This document summarizes information about various parasitic infections including Entamoeba histolytica, Giardia lamblia, Ascaris lumbricoides, Enterobius vermicularis, hookworms, and Schistosoma. For each parasite, it describes the etiology, epidemiology, clinical manifestations, diagnosis, and treatment. Common symptoms include diarrhea, abdominal pain, and anemia. Diagnosis involves examination of stool or other samples for eggs or parasites. Treatment involves antiparasitic drugs like metronidazole, iodoquinol, albendazole, and praziquantel.

1. Parasitic infections
Protozoan diseases
Micheal Mohab Nady Mikael

2. Entamoeba histolytica
Etiology: Infection is established by ingestion of
Entamoeba histolytica cysts which release
trophozoites.
Epidemiology
Food or drink contaminated with E.histolytica
cysts and direct fecal-oral contact are the most
common means of infection.
Untreated water and human feces used as
fertilizer are important sources of infection.
Food handlers carrying amebic cysts may play a
role in spreading the infection.

4. The pathogenecity of E. histolytica is believed to be
dependent on two mechanisms:
1- Cell contact.
2- Toxin exposure.
 Once the trophozoites invade the intestinal mucosa, they
produce tissue destruction (ulcers) with little local
inflammatory response.
 The organisms multiply and spread through the wall
underneath the intestinal epithelium to produce flask
shaped ulcers.
 These lesions are commonly seen in the caecum,
transverse colon, and sigmoid colon.
 Amebae may produce similar lytic lesions if they reach
the liver.
 Rarely the infection may extend extraintestinally to
lungs and brain.

5. Clinical manifestations
1- Intestinal amebiasis
 The onset is usually gradual with colicky abdominal
pain and frequent bowel movements.
 Diarrhea is frequently associated with tenesmus.
 Stools are blood-stained and contain fair amount of
mucus with few leukocytes.
 The attacks of dysentery are recurrent in untreated
cases.
Complications
a- Ameboma.
b- Toxic megacolon.
c- Extraintestinal extension.
d- Local perforation and peritonitis may occur.

6. 2- Hepatic amebiasis
 There is diffuse liver enlargement and
tenderness.
 In few cases liver abscesses develop and are
accompanied by fever and abdominal pain.
 Changes in the base of the right lung, pleural
effusion and elevation of the diaphragm.
 Rupture into the peritoneum, thorax or through
the skin occurs when diagnosis and therapy are
delayed.

7. Laboratory examination of hepatic amebiasis
 Slight leukocytosis and moderate anemia.
 Non-specific elevation of liver enzymes.
 Stool examination for amebae is negative in
more than 50% of patients with liver abscess.
 Ultarsonography, computed tomography (CT),
MRI or isotope scans can localize and
delineate the size of the abscess cavity.

8. Diagnosis
 Patients with invasive colitis show occult blood
in stools.
 Detection of the parasite or cysts in the stools.
 When stool samples are negative for 3 days,
segmoidoscopy is done and biopsy is taken.
 Indirect hemagglutination test may be helpful in
the diagnosis of invasive intestinal amebiasis
and amebic liver abscess.

9. Treatment
All individuals with E. histolytica trophozoites or cysts in their stools
whether symptomatizing or not should be treated.
Asymptomatic cyst carriers: is treated with one of the following drugs:
 Iodoquinol: 30-40mg/kg/day orally in 3 divided doses for 20 days is
the first line agent for treating.
 Diloxanide furoate 10mg/kg/24h divided into 2 doses for 10 days.
The drug should not be used in children < 2 years of age.
Invasive amebiasis is treated by:
 Metronidazole 50 mg/kg/24hr for 10 days orally followed by
iodoquinol 30-40mg/kg/24hr for 20 days.
 In fulminant cases, dehydroemetine (IM or SC and never IV) is
added for the first few days in a dose of 1mg/kg/day.
 Amebic liver abscess is treated with metronidazole. Chloroquine,
which concentrates in the liver, may be used. Aspiration of large
lesions or left lobe abscesses may be necessary if rupture is
imminent or if the response to treatment is poor. Aspiration of the
abscess revealed chocolate brown pus.

10. Giardiasis
Giardia lamblia is a gastrointestinal protozoa that results
in a clinical picture ranging from asymptomatic
colonization to acute or chronic diarrheal illness.
Clinical manifestations
 The majority of the infected individuals are
asymptomatic.
 Symptoms develop 1-3 weeks after exposure to the
parasites.
 The most common presentations are diarrhea, weight
loss, crampy abdominal pain, distension and failure to
thrive.
 Malabsorption occurs in most of the patients.

11. Giardia lamblia

12. Diagnosis
 Stool analysis by several fecal sampling.
 Endoscopy and taking duodenal aspirate and biopsy.
 Antigen detection tests.
Treatment
- Asymptomatic excreters gererally are not treated.
Indication of therapy.
a- children with acute diarrhea.
b- children who manifest failure to thrive.
c- Children who manifest malabsorption or gasterointestinal
tract symptoms such as chronic diarrhea.
One of the following drugs is used:
 Albendazolel (400 mg PO once a day for 5 days among
children 2-12 years of age).
 Metronidazole 15mg/kg/ day divided into 3 doses for 5 days.
 Furazolidone 6mg/kg in 4 divided doses for 10 days.
 Tinidazole single oral dose of 50 mg/kg.

13. Ascariasis: (Ascaris lumbricoides )
Etiology
The infective stage is the mature larva-containing egg.
Clinical manifestations
1- Pulmonary ascariasis: cough, blood stained sputum,
eosinophilia, transient pulmonary infiltrates.
2- Abdominal ascariasis: malnutrition, abdominal pain and
distension. Intestinal obstruction manifested by severe
colicky abdominal pain and vomiting that may be bile
stained and obstruction of billiary tract may occur.
Diagnosis
 Direct fecal smear to detect the characteristic eggs.
 Passage of the mature worms.
Treatment
- Albendazolel (400 mg PO once for all ages), or
- Mebendazole 100mg twice daily for 3 days or 500mg once.

14. Ascaris lumbricoides
• Adult worms live in the lumen of the small
intestine (1). A female may produce
approximately 200,000 eggs per day, which are
passed with the feces (2) .
• Unfertilized eggs may be ingested but are not
infective. Fertile eggs embryonate and become
infective after 18 days to several weeks(3) ,
depending on the environmental conditions
(optimum: moist, warm, shaded soil).
• After infective eggs are swallowed (4) , the
larvae hatch (5), invade the intestinal mucosa,
and are carried via the portal, then systemic
circulation to the lungs (6) .
• The larvae mature further in the lungs (10 to
14 days), penetrate the alveolar walls, ascend
the bronchial tree to the throat (7), and are
swallowed .
• Upon reaching the small intestine, they develop
into adult worms (1) . Between 2 and 3 months
are required from ingestion of the infective
eggs to oviposition by the adult female. Adult
worms can live 1 to 2 years.CDC

15. Ascaris lumbricoides

16. Enterobiasis (pinworm; Enterobius vermicularis)
Etiology
 Humans are infected by ingestion of embryonated eggs which are
usually carried by fingernails, clothing, bedding or house dust.
 Eggs hatch in the stomach and larvae migrate to the cecal region
where they mature into adult worms.
Clinical manifestations
Nocturnal anal pruritus and sleeplessness.
Diagnosis
Detection of eggs by adhesive cellophane tape pressed against the
perianal region early in the morning. Repeated examination may
be needed and worms may be seen in the stools.
Treatment
- Mebendazole 100mg as one dose and also repeated after 2 weeks for
all ages, or
- Single oral dose of albendazole (400mg PO for all ages) repeated
after 2 weeks.

17. Hookworms (Ancylostoma)
 Larvae which are the infective form are found in warm damp soil and infect
the human by penetrating the skin or by drinking contaminated water or
by soil pica.
Clinical manifestations
 Exposure of the skin for the first time to the infective larvae may lead to
pruritis.
 Abdominal pain, indigestion and postprandial fullness.
 Loss of appetite, diarrhea and blood in stool.
 Edema and anemia may lead to heart failure and sudden death.
Diagnosis
Detection of eggs in stool.
Treatment
 In severe anemia (hemoglobin concentration less than 5 gm/dL), iron
therapy should be given before anthelmintic drugs in a dose of 6 mg/kg
/day until anemia is corrected.
 In cases of anemia with heart failure, diuretics and slow transfusion of
packed red cells are indicated.
 Albendazole: 400mg orally once for all ages, or
 Mebendazole: 100mg orally twice daily for 3 days or 500 mg as a single
dose.

19. Schistosomiasis (schistosoma)
 The most common types in Egypt are Schistosoma
haematobium and Schistosoma mansoni.
 Children are infected through contact with water
contaminated with cercariae.
 Cercaria emerge from the infected snails and are
capable to penetrate intact human skin.
 Cercaria they migrate to the lungs and finally to the
liver.
 The adult worms migrate to specific anatomic sites
characteristic of each species.
 Schistosoma haematobium adults are found in the
perivesical and periureteral venous plexus, while
Schistosoma mansoni adults are found in the inferior
mesenterirc veins.

20. Clinical manifestations
 Cercarial penetration of human skin may result in pruritic rash (swimmer’s
itch).
 Acute schistosomiasis (Katayama fever) may occur, particularly in heavy
infection 4-8 weeks after exposure. This is a serum sickness-like syndrome
that is manifested by an acute onset of fever, chills, sweating,
lymphadenopathy, hepatosplenomegaly and eosinophilia.
 Schistosoma haematobium usually manifests by frequency of urine, dysuria
and terminal hematuria.
 Moderate to severe pathologic lesions have been demonstrated in the
urinary tract and the terminal stages of schistosomiasis haematobia are
associated with chronic renal failure and secondary infections.
 Chronic schistosoma mansoni infection presents with colicky abdominal
pain and bloody diarrhea.
 Hepatosplenomegaly, portal hypertension, ascites and hematemesis may be
the initial presentation.
 Schistosome eggs may escape into the lungs, causing pulmonary
hypertension and cor- pulmonale. The schistosome may migrate to the
brain vasculature and produce localized lesions that cause seizures.

21. Diagnosis
Schistosome eggs are found in urine and stool. A volume of 10ml of
urine should be collected around midday, which is the time of
maximal egg excretion, and filtered for diagnosis of S.
haematobium infection.
Treatment
The drug of choice is praziquantel (40 mg/kg/day divided into two
doses for one day).
Prevention
 Transmission of infection may be decreased by reducing the parasite
load in the population. This goal may be achieved by the
availability of oral, single- dose, effective chemotherapeutic agents.
 Other measures, particularly improved sanitation and focal
application of molluscicides, may be useful.
 Control of schistosomiasis is closely linked to economic and social
development.