Medical parasitology
 Parasitology is the
science dealing
know
with parasites.
Parasite: is a living organism that
 Parasites can be
classified into:
1.
2.
3.
Medical terms you should
lives at the expense of its host.
Host: the living organism at which
the parasite lives on his expense.
Helminthes.
Parasitism: relationship between
Protozoa.
two living organisms one gets the
Arthropods.
benefit (parasite) and the other
looses (host).
As regard to the host
 Definitive (final host): The host that
harbors the adult or sexual stages of the
parasite.
 Intermediate host: The host that harbors
the larval or asexual stages of the parasite.
 Vector: an arthropod the carries the
infective stage of the parasite and can
transmit it by active biological sharing in
life cycle.
 Reservoir hosts: other hosts that harbor
the parasite and thus ensure continuity of
As regard to parasite
 Obligate parasite is termed
when the parasite can live
only in a host.
 Facultative parasite when it
can live both in a host as
well as in free form.
 Endoparasites parasites
that live inside the body.
 Ecto-parasites parasites
the parasite's life cycle and act as
that exist on the body
additional sources of human infection.
surface.
Protozoa
General characters of protozoa
 Unicellular organisms that are capable of performing whole
life functions.
 Eukaryotic.
 Complex life cycle involving various stages or forms
 Reproduction : sexual and asexual
 Motility : flagella, cilia, amoeboid movement
 These ways of motility are used to divide them into taxonomic
groups
Asexual reproduction:
Binary fission: longitudinal
or transverse.
Schizogony : Nucleus
undergoes multiple
divisions before the cell
divides.
Sexual reproduction
1. Gametogony: process often
involves production and fusion of
gametes.
2. Conjugation and exchange of
genetic material between different
mating types in Ciliophora
(Balantidium coli).
Cyst formation
 Encystment of some protozoa is essential for
survival outside the body and during the transmision
from host to host.
Intestinal protozoa
Intestinal protozoa significant to human health
include
 Entamoeba histolytica (Amebae).
 Balantidium coli (Ciliates).
 Giardia lamblia (Flagellates).
 Cryptosporidium parvum and Isospora belli
(Sporozoa).
Entamoeba histolytica
Diseases
Amebic dysentery and liver abscess.
Morphology: it has two form stages
Trophozoite:

With the ameboid appearance due to presence of pseudopodia.
Cyst:

cysts are spherical with a cyst wall.

1 to 4 nuclei which are similar to trophozoite.
Life cycle
There are: no intermediate or reservoir hosts.
infective stage: mature cysts.
Mode of infection: feco-orally through contaminated food or hands.
Clinical Findings
# Dysentery.
Laboratory diagnosis

Finding cysts in the stool.
Treatment

Metronidazole (Flagyl)
# Amebic abscess
A: Entamoeba histolytica trophozoite
with one ingested red blood cell and
one nucleus (circle with inner dotted
line represents a red blood cell).
B: E. histolytica cyst with four nuclei
Diseases

Gardia lamblia
Gardiasis= Lambliasis.
Morphology
Trophozoite:

half pear-shaped organism with 8 flagella and 2 axostyles arranged in a bilateral symmetry.

There are two anteriorly located large suction discs. The cytoplasm contains two nuclei and two
parabasal bodies.
Cyst:

The cytoplasm contains four nuclei
with smooth well-defined wall.
Life cycle
Definitive host: Man.
Infective stage: cyst
Mode of infection: ingestion of cysts
Clinical finding
steatorrhia
Laboratory diagnosis
 Cysts (constipation) and trophs ( diarrhea) in the stool.
Treatment
Metronidazole
Balantidium coli
Disease: Balantidiasis.
This is a parasite primarily of cows, pigs and horses
(zoonotic protozoan).
Morphology
 Presence of cilia on the cell surface.
 Macro- and a micro-nucleus.
 Cytostome.
Life cycle:
 Infective stage: cyst.
 Mode of infection: ingestion of cysts in fecal
material of farm animals.
Symptoms and pathogenesis of balantidiasis are
similar to those seen in entamebiasis. However,
extra intestinal abscesses are not seen.
Diagnosis:
 Finding cysts in stool.
Treatment:
 Metronidazole
 Urogenital protozoa
Trichomonas vaginalis (a flagellate)
Disease: Trichomoniasis
Morphology
 Trophoziote is the active and
infective form, no cyst stage.
Life cycle
 Infective stage: trophozoites
 Infection occurs primarily via sexual
contact.
Symptoms
 In Females withheavy infection:
copious foul-smelling yellowish,
frothy discharge.
Treatment
 Metronidazole
 Vinegar douche may be useful.
Blood & Tissue Protozoa
Plasmodium
Disease
Malaria is caused by four plasmodia:
 Plasmodium vivax.
 Plasmodium ovale.
 Plasmodium malariae.
 Plasmodium falciparum.
malaria is one of the most common infectious diseases and a
leading cause of death.
Life cycle
There are two phases in the life cycle:
1. the sexual cycle in mosquitoes, the
final host.
2. asexual cycle “schizogony”, occurs in
humans, the intermediate hosts.
 Infective stage: sporozoites
 Mode of infection:
1. Mosquito bites.
2. Across the placenta.
3. Blood transfusions.
4. Intravenous drug abuse.
Pathogenesis
 Most of the pathologic findings of
malaria result from the destruction of
red blood cells.
 Malaria presents with abrupt onset of
fever and chills.
 The timing of the fever cycle is 72 hours
for P. malariae (quartan malaria) and 48
hours for the other plasmodia (tertian
malaria).
Malaria caused by P. falciparum is more
severe than that caused by other
plasmodia because:
1. It is characterized by infection of more
red cells.
2. Occlusion of the capillaries with
aggregates of parasitized red cells
leading to:
 Cerebral malaria.
 Hemoglobinuria "black water fever”.
Laboratory Diagnosis
Blood films for finding the parasite inside
RBcs
Toxoplasma
Disease
 Toxoplasma gondii causes toxoplasmosis.
Life cycle
Infective stage
1.
Oocysts in animal stools.
2.
True cysts in meat.
3.
Tachyzoites in blood or transplacentally.
Mode of transmission
1.
Ingestion of cysts in uncooked meat or cat feces.
2.
Transplacental transmission: congenital infection of the
fetus occurs only when the mother is infected during
pregnancy for the 1st time.
Clinical Findings
 Asymptomatic in immunocompetent adults.
 Immunosupressed patients (e.g., AIDS patients), lifethreatening disseminated disease.
 Congenital infection.
Laboratory Diagnosis
 Immunofluorescence assay for IgM antibody is used. IgM is
used to diagnose congenital infection, because IgG can be
maternal in origin.
Trypanosoma
The genus Trypanosoma includes three major pathogens:
Trypanosoma cruzi
Disease
 T. cruzi is the cause of Chagas' disease (American
trypanosomiasis).
Life cycle
 Vector: reduviid bug (cone-nose or kissing bug).
 Infective stage: metacyclic trypomastigotes
 Mode of transmission: contamination of bite wound
with bug’s feces leads to infection.
Clinical Findings
 Facial edema and a nodule (chagoma) near
the bite.
 Fever, lymphadenopathy, and
hepatosplenomegaly.
 Some patients progress to the chronic form
with myocarditis and megacolon.
Laboratory Diagnosis
 Acute disease :presence of trypomastigotes
in films of the patient's blood.
 Because the trypomastigotes are not
numerous in the blood, other diagnostic
methods may be required
(1) a stained preparation of a bone marrow
aspirate.
(2) culture of the organism on special
medium.
Trypanosoma gambiense &
Trypanosoma rhodesiense
Disease
 These organisms cause sleeping sickness (African
trypanosomiasis).
Life cycle
 Vector for both is the tsetse fly.
 Infective stage: metacyclic trypomastigotes.
 Mode of transmission: injection of organisms in the
saliva of the insect during biting.
Clinical Findings
 The initial lesion is an indurated skin ulcer
("trypanosomal chancre") at the site of the fly bite.
 Enlargement of the posterior cervical lymph nodes
(Winterbottom's sign).
 The encephalitis is characterized initially by
headache, insomnia and finally coma.
Laboratory Diagnosis
 Microscopic examination of the blood
reveals trypomastigotes.
Leishmania
Disease
 L. donovani is the cause of kalaazar (visceral leishmaniasis).
The life cycle
 Vector: sandfly.
 Infective stage: metacyclic
promastigotes.
 Mode of infection: bite of sand fly.
Visceral leishmaniasis
Clinical Findings
 Symptoms begin with intermittent fever,
weakness, and weight loss.
 The disease affect reticuloendothelial
system leading to enlargement of the
spleen.
 Hyperpigmentation of the skin is seen in
light-skinned patients (kala-azar means
black sickness).
 Post kalazar dermal lishmaniod.
Cutaneous leishmaniasis
New word cutaneous
Old world cutaneous
leishmaniasis
leihmaniasis “oriental
1. Mucocutaneous
sore”: charecterized by
leishmaniasis: skin
uler at the site of bite
lesions which
faceor exposed parts of the
metastasize to
bodythe lesion heals
oropharynx after
spontaneously in 1-2 years
months or years leading
leaving disfiguring scar.
to destruction of
cartilage.
2. Checlero’s ulcer: single
lesions affecting ears
Laboratory Diagnosis
 Diagnosis is usually made by detecting amastigotes in
a bone marrow, spleen, or lymph node biopsy or
"touch" preparation.
Treatment
 Pentavalent antimonial drugs.
Prevention
1. Treatment of cases.
2. Vector control.
3. Active immunization with living organism from an
active ulcer results in life long protection.
Helminthes
3 main classes of medically important helminthes
1. The Nematodes
2. The Trematodes
3. The Cestodes
Nematoda
Elongated.
cylindrical,
round in cross
section & not
segmented
Cestoda
Trematoda
Flattened,
Flattened, leafribbon -shaped & like, Bilaterally
segmented
symmetrical, not
segmented
Digestive
system
Simple straight
tube with anus
Absent
Simple blind
tube(no anus)
Body cavity
Gender(Sex)
Present
separate
Absent
Hermaphrodite
Absent
Hermaphrodite
(except
schistosoma)
Shape
Trematodes
Trematoda (Flukes)
Hepatic flukes: - Fasciola gigantica.
- Fasciola hepatica.
II. Intestinal flukes: - Heterophyes heterophyes.
III. Blood flukes: - Schistosoma haematobium.
- Schistosoma mansoni.
IV. Lung fluke: - Paragonimus
I.
Fasciola gigantica
Disease: Fascioliasis, liver rot.
Morphology
 The adult is a large fleshy worm.
 The adult worms live in the bile ducts of
herbivorous animals & man.
 Fasciola haptica differs from Fasciola gigantica:
- Smaller in size (3 x 1.3 cm).
- Intermediate host: Lymnaea trancatula.
Life cycle
 Final host: herbivorous animals and human.
 Intermediate host: Lymnaea cailliaudi snail
 Infective stage: encysted metacercaria.
 Mode of infection: ingestion of encysted
metacercaria in aquatic vegetables (usually leafy
plants e.g. lettuce) or in water.
Clinical finding:
1. Fever
2. Enlarged tender liver
3. Biliary colic.
4. Jaundice.
Laboratory diagnosis:
Detection of eggs in feces or duodenal aspirate.
Treatment:
Antiparasitic drugs e.g. Bithional.
Heterophyes heterophyes
Morphology: Very small, intestinal flukes.
Disease: Heterophyiasis.
Life cycle:
 Final host: Man & fish eating animals.
 Two intermediate hosts:
1.
Pirenella conica snail .
2.
Bolty & boury fishes.
 Infective stage: encycted metacercaria.
 Mode of infection: eating raw, undercooked or freshly salted fish
containing encysted metacercaria.
Clinical findings
Colicky pain and diarrhea.
Egg emboli
Laboratory diagnosis
Detection of the eggs in faeces.
Treatment
Antiparasitic drugs, Praziquantel
Schistosoma
Disease: Schistosomiasis (Bilharziasis).
It differs from other trematodes in :
1. Separate sexes.
2. Eggs with spine.
3. Cercaria is the infective stage.
3 known schistosomes infect humans:
1. S. haematobium
2. S. mansoni:
3. S. japonicum
 S.mansoni : mesenteric venules of bowel &, rectum. It causes
intestinal schistosomiasis and eggs pass in stool.
 S. haematobium: venous plexus of the bladder, ureter & kidneys. It
causes urinary schistosomiasis and eggs pass in urine.
Life cycle
•Intermediate host is a snail
S. heamatobium (Bulinus trancatus)
S. mansoni (Biomphalaria alexandrina).
•Infective stage: is the cercaria
•Mode of infection: Penetration of the cercaria
(which is attracted to man by the body
temperature) to skin when water begins to dry.
Clinical features
Urinary bilhariziasis: terminal haematuria.
Intestinal bilhariziasis: dysentery.
Laboratory diagnosis:
Detection of eggs in stools or urine.
Treatment:
Praziquantel.
Cestoda
Taenia
saginata
(beef
tapeworm)
Disease: taeniasis saginata.
Morphology:
 Has a scolex.
 Segmented from 1000-2000 segments.
1. Immature segments.
2. Mature segments.
3. Gravid segments.
Life cycle:
Definitive host: human.
Intermediate host: cattle (beef).
Infective stage: Cysticercus bovis.
Mode of infection: ingestion of raw or improperly cooked beef containing the cysticercus bovis.
 Ingestion of eggs is not infective to human.
Clinical finding
#Intestinal obstruction#Loss of weight as the parasite consumes much of patient’s food.
Diagnosis
Detection of the eggs or gravid segments in stool.
T. solium is the same as T. saginata but.
 Intermediate host is the Pork
 Eggs could be infective to human leading to cysticercosis.
Diphyllbothrium latum (fish tapeworm)
Disease: Diphyllobothriasis
Morphology
 Formed of scolex & 3000-4000 immature & mature segments (no gravid
segments).
Life cycle
 Definitive hosts: man, dogs, cats and other fish-eating animals.
 1st intermediate host: Cyclops
 2nd intermediate host: Fresh water fishes e.g. salmon.
 Infective stage is Plerocercoid in infected fish muscles ( the 2nd
intermediate host).
 Mode of infection: by eating infected fishes either raw or improperly
cooked (smoked or pickled).
Clinical features
1.
Intestinal symptoms
2.
Macrocytic hyperchromic anemia
Diagnosis:
1. Detection of eggs in feces.
Treatment:
1. Antiparasitic drugs.
Hymenolepis nana (Dwarf tapeworm)
Disease: hymenolepiasis nana
Life cycle:
 Adult worms live in the small intestine
 Definitive hosts are human, rats & mice More common in children.
 Infective stage: egg.
 Mode of infection:
 Ingestion of eggs through;
1. Contaminated food.
2. Autoinfection either internal or external.
 Clinical picture
 In heavy infection:
1. Intestinal irritation, enteritis
2. Nervous manifestations
Diagnosis:
 Detection of eggs in stool. Peranal swab is more diagnostic.
Treatment:
1. Antiparasitic drugs, praziquantel.
Echinococcus granulosa (Dog tapeworm)
Disease: hydatid cyst disease
Morphology:
 scolex and only three proglottids, making it one of the
smallest tapeworms.
 Humans are almost always dead-end intermediate hosts.
Clinical features
 The cyst acts as a space-occupying lesion, putting pressure on
adjacent tissue.
 The cyst fluid contains parasite antigens, if the cyst ruptures
spontaneously or during trauma or surgical removal, lifethreatening anaphylaxis can occur.
Diagnosis
 Indirect hemagglutination test.
 Surgical removal and microscopic examination of cyst contents.
 Treatment
Treatment
 Albendazole with or without surgical removal of the cyst.
Nematodes
Enterobius vermicularis (pinworm)
Disease: pinworm infection (enterobiasis).
Life cycle:
 Infective stage: Egg.
 Mode of infection: ingesting of the worm eggs.
 At night, the female migrates from the anus and releases
thousands of fertilized eggs on the perianal skin and into the
environment.
Clinical Findings
 Perianal pruritus is the most prominent symptom.
Diagnosis
 The eggs are recovered from perianal skin by using the Scotch
tape technique and can be observed microscopically (Figure
56–3).
 Unlike those of other intestinal nematodes, these eggs are
not found in the stools.
Treatment
 Mebendazole . Whole family must take the treatment as it is
highly infectious.
Trichuris trichiura (whipworm)
Disease: whip worm infection or trichuriasis
Life cycle:
 Infective stage is emberyonated egg.
 Mode of infection: ingesting worm emberyonated
eggs in food or water contaminated with human
feces.
Clinical Findings
 Trichuris may cause rectal prolapse in children
with heavy infection. Prolapse results from
increased peristalsis that occurs in an effort to
expel the worms.
Laboratory Diagnosis
 Diagnosis is based on finding the typical eggs, i.e.,
barrel-shaped with a plug at each end, in the stool
Treatment
 Mebendazole is the drug of choice.
Ascaris lumbricoides
Disease: ascariasis
Life cycle:
 Infective stage: egg.
 Mode of infection: ingesting eggs in food
or water contaminated with human feces
Clinical Findings
 Most infections are asymptomatic
 Malnutrition and intestinal obstruction in a heavy worm
burden patient.
Laboratory Diagnosis
 Microscopically by detecting eggs in the stools.
Treatment
 Both mebendazole and pyrantel pamoate are effective.
Ancylostoma duodenale (hookworm)
Disease: Ancylostomiasis.
Life cycle:
 Infective stage: filariform larvae.
 Mode of infection: penetration of the skin by the
filariform larvae on walking with bared foot on
moist soil.
Clinical Findings
 loss of blood at the site of attachment in the small
intestine will lead to microcytic aneamia.
Laboratory Diagnosis
 Microscopically by finding eggs in the stools.
Treatment
 Both mebendazole and pyrantel pamoate are effective.
Wuchereria
Disease: W. bancrofti leads to elephantiasis.
 Vector: female mosquito (especially Anopheles and Culex
species).
 Infective stage: infective larvae.
 Mode of infection: Humans are infected when the female
mosquito deposits infective larvae on the skin while
biting.
Clinical Findings
 Adult worms in the lymph nodes cause inflammation that
eventually obstructs the lymphatic vessels, causing edema.
Massive edema of the legs is called elephantiasis.
Laboratory Diagnosis
 Thick blood smears taken from the patient at night reveal
the microfilariae.
Treatment
 Diethylcarbamazine is effective only against microfilariae;
no drug therapy for adult worms is available.