clinical pictures:-
1) Intestinal amoebiasis:-
1. Asymptomatic infection: Most common and trophozoites remain in
the intestinal lumen feeding on surrounding nutrients as a commensal
without tissue invasion (Asymptomatic patient known as a healthy
carrier).
2. Symptomatic infection:-
a. Acute amoebic dysentery: Accompanied with fever, abdominal
pain, tenderness, tenesmus (difficult defecation) and frequent
motions of loose stool containing mucus, blood and trophozoites.
b. Chronic infection: Accompanied with low grade fever, recurrent
episodes of diarrhea alternates with constipation. Only cysts are
found in stool.
3. Complications:-
- Haemorrhage due to erosion of large blood vessels.
- Appendicitis.
- Intestinal perforation and peritonitis.
- Amoeboma (Amoebic granuloma): Inflammatory granuloma of the
intestinal wall around the ulcer 🠆 stricture of affected area.
- Pseudopolyposis.
47
Class: Sporozoa
2) Extra-intestinal amoebiasis: Due to invasion of the blood vessels by the

trophozoites in the intestinal ulcer 🠆 reach the blood 🠆 to spread to
different
organs as:-
- Liver: Amoebic liver abscess or diffuse amoebic hepatitis.
- Lung: Lung abscess 🠆 pneumonitis with chest pain, cough, fever.
- Brain: Brain abscess 🠆 encephalitis.
- Skin: Cutaneous amoebiasis (Amoebiasis cutis).
 Diagnosis:-
1) Clinical.
2) Laboratory:-
 Intestinal amoebiasis:-
a. Direct:-
 Macroscopic: Offensive loose stool mixed with mucus and blood.
 Microscopic:-
1. Stool examination: Reveals either trophozoites (in loose stool) or
cysts (in formed stool) by:-
- Direct smear of fresh stool samples to observe the movements
of trophozoite.
- Concentration methods to increase the chance of parasite
detection.
2. Sigmoidoscopy: To see the ulcer or the trophozoites.
3. X-ray after bariun enema: to see the ulcer, deformities or stricture.
b. Indirect:-
 Serological tests: CFT, IHAT, IFAT, ELISA.
 Extra- intestinal amoebiasis: According to the organ affected.
a. Direct:-
1. X- ray:-
78
Class: Sporozoa
- In liver 🠆 space occupying lesion.

- In lung 🠆 pleuritis with elevation of the diaphragm
2. Ultrasonography and CT scan: For liver abscess.
3. Aspiration of abscess content: For liver abscess to detect
trophozoites.
b. Indirect:-
- Serological tests: As intestinal amoebiasis.
- Molecular by PCR.
- Blood examination: Leucocytosis.
- Liver function tests: Increased in amoebic liver abscess.
 Treatment:-
1) Asymptomatic intestinal carrier:-
- Paromomycin.
2) Intestinal amoebiasis:-
- Metronidazol (Flagyl): 750 mg (3 tab.) t.d.s for 5-10 days.
3) Extra-intestinal amoebiasis:
- Metronidazol (Flagyl).
1) Treatment of patients and carriers.
2) Proper washing of vegetables.
3) Pure water supply.
4) Sanitary sewage disposal.
5) Avoid using of human excreta as fertilizer.
6) Fly control.
7) Personal hygienic measures (washing hands after defecation and
before eating) to avoid autoinfection.
78
Class: Sporozoa
III) Class: Zoomastigophora

(Flagellates)
1) Move by one flagellum or multiple flagella.
2) Multiply by longitudinal binary fission.
3) Vesicular nucleus with central karyosome.
4) Some species have a cytostome (mouth).
Classification of Flagellates
According to their habitat
(A) (B) (C) Intestinal flagellates

Atrial flagellates Blood and tissue flagelates
1- Giardia lamblia 1- Trichomonas tenax 1- Leishmania species
(Buccal flagellate) 2- Trypanosoma species
2- Trichomonas vaginalis
(Pathgenic urogenital flagellate)
(A) Intestinal flagellate

(Giardia lamblia)
 Geographical distribution: Cosmopolitan especially tropical and
subtropical regions.
 Habitat: In the small intestine mainly the crypts of the duodenum and
occasionally in the common bile duct and gall bladder.
 D.H: Man.
78
Class: Sporozoa
1) Trophozoite stage:
 Size: 15 8 µm.
 Shape: Pear shaped with convex dorsal surface and flat ventral
surface with 2 sucking discs for attachment to the mucous
membrane.
 Nucleus: Two oval nuclei with central karyosomes anteriorly.
 Four pairs of flagella:-
- One pair anteriorly.
- 2 pairs laterally.
- One pair posteriorly.
 Axostyle: 2 central rods in the middle of the body.
 Parabasal bodies: 2 rode lie across the axostyle in the center just
posterior to the sucking discs.
2) Cyst (I.S):-
 Size: 12 7 µm.
 Shape: Oval with thick cyst wall.
 Contents:-
- 4 nuclei at one pole.
- Fine granular cytoplasm with remnants of flagella, axostyle and
parabasal bodies.
 Life cycle:-
 Giardia (G) lamblia trophozoite lives in the small intestine of man.
 Human infection occurs by ingestion of mature quadrinuclated cyst (I.S)
with faecally contaminated food, water, or hands.
 Cysts are excyst 🠆 2 trophozoites are liberated in the lumen.
 The trophozoites multiply by longitudinal binary fission as the pH of
the duodenum (6-7) is suitable for their growth.
78
Class: Sporozoa
 Encystation takes place. The two trophozoite nuclei divide mitotically so

that the cyst becomes quadrinucleated.
 The cysts pass out with the stool ready to infect another host if
ingested.
Figure (17): Life cycle of Giardia lamblia
 Mode of transmission:-
1) Contaminated foods (ex. green vegetables) or drinks or hands with
human excreta containing mature cyst.
2) Handling food by infected food handlers as cookers and waiters.
3) House flies that carry the cysts from faeces to exposed food.
4) Autoinfection (faeco-oral or hand to mouth infection).
77
Class: Sporozoa

 Disease: Giardiasis.
 Hypogammaglobulinaemia, low level of secretory Ig A in the gut,
achlorhydria (decreased Hcl), vitamin A deficiency and malnutrition are
predisposing factors for the development of infection with Giardia
lamblia.
 Clinical pictures:-
1. Asymptomatic infection: Most common. The trophozoites remain in
the intestinal lumen feeding on surrounding nutrients and mucus
without causing manifestations (Asymptomatic patient known as a
healthy carrier).
2. Symptomatic infection:-
a. Acute giardiasis:-
- Common in children and travelers to endemic areas.
- The patient suffers from fever, abdominal colic, epigastric pain,
anorexia, flatulence, vomiting, watery diarrhoea with excess
mucus (no blood) but later steatorrhoea (fatty stool) occurs
🠆 dehydration and loss of weight. Trophozoites are found in
the stool.
- Invasion of gall bladder 🠆 cholycystitis, jaundice and biliary
colics.
- In immunocompetent patient, giardiasis is self limiting.
- In immunodeficient patient, IgA secreation in the gut is
decreased 🠆 severe infection with persistent diarrhea,
steatorrhoea, malabsorption syndrome and weight loss.
b. Chronic giardiasis:-
- Common in adults.
- The patient suffers from anorexia, epigastric pain, dyspepsia,
77
Class: Sporozoa
nausea, vomiting and diarrhoea alternating with constipation.

Only cysts are found in stool.
c. Complications:-
1. Retardation of growth and development in infant and young
children.
2. Malnutrition and malabsorption syndrome.
3. Biliary tract disease.
 Diagnosis:-
1) Clinical.
2) Laboratory:-
a. Direct:-
 Macroscopic: Foul smelling loose greasy stool mixed with mucus
and usually float on the surface in toilet.
 Microscopic:-
1. Stool examination: Reveals either trophozoites (in loose stool)
or cysts (in formed stool) by:-
- Direct smear of fresh stool samples.
- Concentration methods to increase the chance of parasite
detection.
- Iodine stained smear or permanent staining smear.
2. Examination of duodenal content (enterotest or string test.
b. Indirect:-
 Serological tests.
 PCR: For detection of DNA of Giardia lamblia.
 Treatment:-
1) Metronidazole (Flagyl): 250 mg t.d.s for 10 days.
2) Nitazoxanide: 500 mg twice daily for 3 days.
 Prevention and control: As E. histolytica.
77
Class: Sporozoa
(B) Atrial flagellate

(Trichomonas vaginalis)
 Geographical distribution: Cosmopolitan.
 Habitat: Vagina, cervix and urethra in female & prostate and urethra in
male.
 D.H: Man.
 Morphological characters:
Trophozoite stage (No cyst stage):-
 Size: 15 8 µm.
 Shape: Oval or pear shaped with small cytostome at the anterior end.
 Nucleus: Large oval vesicular at the anterior end.
 Flagella: 5(4 free anterior flagella and one marginal with undulating
membrane that reaches about 1/2 the body).
 Axostyle: One slender rod that extends beyond the posterior end.
 One thick parabasal bodies.
 Life cycle:-
1) The trophozoite of Trichomonas vaginalis lives mainly in the vagina of
female and urethra and prostate in male where it multiplies by
longitudinal binary fission.
2) It is the infective stage (no cyst stage) and does not survive in the
external environment.
74
Class: Sporozoa
Figure (18): Life cycle of Trichomonas vaginalis
1- Direct by sexual intercourse.
2- Indirect by contaminated towels, toilet seats and underwear.
 Disease: Trichomoniasis (sexually transmitted disease).
 In women:-
1. Asymptomatic infection: The trophozoites remain in the vagina without
causing manifestations.
2. Symptomatic infection:
a. Vaginitis: Accompanied with a frothy yellowish - green vaginal
discharge, abnormal vaginal odour, vulvar irritation, itching and
soreness and duspareunia (pain during sexual intercourse).
77
Class: Sporozoa
b. Urethritis: Accompanied with frequency of micturition and dysuria

(pain during urination).
 In men:-
1. Asymptomatic infection is common. Men harbour the organism in their
urinary tract and usually have no symptoms at all.
2. Symptomatic infection includes urethritis, prostatitis with white
discharge and dysuria.
 Diagnosis:-
1) Clinical.
2) Laboratory:-
a.Microscopic:-
 In women: T. vaginalis trophozoite can be detected by:
1. Wet film preparation from vaginal discharge, vaginal scraping or
sedimented urine.
2. Vaginal swab lies in a tube containing 1 ml saline.
 In men: T. vaginalis trophozoite can be detected in urethral
discharge, prostatic secretion or sedimented urine.
b.Culture: More sensitive than microscopic examination but not widely
used.
c. Direct immunofluorescent antibody staining and PCR.
 Treatment:-
1) Systemic:-
 Metronidazole (Flagyl): 2gm (single dose) or 500 mg twice daily for 7
days.
 Antibodies for secondary bacterial infection.
2) Local:-
 Flagyl vaginal insert: 500 mg /day for 10 days.
 Acidifying vaginal douches: Lactic acid douche to maintain the acidity
77
Class: Sporozoa
of the vagina.
N.B. Both partners should be treated simultaneously to avoid re-infection.
1) Treatment of both partners.
2) Personal hygienic measures.
(C) Blood Flagellates

(Haemoflagellates)
Blood flagellates of medical importance to man include:-
1) Genus Leishmania.
2) Genus Trypanosoma.
1) Live in blood and tissues.
2) Move by one flagellum.
3) Need vector for transmission.
4) Require 2 hosts (vertebrate and invertebrate).
Visceral Leishmaniasis
(Kala azar, Dum dum fever, Black sickness)
 Leishmania donovani: India, China & East Africa (common in young
adults of 10 - 25 years old).
 Leishmania infantum: Mediterranean region, Middle East & Africa
(common in children < 4 years).
 Leishmania chagasi: South America (common in children < 4 years).
 Definitive host: Man.
 Reservoir host: Dogs & rodents.
78
Class: Sporozoa
 Vector: Female sand fly (Phlebotomus langeroni for OWVL & Lutzomyia
in
NWVL)
 Life cycle:-
 Leishmaniasis is transmitted by the bite of infected female sand fly. The
female sand fly is infected during tacking the blood meal from the
infected hosts (man or reservoir hosts) which containing amastigotes
inside macrophages (in the stage of parasitaemia).
 In the midgut of the sand fly, amastigotes are transformed into
metacyclic promastigotes (I.S) that multiply by longitudinal binary
fission (cyclopropagative), then migrate forward to the pharynx and
proboscis that become almost blocked with them (blocked sand fly).
The female sand fly is now infective (salivary glands are not
invaded).
 Man and reservoir hosts are infected when female sand fly bites them
🠆 inoculates the metacyclic promastigotes (I.S) 🠆 invade macrophages
and other R.E.Cs where they transformed into amastigotes (D.S).
78
Class: Sporozoa
Figure (19): Life cycle of Leishmaniasis
1) Bite of infected sand fly (cyclopropagative transmission).
2) Blood transfusion.
3) Congenital transmission.
4) Ingestion of contaminated food or drink by excreta of man & animals.
 Pathogenesis and symptomatology: When the female sand fly
injects the infective stage (metacyclic promastigotes) in the skin 🠆 the
parasite engulfed by macrophages 🠆 transformed into amastigotes
(Leishmania form) 🠆 multiply inside the macrophages 🠆 the cells rupture
🠆 the organisms pass to the blood and reach viscera 🠆 invade and
multiply in the RECs of different organs (ex. Spleen, liver, lymph nodes,
bone marrow, skin & intestine) 🠆 hyperplasia and enlargement of the
affected organs.
78
Class: Sporozoa
This leads to the following manifestations:-

1) Local lesion (leishmanioma): A small papule at the site of insect bite.
2) Systemic manifestations:
 Fever: Usually intermitted with double or triple daily rise.
 Loss of weight and cachexia especially in thorax and shoulder girdle.
 Hepatomegaly, splenomegaly and lymph node enlargement.
 Oedema and ascites due to liver and kidney affection (decrease
albumin).
 Pancytopenia: Anaemia (hypoplastic), leucopenia (with relative
monocytosis & lymphocytosis) and thrombocytopenia due to invasion
and depression of bone marrow.
 Diarrhoea or dysentery with ulceration of the intestine 🠆 malabsorption.
 Pigmented skin patches early in the disease 🠆 the skin turns dark (so
the disease is called Kala azar or black sickness).
 Depigmented papules or nodules (Post-kala azar dermal leishmanoid)
may appear later after successful treatment.
 Visceral leishmaniasis is one of the opportunistic infections noted in
AIDS / HIV positive patients.
 Congenital transmission 🠆 abortion.
 Death occurs in untreated severe cases due to:-
- Organ failure and wasting.
- Secondary bacterial infection as pneumonia, tuberculosis due to
immunosuppression.
- Septicemia, severe anaemia and haemorrhage.
N.B. Visceral leishmaniasis is followed by lifelong immunity.
78
Class: Sporozoa
 Diagnosis:-
1) Clinical.
2) Laboratory:-
a. Direct methods: Examination of blood, biopsy from liver, spleen, lymph
nodes or bone marrow puncture for detection of the parasite by:-
1. Smear to detect amastigotes.
2. Culture on Novy Nicol Mac Neal (N.N.N) medium 🠆 for 2 - 3 weeks
🠆 then examined microscopically for detection of motile
promastigotes.
3. Animal inoculation.
b. Indirect methods:-
 Specific tests (immunodiagnosis):-
1- Intradermal test (leishmanin or Montenegro test): Negative in
active disease but became positive late after recovery (6-8 weeks
after treatment).
2- Serological tests: CFT, IHAT, ELISA, IFAT.
c. Molecular method: PCR.
 Treatment:-
1) General (supported treatment):-
- Proper diet rich in proteins, vitamins and iron.
- Blood transfusion for severe anaemia.
- Splenectomy.
- Antibiotics for secondary infection.
2) Specific treatment:
Parenteral therapy:
- Pentamidine, Amphotericin B, Paromomycin.
77
Class: Sporozoa
 Prevention and Control:-

2) Elimination of reservoir hosts (dogs & rodents).
3) Mechanical:-
- Screening of windows and doors.
- Filling cracks in walls and floors (breading places of sand fly).
4) Chemical:-
- Repellants and insecticides against sand fly.
Cutaneous Leishmaniasis
A) Old world cutaneous leishmaniasis
(OWCT)
 Causes: 3 species of leishmania:-
1) Leishmania tropica.
2) Leishmania major.
3) Leishmania aethiopica.
Biological cyclopropagative transmission by female Phlebotomus.
(1) Leishmania tropica

(Dry or urban cutaneous leishmaniasis)
 Geographical distribution: Mediterranean region, Middle East, Asia
and Africa in over populated areas as big cites (urban area).
 R.H: Dog.
A) Oriental sore (Delhi boil or Baghdad boil):-
 Inflammatory reaction occurs at the site of bite 🠆 localized nodule 🠆
undergoes necrosis 🠆 painless ulcers (2 - 3 cm) with sharp edges and
77
Class: Sporozoa
raised indurated margin (oriental sore). Secondary bacterial infection

is common.
 The ulcer heals spontaneously after 1 - 2 years leaving depigmented
disfiguring scare.
 The lesion runs a chronic course in untreated patients with long
incubation period (2 - 12 months), scanty exudate and slow healing
(12 months).
 The lesion develops in exposed parts of the body (face and limbs) and
may be single or multiple and gives solid immunity.
(2) Leishmania major

(Wet or rural cutaneous leishmaniasis)
 Geographical distribution: Middle East, Asia and Africa in highly
inhabited areas as villages at the edge of the desert (rural distribution).
 R.H: Rodents.
 Pathogenesis and symptomatology: Similar to the lesion caused
by Leishmania tropica except that:-
 The disease runs an acute course with short incubation period (2 - 6
weeks), rapid ulceration, serous exudate and rapid healing (3 - 6
months).
 The lesions are multiple, usually on the lower extremities and leaving
large disfiguring scars.
 Infection with Leishmania major protects the host against subsequent L.
tropica infection, but infection with L. tropica does not produce immunity
against L. major.
 Diagnosis:-
1) Clinical.
2) Laboratory:-
77
Class: Sporozoa
a. Direct: Detection of amastigotes in the lesion by:-

 Scraping the edge of the ulcer or aspiration by a needle (not from
the base as contains pus and necrotic tissues) and examined by :-
1. Direct smear stained by Giemsa.
2. Culture on NNN medium (amastigotes changes into
promastigotes).
 Biopsy from the edge of the ulcer and examined by direct smear.
b. Indirect:-
 Immunodiagnosis:-
1. Leishmanin I.D test (Montenegro test).
2. Serological tests: Not useful for the diagnosis.
 Monoclonal antibodies and DNA probe.
 PCR: A reliable diagnostic test. It is highly sensitive than routin
smear and culture and it used also for species differentiation.
 Treatment:-
1) Local:-
 Cryosurgery, curettage or local application of heat to raise the
intra- lesional temperature to 37 - 43 ° C for 12 hours as amastigote
do not grow above 33°C.
 Surgical excision of the lesion.
2) Chemotherapy:-
a. ex. Pentostam
- Dose: 20 mg/kg/day for 10 days.
b. Alternative drugs to antimony compounds:
- Amphotericin B, Imidazoles or Allopurinol.
c. Antibiotics for secondary bacterial infection of lesions.
74
Class: Sporozoa

2) Covering the lesions to protect it from sand fly.
3) Control of sand fly.
4) Destruction of animal reservoir hosts.
5) Vaccination in endemic areas.
IV) Class: Sporozoa

(Palsmodia and Coccidia)
1) No special organs for locomotion (move by gliding).
2) Multiply by alternation of sexual and asexual generations either in the
same host or two different hosts.
1) Plasmodia
(Malaria parasites)
 Malaria parasites of man belong to the genus Plasmodium and include 4
species:
1- Plasmodium vivax 🠆 Causes benign tertian malaria.
2- Plasmodium ovale 🠆 Causes benign tertian malaria.
3- Plasmodium malariae 🠆 Causes benign quartan malaria.
4- Plasmodium falciparum 🠆 Causes malignant malaria.
 Plasmodium vivax has a wider distribution in tropical, subtropical and
temperate areas.
 Plasmodium falciparum is widely prevalent in many tropical and
subtropical areas.
 Plasmodium ovale and Plasmodium malariae are much less
77
Class: Sporozoa
common and are seen mainly in Africa and in some areas of Asia.
 Life cycle:-
 The life cycle of malaria passes in 2 alternate hosts:-
1. Vertebrate host: Man, acts as intermediate host (I.H).
2. Invertebrate host: Mosquito (female Anopheles), acts as definitive
host (D.H).
Figure (20): Life cycle of Malaria
Life cycle of malaria parasites in man

(Intrinsic cycle)
 It includes:
1- Asexual cycle in the liver: Exo-erythrocytic schizogonoy (liver phase).
2- Asexual cycle in RBCs: Erythrocytic schizogony (blood phase).
3- Gametogony (formation of male and female gametocytes in infected
RBCs).
77
Class: Sporozoa
1- Exo-erythrocytic schizogony (liver phase):-

 When an infected female Anopheles bites man, it inoculates the
sporozoite (I.S) with saliva into the skin.
 The sporozoite reaches the blood stream and enters the liver
cells where it grows into trophozoites. The nucleus of the
trophozoite divides 🠆 formation of a schizont containing
thousands of merozoites.
 The schizont ruptures liberating the merozoites in the liver
sinusoids 🠆 then invade the RBCs to start the erythrocytic
schizogony.
2- Erythrocytic schizogony (blood phase):-
 The liver merozoite enters RBC. Inside the RBC, the merozoite
develops into:
 Ring stage: A small chromatin mass (nucleus) attached to a loop of
the cytoplasm enclosing a vacuole.
 Trophozoite stage: The ring stage grows and increases in size.
 Schizont: The nucleus of the trophozoite divides into a large number
of pieces, 🠆 formation of a schizont containing certain number of
merozoites.
 The RBC ruptures releasing the merozoites, malaria pigment and toxins
which are responsible for malaria attack.
3- Gametogony (formation of gametocytes):-
 Some merozoites that invade the RBCs develop into sexual stages
(male and female gametocytes):
 The gametocytes remain within the RBCs without further development
till ingested by female Anopheles mosquito.
Life cycle of malaria parasites in mosquito
(Extrinsic cycle or Sporogony)
888
Class: Sporozoa
 When a female Anopheles bites infected person, it sucks blood

containing all stages of malaria parasite. Except the gametocytes (I.S to
mosquito).
 The male gametocyte (microgametocyte) undergoes exflagellation
process. The nucleus divides (by reduction division) into 6 - 8 pieces that
migrate to the periphery. At the same time, 6-8 thin filaments of the
cytoplasm are extruded out from the cell and the nuclear pieces are
passes to each filament forming 6 - 8 microgamets.
 The female gametocyte (macrogametocyte) undergoes reduction
division of the nucleus to become a macrogamete.
 Fertilization occurs by entering of a microgamete into the macrogamete
forming a zygote.
 The zygote changes into elongated ookinete which penetrates the
stomach wall of the mosquito and develops into a spherical oocyst
between the epithelium and basement membrane. The oocyst grows
rapidly forming sporocyst containing a large number of sickle- shaped
sporozoites (I.S to man).
 The sporocyst ruptures and the sporozoites are liberated into the body
cavity of the mosquito where they migrate to the salivary gland.
 When the mosquito bites the human, the sporozoites pass with the
saliva into the skin through the bite wound.
 The cycle in the female Anopheles takes 10 - 20 days depending on
temperature and humidity.
1) Bite of female Anopheles.
2) Blood transfusion.
3) Congenital transmission.
4) The use of common syringes as in drug addicts.
888
Class: Sporozoa
 Pathogenesis:-
1) Rupture of the parasitized RBCs leading to:
 Malaria paroxysms.
 Anaemia.
2) In P. malariae 🠆 nephrotic syndrome.
3) In P. falciparum, there is a vascular obstruction of small blood vessels
of internal organs 🠆 tissue anoxia of different organs including brain,
kidney, gastrointestinal tract, heart, lung, liver and adrenal.
 Clinical pictures:-
I) General symptoms: In all types of malaria.
a) Prodromal symptoms (few days before rupture of blood schizonts): Low
grade fever, malaise, headache and pain in bone and joints.
b) Malaria paroxysm: It consists of intermittent paroxysmal acute attacks
associated with anaemia, weakness and enlargement of liver and
spleen.
 Every attack passes into 3 stages:-
1- Cold stage (1/2 - one hour): Sensation of cold, shivering and the
patient is feverish. The skin is pale and cyanotic.
2- Hot stage (1 - 4 hours): High fever (40 C° or more), hot dry skin,
flushed face, headache and pain in limbs and back are common.
3-Sweating stage (1 - 4 hours): Profuse sweating with improvement
(temperature falls, disappearance of headache, moist and coal
skin).
2) Specific symptoms:-
A. In quartan malaria (P. malariae ): Nephrotic syndrome.
B. In malignant malaria (P. falciparum):
a. Cerebral malaria: severe headache, high fever, convulsion,
paralysis, coma and death.
888
Class: Sporozoa
b. Algid malaria: shock, collapse and peripheral circulatory failure

(sudden 🠆 in blood pressure) due to adrenal insufficiency.
c. Gastrointestinal malaria: Watery diarrhoea or dysentery with bloody
loose stool 🠆 malabsorption and dehydration resembling cholera.
d. Congenital malaria: Pathological changes in the placenta 🠆
spontaneous abortion.
3) Death may occur due to:-
 Liver damage 🠆 liver failure.
 Pulmonary oedema.
 Acute tubular necrosis and nephritic syndrome 🠆 renal failure.
 Cerebral oedema.
 Haemolysis and toxic effect on bone marrow 🠆 severe anemia.
 Hypotension and shock.
 Diagnosis:-
1) Clinical.
2) Laboratory:-
a. Direct:-
- Microscopic: Thin and thick blood films stained by Giemsa and
Leishman.
b. Indirect:-
1- Serological tests: CFT, IHT, ELISA, FAT.
2- Molecular diagnosis: DNA probes for various malaria species and
PCR.
 Treatment:-
1) Chemotherapy:-
 Chloroquine: 600mg.
 Proguanil: 100 mg daily
888
Class: Sporozoa
2) Treatment of complications:-
 Blood transfusion in severe anaemia.
 Haemodialysis in renal failure.
3) Chemoprophylaxis:-
 Pyrimethamine: 25 mg once a week.

2) Mosquito control.
3) Chemoprophylaxis.
4) Vaccination.
2) Coccidia
1) Single-celled obligate intracellular parasites.
2) Multiply by alternation of sexual and asexual generations either in the
same host or two different hosts.
3) They are opportunistic parasites that common affected
immunosuppressed persons e.g. (Toxoplasma gondii).
I) Tissue coccidian
(Toxoplasma gondii)
 Geographical distribution: Cosmopolitan especially among
immunosuppressed patients.
 D.H: Cats and other felines.
 I.H: Man, other mammals (cattle &pigs), birds and rodents.
 Habitat:-
- In the definitive host (cat): In the columnar epithelium of the small
intestine where sexual cycle occurs.
887
Class: Sporozoa
- In the intermediate host (Man and others): Intracellular especially

cells of RES, brain, retina and muscle where asexual cycle occurs.
1) Trophozoite:
- Obligatory intracellular parasite (toxon=bow or arrow, plasma=form)
- 6 2 µm.
- Crescentic in shape with one pole more pointed than the other.
- Central vesicular nucleus.
- Multiply by longitudinal binary fission.
2) Pseudocyst:
- Intracellular collection of trophozoites in macrophages in acute stage of
infection.
- The trophozoites multiply rapidly (tachyzoites).
- Without cyst wall.
3) Cyst:
- Collection of trophozoites enclosed in a true tissue cyst in chronic stage
of infection when the host immunity develops.
- The trophozoites multiply slowly (bradyzoites).
- With a true cyst wall secreted by the parasite.
- Found in the brain, heart and skeletal muscles for several months or
years.
4) Oocyst:
- 10 12 µm.
- Oval in shape.
- Contents: 2 sporocysts each with 4 sporozoites (disporocystic
tetrazoic).
- Excreted in faeces of infected cat and remains infective in soil for long
time.
887
Class: Sporozoa
 Life cycle:-
A. Sexual cycle in the intestinal epithelium of cat (D.H): Cat is infected by
ingestion of mature oocysts, pseudocysts or cysts. Trophozoites
released in the small intestine where they multiply in the epithelial lining
by schizogony and gametogony resulting in the formation of immature
oocysts that are excreted with faeces of cats 🠆 after 7 days it becomes
mature (disporocystic tetrazoic) and ready for infection.
B. Asexual cycle in man and other mammals (I.H): When man, animals
(other than cat) and birds ingest mature oocyst or meat with
pseudocysts or cyst, the organisms cause extraintestinal infection
only. The trophozoites proliferate in various tissues producing 🠆
pseudocysts in macrophages in acute stage 🠆 cyst formation in viscera
mainly in brain and muscles in chronic stage of infection.
887
Class: Sporozoa
Figure (21): Life cycle of Toxoplasma gondii

1) Congenital (transplacental): When the mother is infected for the 1st time
during pregnancy.
2) Acquired:-
- Ingestion of undercooked meat with pseudocysts and cysts e.g.
beef, pork and lamb.
- Ingestion of oocyst in food and drink contaminated directly with cat
faeces or indirectly by flies.
- Blood transfusion and organs transplants.
- Laboratory exposure to infection with trophozoites.
- Inhalation of oocysts with dust infected with cat faeces.
884
Class: Sporozoa

 Disease: Toxoplasmosis.
A. Congenital toxoplasmosis:-
- If the mother is infected before pregnancy, she will develop
antibodies (IgG) that passes through the placenta and protect the
baby against infection.
- If the mother becomes infected with toxoplasmosis during the
pregnancy for the first time, the infection transmitted through the
placenta to the foetus 🠆 serious complications.
- Infection early in pregnancy results in more severe problems than
later infection.
- Congenital toxoplasmosis produces many symptoms which includes:-
1. Neurological manifestations: Hydrocephalus, cerebral
calcification, microcephalus, macrophalus and mental retardation.
2. Chorioretinitis.
3. Other manifestations: Prematurity, intrauterine growth restriction,
abortion, hepatosplenomegaly, jaundice, skin rash and hearing
loss.
B. Acquired toxoplasmosis:-
a. Immunocompetent patient:-
1- Acute infection:-
 Glandular form with fever and enlarged liver, spleen, lymph
nodes and sore throat (like infectious mononucleosis).
 Acute exanthematous form(Typhus like fever) with high fever,
skin rash and glandular enlargement.
 Cerebrospinal form: Meningeoencephalitis.
2- Chronic (late) infection:-
 Asymptomatic infection: It is the commonest without
887
Class: Sporozoa
manifestations.
 Symptomatic: Low grade fever, lymph node enlargement
(cervical and axillary), muscle pain, myocarditis and
chorioretinitis.
b. Immunocompromised patients:-
 Most cases presented by CNS manifestation (encephalitis, brain
abscess and meningitis), myocarditis and pneumonia.
 Diagnosis:-
1) Clinical.
2) Laboratory:-
a. Direct: Examination of biopsy from enlarged lymph nodes, samples
from blood, CSF or bone marrow for detected of trophozoites,
pseudocyst or cyst.
b. Indirect:-
 Immunodiagnosis:-
1. I.D test ( toxoplasmin, Frenkel test ) : Delayed reaction
,using a killed T. gondii antigen.
2. Serological tests (for IgG & IgM): CFT, IHAT, ELISA, IFAT &
Ig M immunosorbent agglutination assay.
N.B. IgM appears in the early stage and replaced by IgG later on.
Determination of IgM is important in congenital toxoplasmosis as it
indicates active production by the foetus.
1. Antigen detection ELISA.
2. Sabin Feldman dye test.
 Animal inoculation.
 PCR.
 Lymphocytosis.
 CT scan and x-rays of the brain in congenital toxoplasmosis.
887
Class: Sporozoa
 Treatment:-
 Chronic asymptomatic toxoplasmosis 🠆 requires no treatment.
 Acute symptomatic cases are given:-
1. Combination of pyrimethamine (Daraprim): 50 mg/day +
sulphadiazine : 4 mg/ day for 4 - 6 weeks + folic acid.
 For human
1. Proper cooking of meat or freezing to – 20°C.
2. Avoid contamination of food, drink and hands with faeces of cats
especially for pregnant women.
3. Washing of hands after handling raw meat.
4. Protective measures should be used during handling infected
materials in lab and slaughter houses (wearing gloves).
5. Periodic examination of pregnant woman.
6. Keep children away from playing in soil contaminated with cat
faeces.
7. Vaccination.
8. Flies control.
 For cats:-
1. Elimination of stray cats and rodents.
2. Pet cats should eat canned or cooked food.
3. Cat litter box should be emptied every day.
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Collections
Parasites affected different organs
 Parasites in the brain:-

Trematoda: Eggs of H. hetrophyes, Schistosoma.
Cestoda: Hydatid cyst.
Nematoda: Ascaris larva, Disseminated larva of S. stercoralis, T.spiralis.
Protozoa: E. histolytica, African trypanosomes, Plasmodium falciparum,
Toxoplasma.
Arthropoda: Larvae of Sarcophaga & Wohlfahrtia 🠆 aural myiasis.
 Parasites in the eye:-
Nematoda: T. spiralis (in ocular muscle).
Protoza: T. gondii.
Arthropoda: Ocular myasis.
 Parasites in the lung:-
Trematoda: Schistosoma & H. heterophyes eggs.
Nematoda: Migrating larvae (of Ascaris, Hookworms, S. stercoralis).
Protozoa: E. histolytica, Leishmania species (Kala azar), P. falciparum, T.
gondii.
 Parasites of the heart:-
Trematoda: Eggs of H. heterophyes.
Nematoda: T. spiralis larvae.
Protozoa: Toxoplasma gondii.
 Parasites in the liver:-
Trematoda: F. gigantica, F. hepatica & S. mansoni.
Cestoda: Hydatid cyst, multiloular cyst.
Nematoda: Ascaris.
Protozoa: E. histolytica, G. lamblia, Leishmania (Kala azar), Plasmodium
species & T. gondii.
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Collections
 Parasites in the gall bladder:-

Trematoda: Fasciola.
Nematoda: Ascaris.
Protozoa: G. lamblia.
 Parasites in the spleen:-
Trematoda: S. mansoni.
Protozoa: Leishmania (Kala azar), Plasmodium species & T. gondii.
 Parasites in the lymph nodes:-
Nematoda: W. bancrofti.
Protozoa: Leishmania donovani & Toxoplasma gondii.
 Parasites in the kidney:-
Trematoda: S. haematobium.
Protozoa: Plasmodium malariae & Plasmodium falciparum.
 Parasites in the small intestine:-
Trematoda: H.heterophyes.
Cestoda: D. latum, T. Saginata, T. Solium, H. nana, H. diminuta.
Nematoda: A. lumbricoides, Hookworms, S. stercoralis, T. spiralis.
Protozoa: G. lamblia, L. donovani, P. falciparum.
Arthropoda: Intestinal myasis.
 Parasites in the large intestine:-
Trematoda: S. mansoni.
Nematoda: E. vermicularis & T. trichiura.
Protozoa: amoebae except Leishmania donovani, Plasmodium falciparum.
Arthropoda: Intestinal myiasis.
 Parasites in the muscles:-
Nematoda: T. spiralis larvae.
Protozoa: Toxoplasma gondii cyst.
 Parasites in the skin and subcutaneous tissue:-
Trematoda: Schistosoma, Swimmer 's itch.
Nematoda: Filariform larvae of hookworms and S. stercoralis.
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Collections
Protozoa: E. histolytica, and Leishmania .

Arthropoda: Cutaneous myiasis.
 Parasites detected in blood:-
Nematoda: S. stercoralis filariform larvae, T. spiralis larvae, microfilaria of W.
bancrofti (at night).
Protozoa: Plasmodium species, T. gondii.
 Parasites in the sputum:-
Trematoda: Eggs of Schistosoma & Paragonimus.
Cestoda: Hydatid sand (rupture hydatid cyst in lung).
Nematoda: Migrating larvae of Ascaris, Hookworms & S. stercoralis.
Protozoa: E. histolytica trophozoites (lung abscess).
 Parasites in urine:-
Trematoda: S. haematobium eggs (occasionally S. mansoni).
Cestoda: Hydatid cyst (rupture hydatid cyst in the kidney).
Nematoda: Eggs of E. vermicularis in urine of female, microfilaria of W.
bancrofti (chyluria).
Protozoa: T. vaginalis trophozoite & Leishmania donovani.
Arthropoda: Urogenital myiasis.
Mode of transmission of parasitic infections

 Parasites transmitted by eating raw vegetables :-
Eggs: T. solium, H. nana, E. granulosus, A. lumbricoides, E. vermicularis, T.
trichiura.
Larvae: Encysted metacercaria of Fasciola.
Cysts: Amoebae & G. lamblia.
Oocyst: Toxoplasma.
 Parasites transmitted by eating improperly cooked meat, fish or
liver:-
1. Meat: T. solium, T. saginata, T. spiralis, T. gondii.
2. Fish: H. heterophyes.
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 Water- borne parasitic infections:-

1. Ingestion of water contaminated with eggs or larvae of helminthes, cysts or
oocysts of protozoa (see under raw vegetables).
2. Contact with water: Schistosomes, swimmer's itch.
 Parasites transmitted by autoinfection:-
Helminths: H. nana, T. solium, E. vermecularis & S. stercoralis.
Protozoa: Cysts of E. histolytica, G. lamblia.
 Parasites transmitted by inhalation:-
Helminths: A. lumbricoides, E. vermicularis, T. trichiura, T. gondii.
 Parasite transmitted by blood transfusion:-
Blood flagellates: Leishmania (visceral leishmaniasis).
Plasmodium species 🠆 malaria.
Coccidia: T. gondii.
 Parasites transmitted by sexual transmission:-
T. vaginalis trophozoite
 Parasites transmitted congenitally:-
Blood flagellates: Leishmania 🠆 Kala azar.
Plasmodium 🠆 malaria.
Coccidia: T. gondii.
 Parasites transmitted through the skin or mucous membrane:-
1. Helminths: Schistosomes, cercarial dermatitis, Hookworms, S. stercoralis
2. By arthropod vectors: Filariae, Leishmania species, malaria species.
3. By direct infestation: Cutaneous myiasis.
 Parasites transmitted by toilet seats:-
Helminths: E. vermecularis & S. stercoralis.
Arthropoda: Urogenital myiasis.
 Parasites transmitted by animals as a source of infection:-
1- Dogs:-
 Trematoda: H. heterophyes.
 Cestoda: hydatidosis.
 Nematoda: S. stercoralis.
 Protoza: Leishmania.
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2- Cats:-
 Trematoda: H. heterophyes.
 Protozoa: Toxoplasma.
3- Cattle:-
 Trematoda: Fasciola.
 Cestoda: T. saginata, hydatidosis.
 Protozoa: T. gondii, Sarcocystis & Babesia.
4- Pigs:-
 Cestoda: T. solium.
 Nematoda: T. spiralis.
 Protozoa: T. gondii.
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Exam sheet
1-Eneumerate 3 examples of vector porn protozoal infection and

illustrate your answer with diagrams of the infective stage.
2-Classify mayiasis according to affected tissues with 2

examples for each of them .
3-Give reasons:
a-Jaundice may be present in infection with giardiasis .
b-Haemorrhage during amoebiasis infection .
c-Pancytopenia with visceral leishmaniasis .
d-Collaps and shock in malignant malarie .
e-Heart failure in trichinosis .
.
3-A35 female came to the pediatric hospital with 7 days baby .
She asked doctors to examin eye and ear of her baby because
she doubt on his hearing and vision . She gave a history of
unknown fever and lymphadenopathy in early pregnancy .By
clinical examination , it was found an increase in his head
circumference .
a-What was the possible parasitic infection?

b-What are your explanation about history and clinical data?
c-How can you confirm your diagnosis?
4-Choose the most correct answer (single answer).
1- Cutaneous myiasis is caused by:

a-Eristalis .
b-Fannia .
c-Calliphora.
d-Gastrophilus .
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2-Dry leishmaniasis is
a-Leishmania major
b-Leishmania aetheiopica
c-Leishmania tropica
d-veisceral leishmaniasis
3-Itching of perianal region may be due to:
a-Entamobea histolotica .
b-Ascaris lumbricoids .
c-Entrobius vermicularis .
d-giardia lambilia .
4-Autoinfection is one of the mode of transmission :
a( Leishmania donovani .
b-Toxoplasma gondii .
c-T. solium .
d-Fasciola hepatica .
5-Circumoval precipitation test is used for diagnosis of :
a-Malariasis .
b-Entrobiasis .
c-schistosomiasis .
d-Taniasis .
111

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2021-2022

:‫رؤيه كلية التمريض‬

-To provide students with introduction of parasites , biological,

a-knowlage and understanding:

At the end of the program the graduate should be able to:

Students should be according to the faculty by attending laws.

1- Department course books.

II. CHAPTER 2: TREMATODA ............................................... 3

III. CHAPTER 3: NEMATODA ................................................ 18

Fig. (1) Life cycle of Fasciola gigantica 5

Fig. (2) Life cycle of Fasciola hepatica 10

Fig. (3) Life cycle of Schistosomes 14

Fig. (4) Life cycle of Ascaris 25

Fig. (5) Life cycle of Ancylostoma 29

Fig. (6) Life cycle of Strongyloides stercoralis 32

Fig. (7) Life cycle of Trichuris trichiura 36

Fig. (8) Life cycle of Enterobius 39

Fig. (9) Life cycle of Wuchereria bancrofti 43

Fig. (10) Life cycle of Trichinella spiralis 48

Fig. (11) Life cycle of Taenia saginata 54

Fig. (12) Life cycle of Taenia solium 57

Fig. (13) Life cycle of Hymenolepis nana 61

Fig. (14) Life cycle of Hymenolepis diminuta 64

Fig. (15) Life cycle of Echinococcus granulosus 68

Fig. (16) Life cycle of Entamoeba histolytica 78

Fig. (17) Life cycle of Giardia lamblia 84

Fig. (18) Life cycle of Trichomonas vaginalis 88

Fig. (19) Life cycle of Leishmaniasis 92

Fig. (20) Life cycle of Malaria 99

Fig. (21) Life cycle of Toxoplasma gondii 107

 Medical parasitology is classified into:-

 Phylum : Nemathelminthes (round worms) Class: Nematoda

Phylum : Platyhelminthes (Flat worms)

I. Class : Trematoda (Flukes)

Figure (1): Life cycle of Fasciola gigantica

2) Chronic or obstructive phase: Due to adult fluke in the bile duct.

Items F. gigantica F. hepatica

 Morphological characters :-

 Infection is acquired by eating fish containing encysted metacercaria

Figure (2): Life cycle of Fasciola hepatica

 Blood flukes differ from other trematodes in the following :-

Figure (3): Life cycle of Schistosomes

 Pathogenesis and symptomatology :-

3) Stage of egg deposition (acute stage) :-

sedimentation or centrifugation. The last drop must be included in the

- Caused mainly by S.mansoni and S.japonicum. Their defferences are

Item S.haematobium S.mansoni S.japonicum

Testes 3 - 5, big in a line 6 - 9, small and in cluster 6 - 8, in a line

Uterus Long with 20 - 30 Short 1 - 4 ova. Short with 50

spine minute knob

 Pathogenesis and symptomatology :-

1) They are elongated, unsegmented, cylindrical worms with tapering

4) The body is covered by a cuticle made of scleroprotein (resist the

5) The body wall consists of three layers:-

a. Cuticle: Outer laminated non- cellular protective layer. It may be

b. Hypodermis: It is a syncytial layer that secretes the cuticle, it shows

c. Muscle layer: Single layer of non striated fibers divided into 4

b. Oesophagus varies in shape and structure:-

 Double bulbed (anterior club shaped part and posterior

 Rhabditiform (anterior club part and posterior pyriform part

 Cylindrical or filariform (muscular anterior part and glandular

 The oesophagus 🠆 intestine (lined with columnar cells) 🠆

9) Excretory system: Consists of two lateral longitudinal excretory canals

10) Nervous system: Consists of a nerve ring surrounding the oesophagus