Dr.

Dalia El-Shafei
Lecturer, Community Medicine Department,
Zagazig University
Endemic in Egypt & many parts of the world.
Entamoeba Histolytica, found in 2 phases:
• Large trophozoite (vegetative form): pathogenic
form that invades wall of colon, causing ulcerative
lesions.
• Small trophozoite: commensal in the lumen of
large intestine, but potentially pathogenic, and
changes under unknown circumstances into the
pathogenic large trophozoite.
Entamoeba cyst:
While the vegetative form (large pathogenic
trophozoite) is passing with intestinal content
toward the rectum, it secretes a cyst wall &
develops into a 4-nucleate cyst, the infective stage
that passes out with faeces. The cyst is relatively
resistant outside the body, but destroyed by heat,
desiccation and UV.
The vegetative form may pass to the outside with
faeces during acute disease, but is delicate and
perishes rapidly, and so has no infectious role.
1. Man (mainly): chronic cases, or asymptomatic
cyst-passers.
a) Chronic cases: recovered from acute disease
(manifestations disappeared), but infection persists.
Acute cases have no infectious role “fragile
vegetative form perishes rapidly. Even if ingested, it
is destroyed by gastric acidity & digestive enzymes
of stomach & upper intestine.
b) Cyst-passers: asymptomatic, apparently healthy.
2. Rats: frequently infected & pass cysts in their
excreta.
1. Food borne infection: ingestion of food or
water contaminated with entamoeba cysts, from
excreta of man, usually, or may be rats.
2. Hand to mouth infection, when hand gets
contaminated with cysts:
• Hand of contacts.
• From polluted dust, in underdeveloped areas.
Incubation Period: commonly 3-4 weeks.

Amoebiasis:
clinical involvement of the case by E.
histolytica. It may be limited to the colon,
giving- intestinal manifestations (1ry
amoebiasis), or extend from the colon to
other parts of the body (2ry amoebiasis).
 Intestinal amoebiasis:
severe amoebic ulceration may cause
perforation of colon (& intestinal hemorrhage),
and may be peritonitis and appendicitis.
Extra Intestinal amoebiasis:
amoebic abscesses specially the liver (most
frequently affected), “amoebic hepatitis”.
Clinical picture may be suggestive.
Stools examination: 4-nucleate E.
histolytica cysts.
Acute cases, however, are difficult to
diagnose, as the vegetative form perishes
rapidly outside the body.
Giardia Lamblia intestinal protozoon is found in 2
forms:
Trophozoite: inhabits the duodenum and upper intestine,
but not invading the tissues.
Cyst: the infective stage passed with faeces that can
remain viable in the environment for months.
ingestion infection.
• Food borne infection: ingestion of cysts-contaminated food or
water.
• Hand-to-mouth infection, when hand is contaminated with
cysts.
• A high percent of the infected is asymptomatic.
• Gastrointestinal manifestations:
Giardia is an important causative agent of
infective diarrhoeal disease (GE) of infants and
young.

Diagnosis:
stools examined for giardia trophozoite and
cysts.
 Lambliasis Amoebiasis
Site Duodenum & upper Colon
intestine
Main C/P Enteritis Dysentery
Extra intestinal √

Wall invasion √
Protozoal disease of colon, characterized by
dysentery.
Causative Agent:
Balantidium coli ciliated protozoon. Similar to
E.histolytica,
2 forms: trophozoite that inhabits the wall of colon &
cyst.
Reservoirs of Infection: man, swine.
Modes of Infection:
Ingestion infection “food borne & hand-to-mouth
 • Asymptomatic infection.
• Mild colitis.
• Acute dysentery.

Untreated cases become chronic.

 • Worldwide distribution.
• Preschool & School children are
frequently, and may be heavily,
infected & may show prevalence of
25% or more in endemic areas.
Causative Agent: Ascaris Lumbricoides a
nematode that lives in the lumen of small intestine,
with male (15-25 cm) & female (20-40 cm) worms.
Reservoir of Infection: infected person. Each
female worm puts thousands of eggs every day, to
find exit in faeces.
Infective Stage: passed eggs are not infective.
They develop outside the body in 2-3 weeks, to
become embryonated.
"Embryonated egg" in polluted environment is the
infective stage. It is resistant to desiccation and
disinfectants, and remains viable and infective,
under favorable environmental conditions, for around
Food borne Infection: consuming embryonated egg
in contaminated food (salad vegetables) & polluted
water.
Hand-to-mouth infection: when the hand is
contaminated with eggs containing dust. Children
are particularly affected, when hands get
contaminated on playing in the road, and are
infected through either:
• Putting contaminated fingers in the mouth.
• Taking food without hand washing.
 Promiscuous defecation
Fresh human fertilizer.
Salad (fresh) vegetables without thorough
washing.
Neglecting care of children who play in the road,
and get hands contaminated with Eggs-carrying
dust, and not washed.
How Ascaris eggs reach food?
Using fresh human fertilizer for vegetables.
Contamination of food with eggs-containing dust.
Flies may have potential.

Why there is no faeco-oral infection for

ascariasis?
Because eggs passed in faeces are not infective,
except after developing into embryonated egg in 2-
3 weeks.
That is also why infected food handlers do not
spread infection (not directly contaminating food
with ascaris eggs).
Incubation Period: about 2 months, from ingestion
of embryonated eggs, until eggs first appear in
stools.

Clinical Picture:
Mild infection may be in apparent.
Manifest cases :
• Respiratory manifestations.
• Intestinal disorders: abdominal discomfort & colic.
• Nutritional deficiency: due to anorexia, impaired
digestion & protein absorption, loss of nutrients.
• Others: restless sleep & grinding of teeth,
commonly in children.
C/P is not diagnostic, being not specific, except
when adult worms pass & detected in stools.
- Identifying the eggs in faeces.
1. Sanitation of environment:
Safe water supply, food sanitation.
Providing rural areas with sanitary convenient latrines, and
sanitary disposal of wastes
To be used for fertilization of vegetables, human
excreta must be stored, in covered packed heaps, for at
least 6 weeks.
Fly control.
2. Health education of the public:
• Using water closet or latrine, and avoid promiscuous
defecation.
• Thorough washing of uncooked (salad) vegetables.
• Hand washing on returning home, and before food.
• Supervision of children on playing outdoors, and advise
1. Case-finding, on health appraisal: smear of
stools is examined for ascaris eggs.
2. Cases: treatment, and reexamination to be
retreated if necessary.
 ENTEROBIASIS
(Oxyuriasis pinworm
 Prevalence:
The most widespread helminthic infection.
Preschool & school children show the highest
Causative Agent: Enterobius vermicularis, a small
roundworm in the caecum & adjacent part of
colon and small intestine, and the appendix.
Males are few millimeters long, and females
around 10 mm long.
Reservoir of Infection: the infected person.
Infective stage: the egg, almost once deposited
by migrating gravid female worm in the perianal
region (the worm dies after opposition). Eggs
are relatively resistant outside the body.
1. Hand-to-mouth infection: "faeco-oral infection".
■ Autoinfection: fingers and nails of the case get
contaminated by scratching the anal region.
■ Hands of contacts may be contaminated with eggs:
* Playing with the case.
* Handling soiled fomites (e.g. under wears and
bedding)
* Touching soiled toilet fixtures.
2. Ingestion infection: eggs may contaminate food, by
either:
■ Handling food by contaminated hand.
Perianal pruritus & scratching, on migration of
gravid female worms and opposition, usually
nocturnal, causing disturbed sleep and
irritability.
 Worms in perianal region & stools.
■ Perianal swab to demonstrate eggs (using
adhesive tape) when necessary.
■ Stool examination is not diagnostic, and
so not used, as eggs not necessarily show in
stools.
1. Personal cleanliness: most preventive measure.
Keeping hands & nails clean. Nails must also be
regularly trimmed.
2. Health education of the public, specially parents,
for:
♦ Clean hands and habits.
♦ Supervision of children.
3. Food sanitation: clean handling and protection of
food.
♦ Proper antihelminthic therapy.
♦ Prevention of autoinfection during treatment, and
follow clean habits.
♦ Boiling of under wears, clothing and bedding.
♦ Guiding cases (and mothers of young
children) for: treatment, boiling of fomites,
prevention of autoinfection, and protection of
family contacts.
Taeniasis is an intestinal infection with the adult of
large tapeworms.
Infectious agent: T.solium (pork tapeworm) &
T.saginata (beef tapeworm).
Reservoir:
Man is the definitive host of both species of
taenia. He discharges detached gravid segments
which rupture to liberate eggs in human faeces
(remain viable for months). Egg is infective to the
intermediate host (cattle for T.saginata & pig for T.
Solium) where it hatches in the intestine of the animal
& the embryo penetrates the intestinal wall & is
carried by the circulation to various tissues (especially
skeletal muscles where it becomes encysted).
 Man is infected by ingestion of raw or under
cooked infected beef or pork containing the
infective stage (cysticercus bovis in beef &
cysticercus cellulosa in pork). In the intestine the
scolex (in the cysticercus) evaginates, attaches to
the mucosa and develops into mature worm.
Occurrence: World wide.
The prevalence is high wherever beef or pork are
eaten raw or insufficiently cooked and the animal
have access to human faeces.
Man is usually infected with one worm only.
Period of communicability: so long the
worm remains in the intestine sometimes
more than 30 ys. T. saginata is not
directly transmitted from person to
person.

Incubation period:
2-3 months from infection to the appearance
of eggs in faeces.
Clinical picture:
- Many infections are asymptomatic except for
the annoyance from having segments of worms
emerging from the anus.
- Manifestations (if present) include nervousness,
insomnia, anorexia, weight loss, however the
disease is non fatal.
Diagnosis:
based on detection of gravid segment or eggs
of the worm in faeces.
(1) Preventive measures:
a- Health education of the public to:
- avoid promiscus defecation to prevent contamination of soil,
water and animal food.
- cook the meat thoroughly (internal temperature must exceed 60
C) or
freeze it below - 5 C for 5 days to kill the infective stage.
b. Sanitary raising & feeding of cattle.
c. Eliminate source of infection by case finding & treatment.
(2) Control measures:
• Case finding.
• Specific treatment and reexamination of cases.
• Specific measures for cases of T. solium as its eggs are
immediately infective to man causing cysticercosis to avoid auto &/or
contact infection.
N.B: Cysticercosis is a tissue infection with the
larval stage of T. solium, where man acts as a
definitive and intermediate host. Infection
occurs by direct transfer (ingestion) of eggs of T.
solium from faeces of infected person to the mouth
of the same person (auto infection) or another' s
mouth or indirectly through ingestion of contaminated
water or food.
In the intestine the embryo escapes from the egg
shell, penetrates the intestinal wall into lymphatic or
blood vessel and is carried to various tissues to
produce its manifestations which vary according to
the site and intensity.
Cerebral involvement is serious with high case
fatality. Serologic tests and U.S are diagnostic.
Infectious agents: Heterophyes heterophyes, a
minute intestinal trematode, less than 2 mm long that
inhabits the small intestine, deeply embedded in the
villi.

Infective stage: encysted metacercaria (0.3 mm in

diameter), in muscles of infected fish.
• Man: the infected individuals pass eggs in
faeces. Fishermen in endemic areas are
particularly important for pollution of brackish
water channels where intermediate hosts of the
parasite are found.
• Fish-eating animals (cats & dogs): potential
reservoirs.
Ingestion of the infective stage with muscles of
infected fish, when eaten raw, or insufficiently
cooked or grilled. Ingested cysts excyst in the
small intestine, and the liberated metacercariae
develop into adult worms, which pass eggs
infective to the 1st intermediate host brackish-water
snail, pirenella conica, which ingests the eggs
that develop into cercariae, and pass them in
water. Cercaria found in water pierce the skin of the
2nd intermediate host, Some brackish-water fish (e.g.
Mugil cephalus & Tilapia nilotica): to develop and
encyst in muscles, forming the infective stage, the
"encysted metacercaria".
Heterophyiasis is endemic in Egypt around
Lakes Manzala & Borollos where the
intermediate hosts of parasite are found,
and exposure of the people to infection
exists. Other areas may be affected on
consuming infected fish. (Salted raw Mugil fish
is a popular food, named in Arabic
"fessikh". It may transmit infection when
eaten before 10 days of pickling).
Clinical Picture: chronic intermittent
diarrhea, with blood & mucus in stools,
abdominal discomfort and colicky pain.
Diagnosis: Examinations of faeces smear for
ova.
Differential diagnosis: Other causes of
dysentery.
(1) Preventive measures:
Health education of the public for:
- Sufficient cooking or grilling of fish.
- Not to consume salted raw fish before 10 days
of pickling, to ensure that the metacercariae, if any,
are destroyed.
(2) Control of cases:
-Case-finding and treatment.
-Licensing of fishermen after proving to be free
of infection & periodic examination. Avoid pollution
of water with their excreta (may be practically
difficult).
Causative Agent: hymenolepis nana (dwarf
tapeworm), 25-40 mm long, which inhabits
the small intestine. Infective Stage: eggs
passed in faeces, are immediately infective.

Reservoirs of Infection: infected man,

mainly, and rats, occasionally, where eggs
are passed in faeces.
1. Hand-to-mouth infection:
- Contaminated hand of the case: may reinfect
himself (auto-infection), or infect contacts.
- Hand of any person (usually children) may
occasionally be contaminated with eggs when
playing in rat-execreta-contaminated dirt, and gets
infected.
2. Ingestion Infection: ingestion of contaminated food
and water.
3. Internal Autoinfection: ova may not pass in
faeces, but invade the intestinal wall and complete
C/P: varies & may be asymptomatic, mild, or
vague abdominal disturbance. Heavy infection
shows abdominal pain and diarrhea.
Diagnosis: examine smear of faeces for ova.
Occurrence: High in underdeveloped
communities, specially in preschool and school
children, due to poor sanitation (contaminated
food, water and soil) and unclean habits.
(A) Preventive measures:
1- Sanitation of the Environment:
- Sanitary disposal of human excreta.
- Food and water sanitation, to prevent pollution with excreta
of man and rats.
- Rodent eradication or control.
2- Health education of the public for clean habits. Children
must be supervised during playing outdoors, for clean place &
hands.
(B) Control of cases and contacts:
1- Case-finding: examination of stools on health appraisal,
and treatment and re-examination of diagnosed cases.
2- Examination of contacts for case -finding.
A liver disease caused by a large trematode that is
a natural parasite of sheep, cattle and related
animals throughout the world.
Infectious agents: fasciola hepatica & less
commonly F. gigantica. The infective stage is the
encysted metacercaria on aquatic plants.
Reservoir: sheep (f. hepatica), cattle (f.
Gigantica), and other large herbivorous animals.
The infection is maintained in a cycle between
animals, water, snails and aquatic plants. Man is an
accidental host.
Mode of transmission: Infection acquired by
eating uncooked aquatic plants such as water cress
bearing encysted metacercaria.

Occurrence: world wide especially in sheep or

cattle raising areas. F. hepatica is more prevalent in
Europe, America, Australia & Middle east. F. gigantica
(common in Egypt) has restricted distribution in
Africa.
The adult worm lives in liver & bile ducts, eggs pass in
the stool, develop in water where it hatch into
miracidium—► snail (lymenoid) where it develops to
produce large number of cercaria which attach to
and encyst on aquatic plants and when eaten and
reach the intestine larva migrate through the wall
into peritoneal cavity liver and bile duct. Where it
grows and lays eggs.
Period of communicability:
Infection is not transmitted directly from person to
person.
Incubation period: variable.

Clinical picture:
Many cases are asymptomatic, right upper quadrant
pain & hepatomegally, liver function abnormalities &
aesinophilia during liver invasion.
D.D other causes of hepatomegally.
After migration to biliary ducts the worm may cause
biliary colic or obstructive jaundice.
Based on finding characteristic eggs in
faeces or in bile aspirated from the
duodenum.

N.B: detection of non viable eggs in the

faeces occurs after eating liver from
infected animal.
A-preventive measures:
- Educate the public in endemic areas to abstain from
eating aquatic plants.
- Avoid use of sheep or cattle faeces for fertilizing
water plants.
- snail control when feasible.
- Mass treatment of infected animals.
B -Control of patient: by early diagnosis and
treatment.
Causative Agent:
Hydatid cyst, which is the larval (intermediate)
stage of Echinococcus granulosus of dog. The
cyst affects different organs of man.

Reservoir of Infection:
The dog is the definitive host of Echinococcus
granulosus, 3 small tapeworm, some millimeters
long, in the small intestine. Eggs pass in the
faeces of dog.
Intermediate Host:
Sheep, cattle and other herbivorous animals. They
ingest Echinococcus egg-contaminated food, to
form hydatid cysts in different animal organs,
specially the lung & liver. The dog gets infected with
the worm on ingesting hydatid cyst in animal organs,
and the cycle of dog-animal-dog infection continues.
Infection of Man: Man may occasionally be infected
with Echinococcus eggs from dogs, and gets affected
with hydatid cyst.

How man gets infected with eggs:

• Hand-to-mouth infection: the usual method of
infection, when the hand gets contaminated with
eggs, from contact and playing with infected dogs.
• Food-borne infection: ingestion of food or water
which has been accidentally contaminated with
excreta of infected dogs.
C/P: no specific picture, but manifestations of slowly
growing tumor, according to location of hydatid cyst.

Diagnosis:
• Clinical examination: cystic tumor, which is
nonspecific & not diagnostic, but suggestive.
• X-ray: supports suspected disease, but not
conclusive.
• Biopsy or aspiration of cyst: is avoided, for
the risk of anaphylaxis and 2ry infection.
• Casoni test: ID hypersensitivity test. +ve
reaction is diagnostic.
1- Measures for Dogs:
. Prevention of infection: abattoirs must be free of
dogs & affected part(s) of slaughtered animals must
be burnt.
. Elimination of stray dogs, and licensing of the
others after examination for Echinococcus and
treatment of the infected.
2- Protection of Man:
. Personal cleanliness: avoiding contact with
suspected dogs, and keeping the hands clean.
. Supervision of children, as they usually like to play
with dogs.